Lewis's Medical-Surgical Nursing E-Book: Assessment and Management of Clinical Problems [11 ed.] 0323551491, 9780323551496

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Lewis's Medical-Surgical Nursing E-Book: Assessment and Management of Clinical Problems [11 ed.]
 0323551491, 9780323551496

Table of contents :
Title page
Disclaimer
Table of Contents
Copyright
About the Authors
Contributors
Authors of Teaching and Learning Resources
Reviewers
Dedication
Preface
Concepts Exemplars
Special Features
Section One. Concepts in Nursing Practice
1. Professional Nursing
Conceptual Focus
Professional Nursing Practice
Influences on Professional Nursing Practice
Patient-Centered Care
Teamwork and Collaboration
Safety
Quality Improvement
Informatics
Evidence-Based Practice
2. Health Equity and Culturally Competent Care
Conceptual Focus
Determinants of Health
Health Disparities and Health Equity
Culture
Cultural Competence
Cultural Diversity in the Health Care Workplace
Cultural Factors Affecting Health and Health Care
Nursing Management: Promoting Health Equity and Increasing Cultural Competency
3. Health History and Physical Examination
Conceptual Focus
Data Collection
Nursing History: Subjective Data
Physical Examination: Objective Data
Types of Assessment
Problem Identification
4. Patient and Caregiver Teaching
Conceptual Focus
Role of Patient and Caregiver Teaching
Teaching-Learning Process
Process of Patient Teaching
5. Chronic Illness and Older Adults
Conceptual Focus
Chronic Illness
Nursing Management: Chronic Illness
Older Adults
Attitudes Toward Aging
Biologic Aging
Age-Related Physiologic Changes
Special Older Adult Populations
Social Support for Older Adults
Social Services for Older Adults
Medicare and Medicaid
Care Alternatives for Older Adults
Legal and Ethical Issues
Nursing Management: Older Adults
Section Two. Problems Related to Comfort and Coping
6. Stress Management
Conceptual Focus
What is Stress?
Physiologic Response to Stress
Mind-Body-Spirit Connection
Effects of Stress on Health
Coping Strategies
Relaxation Strategies
Nursing Management: Stress
7. Sleep and Sleep Disorders
Conceptual Focus
Sleep
Physiologic Sleep Mechanisms
Insufficient Sleep and Sleep Disturbances
Sleep Disturbances in the Hospital
Sleep Disorders
Nursing Management: Insomnia
Obstructive Sleep Apnea
Nursing and Interprofessional Management: Sleep Apnea
Periodic Limb Movement Disorder
Circadian Rhythm Disorders
Narcolepsy
Parasomnias
Special Sleep Needs of Nurses
8. Pain
Conceptual Focus
Magnitude of Pain Problem
Definitions and Dimensions of Pain
Classification of Pain
Pain Assessment
Pain Treatment
Nursing and Interprofessional Management: Pain
Institutionalizing Pain Education and Management
Ethical Issues in Pain Management
Managing Pain in Special Populations
9. Palliative and End-of-Life Care
Conceptual Focus
Palliative Care
Hospice Care
Death
End-of-Life Care
Legal and Ethical Issues Affecting End-of-Life Care
Nursing Management: End of Life
Special Needs of Caregivers and Nurses in End-of-Life Care
10. Substance Use Disorders
Conceptual Focus
Drugs Associated with Substance Use Disorder
Nursing and Interprofessional Management: Tobacco Use Disorder
Alcohol
Nursing and Interprofessional Management: Alcohol Use Disorder
Use of Other Substances
Nursing and Interprofessional Management: Stimulant Use
Depressants
Nursing and Interprofessional Management: Depressant Use
Inhalants
Cannabis
Caffeine
Nursing Management: Substance Use
Section Three. Problems Related to Homeostasis and Protection
11. Inflammation and Healing
Conceptual Focus
Inflammatory Response
Nursing and Interprofessional Management: Inflammation
Healing Process
Nursing and Interprofessional Management: Wound Healing
Pressure Injuries
Nursing and Interprofessional Management: Pressure Injuries
12. Genetics
Conceptual Focus
Genetics and Genomics
Genetic Disorders
Genetic Screening and Testing
Pharmacogenomics and Pharmacogenetics
Gene Therapy
Stem Cell Therapy
Nursing Management: Genetics and Genomics
13. Immune Responses and Transplantation
Conceptual Focus
Normal Immune Response
Altered Immune Response
Allergic Disorders
Nursing Management: Immunotherapy
Nursing and Interprofessional Management: Latex Allergies
Autoimmunity
Immunodeficiency Disorders
Human Leukocyte Antigen System
Organ Transplantation
Graft-Versus-Host Disease
14. Infection
Conceptual Focus
Infections
Types of Pathogens
Emerging Infections
Health Care–Associated Infections
Infection Prevention and Control
Human Immunodeficiency Virus Infection
Nursing Management: HIV Infection
15. Cancer
Conceptual Focus
Biology of Cancer
Benign Versus Malignant Neoplasms
Classification of Cancer
Prevention and Early Detection of Cancer
Interprofessional Care
Surgical Therapy
Chemotherapy
Radiation Therapy
Nursing Management: Chemotherapy and Radiation Therapy
Late Effects of Radiation and Chemotherapy
Immunotherapy and Targeted Therapy
Nursing Management: Immunotherapy and Targeted Therapy
Hormone Therapy
Hematopoietic Growth Factors
Hematopoietic Stem Cell Transplantation
Gene Therapy
Complications of Cancer
Nutritional Problems
Infection
Oncologic Emergencies
Cancer Pain
Coping with Cancer and Treatment
Cancer Survivorship
16. Fluid, Electrolyte, and Acid-Base Imbalances
Conceptual Focus
Homeostasis
Water Content of the Body
Electrolytes
Mechanisms Controlling Fluid and Electrolyte Movement
Fluid Movement in Capillaries
Fluid Spacing
Regulation of Water Balance
Fluid Volume Imbalances
Fluid Volume Deficit
Fluid Volume Excess
Nursing Management: Fluid Volume Imbalances
Sodium Imbalances
Hypernatremia
Nursing and Interprofessional Management: Hypernatremia
Hyponatremia
Nursing and Interprofessional Management: Hyponatremia
Potassium Imbalances
Hyperkalemia
Nursing and Interprofessional Management: Hyperkalemia
Hypokalemia
Nursing and Interprofessional Management: Hypokalemia
Calcium Imbalances
Hypercalcemia
Nursing and Interprofessional Management: Hypercalcemia
Hypocalcemia
Nursing and Interprofessional Management: Hypocalcemia
Phosphate Imbalances
Hyperphosphatemia
Hypophosphatemia
Magnesium Imbalances
Hypermagnesemia
Hypomagnesemia
Acid-Base Imbalances
pH And Hydrogen ION Concentration
Acid-Base Regulation
Alterations in Acid-Base Balance
Clinical Manifestations of Acid-Base Imbalances
Assessment of Fluid, Electrolyte, and Acid-Base Imbalances
Oral Fluid and Electrolyte Replacement
IV. Fluid and Electrolyte Replacement
Central Venous Access Devices
Nursing Management: Central Venous Access Devices
Section Four. Perioperative Care
17. Preoperative Care
Conceptual Focus
Surgical Settings
Patient Interview
Nursing Assessment of Preoperative Patient
Nursing Management: Preoperative Patient
18. Intraoperative Care
Conceptual Focus
Physical Environment of the Operating Room
Surgical Team
Nursing Management: Patient Before Surgery
Nursing Management: Patient During Surgery
Nursing Management: Patient After Surgery
Anesthesia
Anesthesia Techniques
Perioperative Crisis Events
19. Postoperative Care
Conceptual Focus
Postoperative Care of Surgical Patient
Respiratory Problems
Nursing Management: Respiratory Problems
Cardiovascular Problems
Nursing Management: Cardiovascular Problems
Neurologic and Psychologic Problems
Nursing Management: Neurologic and Psychologic Problems
Pain and Discomfort
Nursing Management: Pain
Temperature Changes
Nursing Management: Temperature Changes
Gastrointestinal Problems
Nursing Management: Gastrointestinal Problems
Urinary Problems
Nursing Management: Urinary Problems
Integumentary Problems
Nursing Management: Surgical Wounds
Discharge from The Pacu
Ambulatory Surgery
Section Five. Problems Related to Altered Sensory Input
20. Assessment and Management: Visual Problems
Conceptual Focus
Visual System
Structures and Functions of Visual System
Visual Pathway
Assessment of Visual System
Diagnostic Studies of Visual System
Visual Problems
Visual Impairment
Nursing Management: Visual Impairment
Eye Trauma
Extraocular Disorders
Nursing Management: Inflammation and Infection
Dry Eye Disorders
Strabismus
Corneal Disorders
Intraocular Disorders
Nursing Management: Cataracts
Retinopathy
Retinal Detachment
Age-Related Macular Degeneration
Glaucoma
Nursing Management: Glaucoma
Intraocular Inflammation and Infection
Ocular Tumors
Enucleation
Ocular Manifestations of Systemic Diseases
21. Assessment and Management: Auditory Problems
Conceptual Focus
Auditory System
Structures and Functions of Auditory System
Assessment of Auditory System
Diagnostic Studies of Auditory System
Auditory Problems: External Ear and Canal
Nursing and Interprofessional Management: External Otitis
Cerumen and Foreign Bodies in External Ear Canal
Trauma
Malignancy of External Ear
Middle Ear and Mastoid
Nursing and Interprofessional Management: Chronic Otitis Media
Otosclerosis
Inner Ear Problems
Ménière’s Disease
Nursing and Interprofessional Management: Ménière’s Disease
Benign Paroxysmal Positional Vertigo
Acoustic Neuroma
Hearing Loss and Deafness
Nursing and Interprofessional Management: Hearing Loss and Deafness
22. Assessment: Integumentary System
Conceptual Focus
Structures and Functions of Skin and Appendages
Assessment of Integumentary System
Diagnostic Studies of Integumentary System
23. Integumentary Problems
Conceptual Focus
Environmental Hazards
Skin Cancer
Nonmelanoma Skin Cancer
Melanoma
Skin Infections and Infestations
Allergic Skin Problems
Benign Skin Problems
Interprofessional Care: Skin Problems
Nursing Management: Skin Problems
Cosmetic Procedures
Nursing Management: Cosmetic Surgery
Skin Grafts
24. Burns
Conceptual Focus
Types of Burn Injury
Classification of Burn Injury
Prehospital and Emergency Care
Phases of Burn Management
Emergent Phase
Nursing and Interprofessional Management: Emergent Phase
Acute Phase
Nursing and Interprofessional Management: Acute Phase
Rehabilitation Phase
Nursing and Interprofessional Management: Rehabilitation Phase
Emotional/Psychologic Needs of Patients and Caregivers
Special Needs of Nurses
Section Six. Problems of Oxygenation: Ventilation
25. Assessment: Respiratory System
Conceptual Focus
Structures and Functions of Respiratory System
Assessment of Respiratory System
Diagnostic Studies of Respiratory System
26. Upper Respiratory Problems
Conceptual Focus
Problems Of Nose And Paranasal Sinuses
Nasal Fracture
Rhinoplasty
Nursing Management: Nasal Surgery
Epistaxis
Allergic Rhinitis
Acute Viral Rhinopharyngitis
Influenza
Sinusitis
Obstruction of Nose and Sinuses
Problems of Pharynx
Peritonsillar Abscess
Problems of Larynx and Trachea
Acute Laryngitis
Airway Obstruction
Tracheostomy
Nursing Management: Tracheostomy
Head and Neck Cancer
Nursing Management: Head and Neck Cancer
27. Lower Respiratory Problems
Conceptual Focus
Lower Respiratory Tract Infections
Acute Bronchitis
Pertussis
Pneumonia
Nursing Management: Pneumonia
Tuberculosis
Nursing Management: Tuberculosis
Atypical Mycobacteria
Pulmonary Fungal Infections
Lung Abscess
Environmental Lung Diseases
Lung Cancer
Nursing Management: Lung Cancer
Other Types of Lung Tumors
Chest Trauma and Thoracic Injuries
Fractured Ribs
Flail Chest
Pneumothorax
Chest Tubes and Pleural Drainage
Nursing Management: Chest Drainage
Chest Surgery
Restrictive Respiratory Disorders
Atelectasis
Pleurisy
Pleural Effusion
Interstitial Lung Diseases
Idiopathic Pulmonary Fibrosis
Sarcoidosis
Vascular Lung Disorders
Pulmonary Embolism
Nursing Management: Pulmonary Embolism
Pulmonary Hypertension
Idiopathic Pulmonary Arterial Hypertension
Secondary Pulmonary Arterial Hypertension
Cor Pulmonale
Lung Transplantation
28. Obstructive Pulmonary Diseases
Cenceptual Focus
Asthma
Nursing Management: Asthma
Chronic Obstructive Pulmonary Disease
Nursing Management: COPD
Cystic Fibrosis
Nursing Management: Cystic Fibrosis
Bronchiectasis
Interprofessional and Nursing Management: Bronchiectasis
Section Seven. Problems of Oxygenation: Transport
29. Assessment: Hematologic System
Conceptual Focus
Structures and Functions of Hematologic System
Assessment of Hematologic System
Diagnostic Studies of Hematologic System
30. Hematologic Problems
Conceptual Focus
Anemia
Nursing and Interprofessional Management: Anemia
Anemia Caused by Decreased Erythrocyte Production
Iron-Deficiency Anemia
Thalassemia
Megaloblastic Anemias
Anemia of Chronic Disease
Aplastic Anemia
Anemia Caused by Blood Loss
Acute Blood Loss
Chronic Blood Loss
Anemia Caused by Increased Erythrocyte Destruction
Sickle Cell Disease
Acquired Hemolytic Anemia
Other Red Blood Cell Disorders
Polycythemia
Problems Of Hemostasis
Thrombocytopenia
Nursing Management: Thrombocytopenia
Hemophilia and Von Willebrand Disease
Nursing Management: Hemophilia
Disseminated Intravascular Coagulation
Nursing Management: Disseminated Intravascular Coagulation
Neutropenia
Myelodysplastic Syndrome
Leukemia
Nursing Management: Leukemia
Lymphomas
Hodgkin’s Lymphoma
Non-Hodgkin’s Lymphoma
Multiple Myeloma
Disorders of the Spleen
Blood Component Therapy
Section Eight. Problems of Oxygenation: Perfusion
31. Assessment: Cardiovascular System
Conceptual Focus
Structures and Functions of Cardiovascular System
Assessment of Cardiovascular System
Diagnostic Studies of Cardiovascular System
32. Hypertension
Conceptual Focus
Normal Regulation of Blood Pressure
Hypertension
Nursing Management: Primary Hypertension
Hypertensive Crisis
33. Coronary Artery Disease and Acute Coronary Syndrome
Conceptual Focus
Coronary Artery Disease
Interprofessional and Nursing Care: Coronary Artery Disease
Chronic Stable Angina
Interprofessional and Nursing Care: Chronic Stable Angina
Acute Coronary Syndrome
Unstable Angina
Myocardial Infarction: St-Elevation and Non–St-Elevation Myocardial Infarction
Diagnostic Studies: Acute Coronary Syndrome
Interprofessional Care: Acute Coronary Syndrome
Nursing Management: Acute Coronary Syndrome
Sudden Cardiac Death
34. Heart Failure
Conceptual Focus
Heart Failure
Nursing Management: Heart Failure
Heart Transplantation
35. Dysrhythmias
Conceptual Focus
Rhythm Identification and Treatment
Syncope
36. Inflammatory and Structural Heart Disorders
Conceptual Focus
Inflammatory Disorders of Heart
Nursing Management: Infective Endocarditis
Acute Pericarditis
Nursing Management: Acute Pericarditis
Chronic Constrictive Pericarditis
Myocarditis
Nursing Management: Myocarditis
Rheumatic Fever and Rheumatic Heart Disease
Nursing Management: Rheumatic Fever and Rheumatic Heart Disease
Valvular Heart Disease
Mitral Valve Stenosis
Mitral Valve Regurgitation
Mitral Valve Prolapse
Aortic Valve Stenosis
Aortic Valve Regurgitation
Tricuspid and Pulmonic Valve Disease
Diagnostic Studies: Valvular Heart Disease
Interprofessional Care: Valvular Heart Disease
Nursing Management: Valvular Disorders
Cardiomyopathy
Dilated Cardiomyopathy
Hypertrophic Cardiomyopathy
Restrictive Cardiomyopathy
37. Vascular Disorders
Conceptual Focus
Peripheral Artery Disease
Peripheral Artery Disease of The Lower Extremities
Nursing Management: Lower Extremity Peripheral Artery Disease
Acute Arterial Ischemic Disorders
Thromboangiitis Obliterans
Raynaud’s Phenomenon
Aortic Aneurysms
Nursing Management: Aortic Aneurysms
Aortic Dissection
Nursing Management: Aortic Dissection
Acute and Chronic Venous Disorders
Venous Thrombosis
Nursing Management: Venous Thromboembolism
Varicose Veins
Nursing Management: Varicose Veins
Chronic Venous Insufficiency and Venous Leg Ulcers
Section Nine. Problems of Ingestion, Digestion, Absorption, and Elimination
38. Assessment: Gastrointestinal System
Conceptual Focus
Structures and Functions of Gastrointestinal System
Assessment of Gastrointestinal System
Diagnostic Studies of Gastrointestinal System
39. Nutritional Problems
Conceptual Focus
Nutritional Problems
Normal Nutrition
Vegetarian Diet
Malnutrition
Nursing and Interprofessional Management: Malnutrition
Specialized Nutritional Support
Nursing Management: Parenteral Nutrition
Eating Disorders
Bulimia Nervosa
40. Obesity
Conceptual Focus
Obesity
Health Risks Associated with Obesity
Nursing and Interprofessional Management: Obesity
Bariatric Surgical Therapy
Nursing Management: Perioperative Care of The Obese Patient
Cosmetic Surgical Therapy
Metabolic Syndrome
Nursing and Interprofessional Management: Metabolic Syndrome
41. Upper Gastrointestinal Problems
Conceptual Focus
Nausea and Vomiting
Nursing Management: Nausea and Vomiting
Oral Inflammation and Infections
Oral Cancer
Nursing Management: Oral Cancer
Esophageal Disorders
Nursing and Interprofessional Management: GERD
Hiatal Hernia
Nursing and Interprofessional Management: Hiatal Hernia
Esophageal Cancer
Nursing Management: Esophageal Cancer
Other Esophageal Disorders
Disorders of the Stomach and Upper Small Intestine
Nursing Management: Peptic Ulcer Disease
Stomach Cancer
Nursing Management: Stomach Cancer
Gastric Surgery
Nursing Management: Gastric Surgery
Gastritis
Nursing and Interprofessional Management: Gastritis
Upper Gastrointestinal Bleeding
Nursing Management: Upper Gastrointestinal Bleeding
Foodborne Illness
42. Lower Gastrointestinal Problems
Conceptual Focus
Diarrhea
Nursing Management: Acute Infectious Diarrhea
Fecal Incontinence
Nursing Management: Fecal Incontinence
Constipation
Nursing Management: Constipation
Acute Abdominal Pain and Laparotomy
Nursing Management: Acute Abdominal Pain
Abdominal Trauma
Chronic Abdominal Pain
Irritable Bowel Syndrome
Inflammatory Disorders
Nursing Management: Appendicitis
Peritonitis
Nursing Management: Peritonitis
Gastroenteritis
Inflammatory Bowel Disease
Nursing Management: Inflammatory Bowel Disease
Intestinal Obstruction
Nursing Management: Intestinal Obstruction
Polyps of Large Intestine
Colorectal Cancer
Nursing Management: Colorectal Cancer
Bowel Resection and Ostomy Surgery
Nursing Management: Bowel Resection and Ostomy Surgery
Diverticulosis and Diverticulitis
Fistulas
Hernias
Malabsorption Syndrome
Celiac Disease
Lactase Deficiency
Short Bowel Syndrome
Gastrointestinal Stromal Tumors
Anorectal Problems
Nursing Management: Hemorrhoids
Anal Fissure
Anorectal Abscess
Anal Fistula
Anal Cancer
Pilonidal Sinus
43. Liver, Biliary Tract, and Pancreas Problems
Conceptual Focus
Disorders of The Liver
Nursing Management: Viral Hepatitis
Drug- and Chemical-Induced Liver Diseases
Autoimmune, Genetic, and Metabolic Liver Diseases
Cirrhosis
Nursing Management: Cirrhosis
Acute Liver Failure
Liver Cancer
Liver Transplantation
Disorders of The Pancreas
Nursing Management: Acute Pancreatitis
Chronic Pancreatitis
Pancreatic Cancer
Nursing Management: Pancreatic Cancer
Disorders of The Biliary Tract
Nursing Management: Gallbladder Disease
Gallbladder Cancer
Section Ten. Problems of Urinary Function
44. Assessment: Urinary System
Conceptual Focus
Structures and Functions of Urinary System
Assessment of Urinary System
Diagnostic Studies of Urinary System
45. Renal and Urologic Problems
Infectious and Inflammatory Disorders of Urinary System
Nursing Management: Urinary Tract Infection
Acute Pyelonephritis
Nursing Management: Acute Pyelonephritis
Chronic Pyelonephritis
Urethritis
Urethral Diverticula
Interstitial Cystitis/Painful Bladder Syndrome
Nursing Management: Interstitial Cystitis/Painful Bladder Syndrome
Genitourinary Tuberculosis
Immunologic Disorders of Kidney
Nursing and Interprofessional Management: Acute Poststreptococcal Glomerulonephritis
Nephrotic Syndrome
Obstructive Uropathies
Urinary Tract Calculi
Nursing Management: Urinary Tract Calculi
Strictures
Renal Trauma
Renal Vascular Problems
Nephrosclerosis
Renal Artery Stenosis
Renal Vein Thrombosis
Hereditary Kidney Diseases
Polycystic Kidney Disease
Medullary Cystic Disease
Alport Syndrome
Urinary Tract Tumors
Bladder Cancer
Nursing and Interprofessional Management: Bladder Cancer
Bladder Dysfunction
Nursing Management: Urinary Incontinence
Urinary Retention
Nursing Management: Urinary Retention
Catheterization
Catheter Construction
Types of Catheters
Surgery of the Urinary Tract
Urinary Diversion
Nursing Management: Urinary Diversion
46. Acute Kidney Injury and Chronic Kidney Disease
Conceptual Focus
Acute Kidney Injury
Nursing Management: Acute Kidney Injury
Chronic Kidney Disease
Nursing Management: Chronic Kidney Disease
Dialysis
Peritoneal Dialysis
Hemodialysis
Continuous Renal Replacement Therapy
Wearable Artificial Kidney
Kidney Transplantation
Nursing Management: Kidney Transplant Recipient
Section Eleven. Problems Related to Regulatory and Reproductive Mechanisms
47. Assessment: Endocrine System
Conceptual Focus
Structures and Functions of Endocrine System
Assessment of Endocrine System
Diagnostic Studies of Endocrine System
48. Diabetes Mellitus
Conceptual Focus
Diabetes Mellitus
Nursing Management: Diabetes
Acute Complications of Diabetes
Diabetic Ketoacidosis
Hyperosmolar Hyperglycemia Syndrome
Nursing Management: Diabetes-Related Ketoacidosis and Hyperosmolar Hyperglycemia Syndrome
Hypoglycemia
Nursing and Interprofessional Management: Hypoglycemia
Chronic Complications Associated with Diabetes
Retinopathy
Nephropathy
Neuropathy
Complications of Feet and Lower Extremities
Skin Complications
Infection
Psychologic Considerations
49. Endocrine Problems
Disorders of Anterior Pituitary Gland
Acromegaly
Interprofessional and Nursing Care
Excesses of Other Tropic Hormones
Hypofunction of Pituitary Gland
Interprofessional and Nursing Care
Pituitary Surgery
Nursing Management: Pituitary Surgery
Disorders of Posterior Pituitary Gland
Syndrome of Inappropriate Antidiuretic Hormone
Interprofessional and Nursing Care
Diabetes Insipidus
Interprofessional and Nursing Care
Disorders of Thyroid Gland
Goiter
Thyroiditis
Hyperthyroidism
Nursing Management: Hyperthyroidism
Hypothyroidism
Nursing Management: Hypothyroidism
Thyroid Nodules and Cancer
Interprofessional and Nursing Care
Multiple Endocrine Neoplasia
Disorders of Parathyroid Glands
Nursing Management: Hyperparathyroidism
Hypoparathyroidism
Interprofessional and Nursing Care
Disorders of Adrenal Cortex
Cushing Syndrome
Nursing Management: Cushing Syndrome
Adrenocortical Insufficiency
Interprofessional and Nursing Care
Corticosteroid Therapy
Hyperaldosteronism
Interprofessional and Nursing Care
Disorders of Adrenal Medulla
Interprofessional and Nursing Care
50. Assessment: Reproductive System
Conceptual Focus
Structures and Functions of Male and Female Reproductive Systems
Assessment of Male and Female Reproductive Systems
Diagnostic Studies of Reproductive Systems
51. Breast Disorders
Conceptual Focus
Assessment of Breast Disorders
Benign Breast Disorders
Breast Infections
Fibrocystic Changes
Fibroadenoma
Nipple Discharge
Atypical Hyperplasia
Intraductal Papilloma
Ductal Ectasia
Male Gynecomastia
Breast Cancer
Nursing Management: Breast Cancer
Mammoplasty
Nursing Management: Breast Augmentation and Reduction
52. Sexually Transmitted Infections
Conceptual Focus
Factors Affecting Incidence of Stis
STIs Characterized by Discharge, Cervicitis, or Urethritis
Gonococcal Infections
Trichomoniasis
STIs Characterized by Genital Lesions or Ulcers
Genital Warts
Syphilis
Nursing Management: STIs
53. Female Reproductive Problems
Conceptual Focus
Infertility
Early Pregnancy Loss
Problems Related to Menstruation
Premenstrual Syndrome
Nursing Management: Premenstrual Syndrome
Dysmenorrhea
Abnormal Uterine Bleeding
Nursing Management: Abnormal Uterine Bleeding
Ectopic Pregnancy
Perimenopause and Postmenopause
Nursing Management: Perimenopause and Postmenopause
Infections of Lower Genital Tract
Nursing Management: Infections of Lower Genital Tract
Pelvic Inflammatory Disease (Pid)
Nursing Management: Pelvic Inflammatory Disease
Chronic Pelvic Pain
Endometriosis
Benign Tumors of the Female Reproductive System
Ovarian Cysts
Cervical Polyps
Cancers of the Female Reproductive System
Endometrial Cancer
Ovarian Cancer
Vaginal Cancer
Vulvar Cancer
Nursing and Interprofessional Management: Cancers of Female Reproductive System
Pelvic Organ Prolapse
Uterine Prolapse
Cystocele and Rectocele
Nursing and Interprofessional Management: Pelvic Organ Prolapse
Fistula
Sexual Assault
Nursing Management: Sexual Assault
54. Male Reproductive Problems
Conceptual Focus
Problems of the Prostate Gland
Nursing Management: Benign Prostatic Hyperplasia
Prostate Cancer
Nursing Management: Prostate Cancer
Prostatitis
Problems of the Penis
Congenital Problems
Problems of Prepuce
Problems of Erectile Mechanism
Cancer of Penis
Problems of Scrotum and Testes
Inflammatory and Infectious Problems
Congenital Problems
Acquired Problems
Testicular Cancer
Sexual Function
Erectile Dysfunction
Hypogonadism
Infertility
Section Twelve. Problems Related to Movement and Coordination
55. Assessment: Nervous System
Conceptual Focus
Structures and Functions of Nervous System
Assessment of Nervous System
Diagnostic Studies of Nervous System
56. Acute Intracranial Problems
Conceptual Focus
Intracranial Regulation
Increased Intracranial Pressure
Nursing Management: Increased Intracranial Pressure
Head Injury
Nursing Management: Head Injury
Brain Tumors
Nursing Management: Brain Tumors
Cranial Surgery
Nursing Management: Cranial Surgery
Inflammatory Conditions of the Brain
Bacterial Meningitis
Nursing Management: Bacterial Meningitis
Viral Meningitis
Brain Abscess
Encephalitis
57. Stroke
Conceptual Focus
Pathophysiology of Stroke
Risk Factors for Stroke
Types of Stroke
Clinical Manifestations of Stroke
Diagnostic Studies for Stroke
Interprofessional Care for Stroke
Nursing Management: Stroke
58. Chronic Neurologic Problems
Conceptual Focus
Headaches
Tension-Type Headache
Migraine Headache
Cluster Headache
Other Types of Headaches
Interprofessional Care for Headaches
Nursing Management: Headaches
Chronic Neurologic Disorders
Nursing Management: Seizure Disorder
Restless Legs Syndrome
Interprofessional and Nursing Care
Degenerative Neurologic Disorders
Nursing Management: Multiple Sclerosis
Parkinson’s Disease
Nursing Management: Parkinson’s Disease
Myasthenia Gravis
Nursing Management: Myasthenia Gravis
Amyotrophic Lateral Sclerosis
Huntington’s Disease
59. Dementia and Delirium
Conceptual Focus
Dementia
Alzheimer’s Disease
Nursing Management: Alzheimer’s Disease
Delirium
Nursing and Interprofessional Management: Delirium
60. Spinal Cord and Peripheral Nerve Problems
Conceptual Focus
Spinal Cord Problems
Nursing Management: Spinal Cord Injury
Spinal Cord Tumors
Cranial Nerve Disorders
Trigeminal Neuralgia
Nursing Management: Trigeminal Neuralgia
Bell’s Palsy
Nursing Management: Bell’s Palsy
Polyneuropathies
Chronic Inflammatory Demyelinating Polyneuropathy
Tetanus
Botulism
61. Assessment: Musculoskeletal System
Conceptual Focus
Structures and Functions of Musculoskeletal System
Assessment of Musculoskeletal System
Diagnostic Studies of Musculoskeletal System
62. Musculoskeletal Trauma and Orthopedic Surgery
Conceptual Focus
Health Promotion
Soft Tissue Injuries
Sprains and Strains
Nursing Management: Sprains and Strains
Dislocation and Subluxation
Repetitive Strain Injury
Carpal Tunnel Syndrome
Rotator Cuff Injury
Meniscus Injury
Anterior Cruciate Ligament Injury
Bursitis
Fractures
Nursing Management: Fractures
Complications of Fractures
Types of Fractures
Humeral Shaft Fracture
Pelvic Fracture
Hip Fracture
Nursing Management: Hip Fracture
Femoral Shaft Fracture
Tibial Fracture
Stable Vertebral Fracture
Facial Fracture
Mandibular Fracture
Nursing Management: Mandibular Fracture
Amputation
Nursing Management: Amputation
Common Joint Surgical Procedures
Types of Joint Surgeries
Nursing and Interprofessional Management: Joint Surgery
63. Musculoskeletal Problems
Conceptual Focus
Osteomyelitis
Nursing Management: Osteomyelitis
Bone Tumors
Benign Bone Tumors
Malignant Bone Tumors
Nursing Management: Bone Cancer
Muscular Dystrophy
Low Back Pain
Acute Low Back Pain
Nursing and Interprofessional Management: Acute Low Back Pain
Chronic Low Back Pain
Intervertebral Disc Disease
Nursing Management: Vertebral Disc Surgery
Neck Pain
Foot Disorders
Nursing Management: Foot Disorders
Metabolic Bone Diseases
Osteomalacia
Osteoporosis
Nursing and Interprofessional Management: Osteoporosis
Paget’s Disease
64. Arthritis and Connective Tissue Diseases
Conceptual Focus
Arthritis
Osteoarthritis
Nursing Management: Osteoarthritis
Rheumatoid Arthritis
Nursing Management: Rheumatoid Arthritis
Gout
Interprofessional and Nursing Management: Gout
Lyme Disease
Septic Arthritis
Spondyloarthropathies
Ankylosing Spondylitis
Psoriatic Arthritis
Reactive Arthritis
Systemic Lupus Erythematosus
Nursing Management: Systemic Lupus Erythematosus
Scleroderma
Nursing Management: Scleroderma
Polymyositis and Dermatomyositis
Interprofessional and Nursing Care
Mixed Connective Tissue Disease
Sjögren’s Syndrome
Myofascial Pain Syndrome
Fibromyalgia
Systemic Exertion Intolerance Disease (SEID)
Section Thirteen. Care in Specialized Settings
65. Critical Care
Conceptual Focus
Critical Care Nursing
Hemodynamic Monitoring
Nursing Management: Hemodynamic Monitoring
Circulatory Assist Devices
Nursing and Interprofessional Management: Circulatory Assist Devices
Noninvasive Ventilation
Artificial Airways
Nursing and Interprofessional Management: Artificial Airway
Mechanical Ventilation
Other Critical Care Content
66. Shock, Sepsis, and Multiple Organ Dysfunction Syndrome
Conceptual Focus
Shock
Nursing Management: Shock
Systemic Inflammatory Response Syndrome and Multiple Organ Dysfunction Syndrome
Nursing and Interprofessional Management: Sirs and Mods
67. Acute Respiratory Failure and Acute Respiratory Distress Syndrome
Conceptual Focus
Acute Respiratory Failure
Nursing and Interprofessional Management: Acute Respiratory Failure
Acute Respiratory Distress Syndrome
Nursing and Interprofessional Management: ARDS
68. Emergency and Disaster Nursing
Conceptual Focus
Care of Emergency Patient
Environmental Emergencies
Heat-Related Emergencies
Cold-Related Emergencies
Submersion Injuries
Stings and Bites
Poisonings
Violence
Agents of Terrorism
Penetrating Trauma
Emergency and Mass Casualty Incident Preparedness
Appendixes
Appendix A. Basic Life Support for Health Care Providers
Appendix B. Nursing Diagnoses
Appendix C. Laboratory Reference Intervals
Index
IBC

Citation preview

Lewis's Medical-Surgical Nursing Assessment and Management of Clinical Problems ELEVENTH EDITION

Mariann M. Harding, RN, PhD, FAADN, CNE Professor of Nursing, Kent State University at Tuscarawas, New Philadelphia, Ohio

Section Editors

Jeffrey Kwong, RN, DNP, MPH, ANP-BC, FAAN, FAANP Professor, Division of Advanced Nursing Practice, School of Nursing, Rutgers University, Newark, New Jersey

Dottie Roberts, RN, EdD, MSN, MACI, OCNS-C, CMSRN, CNE Executive Director, Orthopaedic Nurses Certification Board, Chicago, Illinois

Debra Hagler, RN, PhD, ACNS-BC, CNE, CHSE, ANEF, FAAN Clinical Professor, Edson College of Nursing and Health Innovation, Arizona State University, Phoenix, Arizona

Courtney Reinisch, RN, DNP, FNPBC Undergraduate Program Director, Associate Professor, School of Nursing, Montclair State University, Montclair, New Jersey

Disclaimer This title includes additional digital media when purchased in print format. For this digital book edition, media content may not be included.

Table of Contents Cover image Title page Copyright About the Authors Contributors Authors of Teaching and Learning Resources Reviewers Dedication Preface Concepts Exemplars Special Features

Section One. Concepts in Nursing Practice 1. Professional Nursing Conceptual Focus Professional Nursing Practice Influences on Professional Nursing Practice Patient-Centered Care Teamwork and Collaboration Safety Quality Improvement Informatics Evidence-Based Practice 2. Health Equity and Culturally Competent Care Conceptual Focus Determinants of Health Health Disparities and Health Equity Culture Cultural Competence Cultural Diversity in the Health Care Workplace

Cultural Factors Affecting Health and Health Care Nursing Management: Promoting Health Equity and Increasing Cultural Competency 3. Health History and Physical Examination Conceptual Focus Data Collection Nursing History: Subjective Data Physical Examination: Objective Data Types of Assessment Problem Identification 4. Patient and Caregiver Teaching Conceptual Focus Role of Patient and Caregiver Teaching Teaching-Learning Process Process of Patient Teaching 5. Chronic Illness and Older Adults Conceptual Focus Chronic Illness Nursing Management: Chronic Illness

Older Adults Attitudes Toward Aging Biologic Aging Age-Related Physiologic Changes Special Older Adult Populations Social Support for Older Adults Social Services for Older Adults Medicare and Medicaid Care Alternatives for Older Adults Legal and Ethical Issues Nursing Management: Older Adults

Section Two. Problems Related to Comfort and Coping 6. Stress Management Conceptual Focus What is Stress? Physiologic Response to Stress Mind-Body-Spirit Connection

Effects of Stress on Health Coping Strategies Relaxation Strategies Nursing Management: Stress 7. Sleep and Sleep Disorders Conceptual Focus Sleep Physiologic Sleep Mechanisms Insufficient Sleep and Sleep Disturbances Sleep Disturbances in the Hospital Sleep Disorders Nursing Management: Insomnia Obstructive Sleep Apnea Nursing and Interprofessional Management: Sleep Apnea Periodic Limb Movement Disorder Circadian Rhythm Disorders Narcolepsy Parasomnias Special Sleep Needs of Nurses

8. Pain Conceptual Focus Magnitude of Pain Problem Definitions and Dimensions of Pain Classification of Pain Pain Assessment Pain Treatment Nursing and Interprofessional Management: Pain Institutionalizing Pain Education and Management Ethical Issues in Pain Management Managing Pain in Special Populations 9. Palliative and End-of-Life Care Conceptual Focus Palliative Care Hospice Care Death End-of-Life Care Legal and Ethical Issues Affecting End-of-Life Care Nursing Management: End of Life

Special Needs of Caregivers and Nurses in End-of-Life Care 10. Substance Use Disorders Conceptual Focus Drugs Associated with Substance Use Disorder Nursing and Interprofessional Management: Tobacco Use Disorder Alcohol Nursing and Interprofessional Management: Alcohol Use Disorder Use of Other Substances Nursing and Interprofessional Management: Stimulant Use Depressants Nursing and Interprofessional Management: Depressant Use Inhalants Cannabis Caffeine Nursing Management: Substance Use

Section Three. Problems Related to Homeostasis and Protection

11. Inflammation and Healing Conceptual Focus Inflammatory Response Nursing and Interprofessional Management: Inflammation Healing Process Nursing and Interprofessional Management: Wound Healing Pressure Injuries Nursing and Interprofessional Management: Pressure Injuries 12. Genetics Conceptual Focus Genetics and Genomics Genetic Disorders Genetic Screening and Testing Pharmacogenomics and Pharmacogenetics Gene Therapy Stem Cell Therapy Nursing Management: Genetics and Genomics 13. Immune Responses and Transplantation Conceptual Focus

Normal Immune Response Altered Immune Response Allergic Disorders Nursing Management: Immunotherapy Nursing and Interprofessional Management: Latex Allergies Autoimmunity Immunodeficiency Disorders Human Leukocyte Antigen System Organ Transplantation Graft-Versus-Host Disease 14. Infection Conceptual Focus Infections Types of Pathogens Emerging Infections Health Care–Associated Infections Infection Prevention and Control Human Immunodeficiency Virus Infection Nursing Management: HIV Infection

15. Cancer Conceptual Focus Biology of Cancer Benign Versus Malignant Neoplasms Classification of Cancer Prevention and Early Detection of Cancer Interprofessional Care Surgical Therapy Chemotherapy Radiation Therapy Nursing Management: Chemotherapy and Radiation Therapy Late Effects of Radiation and Chemotherapy Immunotherapy and Targeted Therapy Nursing Management: Immunotherapy and Targeted Therapy Hormone Therapy Hematopoietic Growth Factors Hematopoietic Stem Cell Transplantation Gene Therapy Complications of Cancer Nutritional Problems

Infection Oncologic Emergencies Cancer Pain Coping with Cancer and Treatment Cancer Survivorship 16. Fluid, Electrolyte, and Acid-Base Imbalances Conceptual Focus Homeostasis Water Content of the Body Electrolytes Mechanisms Controlling Fluid and Electrolyte Movement Fluid Movement in Capillaries Fluid Spacing Regulation of Water Balance Fluid Volume Imbalances Fluid Volume Deficit Fluid Volume Excess Nursing Management: Fluid Volume Imbalances Sodium Imbalances

Hypernatremia Nursing and Interprofessional Management: Hypernatremia Hyponatremia Nursing and Interprofessional Management: Hyponatremia Potassium Imbalances Hyperkalemia Nursing and Interprofessional Management: Hyperkalemia Hypokalemia Nursing and Interprofessional Management: Hypokalemia Calcium Imbalances Hypercalcemia Nursing and Interprofessional Management: Hypercalcemia Hypocalcemia Nursing and Interprofessional Management: Hypocalcemia Phosphate Imbalances Hyperphosphatemia Hypophosphatemia Magnesium Imbalances Hypermagnesemia Hypomagnesemia

Acid-Base Imbalances pH And Hydrogen ION Concentration Acid-Base Regulation Alterations in Acid-Base Balance Clinical Manifestations of Acid-Base Imbalances Assessment of Fluid, Electrolyte, and Acid-Base Imbalances Oral Fluid and Electrolyte Replacement IV. Fluid and Electrolyte Replacement Central Venous Access Devices Nursing Management: Central Venous Access Devices

Section Four. Perioperative Care 17. Preoperative Care Conceptual Focus Surgical Settings Patient Interview Nursing Assessment of Preoperative Patient Nursing Management: Preoperative Patient

18. Intraoperative Care Conceptual Focus Physical Environment of the Operating Room Surgical Team Nursing Management: Patient Before Surgery Nursing Management: Patient During Surgery Nursing Management: Patient After Surgery Anesthesia Anesthesia Techniques Perioperative Crisis Events 19. Postoperative Care Conceptual Focus Postoperative Care of Surgical Patient Respiratory Problems Nursing Management: Respiratory Problems Cardiovascular Problems Nursing Management: Cardiovascular Problems Neurologic and Psychologic Problems Nursing Management: Neurologic and Psychologic Problems

Pain and Discomfort Nursing Management: Pain Temperature Changes Nursing Management: Temperature Changes Gastrointestinal Problems Nursing Management: Gastrointestinal Problems Urinary Problems Nursing Management: Urinary Problems Integumentary Problems Nursing Management: Surgical Wounds Discharge from The Pacu Ambulatory Surgery

Section Five. Problems Related to Altered Sensory Input 20. Assessment and Management: Visual Problems Conceptual Focus Visual System Structures and Functions of Visual System

Visual Pathway Assessment of Visual System Diagnostic Studies of Visual System Visual Problems Visual Impairment Nursing Management: Visual Impairment Eye Trauma Extraocular Disorders Nursing Management: Inflammation and Infection Dry Eye Disorders Strabismus Corneal Disorders Intraocular Disorders Nursing Management: Cataracts Retinopathy Retinal Detachment Age-Related Macular Degeneration Glaucoma Nursing Management: Glaucoma Intraocular Inflammation and Infection

Ocular Tumors Enucleation Ocular Manifestations of Systemic Diseases 21. Assessment and Management: Auditory Problems Conceptual Focus Auditory System Structures and Functions of Auditory System Assessment of Auditory System Diagnostic Studies of Auditory System Auditory Problems: External Ear and Canal Nursing and Interprofessional Management: External Otitis Cerumen and Foreign Bodies in External Ear Canal Trauma Malignancy of External Ear Middle Ear and Mastoid Nursing and Interprofessional Management: Chronic Otitis Media Otosclerosis Inner Ear Problems Ménière’s Disease

Nursing and Interprofessional Management: Ménière’s Disease Benign Paroxysmal Positional Vertigo Acoustic Neuroma Hearing Loss and Deafness Nursing and Interprofessional Management: Hearing Loss and Deafness 22. Assessment: Integumentary System Conceptual Focus Structures and Functions of Skin and Appendages Assessment of Integumentary System Diagnostic Studies of Integumentary System 23. Integumentary Problems Conceptual Focus Environmental Hazards Skin Cancer Nonmelanoma Skin Cancer Melanoma Skin Infections and Infestations Allergic Skin Problems

Benign Skin Problems Interprofessional Care: Skin Problems Nursing Management: Skin Problems Cosmetic Procedures Nursing Management: Cosmetic Surgery Skin Grafts 24. Burns Conceptual Focus Types of Burn Injury Classification of Burn Injury Prehospital and Emergency Care Phases of Burn Management Emergent Phase Nursing and Interprofessional Management: Emergent Phase Acute Phase Nursing and Interprofessional Management: Acute Phase Rehabilitation Phase Nursing and Interprofessional Management: Rehabilitation Phase Emotional/Psychologic Needs of Patients and Caregivers

Special Needs of Nurses

Section Six. Problems of Oxygenation: Ventilation 25. Assessment: Respiratory System Conceptual Focus Structures and Functions of Respiratory System Assessment of Respiratory System Diagnostic Studies of Respiratory System 26. Upper Respiratory Problems Conceptual Focus Problems Of Nose And Paranasal Sinuses Nasal Fracture Rhinoplasty Nursing Management: Nasal Surgery Epistaxis Allergic Rhinitis Acute Viral Rhinopharyngitis

Influenza Sinusitis Obstruction of Nose and Sinuses Problems of Pharynx Peritonsillar Abscess Problems of Larynx and Trachea Acute Laryngitis Airway Obstruction Tracheostomy Nursing Management: Tracheostomy Head and Neck Cancer Nursing Management: Head and Neck Cancer 27. Lower Respiratory Problems Conceptual Focus Lower Respiratory Tract Infections Acute Bronchitis Pertussis Pneumonia Nursing Management: Pneumonia

Tuberculosis Nursing Management: Tuberculosis Atypical Mycobacteria Pulmonary Fungal Infections Lung Abscess Environmental Lung Diseases Lung Cancer Nursing Management: Lung Cancer Other Types of Lung Tumors Chest Trauma and Thoracic Injuries Fractured Ribs Flail Chest Pneumothorax Chest Tubes and Pleural Drainage Nursing Management: Chest Drainage Chest Surgery Restrictive Respiratory Disorders Atelectasis Pleurisy Pleural Effusion

Interstitial Lung Diseases Idiopathic Pulmonary Fibrosis Sarcoidosis Vascular Lung Disorders Pulmonary Embolism Nursing Management: Pulmonary Embolism Pulmonary Hypertension Idiopathic Pulmonary Arterial Hypertension Secondary Pulmonary Arterial Hypertension Cor Pulmonale Lung Transplantation 28. Obstructive Pulmonary Diseases Cenceptual Focus Asthma Nursing Management: Asthma Chronic Obstructive Pulmonary Disease Nursing Management: COPD Cystic Fibrosis Nursing Management: Cystic Fibrosis

Bronchiectasis Interprofessional and Nursing Management: Bronchiectasis

Section Seven. Problems of Oxygenation: Transport 29. Assessment: Hematologic System Conceptual Focus Structures and Functions of Hematologic System Assessment of Hematologic System Diagnostic Studies of Hematologic System 30. Hematologic Problems Conceptual Focus Anemia Nursing and Interprofessional Management: Anemia Anemia Caused by Decreased Erythrocyte Production Iron-Deficiency Anemia Thalassemia Megaloblastic Anemias

Anemia of Chronic Disease Aplastic Anemia Anemia Caused by Blood Loss Acute Blood Loss Chronic Blood Loss Anemia Caused by Increased Erythrocyte Destruction Sickle Cell Disease Acquired Hemolytic Anemia Other Red Blood Cell Disorders Polycythemia Problems Of Hemostasis Thrombocytopenia Nursing Management: Thrombocytopenia Hemophilia and Von Willebrand Disease Nursing Management: Hemophilia Disseminated Intravascular Coagulation Nursing Management: Disseminated Intravascular Coagulation Neutropenia Myelodysplastic Syndrome Leukemia

Nursing Management: Leukemia Lymphomas Hodgkin’s Lymphoma Non-Hodgkin’s Lymphoma Multiple Myeloma Disorders of the Spleen Blood Component Therapy

Section Eight. Problems of Oxygenation: Perfusion 31. Assessment: Cardiovascular System Conceptual Focus Structures and Functions of Cardiovascular System Assessment of Cardiovascular System Diagnostic Studies of Cardiovascular System 32. Hypertension Conceptual Focus Normal Regulation of Blood Pressure

Hypertension Nursing Management: Primary Hypertension Hypertensive Crisis 33. Coronary Artery Disease and Acute Coronary Syndrome Conceptual Focus Coronary Artery Disease Interprofessional and Nursing Care: Coronary Artery Disease Chronic Stable Angina Interprofessional and Nursing Care: Chronic Stable Angina Acute Coronary Syndrome Unstable Angina Myocardial Infarction: St-Elevation and Non–St-Elevation Myocardial Infarction Diagnostic Studies: Acute Coronary Syndrome Interprofessional Care: Acute Coronary Syndrome Nursing Management: Acute Coronary Syndrome Sudden Cardiac Death 34. Heart Failure Conceptual Focus

Heart Failure Nursing Management: Heart Failure Heart Transplantation 35. Dysrhythmias Conceptual Focus Rhythm Identification and Treatment Syncope 36. Inflammatory and Structural Heart Disorders Conceptual Focus Inflammatory Disorders of Heart Nursing Management: Infective Endocarditis Acute Pericarditis Nursing Management: Acute Pericarditis Chronic Constrictive Pericarditis Myocarditis Nursing Management: Myocarditis Rheumatic Fever and Rheumatic Heart Disease Nursing Management: Rheumatic Fever and Rheumatic Heart Disease

Valvular Heart Disease Mitral Valve Stenosis Mitral Valve Regurgitation Mitral Valve Prolapse Aortic Valve Stenosis Aortic Valve Regurgitation Tricuspid and Pulmonic Valve Disease Diagnostic Studies: Valvular Heart Disease Interprofessional Care: Valvular Heart Disease Nursing Management: Valvular Disorders Cardiomyopathy Dilated Cardiomyopathy Hypertrophic Cardiomyopathy Restrictive Cardiomyopathy 37. Vascular Disorders Conceptual Focus Peripheral Artery Disease Peripheral Artery Disease of The Lower Extremities Nursing Management: Lower Extremity Peripheral Artery Disease

Acute Arterial Ischemic Disorders Thromboangiitis Obliterans Raynaud’s Phenomenon Aortic Aneurysms Nursing Management: Aortic Aneurysms Aortic Dissection Nursing Management: Aortic Dissection Acute and Chronic Venous Disorders Venous Thrombosis Nursing Management: Venous Thromboembolism Varicose Veins Nursing Management: Varicose Veins Chronic Venous Insufficiency and Venous Leg Ulcers

Section Nine. Problems of Ingestion, Digestion, Absorption, and Elimination 38. Assessment: Gastrointestinal System Conceptual Focus Structures and Functions of Gastrointestinal System

Assessment of Gastrointestinal System Diagnostic Studies of Gastrointestinal System 39. Nutritional Problems Conceptual Focus Nutritional Problems Normal Nutrition Vegetarian Diet Malnutrition Nursing and Interprofessional Management: Malnutrition Specialized Nutritional Support Nursing Management: Parenteral Nutrition Eating Disorders Bulimia Nervosa 40. Obesity Conceptual Focus Obesity Health Risks Associated with Obesity Nursing and Interprofessional Management: Obesity Bariatric Surgical Therapy

Nursing Management: Perioperative Care of The Obese Patient Cosmetic Surgical Therapy Metabolic Syndrome Nursing and Interprofessional Management: Metabolic Syndrome 41. Upper Gastrointestinal Problems Conceptual Focus Nausea and Vomiting Nursing Management: Nausea and Vomiting Oral Inflammation and Infections Oral Cancer Nursing Management: Oral Cancer Esophageal Disorders Nursing and Interprofessional Management: GERD Hiatal Hernia Nursing and Interprofessional Management: Hiatal Hernia Esophageal Cancer Nursing Management: Esophageal Cancer Other Esophageal Disorders Disorders of the Stomach and Upper Small Intestine

Nursing Management: Peptic Ulcer Disease Stomach Cancer Nursing Management: Stomach Cancer Gastric Surgery Nursing Management: Gastric Surgery Gastritis Nursing and Interprofessional Management: Gastritis Upper Gastrointestinal Bleeding Nursing Management: Upper Gastrointestinal Bleeding Foodborne Illness 42. Lower Gastrointestinal Problems Conceptual Focus Diarrhea Nursing Management: Acute Infectious Diarrhea Fecal Incontinence Nursing Management: Fecal Incontinence Constipation Nursing Management: Constipation Acute Abdominal Pain and Laparotomy

Nursing Management: Acute Abdominal Pain Abdominal Trauma Chronic Abdominal Pain Irritable Bowel Syndrome Inflammatory Disorders Nursing Management: Appendicitis Peritonitis Nursing Management: Peritonitis Gastroenteritis Inflammatory Bowel Disease Nursing Management: Inflammatory Bowel Disease Intestinal Obstruction Nursing Management: Intestinal Obstruction Polyps of Large Intestine Colorectal Cancer Nursing Management: Colorectal Cancer Bowel Resection and Ostomy Surgery Nursing Management: Bowel Resection and Ostomy Surgery Diverticulosis and Diverticulitis Fistulas

Hernias Malabsorption Syndrome Celiac Disease Lactase Deficiency Short Bowel Syndrome Gastrointestinal Stromal Tumors Anorectal Problems Nursing Management: Hemorrhoids Anal Fissure Anorectal Abscess Anal Fistula Anal Cancer Pilonidal Sinus 43. Liver, Biliary Tract, and Pancreas Problems Conceptual Focus Disorders of The Liver Nursing Management: Viral Hepatitis Drug- and Chemical-Induced Liver Diseases Autoimmune, Genetic, and Metabolic Liver Diseases

Cirrhosis Nursing Management: Cirrhosis Acute Liver Failure Liver Cancer Liver Transplantation Disorders of The Pancreas Nursing Management: Acute Pancreatitis Chronic Pancreatitis Pancreatic Cancer Nursing Management: Pancreatic Cancer Disorders of The Biliary Tract Nursing Management: Gallbladder Disease Gallbladder Cancer

Section Ten. Problems of Urinary Function 44. Assessment: Urinary System Conceptual Focus Structures and Functions of Urinary System Assessment of Urinary System

Diagnostic Studies of Urinary System 45. Renal and Urologic Problems Infectious and Inflammatory Disorders of Urinary System Nursing Management: Urinary Tract Infection Acute Pyelonephritis Nursing Management: Acute Pyelonephritis Chronic Pyelonephritis Urethritis Urethral Diverticula Interstitial Cystitis/Painful Bladder Syndrome Nursing Management: Interstitial Cystitis/Painful Bladder Syndrome Genitourinary Tuberculosis Immunologic Disorders of Kidney Nursing and Interprofessional Management: Acute Poststreptococcal Glomerulonephritis Nephrotic Syndrome Obstructive Uropathies Urinary Tract Calculi Nursing Management: Urinary Tract Calculi

Strictures Renal Trauma Renal Vascular Problems Nephrosclerosis Renal Artery Stenosis Renal Vein Thrombosis Hereditary Kidney Diseases Polycystic Kidney Disease Medullary Cystic Disease Alport Syndrome Urinary Tract Tumors Bladder Cancer Nursing and Interprofessional Management: Bladder Cancer Bladder Dysfunction Nursing Management: Urinary Incontinence Urinary Retention Nursing Management: Urinary Retention Catheterization Catheter Construction Types of Catheters

Surgery of the Urinary Tract Urinary Diversion Nursing Management: Urinary Diversion 46. Acute Kidney Injury and Chronic Kidney Disease Conceptual Focus Acute Kidney Injury Nursing Management: Acute Kidney Injury Chronic Kidney Disease Nursing Management: Chronic Kidney Disease Dialysis Peritoneal Dialysis Hemodialysis Continuous Renal Replacement Therapy Wearable Artificial Kidney Kidney Transplantation Nursing Management: Kidney Transplant Recipient

Section Eleven. Problems Related to Regulatory and Reproductive Mechanisms

47. Assessment: Endocrine System Conceptual Focus Structures and Functions of Endocrine System Assessment of Endocrine System Diagnostic Studies of Endocrine System 48. Diabetes Mellitus Conceptual Focus Diabetes Mellitus Nursing Management: Diabetes Acute Complications of Diabetes Diabetic Ketoacidosis Hyperosmolar Hyperglycemia Syndrome Nursing Management: Diabetes-Related Ketoacidosis and Hyperosmolar Hyperglycemia Syndrome Hypoglycemia Nursing and Interprofessional Management: Hypoglycemia Chronic Complications Associated with Diabetes Retinopathy Nephropathy Neuropathy

Complications of Feet and Lower Extremities Skin Complications Infection Psychologic Considerations 49. Endocrine Problems Disorders of Anterior Pituitary Gland Acromegaly Interprofessional and Nursing Care Excesses of Other Tropic Hormones Hypofunction of Pituitary Gland Interprofessional and Nursing Care Pituitary Surgery Nursing Management: Pituitary Surgery Disorders of Posterior Pituitary Gland Syndrome of Inappropriate Antidiuretic Hormone Interprofessional and Nursing Care Diabetes Insipidus Interprofessional and Nursing Care Disorders of Thyroid Gland

Goiter Thyroiditis Hyperthyroidism Nursing Management: Hyperthyroidism Hypothyroidism Nursing Management: Hypothyroidism Thyroid Nodules and Cancer Interprofessional and Nursing Care Multiple Endocrine Neoplasia Disorders of Parathyroid Glands Nursing Management: Hyperparathyroidism Hypoparathyroidism Interprofessional and Nursing Care Disorders of Adrenal Cortex Cushing Syndrome Nursing Management: Cushing Syndrome Adrenocortical Insufficiency Interprofessional and Nursing Care Corticosteroid Therapy Hyperaldosteronism

Interprofessional and Nursing Care Disorders of Adrenal Medulla Interprofessional and Nursing Care 50. Assessment: Reproductive System Conceptual Focus Structures and Functions of Male and Female Reproductive Systems Assessment of Male and Female Reproductive Systems Diagnostic Studies of Reproductive Systems 51. Breast Disorders Conceptual Focus Assessment of Breast Disorders Benign Breast Disorders Breast Infections Fibrocystic Changes Fibroadenoma Nipple Discharge Atypical Hyperplasia Intraductal Papilloma

Ductal Ectasia Male Gynecomastia Breast Cancer Nursing Management: Breast Cancer Mammoplasty Nursing Management: Breast Augmentation and Reduction 52. Sexually Transmitted Infections Conceptual Focus Factors Affecting Incidence of Stis STIs Characterized by Discharge, Cervicitis, or Urethritis Gonococcal Infections Trichomoniasis STIs Characterized by Genital Lesions or Ulcers Genital Warts Syphilis Nursing Management: STIs 53. Female Reproductive Problems Conceptual Focus Infertility

Early Pregnancy Loss Problems Related to Menstruation Premenstrual Syndrome Nursing Management: Premenstrual Syndrome Dysmenorrhea Abnormal Uterine Bleeding Nursing Management: Abnormal Uterine Bleeding Ectopic Pregnancy Perimenopause and Postmenopause Nursing Management: Perimenopause and Postmenopause Infections of Lower Genital Tract Nursing Management: Infections of Lower Genital Tract Pelvic Inflammatory Disease (Pid) Nursing Management: Pelvic Inflammatory Disease Chronic Pelvic Pain Endometriosis Benign Tumors of the Female Reproductive System Ovarian Cysts Cervical Polyps Cancers of the Female Reproductive System

Endometrial Cancer Ovarian Cancer Vaginal Cancer Vulvar Cancer Nursing and Interprofessional Management: Cancers of Female Reproductive System Pelvic Organ Prolapse Uterine Prolapse Cystocele and Rectocele Nursing and Interprofessional Management: Pelvic Organ Prolapse Fistula Sexual Assault Nursing Management: Sexual Assault 54. Male Reproductive Problems Conceptual Focus Problems of the Prostate Gland Nursing Management: Benign Prostatic Hyperplasia Prostate Cancer Nursing Management: Prostate Cancer

Prostatitis Problems of the Penis Congenital Problems Problems of Prepuce Problems of Erectile Mechanism Cancer of Penis Problems of Scrotum and Testes Inflammatory and Infectious Problems Congenital Problems Acquired Problems Testicular Cancer Sexual Function Erectile Dysfunction Hypogonadism Infertility

Section Twelve. Problems Related to Movement and Coordination 55. Assessment: Nervous System

Conceptual Focus Structures and Functions of Nervous System Assessment of Nervous System Diagnostic Studies of Nervous System 56. Acute Intracranial Problems Conceptual Focus Intracranial Regulation Increased Intracranial Pressure Nursing Management: Increased Intracranial Pressure Head Injury Nursing Management: Head Injury Brain Tumors Nursing Management: Brain Tumors Cranial Surgery Nursing Management: Cranial Surgery Inflammatory Conditions of the Brain Bacterial Meningitis Nursing Management: Bacterial Meningitis Viral Meningitis

Brain Abscess Encephalitis 57. Stroke Conceptual Focus Pathophysiology of Stroke Risk Factors for Stroke Types of Stroke Clinical Manifestations of Stroke Diagnostic Studies for Stroke Interprofessional Care for Stroke Nursing Management: Stroke 58. Chronic Neurologic Problems Conceptual Focus Headaches Tension-Type Headache Migraine Headache Cluster Headache Other Types of Headaches Interprofessional Care for Headaches

Nursing Management: Headaches Chronic Neurologic Disorders Nursing Management: Seizure Disorder Restless Legs Syndrome Interprofessional and Nursing Care Degenerative Neurologic Disorders Nursing Management: Multiple Sclerosis Parkinson’s Disease Nursing Management: Parkinson’s Disease Myasthenia Gravis Nursing Management: Myasthenia Gravis Amyotrophic Lateral Sclerosis Huntington’s Disease 59. Dementia and Delirium Conceptual Focus Dementia Alzheimer’s Disease Nursing Management: Alzheimer’s Disease Delirium

Nursing and Interprofessional Management: Delirium 60. Spinal Cord and Peripheral Nerve Problems Conceptual Focus Spinal Cord Problems Nursing Management: Spinal Cord Injury Spinal Cord Tumors Cranial Nerve Disorders Trigeminal Neuralgia Nursing Management: Trigeminal Neuralgia Bell’s Palsy Nursing Management: Bell’s Palsy Polyneuropathies Chronic Inflammatory Demyelinating Polyneuropathy Tetanus Botulism 61. Assessment: Musculoskeletal System Conceptual Focus Structures and Functions of Musculoskeletal System Assessment of Musculoskeletal System

Diagnostic Studies of Musculoskeletal System 62. Musculoskeletal Trauma and Orthopedic Surgery Conceptual Focus Health Promotion Soft Tissue Injuries Sprains and Strains Nursing Management: Sprains and Strains Dislocation and Subluxation Repetitive Strain Injury Carpal Tunnel Syndrome Rotator Cuff Injury Meniscus Injury Anterior Cruciate Ligament Injury Bursitis Fractures Nursing Management: Fractures Complications of Fractures Types of Fractures Humeral Shaft Fracture

Pelvic Fracture Hip Fracture Nursing Management: Hip Fracture Femoral Shaft Fracture Tibial Fracture Stable Vertebral Fracture Facial Fracture Mandibular Fracture Nursing Management: Mandibular Fracture Amputation Nursing Management: Amputation Common Joint Surgical Procedures Types of Joint Surgeries Nursing and Interprofessional Management: Joint Surgery 63. Musculoskeletal Problems Conceptual Focus Osteomyelitis Nursing Management: Osteomyelitis Bone Tumors

Benign Bone Tumors Malignant Bone Tumors Nursing Management: Bone Cancer Muscular Dystrophy Low Back Pain Acute Low Back Pain Nursing and Interprofessional Management: Acute Low Back Pain Chronic Low Back Pain Intervertebral Disc Disease Nursing Management: Vertebral Disc Surgery Neck Pain Foot Disorders Nursing Management: Foot Disorders Metabolic Bone Diseases Osteomalacia Osteoporosis Nursing and Interprofessional Management: Osteoporosis Paget’s Disease 64. Arthritis and Connective Tissue Diseases

Conceptual Focus Arthritis Osteoarthritis Nursing Management: Osteoarthritis Rheumatoid Arthritis Nursing Management: Rheumatoid Arthritis Gout Interprofessional and Nursing Management: Gout Lyme Disease Septic Arthritis Spondyloarthropathies Ankylosing Spondylitis Psoriatic Arthritis Reactive Arthritis Systemic Lupus Erythematosus Nursing Management: Systemic Lupus Erythematosus Scleroderma Nursing Management: Scleroderma Polymyositis and Dermatomyositis Interprofessional and Nursing Care

Mixed Connective Tissue Disease Sjögren’s Syndrome Myofascial Pain Syndrome Fibromyalgia Systemic Exertion Intolerance Disease (SEID)

Section Thirteen. Care in Specialized Settings 65. Critical Care Conceptual Focus Critical Care Nursing Hemodynamic Monitoring Nursing Management: Hemodynamic Monitoring Circulatory Assist Devices Nursing and Interprofessional Management: Circulatory Assist Devices Noninvasive Ventilation Artificial Airways Nursing and Interprofessional Management: Artificial Airway Mechanical Ventilation

Other Critical Care Content 66. Shock, Sepsis, and Multiple Organ Dysfunction Syndrome Conceptual Focus Shock Nursing Management: Shock Systemic Inflammatory Response Syndrome and Multiple Organ Dysfunction Syndrome Nursing and Interprofessional Management: Sirs and Mods 67. Acute Respiratory Failure and Acute Respiratory Distress Syndrome Conceptual Focus Acute Respiratory Failure Nursing and Interprofessional Management: Acute Respiratory Failure Acute Respiratory Distress Syndrome Nursing and Interprofessional Management: ARDS 68. Emergency and Disaster Nursing Conceptual Focus Care of Emergency Patient Environmental Emergencies

Heat-Related Emergencies Cold-Related Emergencies Submersion Injuries Stings and Bites Poisonings Violence Agents of Terrorism Penetrating Trauma Emergency and Mass Casualty Incident Preparedness

Appendixes Appendix A. Basic Life Support for Health Care Providers Appendix B. Nursing Diagnoses Appendix C. Laboratory Reference Intervals Index IBC

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About the Authors Mariann M. Harding, RN, PhD, FAADN, CNE

Mariann Harding is a Professor of Nursing at Kent State University Tuscarawas, New Philadelphia, Ohio, where she has been on the faculty since 2005. She received her diploma in nursing from Mt. Carmel School of Nursing in Columbus, Ohio; her Bachelor of Science in nursing from Ohio University in Athens, Ohio; her Master of Science in Nursing as an adult nurse practitioner from the Catholic University of America in Washington, DC; and her doctorate in nursing from West Virginia University in Morgantown, West Virginia. Her 29 years of nursing experience have primarily been in critical care nursing and teaching in licensed practical, associate, and baccalaureate nursing programs. She currently teaches medicalsurgical nursing, health care policy, and evidence-based practice. Her research has focused on promoting student success and health promotion among individuals with gout and facing cancer. Jeffrey Kwong, RN, DNP, MPH, ANP-BC, FAAN, FAANP

Jeffrey Kwong is a Professor at the School of Nursing at Rutgers, the State University of New Jersey. He has worked for over 20 years in the area of adult primary care with a special focus on HIV. He received his undergraduate degree from the University of California— Berkeley, his nurse practitioner degree from the University of California—San Francisco, and completed his doctoral training at the University of Colorado—Denver. He also has a Master of Science Degree in public health with a focus on health education and behavioral sciences from the University of California—Los Angeles, and he was appointed a Hartford Geriatric Interprofessional Scholar while completing his gerontology education at New York University. In addition to teaching, Dr. Kwong maintains a clinical practice at Gotham Medical Group in New York City. He is a Fellow in the American Association of Nurse Practitioners. Dottie Roberts, RN, EdD, MSN, MACI, CMSRN, OCNS-C, CNE

Dottie Roberts received her Bachelor of Science in nursing from Beth-El College of Nursing, Colorado Springs, Colorado; her Master of Science in adult health nursing from Beth-El College of Nursing and Health Sciences; her Master of Arts in curriculum and instruction from Colorado Christian University, Colorado Springs, Colorado; and her EdD in healthcare education from Nova Southeastern University, Ft. Lauderdale, Florida. She has over 25 years of experience in medical-surgical and orthopaedic nursing and holds certifications in both specialties. She has also taught in two baccalaureate programs in the Southeast and is certified as a nurse educator. She currently serves as contributing faculty for the RN-BSN program at Walden University. For her dissertation, Dottie completed a phenomenological study on facilitation of critical-thinking skills by clinical faculty in a baccalaureate nursing program. She has been Executive Director of the Orthopaedic Nurses Certification Board since 2005 and editor of MEDSURG Nursing, official journal of the Academy of MedicalSurgical Nurses, since 2003. Her free time is spent traveling, reading, and cross-stitching. Debra Hagler, RN, PhD, ACNS-BC, CNE, CHSE, ANEF, FAAN

Debbie Hagler is a Clinical Professor in the Edson College of Nursing and Health Innovation at Arizona State University in Phoenix. She is Deputy Editor of The Journal of Continuing Education in Nursing. She received her Practical Certificate in Nursing, Associate Degree in Nursing, and Bachelor of Science in Nursing from New Mexico State University. She earned a Master of Science from the University of Arizona and a doctorate in Learning and Instructional Technology from Arizona State University. Her clinical background is in adult health and critical care nursing. Her current role focuses on supporting students through the Barrett Honors program and helping faculty members develop their scholarly writing for publication. Courtney Reinisch, RN, DNP, FNP-BC

Courtney Reinisch is the Undergraduate Program Director and Associate Professor for the School of Nursing at Montclair State University. She earned her Bachelor of Arts in biology and psychology from Immaculata University. She received her Bachelor of Science in nursing and Masters of Science in family practice nurse practitioner degree from the University of Delaware. She completed her Doctor of Nursing Practice degree at Columbia University School of Nursing. Courtney’s nursing career has focused on providing care for underserved populations in primary care and emergency settings. She has taught in undergraduate and graduate nursing programs in New York and New Jersey. Courtney enjoys playing tennis, snowboarding, reading, and spending time with her family and dogs. She is the biggest fan for her nieces and nephews at their soccer games, crosscountry events, and track meets. She is an active volunteer in the Parents Association of her son’s school and advocates for the needs of students with learning differences and the LGBTQ community.

Contributors Vera Barton-Maxwell, PhD, APRN, FNP-BC, CHFN, Assistant Professor, Advanced Nursing Practice, Family Nurse Practitioner Program, Georgetown University, Washington, District of Columbia Nurse Practitioner, Center for Advanced Heart Failure, West Virginia University Heart and Vascular Institute, Morgantown, West Virginia Cecilia Bidigare, MSN, RN, Professor, Nursing Department, Sinclair Community College, Dayton, Ohio Megan Ann Brissie, DNP, RN, ACNP-BC, CEN Acute Care Nurse Practitioner, Neurosurgery, Duke Health, Durham, North Carolina Adjunct Instructor, College of Nursing, University of Cincinnati, Cincinnati, Ohio Diana Taibi Buchanan, PhD, RN, Associate Professor, Biobehavioral Nursing and Health Systems, University of Washington, Seattle, Washington Michelle Bussard, PhD, RN, RN to BSN Online eCampus Program Director, College of Health and Human Services, Bowling Green State University, Bowling Green, Ohio Kim K. Choma, DNP, APRN, WHNP-BC, Women’s Health Nurse Practitioner, Independent Consultant and Clinical Trainer, Kim Choma, DNP, LLC, Scotch Plains, New Jersey Marisa Cortese, PhD, RN, FNP-BC, Research Nurse Practitioner, Hematology/Oncology, White Plains Hospital, White Plains, New

York Ann Crawford, RN, PhD, CNS, CEN, Professor, Department of Nursing, University of Mary Hardin-Baylor, Belton, Texas Kimberly Day, DNP, RN, Clinical Assistant Professor, Edson College of Nursing and Health Innovation, Arizona State University, Phoenix, Arizona Deena Damsky Dell, MSN, RN, APRN, AOCN(R), LNC, Oncology Advanced Practice Registered Nurse, Sarasota Memorial Hospital, Sarasota, Florida Hazel Dennison, DNP, RN, APNc, CPHQ, CNE, Director of Continuing Nursing Education, College of Health Sciences, School of Nursing, Walden University, Minneapolis, Minnesota , Nurse Practitioner, Urgent Care, Virtua Health System, Medford, New Jersey Jane K. Dickinson, PhD, RN, CDE, Program Director/Lecturer, Diabetes Education and Management, Teachers College Columbia University, New York, New York Cathy Edson, MSN, RN, Nurse Practitioner, Emergency Department, Team Health—Virtua Memorial, Mt. Holly, New Jersey Jonel L. Gomez, DNP, ARNP, CPCO, COE, Nurse Practitioner, Ophthalmic Facial Plastic Surgery , Specialists, Stephen Laquis, MD, Fort Myers, Florida Sherry A. Greenberg, PhD, RN, GNP-BC, FGSA, CourtesyAppointed Associate Professor, Nursing, Rory Meyers College of Nursing, New York University, New York, New York Diana Rabbani Hagler, MSN-Ed, RN, CCRN, Staff Nurse, Intensive Care Unit, Banner Health, Gilbert, Arizona Julia A. Hitch, MS, APRN, FNPCDE,

Nurse Practitioner, Internal

Medicine—Endocrinology, Ohio State University Physicians, Columbus, Ohio Haley Hoy, PhD, APRN, Associate Professor, College of Nursing, University of Alabama in Huntsville, Huntsville, Alabama , Nurse Practitioner, Vanderbilt Lung Transplantation, Vanderbilt Medical Center, Nashville, Tennessee Melissa Hutchinson, MN, BA, RN, Clinical Nurse Specialist, MICU/CCU, VA Puget Sound Health Care System, Seattle, Washington Mark Karasin, DNP, APRN, AGACNP-BC, CNOR, Advanced Practice Nurse, Cardiothoracic Surgery, Robert Wood Johnson University Hospital, New Brunswick, New Jersey , Adjunct Faculty, Center for Professional Development, School of Nursing , Rutgers University, Newark, New Jersey Patricia Keegan, DNP, NP-C, AACC, Director Strategic and Programmatic Initiatives, Heart and Vascular Center, Emory University, Atlanta, Georgia Kristen Keller, DNP, ACNP-BC, PMHNP-BC, Nurse Practitioner, Trauma and Acute Care Surgery, Banner Thunderbird Medical Center, Glendale, Arizona Anthony Lutz, MSN, NP-C, CUNP, Nurse Practitioner, Department of Urology, Columbia University Irving Medical Center, New York, New York Denise M. McEnroe-Petitte, PhD, RN, Associate Professor, Nursing Department, Kent State University Tuscarawas, New Philadelphia, Ohio Amy Meredith, MSN, RN, EM Cert/Residency, APN-C Lead and APN Emergency Department, Emergency Department, Southern Ocean Medical Center, Manahawkin, New Jersey

Helen Miley, RN, PhD, AG-ACNP, Specialty Director of Adult Gerontology, Acute Care Nurse Practitioner Program, School of Nursing, Rutgers University, Newark, New Jersey Debra Miller-Saultz, DNP, FNP-BC, Assistant Professor of Nursing, School of Nursing, Columbia University, New York, New York Eugene Mondor, MN, RN, CNCC(C), Clinical Nurse Educator, Adult Critical Care, Royal Alexandra Hospital, Edmonton, Alberta, Canada Brenda C. Morris, EdD, RN, CNE Clinical Professor, Edson College of Nursing and Health Innovation, Arizona State University, Phoenix, Arizona Janice A. Neil, PhD, RN, CNE, Associate Professor, College of Nursing, Department of Baccalaureate Education, East Carolina University, Greenville, North Carolina Yeow Chye Ng, PhD, CRNP, CPC, AAHIVE, Associate Professor, College of Nursing, University of Alabama in Huntsville, Huntsville, Alabama Mary C. Olson, DNP, APRN, Nurse Practitioner, Medicine, Division of Gastroenterology and Hepatology, New York University Langone Health, New York, New York Madona D. Plueger, MSN, RN, ACNS-BC CNRN, Adult Health Clinical Nurse Specialist, Barrow Neurological Institute, Dignity Health, St. Joseph’s Hospital and Medical Center, Phoenix, Arizona Matthew C. Price, MS, CNP, ONP-C, RNFA, Orthopedic Nurse Practitioner, Orthopedic One, Columbus, Ohio , Director, Orthopedic Nurses Certification Board, Chicago, Illinois Margaret R. Rateau, PhD, RN, CNE,

Assistant Professor, School of

Nursing, Education, and Human Studies, Robert Morris University, Moon Township, Pennsylvania Catherine R. Ratliff, RN, PhD, Clinical Associate Professor and Nurse Practitioner, School of Nursing/Vascular Surgery, University of Virginia Health System, Charlottesville, Virginia Sandra Irene Rome, MN, RN, AOCN, Clinical Nurse Specialist, Blood and Marrow Transplant Program, Cedars–Sinai Medical Center, Los Angeles, California , Assistant Clinical Professor, University of California Los Angeles School of Nursing, Los Angeles, California Diane M. Rudolphi, MSN, RN, Senior Instructor of Nursing, College of Health Sciences, University of Delaware, Newark, Newark, Delaware Diane Ryzner, MSN, APRN, CNS-BC, OCNS-C, Clinical Nursing Transformation Leader, Orthopedics, Northwest Community Healthcare, Arlington Heights, Illinois Andrew Scanlon, DNP, RN, Associate Professor, School of Nursing, Montclair State University, Montclair, New Jersey Rose Shaffer, MSN, RN, ACNP-BC, CCRN, Cardiology Nurse Practitioner, Thomas Jefferson University Hospital, Philadelphia, Pennsylvania Tara Shaw, MSN, RN, Assistant Professor, Goldfarb School of Nursing, Barnes-Jewish College, St. Louis, Missouri Cynthia Ann Smith, DNP, APRN, CNN-NP, FNP-BC, Nurse Practitioner, Renal Consultants, PLLC, South Charleston, West Virginia Janice Smolowitz, PhD, DNP, EdD, Dean and Professor, School of Nursing, Montclair State University, Montclair, New Jersey

Cindy Sullivan, MN, ANP-C, CNRN, Nurse Practitioner, Department of Neurosurgery, Barrow Neurological Institute, Phoenix, Arizona Teresa Turnbull, DNP, RN, Assistant Professor, School of Nursing, Oregon Health and Science University, Portland, Oregon Kara Ann Ventura, DNP, PNP, FNP, Director, Liver Transplant Program, Yale New Haven, New Haven, Connecticut Colleen Walsh, DNP, RN, ONC, ONP-C, CNS, ACNPBC, Contract Assistant Professor of Nursing, College of Nursing and Health Professions, University of Southern Indiana, Evansville, Indiana Pamela Wilkerson, MN, RN, Nurse Manager, Primary Care and Urgent Care, Department of Veterans Affairs, Veterans Administration, Puget Sound, Tacoma, Washington Daniel P. Worrall, MSN, ANP-BC, Nurse Practitioner, Sexual Health Clinic, Nurse Practitioner, General and Gastrointestinal Surgery, Massachusetts General Hospital, Boston, Massachusetts, Clinical Operations Manager, The Ragon Institute of MGH, MIT, and Harvard, Cambridge, Massachusetts

Authors of Teaching and Learning Resources TEST BANK Debra Hagler, RN, PhD, ACNS-BC, CNE, CHSE, ANEF, FAAN, Clinical Professor, Edson College of Nursing and Health Innovation, Arizona State University, Phoenix, Arizona

CASE STUDIES Interactive and Managing Care of Multiple Patients Case Studies Mariann M. Harding, RN, PhD, FAADN, CNE,

Professor of Nursing,

Kent State University at Tuscarawas, New Philadelphia, Ohio

Brenda C. Morris, EdD, RN, CNE,

Clinical Professor, Edson College of Nursing and Health Innovation, Arizona State University, Phoenix, Arizona

POWERPOINT PRESENTATIONS Bonnie Heintzelman, RN, MS, CMSRN,

Assistant Professor of Nursing, Pennsylvania College of Technology, Williamsport, Pennsylvania

Michelle A. Walczak, RN, MSN,

Associate Professor of Nursing, Pennsylvania College of Technology, Williamsport, Pennsylvania

TEACH FOR NURSES Margaret R. Rateau, RN, PhD, CNE,

Assistant Professor, School of Nursing, Education, and Human Studies, Robert Morris University, Moon Township, Pennsylvania

Janice Sarasnick, RN, PhD, CHSE,

Associate Professor of Nursing, Robert

Morris University, Moon Township, Pennsylvania

NCLEX EXAMINATION REVIEW QUESTIONS Mistey D. Bailey, RN, MSN,

Lecturer, Nursing, Kent State University

Tuscarawas, New Philadelphia, Ohio

Shelly Stefka, RN, MSN,

Lecturer, Nursing, Kent State University Tuscarawas, New Philadelphia, Ohio

STUDY GUIDE Collin Bowman-Woodall, RN, MS,

Assistant Professor, Samuel Merritt University, San Francisco Peninsula Campus, San Mateo, California

CLINICAL COMPANION Debra Hagler, RN, PhD, ACNS-BC, CNE, CHSE, ANEF, FAAN, Clinical Professor, Edson College of Nursing and Health Innovation, Arizona State University, Phoenix, Arizona

EVIDENCE-BASED PRACTICE BOXES Linda Bucher, RN, PhD, CEN, CNE,

Emerita Professor, University of

Delaware, Newark, Delaware,

NURSING CARE PLANS Collin Bowman-Woodall, RN, MS,

Assistant Professor, Samuel Merritt University, San Francisco Peninsula Campus, San Mateo, California

Reviewers Kristen Ryan Barry-Rodgers, RN, BSN, CEN, Emergency Department Charge and Staff Nurse, Virtua Memorial Hospital, Mt. Holly, New Jersey Michelle Bussard, PhD, RN, RN to BSN Online eCampus Program Director, College of Health and Human Services, Bowling Green State University, Bowling Green, Ohio Margaret A. Chesnutt, MSN, FNP, BC, CORLN, Nurse Practitioner, Primary Care, Veterans Administration Medical Center, Decatur, Georgia Ann Crawford, RN, PhD, CNS, CEN, Professor, Department of Nursing, University of Mary Hardin-Baylor, Belton, Texas Jonel L. Gomez, DNP, ARNP, CPCO, COE, Nurse Practitioner, Ophthalmic Facial Plastic Surgery Specialists, Stephen Laquis, MD, Fort Myers, Florida Jennifer Hebert, MSN, RN-BC, NE-

BC, Manager, Patient Care Services, Nursing Administration, Sentara Princess Anne Hospital, Virginia Beach, Virginia Haley Hoy, PhD, APRN Associate Professor, College of Nursing, University of Alabama in Huntsville, Huntsville, Alabama Nurse Practitioner, Vanderbilt Lung Transplantation, Vanderbilt Medical Center, Nashville, Tennessee

Coretta M. Jenerette, PhD, RN, CNE, AOCN, Associate Professor, School of Nursing, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina Beth Karasin, MSN, APN, AGACNP-BC, RNFA, CNOR, Advanced Practice Nurse, Neurosurgery, Atlantic Neurosurgical Specialists, Morristown, New Jersey Mark Karasin, DNP, APRN, AGACNP-BC, CNOR Advanced Practice Nurse, Cardiothoracic Surgery, Robert Wood Johnson University Hospital, New Brunswick, New Jersey Adjunct Faculty, Center for Professional Development, School of Nursing, Rutgers University, Newark, New Jersey

Kristen Keller, DNP, ACNP-BC, PMHNPBC, Nurse Practitioner, Trauma and Acute Care Surgery, Banner Thunderbird Medical Center, Glendale, Arizona Suzanne M. Mahon, DNSc, RN, AOCN(R), AGN-BC, Professor, Division of

Hematology/Oncology, Department of Internal Medicine, Adult Nursing, School of Nursing, Saint Louis University, St. Louis, Missouri Helen Miley, RN, PhD, AG-ACNP, Specialty Director of Adult Gerontology, Acute Care Nurse Practitioner Program, School of Nursing, Rutgers University, Newark, New Jersey Linda L. Morris, PhD, APN, CCNS, FCCM, Clinical Nurse Educator, Associate Professor of Physical Medicine and Rehabilitation and Anesthesiology, Academy Department, Shirley Ryan Ability Lab, Northwestern University Feinberg School of Medicine, Chicago, Illinois Louise O’Keefe, PhD, CRNP, Assistant Professor and Director, Faculty and Staff Clinic, College of Nursing, University of Alabama in Huntsville, Huntsville, Alabama Catherine R. Ratliff, RN, PhD, Clinical Associate Professor and Nurse Practitioner, School of Nursing/Vascular Surgery, University of Virginia Health System, Charlottesville, Virginia Lori M. Rhudy, RN, PhD, CNRN, ACNS-BC Clinical Associate Professor, School of Nursing, University of Minnesota, Minneapolis, Minnesota Nurse Scientist, Division of Nursing Research, Mayo Clinic, Rochester, Minnesota

Cynthia Ann Smith, DNP, APRN, CNN-NP, FNP-BC, Nurse Practitioner, Renal Consultants, PLLC, South Charleston, West Virginia Janice Smolowitz, PhD, DNP, EdD, Dean and Professor, School of Nursing, Montclair State University, Montclair, New Jersey Charity L. Tan, MSN, ACNP-BC, Acute Care Nurse Practitioner, Neurological Surgery, University of California Davis Health, Sacramento, California Kara Ann Ventura, DNP, PNP, FNP, Director, Liver Transplant Program, Yale New Haven, New Haven, Connecticut Robert M. Welch, MSN, FNP, CRNO, Nurse Practitioner, Ophthalmology—Retina, Neveda Retina Associates, Reno, Nevada Mary Zellinger, APRN-CCNS, MN, ANP-BC, CCRN-CSC, FCCM, Clinical Nurse Specialist, Cardiovascular Critical Care, Nursing Department, Emory University Hospital, Atlanta, Georgia

Dedication To the Profession of Nursing and to the Important People in Our Lives Mariann My husband Jeff, our daughters Kate and Sarah, and my parents, Mick and Mary. Jeff My parents, Raymond and Virginia, thank you for believing in me and providing me the opportunity to become a nurse. Dottie My husband Steve and my children Megan, E.J., Jessica, and Matthew, who have supported me through four college degrees and countless writing projects; and to my son-in-law Al, our grandsons Oscar and Stephen, and my new daughter-in-law Melissa. Debbie My husband James, our children Matthew, Andrew, Amanda, and Diana, and our granddaughter Emma.

Courtney To future nurses and the advancement of health care globally.

Preface The eleventh edition of Lewis’s Medical-Surgical Nursing: Assessment and Management of Clinical Problems incorporates the most current medical-surgical nursing information in an easy-to-use format. This textbook is a comprehensive resource containing the essential information that students need to prepare for class, examinations, clinical assignments, and safe and comprehensive patient care. The text and accompanying resources include many features to help students learn key medical-surgical nursing content, including patient and caregiver teaching, gerontology, interprofessional care, cultural and ethnic considerations, patient safety, genetics, nutrition and drug therapy, evidence-based practice, and much more. To address the rapidly changing practice environment, all efforts were directed toward building on the strengths of the previous editions while delivering this more effective new edition. To help students and faculty members focus on the most important concepts in patient care, most chapters open with a conceptual focus that introduces students to the common concepts shared by patients experiencing the main exemplars discussed in the chapter. This edition features more body maps and has many new illustrations. Lengthy diagnostic tables in the assessment chapters have been separated into specific categories, including radiologic studies and serology studies. The previously combined visual and auditory content is now in separate chapters focusing on the assessment and management of vision and hearing disorders. New Promoting Population Health boxes address strategies to improve health outcomes. For a text to be effective, it must be understandable. In this edition,

great effort has been put into improving the readability and lowering the reading level. Students will find more clear and easier-to-read language, with an engaging conversational style. The narrative addresses the reader, helping make the text more personal and an active learning tool. The language is more positive. For example, particular side effects and complications are referred to as common, as opposed to not uncommon. International Classification for Nursing Practice (ICNP) nursing diagnoses, one of the terminologies recognized by the American Nurses Association, are used throughout the text and ancillary materials. The language is similar to that of NANDA-I. ICNP nursing diagnoses are used in many facilities worldwide to document nursing care in electronic health records. By introducing students to the ICNP nursing diagnoses, students will learn a more shared vocabulary. This should translate into the more accurate use of diagnostic language in clinical practice across healthcare settings. Contributors were selected for their expertise in specific content areas; one or more specialists in a given subject area have thoroughly reviewed each chapter to increase accuracy. The editors have undertaken final rewriting and editing to achieve internal consistency. The comprehensive and timely content, special features, attractive layout, full-color illustrations, and student-friendly writing style combine to make this the textbook used in more nursing schools than any other medical-surgical nursing textbook.

Organization Content is organized into 2 major divisions. The first division, Sections 1 through 3 (Chapters 1 through 16), discusses general concepts related to the care of adult patients. The second division, Sections 4 through 13 (Chapters 17 through 68), presents nursing assessment and nursing management of medical-surgical problems. At the beginning of each chapter, the Conceptual Focus helps students focus on the key concepts and integrate concepts with exemplars affecting different

body systems. Learning Outcomes and Key Terms assist students in identifying the key content for that chapter. The various body systems are grouped to reflect their interrelated functions. Each section is organized around 2 central themes: assessment and management. Chapters dealing with assessment of a body system include a discussion of the following: 1. A brief review of anatomy and physiology, focusing on information that will promote understanding of nursing care 2. Health history and noninvasive physical assessment skills to expand the knowledge base on which treatment decisions are made 3. Common diagnostic studies, expected results, and related nursing responsibilities to provide easily accessible information Management chapters focus on the pathophysiology, clinical manifestations, diagnostic studies, interprofessional care, and nursing management of various diseases and disorders. The nursing management sections are presented in a consistent format, organized into assessment, nursing diagnoses, planning, implementation, and evaluation. To emphasize the importance of patient care in and across various clinical settings, nursing implementation of all major health problems is organized by the following levels of care: 1. Health Promotion 2. Acute Care 3. Ambulatory Care

Special Features The 6 competencies for registered nursing practice identified by QSEN serve as the foundation of the text and are highlighted in the core content, case studies, and nursing care plans.

• New! Nursing Management tables and boxes focus on the actions nurses need to take to deliver safe, quality, effective patient care. • New! Diagnostic Studies tables focus on the specific type of study, such as interventional, serologic, or radiologic, with more detailed information on interpreting results and associated nursing care. • Cultural and ethnic health disparities content and boxes in the text highlight risk factors and important issues related to the nursing care of various ethnic groups. A special Culturally Competent Care heading denotes cultural and ethnic content related to diseases and disorders. Chapter 2 (Health Equity and Culturally Competent Care) discusses health status differences among groups of people related to access to care, economic aspects of health care, gender and cultural issues, and the nurse’s role in promoting health equity. • Interprofessional care is highlighted in special Interprofessional Care sections in all management chapters and Interprofessional Care tables throughout the text. • Focused Assessment boxes in all assessment chapters provide brief checklists that help students do a more practical “assessment on the run” or bedside approach to assessment. They can be used to evaluate the status of previously identified health problems and monitor for signs of new problems. • Safety Alert boxes highlight important patient safety issues and focus on the National Patient Safety Goals. • Pathophysiology Maps outline complex concepts related to diseases in a flowchart format, making them easier to understand. • Patient and caregiver teaching is an ongoing theme throughout the text. Chapter 4 (Patient and Caregiver Teaching) emphasizes the increasing importance and prevalence of patient management of chronic illnesses and conditions and the role of the caregiver in patient care.

• New! Conceptual Focus at the beginning of each chapter helps students focus on the key concepts and integrate concepts with exemplars affecting different body systems. • Gerontology and chronic illness are discussed in Chapter 5 (Chronic Illness and Older Adults) and included throughout the text under Gerontologic Considerations headings and in Gerontologic Differences in Assessment tables. • Nutrition is highlighted throughout the textbook. Nutritional Therapy tables summarize nutritional interventions and promote healthy lifestyles in patients with various health problems. • New! Promoting Population Health boxes present health care goals and interventions as they relate to specific disorders, such as diabetes and cancer, and to health promotion, such as preserving hearing and maintaining a healthy weight. • Extensive drug therapy content includes Drug Therapy tables and concise Drug Alerts highlighting important safety considerations for key drugs. • Genetics content includes: • Genetics in Clinical Practice boxes that summarize the genetic basis, genetic testing, and clinical implications for genetic disorders that affect adults • A genetics chapter that focuses on practical application of nursing care as it relates to this important topic • Genetic Risk Alerts in the assessment chapters, which call attention to important genetic risks • Genetic Link headings in the management chapters, which highlight the specific genetic bases of many disorders • Gender Differences boxes discuss how women and men are affected differently by conditions such as pain and hypertension. • Check Your Practice boxes challenge students to think critically, analyze patient assessment data, and implement the

appropriate intervention. Scenarios and discussion questions are provided to promote active learning. • Complementary & Alternative Therapies boxes expand on this information and summarize what nurses need to know about therapies such as herbal remedies, acupuncture, and yoga. • Ethical/Legal Dilemmas boxes promote critical thinking for timely and sensitive issues that nursing students may deal with in clinical practice—topics such as informed consent, advance directives, and confidentiality. • Emergency Management tables outline the emergency treatment of health problems most likely to require emergency intervention. • Nursing care plans on the Evolve website focus on common disorders or exemplars. These care plans incorporate ICNP nursing diagnoses, Nursing Interventions Classification (NIC), and Nursing Outcomes Classification (NOC) in a way that clearly shows the linkages among NIC, NOC, and nursing diagnoses and applies them to nursing practice. • Coverage on delegation and prioritization includes: • Specific topics and skills related to delegation and the nurse’s role in working with members of the interprofessional team, which are detailed in Nursing Management tables. • Delegation and prioritization questions in case studies and Bridge to NCLEX Examination Questions. • Nursing interventions throughout the text, listed in order of priority. • Nursing diagnoses in the nursing care plans, listed in order of priority. • Assessment Abnormalities tables in assessment chapters alert the nurse to commonly encountered abnormalities and their possible etiologies. • Nursing Assessment tables summarize the key subjective and

objective data related to common diseases. Subjective data are organized by functional health patterns. • Health History tables in assessment chapters present key questions to ask patients related to a specific disease or disorder. • Evidence-based practice is covered in Applying the Evidence boxes and evidence-based practice-focused questions in the case studies. Applying the Evidence boxes use a case study approach to help students learn to use evidence in making patient care decisions. • Informatics boxes and content in Chapter 4 (Patient and Caregiver Teaching) reflect the current use and importance of technology as it relates to patient self-management. • Bridge to NCLEX® Examination Questions at the end of each chapter are matched to the Learning Outcomes and help students learn the important points in the chapter. Answers are provided just below the questions for immediate feedback, and rationales are provided on the Evolve website. • Case Studies with photos bring patients to life. Management chapters have case studies at the end of the chapters. These cases help students learn how to prioritize care and manage patients in the clinical setting. Unfolding case studies are included in each assessment chapter, and case studies that focus on managing care of multiple patients are included at the end of each section. Discussion questions with a focus on prioritization, delegation, and evidence-based practice are included in all case studies. Answer guidelines are provided on the Evolve website.

Learning Supplements for Students • The handy Clinical Companion presents approximately 200 common medical-surgical conditions and procedures in a concise, alphabetical format for quick clinical reference.

Designed for portability, this popular reference includes the essential, need-to-know information for treatments and procedures in which nurses play a major role. An attractive and functional four-color design highlights key information for quick, easy reference. • An exceptionally thorough Study Guide contains over 500 pages of review material that reflect the content found in the textbook. It features a wide variety of clinically relevant exercises and activities, including NCLEX-format multiple choice and alternate format questions, case studies, anatomy review, critical thinking activities, and much more. It features an attractive four-color design and many alternate-item format questions to better prepare students for the NCLEX examination. An answer key is included to provide students with immediate feedback as they study. • The Evolve Student Resources are available online at http://evolve.elsevier.com/Lewis/medsurg and include the following valuable learning aids organized by chapter: • Printable Key Points summaries for each chapter. • 1000 NCLEX examination Review Questions. • Answer Guidelines to the case studies in the textbook. • Rationales for the Bridge to NCLEX® Examination Questions in the textbook. • 55 Interactive Case Studies with state-of-the-art animations and a variety of learning activities, which provide students with immediate feedback. Ten of the case studies are enhanced with photos and narration of the clinical scenarios. • Customizable Nursing Care Plans for over 60 common disorder or exemplars. • Conceptual Care Map Creator. • Audio glossary of key terms, available as comprehensive alphabetical glossary and organized by chapter.

• Fluids and Electrolytes Tutorial. • Content Updates. • More than just words on a screen, Elsevier eBooks come with a wealth of built-in study tools and interactive functionality to help students better connect with the course material and their instructors. In addition, with the ability to fit an entire library on one portable device, students have the ability to study when, where, and how they want.

Teaching Supplements for Instructors • The Evolve Instructor Resources (available online at http://evolve.elsevier.com/Lewis/medsurg) remain the most comprehensive set of instructor’s materials available, containing the following: • TEACH for Nurses Lesson Plans with electronic resources organized by chapter to help instructors develop and manage the course curriculum. This exciting resource includes: • Objectives • Pre-class activities • Nursing curriculum standards • Student and instructor chapter resource listings • Teaching strategies, with learning activities and assessment methods tied to learning outcomes • Case studies with answer guidelines • The Test Bank features over 2000 NCLEX examination test questions with text page references and answers coded for NCLEX Client Needs category, nursing process, and cognitive level. The test bank includes hundreds of prioritization, delegation, and multiple patient questions. All

alternate-item format questions are included. The ExamView software allows instructors to create new tests; edit, add, and delete test questions; sort questions by NCLEX category, cognitive level, nursing process step, and question type; and administer and grade online tests. • The Image Collection contains more than 800 fullcolor images from the text for use in lectures. • An extensive collection of PowerPoint Presentations includes over 125 different presentations focused on the most common diseases and disorders. The presentations have been thoroughly revised to include helpful instructor notes/teaching tips, unfolding case studies, illustrations and photos not found in the book, new animations, and updated audience response questions for use with iClicker and other audience response systems. • Course management system. • Access to all student resources listed above. • The Simulation Learning System (SLS) is an online toolkit that helps instructors and facilitators effectively incorporate medium- to high-fidelity simulation into their nursing curriculum. Detailed patient scenarios promote and enhance the clinical decision-making skills of students at all levels. The SLS provides detailed instructions for preparation and implementation of the simulation experience, debriefing questions that encourage critical thinking, and learning resources to reinforce student comprehension. Each scenario in the SLS complements the textbook content and helps bridge the gap between lecture and clinical. The SLS provides the perfect environment for students to practice what they are learning in the text for a true-to-life, hands-on learning experience.

Acknowledgments The editors are especially grateful to many people at Elsevier who assisted with this revision effort. In particular, we wish to thank the team of Jamie Blum, Rebecca Leenhouts, Denise Roslonski, Clay Broeker, and Julie Eddy. In addition, we want to thank Kristin Oyirifi in marketing. We also wish to thank our contributors and reviewers for their assistance with the revision process. We are particularly indebted to the faculty, nurses, and student nurses who have put their faith in our textbook to assist them on their path to excellence. The increasing use of this book throughout the United States, Canada, Australia, and other parts of the world has been gratifying. We appreciate the many users who have shared their comments and suggestions on the previous editions. We sincerely hope that this book will assist both students and clinicians in practicing truly professional nursing. Mariann M. Harding Jeffrey Kwong Dottie Roberts Debra Hagler Courtney Reinisch

Concepts Exemplars Acid–Base Balance Chronic Kidney Disease Diarrhea Metabolic Acidosis Metabolic Alkalosis Respiratory Acidosis Respiratory Alkalosis Cellular Regulation Anemia Breast Cancer Cervical Cancer Colon Cancer Endometrial Cancer Head and Neck Cancer Leukemia Lung Cancer Lymphoma Melanoma Prostate Cancer Clotting Disseminated Intravascular Coagulopathy Pulmonary Embolism Thrombocytopenia Venous Thromboembolism Cognition Alzheimer’s Disease Delirium Elimination

Benign Prostatic Hypertrophy Chronic Kidney Disease Constipation Diarrhea Intestinal Obstruction Pyelonephritis Prostatitis Renal Calculi Fluids and Electrolytes Burns Hyperkalemia Hypernatremia Hypokalemia Hyponatremia Gas Exchange Acute Respiratory Failure Acute Respiratory Distress Syndrome Asthma Chronic Obstructive Pulmonary Disease Cystic Fibrosis Lung Cancer Pulmonary Embolism Glucose Regulation Cushing’s Syndrome Diabetes Mellitus Hormonal Regulation Addison’s Disease Hyperthyroidism Hypothyroidism Immunity Allergic Rhinitis Anaphylaxis HIV Infection Organ Transplantation Peptic Ulcer Disease

Infection Antimicrobial Resistant Infections Health Care–Associated Infections Hepatitis Pneumonia Tuberculosis Urinary Tract Infection Inflammation Appendicitis Cholecystitis Glomerulonephritis Pancreatitis Pelvic Inflammatory Disease Peritonitis Rheumatoid Arthritis Intracranial Regulation Brain Tumor Head Injury Meningitis Seizure Disorder Stroke Mobility Fractures Low Back Pain Multiple Sclerosis Osteoarthritis Parkinson’s Disease Spinal Cord Injury Nutrition Gastroesophageal Reflux Disease Inflammatory Bowel Disease Metabolic Syndrome Malnutrition Obesity Perfusion

Acute Coronary Syndrome Atrial Fibrillation Cardiogenic Shock Endocarditis Heart Failure Hyperlipidemia Hypertension Hypovolemic Shock Mitral Valve Prolapse Peripheral Artery Disease Septic Shock Sickle Cell Disease Reproduction Early Pregnancy Loss Ectopic Pregnancy Infertility Sleep Insomnia Sleep Apnea Sensory Perception Cataracts Glaucoma Hearing Loss Macular Degeneration Otitis Media Sexuality Erectile Dysfunction Leiomyomas Menopause Sexually Transmitted Infection Thermoregulation Frostbite Heat Stroke Hyperthyroidism Tissue Integrity

Burns Pressure Injuries Wound Healing

Special Features Assessment Abnormalities Tables Auditory System, 21, p. 382 Breast, 50, p. 1184 Cardiovascular System, 31, p. 665 Endocrine System, 47, p. 1100 Female Reproductive System, 50, p. 1184 Fluid and Electrolyte Imbalances, 16, p. 290 Gastrointestinal System, 38, p. 841 Hematologic System, 29, p. 595 Integumentary System, 22, p. 404 Male Reproductive System, 50, p. 1185 Musculoskeletal System, 61, p. 1439 Nervous System, 55, p. 1294 Respiratory System, 25, p. 468 Urinary System, 44, p. 1016 Vascular Skin Lesions, 29, p. 597 Visual System, 20, p. 356

Case Studies

End-of-Chapter Case Studies Acute Respiratory Distress Syndrome, 67, p. 1603 Alzheimer’s Disease, 59, p. 1400 Benign Prostatic Hyperplasia With Acute Urinary Retention, 54, p. 1276 Breast Cancer, 51, p. 1209 Burn Injury, 24, p. 451 Chronic Kidney Disease, 46, p. 1085 Chronic Obstructive Pulmonary Disease, 28, p. 581 Cirrhosis of the Liver, 43, p. 1003 Colorectal Cancer, 42, p. 966 Critical Care and Mechanical Ventilation, 65, p. 1563 Diabetic-Related Ketoacidosis, 48, p. 1141 Dysrhythmia and Cardiac Arrest, 35, p. 775 Fluid and Electrolyte Imbalance, 16, p. 295 Glaucoma and Diabetic Retinopathy, 20, p. 373 Gonococcal and Chlamydial Infection, 52, p. 1226 Graves’ Disease, 49, p. 1169 Health Disparities, 2, p. 31 Heart Failure, 34, p. 752 HIV Infection, 14, p. 229 Inflammation and Infection, 11, p. 172 Insomnia, 7, p. 100 Intraoperative Patient, 18, p. 326 Laryngeal Cancer, 26, p. 499

Leukemia, 30, p. 652 Melanoma and Dysplastic Nevi, 23, p. 429 Ménière’s Disease, 21, p. 393 Metastatic Bone Tumor/Pathologic Fracture, 63, p. 1496 Myocardial Infarction, 33, p. 731 Obesity, 40, p. 886 Older Adults, 5, p. 74 Pain, 8, p. 125 Painful Bladder and Frequent Urination, 45, p. 1057 Patient and Caregiver Teaching, 4, p. 56 Peptic Ulcer Disease, 41, p. 921 Peripheral Artery Disease, 37, p. 824 Periprosthetic Hip Fracture and Revision Arthroplasty, 62, p. 1475 Pneumonia and Lung Cancer, 27, p. 538 Postoperative Patient, 19, p. 345 Preoperative Patient, 17, p. 311 Primary Hypertension, 32, p. 696 Rheumatoid Arthritis, 64, p. 1529 Seizure Disorder With Headache, 58, p. 1380 Shock, 66, p. 1586 Spinal Cord Injury, 60, p. 1426 Spiritual Distress at End of Life, 9, p. 140 Stress-Induced Illness, 6, p. 86 Stroke, 57, p. 1350 Substance Use Disorder, 10, p. 153

Trauma, 68, p. 1621 Traumatic Brain Injury, 56, p. 1327 Undernutrition, 39, p. 867 Uterine Fibroids and Endometrial Cancer, 53, p. 1251 Valvular Heart Disease, 36, p. 797

Managing Care of Multiple Patients Case Studies Care in Specialized Settings, Section 13, p. 1623 Perioperative Care, Section 4, p. 347 Problems of Ingestion, Digestion, Absorption, and Elimination, Section 9, p. 1006 Problems of Oxygenation: Perfusion, Section 8, p. 827 Problems of Oxygenation: Transport, Section 7, p. 655 Problems of Oxygenation: Ventilation, Section 6, p. 584 Problems of Urinary Function, Section 10, p. 1088 Problems Related to Altered Sensory Input, Section 5, p. 454 Problems Related to Comfort and Coping, Section 2, p. 155 Problems Related to Homeostsis and Protection, Section 3, p. 298 Problems Related to Movement and Coordination, Section 12, p. 1532 Problems Related to Regulatory and Reproductive Mechanisms, Section 11, p. 1278

Assessment Case Studies Auditory System, 21, p. 378 Cardiovascular System, 31, p. 661

Endocrine System, 47, p. 1096 Gastrointestinal System, 38, p. 835 Hematologic System, 29, p. 592 Integumentary System, 22, p. 398 Musculoskeletal System, 61, p. 1434 Nervous System, 55, p. 1288 Reproductive System, 50, p. 1178 Respiratory System, 25, p. 460 Urinary System, 44, p. 1012 Visual System, 20, p. 351

Complementary & Alternative Therapies Boxes Assessment of Use of Herbs and Dietary Supplements, 3, p. 35 Biofeedback, 45, p. 1046 Echinacea, 26, p. 482 Ginger, 41, p. 892 Herbal and Dietary Supplements That May Affect Clotting, 37, p. 818 Herbal Products and Surgery, 17, p. 302 Herbs and Supplements for Menopause, 53, p. 1235 Herbs and Supplements That May Affect Blood Glucose, 48, p. 1129 Lipid-Lowering Agents, 33, p. 705 Melatonin, 7, p. 94 Milk Thistle (Silymarin), 43, p. 974

Music Therapy, 18, p. 317 Supportive Care, 51, p. 1207 Tai Chi, 64, p. 1502 Yoga, 6, p. 82 Zinc, 26, p. 483

Diagnostic Studies Tables Auditory System, 21, p. 383 Cardiovascular System, 31, p. 669 Clotting Studies, 29, p. 599 Common Preoperative Diagnostic Studies, 17, p. 306 Complete Blood Count Studies, 29, p. 599 Electrographic Studies: Nervous System, 55, p. 1298 Fertility Studies, 50, p. 1188 Gastrointestinal System, 38, p. 842 Headaches, 58, p. 1355 Hematologic System, 29, p. 601 Integumentary System, 22, p. 406 Interventional Studies: Cardiovascular System, 31, p. 669 Interventional Studies, 50, p. 1186 Liver Function Tests, 38, p. 847 Miscellaneous Blood Studies, 29, p. 600 Musculoskeletal System, 61, p. 1440 Respiratory System, 25, p. 472 Radiologic Studies: Endocrine System, 47, p. 1106

Radiologic Studies: Male and Female Reproductive Systems, 50, p. 1186 Radiologic Studies: Nervous System, 55, p. 1296 Respiratory System, 25, p. 472 Serology and Urine Studies: Endocrine System, 47, p. 1102 Serology Studies: Cardiovascular System, 31, p. 668 Serology Studies: Male and Female Reproductive Systems, 50, p. 1185 Serology Studies: Musculoskeletal System, 61, p. 1440 Shock, 66, p. 1569 Sputum Studies, 25, p. 471 Stroke, 57, p. 1569 Urinary System, 44, p. 1019 VTE, 37, p. 816 Viral Hepatitis, 43, p. 973 Visual System, 20, p. 358

Drug Therapy Tables Acute and Chronic Glaucoma, 20, p. 371 Acute and Chronic Pancreatitis, 43, p. 995 Adjuncts to General Anesthesia, 18, p. 323 Adjuvant Drugs Used for Pain, 8, p. 116 Alzheimer’s Disease, 59, p. 1392 Androgen Deprivation Therapy for Prostate Cancer, 54, p. 1267 Anticoagulant Therapy, 37, p. 817 Antithrombotic Therapy for Atrial Fibrillation and Atrial Flutter, 35,

p. 764 Antidiarrheal Drugs, 42, p. 926 Antidysrhythmic Drugs, 35, p. 769 Antihypertensive Agents, 32, p. 687 Asthma and Chronic Obstructive Pulmonary Disease (COPD), 28, p. 551 Bacterial Community-Acquired Pneumonia, 27, p. 508 Breast Cancer, 51, p. 1203 Burns, 24, p. 444 Causes of Medication Errors by Older Adults, 5, p. 72 Chemotherapy, 15, p. 244 Chronic Stable Angina and Acute Coronary Syndrome, 33, p. 713 Cirrhosis, 43, p. 986 Combination Therapy for Hypertension, 32, p. 690 Common Bases for Topical Medications, 23, p. 425 Commonly Used Preoperative Medications, 17, p. 309 Constipation, 42, p. 931 Diseases/Disorders Treated With Corticosteroids, 49, p. 1167 Diuretic Agents, 32, p. 689 Drugs That May Cause Photosensitivity, 23, p. 410 Effects and Side Effects of Corticosteroids, 49, p. 1167 GERD and Peptic Ulcer Disease (PUD), 41, p. 899 General Anesthesia, 18, p. 322 Heart Failure, 34, p. 743 H. pylori Infection, 41, p. 908

Hematopoietic Growth Factors Used in Cancer Treatment, 15, p. 258 HIV Infection, 14, p. 221 Hormone Therapy, 15, p. 258 Hyperlipidemia, 33, p. 707 Immunosuppressive Therapy, 13, p. 207 Select Immunotherapies and Targeted Therapies, 15, p. 256 Infertility, 53, p. 1229 Inflammation and Healing, 11, p. 160 Inflammatory Bowel Disease, 42, p. 943 Insomnia, 7, p. 93 Insulin Regimens, 48, p. 1115 Latent Tuberculosis Infection Regimens, 27, p. 513 Leukemia, 30, p. 638 Managing Side Effects of Pain Medications, 8, p. 111 Medication Guidelines, 28, p. 566 Methods of Chemotherapy Administration, 15, p. 245 Multiple Sclerosis, 58, p. 1370 Nausea and Vomiting, 41, p. 891 Obesity, 40, p. 880 Opioid Analgesics, 8, p. 113 Oral Agents and Noninsulin Injectable Agents, 48, p. 1119 Osteoarthritis, 64, p. 1503 Parkinson’s Disease, 58, p. 1375 Pulmonary Hypertension, 27, p. 536 Quick Relief vs. Long-Term Control of Asthma, 28, p. 550

Replacement Factors for Hemophilia, 30, p. 627 Rheumatoid Arthritis, 64, p. 1510 Rhinitis and Sinusitis, 26, p. 481 Safe Medication Use by Older Adults, 5, p. 72 Seizure Disorder, 58, p. 1362 Selected Nonopioid Analgesics, 8, p. 111 Shock, 66, p. 1578 Smoking Cessation, 10, p. 146 Tuberculosis, 27, p. 512 Tuberculosis Treatment Regimens, 27, p. 512 Types of Insulin, 48, p. 1114 Viral Hepatitis B and C, 43, p. 975 Voiding Dysfunction, 45, p. 1050

Emergency Management Tables Abdominal Trauma, 42, p. 936 Acute Abdominal Pain, 42, p. 934 Acute GI Bleeding, 41, p. 919 Acute Soft Tissue Injury, 62, p. 1446 Acute Thyrotoxicosis, 49, p. 1155 Anaphylactic Shock, 13, p. 199 Chemical Burns, 24, p. 438 Chest Injuries, 27, p. 523 Chest Pain, 33, p. 723 Chest Trauma, 27, p. 523

Depressant Toxicity, 10, p. 149 Diabetes-Related Ketoacidosis, 48, p. 1132 Dysrhythmias, 35, p. 760 Electrical Burns, 24, p. 437 Emergency Management Tables, 68, p. 1606 Eye Injury, 20, p. 361 Fractured Extremity, 62, p. 1456 Head Injury, 56, p. 1315 Hyperthermia, 68, p. 1612 Hypoglycemia, 48, p. 1134 Hypothermia, 68, p. 1614 Inhalation Injury, 24, p. 437 Primary Survey, 68, p. 1608 Secondary Survey, 68, p. 1610 Sexual Assault, 53, p. 1250 Shock, 66, p. 1576 Spinal Cord Injury, 60, p. 1409 Stimulant Toxicity, 10, p. 148 Stroke, 57, p. 1340 Submersion Injuries, 68, p. 1616 Thermal Burns, 24, p. 436 Tonic-Clonic Seizures, 58, p. 1361

Ethical/Legal Dilemmas Boxes Advance Directives, 28, p. 576

Allocation of Resources, 46, p. 1081 Board of Nursing Disciplinary Action, 59, p. 1399 Brain Death, 56, p. 1316 Competence, 34, p. 751 Confidentiality and HIPAA, 52, p. 1225 Do Not Resuscitate, 36, p. 791 Durable Power of Attorney for Health Care, 48, p. 1140 End-of-Life Care, 9, p. 135 Entitlement to Treatment, 62, p. 1463 Visitation and Caregiver Presence in the Adult ICU, 65, p. 1537 Genetic Testing, 12, p. 181 Good Samaritan, 68, p. 1621 Health Disparities, 2, p. 18 Individual vs. Public Health Protection, 14, p. 223 Informed Consent, 17, p. 308 Medical Futility, 15, p. 264 Pain Management, 30, p. 619 Patient Adherence, 27, p. 513 Rationing, 43, p. 989 Religious Beliefs, 30, p. 647 Right to Refuse Treatment, 60, p. 1419 Scope and Standards of Practice, 35, p. 767 Social Networking: HIPAA Violation, 1, p. 13 Withdrawing Treatment, 46, p. 1085 Withholding Treatment, 56, p. 1323

Evidence-Based Practice Boxes Adherence to Tuberculosis Treatment Program, 27, p. 515 Condom Use and HIV, 14, p. 224 Early Mobilization and Critically Ill Patients, 65, p. 1562 Exercise and Hematologic Cancer, 30, p. 642 Exercise and Parkinson’s Disease, 58, p. 1374 HPV Vaccine and Young Males, 52, p. 1220 Interactive Self-Management and Diabetes, 48, p. 1127 Lifestyle Changes and Uncontrolled Hypertension, 32, p. 685 Music and Preoperative Anxiety, 17, p. 301 Obesity Interventions and Faith-Based Organizations, 40, p. 878 Pap Test and Cervical Cancer, 53, p. 1242 Participating in Cardiac Rehabilitation, 31, p. 730 Physical Activity and COPD, 28, p. 575 Preventing Recurrent Kidney Stones, 45, p. 1039 Probiotics and Constipation, 42, p. 931 Repositioning and Pressure Injuries, 11, p. 171 Screening and Testing of Hepatitis C, 43, p. 971 Tanning Booths and Skin Cancer, 23, p. 410 Treatment for Breast Cancer, 51, p. 1202 Virtual Reality Training and Stroke, 57, p. 1349

Focused Assessment Boxes Auditory System, 21, p. 381 Cardiovascular System, 31, p. 667

Endocrine System, 47, p. 1101 Gastrointestinal System, 38, p. 840 Hematologic System, 29, p. 598 Integumentary System, 22, p. 403 Musculoskeletal System, 61, p. 1438 Nervous System, 55, p. 1294 Reproductive System, 50, p. 1183 Respiratory System, 25, p. 467 Urinary System, 44, p. 1016 Visual System, 20, p. 355

Gender Differences Boxes Alzheimer’s Disease and Dementia, 59, p. 1386 Asthma, 28, p. 542 Cancer, 15, p. 233 Cholelithiasis, 43, p. 999 COPD, 28, p. 560 Coronary Artery Disease and Acute Coronary Syndrome, 33, p. 701 Effects of Aging on Sexual Function, 50, p. 1178 Endocrine Problems, 49, p. 1150 Gout, 64, p. 1513 Headaches, 58, p. 1353 Heart Failure, 34, p. 736 Hernia, 42, p. 959 Hypertension, 32, p. 679

Irritable Bowel Syndrome (IBS), 42, p. 937 Lung Cancer, 27, p. 517 Older Adults, 5, p. 62 Osteoarthritis (OA), 64, p. 1500 Osteoporosis, 63, p. 1493 Pain, 8, p. 103 Sexually Transmitted Infections, 52, p. 1216 Urinary Incontinence, 45, p. 1046 Urinary Tract Stones, 45, p. 1035 Vascular Disorders, 37, p. 801

Genetics In Clinical Practice Boxes α1-Antitrypsin Deficiency (AATD), 28, p. 561 Alzheimer’s Disease (AD), 59, p. 1387 Ankylosing Spondylitis, 64, p. 1517 Breast Cancer, 51, p. 1195 Cystic Fibrosis (CF), 28, p. 577 Duchenne and Becker Muscular Dystrophy (MD), 63, p. 1484 Familial Adenomatous Polyposis (FAP), 42, p. 948 Familial Hypercholesterolemia, 33, p. 701 Genetic Information Nondiscrimination Act (GINA), 12, p. 181 Genetics in Clinical Practice Boxes Throughout Book, 12, p. 180 Hemochromatosis, 30, p. 620 Hemophilia A and B, 30, p. 626 Hereditary Nonpolyposis Colorectal Cancer (HNPCC) or Lynch

Syndrome, 42, p. 949 Huntington’s Disease (HD), 58, p. 1380 Ovarian Cancer, 53, p. 1244 Polycystic Kidney Disease (PKD), 45, p. 1042 Sickle Cell Disease, 30, p. 616 Types 1 and 2 Diabetes Mellitus and MODY, 48, p. 1110

Gerontologic Assessment Differences Tables Adaptations in Physical Assessment Techniques, 3, p. 41 Auditory System, 21, p. 378 Cardiovascular System, 31, p. 661 Cognitive Function, 5, p. 63 Effects of Aging on Hematologic Studies, 29, p. 591 Effects of Aging on the Immune System, 13, p. 194 Endocrine System, 47, p. 1095 Gastrointestinal System, 38, p. 835 Integumentary System, 22, p. 398 Musculoskeletal System, 61, p. 1434 Nervous System, 55, p. 1287 Reproductive Systems, 50, p. 1178 Respiratory System, 25, p. 460 Summary of Tables, 5, p. 63 Urinary System, 44, p. 1012 Visual System, 20, p. 352

Health History Tables Auditory System, 21, p. 379 Cardiovascular System, 31, p. 663 Endocrine System, 47, p. 1097 Functional Health Pattern Format, 3, p. 37 Gastrointestinal System, 38, p. 836 Hematologic System, 29, p. 593 Integumentary System, 22, p. 399 Musculoskeletal System, 61, p. 1435 Nervous System, 55, p. 1289 Reproductive System, 50, p. 1180 Respiratory System, 25, p. 461 Urinary System, 44, p. 1013 Visual System, 20, p. 353

Informatics in Practice Boxes Chest Drainage System, 27, p. 527 Communication Devices for Patient With Laryngectomy, 26, p. 497 Computer Monitoring of Antibiotic Safety, 46, p. 1065 Computer-Based Timing for Antibiotic Administration, 17, p. 309 Digital Images, 11, p. 171 Discharge Teaching, 19, p. 344 E-Mail and Texting for COPD Patients, 28, p. 574 Heart Surgery Videos, 36, p. 793 Home Monitoring of Asthma, 28, p. 559

Importing Monitor and Ventilator Data, 65, p. 1557 Managing Cancer Patients’ Symptoms, 15, p. 246 Monitoring Blood Pressure, 32, p. 694 Older Adults and Internet Use, 5, p. 64 Patient Teaching Using Smart Phone Apps, 48, p. 1129 Respiratory Monitoring, 19, p. 335 Sleep Apnea Diagnosis and Monitoring, 7, p. 96 Smart Infusion Pumps, 65, p. 1538 Social Media Use for Patients With Migraine Headaches, 58, p. 1355 Staff Training Using Gaming, 24, p. 440 Use of Smart Phone for Weight Loss, 40, p. 884 Use of Internet and Mobile Devices to Manage HIV, 14, p. 225 Use of Translation Applications, 2, p. 30 Using the Internet to Access Information on Unfamiliar Diseases, 30, p. 612 Video Games for Stroke Recovery, 57, p. 1348 Voice Banking Applications For ALS, 58, p. 1379 Web-Based Knee and Hip Replacement Community, 62, p. 1473 Wireless ECG Monitoring, 35, p. 757

Interprofessional Care Tables Abnormal Uterine Bleeding, 53, p. 1233 Acute Kidney Injury, 46, p. 1063 Acute Pancreatitis, 43, p. 994 Acute Pericarditis, 36, p. 784

Acute Pulmonary Embolism, 27, p. 533 Acute Pyelonephritis, 45, p. 1029 Acute Respiratory Distress Syndrome, 67, p. 1601 Acute Respiratory Failure, 67, p. 1594 Acute Stroke, 57, p. 1338 Addison’s Disease, 49, p. 1166 Alzheimer’s Disease, 59, p. 1391 Amputation, 62, p. 1469 Aortic Dissection, 37, p. 812 Asthma, 28, p. 546 Bacterial Meningitis, 56, p. 1325 Benign Prostatic Hyperplasia, 54, p. 1256 Bladder Cancer, 45, p. 1045 Breast Cancer, 51, p. 1199 Burn Injury, 24, p. 441 Cardiomyopathy, 36, p. 794 Cataract, 20, p. 365 Cervical Cord Injury, 60, p. 1410 Chlamydial Infections, 52, p. 1214 Cholelithiasis and Acute Cholecystitis, 43, p. 1000 Chronic Kidney Disease, 46, p. 1070 Chronic Obstructive Pulmonary Disease (COPD), 28, p. 565 Chronic Otitis Media, 21, p. 385 Cirrhosis of the Liver, 43, p. 985 Colorectal Cancer, 42, p. 950

Cor Pulmonale, 27, p. 536 Cushing Syndrome, 49, p. 1163 Diabetes, 48, p. 1113 Diabetes-Related Ketoacidosis (DKA) and Hyperosmolar Hyperglycemia Syndrome (HHS), 48, p. 1132 Diverticulosis and Diverticulitis, 42, p. 958 Endometriosis, 53, p. 1239 Erectile Dysfunction, 54, p. 1274 Esophageal Cancer, 41, p. 901 Fractures, 62, p. 1452 GERD and Hiatal Hernia, 41, p. 897 Genital Herpes, 52, p. 1218 Glaucoma, 20, p. 370 Gonococcal Infections, 52, p. 1216 Gout, 64, p. 1515 Head and Neck Cancer, 26, p. 494 Headaches, 58, p. 1354 Heart Failure, 34, p. 742 Hypertension, 32, p. 685 Hyperthyroidism, 49, p. 1152 Hypothyroidism, 49, p. 1157 Increased Intracranial Pressure, 56, p. 1304 Infertility, 53, p. 1229 Inflammatory Bowel Disease, 42, p. 942 Insomnia, 7, p. 92

Intervertebral Disc Disease, 63, p. 1487 Iron-Deficiency Anemia, 30, p. 611 Lung Cancer, 27, p. 519 Ménière’s Disease, 21, p. 387 Multiple Sclerosis, 58, p. 1369 Myasthenia Gravis, 58, p. 1378 Neurogenic Bladder, 60, p. 1416 Neutropenia, 30, p. 632 Obesity, 40, p. 877 Oral Cancer, 41, p. 895 Osteoarthritis, 64, p. 1502 Osteoporosis, 63, p. 1494 Otosclerosis, 21, p. 386 Ovarian Cancer, 53, p. 1244 Parkinson’s Disease, 58, p. 1374 Peptic Ulcer Disease, 41, p. 907 Peripheral Artery Disease, 37, p. 802 Peritonitis, 42, p. 938 Pneumonia, 27, p. 507 Premenstrual Syndrome (PMS), 53, p. 1231 Prostate Cancer, 54, p. 1265 Pulmonary Tuberculosis, 27, p. 512 Renal Cancer, 45, p. 1043 Retinal Detachment, 20, p. 367 Rheumatic Fever, 36, p. 786

Rheumatoid Arthritis, 64, p. 1508 Scleroderma, 64, p. 1524 Seizure Disorder, 58, p. 1360 Shock, 66, p. 1580 Stomach Cancer, 41, p. 912 Syphilis, 52, p. 1222 Systemic Lupus Erythematosus, 64, p. 1521 Thrombocytopenia, 30, p. 624 Trigeminal Neuralgia, 60, p. 1422 Urinary Tract Infection, 45, p. 1027 Valvular Heart Disease, 36, p. 790 Viral Hepatitis, 43, p. 974

Nursing Assessment Tables Acute Coronary Syndrome, 33, p. 725 Acute Pancreatitis, 43, p. 995 Acute Respiratory Failure, 67, p. 1593 Allergies, 13, p. 198 Alzheimer’s Disease, 59, p. 1393 Anemia, 30, p. 609 Assessment Techniques: Visual System, 20, p. 355 Assessment Variations in Light- and Dark-Skinned Persons, 22, p. 405 Asthma, 28, p. 556 Benign Prostatic Hyperplasia, 54, p. 1260

Breast Cancer, 51, p. 1205 Care of Patient on Admission to Clinical Unit, 19, p. 343 Cholecystitis or Cholelithiasis, 43, p. 1002 Chronic Obstructive Pulmonary Disease, 28, p. 573 Cirrhosis, 43, p. 987 Colorectal Cancer, 42, p. 951 Constipation, 42, p. 932 Cushing Syndrome, 49, p. 1164 Cystic Fibrosis, 28, p. 580 Diabetes, 48, p. 1125 Diarrhea, 42, p. 927 Fracture, 62, p. 1456 Head and Neck Cancer, 26, p. 496 Head Injury, 56, p. 1316 Headaches, 58, p. 1357 Heart Failure, 34, p. 747 Hepatitis, 43, p. 976 HIV-Infected Patient, 14, p. 223 Hypertension, 32, p. 692 Hyperthyroidism, 49, p. 1154 Infective Endocarditis, 36, p. 781 Inflammatory Bowel Disease, 42, p. 944 Leukemia, 30, p. 639 Low Back Pain, 63, p. 1485 Lung Cancer, 27, p. 521

Malnutrition, 39, p. 855 Multiple Sclerosis, 58, p. 1371 Nausea and Vomiting, 41, p. 892 Oral Cancer, 41, p. 895 Osteomyelitis, 63, p. 1480 Pain, 8, p. 108 Parkinson’s Disease, 58, p. 1376 Patients With Obesity, 40, p. 874 Pelvic Inflammatory Disease (PID), 53, p. 1238 Peptic Ulcer Disease, 41, p. 909 Peripheral Artery Disease, 37, p. 805 Pneumonia, 27, p. 508 Pressure Injuries, 11, p. 170 Prostate Cancer, 54, p. 1268 Rheumatic Fever and Rheumatic Heart Disease, 36, p. 787 Rheumatoid Arthritis, 64, p. 1511 Seizure Disorder, 58, p. 1363 STIs, 52, p. 1223 Sleep, 7, p. 94 Spinal Cord Injury, 60, p. 1410 Stroke, 57, p. 1342 Systemic Lupus Erythematosus, 64, p. 1522 Thrombocytopenia, 30, p. 625 Upper GI Bleeding, 41, p. 919 Urinary Tract Stones, 45, p. 1039

Urinary Tract Infection, 45, p. 1027 Valvular Heart Disease, 36, p. 793 VTE, 37, p. 819

Nursing Management Boxes Assessment and Data Collection, 3, p. 34 Assisting With Cardioversion, 35, p. 770 Blood Transfusions, 30, p. 649 Care of the Hospitalized Older Adult, 5, p. 70 Care of the Patient After Pituitary Surgery, 49, p. 1146 Care of the Patient Undergoing Bariatric Surgery, 40, p. 883 Care of the Patient Undergoing Cardiac Catheterization, 31, p. 673 Care of the Patient Undergoing Liver Biopsy, 38, p. 847 Care of the Patient Undergoing Paracentesis, 43, p. 988 Care of the Patient With a Urethral Catheter, 45, p. 1052 Caring for the Patient With Incontinence, 45, p. 1050 Caring for the Patient Requiring Mechanical Ventilation, 65, p. 1560 Caring for the Patient With a Cast or Traction, 62, p. 1457 Caring for the Patient With Alzheimer’s Disease, 59, p. 1395 Caring for the Patient With an Acute Stroke, 57, p. 1344 Caring for the Patient With Chronic Venous Insufficiency, 37, p. 824 Caring for the Patient With Diabetes, 48, p. 1128 Caring for the Patient With Hypertension, 32, p. 693 Caring for the Patient With Neutropenia, 30, p. 633 Caring for the Patient With Osteomyelitis, 63, p. 1481

Caring for the Patient With Rheumatoid Arthritis, 64, p. 1512 Caring for the Patient With Seizure Disorder, 58, p. 1364 Caring for the Patient With Venous Thromboembolism (VTE), 37, p. 821 Caring for the Postoperative Patient, 19, p. 331 Decreasing Enteral Feeding Misconnections, 39, p. 863 EN, 39, p. 862 EN Problems, 39, p. 862 Elder Mistreatment, 5, p. 67 Fluid Volumes Changes, 16, p. 275 Interventions to Promote Health Equity, 2, p. 29 IV Therapy, 16, p. 292 Ostomy Care, 42, p. 955 Oxygen Administration, 28, p. 567 Pain Management, 8, p. 122 PN Parenteral Nutrition Infusions, 39, p. 865 Patient Receiving Bladder Irrigation, 54, p. 1261 Patients Receiving Anticoagulants, 37, p. 820 Percutaneous Coronary Intervention, 33, p. 715 Physical Care at End of Life, 9, p. 138 Postmortem Care, 9, p. 139 Problems Caused by Chemotherapy and Radiation Therapy, 15, p. 249 Psychosocial Care at End of Life, 9, p. 136 Skin Conditions, 23, p. 426 Suctioning and Tracheostomy Care, 26, p. 493

Tracheostomies, 26, p. 489 Troubleshooting Pacemakers, 35, p. 774 Wound Care, 11, p. 166

Nutritional Therapy Tables 1200-Calorie–Restricted Weight Reduction Diet, 40, p. 877 Celiac Disease, 42, p. 961 Chronic Kidney Disease, 46, p. 1072 Effects of Food on Stoma Output, 42, p. 956 Foods High in Iron, 39, p. 851 Foods High in Protein, 39, p. 850 High-Calorie Foods, 15, p. 260 High-Calorie, High-Protein Diet, 39, p. 858 High-Fiber Foods, 42, p. 932 High-Potassium Foods, 16, p. 280 Low-Sodium Diets, 34, p. 747 Maximizing Food Intake in COPD, 28, p. 572 MyPlate Tips for a Healthy Lifestyle, 39, p. 857 Nutrients for Erythropoiesis, 30, p. 610 Postgastrectomy Dumping Syndrome, 41, p. 915 Protein Foods With High Biologic Value, 15, p. 260 Sources of Calcium, 63, p. 1494 Therapeutic Lifestyle Changes to Diet, 33, p. 705 Tips to Make Diet and Lifestyle Changes, 33, p. 705 Urinary Tract Stones, 45, p. 1039

Patient & Caregiver Teaching Tables Addison’s Disease, 49, p. 1166 After Ear Surgery, 21, p. 385 After Eye Surgery, 20, p. 366 Anticoagulant Therapy, 37, p. 821 Antiretroviral Drugs, 14, p. 227 Asthma, 28, p. 559 Automatic Epinephrine Injectors, 13, p. 200 Autonomic Dysreflexia, 60, p. 1415 Avoiding Allergens in Allergic Rhinitis, 26, p. 480 Bowel Management After Spinal Cord Injury, 60, p. 1417 Cancer Survivors, 15, p. 265 Cardiomyopathy, 36, p. 797 Cast Care, 62, p. 1458 Characteristics of Menstruation, 50, p. 1177 Chronic Kidney Disease, 46, p. 1073 Chronic Obstructive Pulmonary Disease, 28, p. 574 Cirrhosis, 43, p. 989 Constipation, 42, p. 933 Corticosteroid Therapy, 49, p. 1168 Decrease Risk for Antibiotic-Resistant Infection, 14, p. 215 Early Warning Signs of Alzheimer’s Disease, 59, p. 1389 Effective Huff Coughing, 28, p. 571 Exercise for Patients With Diabetes, 48, p. 1123 FAST for Warning Signs of Stroke, 57, p. 1331

FITT Activity Guidelines for CAD, Chronic Stable Angina, and ACS, 33, p. 704 Lower Extremity Amputation, 62, p. 1471 Foot Care, 48, p. 1139 GERD, 41, p. 898 Genetic Testing, 12, p. 183 Halo Vest Care, 60, p. 1412 Head Injury, 56, p. 1317 Headaches, 58, p. 1358 Heart Failure, 34, p. 749 Heat and Cold Therapy, 8, p. 121 Home Oxygen Use, 28, p. 570 How to Use a Dry Powder Inhaler (DPI), 28, p. 555 How to Use Your Peak Flow Meter, 28, p. 558 Hypertension, 32, p. 693 Hypothyroidism, 49, p. 1158 Ileal Conduit Appliances, 45, p. 1056 Implantable Cardioverter-Defibrillator (ICD), 35, p. 771 Improving Adherence to Antiretroviral Therapy, 14, p. 227 Instructions for Patients With Diabetes, 48, p. 1130 Preparing an Insulin Injection, 48, p. 1116 Joint Protection and Energy Conservation, 64, p. 1504 Low Back Problems, 63, p. 1485 Management of Diabetes, 48, p. 1130 Mitral Valve Prolapse, 36, p. 789

Neck Exercises, 63, p. 1489 Neutropenia, 30, p. 634 Ostomy Self-Care, 42, p. 955 Pacemaker, 35, p. 775 Pain Management, 8, p. 122 Pelvic Floor Muscle (Kegel) Exercises, 45, p. 1049 Peptic Ulcer Disease (PUD), 41, p. 910 Peripheral Artery Bypass Surgery, 37, p. 806 Posterior Hip Replacement, 62, p. 1465 Postoperative Laparoscopic Cholecystectomy, 43, p. 1003 Preoperative Preparation, 17, p. 307 Pressure Injury, 11, p. 172 Prevention and Early Treatment of Lyme Disease, 64, p. 1516 Prevention of External Otitis, 21, p. 384 Prevention of Food Poisoning, 41, p. 921 Prevention of Hypokalemia, 16, p. 281 Prevention of Musculoskeletal Problems in Older Adults, 62, p. 1445 Protection of Small Joints, 64, p. 1512 Pursed Lip Breathing (PLB), 28, p. 558 Radiation Skin Reactions, 15, p. 253 Reducing Barriers to Pain Management, 8, p. 123 Reducing Risk Factors for Coronary Artery Disease, 33, p. 704 Seizure Disorder, 58, p. 1365 Self-Monitoring of Blood Glucose (SMBG), 48, p. 1124 Sexual Activity after Acute Coronary Syndrome, 33, p. 729

Sexual Assault Prevention, 53, p. 1251 STIs, 52, p. 1224 Signs and Symptoms HIV-Infected Patients Need to Report, 14, p. 227 Skin Care After Spinal Cord Injury, 60, p. 1418 Sleep Hygiene, 7, p. 93 Smoking and Tobacco Use Cessation, 10, p. 145 Systemic Lupus Erythematosus, 64, p. 1522 Thrombocytopenia, 30, p. 626 Urinary Tract Infection, 45, p. 1028

Promoting Health E Alzheimer’s Disease, 59, p. 1386 Arthritis and Connective Tissue Disorders, 64, p. 1505 Blood Studies: Urinary System, 44, 1019 Brain Tumors, 56, p. 1318 Breast Cancer, 51, p. 1204 Cancer, 15, p. 265 Cancers of the Female Reproductive System, 53, p. 1241 Cancers of the Male Reproductive System, 54, p. 1263 Chronic Kidney Disease, 46, p. 1066 Colorectal Cancer, 42, p. 948 Coronary Artery Disease, 33, p. 700 Diabetes Mellitus, 48, p. 1108 Heart Failure, 34, p. 735

Hematologic Problems, 30, p. 607 Hypertension, 32, p. 679 Liver, Pancreas, and Gallbladder Disorders, 43, p. 980 Lung Cancer, 27, p. 518 Obesity, 40, p. 869 Obstructive Pulmonary Diseases, 28, p. 542 Oral, Pharyngeal, and Esophageal Problems, 41, p. 894 Osteoporosis, 63, p. 1492 Promoting Health Equity Boxes Throughout Book, 2, p. 19 Sexually Transmitted Infections, 52, p. 1213 Skin Problems, 23, p. 409 Stroke, 57, p. 1332 Tuberculosis, 27, p. 510 Urologic Disorders, 45, p. 1036 Visual Problems, 20, p. 389

Promoting Population Health Boxes Health Impact of Good Oral Hygiene, 41, p. 896 Health Impact of Maintaining a Healthy Weight, 40, p. 873 Health Impact of Regular Physical Activity, 62, p. 1446 Health Impact of a Well-Balanced Diet, 39, p. 850 Improving the Health and Well-Being of LGBTQ Persons, 2, p. 20 Preventing Diabetes, 48, p. 1126 Preventing Osteoarthritis, 64, p. 1504 Preventing Respiratory Diseases, 27, p. 503

Preventing Sexually Transmitted Infections, 52, p. 1224 Prevention and Detection of Chronic Kidney Disease, 46, p. 1073 Prevention and Early Detection of Cancer, 15, p. 239 Prevention and Early Detection of HIV, 14, p. 224 Promoting Health in Older Adults, 5, p. 70 Promoting Healthy Hearing, 21, p. 389 Reducing the Risk for Head Injuries, 56, 1316 Reducing the Risk for Musculoskeletal Injuries, 62, p. 1444 Responsible Eye Care, 20, p. 360 Strategies to Prevent Burn Injury, 24, p. 432 Stroke Prevention, 57, p. 1338

SECTION ONE

Concepts in Nursing Practice OUTLINE 1. Professional Nursing 2. Health Equity and Culturally Competent Care 3. Health History and Physical Examination 4. Patient and Caregiver Teaching 5. Chronic Illness and Older Adults

1

Professional Nursing Mariann M. Harding

LEARNING OUTCOMES 1. Describe professional nursing practice in terms of domain, definitions, and recipients of care. 2. Compare the different scopes of practice available to professional nurses. 3. Describe the role of critical thinking skills and using the nursing process to provide patient-centered care. 4. Apply the SBAR procedure and effective communication techniques in the clinical setting. 5. Explore the role of the professional nurse in delegating care to licensed practical/vocational nurses and unlicensed assistive personnel. 6. Discuss the role of integrating safety and quality improvement processes into nursing practice. 7. Evaluate the role of informatics and technology in nursing practice. 8. Apply concepts of evidence-based practice to nursing practice.

KEY TERMS

advanced practice registered nurse (APRN), p. 2 case management, p. 7 clinical pathways, p. 9 clinical reasoning, p. 8 critical thinking, p. 8 delegation, p. 9 electronic health records (EHRs), p. 13 evidence-based practice (EBP), p. 13 interprofessional team, p. 8 nursing, p. 2 nursing process, p. 4 SBAR (Situation-Background-Assessment-Recommendation), p. 9 serious reportable event (SRE), p. 10 telehealth, p. 8

Conceptual Focus Care Competencies Leadership Professional Identity Caring is the essence of nursing. Jean Watson http://evolve.elsevier.com/Lewis/medsurg/ This chapter presents an overview of professional nursing practice, discussing the wide variety of roles and responsibilities that nurses fulfill to meet society’s health care needs. This overview includes several key concepts that are part of competent nursing practice.

These include safety, quality, informatics, and collaboration.

Professional Nursing Practice Domain of Nursing Practice Nursing practice today consists of a wide variety of roles and responsibilities necessary to meet society’s health care needs. As a nurse, you are the frontline professional of health care (Fig. 1.1). You can practice in virtually all health care settings and communities. You have never been more important to health care than you are today. As a nurse, you (1) offer skilled care to those recuperating from illness or injury, (2) advocate for patients’ rights, (3) teach patients to manage their health, (4) support patients and their caregivers at critical times, and (5) help them navigate the complex health care system. Although many nurses work in acute care facilities, nurses also practice in longterm care, home care, community health, public health centers, schools, and ambulatory or outpatient clinics. Wherever you practice, recipients of your care include individuals, families, groups, or communities. The American Nurses Association (ANA) states that the authority for nursing practice is based on a contract with society that acknowledges professional rights and responsibilities, as well as mechanisms for public accountability.1 The knowledge and skills that make up nursing practice are based on society’s expectations and needs. Nursing practice continues to evolve according to society’s health care needs and as knowledge and technology expand. This chapter introduces concepts and factors that affect professional nursing practice.

FIG. 1.1 Nurses are frontline professionals of health care. (© Michael Jung/iStock/Thinkstock.)

Definitions of Nursing Well-known definitions of nursing show that the basic themes of health, illness, and caring have existed since Florence Nightingale described nursing. Following are 2 such examples:

• Nursing is putting the patient in the best condition for nature to act (Nightingale).2 • The nurse’s unique function is to aid patients, sick or well, in performing those activities contributing to health or its recovery (or to peaceful death) that they would perform unaided if they had the necessary strength, will, or knowledge —and to do this in such a way as to help them gain independence as rapidly as possible (Henderson).3 In 1980 the ANA defined nursing as “the diagnosis and treatment of human responses to actual and potential health problems.”1 In this context, your care of a person with a fractured hip would focus on the patient’s response to impaired mobility, pain, and loss of independence. The 2010 edition of the ANA’s Nursing: A Social Policy Statement provided a new definition of nursing that reflects the continuing evolution of nursing practice: Nursing is the protection, promotion, and optimization of health and abilities, prevention of illness and injury, alleviation of suffering through the diagnosis and treatment of human response, and advocacy in the care of individuals, families, communities, and populations.1

Nursing’s View of Humanity A person has physiologic (or biophysical), psychologic (or emotional), sociocultural (or interpersonal), spiritual, and environmental components or dimensions. In this book, we consider a person to be in constant interaction with a changing environment. A person is composed of interrelated dimensions and not separate entities. Thus a problem in 1 dimension may affect 1 or more of the other dimensions. A person’s behavior is meaningful and oriented toward fulfilling needs, coping with stress, and developing one’s self. However, at times a person needs help to meet these needs, cope successfully, or develop his or her unique potential.

Scope of Nursing Practice The essential core of nursing practice is to deliver holistic, patientcentered care. It includes assessment and evaluation, giving a variety of interventions, patient and family teaching, and being a member of the interprofessional health care team. The extent that nurses engage in their scope of practice depends on their educational preparation, experience, role, and state law. To enter practice, a nurse must complete an accredited program and pass an examination verifying that the nurse has the knowledge necessary to provide safe care. Entry-level nurses with associate or baccalaureate degrees are prepared to function as generalists. At this level, nurses provide direct health care and focus on ensuring coordinated and comprehensive care to patients in a variety of settings. Nurses work collaboratively with other health care providers to manage the needs of persons and groups. With experience and continued study, nurses may specialize in a specific practice area. Certification is a formal way for nurses to obtain professional recognition for having expertise in a specialty area. A variety of nursing organizations offer certification in nursing specialties.4 Certification usually requires a certain amount of clinical experience and successful completion of an examination. Recertification usually requires ongoing clinical experience and continuing education. Common nursing specialties include critical care, women’s health, geriatric, medical-surgical, perinatal, emergency, psychiatric/mental health, and community health nursing. Additional formal education and experience can prepare nurses for advanced practice. An advanced practice registered nurse (APRN) is a nurse educated at the master’s or doctoral level, with advanced education in pathophysiology, pharmacology, and health assessment and expertise in a specialized area of practice. APRNs include clinical nurse specialists, nurse practitioners, nurse midwives, and nurse anesthetists. APRNs play a vital role in the health care delivery system. In addition to managing and delivering direct patient care, APRNs have roles in leadership, quality improvement, evidencebased practice, and informatics.

The doctor of nursing practice (DNP) degree is a practice-focused terminal nursing degree. With raising the educational preparation for APRNs to the doctoral level, nursing is at the same level as other health professions that offer practice doctorates (e.g., pharmacy [PharmD], physical therapy [DPT]). Nurses with a research-focused doctorate (PhD) typically are used in health care settings as nurse faculty, clinical experts, researchers, and health care system executives.

Standards of Professional Nursing Practice To guide nurses in how to perform professionally, the ANA defined Standards of Professional Nursing Practice. There are 2 parts, Standards of Practice and Standards of Professional Performance.5 The Standards of Practice describe a competent level of nursing care, based on the nursing process. The Standards of Professional Performance describe behavioral competencies expected of a nurse. You are following the performance standards when you practice ethically and use evidence-based practice. Communicating effectively and staying competent in practice are important. You must be able to work in collaboration with other interprofessional team members, patients, and caregivers.

Influences on Professional Nursing Practice Expanding Knowledge and Technology Ever-changing technology and rapidly expanding clinical knowledge add to the complexity of health care. The increased treatment, diagnostic, and care options available are changing care delivery and extending patients’ lives. Discoveries in genetics are changing the way we think about diseases such as cancer and heart disease. For example, genetic information guides breast cancer screening. If a woman has cancer, this information allows for treatment and drug

therapy based on her genetic makeup. Ethical dilemmas and controversies arise about the use of new scientific knowledge and the disparities that exist in patients’ access to technologically advanced health care. Throughout this book, genetics, informatics, and ethical/legal boxes highlight expanding knowledge and technology’s impact on nursing practice.

Diverse Populations Patient populations are more diverse than ever. Americans are living longer, with the number of people with chronic illnesses and multiple co-morbidities increasing. Unlike those who receive acute, episodic care, patients with chronic illnesses have complex needs. They see different health care providers in various settings over an extended period. With care shifting from hospitals and nursing homes to managed care in the community, you need to be able to manage and coordinate care when patients are transitioning among different settings. At the same time, you will be caring for a more culturally and ethnically diverse population. When delivering care, you must consider the patient’s and caregiver’s cultural beliefs and values. Immigrants, particularly undocumented immigrants, often lack the resources necessary to access health care. Inability to pay for health care is related to a tendency to delay seeking care, resulting in illnesses that are more serious at the time of diagnosis. Boxes throughout this book emphasize the influence of such factors as gender, culture, and ethnicity on nursing practice.

Consumerism Health care is a consumer-focused business, and patients today are more involved in their health care. They want more control over their health care and expect high-quality, coordinated, and financially reasonable care. Health information is readily available. Many patients are very knowledgeable about their health and seek information about health problems and health care from media and

Internet sources. They gather information so that they can have a voice in making decisions about their health care. As a nurse, you must be able to help patients access, interpret, and use safe health care information (Fig. 1.2).

Health Care Financing High health care costs are a growing problem. There are many reasons for the continued increase in costs. These include the rising use of prescription medications, administrative costs, and new medical innovations and treatments.6 Many changes in health care systems that influence nursing care delivery are started by the government, employers, insurance companies, and regulating agencies. They are usually in effort to contain spending and provide more cost-effective health care. Historically, the most notable event related to reimbursement was the establishment of prospective payment systems in the Medicare program. With this system, payment for hospital services for Medicare patients are based on flat fees determined by the diseases and problems treated during the admission. For example, if a patient had a total knee replacement, the hospital receives a set sum of money, such as $45,000, for the patient’s care.

FIG. 1.2 The patient, family, and nurse collaborate as part of coordinating high-quality care. (© monkeybusinessimages/iStock/Thinkstock.)

Other health care systems followed by introducing managed care systems that use prospective payment as a means of offering costeffective health care delivery. In health maintenance organizations (HMOs) and preferred provider organizations (PPOs), charges are negotiated before the delivery of care using fixed reimbursement rates or capitation fees for medical care, hospitalization, and other health care services. Now, quality and performance initiatives are driving further changes in health care financing. Value-based purchasing programs base reimbursement to health care providers on their performance on certain quality measures. These quality measures include clinical outcomes, patient safety, patient satisfaction, and the provider’s adherence to evidence-based practice. Those who provide quality care at a lower cost may receive more payment.

As part of value-based purchasing, payment for care can be withheld if a patient experiences events such as developing a pressure injury during a hospital stay or having something happen that is considered preventable (e.g., a fall-related injury, having wrong-site surgery).7 This type of event is considered a serious reportable event (SRE). SREs are discussed later in this chapter on p. 10.

Health Policy Legislation has serious implications for health care delivery and nursing practice. The 2010 Patient Protection and Affordable Care Act (ACA) was the most important health care legislation since the creation of Medicare in 1965. The ACA triggered changes throughout the health care system. The ACA’s main goal was to increase access to health care. The ACA created new health care delivery and payment models that emphasized teamwork, care coordination, and quality care. The ACA encourages the creation of accountable care organizations (ACOs). ACOs are groups of physicians, hospitals, and other health care providers who unite to coordinate care for Medicare patients. The goal of an ACO is to ensure that patients, especially the chronically ill, get the right care at the right time, while avoiding duplicate services and preventing errors. As a nurse, you must take a leadership role in creating health care systems that provide safe, quality, patientcentered care.

Professional Nursing Organizations The ANA is the primary professional nursing organization. There are many professional specialty organizations, such as the American Association of Critical-Care Nurses (AACN), National Association of Orthopedic Nurses (NAON), and Oncology Nursing Society (ONS). Professional organizations play a role in promoting quality patient care and professional nursing practice. These roles include developing standards of practice and codes of ethics, supporting research, and lobbying for legislation and regulations. Major nursing organizations

promote research into the causes of errors, develop strategies to prevent future errors, and address nursing issues that affect the nurse’s ability to deliver patient care safely. Nurses join a professional organization to keep current in their practice and network with others who are interested in a specific practice area. A program that supports nurses is the American Nurses Credentialing Center’s Magnet Recognition Program. The Magnet program “recognizes health care organizations for quality patient care, nursing excellence and innovations in professional nursing practice.”8 Magnet designation shows a high quality of nursing care and achievement of a positive practice environment for nurses. Nurses who work in Magnet facilities have low turnover and burnout rates and more opportunities for professional and personal growth. This leads to better patient outcomes and greater career satisfaction.

Nursing Core Competencies Several high-profile reports over the past 20 years have highlighted problems with the quality of health care. One of these reports, The Future of Nursing: Leading Change, Advancing Health, acknowledged the link between professional nursing practice and health care delivery. The report discussed how health care providers, including nurses, were not being adequately prepared to provide the highest quality care possible. It recommended making changes so that nurses will have the skills to advance health care and play leadership roles in the health care system9 (Table 1.1). To address nursing’s role in solving these problems, the Robert Wood Johnson Foundation funded the Quality and Safety Education for Nurses (QSEN) Institute. QSEN has made a major contribution to nursing by defining specific competencies that nurses need to have to practice safely and effectively in today’s complex health care system. The rest of this chapter describes each of the 6 QSEN nursing core competencies and the knowledge, skills, and attitudes (KSAs) necessary in each area: (1) patient-centered care, (2) teamwork and collaboration, (3) safety, (4) quality improvement, (5) informatics, and

(6) evidence-based practice10 (Table 1.2). When you are licensed as a registered nurse, you accept responsibility to base your practice on these core competencies.

TABLE 1.1 Key Messages for the Future of

Nursing

• Nurses should practice to the full extent of their education and training. • Nurses should achieve high education and training through an improved education system that promotes seamless academic progression. • Nurses should be full partners with physicians and other health professionals in redesigning health care. • Effective workforce planning and policy making require better data collection and information infrastructure.

Source: IOM (now HMD) recommendations. Retrieved from www.thefutureofnursing.org/recommendations.

Patient-Centered Care Nurses have long shown that they deliver patient-centered care based on each patient’s unique needs and understanding of the patient’s preferences, values, and beliefs. Patient-centered care is interrelated with quality and safety. In a patient-centered care model, patients and caregivers seek and receive care from competent and knowledgeable health care professionals. In addition, patients and caregivers are involved in making decisions and coordinating care.

Nursing Process Nurses provide patient-centered care using an organizing framework called the nursing process. The nursing process is a problem-solving approach to the identification and treatment of patient problems that

is the foundation of nursing practice. The nursing process framework provides a structure for delivering nursing care and the knowledge, judgments, and actions that nurses use to achieve best patient outcomes. Once started, the nursing process is continuous and cyclic. The nursing process consists of 5 phases: assessment, diagnosis, planning, implementation, and evaluation (Fig. 1.3). There is a basic order to the nursing process, beginning with assessment. Assessment is the collection of subjective and objective patient information on which you will base your plan of care. Diagnosing is the act of analyzing the assessment data and making a judgment about the nature of the data. It includes your identifying nursing diagnoses or problems and collaborative problems. During planning, you use nursing diagnoses and problems to develop patient outcomes or goals and identify nursing interventions to accomplish the outcomes. Implementation is the activation of the plan with the use of nursing interventions. Evaluation is a continual activity. During evaluation you decide whether the patient outcomes have been met because of the nursing interventions. If the outcomes were not met, a review of the steps of the process is necessary to figure out why not. You may need to revise the assessment (data collection), nursing diagnoses, planning (determining patient outcomes), or implementation (nursing interventions).

Standard Nursing Terminologies The demands of the health care system challenge nursing to define its contribution to health care. The nursing profession can describe its unique role by answering questions such as: What do nurses do? How do they do it? How does it make a measurable difference in the health of those for whom they care? How are nursing’s contributions different from those of medicine? In response to these questions, nursing uses standard terminologies (also called classification systems or taxonomies) to define and evaluate nursing care. This promotes continuity of patient care and gives data showing nursing’s impact on patient outcomes. Instead of using a variety of words to describe the same patient problems and nursing

interventions, nurses use a common language to improve communication.

TABLE 1.2 QSEN Competencies

Source: QSEN competencies. Retrieved from www.qsen.org/competencies.

FIG. 1.3 Nursing process.

Standard languages are essential in exchanging information between different electronic records systems. The need for quality care makes it necessary to be able to share information in a meaningful way across care settings. Using the same language reduces ambiguity and confusion. For example, do the patient problems of pressure injury and skin breakdown mean the same thing? Does turning the patient every 2 hours mean the same thing as repositioning the patient every 2 hours? If you turn or reposition the patient every 2 hours, what is the result? Does placing the patient on a pressure-relieving mattress or a standard mattress change the results? When you use a standard language, each nurse reading and documenting in the electronic record understands the diagnosis, can provide the interventions, and can measure the outcome. The ANA recognizes several nursing and multidisciplinary languages. Three nursing languages focus on specific phases of the nursing process: (1) NANDA International (NANDA-I): Nursing Diagnoses, Definitions, and Classification; (2) the Nursing Outcomes Classification (NOC); and (3) the Nursing Interventions Classification (NIC). Two other nursing languages, each with their own nursing diagnoses, outcomes, and interventions, include the International

Classification of Nursing Practice (ICNP) and the Clinical Care Classification (CCC).

Nursing Diagnoses The ANA defines a nursing diagnosis as the nurse’s clinical judgment about the patient’s response to actual or potential health conditions or needs.11 You determine nursing diagnoses based on your analysis of the assessment data. Delivering care based on accurately identified nursing diagnoses results in more effective and safer patient care. They are the basis for selecting nursing interventions to achieve patient outcomes for which nursing is accountable. This book uses the ICNP nursing diagnosis terminology (see Appendix B).

Outcome Identification The next step is to create the framework for delivering care by identifying outcomes and goal indicators. After choosing an outcome, you need to identify short- and/or long-term measurable goals and then list the behaviors or observations you will use to determine if the goal was attained. By identifying the right outcomes and goals, you can measure and evaluate the impact of the interventions you provide as part of your nursing practice. They also guide the interprofessional team so that we are all working to achieve the same outcomes. The outcomes achieved by patients are the most important indicator of quality in health care.12

Nursing Interventions An intervention is “a single nursing action, treatment, procedure, activity, or service designed to achieve an outcome of a nursing or medical diagnosis for which the nurse is accountable.”13 This includes treatments that you perform in all settings and includes direct and indirect care. The ICNP includes more than 1100 interventions. That many interventions may seem overwhelming. You will discover the interventions you will use most often with your patient population. When planning care for a patient, choose specific interventions for the

patient based on the nursing diagnosis and desired patient outcomes. You make the crucial decision of when and which interventions to use for a specific patient and situation based on your knowledge of the patient and the patient’s condition.

Nursing Care Plans In any clinical setting, you are responsible for providing a custom plan of care that includes nursing diagnoses, outcomes, and interventions. In clinical practice, electronic care plans often follow a standard format that has been adapted for that specific setting. These plans are guides for routine nursing care. You customize each to your patient’s unique needs and problems. In nursing education, the nursing process is often documented differently from clinical practice. The nursing process is often recorded in nursing care plans similar to those found on the website for this book (http://evolve.elsevier.com/Lewis/medsurg). These nursing care plans are teaching and learning tools. You practice and learn the nursing process by collecting assessment data, identifying nursing diagnoses, and selecting patient outcomes and nursing interventions. You usually should give rationales for the selected interventions.;

Nursing Care Plan 1.1 Patient With Heart Failure∗

Nursing Diagnosis†∗ Impaired Gas Exchange Etiology: Increased preload, alveolar-capillary membrane changes Supporting data: Abnormal O2 saturation, hypoxemia, dyspnea, tachypnea, tachycardia, restlessness, patient’s statement, “I am

so short of breath”

Patient Goal Maintains adequate O2/CO2 exchange at the alveolar-capillary membrane to meet O2 needs of the body



This example presents 1 nursing diagnosis for heart failure. The complete nursing care plan for heart failure is available on http://evolve.elsevier.com/Lewis/medsurg. † Nursing diagnoses are listed in order of priority. The nursing care plans associated with this book list nursing diagnoses, in order of priority, based on the ICNP, along with outcomes and interventions (NCP 1.1). When you use these care

plans, you will need to customize the plan for your specific patient. You must use critical thinking to continually evaluate the situation and revise the nursing diagnoses, outcomes, and interventions to fit each patient’s unique care needs. Collaborative problems are certain physiologic complications that nurses must monitor to detect the onset of or changes in patient status.14 Nurses manage collaborative problems using physician and nurse prescribed interventions to prevent morbidity and mortality. You identify these risks during the diagnosis phase of the nursing process. Identifying collaborative problems requires knowledge of pathophysiology and possible complications of medical treatment. Collaborative problem statements are usually written as “potential complication: ______” or “PC: _____” without a related to statement. An example is “PC: pulmonary embolism.” A concept map is another method of recording a nursing care plan. A concept map records the nursing process in a visual diagram. The map displays patient problems and interventions and shows relationships among clinical data. Nurse educators use concept mapping to teach nursing process and care planning. There are various formats for concept maps. Conceptual care maps blend a concept map and a nursing care plan. On a conceptual care map, assessment data used to identify the patient’s primary health concern are centrally positioned. Diagnostic test data, treatments, and medications surround the assessment data. Positioned below are nursing diagnoses or problems that represent the patient’s responses to the health state. Listed with those are the supporting assessment data, outcomes, nursing interventions with rationales, and evaluation. After completing the map, you draw connections between identified relationships and concepts. A conceptual care map creator is available online on the website for this book. Concept maps for select case studies at the end of management chapters are available on the website at http://evolve.elsevier.com/Lewis/medsurg.

Continuum of Patient Care

Nursing is part of health care at all points along the patient care continuum. Depending on their health status, patients often move among a multitude of different health care settings. For example, a young man is in a trauma unit of an acute care hospital following a motor vehicle crash. After he is stable, he is transferred to a general medical-surgical unit and then to an acute rehabilitation facility. After rehabilitation is complete, he is discharged home to continue with outpatient rehabilitation, with follow-up by home health care nurses and care in an ambulatory clinic. Decisions about the best setting for obtaining health care often depend on the cost of care and the patient’s health care insurance plan and personal finances. Although the hospital is the mainstay for acute care interventions, community-based settings offer patients the opportunity to live or recover in settings that maximize their independence and preserve human dignity. Community-based health care settings include ambulatory care, transitional care, and long-term care. Transitional care settings provide care in between the acute care and the home or long-term care setting. Patients may receive transitional care at an acute rehabilitation facility after head trauma or a spinal cord injury. Long-term care refers to the care of patients for a period longer than 30 days. It may be needed for those who are severely developmentally disabled, who are mentally impaired, or who have physical deficits requiring continuous medical and nursing care (e.g., patients who are ventilator dependent or have Alzheimer’s disease). Long-term care facilities include skilled nursing facilities, assisted living facilities, and residential care facilities. There is a new emphasis on care coordination when patients transition between care settings. Transitions of care refer to patients moving among health care practitioners, settings, and home as their condition and care needs change.15 As a nurse, you are an essential part of care coordination by stressing actions that meet patients’ needs and facilitate safe, quality care. Collaborating with other members of the interprofessional team is critical. A lack of communication can result in an ineffective care transition, leading to drug errors and higher hospital readmission rates. For example, you are a nurse in

acute care admitting a long-term care patient who has been receiving propranolol 20 mg/5 mL twice a day. The admitting orders read “propranolol 20 mg/mL, give 5 mL twice a day.” You avert a potential drug error by using communication techniques to reconcile the difference.

Delivery of Nursing Care Nurses deliver patient-centered care in collaboration with the interprofessional health care team and within the framework of a care delivery model. A care delivery model outlines how responsibilities and authority are structured to carry out patient care.16 More positive care outcomes occur when the number and type of care providers match patient needs and there is a designated care coordinator. In acute care settings, 2 basic models are used: team care and total patient care. Team care models involve a group of providers who work together to deliver care. A professional nurse is usually the team leader. As team leader, you manage and coordinate care with others, such as licensed practical/vocational nurses (LPN/VNs) and unlicensed assistive personnel (UAP). You have accountability for the quality of care delivered by team members during a work period. In total patient care models, you are responsible for planning and providing all care. Other care models include case management and telehealth. Case management is “a collaborative process of assessment, planning, facilitation, care coordination, evaluation, and advocacy for options and services to meet an individual’s and family’s comprehensive health needs through communication and available resources to promote quality, cost-effective outcomes.”17 Although health care agencies implement case management in various ways, it involves managing the patient’s care with other interprofessional team members across multiple care settings and levels of care. A professional nurse often serves as the case manager. In this role, the nurse assesses the needs of patients and/or caregivers, coordinates services for them, makes appropriate referrals, and evaluates the

progress toward meeting care goals. For example, a nurse case manager in an outpatient clinic has been working for 3 months with an older male patient who has multiple co-morbidities, including severe coronary artery disease, diabetes, and osteoarthritis. After he is scheduled for a coronary artery bypass, the nurse manager coordinates his care with other members of the interprofessional team. She arranges his preoperative appointments and informs the other team members so that all health care providers understand the patient’s unique needs. After the patient has surgery, he develops a deep venous thrombosis in his leg. The case manager then works with the interprofessional team to evaluate the patient’s discharge needs and decide whether rehabilitation or home health care is necessary for the patient. With the patient and caregiver, the team decides to discharge the patient to a rehabilitation facility. The case manager helps with the transition, again coordinating care so that the providers at the rehabilitation facility are aware of the patient’s needs. Telehealth nursing is the delivery of health care and information through telecommunication technologies, including high-speed Internet, wireless, satellite, and video communications.18 Among the many uses of telehealth are triaging patients, monitoring patients with chronic or critical conditions, helping patients manage symptoms, providing patient and caregiver education and emotional support, and providing follow-up care. Telehealth can increase access to care. The nurse engaged in telehealth can assess the patient’s health status, deliver interventions, and evaluate the outcomes of nursing care while separated geographically from the patient (Fig. 1.4).

Critical Thinking Complex health care environments require that you use critical thinking and clinical reasoning skills to make decisions that lead to the best patient outcomes. Critical thinking, your ability to focus your thinking to get the results you need in various situations, has been described as knowing how to learn, be creative, generate ideas, make decisions, and solve problems.19

FIG. 1.4 An older adult performing remote blood pressure monitoring. From Cooper K, Gosnell K: Foundations of nursing, St Louis, 2015, Elsevier.

Critical thinking is not memorizing a list of facts or the steps of a procedure. Instead, it is the ability to make judgments and solve problems by making sense of information. Learning and using critical thinking is a continual process that occurs inside and outside of the clinical setting. Clinical reasoning is using critical thinking to examine and analyze patient care issues.19 It involves understanding the medical and nursing implications of a patient’s situation when making decisions about patient care. You use clinical reasoning when you identify a change in a patient’s status, consider the context and concerns of the patient and caregiver, and decide what to do about it. Given the complexity of patient care today, nurses need to learn and implement critical thinking and clinical reasoning skills before they gain those skills through experience in professional practice. Various experiences in nursing school offer opportunities for you to learn and make decisions about patient care. Various education activities,

including interactive case studies and simulation exercises, promote practice in critical thinking and clinical reasoning. Throughout this book, select boxes, case studies, and review questions promote your use of critical thinking and clinical reasoning skills.

Teamwork and Collaboration Interprofessional Team To deliver high-quality care, you need to have effective working relationships with members of the health care team. The interprofessional team is made up of providers from various disciplines, working together and sharing their expertise to provide customized care. It may consist of physicians, nurses, pharmacists, occupational and physical therapists, and others (Table 1.3). To be competent in interprofessional practice, you must collaborate in many ways by exchanging knowledge, sharing responsibility for problem solving, and making patient care decisions. You may be responsible for coordinating care among the team members, taking part in interprofessional team meetings or rounds, and making referrals when you need expertise in specialized areas to help the patient. To do so, you must be aware of the knowledge and skills of other team members and be able to communicate effectively with them.

TABLE 1.3 Interprofessional Team Members

Team Member Dentist Dietitian Occupational therapist (OT)

Description of Services Provided Provides preventive and restorative treatments for problems affecting the teeth and mouth Provides general nutrition services, including dietary consultation about health promotion or specialized diets May help patient with fine motor coordination, performing activities of daily living, cognitive-perceptual skills, sensory testing, and the construction or use of assistive or adaptive equipment

Pastoral care

Offers spiritual support and guidance to patients and caregivers

Pharmacist

Prepares medications and infusion products

Physical therapist (PT)

Works with patients on improving strength and endurance, gait training, transfer training, and developing a patient education program

Physician (medical doctor [MD])

Practices medicine and treats illness and injury by prescribing medication, performing diagnostic tests and evaluations, performing surgery, and providing other medical services and advice

Physician assistant

Conducts physical exams, diagnoses and treats illnesses, and counsels on preventive health care in collaboration with a physician

Respiratory therapist

May provide oxygen therapy in the home, give specialized respiratory treatments, and teach the patient or caregiver about the proper use of respiratory equipment Assists patients with developing coping skills, meeting caregiver concerns, securing adequate financial resources or housing, or making referrals to social service or volunteer agencies Focuses on treatment of speech defects and disorders, especially by using physical exercises to strengthen muscles used in speech, speech drills, and audiovisual aids that develop new speech habits

Social worker Speech pathologist

TABLE 1.4 Guidelines for Communicating Using

SBAR

Source: Institute for Health Care Improvement: SBAR technique for communication: A situational briefing model. Retrieved from www.ihi.org/resources/Pages/Tools/SBARTechniqueforCommunicationASituation To help you develop the competencies necessary to practice within an interprofessional clinical environment, you may take part in education activities with students from other disciplines. Throughout this book, case studies and review questions discuss the roles others have in managing patient care.

Coordinating Care Communication Effective communication is key to fostering teamwork and coordinating care. To provide safe, effective care, everyone involved in a patient’s care should understand the patient’s condition and needs. Unfortunately, many issues result from a breakdown in communication. Miscommunication often occurs during transitions of care. One structured model used to improve communication is the SBAR (Situation-Background-Assessment-Recommendation) technique (Table 1.4). This technique offers a way to talk about a patient’s condition among members of the health care team in a predictable, structured manner. Other ways to enhance communication during transitions include using bedside rounds, having standard processes for patient hand-offs, and conducting interprofessional rounds to identify risks and develop a plan for delivering care.

Clinical Pathways Clinical pathways, also known as care maps, are interprofessional care plans that outline the care and desired outcomes for a specific time period for patients with a specific diagnosis. Think of a clinical pathway as a road map the patient and health care team should follow. As the patient progresses along the road, the patient should receive specific care and accomplish specific goals. If a patient’s

progress differs from the planned path, a variance has occurred. A negative variance occurs when specific goals are not met. The nurse usually identifies when a negative variance is present and works with the interprofessional team to create a plan to address the issue.16 The exact content and format of clinical pathways vary among agencies and settings. Each agency usually develops its own pathways based on evidence-based practice guidelines. Common components include assessment guidelines, laboratory and diagnostic testing, medications, activity, diet, and teaching. In acute care, clinical pathways often describe which patient care components are needed at specific times (Fig. 1.5). The case types selected for this type of pathway are usually those that are high volume or high risk and predictable, such as myocardial infarction and surgical procedures (e.g., endoscopy, cholecystectomy, cataract surgery).

Delegation and Assignment As a registered nurse (RN), you will delegate nursing care and supervise those who are qualified to deliver care. Delegation allows a care provider to perform a specific nursing activity, skill, or procedure that is beyond their usual role.20 Delegating and assigning nursing activities is a process that, when used appropriately, results in safe, effective, and efficient patient care. Delegating can allow you more time to focus on complex patient care needs. Delegating care and supervising others will be one of your essential roles as a professional nurse. Delegation usually involves tasks and procedures that licensed practical/vocational nurses (LPN/VNs) and unlicensed assistive personnel (UAP) perform. Nursing interventions that require independent nursing knowledge, skill, or judgment (e.g., initial assessment, patient teaching, evaluating care) are your responsibility and cannot be delegated. State nurse practice acts and agency policies identify activities that you can delegate to LPN/VNs and UAP. You will use professional judgment to select which activities to delegate. Your decision will be based on the patient’s needs, the LPN/VN’s and UAP’s education and training, and the amount of supervision needed.

The most common delegated nursing actions occur during the implementation phase of the nursing process. For example, you can delegate measuring oral intake and urine output to UAP, but you use your nursing judgment to decide if the intake and output are adequate. The general guideline for LPN/VN practice is that they can function independently in a stable, routine situation. However, they must work under the direct supervision of a professional nurse in acute, unstable situations in which a patient’s condition can rapidly change. In most states, LPN/VNs may give medications, perform sterile procedures, and perform a wide variety of interventions planned by the RN. The procedure itself is not the issue when an RN is determining what to delegate. Rather, the stability of the patient determines whether it is appropriate for an RN to delegate a procedure to an LPN/VN. For example, the LPN/VN can change a dressing on an abdominal surgical wound, but the RN should do the first dressing change and wound assessment.

FIG. 1.5 Clinical pathway for endoscopy. From Arnold EC, Boggs KU: Interpersonal relationships, ed 6, St Louis, 2011, Mosby.

UAP hold many titles, including nurse aides, certified medication aides, nursing assistants, patient care assistants, or technicians. The activities UAP perform typically include obtaining routine vital signs on stable patients, feeding and helping patients at mealtimes, ambulating stable patients, and helping patients with bathing and hygiene. Delegation can occur among professional nurses. For example, if 1 RN has accountability for an outcome and asks another RN to perform a specific intervention related to that outcome, that is delegation. This type of delegation typically occurs when 1 RN leaves the unit/work area for a meal break. Assignment is different from delegation. The term assign is used when you direct an LPN/VN or UAP to do an activity or procedure that is part of their everyday job.20 An assignment must be within the authorized scope of practice of the LPN/VN or part of the routine function of the UAP. For example, you can assign an LPN/VN to give

medications to a patient, because this is within the LPN/VN’s scope of practice. You cannot assign an LPN/VN to a patient who needs an admission assessment because an RN must perform the initial patient assessment. Whether you delegate or are working with staff to whom you assign tasks, you are responsible for the patient’s total care during your work period. You need to decide what patient care tasks must be carried out during the given period, identify who will do them, and prioritize the order in which the tasks must be completed. You are responsible for supervising UAP or LPN/VNs. Clearly communicate the tasks that must be done and give necessary guidance. Because you are accountable for ensuring that delegated tasks are completed in a competent manner, evaluate the care given, follow up as needed, and make sure no care was missed. Delegation is a skill that is learned, and you must practice to be proficient in managing patient care. You need to use critical thinking and professional judgment to ensure that you follow the 5 Rights of Delegation (Table 1.5). To help you, information on delegation is presented in the nursing management tables and case study questions at the end of the management chapters.

Safety It is estimated that about 250,000 patients each year die because of preventable medical errors.21 Several groups are addressing this issue by outlining safety goals for health care organizations and identifying safety competencies for health professionals. By implementing various procedures and systems that improve patient safety, health care systems are working to attain a culture that minimizes the risk of harm to the patient. Because of your closeness to patients, you are in a unique position to promote patient safety.

Serious Reportable Events The National Quality Forum (NQF) uses the term serious reportable

event (SRE), also called a never event, to describe serious, largely preventable, and harmful clinical events.22 The current list of SREs consists of 29 events. These events include such things as a patient acquiring a stage III or greater pressure injury while hospitalized and death or disability from a fall or hypoglycemia.

TABLE 1.5 5 Rights of Delegation

Source: National Guidelines for Nursing Delegation. Retrieved from www.ncsbn.org/1625.htm. To reduce the occurrence of SREs, the NQF has a list of effective Safe Practices that health care settings should use to provide safe patient care (www.qualityforum.org). You are implementing NQF practices when you perform a time-out before a surgical procedure, reconcile medication records, and implement interventions to prevent hospitalacquired infections, pressure injuries and falls.

National Patient Safety Goals The Joint Commission (TJC), the accrediting agency for health care organizations, gathers and reports data on serious errors they call sentinel events. A sentinel event is a patient safety event not related to the patient’s illness or underlying condition that reaches a patient and results in death, permanent harm, or severe temporary harm.23 Events are “sentinel” because they signal the need for immediate investigation and response. Many sentinel events are also serious reportable events. If the patient undergoes a wrong-site or wrongprocedure surgery, experiences an assault in the health care setting, or receives an incompatible blood product, the occurrence is both a sentinel event, reportable to TJC, and a serious reportable event, reportable to NQF. To address specific patient safety concerns, TJC issues National Patient Safety Goals (NPSGs).24 NPSGs promote patient safety by offering evidence-based solutions to common safety problems. The 2017 NPSGs are listed in Table 1.6. The latest safety goal, focusing on improving the safety of clinical alarm systems, greatly affects nursing. Patient monitoring systems provide vital information. Alarms that work well improve patient safety and care by telling you when a patient needs your attention. However, so many alarms can go off that alarm fatigue occurs, and nurses can become desensitized to the sounds. By better managing alarms, we reduce alarm fatigue and improve patient safety. Because you have the greatest amount of interaction with patients, you play a key role in promoting safety. Many describe nurses as the patient’s last line of defense. Every nurse has the responsibility to ensure the patient receives care in a manner that prevents errors and promotes patient safety. Throughout this book, safety alerts highlighting patient care issues and NPSGs will help you in learning to apply safety principles.

Quality Improvement

Quality care and safety are related: the higher the culture of safety, the better the quality of care. Health care systems focused on quality outcomes use practice standards and protocols based on best evidence while considering the patient’s unique preferences and needs. Your role is to coordinate the complex aspects of patient care, including the care delivered by others, and identify and correct issues associated with poor quality and unsafe care. Quality improvement (QI) programs involve systematic actions that monitor, assess, and improve health care quality. QI is an interprofessional team effort that is required by accrediting agencies. As part of professional nursing practice, you need to be able to collect data using QI tools, implement interventions to improve quality of care, and monitor patient outcomes. Several public and private groups focusing on improving health care quality have developed standard QI measures. These performance measures assess how well the health care team cares for a patient with a certain condition or receives a specific treatment. They describe what data the team must collect and monitor. Fig 1.6 shows an example of a QI system for adult patients with asthma. In this example, you would review patient medical records to decide if the rate of flu vaccine administration exceeds 90%. You would share the results with the team and, if the identified standard was not met, work as a team to implement measures to correct the deficiency.

TABLE 1.6 National Patient Safety Goals

Adapted from The Joint Commission (TJC): 2016 National patient safety goals, Oakbrook Terrace, IL. Retrieved from www.jointcommission.org/assets/1/6/2017_NPSG_HAP_ER.pdf.

FIG. 1.6 Quality improvement system. Adapted from Courtlandt CD, Noonan L, Leonard GF: Model for improvement—Part 1: A framework for health care quality, Pediatr Clin North Am 56:757, 2009.

National Database of Nursing Quality Indicators

The National Database of Nursing Quality Indicators (NDNQI) provides data on nursing-sensitive measures to evaluate the impact of nursing care on patient outcomes. Patient outcomes are nursing sensitive if they improve with a greater quantity or quality of nursing care. NDNQI outcomes are unique because they identify how nursing workforce factors, including nurse staffing and skill mix, directly influence patient outcomes. NDNQI data show the incidence of falls and health care–associated pressure injuries and infections decreases with adequate staffing and increased nurse education and satisfaction with the work environment. Table 1.7 lists the current NDNQI.

Informatics Nursing is an information-intense profession. Advances in informatics and technology have changed the way nurses plan, deliver, document, and evaluate care. All nurses, regardless of their setting or role, use informatics and technology every day in practice. Informatics has changed how you obtain and review diagnostic information, make clinical decisions, communicate with patients and health care team members, document, and provide care. Technology advances have increased the efficiency of nursing care, improving the work environment and the care nurses provide. Computers and mobile devices allow you to document at the time you deliver care and give you quick and easy access to information, including clinical decision-making tools, patient education materials, and references. Texting, video chat, and e-mail enhance communication among health care team members and help you deliver the right message to the right person at the right time. Technology plays a key role in providing safe, quality patient care. Medication administration applications improve patient safety by flagging potential errors, such as look-alike and sound-alike medications and adverse drug interactions, before they can occur. Computerized provider order entry (CPOE) systems can reduce errors caused by misreading or misinterpreting handwritten orders. Sensor technology can decrease the number of falls in high-risk patients. Care

reminder systems give cues that decrease the amount of missed nursing care.

TABLE 1.7 National Database of Nursing Quality

Indicators • Structure indicators • RN turnover rate • Nursing hours per patient day • RN education and certification • Staff mix: RNs, LPN/VNs, UAP, agency staff • Process and outcome indicators • Patient falls and falls with injury • Pressure injury rate • RN surveys on job satisfaction and practice environment scale • Outcome indicators • Physical/sexual assault rate • Restraint use • Health care–associated infections (HAI) rate Source: National Database of Nursing Quality Indicators. Retrieved from www.nursingquality.org. Being able to use technology skills to communicate and access information is now an essential part of your professional nursing practice. You must be able to use word processing software, communicate by e-mail and book messaging, access information, and follow security and confidentiality rules. You need to have the ability to safely use patient care technologies and navigate electronic documentation systems. Protected health information (PHI) is highly sensitive. The Health

Insurance Portability and Accountability Act (HIPAA) is part of federal legislation that addresses actions for how PHI is used and disclosed. With the increased use of informatics and

Ethical/Legal Dilemmas Social Networking: HIPAA Violation

Situation You log into a closed group on a social networking site and read a posting from a fellow nursing student. The posting describes in detail the complex care the student gave to an older patient in a local hospital the previous day. The student comments on how stressful the day was and asks for advice on how to deal with similar patients in the future.

Ethical/Legal Points for Consideration • Protecting and maintaining patient privacy and confidentiality are basic obligations defined in the Code of Ethics for Nurses, which nurses and nursing students should uphold.1 • As outlined in the Health Insurance Portability and Accountability Act (HIPAA), a patient’s private health information is any information that relates to the person’s past, present, or future physical or mental health. This includes not only specific details such as a patient’s name or picture but also information that gives enough details that someone may be able to identify that person. • You may unintentionally breach privacy or confidentiality by posting patient information (diagnosis, condition, situation) on a social networking site. Using privacy settings or being in a closed group does not guarantee the secrecy of posted information. Others can copy and share any post without your knowledge. • Potential consequences for improperly using social networking

vary based on the situation. These may include (1) disciplinary action by the state board of nursing; (2) being disciplined, suspended, or fired by an employer; (3) dismissal from a nursing program; and (4) civil and/or criminal charges. • A student nurse who experienced a stressful day and is looking for advice and support from peers (e.g., “Today my patient died. I wanted to cry.”) could share the experience by clearly limiting the posts to the student’s personal perspective and not sharing any identifying information. This is 1 area in which it is safest to err on the side of caution to avoid the appearance of impropriety.

Discussion Questions 1. How would you deal with the situation involving the fellow nursing student? 2. How would you handle a situation in which you saw a staff member who violated HIPAA?

Reference 1. Code of Ethics for Nurses. Retrieved from www.nursingworld.org/DocumentVault/Ethics-1/Code-ofEthics-for-Nurses.html. technology come new concerns on how to comply with HIPAA regulations and maintain a patient’s privacy. Wireless technologies, increased use of e-mail and computer networking, and the ongoing threat of computer viruses increase the need for properly protecting a patient’s privacy. We must assure patients of their privacy and that only those with a right to know are accessing protected information.

FIG. 1.7 Members of the interprofessional team review a patient’s electronic health record. From Arnold EC, Boggs KU: Interpersonal relationships, ed 6, St Louis, 2011, Mosby.

As a nurse, you have an obligation to ensure the privacy of your patient’s health information. To do so, you need to understand your agency’s policies about the use of technology. You need to know the rules about accessing patient records and releasing PHI, what to do if information is accidentally or intentionally released, and how to protect any passwords you use. If you are using social networking, you must be careful not to place any individually identifiable PHI online. Throughout this book, Informatics in Practice boxes offer suggestions on how to use informatics in your practice.

Electronic Health Records The largest use of informatics is electronic health records (EHRs), also called electronic medical records. An EHR is a computerized record of patient information. It is shared among all health care team members

involved in a patient’s care and moves with the patient—to other providers and across care settings. The ideal EHR provides a single place for team members to review and update a patient’s health record, document care given, and enter patient care orders, including medications, procedures, diets, and diagnostic and laboratory tests (Fig. 1.7). Several obstacles are still in the way of fully implementing EHRs. Systems are technologically complex, requiring many resources and training to implement and maintain. Communication is still lacking among computer systems and software applications. Finally, perceived challenges in the use of EHRs, including increased workload and the need for workarounds, affect implementation.

Evidence-Based Practice Evidence-based practice (EBP) is a problem-solving approach to clinical decision making. Using the best available evidence (e.g., research findings, QI data), combined with your expertise and the patient’s unique circumstances and preferences, leads to better clinical decisions and improved patient outcomes. EBP closes the gap between research and practice, providing more reliable and predictable care than that based on tradition, opinion, and trial and error.

TABLE 1.8 Steps of Evidence-Based Practice (EBP)

Process 1. Ask the clinical question using the PICOT format: Patients/population Intervention Comparison or comparison group Outcome(s) Time (as applicable)

2. Search for the best evidence based on the clinical question. 3. Critically appraise and synthesize the evidence. 4. Implement the evidence in practice. 5. Evaluate the practice decision or change. 6. Share the outcomes of the decision or change. EBP does not mean that you conduct a research study. Instead, EBP depends on you to take an active role in using the best available evidence when delivering care. You need to have an ongoing curiosity about what are the best nursing practices and routinely ask questions about your patient’s care. Recognize when you need more information. When you base your practice on valid evidence, you are solving problems and supporting best patient outcomes.

Steps of EBP Process The EBP process has 6 steps (Table 1.8).

Step 1 Step 1 is asking a clinical question in the PICOT format. Developing the clinical question is the key step in the EBP process.25 A good clinical question sets the context for integrating evidence, clinical judgment, and patient preferences. In addition, the question guides the literature search for the best evidence to influence practice. An example of a clinical question in PICOT format is, “In adult abdominal surgery patients (P = patients/population) is splinting with an elasticized abdominal binder (I = intervention) or a pillow (C = comparison) more effective in reducing pain associated with ambulation (O = outcome) on the first postoperative day (T = time period)?” A clinical question may not have all components of PICOT. Some only include 4 components. The (T) timing or (C) comparison components are not appropriate for every question. The (C) component of PICOT may include a comparison with a specific intervention, the usual standard of care, or no intervention at all.

Step 2 Step 2 is searching for the best evidence that applies to the clinical question. Technology provides you with ready access to data. You can easily search several online resources and collect large amounts of clinical information and evidence. It is important to evaluate all data sources for their credibility and reliability. Not all evidence is equal. Fig. 1.8 presents the hierarchy of evidence. As you go down the pyramid, the strength of the evidence becomes weaker. Systematic reviews and evidence-based clinical practice guidelines save time and effort in the EBP process. However, they are available for only a limited number of clinical topics and may not suit all types of clinical questions. When insufficient research exists to guide practice, recommendations from expert panels and authority figures may be the best evidence available.

FIG. 1.8 Hierarchy of evidence. Modified from Melnyk BM, Fineout-Overholt E: Evidence-based practice in nursing and healthcare: A guide to best practice, ed 3, Philadelphia, 2014, Lippincott Williams & Wilkins.

Step 3 Step 3 is to critically appraise the evidence you found. A successful critical appraisal process focuses on 3 essential questions: (1) What are the results? (2) Are the results reliable and valid? and (3) Will the results help me in caring for my patients? You decide the strength of the evidence and synthesize the findings related to the clinical question to conclude what is the best practice. For example, you find

strong evidence supporting effectiveness of elasticized binders and pillows in reducing pain associated with ambulation. However, the binder appears to be more effective if the patient is obese or has had prior abdominal surgery.

Step 4 Step 4 involves implementing the evidence in practice. The decision to implement change is made by combining the evidence, clinical judgment, and preferences and values of patients and caregivers. You may be part of an interprofessional team charged with implementing a practice change or applying evidence in a specific patient care situation. This may include developing clinical practice guidelines, policies and procedures, or new assessment, teaching, or documentation tools. For example, you may be part of a team implementing a new postoperative protocol focused on using elasticized abdominal binders with patients who are obese or had prior abdominal surgery.

Step 5 Step 5 is evaluating the outcome of the practice change. After implementing the change for a specific period, you should monitor outcomes to determine whether the change has improved patient outcomes. Accrediting bodies require documentation of outcome measures to show that the organization is using evidence to improve patient care.

Step 6 Step 6 is sharing the results of the EBP change. If you do not share the outcomes of EBP, then other health care providers and patients cannot benefit from what you learned from your experience. You can share information locally using unit- or hospital-based newsletters and posters and regionally and nationally through journal publications and presentations at conferences.

Implementing EBP To implement EBP, you must develop the skills to be able to seek and incorporate into practice scientific evidence that supports best patient outcomes. Throughout this book, Evidence-Based Practice boxes provide an opportunity for you to practice your critical thinking skills in applying EBP to patient scenarios. To help you identify the use of evidence in this book, an asterisk (∗) in the reference list at the end of each chapter indicates evidence-based information for clinical practice.

Bridge to Nclex Examination The number of the question corresponds to the same-numbered outcome at the beginning of the chapter.

1. An example of a nursing activity that best reflects the American Nurses Association’s definition of nursing is a. treating dysrhythmias that occur in a patient in the coronary care unit. b. diagnosing a patient with a feeding tube as being at risk for aspiration. c. setting up protocols for treating patients in the emergency department. d. offering antianxiety drugs to a patient with a disturbed sleep pattern. 2. A nurse working on the medical-surgical unit at an urban hospital would like to become certified in medical-surgical nursing. The nurse knows that this process would most likely require a. a bachelor’s degree in nursing. b. formal education in advanced nursing practice.

c. experience for a specific period in medical-surgical nursing. d. membership in a medical-surgical nursing specialty organization. 3. The nurse is assigned to care for a newly admitted patient. Number in order the steps for using the nursing process to prioritize care. (Number 1 is the first step, and number 5 is the last step.) ___ Evaluate whether the plan was effective. ___ Identify any health problems. ___ Collect patient information. ___ Carry out the plan. ___ Decide a plan of action. 4. Using the SBAR format, number in order the steps for how the nurse would communicate information with the provider. (Number 1 is the first step, and number 4 is the last step.) ____ “I would like you to order an IV medication and come evaluate the patient as soon as possible.” ____ “This is Nurse M.H. I am calling from the unit because your patient, D.R., has a new onset of atrial fibrillation.” ____ “The atrial fibrillation started about 10 minutes ago. The heart rate is 124; BP 90/60. The patient is experiencing dizziness.” ____ “D.R., who is 2 days postoperative for a bowel resection for diverticulitis, has a history of mitral valve disease.”

5. The nurse is caring for a diabetic patient in the ambulatory surgical unit who has undergone wound debridement. Which task is appropriate for the nurse to delegate to unlicensed assistive personnel (UAP)? a. Check the patient’s vital signs. b. Assess the patient’s pain level. c. Palpate the patient’s pedal pulses. d. Monitor the patient’s IV catheter site. 6. The nurse’s role in addressing the National Patient Safety Goals established by The Joint Commission includes (select all that apply) a. answering all patient monitoring alarms promptly. b. memorizing all the rules published by The Joint Commission. c. obtaining a correct list of the patient’s medications on admission. d. encouraging patients to be actively involved in their own health care. e. using side rails and alarm systems as necessary to prevent patient falls. 7. Advantages of using informatics in health care delivery are (select all that apply) a. reduced need for nurses in acute care. b. increased patient anonymity and confidentiality. c. the ability to achieve and maintain high standards of care. d. access to standard plans of care for many health problems.

e. improved communication of the patient’s health status to the health care team. 8. When using evidence-based practice, the nurse a. must use clinical practice guidelines developed by national health agencies. b. should use findings from randomized controlled trials to plan care for all patient problems. c. uses clinical decision making and judgment to decide what evidence is appropriate for a specific clinical situation. d. analyzes the relationship of nursing interventions to patient outcomes to discover evidence for patient interventions. 1. b, 2. c, 3. 5, 2, 1, 4, 3, 4. 4, 1, 3, 2, 5. a, 6. a, c, e, 7. c, d, e, 8. c. For rationales to these answers and even more NCLEX review questions, visit http://evolve.elsevier.com/Lewis/medsurg.

Evolve Website/Resources List http://evolve.elsevier.com/Lewis/medsurg

Review Questions (Online Only) Key Points Answer Key for Questions • Rationales for Bridge to NCLEX Examination Questions Conceptual Care Map Creator Audio Glossary Content Updates

References 1. American Nurses Association: Nursing: A social policy statement, 3rd ed, Washington, DC, 2010, The Association. (Classic) 2. Nightingale F: Notes on nursing: What it is and what it is not (facsimile edition), Philadelphia, 1946, Lippincott. (Classic) 3. Henderson V: The nature of nursing, New York, 1966, Macmillan. (Classic) 4. American Nurses Credentialing Center. Certification. Retrieved from www.nursingworld.org/ancc/ 5. American Nurses Association. Nursing: Scope and standards of practice, Washington, DC, 2010, The Association. (Classic) 6. Thorpe KE The rise in health care spending and what to do about it, Health Affairs 24:1436, 2017. 7. Robert Wood Johnson Foundation. Achieving the potential of health care performance measures. Retrieved from www.rwjf.org. 8. ANCC Magnet Recognition Program. Retrieved from www.nursingworld.org/organizational-programs/magnet/. 9. Committee on the Robert Wood Johnson Foundation Initiative on the Future of Nursing at the Institute of Medicine. The future of nursing: Leading change, advancing health, Washington, DC, 2011, National Academies Press. (Classic) 10. QSEN Institute. Retrieved from http://qsen.org. 11. American Nurses Association: The nursing process. Retrieved from www.nursingworld.org/practicepolicy/workforce/what-is-nursing/the-nursing-process/. 12. Rabelo-Silva ER, Dantas Cavalcanti AC, Ramos MC,

et al: Advanced nursing process quality: Comparing the ICNP with the NANDA-International and Nursing Interventions Classification, J Clinical Nurs 26:379, 2017. 13. Clinical Care Classification. Nursing interventions. Retrieved from www.sabacare.com/framework/nursinginterventions/. 14. Carpenito LJ: Handbook of nursing diagnoses. 17th ed, Philadelphia, 2017, Lippincott Williams & Wilkins. 15. The Joint Commission: Transitions of care portal. Retrieved from www.jointcommission.org/toc.aspx. 16. Motacki K, Burke K. Nursing delegation and management of patient care. 2nd ed, St Louis, 2016, Elsevier. 17. What is a case manager? Retrieved from www.cmsa.org. 18. Zerwekh J, Garneau AZ. Nursing today: Transitions and trends, 9th ed, St Louis, 2017, Elsevier. 19. Alfaro-LeFevre R. Critical thinking, clinical reasoning, and clinical judgment, 6th ed, St Louis, 2017, Saunders. 20. Delegation. Retrieved from www.ncsbn.org/1625.htm. Makary MA, Daniel M: Medical error—The third leading cause of death in the US, BMJ 3:353, 2016.

22. Safe practices for better healthcare. Retrieved from www.qualityforum.org/Topics/Patient_Safety.aspx. 23. Sentinel events policy and procedures. Retrieved from www.jointcommission.org/sentinel_event_policy_and_procedures/ 24. National patient safety goals. Retrieved from www.jointcommission.org/standards_information/npsgs.aspx 25. Melnyk BM, Gallagher-Ford L, Fineout-Overholt E:

Implementing the evidence-based practice competencies in healthcare: A practical guide for improving quality, safety, and outcomes, Indianapolis, 2016, Sigma Theta Tau. Evidence-based information for clinical practice.

2

Health Equity and Culturally Competent Care Andrew Scanlon

LEARNING OUTCOMES 1. Identify the key determinants of health and equity. 2. Describe the factors that contribute to health disparities and health equity. 3. Define the terms culture, values, acculturation, ethnicity, race, stereotyping, ethnocentrism, cultural imposition, cultural competency, and culture-bound syndrome. 4. Explain how culture and ethnicity may affect a person’s physical and psychologic health. 5. Apply strategies for incorporating cultural information in the nursing process with all patients. 6. Describe the role of nursing in promoting health equity. 7. Examine ways that your own cultural background may influence nursing care. 8. Describe strategies for successfully communicating with a person who speaks a language that you do not understand.

KEY TERMS

acculturation, p. 21 cultural competence, p. 22 culture, p. 20 culture-bound syndromes, p. 27 determinants of health, p. 17 ethnicity, p. 18 ethnocentrism, p. 21 folk healers, p. 23 health disparities, p. 18 health equity, p. 18 health status, p. 17 lesbian, gay, bisexual, transgender, and queer or questioning (LGBTQ), p. 20 place, p. 19 race, p. 18 sexuality, p. 20 stereotyping, p. 21 transcultural nursing, p. 22 values, p. 20

Conceptual Focus Culture Health Disparities We may have different religions, different languages, different colored skin, but we all belong to one human race. We all share the same basic values.

Kofi Annan http://evolve.elsevier.com/Lewis/medsurg/ This chapter discusses health disparities and culture. Health is a cultural concept because culture frames and shapes our experiences. Cultural beliefs influence health promotion practices and attitudes about seeking health care. Cultural differences can lead to problems that decrease the chance of receiving equitable health care. Nurses play a key role in recognizing and reducing health disparities. Understanding the concept of culture is important in your ability to provide patient-centered care.

Determinants of Health Why are there differences in people’s health status? How do these differences occur? The determinants of health are factors that (1) influence the health of individuals and groups and (2) help explain why some people experience poorer health than others.1 Where people are born, grow up, live, work, and age helps determine their health status, behaviors, and care. Health status is a holistic concept that is more than the presence or absence of disease. It encompasses life expectancy as well as selfassessment of health. As such, many measures make up the concept of health status. For individuals, this means the sum of their current health problems plus their coping resources (e.g., family, financial resources). For a community, health status is the combination of health measures for all people living in the community. Community health measures include birth and death rates, life expectancy, access to care, and morbidity and mortality rates related to disease and injury. Factors in a person’s social and physical environment, including personal relationships, workplace, housing, transportation, and neighborhood violence, contribute to health status.1 For example, the risk of youth homicide is much higher in neighborhoods with gang activity and high crime rates. The physical environment in which one

lives, works, and plays may expose a person to such risks as environmental hazards (workplace injuries), toxic agents (chemical spills, industrial pollution), unsafe traffic patterns (lack of sidewalks), or absence of fresh and healthy food choices. A person’s behavior is influenced by his or her environment, education, and economic status. Behaviors such as tobacco and illicit drug use are strongly linked to many health conditions (e.g., lung cancer, liver disease). A person’s biologic makeup, such as genetics and family history of disease (e.g., heart disease), can increase the risk for specific diseases. The availability of health care also contributes to a person’s health. Though government initiatives are striving to reduce the number of uninsured Americans, millions remain uninsured and have limited access to care. This affects both individual and community health.

Health Disparities and Health Equity Health disparities are differences in the incidence, prevalence, mortality rate, and burden of diseases that exist among specific population groups. In the United States this is because of social, economic, or environmental disadvantages. Health disparities can affect population groups based on gender, age, ethnicity, socioeconomic status, education, location, sexual orientation, or disability status.2 Health equity is achieved when every person has the opportunity to attain his or her health potential, and no one is disadvantaged.

Ethical/Legal Dilemmas Health Disparities

Situation E.M., a 47-yr-old Mexican American woman living with type 2 diabetes mellitus, comes to the clinic to have her blood glucose

measured. It has been 12 months since her last visit. At that time, the nurse asked that she bring along her glucometer and strips to show how she checks her blood glucose because her glucose values were high at her previous visits. When you check E.M.’s equipment and glucose strips, you find that the strips are for a different machine and they expired more than 2 years ago. When you inquire about the situation, E.M. explains that she cannot afford to come to the clinic or to buy new equipment and supplies to check her blood glucose level. During the day, E.M. cares for her 3 grandchildren so her daughter can work. E.M. spends most of her income on food for her family, so she has little money left for her health care.

Ethical/Legal Points for Consideration • Ethnic minorities and other vulnerable or disadvantaged groups experience certain chronic illnesses at higher rates. Limited access to high-quality, accessible, and affordable health care services is associated with an increased incidence of illness and complications, as well as a reduced life span. • People with certain health problems such as diabetes may have difficulty obtaining health care insurance. Consider these issues in the broader context of social justice. • In many states, the legal definition of the role of the professional nurse includes patient advocacy. Advocacy includes the obligation to provide adequate follow-up care for all patients, especially those who are experiencing health care disparities. • A nurse who observes disparities must consider the possibility of discrimination and abuse. Professional nurses are legally and ethically responsible for patient advocacy. The nurse may incur legal liability if failure to fulfill this obligation results in patient harm.

Discussion Questions

1. How would you work with E.M. to help her obtain the necessary resources and knowledge to care for her diabetes? 2. What can you do to begin working on the problems of health disparities in your community?

Factors and Conditions Leading to Health Disparities Many factors and conditions can lead to the development of health disparities (Table 2.1). Awareness of these factors will help you provide optimal care for your patients.

Ethnicity and Race The terms ethnicity and race are subjective and based on self-report. These terms are used interchangeably in conversation and are not defined by genetic markers. Social context and lived experiences influence people’s decision about the ethnic and race category to which they identify or are assigned. For example, ethnic and race categories may differ on a person’s birth certificate and death certificate. People often identify their own ethnicity and race for health data collection (e.g., health plans, birth certificates). Collection of health data based on self-reported ethnic and race categories is important for research, to inform policy, and to understand and eliminate disparities. People identify their race using 1 or more categories. Law requires federal agencies to list a minimum of 5 race categories: white, black, American Indian or Alaska Native, Asian, and Native Hawaiian or other Pacific Islander. Federal agencies must also list a minimum of 2 ethnicities for people who self-identify as either Hispanic or Latino and Not Hispanic or Latino. A Hispanic or Latino is typically a person of Cuban, Mexican, Puerto Rican, South or Central American, or other Spanish descent, regardless of race. In this book, we use the terms ethnicity and race interchangeably or together. Although dramatic improvements in treatments have prolonged life and improved quality of life for many, racial and ethnic minorities

have benefited far less from these advances. Disparities are generally determined by comparing population groups. In the United States, minority groups include Hispanics/Latinos (17.8% of the U.S. population), blacks (13.3%), Asian Americans (5.7%), Native Hawaiians and other Pacific Islanders (0.2%), Native Americans and Native Alaskans (1.3%), and 2 or more races (2.6%) population.3 The number for most of these groups is expected to increase in the coming decades. Obesity and chronic illness rates for diabetes, hypertension, chronic obstructive pulmonary diseases, cancer, and stroke are higher among minority people. Racial, ethnic, and cultural differences exist in health services, treatments provided, and access to health care providers (HCPs). Race and ethnicity also influence disease risk and outcomes. For example, after myocardial infarction, minority patients are at greater risk of rehospitalization and death but are less likely than nonminority patients to receive potentially beneficial treatments.4 Native Americans have a higher incidence of several types of cancers and are often diagnosed at later stages of disease, resulting in a poorer prognosis.5 Numerous strategies are being developed to promote health equity and reduce disparities.

TABLE 2.1 Factors and Conditions Leading to

Health Disparities • Age • Disability status • Education • Ethnicity and race • Gender • Health care provider attitudes/biases • Health literacy • Income status

• Lack of health care services access • Language barrier • Occupation or unemployment • Place • Sexual orientation

Promoting Health Equity Promoting Health Equity Boxes Throughout Book Title Alzheimer’s Disease

Chapter 59

Page 1386

Arthritis and Connective Tissue Disorders

64

1505

Brain Tumors

56

1318

Breast Cancer

51

1204

Cancer

15

265

Cancers of the Female Reproductive System

53

1241

Cancers of the Male Reproductive System

54

1263

Chronic Kidney Disease

46

1066

Colorectal Cancer

42

948

Coronary Artery Disease

33

700

Diabetes

48

1110

Heart Failure

34

735

Hematologic Problems

30

607

Hypertension

32

679

Liver, Pancreas, and Gallbladder Disorders

43

980

Lung Cancer

27

518

Obesity

40

869

Obstructive Pulmonary Diseases

28

542

Oral, Pharyngeal, and Esophageal Problems

41

894

Osteoporosis

63

1492

Sexually Transmitted Infections

52

1213

Skin Problems

23

411

Stroke

57

1332

Tuberculosis

27

510

Urologic Disorders

45

1036

Visual Problems

20

359

Place Place refers to the geographic and environmental location where a person is born, grows, lives, works, and ages. Place affects the use of health services, health status, and health behaviors. About 20% of Americans live in nonurban or rural areas.6 Differences in access to health care services between rural and urban settings can create geographic health disparities. For example, rural populations and Native Americans living on reservations may need to travel long distances to receive health care. This can result in inadequate or less-frequent access to health care services. Some parts of the rural United States are “medically underserved” because of decreased numbers of HCPs per population. People living in rural areas have higher rates of cancer, heart disease, diabetes, depression, and injury-related deaths than people living in urban areas. For example, in rural Appalachia the rates of lung, colon, cervical, and colorectal cancer are higher than the national average. Rural populations tend to be older than urban populations. Many rural areas have higher rates of obesity and chronic disease. The impact of social and physical environment on health choices can be illustrated by the problem of intimate partner violence in rural communities.7 The decision to seek help is affected by geographic isolation, traditional gender roles, patriarchal attitudes, fear of lack of confidentiality, and economic factors that exist in some small rural communities. Living in urban centers may also predispose a person to health disparities. Concerns about personal safety (e.g., clinics located in high-crime neighborhoods) can make patients reluctant to visit HCPs. High rates of chronic health problems and premature deaths occur in

neighborhoods with social inequalities, including high poverty rates and residential segregation. Among the most obvious health behaviors affected by place are physical activity and nutrition. Safe, walkable neighborhoods with playgrounds and sources of healthy foods promote physical activity and healthy eating. Social support positively affects coping with illness. Social networks are more likely to be found in communities where neighbors interact and rely on one another.

Income, Education, and Occupation People of lower income, education, or occupational status experience worse health. In addition, they die at a younger age than those who are more affluent. Adults without a high school diploma or equivalent are 3 times more likely to die before age 65 than those with a college degree. Health care costs are 1 of the key factors that contribute to health disparities. People who have no insurance, are underinsured, or lack financial resources to pay for treatment of diseases may forgo health care visits, screenings, and treatments. Patients who lack the knowledge and/or access to apply for government assistance programs (e.g., Medicaid) are also at risk. Hazardous work environments and high-risk occupations of laborers increase health risk and contribute to higher rates of illness, injury, and death.

Health Literacy Health literacy is defined as the degree to which a person has the capacity to obtain, process, and understand basic health information and services needed to make appropriate health decisions. This includes the ability to (1) read, understand, and analyze information; (2) understand instructions; (3) weigh risks and benefits; and (4) make decisions and take action. Low health literacy is associated with more hospitalizations, greater use of emergency department care, decreased use of cancer screening and influenza vaccine, decreased ability to use medications correctly, and higher mortality rates among older adults. On a daily basis, patients need to self-manage conditions such as diabetes and asthma. For example, patients with diabetes may not be

able to maintain adequate blood glucose levels if they cannot read or understand the numbers on the home glucose monitoring system. The inability to read and understand medication labels can result in taking medications at the wrong time or in the wrong dose. See Chapter 4 for more about health literacy.

Gender Health disparities exist between men and women. Adult women use health care services more than men. Women may not receive the same quality of care (Fig. 2.1). For example, women are less likely than men to receive procedures (e.g., coronary angiography) for cardiovascular disease.8 When gender is combined with racial and ethnic differences, the disparities are even greater. Gender Differences boxes throughout this book highlight gender differences in disease risk, manifestations, and treatment.

FIG. 2.1 Older Asian women are especially at risk for health disparities.

© szefei/iStock/Thinkstock.

Age Older adults are at risk for experiencing health disparities in the number of diagnostic tests done and aggressiveness of treatments used. Biases toward older adults that affect their care, or ageism, are discussed in Chapter 5. Older people of low socioeconomic status experience greater disability, more limitations in activities of daily living, and more frequent and rapid cognitive decline. Black and Latino older adults, in particular, are disproportionately affected by chronic illnesses, disability, depression, and substandard quality of life.9

Sexual Orientation Sexuality is defined as a person’s romantic, emotional, or sexual attraction to another person.

Lesbian, Gay, Bisexual, Transgender, and Queer or Questioning Lesbian, gay, bisexual, transgender, and queer or questioning (LGBTQ) is a term that refers to the sexual orientation of these groups of people. LGBTQ persons encompass all races and ethnicities, religions, and social classes. Being LGBTQ places a person at risk for health disparities resulting from social, economic, or environmental disadvantages. Personal, family, and social acceptance of sexual orientation and gender identity affects the mental health and personal safety of LGBTQ persons. Discrimination against LGBTQ people has been associated with high rates of psychiatric disorders, substance abuse, and suicide. LGBTQ people are more likely to be obese when compared with their heterosexual counterparts. Lesbian and bisexual women have higher rates of breast cancer and increased risk factors for cardiovascular disease. Gay and bisexual men have higher rates of human immunodeficiency virus and hepatitis infections than other

groups.10 Older LGBTQ persons may face added barriers to health because of isolation and a lack of social services and culturally competent providers.9 Understanding the cause of disparities among LGBTQ persons is essential to providing safe and high-quality care. One of the barriers to accessing high-quality health care by LGBTQ adults is the current lack of HCPs who are knowledgeable about their health needs. LGBTQ people may also experience fear of discrimination in health care settings. Some health care settings are addressing the negative stereotypes that health care professionals may have, but of which they may not be aware. The Joint Commission (TJC) requires that patients be allowed the presence of a support person of their choice. In addition, hospitals must adopt policies that bar discrimination based on factors such as sexual orientation and gender identification and expression.

Promoting Population Health Improving the Health and Well-Being of LGBTQ Persons • Provide supportive social services to reduce suicide among young LGBTQ persons. • Inquire about and be supportive of a patient’s sexual orientation to enhance the patient-provider interaction and patient’s regular use of care. • Implement antibullying policies in schools. • Provide health care professionals with knowledge of the health needs of the LGBTQ community and training on LGBT mental health issues. • Continue efforts to expand domestic partner health insurance coverage. • Establish community advisory boards and LGBTQ health centers.

• Disseminate effective HIV and sexually transmitted infections interventions.

Health Care Provider Attitudes Certain behaviors and biases of the HCP can contribute to health disparities. Factors such as bias and prejudice can affect health careseeking behavior in minority populations. The health care system may also contribute to the problem of health disparities. For example, a clinic located in an area with a large population of Vietnamese immigrants that does not provide interpreters or educational materials and financial forms in Vietnamese may limit these families’ ability to understand how to access health care. Discrimination and bias based on a patient’s race, ethnicity, gender, age, body size, sexual orientation, or ability to pay are likely to result in less aggressive or negative treatment practices. Discrimination can result in the delay of a proper diagnosis due to assumptions made about the patient. Sometimes discrimination is hard to recognize, especially when it occurs at the institutional level. Because an HCP’s overt discriminatory behavior may not be clear to the patient or yourself, it may be difficult to confront. Even wellintentioned providers who try to eliminate bias in their care can show their prior beliefs or prejudices through nonverbal communication. Many policies are in place to eliminate discrimination, but it still exists.

Culture Culture is a way of life for a group of people. It includes the behaviors, beliefs, values, traditions, and symbols that the group accepts, generally without thinking about them. This way of life is passed along by communication and imitation from 1 generation to the next. You can also think of culture as cultivated behavior that one acquires through social learning. It is the totality of a person’s learned, accumulated experience that is socially transmitted. The 4 classic

characteristics of culture are described in Table 2.2. Values are the sets of rules by which persons, families, groups, and communities live. They are the principles and standards that serve as the basis for beliefs, attitudes, and behaviors. Although all cultures have values, the types and expressions of those values differ from 1 culture to another. These cultural values develop over time, guide decision making and actions, and may affect a person’s self-esteem. Cultural values often unconsciously develop early in life as a child learns about acceptable and unacceptable behaviors. The extent to which a person’s cultural values are internalized influences that person’s tendency toward judging other cultures, while usually using his or her own culture as the accepted standard. Table 2.3 provides some examples of cultural characteristics of different ethnic groups in the United States. Although persons within a cultural group may have many similarities through their shared values, beliefs, and practices, there is also diversity within groups (Fig. 2.2). Each person is culturally unique. Such diversity may result from different perspectives and interpretations of situations. These differences may be based on age, gender, marital status, family structure, income, education level, religious views, and life experiences. Within any cultural group, there are smaller groups that may not hold all the values of the dominant culture. These smaller cultural groups have experiences that differ from those of the dominant group. These differences may be related to ethnic background, residence, religion, occupation, health, age, gender, education, or other factors that unite the group. Members of a subculture share certain aspects of culture that are different from those of the overall cultural group. For example, among Hispanics some seek professional health care right away when symptoms appear. Other Hispanics rely first on folk healers. Others first seek the opinion of family and friends before seeking formal health care.

TABLE 2.2 Basic Characteristics of Culture

• Dynamic and ever-changing • Not always shared by all members of a cultural group • Adapted to specific conditions such as environmental factors • Learned through oral and written histories, as well as socialization

TABLE 2.3 Cultural Characteristics of Different

Ethnic Groups

Asian American • Cultural foods • Family loyalty • Folk healing • Harmonious relationships • Harmony and balance within body vital for preservation of life energy • Respect for elders • Respect for one’s parents and ancestors

Black • Cultural foods • Family networks • Folk healing • Importance of religion • Interdependence within ethnic group • Music and physical activities valued

European American

• Equal rights of genders • Independence and freedom • Individualistic and competitive • Materialistic • Self-reliance valued • Youth and beauty valued

Hispanic/Latino • Cultural foods • Folk healing • Extended family valued • Interdependence and collectivism • Involvement of family in social activities • Religion and spirituality highly valued • Respect for elders and authority

Native American • Doing the honorable thing • Folk healing • Living in harmony with people and nature • Respect for tribal elders and children • Respect for all things living • Return what is taken from nature • Spiritual guidance

Pacific Islander American • Collective concern and involvement

• Kinship alliance among nuclear and extended family • Knowledge is collective; belongs to group, not a person • Natural order and balanced relationships Adapted from Andrews MM, Boyle JS: Transcultural concepts in nursing care, ed 7, Philadelphia, 2016, Lippincott Williams & Wilkins; and Giger JN, Davidhizar RE: Transcultural nursing: Assessment and intervention, ed 7, St Louis, 2016, Mosby. Cultural beliefs about symptom tolerance and health care–seeking behavior can contribute to health disparities. Some cultures consider pain something to be endured or ignored, and as a result, the patient does not seek help. Some cultures may view diseases or problems fatalistically; that is, people see no reason to seek treatment because they believe it is unlikely to have any benefit. Some cultures view the signs and symptoms of an illness as “God’s will” or as a punishment for some prior behavior. In some cultures, it may not be acceptable to see an HCP who is not of the same gender or ethnic group. Such beliefs can result in delays in seeking health care or inadequate treatment.

FIG. 2.2 Members of this family share a common heritage. © Jack Hollingsworth/Photodisc/Thinkstock.

Acculturation is the lifelong process of incorporating cultural aspects of the contexts in which a person grows, lives, works, and ages.11 Acculturation is often bidirectional. In other words, the context changes as a person’s culture influences it. Change may be in attitudes, behaviors, and values. For example, a sedentary person who loves to cook may change his or her attitude toward exercise when living with athletic roommates, who in turn also change as they begin to appreciate cooking. Behaviors change when an immigrant child learns the local language while influencing the conduct of classmates. A deeply held value such as self-sufficiency may change for a person exposed to a culture in which reliance on others dominates. Newcomers may adopt both the strengths and limitations of the dominant culture. This is relevant when considering health behaviors and the quality of health care delivered by professionals. For example, an immigrant may be negatively influenced by a dominant cultural context in which unhealthy eating habits prevail.12

The result of acculturation may be new cultural variations in attitudes, behaviors, and values. All people take part in this process over their lives. People who move to a new cultural context are more aware of the acculturation experience than people who are not exposed to new experiences. Exposure to new cultural contexts increases a nurse’s cultural competency. Stereotyping refers to an overgeneralized viewpoint that members of a specific culture, race, or ethnic group are alike and share the same values and beliefs. This oversimplified approach does not consider the individual differences that exist within a culture. Being a member of a particular cultural, ethnic, or racial group does not make the person an expert on other members of that same group. Such stereotyping can lead to false assumptions and affect a patient’s care. For example, it would be inappropriate for you to assume that just because a nurse is Mexican American, he would know how a Mexican American patient’s beliefs may affect that patient’s health care practices. As another example, a young Mexican American nurse born and raised in a large city has experienced a different culture than the older patient who was born and raised in a rural area of Mexico. Ethnocentrism refers to the belief that one’s own culture and worldview are superior to those of others from different cultural, ethnic, or racial backgrounds.11 Comparing others’ ways to your own can lead to seeing others as different or inferior. HCP’s ethnocentrism can result in poor communication, patient alienation, and potentially inadequate treatment. To avoid ethnocentrism, you need to remain open to a variety of perspectives and maintain a nonjudgmental view of the values, beliefs, and practices of others. Failure to do this can result in ethnic stereotyping or cultural imposition. Cultural imposition occurs when we impose our own cultural beliefs and practices on another person or group of people. In health care, it can result in disregarding or trivializing a patient’s health care beliefs or practices. Cultural imposition may happen when an HCP is unaware of the patient’s cultural beliefs and plans and implements care without taking them into account. Cultural safety describes care and advocacy for a person of another

culture determined by that person or family. Care that is culturally safe prevents cultural imposition. Culturally safe practice requires cultural competency and action to ensure that cultural histories, experiences, and traditions of patients, their families, and communities are valued and shape health care approaches and policies.13 Madeleine Leininger coined the term transcultural nursing in the 1950s. Transcultural nursing is a specialty that focuses on the comparative study and analysis of cultures and subcultures. The goal of transcultural nursing is the discovery of culturally relevant facts that can guide the nurse in providing culturally appropriate care.11

Cultural Competence Cultural competence is the ability to understand, appreciate, and work with people from cultures other than your own. It involves an awareness and acceptance of cultural differences, self-awareness, knowledge of the patient’s culture, and adaptation of skills to meet the patient’s needs. The 4 components of cultural competence are (1) cultural awareness, (2) cultural knowledge, (3) cultural skill, and (4) cultural encounter (Table 2.4). We present specific information throughout this book to help you develop an awareness of cultural differences and learning assessment skills for different cultural groups. Table 2.8 (later in this chapter) presents a cultural assessment guide. It may be helpful to review general cultural characteristics associated with a cultural group when preparing to interview a patient. However, recognize that the patient may not identify with the assumed cultural group and the provider’s own biases and stereotypes may affect the patient and result in more patient-provider barriers. Providing culturally competent care may increase patient satisfaction, promote health equity, increase patient safety, and prevent misunderstandings between you and your patients.14 It also involves integrating cultural practices into Western medicine. For example, before some diagnostic procedures and interventions, it is

typical to have patients remove personal objects they are wearing on the body. Ask patients whether they wear personal objects and the significance of their removal, since they may have cultural or spiritual significance. You should know whether wearing these objects will compromise patient safety, test results, or outcomes of the intervention.

Cultural Diversity in the Health Care Workplace Poorer health outcomes for minorities are linked to the shortage of culturally and ethnically diverse HCPs, who have historically been underrepresented in the health professions. A diversity gap exists between the ethnic composition of the interprofessional health care team and the overall population in the United States (Fig. 2.3). For example, the diversity of nurses in the United States is increasing but still lags that of the overall population. Blacks, Hispanic/Latino Americans, and Native Americans make up more than 35% of the population but only 24% of the nation’s nurses.3,15 Biased behaviors against nurses of diverse cultural and ethnic backgrounds by patients and health care professionals may contribute to their underrepresentation.

TABLE 2.4 How to Develop Cultural Competence

FIG. 2.3 Interprofessional team working together in a multicultural health care environment. © Thinkstock/Stockbyte/Thinkstock.

Cultural differences exist in how well patients think they can communicate with their HCP. In the United States, minority patients are more likely to have difficulty communicating with their HCP.16 Communication issues include not understanding the HCP, feeling that they are not listened to, and having questions but not asking them. As more internationally educated nurses join the workforce, sufficient training and transitional support must be in place to ensure communication and quality of care. When HCPs from different cultures work together as members of the health care team, opportunities for miscommunication and conflict can occur. This is termed cultural conflict. The cultural origins of miscommunication and conflict in the workplace are often

interconnected with cultural beliefs, values, and etiquette. Seeking clarification about misperceptions and misunderstandings is a communication strategy to foster effective teamwork among a multicultural health care team. To ensure the recruitment and retention of nurses from minority populations, all members of the health care team and leadership must create an environment that promotes effective cross-cultural communication and reduces bias and discrimination.

Cultural Factors Affecting Health and Health Care Many cultural factors affect the patient’s health and health care. Several potential factors are outlined in Table 2.5.

Folk Healers and Traditions Many cultures have folk healers, who are also known as traditional healers. Most folk healers speak the person’s native language and cost less than conventional HCPs. Among the many folk healers found worldwide, Hispanics, particularly from regions in Mexico and Central and South America, may choose to use a curandero (or curandera); blacks may visit a hougan; Native Americans may seek help from a medicine man or shaman; and Asian Americans may use folk healers such as a Chinese herbal therapist. In addition to folk healers, some cultures involve lay midwives (e.g., parteras for Hispanic women) in the care of pregnant women.

TABLE 2.5 Cultural Factors Affecting Health and

Health Care

Beliefs and Practices

• Care provided in established health care programs may not be perceived as culturally relevant. • Religious reasons, beliefs, or practices may affect a person’s decision to seek (or not seek) health care. • Patients may delay seeking health care because of fear or dependence on folk medicine and herbal remedies. • Patients may stop treatment or visits for health care because the symptoms are no longer present and they think that further care is not needed. • Some patients associate hospitals and extended care facilities with death. • The patient may have had a previous negative experience with culturally incompetent HCPs or discriminatory practices. • Some people mistrust the majority population and institutions dominated by them. • Some patients may feel apprehensive about unfamiliar diagnostic procedures and treatment options.

Communication and Language • Patients may not speak English and may not be able to communicate with the HCP. • It may be hard to communicate, even with interpreters.

Economic Factors • Patients may not get health care because they cannot pay for it or because of the costs associated with travel for health care. • Refugee or undocumented immigrant status may deter some patients from using the health care system. • Immigrant women who are heads of households or single mothers may not seek health care for themselves because of child

care costs. • Patients may lack health insurance.

Health Care System • Patients may not make or keep appointments because of the time lag between the onset of an illness and an available appointment. • Hours of operation of health care facilities may not accommodate patients’ need to work or use public transportation. • Requirements to access some types of care may discourage some patients from taking the steps to qualify for health care or health care payment assistance. • Some patients have a general distrust of HCPs and health care systems. • Lack of ethnic-specific health care programs may deter some people from seeking health care. • Transportation may be a problem for patients who must travel long distances for health care. • Adequate interpreter services may be unavailable. • Patients may not have a primary HCP and may use emergency departments or urgent care centers for health care. • Shortages of HCPs from specific ethnic groups may deter some people from seeking health care. • Patients may lack knowledge about the availability of existing health care resources. • Facility policies may not be culturally competent (e.g., hospital policy may limit the number of visitors, which is problematic for cultures that value having many family members present).

Time Orientation • For some cultures, it is more important to attend to a social role

than to arrive on time for an appointment with an HCP. • Some cultures are future oriented; others are past or present oriented.

TABLE 2.6 Health-Related Beliefs and Practices

of Selected Religious Groups

Amish • Prohibit drinking alcoholic beverages • Prohibit abortion, artificial insemination, and stem cell use • Seldom buy commercial health insurance • Prohibit drugs unless prescribed by HCPs

Buddhism • Prohibit drinking alcoholic beverages and using illicit drugs • Practice moderation in diet and avoidance of extremes • Central tenets are maintaining right views, intentions, speech, actions, livelihood, effort, mindfulness, and concentration

Catholicism • Fast and abstain from meat and meat products on Ash Wednesday and the Fridays of Lent • Prohibit artificial contraception and direct abortion • Indirect abortion (e.g., treatment of uterine cancer in a pregnant woman) may be morally justified • Sacrament of the Sick includes anointing of sick with oil, blessing by a priest, and communion (unleavened wafer made of flour and water)

Church of Jesus Christ of Latter-Day Saints (Mormons) • Strict dietary code called Word of Wisdom prohibits all alcoholic beverages, hot drinks (nonherbal teas and coffee), tobacco, and recreational drugs • Fast for a 24-hour period each month on “Fast Sunday” • During hospitalization or serious illness, an elder anoints the ill person with oil while a second elder seals the anointing with a prayer and blessing (laying on of hands) • Prohibit abortion except when the mother’s life is in danger

Hinduism • Prohibit eating meat because it involves harming a living creature • Cremation is the usual form of body disposal, but fetuses or newborns are sometimes buried

Islam • Fasting during daytime hours occurs during a month-long period called Ramadan • Perform a ritual cleansing with water before eating and before prayer • Prohibit eating pork or taking medicines with pork derivatives • Prohibit drinking alcoholic beverages • Artificial insemination is permissible only if from the husband to his own wife

Jehovah’s Witness

• Prohibit transfusions of blood in any form or agents in which blood is an ingredient • Blood volume expanders are acceptable if they are not derivatives of blood • Prohibit transplants that involve bodily mutilation • Prohibit artificial insemination and therapeutic and on-demand abortions

Judaism • Prohibit eating pork, shellfish, or predatory fowl or mixing milk dishes and meat dishes when preparing foods • Certain foods and drinks are designated as kosher, which means “proper.” All animals must be ritually slaughtered • On the eighth day after birth, boys are circumcised in a ritual called Brit Milah. Girls are given a dedication ceremony involving prayers and blessings • Prohibit abortion except when the mother’s life is in danger • Organized support system for the sick includes a visit from the rabbi. The rabbi may pray with the sick person alone or in a minyan, a group of 10 adults over age 13 • If an autopsy is done, all body parts must be returned for burial

Seventh-Day Adventism • Encourage a vegetarian diet • Nonvegetarian members do not eat foods derived from any animal having a cloven hoof that chews its cud (e.g., pigs, goats). • Prohibit eating shellfish; eating fish with fins and scales is acceptable • Prohibit drinking alcoholic beverages • Healthy church members practice voluntary fasting

Data from Andrews MM, Boyle JS: Transcultural concepts in nursing care, ed 7, Philadelphia, 2016, Lippincott Williams & Wilkins. Folk medicine and traditions are culturally based forms of prevention and treatment. They traditionally rely on oral transmission of healing techniques from 1 generation to the next. The patient may not use the term folk medicine but thinks of these as cultural home remedies or treatment practices. A patient can be practicing folk medicine at home without using a folk healer. It is important to assess whether the patient is practicing traditional or folk healing. Some traditions that are practiced as a rite of passage in some cultures are considered harmful in the dominant culture in the United States. For example, female genital cutting is a tradition that is illegal in most countries yet still practiced in many countries in Africa and the Middle East. It results in physical and emotional trauma and may affect childbirth. Nurses can advocate for immigrant women who have experienced this trauma and to prevent return of young girls to their country of origin for the procedure.

Spirituality and Religion Spirituality and religion are aspects of culture that may affect a person’s beliefs about health, illness, and end-of-life care. They may also play a role in nutrition and decisions related to health, wellness, and how to respond to or treat an illness. Spirituality refers to a person’s effort to find purpose and meaning in life. It is influenced by a person’s unique life experiences and reflects one’s personal understanding of life’s mysteries. Spirituality relates to the soul or spirit more than to the body, and it may provide hope and strength for a person during an illness. Religion is a more formal and organized system of beliefs, including belief in or worship of God or gods. Religious beliefs include the cause, nature, and purpose of the universe and involve prayer and rituals. Religion is based on beliefs about life, death, good, and evil. You can use several interventions to meet a patient’s religious and

spiritual needs, including prayer, scripture reading, listening, and referral to a chaplain, rabbi, or priest. Many patients find that rituals help them during times of illness. Rituals help a person make sense of life experiences and may take the form of prayer, meditation, or other rituals that the patient may create. You should include spiritual questions in your patient assessment and plan care accordingly. Table 9.5 has a spiritual assessment guide that may be used with patients. Table 2.6 summarizes health-related beliefs and practices of selected religious groups.

Cross-Cultural Communication Communication refers to an organized, patterned system of behavior that may be verbal or nonverbal (Fig. 2.4). Verbal communication includes not only one’s language or dialect, but also voice tone, volume, timing, and ability to share thoughts and feelings. More than 45 million people in the United States speak a language other than English in their home, with Spanish being the most common. Hispanic people who do not speak English at home are less likely to receive a variety of health care services even if they are comfortable speaking English.

FIG. 2.4 Co-workers from different cultures communicate with verbal and nonverbal cues. © BananaStock/Thinkstock.

Nonverbal communication may take the form of writing, gestures, body movements, posture, facial expressions, and personal dress in some cultures. It also includes eye contact, use of touch, body language, style of greeting, and spatial distancing. Eye contact varies greatly among cultural groups. Patients who are Asian, Arab, or Native American may avoid direct eye contact and consider it disrespectful or aggressive. Hispanic patients may expect you to look directly at them but may not return that direct gaze. Other variables to consider include the role of gender, age, acculturation, status, or appropriate eye contact. For example, Muslim-Arab women exhibit modesty when avoiding eye contact with men other than their husbands and when in public situations.

Silence has many meanings. It is important to understand the meaning of silence for different cultural groups. Some people are comfortable with silence. Others become uncomfortable and may speak to decrease the amount of silent time. It is important to clarify what silence means in an interaction with a patient. Patients sometimes nod their head or say “yes” as if agreeing with you or to show they understand. Actually, they may be doing this because it is a culturally acceptable manner of showing respect, not because they understand or agree. Many Native Americans are comfortable with silence and interpret silence as essential for thinking and carefully considering a response. In these interactions, silence shows respect for the other person and shows the importance of the remarks. In traditional Japanese and Chinese cultures, the speaker may stop talking and leave a period of silence for the listener to think about what was said before continuing. Silence may show respect for the speaker’s privacy. In some cultures (e.g., French, Spanish, and Russian) the person may interpret silence as meaning agreement. Asian Americans may use silence to show respect for elders. Blacks may use silence as a response to what they perceive to be an inappropriate question. Racism and microaggression affect communication. Racism is a belief that differences among the various racial/ethnic groups determine cultural or individual achievement. It usually involves the idea that one’s own race/ethnicity is superior and has the right to dominate others or that a particular racial/ethnic group is inferior to the others.

FIG. 2.5 Family roles and relationships differ from 1 culture to another. © Jupiterimages/Photos.com/Thinkstock.

Microaggression is social exchanges in which a person says or does something that can either intentionally or unintentionally belittle or alienate a person, especially someone of a different racial/ethnic

group. It is imperative that nurses seek to understand racism and microaggression through education, self-awareness, and open dialogue with peers.17

Family Roles and Relationships Family roles differ from 1 culture to another (Fig. 2.5). It is important for you to determine who should be involved in communication and decision making related to health care. Some cultural groups emphasize interdependence rather than independence. In the United States, many in the mainstream culture have strong beliefs related to autonomy. We expect a patient to sign consent forms when receiving health care. In some cultural groups, the patient may expect a family member to make health care decisions. When you encounter a patient who values interdependence over independence, the health care system may have difficulty with how the patient makes decisions. We may have to delay treatment while the patient waits for family members to arrive before giving consent for a procedure or treatment. In other instances, the patient may make a decision that is best for the family despite adverse outcomes for the patient. Being aware of such values will better prepare you to advocate for the patient. Some cultural differences relate to expectations of family members in providing care. In some cultures, family members expect to provide care for the patient even in the hospital. The patient may expect that the family, along with the HCPs, will provide all care. This view is the opposite of the predominant Western expectation that the patient will assume self-care as quickly as possible. Ask about culturally relevant gender relationships. For example, in some cultures, such as many Arab groups, it is not appropriate for a man to be alone with a woman other than his wife. Nor is it appropriate for a woman other than a man’s wife to provide physical care for him. The clinical implication of this cultural belief is that for many patients from Arab cultures, nurses cannot provide direct physical care for patients of the opposite gender. In some instances, patients may only receive procedures or treatments from providers of

the opposite gender if a third party is present.

FIG. 2.6 Personal space zones.

Personal Space Personal space zones are the variable and subjective distance at which 1 person feels comfortable talking to another. A representative example of personal space zones for European Americans is shown in Fig. 2.6. Personal space distances vary from culture to culture, as well as within a culture. As a nurse, you often interact with patients in the intimate or personal distance, which may be uncomfortable for the patient. Cultural groups have wide variations in their perception of appropriate distances. An American nurse of European descent may be comfortable with a certain distance. A person from a Hispanic or

Middle Eastern background may believe that the distance is too far and will move closer, perhaps causing you to feel uncomfortable. If you then move away to a more comfortable distance, this may cause the other person to think that you are unfriendly or the person may be offended.

Touch Physical contact with patients conveys various meanings depending on the culture. Performing a comprehensive assessment requires touching a patient. Many people of Asian and Hispanic heritage believe that touching a person’s head is a sign of disrespect because the head is the source of one’s strength and/or soul. Many people in the world believe in the evil eye, or mal ojo. In this culture-bound syndrome, the illness—usually in a child or a woman—resulted from excessive admiration by another person. In some cultures, the proper way to ward off the evil eye is to touch the area of admiration. For example, if the person admires the hair, the top of the head may be touched. It is important for you to ask permission before touching anyone, particularly if it is necessary to touch the person’s head.

Nutrition An important part of cultural practices is food, including both the foods that are eaten and rituals and practices associated with food. Muslims fast during the daytime during the Islamic month of Ramadan. Such practices may affect when and how patients take medications. Patients may need to make major changes in their diets because of health problems. A person may use food to cope with life changes such as homesickness. Specific foods may be considered essential to good health during pregnancy or other life stages. The HCP should consider food-related cultural beliefs, practices, and habits when discussing nutrition with patients and planning their diets. When people immigrate to an area that is very different from their country of origin, they may experience unfamiliar foods, food-storage

systems, and food-buying habits. They may come from countries that have limited food supplies because of poverty, wars, and poor sanitation. They may arrive with conditions such as malnutrition, diarrhea, and dental caries. Other problems may develop after the person arrives in the new country. For example, second-generation Hispanic immigrants have a greater chance of becoming overweight than their first-generation counterparts. The increase in weight is related to the degree of acculturation experienced by the immigrant.

Immigrants and Immigration Several conditions drive migration, such as overcrowding, natural disasters, geopolitical conflict, persecution, and economic forces. Because of these migrations, a rich diversity of cultures exists in many communities and countries today (Fig. 2.7). Recent immigrants may be at risk for physical and mental health problems for many reasons. Conditions in their countries of origin (e.g., malnutrition, poor sanitation, civil war) may have resulted in chronic health problems. In addition, recent immigrants are at increased risk for health problems after arriving in a new area. Relocation is associated with many losses and can cause economic hardship, physical stress, and mental distress. As new immigrants go through the acculturation process, many have cultural stress as they adjust to their new environment, especially if they have left relatives behind or are unable to return to their home country. Older immigrants are especially affected by changes in role and social position. This may result in depression. Immigrants who have survived wars and violence may have posttraumatic stress disorder. Immigrants may face barriers to social acceptance, such as prejudice or discrimination, and experience a lack of ethnic and cultural resources. For some, it may mean loss of the social status that they experienced in their countries of origin. Another potential problem is tuberculosis (TB). Two-thirds of the TB cases in the United States occur in people born outside the country.18 Those who have recently immigrated from areas that have

a high endemic rate of TB are more likely to have TB. Foreign-born Hispanics and Asians combined account for 48% of the nation’s TB cases. The top 5 countries of the origin of foreign-born people with TB are Mexico, Philippines, Vietnam, India, and China. The Refugee Health Guidelines from the Centers for Disease Control and Prevention supports early identification and treatment.19 During the past 45 years, the migration pattern of North America has shifted. Once most immigrants came from Europe. Now, most originate from Asia, Latin America, and Africa. Additionally, an increased number of first- and second-generation immigrants enter the United States after visiting friends and relatives. They have a higher risk for malaria, typhoid fever, cholera, and hepatitis A than people born in the United States. Many immigrants lack health insurance and may primarily obtain their health care in emergency departments and urgent care clinics. Therefore nurses in all settings need to be aware of refugee health screening, treatment recommendations, and resources for access to health care and social services.

Drugs Genetic differences among people from diverse ethnic or racial groups may explain differences in drug choice, dosage, or administration. For example, some drugs are more effective in certain ethnic groups than others. Side effects may vary among persons from diverse backgrounds. Genetic variations can affect how the body processes a drug and the overall effect of selected drugs on the body. Although race and ethnicity are imprecise indicators of genetic differences, they can be helpful in predicting variations in the response to drugs. For example, European Americans respond better to angiotensin-converting enzyme (ACE) inhibitors and β-blockers than blacks. Genetics and drug metabolism are discussed in Chapter 12.

FIG. 2.7 Recently arrived immigrants join a neighbor for a barbecue, a common American tradition. © Jack Hollingsworth/Photodisc/Thinkstock.

Regardless of their cultural origins, many people use cultural remedies and prescription drugs to treat illness. Problems can result from interactions of these substances. For example, some Mexican Americans may treat gastrointestinal problems with preparations that contain lead. Some people may self-treat their depression with St. John’s wort, which can result in adverse effects if taken with prescription antidepressants. Patients may avoid standard Western medicine until herbs and other remedies become ineffective or the illness becomes acute. The

challenge for you is to try to accommodate the patient’s desire for traditional aspects of care while using evidence-based approaches that are appropriate and acceptable to the patient. Evaluate the safety and appropriateness of the patient’s traditional cultural healing therapies. Develop a collaborative, trusting relationship with patients and encourage them to discuss their traditional approaches to healing. Seek out information on potential drug and herbal product interaction from the pharmacist. Honor the patient’s choices, if safe and effective, since this will enhance collaboration and may have a positive impact on health outcomes.

Psychologic Factors Symptoms are interpreted through a person’s cultural norms and may vary from the recognized interpretations of Western medicine. All symptoms have meaning, and the meanings may vary from 1 culture to another. For example, the degree of depression following a cardiac diagnosis is mediated by cultural views. It is important to ask patients what their illness means to them, what they believe is the cause, and what they think is the best treatment. Culture-bound syndromes are illnesses or afflictions that are recognized only within a cultural group (Table 2.7). The symptoms, course of the illness, and people’s reactions to the illness are limited to specific cultures. Culture-bound syndromes are expressed through psychologic or physical symptoms.

TABLE 2.7 Culture-Bound Syndromes

Nursing Management: Promoting Health Equity and Increasing Cultural Competency Nurse’s Self-Assessment The first step in promoting health equity and providing culturally competent care is for you to assess your own cultural background, values, and beliefs, especially those that are related to health and health care. Many tools are available to help you with this process (http://nccc.georgetown.edu). Table 2.4 suggests ways for you to improve your cultural competence. This information can help you better understand patients and provide culturally competent care. It is important to understand that cultures evolve and change over time. Culturally competent care requires continual learning and self-reflection. Many other important

aspects of culture related to health care are included in the Culturally Competent Care sections throughout this book. In today’s increasingly multicultural environment, you will meet patients, families, significant others, and members of the health care team from many different cultures. You will find yourself in patient care situations that require an understanding of the patient’s cultural beliefs and practices. Even when you provide care for patients from your own cultural background, you may be from a different subculture than the patient. For example, there are more than 550 federally recognized Native American tribes in the United States. It would be inappropriate for you to assume that a Native American nurse can give culturally appropriate care to a Native American patient when the nurse may be from a different tribe. A white nurse from an urban upbringing may find cultural differences with a white patient from a rural community. Cultural competence is a lifelong process that involves self-reflection and continual learning.20

Patient Assessment HCPs play a key role in promoting health equity. However, the causes of health disparities are not always easy to identify. Assess patients for their risk for reduced health care services because of limited access, inadequate resources, age, or low health literacy. A cultural assessment should be included in the nursing process.21 Table 2.8 lists important components of the assessment. Determine the patient’s (1) health beliefs and health care practices and (2) perspective of the meaning, cause, and preferred treatment of illness. Ask questions that you are comfortable with based on your own culture. How can you be aware of the differences among ethnic groups? Using guides for cultural assessment will facilitate the nursing process when working with patients, families, or other groups who are from different cultures. Although guides can help in this process, you need to be careful not to stereotype or assume that common cultural characteristics pertain to each patient. Use guides to explore the

degree to which patients share commonalities with the traits attributed to their cultural group. You need to know about traditional characteristics of cultural groups while recognizing that culture is constantly evolving and unique for each person.

Nursing Implementation Although the issues associated with health disparities can seem overwhelming, several strategies are available to reduce and eliminate health disparities. Table 2.9 presents nursing interventions to promote health equity.

Advocacy The solutions to reduce health disparities often rest with the policymakers. Economic issues often determine health care delivery. Access and public policy decisions determine who is eligible for federal and state health insurance coverage. You, along with the social worker, can help by identifying key resources in the community, including transportation services, reduced-fee screening programs, and appropriate federal and state offices for Medicaid and Medicare.

TABLE 2.8 Cultural Assessment A cultural assessment should include the following: • Brief history of the cultural group with which person identifies • Communication • Cultural sanctions and restrictions • Educational background • Health-related beliefs and practices • Nutrition • Organizations providing cultural support • Religious affiliation

• Socioeconomic considerations • Spiritual considerations • Values orientation Adapted from Jarvis C: Physical examination and health assessment, ed 7, Philadelphia, 2016, Saunders.

TABLE 2.9 Nursing Management

Interventions to Promote Health Equity • Treat all patients equally. • Be aware of your own biases or prejudices and work toward eliminating them. • Learn about services and programs that focus on specific cultural/ethnic groups. • Inform patients about health care services available for their specific cultural/ethnic group. • Make sure the same standards of care are followed for all patients regardless of culture or ethnicity. • Recognize health care practices and cultural practices that are important to cultural and ethnic identity. • Take part in research focused on understanding and improving care to culturally and ethnically diverse populations. • Identify stereotypic attitudes toward a culture/ethnic group that may interfere with getting appropriate health care. • Support patients who are fearful about traveling outside the accepted neighborhood for health care services. • Advocate for patients of specific cultural/ethnic groups to receive health care services that pay special attention to English-language

limitations and cultural health practices. • Learn advocacy and interpersonal strategies from leaders of specific cultural/ethnic groups. For example, blacks may respond to themes such as “do it for your loved ones.” Asian Americans may respond to fear of dependency themes. • Ensure availability of culturally appropriate patient educational resources. You can be an advocate in your health care setting by helping to create a community advisory group. Such a group can be very helpful when setting up health programs within a community. This can increase the distribution of culturally sensitive information. Another powerful strategy is to increase the number of underrepresented populations in the health care professions (Fig. 2.8).

Standardized Guidelines The use of standardized, evidence-based care guidelines can reduce disparities in diagnosis and treatments. For example, the management of hypertension should be based on guidelines and the patient’s BP, symptoms, history, and laboratory values rather than other characteristics such as gender, age, or culture. Following the guidelines reduces racial or cultural differences in outcomes. In addition, recommendations related to cultural competency will guide you in your learning and practice.

FIG. 2.8 A Navajo nurse teaching a Navajo patient. From Giger JN: Transcultural nursing, ed 7, St Louis, 2016, Mosby.

The National Standards for Culturally and Linguistically Appropriate Services in Health Care (CLAS standards) are guidelines that improve the quality of health care.22 The CLAS standards provide practical guidance for care of people with limited English proficiency and of diverse cultural backgrounds.

Communication Improving interpersonal skills is an important first step in providing culturally competent care. To show respect for the patient, consider the patient’s usual communication style. For instance, conduct a health history in an unhurried manner and in a way that is appropriate for the culture. In some cultures, it is best to start with general rather than direct questions. For some cultures, it is most effective to engage in “small talk,” with the discussion including

answers that may seem to be unrelated to the questions. If you appear to be “too busy,” communication may be impaired. When meeting patients or family members, introduce yourself and indicate how you would like them to address you—whether they should use first names; Mr., Ms., or Mrs.; or a title, such as Nurse. Ask the patient how he or she prefers to be addressed. This shows respect and will help you begin the relationship in a culturally appropriate manner. If you need to gather personal information, it is important to understand the most effective approach to use. For instance, when talking with people from some cultural groups, it is imperative that you take time to establish trust and listen to the patient’s responses to questions. There may be long silences as the person thinks about the question, showing respect by giving the question proper consideration before answering. Take time to listen and help establish trust. Consider how the patient’s age may affect his or her views and communication. For example, black older adults with mental health concerns may struggle with shame, uncertainty, and lack of trust in the system. Do not try to serve as an interpreter if your patient does not understand English, because this could lead to misunderstandings. Get the help of a person who is qualified to do medical interpretation when you cannot speak the patient’s primary language (Table 2.10). Interpreters are available by phone anywhere in the United States through a fee-based service. Use them rather than a family member. Table 2.11 offers guidelines for communicating when no interpreter is available.

TABLE 2.10 Using a Medical Interpreter

Choosing an Interpreter • Use an agency interpreter if possible. • Use a trained medical interpreter who knows how to interpret,

has a health care background, understands patients’ rights, and can help with advice about the cultural relevance or appropriateness of the health care plan and instructions. • Use a family member only if necessary. Be aware of limitations if the family member does not understand medical terms, is younger or a different gender from the patient, or is not aware of the health care procedures or medical ethics. • Interpreter should be able to do the following: • Interpret the patient’s nonverbal as well as verbal communication. • Translate the message into understandable terms. • Act as a patient advocate to represent the patient’s needs to the health care team. • Be culturally competent and understand how to give teaching instructions.

Strategies for Working With an Interpreter • If possible, have the interpreter meet with the patient ahead of time to establish rapport before the interpreting begins. • Speak slowly. • Maintain eye contact with the patient. • Talk to the patient, not the interpreter. • Use simple language with as few medical terms as possible. • Speak 1 or 2 sentences at a time to allow for easier interpretation. • Avoid raising your voice during the interaction. • Obtain feedback to be certain the patient understands. • Plan to take twice as long to complete the interaction.

Informatics in Practice

Use of Translation Applications • Communication barriers can negatively affect the type of care received by non–English-speaking patients. • Use a language translation app to help you translate 1 language into another language. • Some apps allow you to speak critical phrases and the translation is immediately spoken back to you or the patient in a natural human voice with the proper accent. • Check the policy of the health care institution on the use of medical interpreters or translators, including the use of translation apps. A dictionary that translates from both your language and the patient’s language (e.g., Spanish-English/English-Spanish dictionary) is useful. Patients may find it helpful if you have a list of questions and potential answers in several languages prepared by using these types of dictionaries. Many websites and applications translate words and documents from 1 language into another (see Informatics in Practice box). It is helpful to have resources for persons from cultural groups who often use the health care facility. This is especially beneficial when a qualified medical interpreter is not readily available, and you need to learn important phrases in another language.

TABLE 2.11 Overcoming Language Barriers 1. Be polite and formal. 2. Pronounce name correctly. If unsure, ask about the correct pronunciation of the name. Use proper titles of respect, such as “Mr.,” “Mrs.,” “Ms.,” “Dr.” Greet the person using the last or complete name. 3. Gesture to yourself and say your name.

4. Offer a handshake or nod. Smile. 5. Proceed in an unhurried manner. Pay attention to any effort by the patient or family to communicate. 6. Speak in a low, moderate voice and avoid excess hand gestures. Remember that there is a tendency to raise the volume and pitch of your voice when the listener appears not to understand. The listener may perceive that you are shouting or angry. 7. Use any words that you might know in the person’s language. This shows that you are aware of and respect his or her culture. 8. Use simple words such as “pain” instead of “discomfort.” Avoid medical jargon, idioms, and slang. Avoid using contractions (e.g., don’t, can’t, won’t). Use nouns repeatedly instead of pronouns. Example: Do not say: “He has been taking his medicine, hasn’t he?” Do say: “Does Juan take medicine?” 9. Pantomime words and simple actions while you say them. 10. Give instructions in the proper sequence. Example: Do not say: “Before you rinse the bottle, sterilize it.” Do say: “First, wash the bottle. Second, rinse the bottle.” 11. Discuss 1 topic at a time. Avoid using conjunctions. Example: Do not say: “Are you cold and in pain?” Do say: “Are you cold [while pantomiming]? Are you in pain?” 12. Validate whether the person understands by having him or her repeat instructions, demonstrate the procedure, or act out the meaning. 13. Write out several short sentences in English and determine the person’s ability to read them. 14. Try a third language. Many Indochinese people speak French. Europeans often know 2 or more languages. Try Latin words or phrases. Use English words that have Latin roots (e.g., use precipitation instead of rain). 15. Ask the person’s family and friends who could serve as an interpreter.

16. Use websites that translate words from 1 language to another. Some of them also have audio to help you know how to say the word correctly. 17. Obtain phrase books from a library or bookstore, make or purchase flash cards, contact hospitals for a list of interpreters, and use both a formal and an informal network to find a suitable interpreter. Source: Jarvis C: Physical examination and health assessment, ed 7, Philadelphia, 2016, Saunders.

Case Study Health Disparities

© Luevanos/iStock/Thinkstock.

Patient Profile M.S. is an 81-yr-old woman who came to the United States from India 4 years ago with her son and daughter-in-law and their 4 children. She has several health problems, including coronary artery disease,

hypertension, osteoarthritis in her right hip, and diabetes. Her daughter-in-law is the primary caregiver and often brings her to the urban community health clinic for a variety of health-related problems. Recently, M.S. has been having memory problems. The entire family comes to the health clinic with M.S. Because English is a second language (Hindustani is their first language) for all the adult family members, the staff relies on the oldest granddaughter to interpret. At this clinic visit, M.S. is presenting with shortness of breath. Through her granddaughter’s interpretation, she tells the nurse that she is having trouble walking up the stairs in the apartment building. The nurse does the history and assessment, checks her blood glucose (which is within normal limits), and tells her that she should get more exercise. Given M.S.’s memory problems and limited English, the nurse does not complete a 24-hour dietary recall or teach her or the family about diabetes management. M.S. is scheduled for an appointment with the cardiologist for an evaluation of her hypertension and heart disease. Two weeks later, when she sees the cardiologist, her shortness of breath is much worse, and she is having chest pain. She is hospitalized immediately. Meanwhile, the clinic supervisor is completing a chart audit for the clinic’s quality review program. She is reviewing M.S.’s chart and notices that, although she has been a patient in the clinic for 3 years, she has never received instructions on blood glucose monitoring or general diabetes management. The clinic has a nurse diabetes educator who teaches individual patients and groups of patients with diabetes. The clinic manager reviews these findings with the nurse and asks why she has not recommended that M.S. see the diabetes educator. The nurse states that with M.S.’s memory problems and the language barrier, she assumed that M.S. and her family would not benefit from the consultation.

Discussion Questions 1. What type of health disparity has M.S. experienced? 2. What factors led to her not receiving the standard of care?

3. What other assessment should have been done at the initial visit? 4. Patient-Centered Care: What strategies may have worked to enhance patient education? 5. Patient-Centered Care: How would you assess M.S.’s religious and spiritual needs? 6. Quality Improvement: If you were the clinic manager, how would you recommend that the nurse improve her practice? Answers available at http://evolve.elsevier.com/Lewis/medsurg.

Bridge to Nclex Examination The number of the question corresponds to the same-numbered outcome at the beginning of the chapter.

1. What are the leading determinants of a patient’s health (select all that apply)? a. Genetics b. Health behaviors c. Family history of disease d. Social and physical environment e. Type and quality of medical care received 2. In identifying patients at the greatest risk for health disparities, the nurse would note that a. patients who live in urban areas have readily available access to health care services. b. cultural differences exist in patients’ ability to communicate with their health care provider. c. a patient receiving care from a health care provider of a different culture will have decreased quality of care.

d. men are more likely than women to have their cardiovascular disease symptoms ignored by a health care provider. 3. Forcing one’s own cultural beliefs and practices on another person is an example of a. stereotyping. b. ethnocentrism. c. cultural relativity. d. cultural imposition. 4. Which statement most accurately describes cultural factors that may affect health? a. Diabetes and cancer rates differ by cultural/ethnic groups. b. There are limited ethnic variations in physiologic responses to drugs. c. Most patients find that religious rituals help them during times of illness. d. Silence during a nurse-patient interaction means the patient understands the instructions. 5. As part of the nursing process, cultural assessment is best accomplished by a. judging the patient’s cultural values based on observations. b. using a cultural assessment guide as part of the nursing process. c. seeking guidance from a nurse from the patient’s cultural background. d. relying on the nurse’s previous experience with patients

from that cultural group. 6. Nurses play a key role in promoting health equity. An important mechanism to do this is to a. discourage use of evidence-based practice guidelines. b. insist that patients adhere to established clinical guidelines. c. teach patients to use the Internet to find resources related to their health. d. engage in active listening and establish relationships with patients and families. 7. What is the first step in developing cultural competence? a. Create opportunities to interact with a variety of cultural groups. b. Examine the nurse’s own cultural background, values, and beliefs about health and health care. c. Learn about a multitude of folk medicines and herbal substances that different cultures use for self-care. d. Learn assessment skills for different cultural groups, including cultural beliefs and practices and physical assessments. 8. When communicating with a patient who speaks a language that the nurse does not understand, it is important to first attempt to a. have a family member interpret. b. use a trained medical interpreter. c. use specific medical terminology so there will be no mistakes. d. focus on the translation rather than nonverbal

communication. 1. a, b, d, 2. b, 3. d, 4. a, 5. b, 6. d, 7. b, 8. b For rationales to these answers and even more NCLEX review questions, visit http://evolve.elsevier.com/Lewis/medsurg.

Evolve Website/Resources List http://evolve.elsevier.com/Lewis/medsurg

Review Questions (Online Only) Key Points Answer Keys for Questions • Rationales for Bridge to NCLEX Examination Questions • Answer Guidelines for Case Study on p. 31 Conceptual Care Map Creator Audio Glossary Content Updates

References 1. World Health Organization: Health impact assessment. Retrieved from www.who.int.hia.en. 2. Kaiser Family Foundation: Disparities in health and health care. Retrieved from www.kff.org/disparitiespolicy/issue-brief/disparities-in-health-and-health-carefive-key-questions-and-answers/. 3. U.S. Census Bureau : Population estimates. Retrieved from www.census.gov/programssurveys/popest.html. Hess CN, Kaltenbach LA, Doll JA, et al Race and sex differences in

post-myocardial infarction angina frequency and risk of 1-year unplanned rehospitalization, Circulation 135:532, 2017. Willman CL: Cancer health disparities in American Indian and Alaskan Native populations, Cancer 77:13, 2017.

6. U.S. Census Bureau: Measuring America, our changing landscape. Retrieved from www.census.gov/library/visualizations/2016/comm/acsrural-urban.html. DeKeseredy WS, Hall-Sanchez A, Dragiewicz M, et al Intimate violence against women in rural communities. In Donnermeyer JF, editor: The Routledge international handbook of rural criminology, London, 2016, Routledge. Shaw LJ, Pepine CJ, Xie J, et al Quality and equitable health care gaps for women: Attributions to sex differences in cardiovascular medicine, J Am Coll Cardiol 70:373, 2017.

9. Correa-de-Araujo R: Health disparities: Access and utilization, New York, 2017, Springer. 10. Cigna: LGBT and health disparities. Retrieved from www.cigna.com/healthwellness/lgbt/lgbt-disparities. 11. Giger JN: Transcultural nursing: Assessment and intervention, ed 7, St Louis. 2016, Mosby. 12. Schwartz SJ, Unger J. The Oxford handbook of acculturation and health, New York, 2017, University Press. Darroch F, Giles A, Sanderson P, et al The United States does CAIR about cultural safety, J Transcult Nurs 28:269, 2017. Betancourt JR, Green AR, Carrillo JE, et al Defining cultural competence: A practical framework for addressing racial/ethnic disparities in health and health care, Public Health Rep 118:293, 2016.

15. Minority Nurse: Nursing statistics. Retrieved from http://minoritynurse.com/nursing-statistics/. Han W, Lee S: Racial/ethnic variation in health care satisfaction: The

role of acculturation, Soc Work Health Care 55:694, 2016. Hall JM, Carlson K: Marginalization, Adv Nurs Sci 39:200, 2016. Schmit KM: Tuberculosis—United States 2016, MMWR 66:289, 2017.

19. Centers for Disease Control and Prevention: Refugee health guidelines. Retrieved from www.cdc.gov/immigrantrefugeehealth/guidelines/refugeeguidelines.html. 20. American Association of Colleges in Nursing: Cultural competency in baccalaureate nursing education. Retrieved from www.aacnnursing.org/Education-Resources/ToolKits/Cultural-Competency-in-Nursing-Education. 21. Jarvis C: Physical examination and health assessment, ed 7, Philadelphia, 2016, Saunders. 22. U.S. Department of Health and Human Services: Think cultural health. Retrieved from www.ThinkCulturalHealth.hhs.gov. Evidence-based information for clinical practice.

3

Health History and Physical Examination Courtney Reinisch

LEARNING OUTCOMES 1. Explain the purpose, components, and techniques of a patient’s health history and physical examination. 2. Obtain a nursing history using a functional health pattern format. 3. Select appropriate techniques of inspection, palpation, percussion, and auscultation for physical examination of a patient. 4. Distinguish among emergency, comprehensive, and focused types of assessment in terms of indications, purposes, and components.

KEY TERMS auscultation, p. 38 database, p. 33 functional health patterns, p. 35 inspection, p. 38 nursing history, p. 34

objective data, p. 34 palpation, p. 38 percussion, p. 38 subjective data, p. 34 We make a living by what we get, but we make a life by what we give. Winston Churchill http://evolve.elsevier.com/Lewis/medsurg/

Conceptual Focus Clinical Judgment Collaboration Communication During the assessment phase of the nursing process, you will obtain a patient’s health history and perform a physical examination. This serves as part of the interprofessional team evaluation. The interprofessional team, also known as an interdisciplinary, transdisciplinary, or multidisciplinary team, is made up of a number of health care professionals who provide care to a patient. The findings of your nursing assessment (1) contribute to a database that identifies the patient’s current and past health status and (2) provide a baseline against which future changes can be evaluated. The purpose of the nursing assessment is to enable you to make clinical judgments about your patient’s health status.1 Assessment is the first step of the nursing process. It is performed continually throughout the nursing process to validate nursing diagnoses, evaluate nursing interventions, and determine whether patient outcomes and goals have been met. The language of assessment is complex, with many overlapping and confusing terms. In this text, assessment describes a hands-on data

collection process and a database identifies a specific list of information (data) to collect.

Data Collection The database is all the health information about a patient. It includes (1) nursing history and physical examination, (2) the medical history and physical examination, and (3) laboratory and diagnostic test results. A nurse and health care provider (HCP) perform a patient history and a physical examination using formats and data based on each discipline’s focus.

Medical Focus A medical history is designed to collect data to be used primarily by the HCP to determine risk for disease and diagnose medical conditions. The medical history is usually collected by a member of the health care team (e.g., physician, advanced practice nurse [APN], resident, physician’s assistant, medical student). The HCP’s physical examination and diagnostic tests aid in establishing medical diagnoses and implementing and monitoring the medical treatment plan. The information collected and reported by the HCP is used by nurses and other health care team members (e.g., pharmacist, physical therapist, dietitian, social worker) based on the focus of their care. For example, the abnormal results of a neurologic examination by an APN may aid in diagnosing a stroke. You may use the same results to identify a priority nursing diagnosis of fall risk. A physical therapist may use this information to plan therapy involving range-of-motion exercises.

Nursing Focus The focus of nursing care is the diagnosis and treatment of human responses to actual or potential health problems or life processes. The information obtained from the nursing history and physical

examination is used to determine the patient’s strengths and responses to a health problem. For example, a patient with a diagnosis of diabetes may respond with anxiety or a lack of knowledge about self-managing the condition. This patient may experience the physical response of fluid volume deficit because of the abnormal fluid loss caused by hyperglycemia. These human responses to the condition of diabetes are diagnosed and treated by nurses. During the nursing history interview and physical examination, you will obtain and record the data to support the identification of nursing diagnoses (Fig. 3.1).

Types of Data The database includes subjective and objective data. Subjective data, also known as symptoms, are collected by interviewing the patient and/or caregiver during the nursing history. This type of data includes information that can be described or verified only by the patient or caregiver. It is what the person tells you either spontaneously or in response to a direct question. Objective data, also known as signs, are data that can be observed or measured. You obtain this type of data using inspection, palpation, percussion, and auscultation during the physical examination. Objective data are also acquired by diagnostic testing. Patients often provide subjective data while you are performing the physical examination. You will observe objective signs while interviewing the patient. All the findings related to a specific problem, whether subjective or objective, are known as clinical manifestations of that problem.

Interview Considerations The purpose of the patient interview is to obtain a health history (i.e., subjective data) about the patient’s past and present health state. Effective communication is needed in the interview process. Creating a climate of trust and respect is critical to establishing a therapeutic relationship.2 You need to communicate acceptance of the patient as a

person by using an open, responsive, nonjudgmental approach. You communicate through spoken language, as well as in your manner of dress, gestures, and body language. Culture influences the words, gestures, and postures one uses and the information that is shared with others (see Chapter 2).

FIG. 3.1 Conducting a nursing focused interview. Courtesy Linda Bucher, RN, PhD, CEN, CNE, Staff Nurse, Virtua Memorial Hospital, Mt. Holly, N.J.

In addition to understanding the principles of effective communication, you will develop a personal style of relating to patients. One style of communication does not fit all. The wording of questions can increase the likelihood of obtaining the needed information. The ease of asking questions, particularly those related to sensitive areas such as sexual functioning, comes with training and experience. The amount of time you need to complete a nursing history varies with the format used and your experience. The nursing history may

be completed in 1 or several sessions, depending on the setting and patient. For example, an older adult patient with a low energy level may need a few brief interviews to allow time for the patient to give the needed information. You must make a judgment about the amount of information to collect on initial contact with the patient. In interviews with patients with chronic disease, patients in pain, and patients in emergency situations, ask only those questions that are pertinent to a specific problem. You can complete the health history interview at a more appropriate time. Judge the reliability of the patient as a historian. An older adult may give a false impression about his or her mental status because of a prolonged response time or visual and hearing impairments. The complexity and long duration of health problems may make it hard for an older adult or a chronically ill younger patient to be an accurate historian. It is important for you to determine the patient’s priority concerns and expectations, since your priorities may be different from the patient’s. For example, your priority may be to complete the health history, while the patient is interested only in relief from symptoms. Until the patient’s priority need is met, you will probably be unsuccessful in obtaining complete and accurate data.

Nursing Management Assessment and Data Collection In acute care, a registered nurse (RN) must complete the initial (admission) nursing assessment within the timeframe determined by the agency. Ongoing data collection is expected of all members of the health care team. • On admission, complete a comprehensive assessment (Table 3.4). • Obtain patient’s health history by interviewing patient and/or caregiver.

• Perform physical examination using inspection, palpation, percussion, and auscultation as appropriate. • Document findings from the health history and physical examination in the patient’s record. • Organize patient data into functional health patterns (Table 3.2). • Develop and prioritize nursing and collaborative problems for the patient. • Throughout hospitalization, perform focused assessments based on patient’s history or clinical manifestations (Table 3.7). • Oversee aspects of data collection by UAP. • Vital signs, including oxygen saturation • Height and weight, oral intake, and output • Per agency policy, point-of-care testing (e.g., glucose)

Symptom Investigation At any time during the assessment the patient may report a symptom such as pain, fatigue, or weakness. Because we do not observe symptoms patients experience, the symptoms must be explored. Table 3.1 shows a mnemonic (PQRST) to help you remember the areas to explore when a symptom is reported. The information you receive may help determine the cause of the symptom. A common symptom that you will assess is pain (see Chapter 8). For example, if a patient states that he has “pain in his leg,” you would assess and record the data using PQRST. Has right midcalf pain that usually occurs at work when climbing stairs after lunch (P). Pain is alleviated by stopping and resting for 2 to 3 minutes. Patient states he has been “eating a banana every day for extra potassium” but “it hasn’t helped” (P). Pain is described as “stabbing” and is non-radiating (Q, R). Pain is so severe (rating 9 on 010 scale) that patient cannot continue activity (S). Onset is abrupt, occurring once or twice daily. It last occurred yesterday while cutting the lawn (T).

Data Organization You must systematically obtain and organize assessment data so you can readily analyze and make judgments about the patient’s health status and any health problems. Some assessment forms are organized using body systems. Although helpful, these types of forms may be incomplete because they may omit areas such as health promotion behaviors, sleep, coping, and values. Functional health patterns, developed by Gordon,3 provide the framework used throughout this book for obtaining a nursing history. This format includes an initial collection of important health information followed by assessment of 11 areas of health status or function (Table 3.2). Data organized in this format allow for the identification of areas of wellness (or positive function) and health problems.2

Culturally Competent Care: Assessment The process of obtaining a health history and performing a physical examination is an intimate experience for you and the patient. Culture influences patterns of communication and the information one shares with others. During the interview and physical examination, be sensitive to issues of eye contact, space, modesty, and touching, as discussed in Chapter 2. Knowing the cultural norms related to malefemale relationships is especially important during the physical examination. To avoid violating any culturally based practices, ask the patient about cultural values. Determine if the patient would like to have someone present during the history or physical examination or someone of the same gender to perform the history and physical examination.1

Nursing History: Subjective Data Important Health Information Important health information offers an overview of past and present

medical conditions and treatments. Past health history, medications, allergies, and surgery or other treatments are included in this part of the history.

Past Health History The past health history provides information about the patient’s prior state of health. Ask the patient about major childhood and adult illnesses, injuries, hospitalizations, and surgeries. Specific questions are more effective than simply asking whether the patient has had any illness or health problems in the past. For example, asking “Do you have a history of diabetes?” elicits better information than asking “Do you have any chronic health problems?”

Medications Ask the patient for specific details related to past and current medications, including prescription and illicit drugs, over-the-counter (OTC) drugs, vitamins, herbs, and dietary supplements. Patients often do not consider herbs and dietary supplements as drugs. It is important to specifically ask about their use because they can interact adversely with existing or newly prescribed medications (see the Complementary & Alternative Therapies box).

Complementary & Alternative Therapies Assessment of Use of Herbs and Dietary Supplements

Why Assessment Is Important • Herbs and dietary supplements may have side effects or may interact adversely with prescription or OTC drugs. • Patients at high risk for drug-herb interactions include those taking anticoagulant, antihypertensive, antidepressant, or immune-regulating therapy and patients undergoing anesthesia.

Most herbs must be stopped 2 to 3 weeks before surgery. • Many patients do not tell HCPs that they are using herbs and dietary supplements. They may fear HCPs will disapprove of their use. • Many herbal preparations have a variety of ingredients. Ask the patient or caregiver to bring labeled containers to the health care site to determine product composition.

Nurse’s Role • Patients typically share information about the use of herbs and dietary supplements with you if you ask them. • Create an accepting and nonjudgmental attitude when assessing use or interest in herbs or dietary supplements. • Use open-ended questions such as, “What types of herbs, vitamins, or supplements do you take?” and “What effects have you noticed from using them?” • Document the use of any herb(s) or dietary supplements in the patient record, including the name, amount, frequency of use, and any side effects. • Inform patients of the following: • Risks and benefits associated with herbal use, including drug-herb interactions • Health food store employees are not licensed HCPs • Importance of carefully reading the labels of herbal therapies and dietary supplements and taking only the recommended amount • Moisture, sunlight, and heat may change the components of herbs • Many herbal therapies have side effects. Report these to the HCP at once. Question older adult and chronically ill patients about medication

routines. Look for issues related to medication cost and polypharmacy. Changes in absorption, metabolism, and elimination of drugs can pose serious potential problems for these patients.4

Allergies Explore the patient’s history of allergies to drugs, latex, contrast media, food, and the environment (e.g., pollen). Include a detailed description of any allergic reaction(s) reported by the patient.

Surgery or Other Treatments Record all surgeries, along with the date, reason for the surgery, and outcome. The outcome includes whether the problem was resolved or has residual effects. Ask about and record any blood products the patient has received.

Table 3.1 Investigation of Patient-Reported

Symptom

Functional Health Patterns Assess the patient’s functional health patterns to identify effective, dysfunctional, and potential dysfunctional health patterns. Dysfunctional health patterns occur with disease. Potential dysfunctional

patterns identify risk conditions for problems. You may identify patients with effective health function who want a higher level of wellness. Table 3.2 gives examples of possible questions to ask the patient related to functional health patterns.

Health Perception–Health Management Pattern This pattern focuses on the patient’s perceived level of health and well-being and on personal practices for maintaining health. Ask the patient to describe his or her personal health and any concerns about it. Explore the patient’s feelings of effectiveness at staying healthy by asking what helps and what hinders his or her well-being. Ask the patient to rate his or her health as excellent, good, fair, or poor. When possible, record this information in the patient’s own words. Next, ask about the type of HCP the patient uses. For example, if the patient is Native American, a medicine man may be considered the primary HCP. If the patient is of Hispanic origin, a curandero, a Hispanic healer who uses folk medicine and herbs to treat patients, may be the primary HCP (see Chapter 2). Other questions seek to identify risk factors by obtaining a thorough family history (e.g., heart disease, cancer, genetic disorders), history of personal health habits (e.g., tobacco, alcohol, drug use), and history of exposure to environmental hazards (e.g., asbestos). If the patient is hospitalized, ask about the expectations for this experience. Have the patient describe his or her understanding of the current health problem, including its onset, course, and treatment. These questions obtain information about a patient’s knowledge of the health problem and ability to use appropriate resources to manage the problem.

Nutritional-Metabolic Pattern This pattern assesses the processes of ingestion, digestion, absorption, and metabolism. Obtain a 24-hour diet recall from the patient to evaluate the quantity and quality of foods and fluids consumed. If a problem is found, ask the patient to keep a 3-day food diary for a more careful analysis of dietary intake. Assess the impact of psychologic factors such as depression, anxiety, stress, and self-

concept on nutrition. Evaluate socioeconomic and cultural factors such as food budget, who prepares the meals, and food preferences. Determine whether the patient’s present condition has interfered with eating and appetite by exploring any symptoms of nausea, intestinal gas, or pain. Food allergies should be distinguished from food intolerances, such as lactose or gluten intolerance.

Elimination Pattern This pattern involves bowel, bladder, and skin function. Ask the patient about the frequency of bowel and bladder activity. Ask about urgency, incontinence, and diuretic use. Inquire about stool consistency, color, and laxative use. Assess the skin in the elimination pattern in terms of its excretory function.

Activity-Exercise Pattern Assessing this pattern looks at the patient’s usual pattern of exercise, work activity, leisure, and recreation. Question the patient about his or her ability to perform activities of daily living (ADLs) and note any specific problems. Table 3.2 includes a scale for rating the functional levels of common activities.

Sleep-Rest Pattern This pattern describes the patient’s perception of his or her pattern of sleep, rest, and relaxation in a 24-hour period. Elicit this information by asking, “Do you feel rested when you wake up?”

Cognitive-Perceptual Pattern Assessing this pattern involves a description of all the senses and cognitive functions. Assess pain as a sensory perception (see pain assessment in Chapter 8). Ask the patient about any sensory deficits that affect the ability to perform ADLs. Record ways in which the patient compensates for any sensory-perceptual problems. Ask the patient how he or she learns best and in what language. Ask what he or she understands about the illness and treatment plan. Plan patient

teaching according to identified needs and preferences (see Chapter 4 for details on patient teaching).

Self-Perception–Self-Concept Pattern This pattern describes the patient’s self-concept, which is critical in determining the way the person interacts with others. Included are attitudes about self, perception of personal abilities, body image, and general sense of worth. Ask the patient for a self-description and about how his or her health condition affects self-concept. Patients’ expressions of hopelessness or loss of control often reflect an inability to care for one’s self.

TABLE 3.2 Health HistoryFunctional Health

Pattern Format

CPAP, Continuous positive airway pressure. ∗

If appropriate.



For women.

Modified from Gordon M: Manual of nursing diagnosis, ed 13, Boston, 2014, Jones & Bartlett.

Role-Relationship Pattern This pattern reveals the patient’s roles and relationships, including major responsibilities. Ask the patient to describe family, social, and work roles and relationships and to rate his or her performance of the expected behaviors related to these. Determine whether patterns in these roles and relationships are satisfactory or whether strain is evident. Note the patient’s feelings about how the present condition affects his or her roles and relationships.

Sexuality-Reproductive Pattern This pattern describes satisfaction or dissatisfaction with personal sexuality and describes reproductive issues. Assessing this pattern is important because many illnesses, surgical procedures, and drugs affect sexual function. A patient’s sexual and reproductive concerns may be expressed. Teaching needs may be identified through information obtained in this pattern. You may feel uncomfortable obtaining information related to sexuality. However, it is important to take a health history and screen for sexual function and dysfunction in a nonjudgmental way. Provide appropriate information or refer the patient to a more experienced HCP.

Coping–Stress Tolerance Pattern This pattern describes the patient’s general coping and the effectiveness of the coping mechanisms. Assessing this pattern involves analyzing the specific stressors or problems that confront the patient, the patient’s perception of the stressors, and the patient’s response to the stressors. Document any major losses or stressors

experienced by the patient in the previous year. Note strategies used by the patient to deal with stressors and relieve tension. Ask about persons and groups that make up the patient’s social support networks.

Value-Belief Pattern This pattern describes the values, goals, and beliefs (including spiritual) that guide health-related choices. Document the patient’s ethnic background and effects of culture and beliefs on health practices. Note and respect the patient’s wishes about continuation of religious or spiritual practices and the use of religious articles.

Physical Examination: Objective Data General Survey After the nursing history, make a general survey statement. This is your general impression of a patient, including behavioral observations. The initial survey begins with your first encounter with the patient and continues during the health history interview. The major areas included in the general survey statement are (1) body features, (2) mental state, (3) speech, (4) body movements, (5) obvious physical signs, (6) nutritional status, and (7) behavior. Vital signs and body mass index (BMI) (calculated from height and weight [kg/m2]) may be included. The following is a sample of a general survey statement: A.H. is a 34-yr-old Hispanic woman, BP 130/84, P 88, R 18. No distinguishing body features. Alert but anxious. Speech rapid with trailing thoughts. Wringing hands and shuffling feet during interview. Skin flushed, hands clammy. Overweight relative to height (BMI = 28.3 kg/m2). Sits with eyes downcast, shoulders slumped, and avoids eye contact.

Physical Examination

The physical examination is the systematic assessment of a patient’s physical status. Explore any positive findings using the same criteria used when investigating a symptom in the nursing history (Table 3.1). A positive finding shows that the patient has or has had the particular problem or sign under discussion (e.g., if the patient with jaundice has an enlarged liver, it is a positive finding). Relevant information about this problem should then be gathered. Negative findings may be significant. A pertinent negative finding is the absence of a sign or symptom usually associated with a problem. For example, peripheral edema is common with advanced liver disease. If edema is not present in a patient with advanced liver disease, specifically note this as “no peripheral edema.”

Techniques Four major techniques are used in performing the physical examination: inspection, palpation, percussion, and auscultation. The techniques are usually performed in this sequence: inspection, palpation, percussion, and auscultation. The abdominal examination is an exception. Inspection is first, followed by auscultation, percussion, and palpation. Performing percussion and palpation before auscultation can alter bowel sounds and produce false findings. Not every assessment area requires the use of all 4 assessment techniques (e.g., musculoskeletal system requires only inspection and palpation).

Inspection Inspection is the visual examination of a part or region of the body to assess normal conditions or deviations. Inspection is more than just looking. This technique is deliberate, systematic, and focused. Compare what is seen with the known, generally visible characteristics of the body part that you are inspecting. For example, most 30-yr-old men have hair on their legs. Absence of hair may indicate a vascular problem and the need for further investigation, or it may be normal for a patient of a particular ethnicity (e.g., Filipino men have little body hair). Always compare 1 side of the patient’s

body to the other to assess bilaterally for any abnormal findings.

Palpation Palpation is the examination of the body using touch. Using light and deep palpation can yield information related to masses, pulsations, organ enlargement, tenderness or pain, swelling, muscular spasm or rigidity, elasticity, vibration of voice sounds, crepitus, moisture, and texture. Different parts of the hand are more sensitive for specific assessments. For example, use the palmar surface (base of fingers) to feel vibrations, the dorsa (backs) of your hands and fingers to assess skin temperature, and tips of your fingers to palpate the abdomen1 (Fig. 3.2).

Percussion Percussion is a technique that produces a sound and vibration to obtain information about the underlying area (Fig. 3.3). The sounds and vibrations are relative to the underlying structures. A change from an expected sound may indicate a problem. For example, dullness in the right lower quadrant instead of the normal sound of tympany should be explored. Specific percussion sounds of various body parts and regions are discussed in the appropriate assessment chapters.

Auscultation Auscultation involves listening to sounds produced by the body with a stethoscope to assess normal and abnormal conditions. This technique is useful in evaluating sounds from the heart, lungs, abdomen, and vascular system. The bell of the stethoscope is more sensitive to low-pitched sounds (e.g., heart murmurs). The diaphragm of the stethoscope is more sensitive to high-pitched sounds (e.g., bowel sounds). Some stethoscopes have only a diaphragm, designed to transmit low- and high-pitched sounds. To listen for low-pitched sounds, hold the diaphragm lightly on the skin. For high-pitched sounds, press the diaphragm firmly on the skin (Fig. 3.4).1 Specific

sounds and auscultation techniques are discussed in the appropriate assessment chapters.

FIG. 3.2 Palpation is the examination of the body using touch. From Jarvis C: Physical examination and health assessment, ed 7, St Louis, 2015, Saunders.

FIG. 3.3 Percussion is tapping of the patient’s skin with the middle finger or striking finger of the dominant hand. Hyperextend the middle finger of the nondominant hand and place its distal joint and tip firmly on the patient’s skin. Normal percussion sounds: resonant—lung tissue; tympany—air-filled viscus (e.g., intestines); dull—dense organs (e.g., liver); flat—no air present (e.g., bone, muscle). Adapted from Jarvis C: Physical examination and health assessment, ed 7, St Louis, 2015, Saunders.

Equipment

Collect the equipment needed for the physical examination before you begin (Table 3.3). This saves time and energy for you and the patient. It promotes trust by showing a level of professionalism. The use of specific equipment is discussed in the appropriate assessment chapters.

Organization of Examination Perform the physical examination systematically and efficiently. Give explanations to the patient as the examination proceeds and consider the patient’s comfort, safety, and privacy. Follow the same sequence every time to avoid omitting a procedure, a step in the sequence, or a part of the body. Table 3.4 presents a comprehensive, organized physical examination outline.

FIG. 3.4 Auscultation is listening to sounds produced by the body to assess normal conditions and deviations from normal.

Courtesy Linda Bucher, RN, PhD, CEN, CNE, Staff Nurse, Virtua Memorial Hospital, Mt. Holly, N.J.

TABLE 3.3 Common Physical Examination

Equipment

• Alcohol swabs • Blood pressure cuff • Cotton balls • Examining table or bed • Eye chart (e.g., Snellen eye chart) • Paper cup with water • Patient gown • Pocket flashlight • Reflex hammer • Stethoscope (with bell and diaphragm or a dual-purpose diaphragm; tubing 15–18 inches [38–46 cm]) • Tongue blades • Watch (with second hand or digital)

Adapting the physical examination is often useful for the older adult patient, who may have age-related problems such as decreased mobility, limited energy, and perceptual changes.5 An outline listing some useful adaptations is found in Table 3.5. A nurse with appropriate education can perform advanced techniques. A retinal reflex examination would be done with an eye examination. Speculum and bimanual examination of women and the prostate gland examination of men would be performed after inspecting the genitalia.

Recording Physical Examination At the end of the examination, record the normal and abnormal findings in the patient’s health record. See Table 3.6 for an example of

how to record findings of a normal physical examination of a healthy adult. See Table 5.5 to find age-related assessment findings in the book.

Types of Assessment Different types of assessment are used to obtain information about a patient. These approaches are divided into 3 types: emergency, comprehensive, and focused (Table 3.7). Decide what type of assessment to perform based on the clinical situation. Sometimes the health care agency provides guidelines, and other times it is a nursing judgment.

Emergency Assessment An emergency assessment may be done in an emergency or lifethreatening situation. This involves a rapid history and examination of a patient while supporting vital functions.

TABLE 3.4 Physical Examination Outline

1. General Survey Observe general state of health (patient is seated). • Body features • Mental state and level of orientation • Speech • Body movements • Physical appearance • Nutritional status • Behavior

2. Vital Signs Record vital signs. • Blood pressure—both arms for comparison • Apical/radial pulse • Respiration • Temperature • Oxygen saturation Record height and weight; calculate body mass index (BMI).

3. Integument Inspect and palpate skin for the following: • Color • Integrity (e.g., lacerations, lesions, breakdown) • Scars, tattoos, piercings • Bruises, rash • Edema • Moisture • Texture • Temperature • Turgor • Vascularity Inspect and palpate nails for the following: • Color • Lesions • Size • Shape • Angle

• Capillary refill time

4. Head and Neck Inspect and palpate head for the following: • Shape and symmetry of skull • Masses • Tenderness • Condition of hair and scalp • Temporal arteries • Temporomandibular joint • Sensory (CN V, light touch, pain) • Motor (CN VII, shows teeth, purses lips, raises eyebrows) • Looks up, wrinkles forehead (CN VII) • Raises shoulders against resistance (CN XI) Inspect and palpate (occasionally auscultate) neck for the following: • Skin (vascularity and visible pulsations) • Symmetry • Range of motion • Pulses and bruits (carotid) • Midline structure (trachea, thyroid gland, cartilage) • Lymph nodes (preauricular, postauricular, occipital, mandibular, tonsillar, submental, anterior and posterior cervical, infraclavicular, supraclavicular) Test visual acuity. Inspect and lightly palpate eyes/eyebrows for the following: • Position and movement of eyelids (CN VII)

• Visual fields (CN II) • Extraocular movements (CN III, IV, VI) • Cornea, sclera, conjunctiva • Pupillary response (CN III) • Red reflex Inspect and palpate nose and sinuses for the following: • External nose: Shape, blockage • Internal nose: Patency of nasal passages, shape, turbinates or polyps, discharge • Frontal and maxillary sinuses Inspect and palpate ears for the following: • Placement • Pinna • Auditory acuity (whispered voice, ticking watch) (CN VIII) • Mastoid process • Auditory canal • Tympanic membrane Inspect and palpate mouth for the following: • Lips (symmetry, lesions, color) • Buccal mucosa (Stensen’s and Wharton’s ducts) • Teeth (absence, state of repair, color) • Gums (color, receding from teeth) • Tongue for strength (asymmetry, ability to stick out tongue, side to side, fasciculations) (CN XII) • Palates

• Tonsils and pillars • Uvular elevation (CN IX) • Posterior pharynx • Gag reflex (CN IX and X) • Jaw strength (CN V) • Moisture • Color • Floor of mouth

5. Extremities Observe size and shape, symmetry and deformity, involuntary movements. Inspect and palpate arms, fingers, wrists, elbows, shoulders for the following: • Strength • Range of motion • Joint pain • Swelling • Pulses (radial, brachial) • Sensation (light touch, pain, temperature) • Test reflexes: Triceps, biceps, brachioradialis Inspect and palpate legs for the following: • Strength • Range of motion • Joint pain • Swelling, edema • Hair distribution • Sensation (light touch, pain, temperature) • Pulses (dorsalis pedis, posterior tibialis) • Test reflexes: Patellar, Achilles, plantar

6. Posterior Thorax Inspect for muscular development, scoliosis, respiratory movement, approximation of AP diameter. • Palpate for symmetry of respiratory movement, tenderness of CVA, spinous processes, tumors or swelling, tactile fremitus • Percuss for pulmonary resonance • Auscultate for breath sounds • Auscultate for egophony, bronchophony, whispered pectoriloquy

7. Anterior Thorax • Assess breasts for configuration, symmetry, dimpling of skin • Assess nipples for rash, direction, inversion, retraction • Inspect for apical impulse, other precordial pulsations • Palpate the apical impulse and the precordium for thrills, lifts, heaves, tenderness • Inspect neck for venous distention, pulsations, waves • Palpate lymph nodes in the subclavian, axillary, brachial areas • Palpate breasts • Auscultate for rate and rhythm; character of S1 and S2 in the aortic, pulmonic, Erb’s point, tricuspid, mitral areas; bruits at carotid, epigastrium

8. Abdomen • Inspect for scars, shape, symmetry, bulging, muscular position and condition of umbilicus, movements (respiratory, pulsations, presence of peristaltic waves) • Auscultate for peristalsis (i.e., bowel sounds), bruits • Percuss then palpate to confirm positive findings; check liver

(size, tenderness), spleen, kidney (size, tenderness), urinary bladder (distention) • Palpate femoral pulses, inguinofemoral nodes, abdominal aorta

9. Neurologic Observe motor status: • Gait • Toe walk • Heel walk • Drift Observe coordination: • Finger to nose • Romberg sign • Heel to opposite shin Observe the following: • Proprioception (position sense of great toe)

10. Genitalia Male External Genitalia • Inspect penis, noting hair distribution, prepuce, glans, urethral meatus, scars, ulcers, eruptions, structural changes, discharge • Inspect epidermis of perineum, rectum • Inspect skin of scrotum; palpate for descended testes, masses, pain

Female External Genitalia • Inspect hair distribution; mons pubis, labia (minora and majora); urethral meatus; Bartholin’s, urethral, Skene’s glands (may be palpated, if indicated); introitus; any discharge • Assess for presence of cystocele, prolapse • Inspect perineum, rectum AP, Anteroposterior; CN, cranial nerve; CVA, costovertebral angle.

TABLE 3.5 Gerontologic Assessment

DifferencesAdaptations in Physical Assessment Techniques

General Approach Keep patient warm and comfortable because loss of subcutaneous fat decreases ability to stay warm. Adapt positioning to physical limitations. Avoid unnecessary changes in position. Perform as many activities as possible in the position of comfort for the patient.

Skin Handle with care because of fragility and loss of subcutaneous fat.

Head and Neck Provide a quiet environment free from distraction because of possible sensory impairments (e.g., decreased vision, hearing).

Extremities Use gentle movements and reinforcement techniques. Avoid having patient hop on 1 foot or perform deep knee bends if patient has limited range of motion of the extremities, decreased reflexes, or diminished sense of balance.

Thorax Adapt examination for changes related to decreased force of

expiration, weakened cough reflex, and shortness of breath.

Abdomen Use caution in palpating patient’s liver because it is readily accessible because of a thinner, softer abdominal wall. The older adult patient may have diminished pain perception in the abdominal wall.

Comprehensive Assessment A comprehensive assessment includes a detailed health history and physical examination of all body systems. This is typically done on admission to the hospital or onset of care in a primary care setting.

Focused Assessment A focused assessment is an abbreviated health history and examination. It is used to evaluate the status of previously identified problems and monitor for signs and symptoms of new problems. It can be done when a specific problem (e.g., pneumonia) is identified. The patient’s clinical manifestations guide a focused assessment. For example, abdominal pain signals the need for a focused assessment of the abdomen. Some problems need a focused assessment of more than 1 body system. A patient with a headache may need musculoskeletal, neurologic, and head and neck examinations. Examples of focused assessments for the various body systems are found in each assessment chapter of this book.

Using Assessment Approaches Assessment in an inpatient, acute care hospital setting is different from assessment in other settings. Focused assessment of the hospitalized patient is frequent and performed by many different HCPs. A team approach demands a high degree of consistency among HCPs from a variety of disciplines. As you gain experience, you will be able to form a mental image of a patient’s status from a few basic details, such as “85-yr-old Hispanic

woman admitted for COPD exacerbation.” Details from a complete verbal report, including length of stay, laboratory results, physical findings, and vital signs will help you make a clearer picture. Next, perform your own assessment using a focused approach. During your assessment, you will confirm or revise the findings that you read in the medical record and what you heard from other HCPs. Remember, the process does not end once you have done your first assessment on a patient during rounds. Continue to gather information about all your patients throughout your shift. Everything you learned previously about each patient is considered in light of new information. For example, when you are doing a respiratory assessment on your patient with COPD, you hear crackles in her lungs. This finding should lead you to do a cardiovascular assessment because heart problems (e.g., heart failure) can also cause crackles. As you gain experience, the importance of new findings will be more obvious to you. Assessment case studies integrated into all the assessment chapters will help you develop your assessment skills and knowledge.

TABLE 3.6 Findings From a Physical Examination

of a Healthy AdultExample

General Status Well-nourished, well-hydrated, well-developed white (woman) or (man) in NAD, appears stated age, speech clear and evenly paced; is alert and oriented ×3; cooperative, calm; BMI 23.8

Skin Clear lesions, warm and dry, trunk warmer than extremities, normal skin turgor, no ↑ vascularity, no varicose veins

Nails Well-groomed, round 160-degree angle lesions, nail beds pink, capillary refill 15 apnea/hypopnea events/hour), continuous positive airway pressure (CPAP) by mask is the treatment of choice. With CPAP, the patient applies a nasal mask that is attached to a high-flow blower (Fig. 7.5). The blower is adjusted to maintain enough positive pressure (5–25 cm H2O) in the airway during inspiration and expiration to prevent airway collapse. Some patients cannot adjust to wearing a mask over the nose or mouth or to exhaling against the high pressure. A technologically more sophisticated therapy, bilevel positive airway pressure (BiPAP), can deliver a higher inspiration pressure and a lower pressure during expiration. With BiPAP, the apnea can be relieved with a lower mean pressure and may be better tolerated. CPAP reduces apnea episodes, daytime sleepiness, and fatigue. It improves quality of life ratings and returns cognitive functioning to normal. Benefits of CPAP are dose-dependent based on how long the device is used during the night. It must be used a minimum of 4 hours each night to reduce/reverse the negative cardiovascular effects of OSA.20 Although CPAP is a highly effective treatment, patients have problems with using it every day. About two-thirds of those using CPAP report side effects such as nasal stuffiness.

FIG. 7.5 Examples of positive airway pressure devices for sleep apnea. A, Patient wearing a nasal mask and headgear (positive pressure only through nose). B, Patient wearing nasal pillows (positive pressure only through nose). C, Patient wearing a full face mask (positive pressure to nose and mouth). From Goldman L, Schafer AI: Goldman’s Cecil medicine, ed 24, Philadelphia, 2012, Saunders.

First, assess the patient’s knowledge about OSA and CPAP. Involve the bed partner in teaching. Assess the patient for nasal resistance. To ensure successful adherence to CPAP treatment, patients need to be involved in choosing the mask and device before the start of therapy. Patient-centered care may improve patient outcomes given that OSA treatment requires behavioral and lifestyle changes. You can facilitate goal-setting discussions between patients and HCPs to arrive at treatment plans that are feasible and mutually agreed upon. When patients with a history of OSA are hospitalized, be aware that giving opioid analgesics and sedating medications (benzodiazepines, hypnotics) may worsen OSA symptoms by depressing respirations. Check with the HCP in charge of the patient’s care to determine if a patient who uses home CPAP or BiPAP should continue this therapy in the hospital. If so, it is important for these patients to wear the device when resting or sleeping. Many patients can use their own equipment but check hospital policy to be certain it can be used.

Surgical Treatment If other measures fail, OSA can be managed surgically. The goal of OSA surgery is to reduce collapsibility and increase patency of the upper airway, including oral, nasal, and pharyngeal passages. The most common procedures are uvulopalatopharyngoplasty (UPPP or UP3) and genioglossal advancement and hyoid myotomy (GAHM). UPPP involves excision of the tonsillar pillars, uvula, and posterior soft palate to remove the obstructing tissue. GAHM involves advancing the attachment of the muscular part of the tongue on the mandible. When GAHM is performed, UPPP is generally done as well. Depending on the site of the obstruction, symptoms are relieved in up to 80% of patients. Radiofrequency ablation (RFA) of obstructive tissues alone or in combination with other surgical techniques is also used. RFA is the least invasive surgical intervention. New treatments involve surgically implanted neurostimulators. One type stimulates the hypoglossal nerve to increase the tone of airway muscles. This treatment for OSA is still being tested for effectiveness and safety.19 After surgery, complications of airway obstruction or hemorrhage occur most often in the immediate postoperative period. Patients are usually discharged home within 1 day after the procedure. Before going home, teach the patient what to expect during the postoperative recovery period. Tell patients that their throat will be sore. They may have a foul breath odor that may be reduced by rinsing with diluted mouthwash and then salt water for several days. Snoring may persist until the inflammation has subsided. Follow-up after surgery is important. A repeat PSG is done 3 to 4 months after surgery.

Periodic Limb Movement Disorder Periodic limb movement disorder (PLMD) is characterized by periodic limb movements in sleep (PLMS): involuntary, repetitive movement of the limbs that affects people only during sleep.21 PLMD usually involves the legs and rarely involves the arms. Sometimes

abdominal, oral, and nasal movement accompanies PLMD. Movements typically occur for 0.5 to 10 seconds, in intervals separated by 5 to 90 seconds. PLMD causes poor-quality sleep and excessive daytime sleepiness. The causes of PLMD are not fully understood. Iron deficiency and dopamine dysfunction in the CNS have been implicated.21 PLMS can occur with medical disorders (e.g., sleep apnea, narcolepsy) and certain medications. For a diagnosis of PLMD, the occurrence of PLMS must not be due to another disorder. PLMS affects many people with restless legs syndrome (RLS). RLS is discussed in Chapter 58. PLMD is diagnosed using a detailed history from the patient and/or bed partner and doing PSG. PLMD is treated by medications aimed at reducing or eliminating the limb movements or the arousals. Clonazepam, a benzodiazepine, is used to treat PLMD. It likely helps patients by improving sleep quality rather than reducing limb movements. Other medications shown to be effective are valproic acid, an antiseizure drug that reduces muscle activity, and selegiline, a dopaminergic agent. Dopamine agonists (pramipexole, ropinirole) are used to treat RLS, but there is little research on their efficacy for PLMD. However, it is common practice for HCPs to prescribe these drugs treat PLMD.

Circadian Rhythm Disorders Circadian rhythm disorders can occur when the circadian time-keeping system loses synchrony with the environment. Lack of synchrony between the circadian time-keeping system and environment disrupts the sleep-wake cycle and affects the patient’s ability to have quality sleep. The common symptoms are insomnia and excessive sleepiness. Jet lag disorder and shift work sleep disorder (see Special Sleep Needs of Nurses section on p. 99) are the most common types of circadian rhythm disorders. Jet lag disorder occurs when a person travels across multiple time zones. The result is your body’s time is not synchronized with

environmental time. Most persons crossing at least 3 time zones get jet lag. The number of time zones crossed affects the severity of symptoms and the time it takes to recover. Resynchronization of the body’s clock occurs at a rate of about 1 hr/day when traveling eastward and 1.5 hr/day when traveling westward. Melatonin and exposure to daylight help to synchronize the body’s rhythm. Several strategies may help to reduce the risk for developing jet lag. Before travel the person can start to get in harmony with the time schedule of the destination. When time at destination is brief (i.e., 2 days or less), keeping home-based sleep hours rather than adopting destination sleep hours may reduce sleepiness and jet lag symptoms.

Narcolepsy Narcolepsy is a chronic neurologic disorder caused by the brain’s inability to regulate sleep-wake cycles normally. At various times throughout the day, people with narcolepsy have uncontrollable urges to sleep. Patients with narcolepsy often go directly into REM sleep from wakefulness.21 This does not occur in normal sleep and is a unique feature of narcolepsy. Patients with narcolepsy also have fragmented and disturbed nighttime sleep. There are 2 types of narcolepsy: with cataplexy (type 1) and without cataplexy (type 2).21 Cataplexy is a brief and sudden loss of skeletal muscle tone. It can manifest as a brief episode of muscle weakness or complete postural collapse and falling. Laughter, anger, or surprise often triggers episodes. The onset of narcolepsy typically occurs in adolescence or early in the third decade. Head trauma, a sudden change in sleep-wake habits, and infection may trigger the onset of narcolepsy symptoms. The cause of narcolepsy is unknown. It is associated with destruction of neurons that make orexin. The resulting deficiency of orexin causes instability of wake and transitions from wake to sleep that occur unpredictably. The loss of neurons may be due to an autoimmune process.22 Narcolepsy is diagnosed based on a history of sleepiness, PSG, and

daytime multiple sleep latency tests (MSLTs).21 For the MSLT, patients undergo an overnight PSG evaluation followed by 4 or 5 naps scheduled every 2 hours during the next day. Short sleep latencies and onset of REM sleep in more than 2 MSLTs are diagnostic signs of narcolepsy. Narcolepsy cannot be cured. Management is focused management of common symptoms: excessive daytime sleepiness, nighttime sleep disturbance, and cataplexy (Table 7.3). Provide teaching about sleep and sleep hygiene. Advise the patient to take 3 or more short (15minute) naps throughout the day and to avoid large or heavy meals and alcohol.22 You can play a key role in ensuring patient safety by teaching safety behaviors and encouraging adherence to the prescribed medication regimen. Safety precautions, especially when driving, are critically important for patients with narcolepsy. The behavioral therapies for insomnia are also used to address the sleep disturbances. Stimulants are used to counter daytime sleepiness. Modafinil (Provigil) and armodafinil (Nuvigil) are nonamphetamine wake-promotion drugs that are considered a firstline drug therapy. Sodium oxybate (Xyrem), a metabolite of GABA, is another wake-promoting medication that is effective for treating both daytime sleepiness and cataplexy. Antidepressants are used to treat cataplexy. Tricyclic antidepressants used to be commonly used, but selective serotonin reuptake inhibitors (SSRIs) (e.g., fluoxetine [Prozac], venlafaxine) are becoming favored for the management of cataplexy.22

Parasomnias Parasomnias are unusual and often undesirable behaviors that occur while falling asleep, transitioning between sleep stages, or arousing from sleep.21 They are due to CNS activation and often involve complex behaviors. The parasomnia is generally goal directed, although the person is not aware or conscious of the act. Parasomnias may result in fragmented sleep and fatigue. Sleepwalking and sleep terrors are arousal parasomnias that occur

during NREM sleep. Sleepwalking behaviors can range from sitting up in bed, moving objects, and walking around the room to driving a car. During a sleepwalking event the person may not speak and may have limited or no awareness of the event. On awakening, the person does not remember the event. In the ICU, a parasomnia may be misinterpreted as ICU psychosis. Sedated ICU patients can have manifestations of a parasomnia. Sleep terrors (night terrors) are characterized by a sudden awakening from sleep along with a loud cry and signs of panic. The person has marked increases in heart rate and respiration and diaphoresis. Factors in the ICU such as sleep disruption and deprivation, fever, stress, and exposure to noise and light can contribute to sleep terrors. Nightmares are a parasomnia characterized by recurrent awakening with recall of a frightful or disturbing dream. These normally occur during REM sleep during the final third of sleep. In critically ill patients, nightmares are common and likely due to medications. Drug classes most likely to cause nightmares are sedative-hypnotics, βadrenergic antagonists, dopamine agonists, and amphetamines.

Gerontologic Considerations: Sleep Older age is associated with overall shorter total sleep time, decreased sleep efficiency, and more awakenings (Fig. 7.6). A common misconception is that older people need less sleep than younger people. In fact, the amount of sleep needed as a person ages stays relatively constant. Other sleep disorders (e.g., sleep-disordered breathing) increase with age and may manifest with symptoms of insomnia. Some older adults have a shift in their circadian sleep timing so that they get sleepy earlier in the evening and awaken early in the morning.23 Multiple factors impair older adults’ ability to obtain quality sleep. Insomnia symptoms in older adults often occur with depression, cardiovascular disease, pain, and cognitive problems. Chronic conditions that are common in older adults (chronic obstructive pulmonary disease [COPD], diabetes, dementia, chronic pain, cancer)

can affect sleep quality. Medications used to treat these conditions can contribute to sleep problems. OTC medications can lead to sleep problems. Stimulating OTC medications include cough and cold medications, especially those containing pseudoephedrine; caffeinecontaining drugs; and drugs containing nicotine (e.g., nicotine gum, transdermal patches). Awakening and getting out of bed during the night (e.g., to use the bathroom) increase the risk for falls. Older adults may use OTC medications or alcohol as a sleep aid. This practice can further increase the risk for falls at night. Chronic disturbed sleep in older adults can result in disorientation, delirium, impaired intellect, disturbed cognition, and increased risk for accidents and injury.

FIG. 7.6 Many older people have sleep problems. © Studio-Annika/iStock/Thinkstock.

Because older adults may attribute their disturbed sleep to normal aging, they may fail to report symptoms of sleep disorders to their HCPs. Use a sleeping assessment (Table 7.5) to detect sleep disturbances in older adults. Sleep medications should be used with great caution in older adults. Diphenhydramine, alone or in combination with other drugs, is sedating with anticholinergic effects. Any OTC medication labeled

“PM” probably has diphenhydramine and should be used cautiously by older adults. Metabolism of most hypnotic drugs decreases with aging. Older adults have increased sensitivity to hypnotic and sedative medications. Thus drug therapies for sleep disturbances are started at lower doses and monitored carefully.17 Whenever possible, long-acting benzodiazepines should be avoided. Older adults receiving benzodiazepines are at increased risk of daytime sedation, falls, and cognitive and psychomotor impairment.

Special Sleep Needs of Nurses Nursing is 1 of several professions that needs night shift and rotating shift schedules. In many settings, nurses work a variety of day and night shifts, often alternating and rotating them. Unfortunately, nurses who do shift work often report less job satisfaction and more job-related stress.24 Nurses on permanent night or rapidly rotating shifts are at increased risk for experiencing shift work sleep disorder. It is characterized by insomnia, sleepiness, and fatigue. Nurses on rotating shifts get the least amount of sleep. With repeated periods of inadequate sleep, the sleep debt grows. Chronic fatigue in nurses doing shift work poses challenges for the individual nurse’s health and for patient safety (Fig. 7.7).24

FIG. 7.7 Sleep disturbances are common among nurses. © iStock.com/kupicoo.

Shift work alters the synchrony between circadian rhythms and the environment, leading to sleep disruption. Nurses working the night shift are often too sleepy to be fully alert at work and too alert to sleep soundly the next day. Sustained changes in circadian rhythms such as those imposed by rotating shift work are linked to increased morbidity and mortality risks associated with cardiovascular problems. Mood disorders such as anxiety are higher in nurses who work rotating shifts. From a safety perspective, disturbed sleep and subsequent fatigue can result in errors and accidents for nurses as well as for their patients. Fatigue diminishes or distorts perceptual skills, judgment, and decision-making capabilities. Lack of sleep reduces the ability to cope and handle stress and may result in physical, mental, and emotional exhaustion. The problem of sleep disruption is critically important to nursing. Several strategies may help reduce the distress associated with rotating shift work. These include brief periods of on-site napping.

Maintaining a consistent sleep-wake schedule even on days off is best but somewhat unrealistic. For night shift work, scheduling the sleep period just before going to work increases alertness and vigilance, improves reaction times, and decreases accidents during night shift work. Nurses who have control over their work schedules appear to have less sleep disruption than those whose schedule is imposed. As a nurse, you need to manage the impact of sleep disruption by using sleep hygiene practices.

Case Study Insomnia

© JackF/iStock/Thinkstock.

Patient Profile G.P., a 49-yr-old black woman, is seen in the primary care clinic for chronic fatigue and disturbed sleep. She is postmenopausal based on self-report. In the past year, since the end of her periods, she has had daily hot flashes and sleep problems. She denies any other health problems. On a usual workday she drinks 2 cups of hot tea in the morning and a can of diet cola in the late afternoon. Currently she is

taking OTC diphenhydramine for sleep. Her partner, who has accompanied her to the clinic, states that her snoring has gotten worse, and it is interfering with his sleep.

Subjective Data • Reports hot flashes and nighttime sweating • Reports daytime tiredness and fatigue • States she has trouble getting to sleep and staying asleep

Objective Data Physical Examination • Laboratory evaluations within normal limits • Height 5′6″ • Weight 190 lb

Diagnostic Studies • Nighttime PSG study reveals episodes of obstructive sleep apnea

Interprofessional Care • CPAP nightly • Referred for weight reduction counseling • Education about sleep hygiene

Discussion Questions 1. What are G.P.’s risk factors for sleep apnea? 2. What are the major health risks for G.P. from sleep apnea? 3. Priority Decision: Based on the assessment data provided, what

are the priority nursing diagnoses? 4. How does CPAP work? 5. Priority Decision: Based on your assessment of G.P., what are the priority nursing interventions for her? 6. Collaboration: For the interventions that you identified in the previous question, which can you delegate to unlicensed assistive personnel (UAP)? 7. Patient-Centered Care: What specific sleep hygiene practices could G.P. use to improve the quality of her sleep? 8. Collaboration: What referrals may be indicated for G.P.? Answers available at http://evolve.elsevier.com/Lewis/medsurg.

Bridge to Nclex Examination The number of the question corresponds to the same-numbered outcome at the beginning of the chapter.

1. Sleep is best described as a a. loosely organized state similar to coma. b. quiet state in which there is little brain activity. c. state in which a person has reduced sensitivity to pain. d. state in which a person lacks conscious awareness of the environment. 2. Which statements are true about rapid eye movement (REM) sleep (select all that apply)? a. The EEG pattern is quiescent. b. Muscle tone is greatly reduced. c. It occurs only once in the night. d. It is physiologically similar to NREM sleep. e. The most vivid dreaming occurs during this phase.

3. Insufficient sleep is associated with (select all that apply) a. increased body mass index. b. increased insulin resistance. c. impaired cognitive functioning. d. improved immune responsiveness. e. increased daytime body temperature. 4. When teaching the patient with primary insomnia about sleep hygiene, the nurse should emphasize a. the importance of daytime naps. b. the need for long-term use of hypnotics. c. the need to exercise about 1 hour before bedtime. d. the importance of avoiding caffeine 6 to 9 hours before bedtime. 5. An overweight patient with sleep apnea would like to avoid using a nasal CPAP device. To help him reach this goal, the nurse suggests that the patient a. lose excess weight. b. take a nap during the day. c. eat a high-protein snack at bedtime. d. use mild sedatives or alcohol at bedtime. 6. While caring for a patient with a history of narcolepsy with cataplexy, the nurse can delegate which activity to the unlicensed assistive personnel (UAP)? a. Teaching about the timing of medications b. Walking the patient to and from the bathroom c. Developing a plan of care with a family member d. Planning an appropriate diet that avoids caffeine-

containing foods 7. Strategies to reduce sleepiness during nighttime working include a. exercising before work. b. taking melatonin before working the night shift. c. sleeping for at least 2 hours immediately before work time. d. walking for 10 minutes every 4 hours during the night shift. 1. d, 2. b, e, 3. a, b, c, 4. d, 5. a, 6. b, 7. c For rationales to these answers and even more NCLEX review questions, visit http://evolve.elsevier.com/Lewis/medsurg.

Evolve Website/Resources List http://evolve.elsevier.com/Lewis/medsurg

Review Questions (Online Only) Key Points Answer Keys for Questions • Rationales for Bridge to NCLEX Examination Questions • Answer Guidelines for Case Study on p. 100 Conceptual Care Map Creator Audio Glossary Content Updates

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23. National Sleep Foundation: Aging and sleep. Retrieved from www.sleepfoundation.org/sleeptopics/aging-and-sleep.

Tahghighi M, Rees CS, Brown JA, et al: What is the impact of shift work on the psychological functioning and resilience of nurses? An integrative review, J Adv Nurs 73:2065, 2017. Evidence-based information for clinical practice.

8

Pain Debra Miller-Saultz

LEARNING OUTCOMES 1. Define pain. 2. Describe the neural mechanisms of pain and pain modulation. 3. Distinguish between nociceptive and neuropathic types of pain. 4. Explain the physical and psychologic effects of unrelieved pain. 5. Interpret the subjective and objective data that are obtained from a comprehensive pain assessment. 6. Describe effective interprofessional pain management techniques. 7. Describe drug and nondrug methods of pain relief. 8. Explain your role and responsibility in pain management. 9. Discuss ethical and legal issues related to pain and pain management. 10. Evaluate the influence of one’s own knowledge, beliefs, and attitudes about pain assessment and management.

KEY TERMS analgesic ceiling, p. 111

breakthrough pain (BTP), p. 108 central sensitization, p. 105 complex regional pain syndrome (CRPS), p. 107 equianalgesic dose, p. 117 modulation, p. 106 multimodal analgesia, p. 110 neuropathic pain, p. 106 nociception, p. 103 nociceptive pain, p. 106 pain, p. 102 patient-controlled analgesia (PCA), p. 119 patient-controlled epidural analgesia (PCEA), p. 119 peripheral sensitization, p. 104 transduction, p. 104 transmission, p. 104 trigger point, p. 120

Conceptual Focus Coping Functional Ability Pain One word frees us of all the weight and pain of life. That word is love. Sophocles http://evolve.elsevier.com/Lewis/medsurg/ Pain is a complex, multidimensional experience that can cause

suffering and decreased quality of life. Pain is 1 of the major reasons that people seek health care. To effectively assess and manage patients with pain, you need to understand the physiologic and psychosocial dimensions of pain. Pain is interrelated with many concepts. Culture and spirituality influence the expression of pain. Acute pain adversely affects mobility and sleep, leading to fatigue. Having pain is a stressor that can lead to depression. Those with severe or chronic pain are more likely to describe their health as poor and have increased mortality. This chapter presents evidence-based information to help you assess and safely manage pain in collaboration with other interprofessional team members.

Magnitude of Pain Problem Millions of people suffer from pain. Each year in the United States, at least 25 million people have acute pain because of injury or surgery. Common chronic pain conditions, such as arthritis, migraine headache, and back pain, affect more than 1 million American adults.1 Of the 1.7 million people diagnosed with cancer each year, about 60% have pain during treatment.2 Despite the high prevalence and costs of acute and chronic pain, inadequate pain management occurs. Consequences of unrelieved acute pain are shown in Table 8.1.

Definitions and Dimensions of Pain In 1968 Margo McCaffery, a nurse and pioneer in pain management, defined pain as “whatever the person experiencing the pain says it is, existing whenever the person says it does.”3 The International Association for the Study of Pain (IASP) defines pain as “an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.”1

TABLE 8.1 Negative Consequences of Unrelieved

Acute Pain

These definitions emphasize the subjective nature of pain, in which the patient’s self-report is the most valid means of assessment. Although understanding the patient’s experience and relying on his or her self-report is essential, this view is problematic for many patients. For example, patients who are comatose or who have dementia, patients who are mentally disabled or challenged, and patients with expressive aphasia have varying abilities to report pain. In these instances, you must include nonverbal information, such as observed

behaviors, into your pain assessment. The emotional distress of pain can cause suffering, which is the state of distress associated with loss. Suffering can result in a sense of insecurity, lack of control, and spiritual distress. It is important to assess the ways in which a person’s spirituality influences and is influenced by pain.4 The meaning of the pain to the person is important. For example, a woman in labor may have severe pain but can manage it without analgesics because for her it is associated with a joyful event. Moreover, she may feel control over her pain because of the training she received in prenatal classes and the knowledge that the pain is time-limited. In contrast, a woman with chronic, undefined musculoskeletal pain may be stressed

TABLE 8.2 Dimensions of Pain

Gender Differences Pain

Men • Are less likely to report pain than women

• Report more control over pain • Are less likely to use alternative treatments for pain

Women • More often have migraine headache, back pain, arthritis, fibromyalgia, irritable bowel syndrome, neuropathic pain, abdominal pain, and foot ache • Are more likely to be diagnosed with a nonspecific, somatic disorder • Are less likely to receive analgesics for symptoms of chest and abdominal pain by thoughts that her pain is “not real,” is uncontrollable, or is caused by her own actions. Perceptions influence the ways in which a person responds to pain and must be included in a comprehensive treatment plan. Some people cope with pain by distracting themselves. Others convince themselves that the pain is permanent, untreatable, and overwhelming. People who believe their pain is uncontrollable and overwhelming are more likely to have poor outcomes.5 The biopsychosocial model of pain includes the physiologic, affective, cognitive, behavioral, and sociocultural dimensions of pain (Table 8.2). Families and caregivers influence the patient’s response to pain through their beliefs and behaviors. For example, families may discourage the patient from taking opioids because they have preconceived notions and fears that the patient may become addicted. Understanding these beliefs helps you address them through patient and family teaching.

Pain Mechanisms Nociception is the physiologic process by which information about

tissue damage is communicated to the central nervous system (CNS). It involves 4 processes: (1) transduction, (2) transmission, (3) perception, and (4) modulation (Fig. 8.1).

FIG. 8.1 Nociceptive pain originates when the tissue is injured. 1, Transduction occurs when there is release of chemical mediators. 2, Transmission involves the conduct of the action potential from the periphery (injury site) to the spinal cord and then to the brainstem, thalamus, and cerebral cortex. 3, Perception is the conscious awareness of pain. 4, Modulation involves signals from the brain going back down the spinal cord to modify incoming impulses. Developed by McCaffery M, Pasero C, Paice JA. Modified from McCaffery M, Pasero C: Pain: Clinical manual, ed 2, St Louis, 1999, Mosby.

Transduction Transduction involves the conversion of a noxious mechanical, thermal, or chemical stimulus into an electrical signal called an action potential. Noxious (tissue-damaging) stimuli, including thermal (e.g., sunburn), mechanical (e.g., surgical incision), or chemical (e.g., toxic substances) stimuli, cause the release of chemicals, such as substance P and adenosine triphosphate (ATP), into the damaged tissues. Other chemicals are released from mast cells (e.g., serotonin, histamine,

prostaglandins) and macrophages (e.g., cytokines). These chemicals activate nociceptors, which are specialized receptors, or free nerve endings, which respond to painful stimuli. Activation of nociceptors results in an action potential that is carried from the nociceptors to the spinal cord primarily by small, rapidly conducting, myelinated Adelta fibers and slowly conducting unmyelinated C fibers. In addition to stimulating nociceptors, inflammation and the subsequent release of chemical mediators lower nociceptor thresholds. As a result, nociceptors may fire in response to stimuli that previously were insufficient to elicit a response. They may also fire in response to non-noxious stimuli, such as light touch. We call this increased susceptibility to nociceptor activation peripheral sensitization. Leukotrienes, prostaglandins, cytokines, and substance P are involved in peripheral sensitization. Cyclooxygenase (COX), produced in the inflammatory response, also plays a key role in peripheral sensitization. A clinical example of this process is sunburn. This thermal injury causes inflammation that results in a sensation of pain when the affected skin is lightly touched. Peripheral sensitization amplifies signal transmission, which in turn contributes to central sensitization (discussed under Dorsal Horn Processing). The pain from activation of peripheral nociceptors is called nociceptive pain (described later in the chapter on p. 106). Therapies that change either the local environment or sensitivity of the peripheral nociceptors can prevent transduction and initiation of an action potential. Decreasing the effects of chemicals released at the periphery is the basis of several drug approaches to pain relief. For example, nonsteroidal antiinflammatory drugs (NSAIDs), such as ibuprofen (Advil), exert their analgesic effects by blocking the action of COX (see Fig. 11.4).

Transmission Transmission is the process by which pain signals are relayed from the periphery to the spinal cord and then to the brain. Nerves that carry pain impulses from the periphery to the spinal cord are called primary afferent fibers. These include A-delta and C fibers. Each is

responsible for a different pain sensation. A-delta fibers conduct pain rapidly and are responsible for the initial, sharp pain that accompanies tissue injury. C fibers transmit painful stimuli more slowly and produce pain that is typically aching or throbbing. Primary afferent fibers end in the dorsal horn of the spinal cord. Activity in the dorsal horn integrates and modulates pain inputs from the periphery. The movement of pain impulses from the site of transduction to the brain is shown in Fig. 8.1. Three segments are involved in nociceptive signal transmission: (1) transmission along the peripheral nerve fibers to the spinal cord, (2) dorsal horn processing, and (3) transmission to the thalamus and cerebral cortex. Drugs that stabilize the neuronal membrane act on peripheral sodium channels to inhibit movement of nerve impulses. These medications include local anesthetics (e.g., injectable or topical lidocaine, bupivacaine [Sensorcaine]) and antiseizure drugs (e.g., gabapentin [Neurontin]).

Transmission to Spinal Cord The first-order neuron extends the entire distance from the periphery to the dorsal horn with no synapses. For example, an afferent fiber from the great toe travels from the toe through the fifth lumbar nerve root into the spinal cord; it is 1 cell. Once generated, an action potential travels all the way to the spinal cord unless it is blocked by a sodium channel inhibitor (e.g., local anesthetic) or disrupted by a lesion, such as a dorsal root entry zone lesion.

FIG. 8.2 Sequence of mechanisms leading to peripheral and central sensitization. Increased susceptibility to nociceptor activation is called peripheral sensitization. Increased sensitivity and hyperexcitability of neurons in the CNS is called central sensitization.

The way nerve fibers enter the spinal cord is central to the notion of spinal dermatomes. Dermatomes are areas on the skin that are innervated primarily by a single spinal cord segment. The distinct pattern of the rash caused by herpes zoster (shingles) across the back and trunk is determined by dermatomes (see Fig. 23.7). Different dermatomes and their innervations are shown in Fig. 55.7.

Dorsal Horn Processing Once a nociceptive signal arrives in the spinal cord, it is processed within the dorsal horn. Neurotransmitters released from the afferent fiber bind to receptors on nearby cells. Some of these neurotransmitters (e.g., glutamate, substance P) produce activation. Others (e.g., γ-aminobutyric acid [GABA], serotonin) inhibit activation of nearby cells. In this area, exogenous and endogenous

opioids (e.g., encephalin, β-endorphin) play a vital role by binding to opioid receptors and blocking the release of neurotransmitters, especially substance P. They produce analgesic effects similar to those of exogenous opioids, such as morphine. The neurons that project to the thalamus are called second-order neurons. Increased sensitivity and hyperexcitability of neurons in the CNS is called central sensitization. With central sensitization, the central processing circuits are altered. Peripheral tissue damage or nerve injury can cause central sensitization. Continued nociceptive input from the periphery maintains it (Fig. 8.2). In some cases, central sensitization can be long-lasting due to multiple changes that occur in the periphery and CNS.6 Because of the increased excitability of CNS neurons, normal sensory inputs cause abnormal sensing and responses to painful and other stimuli. This explains why some people have significant pain from touch or tactile stimulation in and around the areas of tissue or nerve injury. We call this allodynia, pain from a stimulus that is not typically painful. It also explains why some people have hyperalgesia, an exaggerated or increased pain response to noxious stimuli. With ongoing stimulation of slowly conducting unmyelinated Cfiber nociceptors, firing of specialized dorsal horn neurons gradually increases. These inputs can lead to the sprouting of wide dynamic range (WDR) neuron dendrites and the induction of glutamatedependent N-methyl-D-aspartate (NMDA) receptors. This results in an increased capacity to transmit a broader range of stimuli-producing signals, which are then passed up the spinal cord and to the brain. This process is known as wind-up.7 Activation of NMDA receptors also plays a role in wind-up. NMDA receptor antagonists, such as ketamine (Ketalar), potentially interrupt or block mechanisms that lead to or sustain central sensitization. Wind-up is like central sensitization and hyperalgesia in that it occurs in response to C-fiber inputs. Wind-up is different, however, in that it can be short-lasting, while central sensitization and hyperalgesia persist over time.

FIG. 8.3 Typical areas of referred pain.

It is important for you to understand that acute, unrelieved pain leads to chronic pain through central sensitization. Even brief intervals of acute pain can induce long-term neuronal remodeling and sensitization (plasticity), chronic pain, and lasting psychologic distress. Neuroplasticity refers to processes that allow neurons in the brain to compensate for injury and adjust their responses to new situations or changes in their environment.8 Neuroplasticity contributes to adaptive mechanisms for reducing pain but can result in maladaptive mechanisms that enhance pain sensitivity. Genetic variability may play a key role in changes that occur in the CNS and the response to different analgesic therapies to treat pain.

Understanding this phenomenon helps explain individual differences in response to pain and why some patients develop chronic pain conditions and others do not.9 Referred pain must be considered when interpreting the location of pain reported by the person with an injury or a disease involving visceral organs. The location of a stimulus may be distant from the pain location reported by the patient (Fig. 8.3). For example, pain from liver disease often occurs in the right upper abdominal quadrant. It also can be referred to the anterior and posterior neck region, shoulder area, and posterior flank area. If we do not consider referred pain when evaluating a pain location report, diagnostic tests and therapy could be misdirected.

TABLE 8.3 Comparison of Nociceptive and

Neuropathic Pain



Some types of neuropathic pain (e.g., postherpetic neuralgia) are caused by more than 1 neuropathologic mechanism.

Transmission to Thalamus and Cortex From the dorsal horn, nociceptive stimuli are communicated to the third-order neuron, primarily in the thalamus. Fibers of dorsal horn

projection cells enter the brain through several pathways, including the spinothalamic tract and spinoreticular tract. Distinct thalamic nuclei receive nociceptive input from the spinal cord and have projections to several regions in the cerebral cortex, where the perception of pain is presumed to occur. Therapeutic approaches that target pain transmission include opioid analgesics that bind to opioid receptors on primary afferent and dorsal horn neurons. These agents mimic the inhibitory effects of endogenous opioids. Another medication, baclofen (Lioresal), inhibits pain transmission by binding to GABA receptors, thus mimicking the inhibitory effects of GABA.

Perception Perception occurs when pain is recognized, defined, and assigned meaning by the person experiencing the pain. In the brain, nociceptive input is perceived as pain. There is no single, precise location where pain perception occurs. Instead, pain perception involves several brain structures. For example, it is thought that the reticular activating system is responsible for warning the person to attend to the pain stimulus; the somatosensory system is responsible for localization and characterization of pain; and the limbic system is responsible for the emotional and behavioral responses to pain. Cortical structures are crucial to constructing the meaning of the pain. Therefore behavioral strategies, such as distraction and relaxation, are effective pain-reducing therapies for many people. Meditation and imagery can affect pain perception. By directing attention away from the pain sensation, patients can reduce the sensory and affective components of pain.

Modulation Modulation involves the activation of descending pathways that exert inhibitory or facilitatory effects on the transmission of pain (Fig. 8.1). Depending on the type and degree of modulation, nociceptive stimuli may or may not be perceived as pain. Modulation of pain signals can occur at the level of the periphery, spinal cord, brainstem, and

cerebral cortex. Descending modulatory fibers release chemicals, such as serotonin, norepinephrine, GABA, and endogenous opioids, which can inhibit pain transmission. Several antidepressants exert their effects through the modulatory systems. For example, tricyclic antidepressants (e.g., amitriptyline) and serotonin norepinephrine reuptake inhibitors (SNRIs) (e.g., venlafaxine) are used to manage chronic noncancer and cancer pain. These agents interfere with the reuptake of serotonin and norepinephrine, thereby increasing their availability to inhibit noxious stimuli.

Classification of Pain We categorize pain in several ways. Most often, pain is categorized as nociceptive or neuropathic based on underlying pathology (Table 8.3). Another useful scheme is to classify pain as acute or chronic (Table 8.4).

Nociceptive Pain Nociceptive pain is caused by damage to somatic or visceral tissue. Somatic pain often is further categorized as superficial or deep. Superficial pain arises from skin, mucous membranes, and subcutaneous tissues. It is often described as sharp, burning, or prickly. Deep pain is often described as aching or throbbing. It originates in bone, joint, muscle, skin, or connective tissue. Visceral pain comes from the activation of nociceptors in the internal organs and lining of the body cavities, such as the thoracic and abdominal cavities. Visceral nociceptors respond to inflammation, stretching, and ischemia. Stretching of hollow viscera in the intestines and bladder that occurs from tumor involvement or obstruction can produce intense cramping pain. Examples of visceral nociceptive pain include pain from a surgical incision, pancreatitis, and inflammatory bowel disease.

Neuropathic Pain Neuropathic pain is caused by damage to peripheral nerves or structures in the CNS. Although neuropathic pain is often associated with diabetic neuropathy and other neuropathic pain syndromes, around 8% of the general population has pain with neuropathic characteristics.9 Typically described as numbing, hot, burning, shooting, stabbing, sharp, or electric shock–like, neuropathic pain can be sudden, intense, short lived, or lingering. Paroxysmal firing of injured nerves is responsible for shooting and electric shock-like sensations. Common causes of neuropathic pain include trauma, inflammation, metabolic diseases (e.g., diabetes), alcoholism, nervous system infections (e.g., herpes zoster, human immunodeficiency virus), tumors, toxins, and neurologic diseases (e.g., multiple sclerosis). Examples of neuropathic pain conditions include phantom limb sensation, diabetic neuropathy, and trigeminal neuralgia. No single sign or symptom is diagnostic for neuropathic pain.

TABLE 8.4 Differences Between Acute and

Chronic Pain

CNS lesions or dysfunction cause central pain. Deafferentation pain results from loss of or altered afferent input secondary to either peripheral nerve injury (e.g., amputation) or CNS damage, including a spinal cord injury. Painful peripheral polyneuropathies (pain felt along the distribution of multiple peripheral nerves) and painful mononeuropathies (pain felt along the distribution of a damaged nerve) arise from damage to peripheral nerves. They generate pain that people may describe as burning, paroxysmal, or shock-like. The patient may have positive or negative motor and sensory signs, including numbness, allodynia, or change in reflexes and motor strength. Sympathetically maintained pain is associated with a group of conditions that have a degree of changes in autonomic nervous system. One particularly debilitating type is complex regional pain syndrome (CRPS). Typical features include dramatic changes in the color and temperature of the skin over the affected limb or body part, accompanied by intense burning pain, skin sensitivity, sweating, and swelling. CRPS type I is often triggered by tissue injury, surgery, or a vascular event, such as stroke.10 CRPS type II includes all these features and a peripheral nerve lesion. Neuropathic pain is often not well controlled by opioid analgesics alone. Treatment often requires a multimodal approach combining various adjuvant analgesics from different drug classes. These include tricyclic antidepressants (e.g., amitriptyline), SNRIs (e.g., bupropion [Wellbutrin, Zyban]), antiseizure drugs (e.g., pregabalin [Lyrica]), transdermal lidocaine, and α2-adrenergic agonists (e.g., clonidine). NMDA receptor antagonists, such as ketamine, have shown promise in alleviating neuropathic pain refractory to other drugs.

Acute and Chronic Pain Acute pain and chronic pain differ in their cause, course, manifestations, and treatment (Table 8.4). Examples of acute pain include postoperative pain, labor pain, pain from trauma (e.g., lacerations, fractures, sprains), pain from infection (e.g., dysuria from

cystitis), and pain from acute ischemia. For acute pain, treatment includes analgesics for symptom control and treatment of the underlying cause (e.g., splinting for a fracture, antibiotic therapy for an infection). Normally, acute pain decreases over time as healing occurs. However, acute pain that persists can lead to disabling chronic pain states. For example, pain associated with herpes zoster subsides as the acute infection resolves, usually within a month. However, sometimes the pain persists and develops into a chronic pain state called postherpetic neuralgia. Because of the connection between inadequately treated acute pain and chronic pain, it is important to treat acute pain aggressively. Chronic pain, or persistent pain, lasts for longer periods, often defined as longer than 3 months or past the time when an expected acute pain or acute injury should subside. The severity and functional impact of chronic pain often are disproportionate to objective findings because of changes in the nervous system not detectable with standard tests. Although acute pain functions as a signal, warning the person of potential or actual tissue damage, chronic pain does not appear to have an adaptive role. Chronic pain can be disabling and often is accompanied by anxiety and depression.

Pain Assessment Assessment is an essential, although often overlooked, step in pain management. Regularly screen all patients for pain and, when present, perform a more thorough pain assessment. The key to accurate and effective pain assessment is to consider the principles of pain assessment (Table 8.5). The goals of a nursing pain assessment are to (1) describe the patient’s pain experience to identify and implement appropriate pain management techniques and (2) identify the patient’s goal for therapy and resources for self-management.

Elements of a Pain Assessment

Most components of a pain assessment involve direct interview or observation of the patient. Diagnostic studies and physical examination findings complete the initial assessment. Although the assessment differs according to the clinical setting, patient population, and point of care (i.e., whether the assessment is part of an initial workup or a reassessment of pain following therapy), the evaluation of pain should always be multidimensional (Table 8.6). Before beginning any assessment, recognize that patients may use words other than “pain.” For example, older adults may deny that they have pain but respond positively when asked if they have soreness or aching. Document the specific words that the patient uses to describe pain. Then consistently ask the patient about pain using those words.

TABLE 8.5 Principles of Pain Assessment

Pain Pattern Assessing pain onset involves determining when the pain started. Patients with acute pain resulting from injury, acute illness, or

treatment (e.g., surgery) typically know exactly when their pain began. Those with chronic pain may be less able to relate when the pain started. Establish the duration of the pain (how long it has lasted). This information helps to determine whether the pain is acute or chronic and helps identify the cause of the pain. For example, a patient with advanced cancer who has chronic low back pain from spinal stenosis reports a sudden, severe pain in the back that began 2 days ago. Knowing the onset and duration can lead to a diagnostic workup that may reveal new metastatic disease in the spine. The pain pattern gives clues about the cause of the pain and directs its treatment. Many types of chronic pain (e.g., arthritis pain) can increase and decrease over time. A patient may have pain all the time (around-the-clock pain), as well as discrete periods of intermittent pain. Breakthrough pain (BTP) is transient, moderate to severe pain that occurs in patients whose baseline persistent pain is otherwise mild to moderate and fairly well controlled. The average peak of BTP can be 3 to 5 minutes and can last up to 30 minutes or even longer. BTP can be either predictable or unpredictable. Patients can have 1 to many episodes per day. Several transmucosal fentanyl products are used specifically to treat BTP. End-of-dose failure is pain that occurs before the expected duration of a specific analgesic. It should not be confused with BTP. Pain that occurs at the end of the duration of an analgesic often leads to a prolonged increase in the baseline persistent pain. For example, in a patient on transdermal fentanyl (Duragesic patches) the typical duration of action is 72 hours. An increase in pain after 48 hours on the drug would be an end-of-dose failure. End-of-dose failure signals the need for changes in the dose or scheduling of the analgesic. Episodic, procedural, or incident pain is a transient increase in pain that is caused by a specific activity or event that precipitates pain. Examples include dressing changes, movement, position changes, and procedures, such as catheterization.

TABLE 8.6 Nursing Assessment

Pain Subjective Data Important Health Information Health history: Pain history includes onset, location, intensity, quality, patterns, aggravating and alleviating factors, and expression of pain. Coping strategies. Past treatments and their effectiveness. Review health care use related to the pain problem (e.g., emergency department visits, treatment at pain clinics, visits to primary HCPs and specialists) Medications: Use of any prescription or over-the-counter, illicit, or herbal products for pain relief. Alcohol use Nondrug measures: Use of therapies, such as massage, heat or ice, Reiki, aromatherapy, acupuncture, hypnosis, yoga, or meditation

Functional Health Patterns Health perception–health management: Social and work history, mental health history, smoking history. Effects of pain on emotions, relationships, sleep, and activities. Interviews with family members. Records from psychologic/psychiatric treatment related to the pain Elimination: Constipation related to opioid drug use, other medication use, or pain related to elimination Activity-exercise: Fatigue, limitations in ability to perform activities of daily living (ADLs), instrumental activities of daily living (IADLs), and pain related to use of muscles Sexuality-reproductive: Decreased libido Coping–stress tolerance: Psychologic evaluation using standardized measures to examine coping style, depression,

anxiety

Objective Data Physical examination, including evaluation of functional limitations Psychosocial evaluation, including mood

Location Determining the location of pain helps us identify possible causes and treatment. Some patients may be able to specify the precise location(s) of their pain. Others may describe general areas or comment that they “hurt all over.” The location of the pain may be referred from its origin to another site (Fig. 8.3). For example, myocardial infarction can result in pain in the left shoulder. Pain can radiate from its origin to another site. For example, angina pectoris can radiate from the chest to the jaw or down the left arm. We refer to this as radiating pain. Sciatica is pain that follows the course of the sciatic nerve. It may originate from joints or muscles around the back or from compression or damage to the sciatic nerve. The pain is projected along the course of the peripheral nerve, causing painful shooting sensations down the back of the thigh and inside of the leg to the foot.

FIG. 8.4 Pain intensity scales. A, 0 to 10 numeric scale. B, Visual analog scale. C, Descriptive scale. D, Faces Pain Scale. Modified from Baird M: Manual of critical care nursing: Nursing interventions and collaborative management, ed 2, St Louis, 2015, Elsevier.

Obtain information about the location of pain by asking the patient to (1) describe the site(s) of pain, (2) point to painful areas on the body, or (3) mark painful areas on a pain map. Because many patients have more than 1 site of pain, make certain that the patient describes every location.

Intensity Assessing the severity, or intensity, of pain provides a reliable measure to determine the type of treatment and its effectiveness. Pain scales help the patient communicate pain intensity. Base your choice of a scale on the patient’s developmental needs and cognitive status (Fig. 8.4). Most adults can rate the intensity of their pain using a numeric rating scale (e.g., 0 = no pain, 10 = the worst pain). Patients who wish

to have word choices to quantify pain may prefer a verbal descriptor scale (e.g., none, mild, moderate, severe). For those oriented to vertical representations, the Pain Thermometer Scale is an option. Other visual pain measures, such as the Wong-Baker FACES pain tool, are useful for patients with cognitive or language barriers to describe their pain.11 Pain assessment measures for cognitively impaired adults and nonverbal adults are addressed later in this chapter. Although intensity is an important factor in determining analgesic approaches, do not dose patients with opioids solely based on reported pain scores.12 Opioid “dosing by numbers” without considering a patient’s sedation level and respiratory status can lead to unsafe practices and serious adverse events. Safer analgesic administration can be achieved by balancing an amount of pain relief with analgesic side effects and using a multimodal approach. (Multimodal approach is described later in this chapter.) Adjustments in therapy can be made to promote better pain control and minimize adverse outcomes.

Quality The pain quality refers to the nature or characteristics of the pain. For example, patients often describe neuropathic pain as burning, numbing, shooting, stabbing, electric shock–like, or itchy. Nociceptive pain may be described as sharp, aching, throbbing, dull, and cramping. Since the quality of pain relates to a degree to the classification of pain (e.g., neuropathic, nociceptive), these descriptors can help to guide treatment options that best address the specific mechanism of pain.

Associated Symptoms Associated symptoms, such as anxiety, fatigue, and depression, may worsen or be worsened by pain. Patients with pain often report poor sleep and subsequent daytime sleepiness. Poor sleep can further increase pain perception. Ask about aggravating factors that increase pain as well as activities and situations that alleviate pain. For example, musculoskeletal pain may be increased or decreased with

movement and ambulation. Resting or immobilizing a painful body part can decrease pain. Knowing what makes pain better or worse can help characterize the type of pain and be helpful in selecting treatments.

Management Strategies As people experience and live with pain, they may cope differently and be more or less willing to try different strategies to manage it. Some strategies are successful, while others are not. To maximize the effectiveness of the pain treatment plan, ask patients what they are using now to control pain, what they have used in the past, and the outcomes of these methods. Strategies include prescription and nonprescription drugs and nondrug therapies, such as hot and cold applications, complementary and alternative therapies (e.g., acupuncture), and relaxation strategies (e.g., imagery). It is important to document both those that work and those that are ineffective.

Impact of Pain Pain can have a profound influence on a patient’s quality of life and functioning. Assess the effect of the pain on the patient’s ability to sleep, enjoy life, interact with others, perform work and household duties, and engage in physical and social activities. Assess the impact of pain on the patient’s mood. In an acute care setting, time limitations may dictate a shortened assessment. At a minimum, assess the effects of the pain on the patient’s sleep and daily activities, relationships with others, physical activity, and emotional well-being. Include the ways in which the patient describes the pain and strategies used to cope with and control the pain.

Patient’s Beliefs, Expectations, and Goals Patient and family beliefs, attitudes, and expectations influence responses to pain and pain treatment. Assess for attitudes and beliefs that may hinder effective treatment (e.g., belief that opioid use will

result in addiction). Ask about expectations and goals for pain management.

Documentation Document the pain assessment, since this is critical to ensure safe, effective communication among interprofessional team members. Many health care facilities have adopted specific tools to record an initial pain assessment, treatment, and reassessment. There also are many multidimensional pain assessment tools, such as the Brief Pain Inventory, the McGill Pain Questionnaire, and the Neuropathic Pain Scale.

Reassessment It is critical for you to reassess pain at appropriate intervals. The frequency and scope of reassessment are guided by factors such as pain severity, physical and psychosocial condition, type of intervention and risks for adverse effects, and institutional policy. For example, reassessment of a postoperative patient may be done frequently, such as at the time of peak effect for each analgesic dose. In a long-term care facility, residents with chronic pain are reassessed at least quarterly or with a change in condition or functional status.

Pain Treatment Basic Principles All pain treatment plans are based on the following 10 principles and practice standards: 1. Follow the principles of pain assessment (Table 8.5). Remember that pain is a subjective experience. The patient is not only the best judge of his or her own pain but also the expert on the effectiveness of each pain treatment.

2. Use a holistic approach to pain management. The pain experience affects all aspects of a person’s life. Thus a holistic approach to assessment, treatment, and evaluation is required. 3. Every patient deserves adequate pain management. Many patient populations, including ethnic minorities, cognitively impaired adults, and people with past or current substance abuse, are at risk for inadequate pain management. Be aware of your own biases and ensure that all patients are treated respectfully. 4. Base the treatment plan on the patient’s goals. Discuss with the patient realistic goals for pain relief during the initial pain assessment. Although goals can be described in terms of pain intensity (e.g., the desire for average pain to decrease from “8/10” to “3/10”), with chronic pain conditions, encourage functional goal setting (e.g., a goal of performing certain daily activities, such as socializing and recreational activities). Encourage functional activities for the patient with acute pain as well. For example, the pain must be at a level that allows the patient to use the incentive spirometer, get out of bed, and ambulate. Over time, reassess these goals and progress made toward meeting them. The patient, in collaboration with the interprofessional team, determines new goals. If the patient has unrealistic goals for therapy, such as wanting to be completely rid of all chronic arthritis pain or be completely pain free after a major surgery, work with the patient to establish a more realistic goal. 5. Use both drug and nondrug therapies. Although drugs are considered the mainstay of therapy, include self-care activities and nondrug therapies to increase the overall effectiveness of therapy and to allow for the reduction of drug dosages to minimize adverse drug effects. 6. When appropriate, use a multimodal approach to analgesic therapy. Multimodal analgesia employs the use of 2 or more classes of analgesic agents to take advantage of the various mechanisms of action. For acute, postoperative pain, a multimodal approach may include the use of an opioid

(morphine), nonopioid (nonsteroidal antiinflammatory drug), and/or antiseizure drug (e.g., gabapentin). Regional anesthesia and continuous peripheral neural blockade can be used with local anesthetics as part of multimodal regimens.13 Factors such as age, type of surgery, risk for developing chronic pain, and coexisting conditions are all considered when designing a multimodal analgesic regimen. Multimodal analgesia is used to treat chronic or persistent pain. Similar to the strategies for acute postoperative pain, the goal is to combine classes of analgesics for the maximum benefit of relieving pain with minimum doses to achieve relief and reduce adverse events from analgesics. Multimodal regimens achieve superior pain relief, enhance patient satisfaction, and decrease adverse effects of individual drugs.14 7. Address pain using an interprofessional approach. The expertise and perspectives of an interprofessional team are often necessary to provide effective assessment and therapies for patients with both acute and chronic pain. For hospitalized patients or those with complex acute or chronic pain issues, anesthesiology-based pain services may be available to manage patients with technology-supported pain care (e.g., patient-controlled analgesia or regional analgesia). Team members for these services can include pain management nurses, nurse practitioners, clinical nurse specialists, anesthesiologists, and clinical pharmacists. These teams help to establish realistic goals with patients and families to facilitate recovery and discharge. Many outpatient pain management centers or clinics are available. Some provide comprehensive pain care and employ multiple providers, including anesthesiologists, rehabilitation physicians, nurses, psychologists, physical and occupational therapists, and social workers. Services may focus on medication management, pain interventional therapies, psychologic counseling, cognitive and behavioral therapies, rehabilitative therapies (physical and occupational therapy), and social services. Specialized pain

treatment centers may also offer more holistic therapies, such as massage, music and art therapy, and acupuncture. Advise patients seeking specialized pain care from outpatient treatment centers to check about services that are provided. 8. Evaluate the effectiveness of all therapies to ensure that they are meeting the patient’s goals. Achievement of an effective treatment plan often requires trial and error. Adjustments in drug, dosage, or route are common to achieve maximal benefits while minimizing adverse effects. This trial-and-error process can become frustrating for the patient and caregivers. Reassure them that pain relief, if not pain cessation, is possible and that the interprofessional team will continue to work with them to achieve adequate pain relief.

TABLE 8.7 Drug Therapy

Managing Side Effects of Pain Medications Side effects can be managed by 1 or more of the following methods:

• Decreasing the dose of analgesic by 10% to 15% • Changing to a different medication in the same class • Adding a drug to counteract the adverse effect of the analgesic (e.g., using a stool softener for patients experiencing opioid-induced constipation) • Using an administration route that

minimizes drug concentrations (e.g., intraspinal administration of opioids used to minimize high drug levels that produce sedation, nausea, and vomiting) 9. Prevent and/or manage medication side effects. Side effects or adverse events are a major reason for treatment failure and nonadherence. Side effects are managed in 1 of several ways, as described in Table 8.7. You play a key role in monitoring for and treating side effects and in teaching patients and caregivers how to minimize these effects. 10. Include patient and caregiver teaching throughout assessment and treatment. Content should include information about the causes of the pain, pain assessment methods, treatment goals and options, expectations of pain management, proper use of drugs, side effect management, and nondrug and self-help pain relief measures. Document the teaching and include evaluation of patient and caregiver comprehension.

Drug Therapy for Pain Pain medications generally are divided into 3 categories: nonopioids, opioids, and adjuvant drugs. Patient-centered treatment regimens may include medications from 1 or more of these groups. Mild pain often can be relieved using nonopioids alone. Moderate to severe pain usually requires an opioid. Certain types of pain, such as neuropathic pain, typically require adjuvant drug therapy alone or in combination with an opioid or another class of analgesics. Pain caused by cancer may be treated with chemotherapy or radiation therapy, as well as pain medications.

Nonopioids

Nonopioid analgesics include acetaminophen, aspirin and other salicylates, and NSAIDs (Table 8.8). These agents are characterized by (1) their analgesic properties have an analgesic ceiling; that is, increasing the dose beyond an upper limit provides no greater analgesia; (2) they do not produce tolerance or physical dependence; and (3) many are available without a prescription. To provide safe care, monitor over-the-counter (OTC) analgesic use to avoid serious problems related to drug interactions, side effects, and overdose. Nonopioids are effective for mild to moderate pain. They are often used in conjunction with opioids because they allow for effective pain relief using lower opioid doses (thereby causing fewer opioid side effects). This phenomenon is called the opioid-sparing effect. Aspirin is effective for mild pain, but its use is limited by its common side effects, including increased risk for bleeding, especially gastrointestinal (GI) bleeding. Other salicylates, such as choline magnesium trisalicylate (Trilisate), cause fewer GI problems and bleeding abnormalities. Similar to aspirin, acetaminophen (Tylenol) has analgesic and antipyretic effects. Unlike aspirin, it has no antiplatelet or antiinflammatory effects. Acetaminophen is well tolerated. It is metabolized by the liver. Hepatotoxicity may result from chronic dosing of more than 3 g/day, acute overdose, or use by patients with severe preexisting liver disease.15 Adding acetaminophen to opioid therapy produces an opioid-sparing effect, lower pain scores, and fewer side effects. This is the reason for opioidacetaminophen combinations.

TABLE 8.8 Drug Therapy

Selected Nonopioid Analgesics

FIG. 8.5 Arachidonic acid is oxidized by 2 different pathways: lipoxygenase and cyclooxygenase. The cyclooxygenase pathway leads to 2 forms of the enzyme cyclooxygenase: COX-1 and COX-2. COX-1 is known as constitutive (always present), and COX-2 is known as inducible (its expression varies markedly depending on the stimulus). Nonsteroidal antiinflammatory drugs (NSAIDs) differ in their actions, with some having more effects on COX-1 and others more on COX-2. Indomethacin acts primarily on COX-1. Ibuprofen is equipotent on COX-1 and COX-2. Celecoxib primarily inhibits COX-2.

IV acetaminophen (Ofirmev) is used alone for the treatment of acute mild to moderate pain and as an adjunct to opioid analgesics or part of a multimodal analgesic regimen for moderate to severe pain. It must be given over 15 minutes and has a short duration of action. The daily dose should not exceed 4 g/day. NSAIDs represent a broad class of drugs with varying efficacy and side effects. All NSAIDs inhibit COX, the enzyme that converts arachidonic acid into prostaglandins and related compounds. The

enzyme has 2 forms: COX-1 and COX-2. COX-1 is found in almost all tissues. It is responsible for several protective physiologic functions. In contrast, COX-2 is made mainly at the sites of tissue injury, where it mediates inflammation (Fig. 8.5). Inhibition of COX-1 causes many of the untoward effects of NSAIDs, such as impairment of renal function, bleeding tendencies, GI irritation, and ulceration. COX-2 inhibition is associated with the therapeutic, antiinflammatory effects of NSAIDs. (Celecoxib [Celebrex] is a COX-2 inhibitor.) Older NSAIDs, such as ibuprofen, inhibit both forms of COX. We refer to them as nonselective NSAIDs. Patients vary greatly in their responses to a specific NSAID. So, when 1 NSAID does not provide relief, another should be tried. NSAIDs are associated with many side effects, including GI problems ranging from dyspepsia to life-threatening ulceration and hemorrhage. NSAIDs can cause cognitive impairment and hypersensitivity reactions with asthma-like symptoms. Patients at risk for NSAID-associated GI toxicity include those who have a recent history of peptic ulcer disease, patients who are older than 65, and those concurrently using corticosteroids or anticoagulants. If NSAIDs are used in patients at risk for GI bleeding, they should have concomitant therapy with misoprostol (Cytotec) or a proton pump inhibitor, such as omeprazole. NSAIDs should not be given concurrently with aspirin since this increases the risk for GI bleeding.

Drug Alert Nonsteroidal Antiinflammatory Drugs (NSAIDs) • NSAIDs, except aspirin, have been linked to a higher risk for cardiovascular events, such as myocardial infarction, stroke, and heart failure. • Patients who have just had heart surgery should not take

NSAIDs.

Opioids Opioids (Table 8.9) produce their effects by binding to receptors in the CNS. This results in (1) inhibition of the transmission of nociceptive input from the periphery to the spinal cord, (2) altered limbic system activity, and (3) activation of the descending inhibitory pathways that modulate transmission in the spinal cord. Thus opioids act on several nociceptive processes.

Types of Opioids Opioids are categorized according to their physiologic action (i.e., agonist, antagonist) and binding at specific opioid receptors (e.g., mu, kappa, delta). The most commonly given subclass of opioids is the pure opioid agonists, or morphine-like opioids, which bind to mu receptors. Opioid agonists are used for acute and chronic pain. Although nociceptive pain seems to be more responsive to opioids than neuropathic pain, opioids may be used to treat both types of pain. In the treatment of neuropathic pain, antineuropathic pain drugs, such as antidepressants and antiseizure drugs, are recommended as firstline agents. Pure opioid agonists include morphine, oxycodone (OxyContin), hydrocodone, codeine, methadone, hydromorphone (Dilaudid), and levorphanol (Table 8.9). These drugs are effective for moderate to severe pain because they are potent, theoretically have no analgesic ceiling, and can be given by several routes. When opioids are prescribed for moderate pain, they are usually combined with a nonopioid analgesic, such as acetaminophen with codeine or hydrocodone plus acetaminophen or ibuprofen. Adding acetaminophen limits the total daily dose that we can give.

Drug Alert

Morphine • Morphine may cause respiratory depression. • If respirations are 12 or fewer breaths per minute, withhold medication and contact the health care provider (HCP). Methadone has a unique mechanism of action as an NMDA receptor antagonist and mu opioid receptor agonist. It is used primarily in the treatment of chronic pain but can be used for acute pain. It produces analgesic effects independent of its action as an opioid.16

Drug Alert Methadone (Dolophine) • Methadone may cause respiratory depression. • Methadone can cause cardiac toxicity, specifically QT prolongation. Mixed agonist-antagonists (e.g., pentazocine [Talwin], butorphanol) bind as agonists on kappa receptors and as weak antagonists or partial agonists on mu receptors. Because of this difference in binding, mixed agonist-antagonists produce less respiratory depression than drugs that act only at mu receptors. These drugs cause more dysphoria and agitation. In addition, opioid agonist-antagonists have an analgesic ceiling and can precipitate withdrawal if used by a patient who is physically dependent on mu agonist drugs. Partial opioid agonists (e.g., buprenorphine [Buprenex]) can produce some pain relief but bind tightly to mu receptors and can block the effect of other drugs. Agonist-antagonists and partial agonists currently have limited clinical application in pain management.

TABLE 8.9 Drug Therapy

Opioid Analgesics

Dual-Mechanism Agents Some analgesics have 2 distinct actions, or dual mechanisms. Tramadol (Ultram) is a weak mu agonist and inhibits the reuptake of norepinephrine and serotonin. It is effective in low back pain, osteoarthritis, fibromyalgia, diabetic peripheral neuropathic pain, polyneuropathy, and postherpetic neuralgia. The most common side effects are like those of other opioids, including nausea, constipation, dizziness, and sedation. As with other medications that increase serotonin and norepinephrine, avoid this drug in patients with a history of seizures because it lowers seizure threshold. Tapentadol (Nucynta) is a centrally acting analgesic that works at mu receptors and inhibits norepinephrine reuptake. It is approved for management of moderate to severe acute pain. For chronic moderate to severe pain, an extended-release formula is available. The side effects are like those of conventional opioids, except that this drug is associated with less nausea and constipation.

Opioids to Avoid Some opioids should be avoided for pain relief because of limited efficacy and/or toxicities. Meperidine (Demerol), or pethidine, is associated with neurotoxicity (e.g., seizures) caused by accumulation of its metabolite, normeperidine. Its use is limited for very short-term (i.e., less than 48 hours) treatment of acute pain when other opioid agonists are contraindicated.

Drug Alert

Meperidine (Demerol) The American Pain Society does not recommend the use of meperidine as an analgesic.

Side Effects of Opioids Common side effects of opioids include constipation, nausea and vomiting, sedation, respiratory depression, and pruritus. With continued use, many side effects diminish; the exception is constipation. Less common side effects include urinary retention, myoclonus, dizziness, confusion, and hallucinations. Constipation is the most common side effect of opioids. Left untreated, it may increase the person’s pain and can lead to fecal impaction and paralytic ileus. Because tolerance to opioid-induced constipation does not develop, a bowel regimen should be started at the beginning of opioid therapy and continued for as long as the person takes opioids. Although dietary fiber, fluids, and exercise should be encouraged, these measures alone may not be enough. Most patients should use a gentle stimulant laxative (e.g., senna) plus a stool softener (e.g., docusate sodium [Colace]). Other agents (e.g., Milk of Magnesia, bisacodyl, polyethylene glycol, lactulose) can be added if needed. Methylnaltrexone (Relistor), naldemedine (Symproic), and naloxegol (Movantik) are peripheral opioid receptor antagonists used for opioidinduced constipation when the response to traditional laxative and stool softener therapy is insufficient. Nausea is often a problem in opioid-naive patients. The use of an antiemetic, such as ondansetron (Zofran), metoclopramide (Reglan), transdermal scopolamine, or hydroxyzine (Vistaril), can prevent or minimize nausea and vomiting until tolerance develops, usually within 1 week. Opioids delay gastric emptying (patient relates gastric fullness). Metoclopramide can reduce this effect. If nausea and vomiting are severe and persistent, changing to a different opioid may be needed. Sedation is usually seen in opioid-naive patients being treated for

acute pain. Regularly monitor patients receiving opioid analgesics for acute pain, especially in the first few days (e.g., after surgery). Be aware that the risk for unintended sedation in postoperative patients is greatest within 4 hours after leaving the postanesthesia care unit. Opioid-induced sedation resolves with the development of tolerance. Persistent sedation with chronic opioid use can be effectively treated with psychostimulants, such as caffeine, dextroamphetamine (Dexedrine), methylphenidate (Ritalin), or the anticataleptic drug modafinil (Provigil). The risk for respiratory depression is higher in opioid-naive, hospitalized patients who are treated for acute pain. Clinically significant respiratory depression is rare in opioid-tolerant patients and when opioids are titrated to analgesic effect. Patients most at risk for respiratory depression include those who are age 65 or older, have a history of snoring or witnessed apneic episodes, report excessive daytime sleepiness, have underlying heart or lung disease, are obese (body mass index greater than 30 kg/m2), have a history of smoking (more than 20 pack-years), or are receiving other CNS depressants (e.g., sedatives, benzodiazepines, antihistamines). For postoperative patients the greatest risk for opioid-related respiratory adverse events is within the first 24 hours after surgery. Clinically significant respiratory depression cannot occur in patients who are fully awake.

Check Your Practice A 74-yr-old male patient returned to the clinical unit after surgery for a hip replacement. You are having difficulty arousing him with either verbal or physical stimulation. His wife tells you to just let him sleep. His respiratory rate ranges from 8 to 10 breaths/min. • What should you do? Frequently monitor both the sedation level and respiratory rate in patients receiving opioid analgesics.17 A sedation scale can be used for

monitoring and providing appropriate interventions based on the level of sedation (Table 8.10).

Safety Alert Sedation and Respiratory Depression • If the patient’s respiratory rate falls below 8 or 10 breaths/min and the sedation level is 3 or greater, you should vigorously stimulate the patient and try to keep the patient awake. • If the patient becomes oversedated, apply oxygen. • In this situation, the opioid dose should be reduced. For patients who are excessively sedated or unresponsive, we can give naloxone, an opioid antagonist that rapidly reverses the effects of opioids. Naloxone can be given IV, subcutaneously, or intranasally. Evzio (hand-held autoinjector containing naloxone) can be used by a caregiver or family member to treat a person known or suspected to have had an opioid overdose. If the patient has been taking opioids regularly for more than a few days, use naloxone carefully because it can precipitate severe, agonizing pain; profound withdrawal symptoms; hypertension; and pulmonary edema. Because naloxone’s half-life is shorter than that of most opioids, frequently monitor the patient. Pruritus (itching) is another common side effect of opioids. It occurs most often when opioids are given by neuraxial (i.e., epidural, intrathecal) routes. Managing opioid-induced pruritus in noncancer patients may include low-dose infusions of naloxone.

TABLE 8.10 Pasero Opioid-Induced Sedation

Scale (POSS) With Interventions

Adapted from Pasero C: Assessment of sedation during opioid administration for pain management, J PeriAnesthesia Nurs 24:186, 2009. A rare but concerning problem with long-term and even short-term use of high-dose opioids is opioid-induced hyperalgesia (OIH). OIH is a state of nociceptive sensitization caused by exposure to opioids. It is characterized by a paradoxical response in which patients become more sensitive to certain painful stimuli and report increased pain with opioid use. The exact mechanism is not clearly understood, but it may be due to neuroplasticity changes. This may explain why opioids tend to lose their effectiveness in certain patients over time.

Adjuvant Analgesic Therapy Analgesic adjuvants are drugs that can be used alone or in conjunction with opioid and nonopioid analgesics (Table 8.11). Generally, these agents were developed for other purposes (e.g., antiseizure drugs, antidepressants) and found to be effective for treating pain.

α2-Adrenergic Agonists We think clonidine and tizanidine (Zanaflex), the most widely used

α2-adrenergic agonists, work on the central inhibitory α-adrenergic receptors. These agents may also decrease norepinephrine release peripherally. They are given for chronic headache and neuropathic pain.

Antidepressants Tricyclic antidepressants (TCAs) enhance the descending inhibitory system by preventing the cellular reuptake of serotonin and norepinephrine. Higher levels of serotonin and norepinephrine in the synapse inhibit the transmission of nociceptive signals in the CNS. Other potential beneficial actions of TCAs include sodium channel modulation, α1-adrenergic antagonist effects, and a weak NMDA receptor modulation. They are effective for a variety of pain syndromes, especially neuropathic pain syndromes. However, side effects, such as sedation, dry mouth, blurred vision, and weight gain, limit their usefulness. Antidepressants that selectively inhibit reuptake of serotonin and norepinephrine (SNRIs) are effective for many neuropathic pain syndromes and have fewer side effects than the TCAs. These agents include venlafaxine, desvenlafaxine (Pristiq), milnacipran (Savella), and bupropion.

Antiseizure Drugs Antiseizure drugs affect peripheral nerves and the CNS in several ways, including sodium channel modulation, central calcium channel modulation, and changes in excitatory amino acids and other receptors. Agents such as gabapentin, lamotrigine, and pregabalin are valuable adjuvant agents in chronic pain therapy and are being used more in the treatment of acute pain.

GABA-Receptor Agonist Baclofen, an agonist at GABA receptors, can interfere with the transmission of nociceptive impulses. It is used for muscle spasms and neuropathic pain. It crosses the blood-brain barrier poorly and is much more effective for spasticity when delivered intrathecally.

Corticosteroids Corticosteroids include dexamethasone, prednisone, and methylprednisolone (Medrol). They are used for managing acute and chronic cancer pain, pain secondary to spinal cord compression, and inflammatory joint pain syndromes. Mechanisms of action may be related to the ability of corticosteroids to decrease edema and inflammation. Corticosteroids have many side effects, especially when given chronically in high doses. These include hyperglycemia, fluid retention, dyspepsia and GI bleeding, impaired healing, muscle wasting, osteoporosis, adrenal suppression, and susceptibility to infection. Because they act through the same final pathway as NSAIDs, do not give corticosteroids at the same time as NSAIDs.

Local Anesthetics For acute pain from surgery or trauma, local anesthetics, such as bupivacaine and ropivacaine, can be given epidurally by continuous infusion or by intermittent or continuous infusion with regional nerve blocks. Systemic lidocaine given in an IV infusion is sometimes used for neuropathic and postoperative visceral pain. Topical applications are used to interrupt transmission of pain signals to the brain. For example, 5% lidocaine patch (Lidoderm) is a first-line agent for the treatment of several types of neuropathic pain. In the treatment of chronic severe neuropathic pain that is refractory to other analgesics, oral therapy with mexiletine (Mexitil) may be tried.

Cannabinoids Cannabinoid-derived medications show promise in the treatment of neuropathic pain, certain pain syndromes, and some symptoms. However, these preparations have sparked considerable controversy and confusion, mostly because cannabinoids are related to the cannabis plant, also known as marijuana. Synthetic cannabinoids (e.g., dronabinol [Marinol]) have been approved for medical use. Smoking marijuana or cannabis rapidly increases plasma levels of tetrahydrocannabinol (THC). The increase depends on composition of

the marijuana cigarette and inhalation technique. As a result, this form of use is associated with variable pain relief. With commercially available oral preparations, the absorption and bioavailability are more reliable and predictable. Cannabinoids exert their analgesic effects primarily through the cannabinoid-l (CB1) and CB2 receptors. Activation of cannabinoid receptors modulates neurotransmission in the serotoninergic, dopaminergic, and glutamatergic systems, as well as other systems. Cannabinoids also enhance the endogenous opioid system. Other beneficial effects include alleviating nausea and increased appetite. They may have opioid-sparing effects, possibly reducing opioid tolerance and symptoms of opioid withdrawal.18

TABLE 8.11 Drug Therapy

Adjuvant Drugs Used for Pain

Adapted from Pasero C, Polomano RC, McCaffery M, et al: Adjuvant analgesics. In Pasero C, McCaffery M, editors: Pain: Assessment and pharmacological management, New York,

2011, Mosby.

Administration Scheduling Appropriate analgesic scheduling focuses on preventing or controlling pain, rather than providing analgesics only after the patient’s pain has become severe. Premedicate a patient before procedures and activities that will likely produce pain. Similarly, a patient with constant pain should receive analgesics around the clock rather than on an “as needed” (PRN) basis. These strategies control pain before it starts and usually result in lower analgesic requirements. Use fast-acting drugs for incident or breakthrough pain, while long-acting analgesics are more effective for constant pain. Examples of fast-acting and sustained-release analgesics are described later in this section.

Titration Analgesic titration is dose adjustment based on assessment of the adequacy of analgesic effect versus the side effects produced. The amount of analgesic needed to manage pain varies widely, and titration is an important strategy in addressing this variability. An analgesic can be titrated upward or downward, depending on the situation. For example, in a postoperative patient the dose of analgesic decreases over time as the acute pain resolves. On the other hand, opioids for chronic, severe cancer pain may be titrated upward many times over the course of therapy to maintain adequate pain control. The goal of titration is to use the smallest dose of analgesic that provides effective pain control with the fewest side effects.

Equianalgesic Dosing The term equianalgesic dose refers to a dose of 1 analgesic that is equivalent in pain-relieving effects to a given dose of another analgesic (Table 8.12). This equivalence helps guide opioid dosing

when changing routes or opioids when a specific drug is ineffective or causes intolerable side effects. Equianalgesic charts and conversion programs are widely available in clinical guidelines, in health care facility pain protocols, and on the Internet. They are useful tools, but you need to understand their limitations since these doses are estimates. To ensure safety, all changes in opioid therapy must be carefully monitored and adjusted for the individual patient.

Administration Routes We can deliver opioids and other analgesic agents by many routes. This flexibility allows the HCP to (1) target a particular anatomic source of the pain, (2) achieve therapeutic blood levels rapidly when necessary, (3) avoid certain side effects through localized administration, and (4) provide analgesia when patients are unable to swallow. The following discussion highlights the uses and nursing considerations for analgesic agents delivered through a variety of routes.

TABLE 8.12 Opioid Equianalgesic Doses∗



All equivalencies are approximations. These amounts can be affected by many factors, including interpatient variability, type of pain, and tolerance. Monitor patients for effectiveness and adverse reactions and adjust the dose accordingly.

Oral

Generally, oral administration is the route of choice for the person with a functioning GI system. Most pain medications are available in oral preparations, such as liquid and tablet. For opioids, larger oral doses are needed to achieve the equivalent analgesia of doses given IM or IV (Table 8.12). For example, 10 mg of parenteral morphine is equivalent to around 30 mg of oral morphine. The reason larger doses are needed is related to the first-pass effect of hepatic metabolism. This means that oral opioids are absorbed from the GI tract into the portal circulation and shunted to the liver. Partial metabolism in the liver occurs before the drug enters the systemic circulation and becomes available to peripheral receptors or can cross the blood-brain barrier and access CNS opioid receptors, which is needed to produce analgesia. Oral opioids are as effective as parenteral opioids if the dose is large enough to compensate for the first-pass metabolism. Many opioids are available in short-acting (immediate-release) and long-acting (sustained-release or extended-release) oral preparations. Immediate-release products are effective in providing rapid, shortterm pain relief. Sustained-release or extended-release preparations generally are given every 8 to 12 hours, although some preparations (e.g., Kadian, Exalgo) may be dosed every 24 hours.

Safety Alert Sustained-Release or Extended-Release Preparations • These should not be crushed, broken, dissolved, or chewed. These drugs are to be swallowed whole. • If all the medicine is released into a person at once, serious side effects can occur, including death from overdose. Transmucosal and buccal routes Although morphine has historically been given sublingually to people with cancer pain who have difficulty swallowing, little of the drug is

absorbed from the sublingual tissue. Instead, most of the drug dissolves in saliva and is swallowed, making its absorption similar to that of oral morphine. Several transmucosal fentanyl products are used for the treatment of breakthrough pain. These include (1) oral transmucosal fentanyl citrate (OTFC) (Actiq), with the fentanyl embedded in a flavored lozenge on a stick that is absorbed by the buccal mucosa after being rubbed actively over it when given as the lozenge (not sucked as a lollipop); (2) fentanyl buccal tablet (FBT) (Fentora) in the form of a buccal tablet that disintegrates; and (3) fentanyl sublingual (Abstral). Transmucosal absorption allows the drug to enter the bloodstream and travel directly to the CNS. Pain relief typically occurs 5 to 7 minutes after administration. These formulations should be used only for patients who are already receiving and are tolerant to opioid therapy.19 Intranasal route Intranasal administration allows delivery of medication to highly vascular mucosa and avoids the first-pass effect. Butorphanol is given for acute headache and other intense, recurrent types of pain. A transmucosal fentanyl nasal spray (Lazanda) is available for the treatment of breakthrough pain. Rectal The rectal route is often overlooked but is particularly useful when the patient cannot take an analgesic by mouth, such as with severe nausea and vomiting. Analgesics that are available as rectal suppositories include hydromorphone, oxymorphone, morphine, and acetaminophen. If rectal preparations are not available, many oral formulations can be given rectally if the patient is unable to take medications by mouth. Transdermal route Transdermal patches are designed for systemic drug delivery (e.g., Duragesic) or for topical or local delivery (e.g., Lidoderm). Fentanyl

(Duragesic) is useful for the patient who cannot tolerate oral analgesic drugs. Absorption from the patch is slow. It takes 12 to 17 hours to reach full effect with the first application. Therefore transdermal fentanyl is not suitable for rapid dose titration but can be effective if the patient’s pain is stable and the dose needed to control it is known. Patches may have to be changed every 48 hours rather than the recommended 72 hours based on individual patient responses. Patches are applied to intact, nonhairy skin. Rashes caused by the patch’s adhesive may be reduced by preparing the skin 1 hour before placement with a weak corticosteroid cream. Bioocclusive dressings are available if the patch keeps falling off because of sweating. A transdermal patient-controlled analgesia (PCA) system (iontophoretic transdermal system [ITS]) is available.

Drug Alert Fentanyl Patches • Fentanyl patches (Duragesic) may cause death from overdose. • Signs of overdose include trouble breathing or shallow respirations; tiredness, extreme sleepiness, or sedation; inability to think, talk, or walk normally; and faintness, dizziness, or confusion. A 5% lidocaine-impregnated transdermal patch (Lidoderm patch) is used for postherpetic neuralgia. The patch is placed directly on the intact, nonhairy skin in the area of postherpetic pain and left in place for up to 12 hours. There are few systemic side effects, even with chronic use. Creams and lotions containing 10% trolamine salicylate (Aspercreme, Myoflex Creme) are available for joint and muscle pain. This aspirin-like substance is absorbed locally. This route avoids GI irritation but not the other side effects of high-dose salicylates. Topical

diclofenac solution and a diclofenac patch (Flector) are effective for osteoarthritic pain of the knee. Other topical analgesic agents, such as capsaicin (e.g., Zostrix) and lidocaine (L-M-X cream), also provide analgesia. Derived from red chili pepper, capsaicin acts on C-fiber heat receptors. If used 3 or 4 times a day for 4 to 6 weeks, it will cause the C nociceptor fibers to become inactive. The result is neuronal resistance to painful stimuli. Capsaicin may control pain associated with diabetic neuropathy, arthritis, and postherpetic neuralgia. L-M-X cream is useful for control of pain associated with venipunctures. Cover the targeted area of intact skin with a layer of L-M-X for at least 20 to 30 minutes, then wipe it off prior to beginning a painful procedure. Parenteral routes The parenteral routes include IV and subcutaneous administration. Single, repeated, or continuous dosing (IV or subcutaneous) is possible with parenteral routes. IV administration is the best route when immediate analgesia and rapid titration are needed. Continuous IV infusions provide excellent steady-state analgesia through stable blood levels. Onset of analgesia after subcutaneous administration is slow, and thus the subcutaneous route is rarely used for acute pain management. However, continuous subcutaneous infusions are effective for pain management at the end of life. This route is especially helpful for people with abnormal GI function and limited venous access. The IM route is not recommended because injections cause significant pain and result in unreliable absorption. With chronic use, IM injections can result in abscesses and fibrosis.

FIG. 8.6 Cross section of spinal cord with placement of catheters into the subarachnoid space (intrathecal delivery) and the epidural space (epidural delivery). From Urden LD, Stacy KM, Lough ME: Critical care nursing: Diagnosis and management, ed 8, St Louis, 2018, Elsevier.

Intraspinal delivery Intraspinal or neuraxial opioid therapy involves inserting a catheter into the subarachnoid space (intrathecal delivery) or the epidural space (epidural delivery) (Fig. 8.6). Analgesics are injected either by

intermittent bolus doses or continuous infusion. Percutaneously placed temporary catheters are used for short-term therapy (2 to 4 days), and surgically implanted catheters are used for long-term therapy. Although the lumbar region is the most common site of placement, epidural catheters may be placed at any point along the spinal column (cervical, thoracic, lumbar, or caudal). The tip of the epidural catheter is placed as close to the nerve supplying the painful dermatome as possible. For example, a thoracic catheter is placed for upper abdominal surgery, and a high lumbar catheter is used for lower abdominal surgery. Fluoroscopy ensures correct placement of the catheter. Intraspinal analgesics are highly potent because they are delivered close to the receptors in the spinal cord dorsal horn. Smaller doses of analgesics are needed than with other routes, including IV. For example, 1 mg of intrathecal morphine equals 10 mg of epidural morphine, 100 mg of IV morphine, and 300 mg of oral morphine. Drugs delivered intraspinally include morphine, fentanyl, sufentanil (Sufenta), alfentanil (Alfenta), hydromorphone, clonidine, and ziconotide, a calcium channel receptor modulator for use in neuropathic pain syndromes. Nausea, itching, and urinary retention are common side effects of intraspinal opioids. Complications of intraspinal analgesia include catheter displacement and migration, accidental infusions of neurotoxic agents, epidural hematomas, and infection. Clinical manifestations of catheter displacement or migration depend on catheter location and the drug being infused. A catheter that migrates out of the intrathecal or epidural space causes a decrease in pain relief with no improvement with more boluses or increases in the infusion rate. If an epidural catheter migrates into the subarachnoid space, increased side effects become quickly apparent. Somnolence, confusion, and increased anesthesia (if the infusate contains an anesthetic) occur. Check with institutional policy before aspirating cerebrospinal fluid to determine intrathecal catheter placement. Migration of a catheter into a blood vessel may cause an increase in side effects because of systemic drug distribution.

Many drugs and chemicals are highly neurotoxic when given intraspinally. These include antibiotics, chemotherapy agents, potassium, parenteral nutrition, and many preservatives, such as alcohol and phenol. To avoid inadvertent injection of IV drugs into an intraspinal catheter, the catheter should be clearly marked as an intraspinal access device. Only preservative-free drugs should be used. Infection is a rare but serious complication of intraspinal analgesia. Assess the skin around the exit site for inflammation, drainage, or pain. Manifestations of an intraspinal infection include diffuse back pain, pain or paresthesia during bolus injection, and unexplained sensory or motor deficits in the lower limbs. Fever may or may not be present. Acute bacterial infection (meningitis) is manifested by photophobia, neck stiffness, fever, headache, and altered mental status. Regular, meticulous wound care and using sterile technique when caring for the catheter and injecting drugs reduces infection risk. Long-term epidural catheters may be placed for terminal cancer patients or patients with certain pain syndromes that are unresponsive to other treatments. If a long-term indwelling epidural catheter is used, bacterial filters are recommended. Implantable pumps Intraspinal catheters can be surgically implanted for long-term pain relief. The surgical placement of an intrathecal catheter to a subcutaneously placed pump and reservoir allows for the delivery of drugs directly into the intrathecal space. The pump, which is normally placed in a pocket made in the subcutaneous tissue of the abdomen, may be programmable or fixed. We make changes reprogramming the pump, changing the mixture, or concentration of drug in the reservoir. The pump is refilled every 30 to 90 days depending on flow rate, mixture, and reservoir size. Patient-controlled analgesia Patient-controlled analgesia (PCA) (demand analgesia) is a method

that allows the patient to self-administer preset doses of an analgesic within a prescribed time period by activating an infusion pump. Routes of administration include oral, IV, epidural, inhaled, nasal, and transcutaneous. In acute care, PCA often refers to an electronically controlled infusion pump that delivers the medication by an IV or epidural route (patient-controlled epidural analgesia [PCEA]). PCEA often combines an opioid and local anesthetic. PCA also can be adapted for oral administration. With PCA/PCEA, a dose of opioid is delivered when the patient decides a dose is needed. PCA/PCEA uses an infusion system in which the patient pushes a button to receive a bolus infusion of an analgesic. PCA/PCEA is used widely for the management of acute pain, including postoperative pain and cancer pain. Opioids, such as morphine and hydromorphone, are often given via PCA therapy for acute and chronic pain. Sometimes IV PCA is given with a continuous or background infusion called a basal rate, depending on the patient’s opioid requirement. Adding a basal rate in opioid-naive patients and those at risk for adverse respiratory outcomes (e.g., older age, obstructive sleep apnea, lung disease) may lead to serious respiratory events. Basal rates are often used with epidural catheter pain management. Because the medication is delivered directly into the epidural space, the amount of opioid is 10 times less than is needed by IV route. This lessens the risk for respiratory depression but does not eliminate it. Patient teaching is very important with the use of PCA/PCEA. Help the patient understand the mechanics of getting a drug dose and how to titrate the drug to achieve good pain relief. Teach the patient to selfadminister the analgesic before pain is severe. Assure the patient that he or she cannot “overdose” because the pump is programmed to deliver a maximum number of doses per hour. The patient will not receive more analgesic once the maximum dose has been reached. If the maximum dose is inadequate to relieve pain, the pump can be reprogrammed to increase the amount or frequency of dosing. In addition, you can give bolus doses if they are part of the HCP’s orders. To make a smooth transition from infusion PCA to oral drugs,

the patient should receive increasing doses of oral drug as the PCA analgesic is tapered. Patient-controlled delivery systems are intended for use by the patient. An authorized agent controlled analgesia (AACA) is a method of delivery performed by a consistently available and competent person for patients who are unable to independently activate PCA devices.20 This authorized agent must be carefully selected, taught the principles of PCA, and capable of recognizing pain and the appropriate times to give medication via the PCA device. Understand your institution’s policies about PCA and AACA.

Interventional Therapy Therapeutic Nerve Blocks Nerve blocks involve 1-time or continuous infusion of local anesthetics into a particular area to produce pain relief. These techniques are also called regional anesthesia. Nerve blocks interrupt all afferent and efferent transmission to the area and thus are not specific to nociceptive pathways. They include local infiltration of anesthetics into a surgical area (e.g., chest incisions, inguinal hernia) and injection of anesthetic into a specific nerve (e.g., occipital, pudendal nerve) or nerve plexus (e.g., brachial, celiac plexus). Nerve blocks can be used during and after surgery to manage pain. For longer term relief of chronic pain syndromes, local anesthetics can be given by a continuous infusion. Adverse effects of nerve blocks are similar to those for local anesthetics delivered by other systemic routes. Effects include systemic toxicity resulting in dysrhythmias, confusion, nausea and vomiting, blurred vision, tinnitus, and metallic taste. Temporary nerve blocks affect motor function and sensation and typically last 2 to 24 hours, depending on the agent and the site of injection. Motor ability generally returns before sensation.

Neuroablative Techniques Neuroablative interventions are done for severe pain that is

unresponsive to all other therapies. They involve destroying nerves, thereby interrupting pain transmission. Destruction is by surgical resection or thermocoagulation, including radiofrequency coagulation. Neuroablative interventions that destroy the sensory division of a peripheral or spinal nerve are classified as neurectomies, rhizotomies, and sympathectomies. Neurosurgical procedures that ablate the lateral spinothalamic tract are classified as cordotomies if the tract is interrupted in the spinal cord or tractotomies if the interruption is in the medulla or midbrain of the brainstem (Fig. 8.7). Cordotomy and tractotomy can be done with the aid of local anesthesia by a percutaneous technique under fluoroscopy.

FIG. 8.7 Sites of neurosurgical procedures for pain relief.

Neuroaugmentation Neuroaugmentation involves electrical stimulation of the brain and spinal cord. Spinal cord stimulation (SCS) is done much more often than brain stimulation. The most common use of SCS is for chronic back pain secondary to nerve damage that is unresponsive to other therapies. Other uses include CRPS, spinal cord injury pain, and interstitial cystitis. Potential complications include those related to the surgery (bleeding and infection), migration of the generator (which usually is implanted in the subcutaneous tissues of the upper gluteal or pectoralis area), and nerve damage.

Nondrug Therapies for Pain Nondrug strategies play an important role in pain management (Table 8.13). They can reduce the dose of an analgesic needed to relieve pain and thereby minimize side effects of drug therapy. Moreover, they increase the patient’s sense of personal control about managing pain and increase coping skills. Some strategies are thought to alter ascending nociceptive input or stimulate descending pain modulation mechanisms. These nondrug therapies are useful for both acute and chronic pain.

Physical Pain Relief Strategies Massage Massage is useful for acute and chronic pain. Many different massage techniques exist, including moving the hands or fingers over the skin slowly or briskly with long strokes or in circles (superficial massage) or applying firm pressure to the skin to maintain contact while massaging the underlying tissues (deep massage). Another type is trigger point massage. A trigger point is a circumscribed hypersensitive area within a tight band of muscle. It is caused by acute or chronic muscle strain. It feels like a tight knot under the skin. Trigger point massage is done by applying strong, sustained digital pressure; deep massage; or gentler massage with ice followed by

muscle heating. Massage is discussed in Chapter 6.

TABLE 8.13 Nondrug Therapies for Pain

Physical Therapies • Acupuncture • Application of heat and cold (Table 8.14) • Exercise • Massage • Transcutaneous electrical nerve stimulation (TENS)

Cognitive Therapies • Distraction • Hypnosis • Imagery • Relaxation strategies (see Chapter 6) • Art therapy • Imagery • Meditation • Music therapy • Relaxation breathing

FIG. 8.8 Treatment of pain with transcutaneous electrical nerve stimulation (TENS) treatment after shoulder surgery. © Noel Moore/Hemera/Thinkstock.

Exercise Exercise is an essential part of the treatment plan for patients with chronic pain, particularly those with musculoskeletal pain. Many patients become physically deconditioned from their pain, which in turn leads to more pain. Exercise acts via many mechanisms to relieve pain. It enhances circulation and cardiovascular fitness, reduces edema, increases muscle strength and flexibility, and enhances physical and psychosocial functioning. Tailor an exercise program to the patient’s physical needs and lifestyle. It may include aerobic exercise, stretching, and strengthening exercises. Trained personnel (e.g., physical therapist) should supervise the program.

Transcutaneous Electrical Nerve Stimulation Transcutaneous electrical nerve stimulation (TENS) involves the delivery of an electric current through electrodes applied to the skin surface

over the painful region, at trigger points, or over a peripheral nerve. A TENS system consists of 2 or more electrodes connected by lead wires to a small, battery-operated stimulator (Fig. 8.8). Usually a physical therapist is responsible for delivering TENS therapy, although nurses can be trained in the technique. TENS may be used for acute pain, including postoperative pain and pain associated with physical trauma. The effects of TENS on chronic pain are less clear, but it may be effective in these cases.21

TABLE 8.14 Patient & Caregiver Teaching

Heat and Cold Therapy Include the following instructions when teaching the patient and caregiver about superficial heat or cold techniques:

Heat Therapy • Do not use heat on an area that is being treated with radiation therapy, is bleeding, has decreased sensation, or has been injured in the past 24 hours. • Do not use any menthol-containing products (e.g., Ben-Gay, Vicks, Icy Hot) with heat applications because this may cause burns. • Cover the heat source with a towel or cloth before applying to the skin to prevent burns.

Cold Therapy • Cover the cold source with a cloth or towel before applying to the skin to prevent tissue damage. • Do not apply cold to areas that are being treated with radiation therapy, have open wounds, or have poor circulation.

• If it is not possible to apply the cold directly to the painful site, try applying it right above or below the painful site or on the opposite side of the body on the corresponding site (e.g., left elbow if the right elbow hurts).

Acupuncture Acupuncture is a technique of Traditional Chinese Medicine in which very thin needles are inserted into the body at designated points. Acupuncture is used for many kinds of pain. Acupuncture is described in Chapter 6.

Heat Therapy Heat therapy is the application of either moist or dry heat to the skin. Heat therapy can be either superficial or deep. We can apply superficial heat using an electric heating pad (dry or moist), a hot pack, hot moist compresses, warm wax (paraffin), or a hot water bottle. To expose large areas of the body, patients can immerse themselves in a hot bath, shower, or whirlpool. Physical therapy departments provide deep-heat therapy through techniques such as short-wave diathermy, microwave diathermy, and ultrasound therapy. Patient and caregiver teaching about heat therapy is described in Table 8.14.

Cold Therapy Cold therapy involves the application of either moist or dry cold to the skin. Dry cold can be applied by using an ice bag, moist cold by using towels soaked in ice water, cold hydrocollator packs, or immersion in a bath or under running cold water. Icing with ice cubes or blocks of ice made to resemble Popsicles is another technique used for pain relief. Cold therapy is thought to be more effective than heat for a variety of painful conditions, including acute pain from trauma or surgery, acute flare-ups of arthritis, muscle spasms, and headache. Patient and caregiver teaching about cold therapy is described in Table 8.14.

Cognitive Therapies Techniques to alter the affective, cognitive, and behavioral components of pain include a variety of cognitive strategies and behavioral approaches. For example, patients can identify and challenge negative pain-related thoughts and replace them with more positive coping thoughts. Some techniques need little training and often are adopted independently by the patient. For others, a trained therapist is needed.

Distraction Distraction involves redirection of attention away from the pain and onto something else. It is a simple but powerful strategy to relieve pain. Distraction involves engaging the patient in any activity that can hold his or her attention (e.g., watching TV or a movie, conversing, listening to music). It is important to match the activity with the patient’s energy level and ability to concentrate.

Hypnosis Hypnotherapy is a structured technique that enables a patient to achieve a state of heightened awareness and focused concentration that can be used to alter the patient’s pain perception. Hypnosis should be delivered and monitored only by specially trained clinicians.

Relaxation Strategies Relaxation strategies reduce stress, decrease acute anxiety, distract from pain, ease muscle tension, combat fatigue, promote sleep, and enhance the effectiveness of other pain relief measures.22 Relaxation strategies include relaxation breathing, music, imagery, meditation, muscle relaxation, and art (see Chapter 6).

Nursing and Interprofessional

Management: Pain You are an important member of the interprofessional pain management team. You provide input into the assessment and reassessment of pain. You help in planning and implementing treatments, including teaching, advocacy, and support of the patient, caregiver, and family. Because patients in any care setting can have pain, you must be knowledgeable about current therapies and flexible in trying new approaches to pain management. Together with the patient, develop a written agreement or treatment plan that describes the pain management. The plan should ensure that pain will be treated based on the patient’s perception and report of pain. When appropriate, the plan outlines the gradual tapering of the analgesic dose, with eventual substitution of parenteral analgesics with long-acting oral preparations and possibly cessation of opioids. Many nursing roles are described earlier in this chapter, including assessing pain, giving treatment, monitoring for side effects, and teaching patients and caregivers. However, the success of these actions depends on your ability to establish a trusting relationship with the patient and caregiver and to address their concerns about pain and its treatment.

Effective Communication Because pain is a subjective experience, patients need to feel confident that their reporting of pain will be believed and will not be perceived as “complaining.” The patient and caregiver need to know that you consider the pain significant and understand that pain may profoundly disrupt a person’s life. Communicate concern and commit to helping the patient obtain pain relief and cope with any unrelieved pain. Support the patient and caregiver through the period of trial and error that may be necessary to implement an effective therapeutic plan. It is important to clarify responsibilities in pain relief. Help the patient understand the role of the interprofessional team members, as well as the patient’s roles and expectations.

In addition to addressing specific aspects of pain assessment and treatment, evaluate the impact that the pain has on the lives of the patient and caregiver. Table 8.15 addresses teaching needs of patients and caregivers related to pain management.

Challenges to Effective Pain Management Common challenges to effective pain management include misunderstandings about tolerance, physical dependence, and addiction. It is important for you to understand and be able to explain these concepts. Table 8.16 lists barriers to pain management and strategies to address them.

Nursing Management Pain Management • Assess pain characteristics (pattern and onset, area or location, intensity, quality, associated symptoms, and management strategies). • Develop treatment plan for patient’s pain (including drug and nondrug therapies). • Give ordered pain medications. • Evaluate whether current treatment plan is effective. • Teach patient and caregiver about treatment plan. • Implement discharge teaching about pain management. • Provide effective supervision of UAP: • Help with screening for pain and notify RN if patient expresses pain. • Take and report vital signs before and after pain medications are given. • Note and report if patient is refusing to take part in ordered activities, such as ambulation (since this may

indicate inadequate pain management).

TABLE 8.15 Patient & Caregiver Teaching

Pain Management Include the following information in the teaching plan for the patient with pain and caregiver: • Self-management techniques • Realistic goals for pain control • Negative consequences of unrelieved pain • Need to maintain a record of pain level and effectiveness of treatment • Treat pain with drugs and/or nondrug therapies before it becomes severe • Medication may stop working after it is taken for a period of time, and dosages may have to be adjusted • Potential side effects and complications associated with pain therapies can include nausea and vomiting, constipation, sedation and drowsiness, itching, urinary retention, and sweating. • Need to report when pain is not relieved to tolerable levels

Tolerance Tolerance occurs with chronic exposure to a variety of drugs. In the case of opioids, tolerance to analgesia is characterized by the need for an increased opioid dose to maintain the same degree of analgesia. Although the development of tolerance to side effects (except constipation) is more predictable, the incidence of clinically significant analgesic opioid tolerance in chronic pain patients is unknown, since dosage needs may increase as the disease (e.g., cancer) progresses. It is

essential to assess for increased analgesic needs in patients on longterm therapy. The interprofessional team must evaluate and rule out other causes of increased analgesic needs, such as disease progression or infection. If significant tolerance to opioids develops and the opioid is losing its effectiveness, or intolerable side effects are associated with escalation of doses, the practice of opioid rotation may be considered. This involves switching from 1 opioid to another, assuming that the new opioid will be more effective at lower equianalgesic doses. However, very high opioid doses can result in OIH rather than pain relief. This means that increases in the dose can lead to higher pain levels. (OIH is discussed on p. 115.)

Physical Dependence Like tolerance, physical dependence is a normal physiologic response to ongoing exposure to drugs. It is manifested by a withdrawal syndrome when the drug is abruptly decreased. Manifestations of opioid withdrawal are listed in Table 8.17. When opioids are no longer needed to provide pain relief, a tapering schedule should be used in conjunction with careful monitoring. A typical tapering schedule may involve reducing the dose by 20% to 50% per day. The goal is to reduce the amount of medication and at the same time minimize adverse and withdrawal effects.

Pseudoaddiction Inadequate treatment of pain can lead to a phenomenon called pseudoaddiction. This occurs when patients show behaviors associated with addiction (e.g., frequent requests for analgesic refills or higher dosages), but the behaviors resolve with adequate treatment of the patient’s pain. These patients are often labeled as drug seeking, which can result in mistrust between the patient and HCP. This problem can be avoided by effective communication strategies and optimal pain management.

Addiction

Addiction is a complex neurobiologic condition characterized by aberrant behaviors arising from a drive to obtain and take substances for reasons other than the prescribed therapeutic value (see Chapter 10). Tolerance and physical dependence are not indicators of addiction. Rather, they are normal physiologic responses to chronic exposure to certain drugs, including opioids. Addiction rarely occurs in patients who receive opioids for pain control. If addiction is suspected, it must be investigated and appropriately diagnosed. It should not be implied without evidence because this interferes with pain management. The hallmarks of addiction include (1) compulsive use, (2) loss of control of use, and (3) continued use despite risk of harm.

Risk Monitoring Several opioid risk assessments are available to help clinicians assess patients for abuse, misuse, and addiction. A controlled substance agreement for those at risk for addiction may be used. Addiction risk assessment tools, such as the Opioid Risk Tool (www.drugabuse.gov/sites/default/files/files/OpioidRiskTool.pdf) and the Screener and Opioid Assessment for Patient Pain (www.nhms.org/sites/default/files/Pdfs/SOAPP-14.pdf) are available. Patient monitoring with urine drug screens and access to state prescription monitoring programs to track prescriptions are effective in detecting misuse of drugs. The risk for addiction should not prevent HCPs from using opioids to effectively treat moderate to severe acute and chronic pain.

Institutionalizing Pain Education and Management Besides patient and caregiver barriers, other barriers to effective and safe pain management include inadequate HCP education and lack of institutional support. Traditionally, medical and nursing school curricula have spent little time teaching future physicians and nurses

about pain and symptom management. The lack of emphasis on pain has contributed to inadequate training of HCPs. We have made progress overcoming these barriers. Medical and nursing schools devote more time to addressing pain. Numerous professional organizations have published evidence-based guidelines for assessing and managing pain in many patient populations and clinical settings. Institutional commitment and practices are changing clinical practice. One major step in institutionalizing pain management is the development and adoption of The Joint Commission (TJC) guideline on pain.23 TJC is the accrediting body for most health care facilities (hospitals, nursing homes, and health care clinics). Under these standards, health care facilities are required to (1) recognize the patient’s right to appropriate assessment and management of pain; (2) identify pain in patients during their initial assessment and as needed, during ongoing, periodic reassessments; (3) teach HCPs about pain assessment and management and ensure competency; and (4) teach patients and their families about pain management.

TABLE 8.16 Patient & Caregiver Teaching

Reducing Barriers to Pain Management

TABLE 8.17 Manifestations of Opioid Withdrawal

Syndrome

Ethical Issues in Pain Management Fear of Hastening Death by Giving Analgesics A common concern of health care professionals and caregivers is that giving a sufficient amount of drug to relieve pain will hasten or precipitate death of a terminally ill person. However, there is no scientific evidence that opioids can hasten death, even among patients at the very end of life. Moreover, you have a moral obligation to provide comfort and pain relief at the end of life. Even if there is a concern about the possibility of hastening death, the rule of double effect provides ethical justification. This rule states that if an unwanted consequence (i.e., hastened death) occurs because of an action taken to achieve a moral good (i.e., pain relief), the action is justified if the nurse’s intent is to relieve pain and not to hasten death.

Requests for Assisted Suicide Unrelieved pain is 1 of the reasons that patients make requests for assisted suicide. Aggressive and adequate pain management may decrease the number of such requests. Assisted suicide is a complex issue that extends beyond pain and pain management. Physicianassisted suicide is legal in some states (e.g., Oregon, Washington). To address the legal and ethical issues about this situation, the International Association for Hospice and Palliative Care prepared a position paper on this topic.24

Use of Placebos in Pain Assessment and Treatment Placebos are still sometimes used to assess and treat pain. Using a placebo involves deceiving patients by making them think they are receiving an analgesic when they are receiving an inert substance, such as saline. Many professional organizations condemn the use of

placebos to assess or treat pain.

Gerontologic Considerations: Pain Persistent pain is a common problem in older adults and is often associated with physical disability and psychosocial problems. The prevalence of chronic pain among community-dwelling older adults exceeds 50% and among older nursing home patients is around 80%. The most common painful conditions among older adults are musculoskeletal conditions, such as osteoarthritis and low back pain. Chronic pain often results in depression, sleep problems, decreased mobility, increased health care use, and physical and social role dysfunction. Despite its high prevalence, pain in older adults is often inadequately assessed and treated. Several barriers to pain assessment in the older patient exist. Older adults and their HCPs often believe that pain is a normal, inevitable part of aging and that nothing can be done to relieve the pain. Older adults may not report pain for fear of being a “burden” or a “complainer.” They may fear taking opioids. In addition, older patients are more likely to use words such as “aching,” “soreness,” or “discomfort” rather than “pain.” Be persistent in asking older adults about pain. Carry out the assessment in an unhurried, supportive manner. Another barrier is the increased prevalence of cognitive, sensoryperceptual, and motor problems that interfere with a person’s ability to process information and communicate. Examples include dementia and delirium, poststroke aphasia, and other communication barriers. Hearing and vision deficits may complicate assessment. Therefore pain assessment tools may have to be adapted for older adults. For example, you many need to use a large-print pain intensity scale. Most older adults, even those with mild to moderate cognitive impairment, can use quantitative scales accurately and reliably. In older patients with chronic pain, perform a thorough physical examination and history to identify causes of pain, possible therapies, and potential problems. Assess for depression and functional impairments, because they are also common among older adults with

pain. Treatment of pain in older adults is complicated by several factors. First, older adults metabolize drugs more slowly than younger people and thus are at greater risk for higher blood levels and adverse effects. The adage “start low and go slow” must be applied to analgesic therapy in this age group. Second, the use of NSAIDs in older adults is associated with a high frequency of GI bleeding. Third, older adults often are taking many drugs for 1 or more chronic conditions. The addition of analgesics can result in dangerous drug interactions and increased side effects. Fourth, cognitive impairment and ataxia can be worsened by analgesics, such as opioids, antidepressants, and antiseizure drugs. This requires that HCPs titrate drugs slowly and monitor carefully for side effects. Treatment regimens for older adults must include nondrug modalities. Exercise and patient teaching are important nondrug interventions for older adults with chronic pain. Include family and caregivers in the treatment plan (Tables 8.15 and 8.16).

Managing Pain in Special Populations Patients Unable to Self-Report Pain Although the patient’s self-report is the gold standard of pain assessment, many illnesses and conditions affect a patient’s ability to report pain. These diagnoses and conditions include dementia and delirium. For these people, behavioral and physiologic changes may be the only indicators of pain. You must be astute at recognizing behavioral symptoms of pain.

TABLE 8.18 Assessing Pain in Nonverbal Patients The following assessment techniques are recommended: • Obtain a self-report when possible.

• Never assume a nonverbal person is unable to communicate pain; blinking, writing, hand gestures, or nodding can be ways to express pain or the absence of pain. • Investigate potential causes of pain. • Observe patient behaviors that indicate pain (e.g., grimacing, frowning, rubbing a painful area, groaning, restlessness). • Obtain surrogate reports of pain from professional and family caregivers. • Try to use analgesics and reassess the patient to observe for a decrease in pain-related behaviors.

Modified from Herr K, Coyne PJ, McCaffery M, et al: Position statement from the American Society for Pain Management Nursing (ASPMN): Pain assessment in the patient unable to self-report— Position statement with clinical practice recommendations, Pain Manag Nurs 12:230, 2011. A guide for assessing pain in nonverbal patients is outlined in Table 8.18. Several scales are available to assess pain-related behaviors in nonverbal patients, particularly those with advanced dementia and the critically ill. Links to several pain assessment tools are available at the City of Hope Pain and Palliative Care Resource Center website (http://prc.coh.org).

Patients With Substance Use Problems HCPs are often reluctant to give opioids to patients at risk for addiction or those with substance-abuse disorders for fear of promoting or worsening addictions. However, there is no evidence that providing opioid analgesia to these patients in any way worsens their addictive disease. In fact, the stress of unrelieved pain may contribute to relapse in the recovering patient or increased drug use in the patient who is actively abusing drugs.

Check Your Practice A 36-yr-old male patient is recovering from abdominal surgery to remove his spleen after an automobile accident. He is a known drug user. You are taking care of him, and he is very irritable because he is not getting enough pain medication. You are reluctant to give him his PRN morphine for fear that you will contribute to his addiction problem. • What should you do? Guidelines for pain management in patients with addictive disease have been established by the American Society for Pain Management Nursing (ASPMN). These guidelines reflect your role in a team approach in which patients with addictive disease and pain have the right to be treated with dignity, respect, and the same quality of pain assessment and management as all other patients. If the patient acknowledges substance use, determine the types and amounts of drugs used. Avoid exposing the patient to the misused drug. Effective equianalgesic doses of other opioids may be determined if daily drug doses are known. If a history of drug use is unknown or if the patient does not acknowledge substance use, be suspect when normal doses of analgesics do not relieve the patient’s pain. Aggressive behavior patterns and signs of withdrawal may occur. Withdrawal symptoms can worsen pain and lead to drug-seeking behavior or illicit drug use. Toxicology screens may be helpful in determining recently used drugs. Discussing these findings with the patient may help gain the patient’s cooperation in pain control. Severe pain should be treated with opioids and at much higher doses than those used with drug-naive patients. The use of a single opioid is preferred. Avoid using a mixed opioid agonist-antagonist (e.g., butorphanol) or a partial agonist (e.g., buprenorphine) because these drugs may precipitate withdrawal symptoms. Nonopioid and

adjuvant analgesics and nondrug pain relief measures may be used as needed. To maintain opioid blood levels and prevent withdrawal symptoms, provide analgesics around the clock. Use supplemental doses to treat breakthrough pain. IV or PCA infusions may be considered for acute pain management. Pain management for people with addiction is challenging and needs an interprofessional team approach. When possible, the team includes pain management and addiction specialists. Team members need to be aware of their own attitudes about people with substance use problems, which may result in undertreatment of pain.

Case Study Pain

© iStock.com/XiXinXing.

Patient Profile K.C. is a 280-lb (127-kg) 68-yr-old black man with diabetes, peripheral neuropathy, hypertension, and gout, who was admitted for an

incision and drainage of a right abdominal abscess. He is being discharged on his second postoperative day. His daughter will perform dressing changes at home.

Subjective Data • Lives alone • Desires 0 pain but will accept 1 or 2 on a scale of 0 to 10 • Reports incision area pain as a 2 or 3 between dressing changes and as a 6 during dressing changes • States sharp pain persists 1 to 2 hours after dressing change • Reports pain between dressing changes controlled by 2 oxycodone tablets • Has history of peripheral neuropathy and describes chronic pain in his feet

Objective Data • Needs dressing changes 4 times per day after discharge • For discharge, oxycodone (2 tablets q4hr for pain PRN) is prescribed.

Discussion Questions 1. Describe the assessment data that are important for determining whether K.C. has adequate pain management. 2. Priority Decision: Based on the data presented, what are the priority nursing diagnoses? Are there any collaborative problems? 3. Priority Decision: What are the priority nursing interventions for K.C.? 4. How long should the daughter wait after the oxycodone is given to begin the dressing change?

5. Patient-Centered Care: What other pain therapies might you plan to help K.C. through the dressing change? 6. Safety: What side effects might he have because of his pain medication? How can these be safely managed? 7. Collaboration: To whom can you delegate teaching K.C. and his daughter the plan of care at home? 8. Evidence-Based Practice: K.C.’s daughter asks you if any other strategies could be used to help decrease her father’s incisional pain and his peripheral neuropathy pain. Answers available at www.evolve.elsevier.com/Lewis/medsurg.

Bridge to Nclex Examination The number of the question corresponds to the same-numbered outcome at the beginning of the chapter.

1. Pain is best described as a. a creation of a person’s imagination. b. an unpleasant, subjective experience. c. a maladaptive response to a stimulus. d. a neurologic event resulting from activation of nociceptors. 2. A patient is receiving a PCA infusion after surgery to repair a hip fracture. She is sleeping soundly but awakens when the nurse speaks to her in a normal tone of voice. Her respirations are 8 breaths/min. The most appropriate nursing action in this situation is to a. stop the PCA infusion. b. obtain an oxygen saturation level. c. continue to closely monitor the patient.

d. administer naloxone and contact the provider. 3. Which words are most likely to be used to describe neuropathic pain (select all that apply)? a. Dull b. Itching c. Burning d. Shooting e. Shock-like 4. Unrelieved pain is a. not expected after major surgery. b. expected in a person with cancer. c. dangerous and can lead to many physical and psychologic complications. d. an annoying sensation, but it is not as important as other physical care needs. 5. A cancer patient who reports ongoing, constant moderate pain with short periods of severe pain during dressing changes is a. probably exaggerating his pain. b. in need of a referral for surgical treatment of his pain. c. best treated by receiving a long-acting and a short-acting opioid. d. best treated by regularly scheduled short-acting opioids plus acetaminophen. 6. An example of distraction to provide pain relief is a. TENS. b. music.

c. exercise. d. biofeedback. 7. Appropriate nonopioid analgesics for mild pain include (select all that apply) a. oxycodone. b. ibuprofen (Advil). c. lorazepam (Ativan). d. acetaminophen (Tylenol). e. codeine with acetaminophen (Tylenol #3). 8. An important nursing responsibility related to pain is to a. leave the patient alone to rest. b. help the patient appear to not be in pain. c. believe what the patient says about the pain. d. assume responsibility for eliminating the patient’s pain. 9. Giving opioids to an actively dying patient who has moderate to severe pain a. may cause addiction. b. will likely be ineffective. c. is an appropriate nursing action. d. will likely hasten the person’s death. 10. A nurse believes that patients with the same type of tissue injury should have the same amount of pain. This statement reflects a. a belief that will contribute to appropriate pain management. b. an accurate statement about pain mechanisms and

expected goals of pain therapy. c. a belief that will not have any effect on the type of care provided to people in pain. d. a lack of knowledge about pain mechanisms, which is likely to contribute to poor pain management. 1. b, 2. c, 3.b, c, d, e, 4. c, 5. c, 6. b, 7. b, d, 8. c, 9. c, 10. d. For rationales to these answers and even more NCLEX review questions, visit http://evolve.elsevier.com/Lewis/medsurg.

Evolve Website/Resources List http://evolve.elsevier.com/Lewis/medsurg Review Questions (Online Only) Key Points Answer Keys for Questions • Rationales for Bridge to NCLEX Examination Questions • Answer Guidelines for Case Study on p. 125 Student Case Study • Patient With Pain Conceptual Care Map Creator Audio Glossary Content Updates

References 1. Centers for Disease Control and Prevention. Guideline for prescribing opioids for chronic pain. Retrieved from

www.cdc.gov/drugoverdose/prescribing/guideline.html. Van den Beuken-Van Everdingen MH, Hochstenbach LM, Joosten EA, et al: Update on prevalence of pain in patients with cancer: Systematic review and meta-analysis, J Pain Symptom Manage 51:6, 2016.

3. McCaffery M. Nursing practice theories related to cognition, bodily pain and man-environmental interactions, Los Angeles, 1968, UCLA Students Store. (Classic) Goncalves JPB, Lucchetti G, Menezes PR, et al: Complimentary religious and spiritual interventions in physical health and quality of life: A systematic review of randomized controlled clinical trials, PLoS One 12:10, 2017.

5. Jensen MP, Tomé-Pires C, de la Vega C, et al: What determines whether a pain is rated as mild, moderate, or severe? Clin J Pain 33:414, 2017. 6. Nix WA: Muscles, nerves, and pain. Berlin, 2017, Springer. Tesarz J, Eich W, Treede RD, et al: Altered pressure pain thresholds and increased wind-up in adult patients with chronic back pain with a history of childhood maltreatment: A quantitative sensory testing study, Pain 157:1799, 2016. Parker RS, Lewis, GN, Rice DA, et al: Is motor cortical excitability altered in people with chronic pain? A systematic review and metaanalysis, Brain Stimul 9:4, 2016. Blyth FM: The global burden of neuropathic pain, Pain 159:614, 2018. Kuttikat A, Maliha S, Oomatia A, et al: Novel signs and their clinical utility in diagnosing complex regional pain syndrome: A prospective observational cohort study, Clin J Pain 33:496, 2017.

11. Hale D, Marshall K. Assessing and treating pain in the cognitively impaired geriatric home care patient, Home Health Now 25:116, 2017. Gordon DB, Dahl J, Phillips P, et al: The use of “as-needed” range

orders for opioid analgesic in the management of acute pain: A consensus statement of the American Society of Pain Management Nurses and the American Pain Society, Pain Manag Nurs 5:53, 2004. (Classic) Kumar K, Kirksey MA, Duong S, et al: A review of opioid-sparing modalities in perioperative pain management: methods to decrease opioid use postoperatively, Anesth Analg 125:1749, 2017.

14. Tawfic Q, Kumar K, Pirani Z, et al: Prevention of chronic post-surgical pain: The importance of early identification of risk factors, J Anesth 31:424, 2017. 15. Yoon E, Barbar A, Choudhary M, et al: Acetaminophen-induced hepatotoxicity: A comprehensive update, J Clin Transl Hepatol 4:131, 2016. 16. Kharasch ED: Current concepts in methadone metabolism and transport, Clin Pharmacol Drug Dev 6:125, 2017. Gupta K, Prasad A, Nagappa M, et al: Risk factors for opioid-induced respiratory depression and failure to rescue, Curr Opin Anaesthesiol 31:110, 2018. Mu A, Weinberg E, Moulin DE, et al: Pharmacologic management of chronic neuropathic pain: Review of the Canadian Pain Society consensus statement, Can Fam Physician 63:844, 2017.

19. Janknegt R, van den Beuken M, Schiere S, et al: Rapid acting fentanyl formulations in breakthrough pain in cancer: Drug selection by means of the System of Objectified Judgement Analysis. Eur J Hosp Pharm Sci Pract, 25:e2, 2018. 20. Webb RJ, Shelton CP: The benefits of authorized agent controlled analgesia (AACA) to control pain and other symptoms at the end of life, J Pain Symptom Manage 50:371, 2015.

21. Coutaux A. Non-pharmacological treatments for pain relief: TENS and acupuncture, Joint Bone Spine 84:657, 2017. Felix MM, Ferreira MB, da Cruz LF, et al: Relaxation therapy with guided imagery for postoperative pain management: An integrative review, Pain Manag Nurs 35:342, 2017.

23. The Joint Commission: Revised standard on pain assessment and management, 2018. Retrieved from www.jointcommission.org. 24. De Lima L, Woodruff R, Pettus K, et al: International Association for Hospice and Palliative Care position statement: Euthanasia and physician-assisted suicide, J Palliat Med 20:8, 2017. Evidence-based information for clinical practice.

9

Palliative and End-of-Life Care Denise M. McEnroe-Petitte

LEARNING OUTCOMES 1. Distinguish the purpose of palliative care at the end of life and hospice care. 2. Describe the physical and psychologic manifestations at the end of life. 3. Explain the process of grief and bereavement at the end of life. 4. Examine the cultural and spiritual issues related to end-of-life care. 5. Discuss ethical and legal issues in end-of-life care. 6. Describe the nursing management of the dying patient. 7. Explore the special needs of family caregivers in end-of-life care. 8. Discuss the special needs of the nurse who cares for dying patients and their families.

KEY TERMS advance directives, p. 133 bereavement, p. 131 brain death, p. 129

Cheyne-Stokes respiration, p. 130 death, p. 129 death rattle, p. 130 end of life, p. 129 grief, p. 131 hospice, p. 128 palliative care, p. 127 spirituality, p. 132

Conceptual Focus Coping Ethics Family Dynamics Health Care Organizations Palliation Spirituality Those who have the strength and the love to sit with a dying patient in the silence that goes beyond words will know that this moment is neither frightening nor painful, but a peaceful cessation. Elisabeth Kübler-Ross http://evolve.elsevier.com/Lewis/medsurg/

Palliative Care Palliative care is any form of care or treatment that focuses on reducing the severity of disease symptoms. The overall goals of palliative care are to (1) prevent and relieve suffering and (2) improve

quality of life for patients with serious life-limiting illnesses1 (Fig. 9.1). Specific goals of palliative care are listed in Table 9.1. Ideally, all patients receiving curative or restorative health care should receive palliative care at the same time. Palliative care extends into the period of end-of-life (EOL) care and offers patient and family support while planning for EOL needs.2 Bereavement care follows the patient’s death (Fig. 9.2). Palliative care originated as EOL care in the 1960s. Initially, this care focused on providing symptom relief and emotional support to the patient, family, and significant others during the terminal phases of a serious life-limiting disease. We now call that phase of palliative care palliative care at the end of life, which is the focus of this chapter. The role of palliative care at the EOL is increasing in our current health care environment. Demographic changes are increasing the demand for palliative care. A growing number of Baby Boomers are turning 65. Improvements in health care technology have led to longer life expectancies and an increased number of older adults. The growing number of people with conditions such as diabetes and heart disease contribute to the increased use of palliative care.2 Older adults often have multiple chronic illnesses resulting in increased health care use.3 Palliative care has been shown to (1) improve quality of life for those with chronic illness, (2) decrease the associated economic costs for their health care, and (3) ease caregiver burden for those with chronic and terminal illnesses.

FIG. 9.1 One goal of palliative care is to improve the quality of the patient’s remaining life. Courtesy Kathleen A. Pollard, RN, MSN, CHPN, Phoenix, AZ.

TABLE 9.1 Goals of Palliative Care • Regard dying as a normal process • Provide relief from symptoms, including pain • Affirm life and neither hasten nor postpone death • Support holistic patient care and enhance quality of life • Offer support to patients to live as actively as possible until death • Offer support to the family during the patient’s illness and in their own bereavement Adapted from World Health Organization: WHO definition of

palliative care. Retrieved from www.who.int/cancer/palliative/definition/en.

FIG. 9.2 Continuum-of-care model showing integration of curative care, palliative and end-of-life/hospice care, and bereavement care. Redrawn from Robert Wood Johnson Foundation: The EPEC Project: Elements and models of end-of-life care, 1999.

To optimize the benefits of palliative care, it should be started after a person receives a diagnosis of a life-limiting illness, such as cancer, heart failure, chronic obstructive pulmonary disease, dementia, or end-stage kidney disease. The palliative care team is an interprofessional collaboration involving physicians, nurses, social workers, pharmacists, chaplains, and other health care professionals. Communication among the patient, family, and interprofessional palliative team is important to provide optimal care. Patients may receive palliative care services in multiple settings, including the home, long-term and acute care, mental health facilities, rehabilitation centers, and prisons. Many institutions have established interprofessional palliative and hospice care teams.1

Hospice Care Palliative care often includes hospice care before or at the EOL (Fig.

9.3). Hospice is a concept of care that provides compassion, concern, and support for persons in the last phases of a terminal disease (Fig. 9.4). The main goals of hospice care are to assist the patient to live as fully and comfortably as possible while dying with dignity. Hospice programs provide care with an emphasis on symptom management, advance care planning, spiritual care, and family support.

FIG. 9.3 Relationship of palliative care and end-of-life care/hospice. From Rosenberg M, Lamba S, Misra S: Palliative medicine and geriatric emergency care: Challenges, opportunities, and basic principles, Clin Geriatr Med 29:1, 2013.

FIG. 9.4 Hospice care is designed to provide compassion, concern, and support for the dying. From Rick Brady, Riva, MD.

The major difference between palliative care and hospice care is that palliative care allows a person to simultaneously receive curative and palliative treatments. Hospice care is an option when the physician determines a person has 6 months or less to live and that person or health care proxy decides to forgo curative treatments. Hospice is often underused, as many assume the person must be actively dying before hospice is necessary. On the contrary, it is important that the person be referred to hospice as soon as possible to ease the physical, emotional, and spiritual distress so common at the EOL. Almost half of the patients who die in the United States are under the care of a hospice program.4 More than three-quarters of persons in hospice programs are over the age of 65 years, and the majority are white. Most patients have cancer, dementia, stroke, or heart or respiratory conditions.4 Hospice programs are organized under a variety of models. Some are hospital-based programs, others are part of existing home health care agencies, and others are freestanding or community-based programs. Like palliative care, hospice care is provided in a variety of

locations, including the home, inpatient settings, acute and long-term care facilities, and rehabilitation centers. Hospice services are available 24 hours a day, 7 days a week to help patients and families in their homes. Inpatient hospice settings often have a relaxed and homelike atmosphere (Fig. 9.5). Staff and volunteers are available for the patient and family.

FIG. 9.5 Inpatient hospice settings are designed to make the atmosphere as relaxed and homelike as possible.

© Photodisc/Thinkstock.

A medically supervised interprofessional team and volunteers provide holistic hospice services. The hospice nurse plays a pivotal role in coordination of the hospice team.5 Hospice nurses work with other interprofessional team members to provide care and support to the patient and family. Hospice nurses focus on pain control and symptom management, spiritual assessment, and assessment and management of family needs. To meet patient and family needs, the hospice nurse needs excellent teaching skills, compassion, flexibility, cultural competence, and adaptability. The decision to begin hospice care is hard for several reasons. Many patients, families, physicians, and other health care providers (HCPs) lack information about hospice care. Some cultural/ethnic groups may not use hospice because of a lack of awareness of hospice services, a desire to continue with potentially curative therapies, and concerns about lack of minority hospice workers. Physicians may be reluctant to give referrals because they sometimes view a patient’s decline as their personal failure. Some patients or family members see hospice care as “giving up” or receiving second-rate care. It is important to consider potential barriers to hospice care in vulnerable populations. These may include veterans, homeless, immigrants, impoverished, disabled, or institutionalized persons. In these populations, besides the hospice team, you may need to collaborate with community partners to facilitate support services to meet the needs of the patient and family.5 Medicare, Medicaid, and many private insurance agencies cover hospice services. Admission to a hospice program has 2 criteria. The first criterion is that the patient must want the services and agree in writing to use only hospice care, not curative care, to treat the terminal illness. The second criterion is that the patient must be medically eligible for hospice. Medicare, Medicaid, and other insurers require that 2 physicians certify that the patient’s prognosis is terminal, with less than 6 months to live. After this initial certification, only 1 physician (e.g., the hospice medical director) is needed to

recertify the patient. It is important to realize that the physician who certified that a hospice patient is terminal does not “guarantee” death within 6 months. If a patient in hospice survives beyond 6 months, Medicare and other reimbursement organizations will continue to reimburse for an extended period if the patient still meets enrolment criteria. Hospice patients can receive care for other health problems that are not related to the terminal illness. However, the hospice, Medicare, Medicaid, or patient’s insurance company may not cover those services.6 They can voluntarily withdraw from the program at any time. Occasionally, a patient’s condition stabilizes, and the patient may be discharged from hospice care. This decision is made after review of the current treatment plan and input from members of the interprofessional hospice team.

Death Death occurs when all vital organs and body systems cease to function. It is the irreversible cessation of cardiovascular, respiratory, and brain function. Brain death is an irreversible loss of all brain functions, including those of the brainstem. Brain death is a clinical diagnosis. It occurs when the cerebral cortex stops functioning or is irreversibly destroyed. With the growing use of technology that assists in supporting life, controversies have arisen over the exact definition of death. Questions and discussions have focused on whether brain death occurs when the whole brain (cortex and brainstem) ceases activity or when function of the cortex alone stops. The American Academy of Neurology developed the diagnostic criteria guidelines for clinical diagnosis of brain death. The criteria include coma or unresponsiveness, absence of brainstem reflexes, and apnea. Physicians must perform specific assessments to confirm each of the criteria.7 Currently, legal and medical standards require that all brain function must cease to be able to pronounce brain death and

disconnect life support. Diagnosing brain death is of special importance when organ donation is an option. In some states and under specific circumstances, a registered nurse is legally allowed to pronounce death. Policies and procedures may vary from state to state and among health care institutions.

End-of-Life Care End of life generally refers to the final phase of a patient’s illness when death is imminent. The time from diagnosis of a terminal illness to death varies depending on the patient’s diagnosis and extent of disease. The National Academy of Medicine defines end of life as the period during which a person copes with declining health from a terminal illness or from the frailties associated with advanced age, even if death is not clearly imminent.8 In some cases it is obvious to HCPs that the patient is at the EOL. In other cases, they may be uncertain if the EOL is near. This uncertainty adds to the challenge of answering the common question asked by the patient and family, “How much time is left?” End-of-life care (EOL care) is the term used for issues and services related to death and dying. EOL care focuses on physical and psychosocial needs for the patient and family. The goals for EOL care are to (1) provide comfort and supportive care during the dying process, (2) improve the quality of the patient’s remaining life, (3) help ensure a dignified death, and (4) provide emotional support to the family.

TABLE 9.2 Physical Manifestations at End of Life

Physical Manifestations at End of Life As death approaches, metabolism reduces and the body gradually slows down until all functions end. Respiratory changes are common. Respirations may be rapid or slow, shallow, and irregular. Breath sounds may become wet and noisy, both audibly and on auscultation. Mouth breathing and accumulation of mucus in the airways cause noisy, wet-sounding respirations, termed the death rattle or terminal secretions. Cheyne-Stokes respiration is a pattern of breathing characterized by alternating periods of apnea and deep, rapid breathing. When respirations cease, the heart stops beating within a few minutes. The physical manifestations of approaching death are listed in Table 9.2.

Psychosocial Manifestations at End of Life A variety of feelings and emotions can affect the dying patient and family at the EOL (Table 9.3). Most patients and families struggle with a terminal diagnosis and the realization that there is no cure. The patient and family may feel overwhelmed, fearful, powerless, and fatigued. The family’s response depends in part on the type and length of the illness and their relationship with the person. The patient’s needs and wishes must be respected. Patients need time to think and express their feelings. Response time to questions may be sluggish because of fatigue, weakness, and confusion.

TABLE 9.3 Psychosocial Manifestations at End of

Life • Altered decision making • Anxiety about unfinished business • Decreased socialization • Fear of loneliness • Fear of meaninglessness of one’s life • Fear of pain • Helplessness • Life review • Peacefulness • Restlessness • Saying goodbyes • Unusual communication • Vision-like experiences • Withdrawal

Bereavement and Grief

Although we often use the terms interchangeably, bereavement refers to the state of loss and grief refers to the reaction to loss. Bereavement is the period after the death of a loved one during which we experience grief and mourning occurs. The time spent in bereavement depends on several factors, including how attached one was to the person who died and how much time one spent expecting the loss.

TABLE 9.4 Kübler-Ross Model of Grief

Stage Denial

Anger

What Person May Say No, not me. It cannot be true. Why me?

Characteristics Denies the loss has taken place and may withdraw. This response may last minutes to months May be angry at the person who inflicted the hurt (even after death) or at the world for letting it happen. May be angry with self for letting an event (e.g., car accident) take place, even if nothing could have stopped it May make bargains with God, asking, “If I do this, will you take away the loss?” Feels numb, although anger and sadness may remain underneath

Yes me, but . . . Depression Yes me, and I am sad. Acceptance Yes me, Anger, sadness, and mourning have tapered off. Accepts the reality of the but it is loss okay. Bargaining

Adapted from Kübler-Ross E: On death and dying, New York, 1969, Macmillan. (Classic) Grief is a normal reaction to loss. Grief occurs in response to the real loss of a loved one and the loss of what might have been. Grief is dynamic and includes both psychologic and physiologic responses after a loss. Psychologic responses include anger, guilt, anxiety, sadness, depression, and despair. Physiologic reactions include sleeping problems, changes in appetite, physical problems, and illness.

Grief is a powerful emotional state that affects all aspects of a person’s life. It is a complex and intense emotional experience. In the Kübler-Ross model of grief, there are 5 stages9 (Table 9.4). Not every person experiences all the stages of grieving, and they are not always progressive. It is common to reach a stage and then go backward. For example, a person may have reached the stage of bargaining and then revert to the denial or anger stage. Another model of grief is the grief wheel (Fig. 9.6). After a person has a loss, he or she feels shock (numbness, denial, inability to think straight). Next is the protest stage, in which a person may have anger, guilt, sadness, fear, and searching. Then comes the disorganization stage, in which a person feels despair, apathy, anxiety, and confusion. The next stage is reorganization, in which a person gradually returns to normal functioning, but he or she feels different. The last stage is the new normal. Eventually the destabilization experienced in grief resolves and a normal state can begin. However, because of the loss, the normal state is different from before. The challenge is to accept the new normal. Trying to go back to the “old” normal (which is not there anymore) is what causes a great deal of anxiety and stress.

FIG. 9.6 The grief wheel model begins with the normal state at the bottom. After a person goes through the grief process, eventually the grief will resolve. However, because of the loss, the normal state is different from before. The challenge is to accept the “new normal.”

The way a person grieves depends on factors such as the relationship with the person who has died (e.g., spouse, parent), physical and emotional coping resources, concurrent life stresses, cultural beliefs, and personality. Other factors that affect the grief response include mental and physical health, economic resources, religious influences or spiritual beliefs, family relationships, social support, and time spent preparing for the death. Issues that occurred before the death (e.g., marital problems) may affect the grief response.10 The grief experience for the caregiver of the patient with a chronic illness often begins long before the actual death event. This is called anticipatory grief. Patients at the EOL also can have anticipatory grief. Working in a positive way through the grief process helps to adapt to the loss. Grief that helps the person accept the reality of death is called adaptive grief. It is a healthy response. It may be associated with

grieving before death occurs or when the inevitability of the death is known. Indicators of adaptive grief include the ability to see some good resulting from the death and positive memories of the deceased person. Dysfunctional reactions to loss can occur, and the physical and psychologic impact of the loved one’s death may persist for years. Prolonged grief disorder, formerly called complicated grief, is a term used to describe prolonged and intense mourning. Prolonged grief disorder can include symptoms such as recurrent and severe distressing emotions and intrusive thoughts related to the loss of a loved one, self-neglect, and denial of the loss for longer than 6 months. About 1 in 5 bereaved persons has prolonged grief disorder. Those with prolonged grief disorder have a higher risk for illness and may have work and social impairments. Bereavement and grief counseling are core parts of patient- and family-centered palliative care. The goal of a bereavement program is to provide support and to help survivors in the transition to a life without the deceased person. Incorporate grief support into the plan of care for the family and significant others during the patient’s illness and after the death.

TABLE 9.5 Spiritual Assessment 1. Who or what provides you strength and hope? 2. Do you use prayer in your life? 3. How do you express spirituality? 4. How would you describe your philosophy of life? 5. What type of spiritual or religious support do you wish? 6. What is the name of your clergy, minister, chaplain, pastor, rabbi? 7. What does suffering mean to you? 8. What does dying mean to you? 9. What are your spiritual goals?

10. Is there a role of a church, synagogue, mosque, or temple in your life? 11. Has belief in God been important in your life? 12. How does your faith help you cope with illness? 13. How do you keep going day after day? 14. What helps you get through this health care experience? 15. How has illness affected you and your family? © The Joint Commission. Adapted with permission.

FIG. 9.7 Spiritual needs are an important consideration in end-of-life care. © Photodisc/Thinkstock.

Priority interventions for grief focus on providing an environment that allows the patient and family to express their feelings, such as anger, fear, and guilt. Discussing feelings helps the patient and family work toward resolution of the grief process. Respect for the patient’s privacy and need or desire to talk (or not to talk) is important.

Honesty in answering questions and giving information is essential.

Spiritual Needs Assessment of spiritual needs in EOL care is a key consideration (Table 9.5). Spirituality is a broad concept that encompasses beliefs, values, and purpose that relate to the search for existential meaning and purpose.11 Some define spirituality as a relationship with a supreme being that directs beliefs and practices. Spiritual needs do not necessarily equate to religion or belief in a higher power. A person may not be part of a particular religion but have a deep spirituality. Assess the patient’s and family’s preferences related to spiritual guidance or pastoral care services and make appropriate referrals. Deep-seated spiritual beliefs may surface for some patients when they deal with their terminal diagnosis and related issues. Patients may question their beliefs about a higher power, their journey through life, religion, and an afterlife (Fig. 9.7). Spiritual distress may occur.11 Characteristics of spiritual distress include anger toward God or a higher being, change in behavior and mood, desire for spiritual assistance, or displaced anger toward clergy. Spirituality has been associated with decreased despair in patients at EOL. Some dying patients are secure in their faith about the future. It is common to see patients relinquish material possessions of life and focus on values that they believe will lead them on to another place. Many turn to religion because it gives order to the world even in the presence of physical decline, social losses, suffering, and impending death. Religion may offer an existential meaning that offers a sense of peace and recognition of one’s place in the broader cosmic context.11

Culturally Competent Care: End of Life Culture and ethnicity are important considerations for patients who are receiving palliative and EOL care and their families. Cultural beliefs affect a person’s understanding of and reaction to death or loss. In some cultural/ethnic groups, death and dying are private matters

shared only with significant others. Often feelings are repressed or internalized. People who believe in “toughing it out” or “being strong” may not express themselves when they are experiencing a loss. Some cultural groups, such as blacks and Hispanic/Latinos, may easily express their feelings and emotions. Kinship tends to be strong in the Hispanic culture, and immediate and extended family provide support for one another. Expressing feelings of loss is encouraged and accepted easily. Culture and ethnicity affect decision making about life support, withholding and withdrawing treatments, and using palliative or hospice care.12 In some cultures, such as the Filipino American culture, it may be appropriate to first discuss a terminal diagnosis with the family before informing the patient. For Hispanics, often spouses and daughters are involved in decisions about palliative care and hospice. Blacks and Asian Americans use hospice care less often, with blacks being more likely to prefer aggressive treatment. Rituals associated with dying are part of all cultures. In certain cultures, the family may want to keep constant vigil in the room of a dying patient or in the waiting area. For example, some Jewish Americans believe that the spirit should not be alone when it leaves the body at the time of death. Therefore someone who is terminally ill should never be alone. The Jewish culture believes all body tissues must be buried with the person. Once a death has occurred, some cultures, such as the Puerto Rican American culture, may want to kiss and touch the body to say goodbye. In the Islamic cultures, the traditional rites of washing, shrouding, funeral prayers, and burial are done as soon as possible. Cultural variations exist in symptom expression (e.g., pain expression) and use of health care services. Providing culturally competent care requires assessment of nonverbal cues, such as grimaces, body position, and decreased or guarded movements. See Chapter 8 for issues related to pain assessment and management. Many differences exist among cultural beliefs and values in relation to death and dying. Assess beliefs and preferences on an individual basis to avoid stereotyping patients with different cultural belief

systems. Assess and document the patient’s cultural background, concerns, health practices, and attitudes about suffering. Ask the patient and family to describe their desires for care before death and care of the body after death. Use this assessment to guide the patient’s plan of care and evaluation. You can suggest or plan grief and bereavement counseling for the family. Make accommodations related to the patient’s language, diet, and cultural beliefs and practices. Families with non–English-speaking members are at risk for receiving less information about their family member’s critical illness and prognosis.13 When appropriate, access medical interpreter services so that the patient’s wishes are known. Culturally competent care is discussed in Chapter 2.

Legal and Ethical Issues Affecting Endof-Life Care Patients and families struggle with many decisions during the terminal illness and dying experience. Many people decide that the outcomes related to their care should be based on their own wishes and values. It is important to provide information to help patients with these decisions. The decisions may involve the choice for (1) organ and tissue donations, (2) advance directives (e.g., medical power of attorney, living wills), (3) resuscitation, (4) mechanical ventilation, and (5) feeding tube placement. Decisional capacity refers to the ability to consent to or refuse care. It means that the person has an understanding and appreciation of the information received and has the capacity to engage in the reasoning process.

Organ and Tissue Donation Persons who are legally competent may choose organ donation. You can donate any body part or the entire body. The decision to donate organs or to provide anatomic gifts may be made by a person before

death or by immediate family after death. Family permission must be obtained at the time of donation.14 Some people carry donor cards. Some states mark organ donation wishes on drivers’ licenses. The names of agencies that handle organ donation vary by state and community. Common names for such an agency may be the organ bank, organ-sharing network, and organsharing alliance. Organ and tissue donations follow specific legal guidelines. Follow those requirements and facility policies for organ or tissue donation. Notify the proper personnel at once when organ donation is intended, because some tissues must be used within hours after death.

Advance Care Planning and Advance Directives Advance care planning is a process that involves having patients (1) think through their values and goals for treatment, (2) talk about their values and goals with others, and (3) document them. Advance directives are the written documents that provide information about the patient’s wishes and his or her designated spokesperson (Table 9.6). The first advance directive was known by laypersons as a living will. Most states have replaced the idea of living wills with natural death acts, which may include directive to physicians (DTPs), durable power of attorney for health care (DPAHC), medical power of attorney (MPOA), and power of attorney for health care (POAH). Under the natural death acts, a person can tell the HCP exactly what treatment is or is not desired. Each state has its own unique requirements. Patients often change their minds about desired treatments as their disease state progresses. It is important to reassess a patient’s advance directives. For cognitively impaired older adults, consider the person’s values and manner of life to make health care decisions consistent with decisions they made when they were cognitively intact. People can get copies of state-specific forms from local medical associations and on the Internet. However, a person may write his or

her wishes without special forms. Verbal directives can be given to the attending physician in the presence of 2 witnesses. The physician may use a Physician Order for Life-Sustaining Treatment (POLST) or Medical Order for Life-Sustaining Treatment (MOLST) to outline current treatment options that honor the person’s desire for treatment (Table 9.6). The person should keep a copy of the order to use in case of an emergency in which the primary physician is not available for consultation. Attorneys and notaries may not be needed to develop these directives. If the person is not capable of communicating his or her wishes, the surrogate decision maker (most often family or significant other) decides the measures that will or will not be taken. In this case, the physician and nurse can discuss the available options with the family. Then it is important to document the family’s decision. This is important because often nurses and other medical professionals do not know who can legally make EOL decisions for patients when they no longer have decisional capacity.

Resuscitation Cardiopulmonary resuscitation (CPR) is common practice in health care. Patients who have respiratory or cardiac arrest receive CPR unless the physician gives a do-not-resuscitate (DNR) order. A DNR order is a written medical order that documents a patient’s wishes about resuscitation and, more important, the patient’s desire to avoid CPR.15 There are several types of CPR decisions. Complete and total heroic measures, which may include CPR, drugs, and mechanical ventilation, can be referred to as a full code. Some people choose variations of the full code. A chemical code involves the use of drugs for resuscitation without the use of CPR. A “no code,” or a DNR order, allows the person to die with comfort measures only and without the interference of technology. Some states have implemented a form called out-of-hospital DNR for use by terminally ill patients who wish to have no heroic measures used to prolong life after they leave an

acute care facility. Allow natural death (AND) is a term being used to replace “no code” or DNR. This term more accurately conveys our actions. It is sometimes referred to as “comfort measures only” status. The patient receives all comfort measures associated with pain control and symptom management, but the natural physiologic progression to death is not delayed or interrupted. The use of this type of language means that we do not withhold care, but care is supportive while allowing nature to take its course. It is meant to promote comfort and dignity at the EOL. An advance directive includes whether to withhold or withdraw certain treatments. The directive must clearly state what is to be done and what is not to be done. The American Nurses Association (ANA) states that the decision to withhold artificial nutrition and hydration should be made by the patient or surrogate together with the interprofessional team. It is important we continue to provide expert nursing care for patients who are no longer receiving artificial nutrition and hydration. You need to be aware of legal issues and have a primary role in supporting the patient’s wishes. Advance directives and organ donor information should be in the medical record and identified on the patient’s record and/or the nursing care plan. All caregivers responsible for the patient need to know the patient’s wishes. Additionally, you need to be familiar with state, local, and agency procedures in EOL care documentation.

TABLE 9.6 Common Documents Used in End-of-

Life Care

Euthanasia is the deliberate act of hastening death. The ANA statement on active euthanasia states that the nurse should not take part in active euthanasia, because such an act is in direct violation of the Code for Nurses, ethical traditions and goals of the profession, and its covenant with society. Physician-assisted suicide is legal in some states. In this case, the physician provides the means and/or information about how the patient can commit suicide. As a nurse, you have an obligation to provide prompt, humane, comprehensive, and compassionate EOL care. Some confuse euthanasia with palliative sedation, which is the use of medications to intentionally produce sedation to relieve intractable symptoms and distress in a patient who is imminently dying. The intent of palliative sedation is to relieve pain and suffering and not to

shorten life or to hasten death, as is the case with euthanasia. The use of opioids for symptom management at the EOL is often misunderstood and feared by patients, families, and HCPs. For this reason, many patients refuse to take opioids, which leads to physical and emotional suffering due to uncontrolled pain and symptoms. Your ethical obligation is to relieve suffering. This includes giving medications that have the potential of producing harm, such as with opioids. The principle of double effect refers to a principle that regards it morally permissible to give a medication that has the potential for harm if it is given with the intent of relieving pain and suffering and not intended to hasten death. As a nurse, your role is to teach the patient and family about addiction and tolerance to and dependence on medications. The person with terminal illness should not be concerned with addiction when the goal of treatment is comfort. Pain management is discussed in Chapter 8.

Ethical/Legal Dilemmas End-of-Life Care

Situation A.P. is a terminally ill 50-yr-old woman with metastatic breast cancer who is hospitalized with severe bone pain. She moans at rest and shows severe pain with any movement to reposition her. The present dose of IV morphine is not controlling her pain. At the team conference, the nurses discuss the need for more effective pain control but are concerned that more pain medicine could hasten her death.

Ethical/Legal Points for Consideration • Adequate pain relief is an important outcome for all patients, especially patients who are terminally ill.

• The Code of Ethics for Nurses addresses the responsibility of the nurse to relieve suffering and have conversations with patients and families about pain and symptom management.1 • The principle of beneficence means that we provide care to benefit patients. The goal of adequate pain control in the terminally ill to ease suffering is based on the principle of nonmaleficence (preventing or reducing harm to the patient). The secondary effect of hastening the patient’s death is ethically justified and known as the double effect. • Legally, the standard of care is used to define the nursing acts that are required for safe and competent nursing practice. When the actual nursing care falls below the standard of care, it is considered negligent and unsafe, and the nurse is at risk for being found incompetent. • In a court of law, the standard of care in nursing is determined by nursing experts and evidence-based practices. The increasing use of technology to access the latest scientific findings is changing the standard of nursing care to a national, if not global, standard defined by research findings and nationally recognized expert testimony. Standards for providing expert nursing care and counseling at EOL are available.1 • In A.P.’s situation the standard of care is that the patient will have pain relief. Failure of the nurse to act assertively to achieve pain relief for the patient and failure to effectively use resources to obtain that pain relief will be considered below the standard of care and unsafe and incompetent practice.

Discussion Questions 1. What types of discussions need to occur among the health care team, patient, and family as the terminally ill patient approaches this phase of care? 2. Distinguish between promotion of comfort and relief of pain in dying patients and between assisted suicide and euthanasia.

Reference 1. ANA: Code of ethics for nursing. Retrieved from www.nursingworld.org/DocumentVault/Ethics-1/Code-ofEthics-for-Nurses.html.

Nursing Management: End of Life Nurses spend more time with patients near the EOL than any other health care professionals. Nursing care of terminally ill and dying patients is holistic and encompasses all psychosocial and physical needs. Respect, dignity, and comfort are important for the patient and family. Although there is no cure for the person’s disease, the treatment plan still consists of assessment, planning, implementation, and evaluation. The main difference is that the focus of care is on the management of the symptoms of the disease, not necessarily the disease itself. Nurses who care for the dying need to recognize their own needs when dealing with grief and dying.

Nursing Assessment Assessment of the terminally ill or dying patient varies with the patient’s condition. Be sensitive and do not impose repeated, unnecessary assessments on the dying patient. When possible, use health history data that are available in the medical record rather than tiring the patient with an interview. Document the specific event or change that brought the patient into the health care setting. Record the patient’s medical diagnoses, medication profile, and allergies. If the patient is alert, do a brief review of the body systems. Assess for discomfort, pain, nausea, and dyspnea so that you can implement interventions using evidence-based tools for symptom assessment. These include numeric scales or visual analog scales for pain rating. Evaluate and manage co-morbidities or acute episodes of problems, such as diabetes mellitus or headache. Elicit information about the

patient’s abilities, food and fluid intake, patterns of sleep and rest, and response to the stress of terminal illness. Assess the patient’s ability to cope with the diagnosis and prognosis of the illness. Determine the family’s ability to manage the needed care and to cope with the illness and its consequences. The physical assessment is abbreviated and focuses on changes that accompany terminal illness and the specific disease process. Pay attention to patients who are nonverbal for subtle changes in their condition.16 The frequency of assessment depends on the patient’s stability. Assessment is done at least every 8 hours in the institutional setting. For patients cared for in their homes by hospice programs, assessment may occur weekly. As changes occur, you may have to complete assessment and documentation more often. If the patient is in the final hours of life, we may limit the physical assessment to essential data. Key elements of a social assessment include determining the relationships and patterns of communication among the family. If multiple family members are present, listen to concerns from different members. Differences in expectations and interpersonal conflict can produce disruptions during the dying process and after the death of the loved one. Social assessment also includes evaluating the goals of the patient and family. As death approaches, monitor the patient for multiple systems that often are failing during the EOL period. This requires vigilance and attention to often subtle physical changes. Neurologic assessment is especially important and includes level of consciousness, presence of reflexes, and pupil responses. Evaluation of vital signs, skin color, and temperature shows changes in circulation. Monitor and describe respiratory status, character and pattern of respirations, and characteristics of breath sounds. Assess nutritional and fluid intake, urine output, and bowel function, since this gives data about renal and gastrointestinal functioning. Assess skin condition on an ongoing basis, because skin becomes fragile and may easily break down. In the last hours of life, limit assessments to only those that you need to determine patient comfort. Assessment of pain and

respiratory status may be the most important during this time. It may be more peaceful and comforting to the patient and family to refrain from overstimulation that may occur from certain types of assessments, such as measuring BP or checking for pupillary response. As death approaches, your efforts may be better spent providing emotional support to the patient and family rather than performing tasks that will have no impact on the patient’s physical care.

Planning The patient and family need to be involved in planning and coordinating EOL care. In some cases, a family conference may be helpful to develop a coordinated plan of care. Develop a comprehensive plan to support, teach, and evaluate patients and families. Nursing care goals during the last stages of life involve comfort and safety measures and care of the patient’s emotional and physical needs. These goals may include determining where the patient would like to die and whether this is possible. For example, the patient may want to die at home, but the family may object. Many factors contribute to the patient and family’s decision. Interprofessional EOL care that includes the physician, social worker, chaplain, and other members of the palliative and/or hospice care team is important. Advocate for the patient so that their wishes are met as much as possible. The last hours or days of the patient experiencing brain death (e.g., from trauma) are often spent in the ICU. Planning for EOL care may be particularly challenging in the ICU environment. At this time, some families are approached about organ donation. Consultation from palliative care specialists may help the family plan and cope with EOL issues.

Nursing Implementation Psychosocial care and physical care are interrelated for both the dying patient and family. Teaching them is an important part of EOL care.

Families need ongoing information on the disease, the dying process, and any care you will be providing. They need information on how to cope with the many issues during this period of their lives. Denial and grieving may be barriers to learning and understanding at the EOL for both the patient and family.

Psychosocial Care As death approaches, respond appropriately to the patient’s psychosocial manifestations at the EOL (Table 9.7).

Anxiety and Depression Patients often show signs of anxiety and depression during the EOL period. Causes of anxiety and depression may include uncontrolled pain and dyspnea, psychosocial factors related to the disease process or impending death, altered physiologic states, and drugs used in high dosages. Anxiety is often related to fear. Encouragement, support, and teaching decrease some of the anxiety and depression. Management of anxiety and depression may include both medications and nonpharmacologic interventions. Relaxation strategies, such as relaxation breathing, muscle relaxation, music, and imagery, may be useful (see Chapter 6).

Anger Anger is a common and normal response to grief. A grieving person cannot be forced to accept the loss. The surviving family members may be angry with the dying loved one who is leaving them. Encourage the expression of feelings, but at the same time realize how hard it is to come to terms with loss. As a nurse, you may be the target of the anger. You need to understand what is happening and not react on a personal level.

Hopelessness and Powerlessness Feelings of hopelessness and powerlessness are common during the EOL period. Encourage realistic hope within the limits of the

situation. Allow the patient and family to deal with what is within their control and help them recognize what is beyond their control. When possible, support the patient’s involvement in decision making about care to foster a sense of control and autonomy.

TABLE 9.7 Nursing Management

Psychosocial Care at End of Life

Fear Fear is a typical feeling associated with dying. Specific fears associated with dying are fear of pain, fear of shortness of breath, fear of loneliness and abandonment, and fear of meaninglessness. Fear of pain Many people assume that pain always accompanies death. Physiologically, there is no absolute indication that death is always painful. Psychologically, pain may occur based on the anxieties and

separations related to dying. Patients can take part in their own pain relief by discussing pain relief measures and their effects. Most patients want their pain relieved without the side effects of grogginess or sleepiness. Pain relief measures do not have to deprive the patient of the ability to interact with others. Patients with physical pain should have pain-relieving drugs available. Assure the patient and family that drugs will be given promptly when needed and that side effects of drugs can and will be managed. As many EOL patients are unable to swallow, other routes, such as patches, sublingual, and rectal routes, may be used.17 Consider alternative methods like massage, music, aromatherapy, and mindfulness. Fear of shortness of breath Respiratory distress and dyspnea are common near the EOL. The sensation of air hunger results in anxiety for the patient and family. Current therapies include opioids, bronchodilators, and oxygen, depending on the cause of the dyspnea. Anxiety-reducing agents (e.g., anxiolytics) may help produce relaxation.

FIG. 9.8 Dying patients typically want someone whom they know and trust to stay with them. © iStockphoto/Thinkstock.

Fear of loneliness and abandonment Most terminally ill and dying people fear loneliness and do not want to be alone. Many dying patients are afraid that loved ones who are unable to cope with the patient’s imminent death will abandon them. Simply being present offers support and comfort (Fig. 9.8). Holding hands, touching, and listening are important nursing interventions. Providing companionship allows the dying person a sense of security. Fear of meaninglessness Fear of meaninglessness leads people to review their lives. They review their intentions during life, examining actions and expressing regrets about what might have been. Life review helps patients recognize the value of their lives. Assist patients and their families to identify the positive qualities of the patient’s life. Practical ways of helping may include looking at photo albums or collections of

important mementos. Sharing thoughts and feelings may enhance spirituality and provide comfort. Respect and accept the practices and rituals associated with the patient’s life review while staying nonjudgmental.

Communication Communication among the interprofessional team, patient, and family is essential at the EOL. Empathy and active listening are essential parts of communication in care. Empathy is the identification with and understanding of another’s situation, feelings, or motives. Active listening is paying attention to what is said, observing the patient’s nonverbal cues, and not interrupting. There may be silence. Often silence is related to the overwhelming feelings experienced at the EOL. Silence can also allow time to gather thoughts. Listening to the silence sends a message of acceptance and comfort. Communication must be respectful of the patient’s ethnic, cultural, and religious backgrounds. Patients and family members may have difficulties expressing themselves emotionally. Allow time for them to express their feelings and thoughts. Make time to listen and interact in a sensitive way to enhance the relationship among you, the patient, and the family. A family conference is 1 way to create a good environment for communication. Prepare family members for changes in emotional and cognitive function that occur as death nears. Unusual communication by the patient may take place. The patient’s speech may become confused, disoriented, or garbled. Patients may speak to or about family members or others who have predeceased them or give instructions to those who will survive them. Active, careful listening allows for the identification of specific patterns in the dying person’s communication and decreases the risk for inappropriate labeling of behaviors.

Physical Care Nursing management related to physical care at the EOL focuses on symptom management and comfort rather than treatment for curing a

disease or disorder (Table 9.8). The priority is meeting the patient’s physiologic and safety needs. Physical care focuses on the needs for oxygen, nutrition, pain relief, mobility, elimination, and skin care. People who are dying deserve and require the same physical care as people who are expected to recover. If possible, it is important to discuss with the patient and family the goals of care before treatment begins. An advance directive should be completed so that the patient and family wishes are followed.

Postmortem Care After the patient is pronounced dead, prepare or delegate preparing the patient’s body for immediate viewing by the family with consideration for cultural customs and in accord with state law and agency policies and procedures (Table 9.9). In some cultures and in some types of death, it may be important to allow the family to prepare or help in caring for the patient’s body. When the death is unexpected, preparing the patient’s body for viewing or release to a funeral home depends on state law and agency policies and procedures. Care of and discussion related to the person should continue to be respectful even after death. Allow the family privacy and as much time as they need with the deceased person. Never refer to the deceased person as “the body.”

Special Needs of Caregivers and Nurses in End-of-Life Care Special Needs of Family Caregivers Family caregivers are important in meeting the patient’s physical and psychosocial needs. Their role includes working and communicating with the patient and other family members, supporting the patient’s concerns, and helping the patient resolve any unfinished business. Families often face emotional, physical, and economic consequences

from caring for a family member who is dying. The caregiver’s responsibilities do not end when the patient is admitted to an acute care, inpatient hospice, or long-term care facility.18 An understanding of the grieving process as it affects both the patient and family is important. Being present during a family member’s dying process can be highly stressful. Recognize signs and behaviors among family members who may be at risk for abnormal grief reactions and be prepared to intervene if needed. Warning signs may include dependency and negative feelings about the dying person, inability to express feelings, sleep disturbances, a history of depression, difficult reactions to previous losses, perceived lack of social or family support, low self-esteem, multiple previous bereavements, alcoholism, or substance abuse. Caregivers with concurrent life crises (e.g., divorce) are especially at risk. Family caregivers and other family members need encouragement to continue their usual activities as much as possible. They need to discuss their activities and maintain some control over their lives. Inform caregivers about resources for support, including respite care. Community counseling and local support may help some people in working through their grief. Encourage caregivers to build a support system of extended family, friends, faith community, and clergy. The caregivers should have people to call on at any time to express any feelings they are experiencing.

TABLE 9.8 Nursing Management

Physical Care at End of Life

TABLE 9.9 Nursing Management

Postmortem Care • Close the patient’s eyes and jaw. • Replace dentures; remove jewelry and eyeglasses. • Wash the body as needed then apply a clean gown and bed linen. • Place a waterproof pad or incontinence brief to absorb urine and feces. • Comb and arrange the hair neatly. • Remove tubes and dressings (if appropriate). • Straighten the body, placing the arms at their sides or across the abdomen with palms down. • Place a pillow under the head.

Special Needs of Nurses Many nurses who care for dying patients do so because they are passionate about providing high-quality EOL care. Caring for patients and their families at the EOL is challenging and rewarding but also intense and emotionally charged. A bond or connection may develop between you and the patient or family. Be aware of how grief personally affects you. When you provide care for terminally ill or dying patients, you are not immune to feelings of loss. It is common to feel helpless and powerless when dealing with death. Express feelings of sorrow, guilt, and frustration. It is important to recognize your own values, attitudes, and feelings about death. Common ethical concerns include lack of adequate communication, lack of effective decision making, when to stop life-prolonging interventions, and concerns with symptom treatment, especially with use of opioids. Interventions are available that may help ease your physical and emotional stress. Be aware of what you can and cannot control.

Recognizing personal feelings allows openness in exchanging feelings with the patient and family. Realizing that it is okay to cry with the patient or family during the EOL may be important for your wellbeing. To meet your personal needs, focus on interventions that will help decrease your stress. Get involved in hobbies or other interests, schedule time for yourself, ensure time for sleep, maintain a peer support system, and develop a support system beyond the workplace. Many hospice agencies offer support groups and discussion sessions that can help you cope.

Case Study Spiritual Distress at End of Life

© Mocker_bat/iStock/Thinkstock.

Patient Profile G.M. is a 42-yr-old Orthodox Jewish man. He is being seen by the hospice nurse for increasing abdominal pain, nausea, vomiting, lack of appetite, and constipation. He was diagnosed 6 months ago with pancreatic cancer that has metastasized to the liver and lungs. He quit work 1 month later. Two weeks ago, he ended the drug trial he was on for 5 months and enrolled in hospice. Currently, he is taking oral opioids for pain, ondansetron for nausea and vomiting, sertraline for depression, and megestrol for appetite. His wife is worried that he will become addicted to the pain medication.

Subjective Data

• States that he is angry at God for giving him this illness • Reports fatigue and lack of appetite • Reports pain at 7 (0–10 point scale) not relieved by medication • States he is worried about the loss of his health benefits and what will happen to his young family, including a son age 3, when he is gone

Objective Data Physical Examination • Underweight (20% less than ideal body weight for height) • Skin is jaundiced • Yellow sclera

Interprofessional Care • Review pain medications for dosage adjustment. • Hospice social worker to review medical benefits and disability application • Ensure that advance directives are in place.

Discussion Questions 1. What are G.M.’s risk factors for spiritual distress? 2. Based on the data given, what are the major health problems for G.M.? 3. Patient-Centered Care: What specific palliative care needs does G.M. have? 4. Priority Decision: Based on your assessment of G.M., what are the priority nursing interventions for him? 5. Collaboration: For the interventions that you identified in the previous question, which personnel could be responsible for

implementing them: RN, LPN/VN, unlicensed assistive personnel (UAP)? 6. Collaboration: What referrals may be indicated? Answers available at http://evolve.elsevier.com/Lewis/medsurg.

Bridge to Nclex Examination The number of the question corresponds to the same-numbered outcome at the beginning of the chapter.

1. An 80-yr-old female patient is receiving palliative care for heart failure. The primary purpose(s) of her receiving palliative care is (are) to (select all that apply) a. improve her quality of life. b. assess her coping ability with disease. c. have time to teach patient and family about disease. d. focus on reducing the severity of disease symptoms. e. provide care that the family is unwilling or unable to give. 2. A 67-yr-old woman was recently diagnosed with inoperable pancreatic cancer. Before the diagnosis, she was very active in her neighborhood association. Her husband is concerned because his wife is staying at home and missing her usual community activities. Which common EOL psychologic manifestation is she most likely demonstrating? a. Peacefulness b. Decreased socialization c. Decreased decision making

d. Anxiety about unfinished business 3. For the past 5 years, Tom has repeatedly asked his mother to donate his deceased father’s belongings to charity, but his mother has refused. She sits in the bedroom closet, crying and talking to her long-dead husband. What type of grief is Tom’s mother experiencing? a. Adaptive grief b. Disruptive grief c. Anticipatory grief d. Prolonged grief disorder 4. While caring for his dying wife, the husband states that his wife is a devout Roman Catholic, but he is a Baptist. Who is considered the most reliable source for spiritual preferences concerning EOL care for the dying wife? a. A priest b. Dying wife c. Hospice staff d. Husband of dying wife 5. The family attorney informed a patient’s adult children and wife that the patient did not have an advance directive after he suffered a serious stroke. Who is responsible for making the decision about EOL measures when the patient cannot communicate his or her specific wishes? a. Notary and attorney b. Physician and family c. Wife and adult children d. Physician and nursing staff

6. The home health nurse visits a 40-yr-old patient with metastatic breast cancer who is receiving palliative care. The patient has pain at a level of 7 (0–10 point scale). In prioritizing activities for the visit, what should the nurse do first? a. Auscultate for breath sounds. b. Give as needed pain medication. c. Check pressure points for skin breakdown. d. Ask family about patient’s food and fluid intake. 7. The children caregivers of an older patient whose death is imminent have not left the bedside for the past 36 hours. In the nurse’s assessment of the family, what findings indicate the potential for an abnormal grief reaction to occur (select all that apply)? a. Family cannot express their feelings to one another. b. Dying patient is becoming more restless and agitated. c. A family member is going through a difficult divorce. d. Family talks with and reassures the patient at frequent intervals. e. Siblings who were estranged from each other have now reunited. 8. A nurse has been working full-time with terminally ill patients for 3 years. He has been experiencing irritability and mixed emotions when expressing sadness since 4 of his patients died on the same day. To optimize the quality of his nursing care, he should examine his own a. full-time work schedule. b. past feelings toward death.

c. patterns for dealing with grief. d. demands for involvement in patient care. 1. a, d, 2. b, 3. d, 4. b, 5. c, 6. b, 7. a, c, 8. c. For rationales to these answers and even more NCLEX review questions, visit http://evolve.elsevier.com/Lewis/medsurg.

Evolve Website/Resources List http://evolve.elsevier.com/Lewis/medsurg

Review Questions (Online Only) Key Points Answer Keys for Questions • Rationales for Bridge to NCLEX Examination Questions • Answer Guidelines for Case Study on p. 140 Student Case Study • Patient With Chronic Myelogenous Leukemia Including End-of-Life Care Conceptual Care Map Creator Audio Glossary Content Updates

References 1. National Coalition for Hospice and Palliative Care: Clinical practice guidelines for quality palliative care. Retrieved from www.nationalcoalitionhpc.org/ncp/. Cleary A: Integrating palliative care into primary care for patients with chronic, life-limiting conditions, TNP 41:42, 2016.

3. Centers for Disease Control and Prevention: Healthy aging. Retrieved from www.cdc.gov/aging. 4. National Hospice and Palliative Care Organization: Facts on hospice and palliative care. Retrieved from www.nhpco.org/hospice-statistics-research-pressroom/facts-hospice-and-palliative-care. 5. Hospice and Palliative Nurses Association: HPNA position statements. Retrieved from https://advancingexpertcare.org/HPNA/Leadership/Position_Stateme hkey=a794c17f-c88f-42d9-a09f-caf413e42aa3. 6. National Hospice and Palliative Care Organization: Palliative care costs and benefits. Retrieved from www.caringinfo.org/i4a/pages/index.cfm?pageid=3297. 7. Lungu M, Lupu MN, Voinescu CD: The neurologist’s responsibilities in declaring the time of brain death and organ donation, Acta Medica 22:15, 2017. 8. Field M, Cassel C: Approaching death: Improving care at the end of life, Washington, DC, 1997, National Academy Press. (Classic) 9. Kübler-Ross E: On death and dying, New York, 1969, Macmillan. (Classic). 10. National Cancer Institute: PDQ: Grief, bereavement, and coping with loss. Retrieved from www.cancer.gov/cancertopics/pdq/supportivecare/bereavement/Health 11. O’Brien ME: Spirituality in nursing, 3rd ed, Burlington, MA, 2017, Jones & Bartlett Learning. LoPresti MA, Dement F, Gold HT: End-of-life care for people from ethnic minority groups: A systematic review, Am J Hosp Palliat Care 33:291, 2016. Hagerty TA, Velázquez Á, Schmidt JM, et al: Assessment of satisfaction with care and decision-making among English and Spanish-speaking family members of neuroscience ICU patients,

App Nurs Res. 29:262, 2016.

14. U.S. Department of Health and Human Services: U.S. government information on organ donation and transplantation. Retrieved from www.organdonor.gov/index.html. Robinson EM, Cadge W, Zollfrank AA, et al: After the DNR: Surrogates who persist in requesting cardiopulmonary resuscitation, Hastings Center Report 47:10, 2017. Davies P: Pharmacologic pain management at the end of life, TNP 41:26, 2016. Paez K, Gregg M, Massion C, et al: A new intervention for rapid endof-life symptom control in the home setting, JHPN 18:498, 2016.

18. Marrelli T: Caregivers and caregiving: An important part of the healthcare team, Home Healthcare Now 35:427, 2017. Evidence-based information for clinical practice.

10

Substance Use Disorders Mariann M. Harding

LEARNING OUTCOMES 1. Relate the effects of substance use to its resulting major health complications. 2. Distinguish among the effects of the use of stimulants, depressants, and cannabis. 3. Explain your role in promoting the cessation of smoking and tobacco use. 4. Summarize the nursing and interprofessional management of patients who experience toxicity or withdrawal from stimulants and depressants. 5. Apply the Screening, Brief Intervention, and Referral to Treatment approach in clinical situations. 6. Describe the incidence and effects of substance use in the older adult.

KEY TERMS acute alcohol toxicity, p. 147 alcohol use disorder (AUD), p. 145

alcohol withdrawal syndrome (AWS), p. 147 binge drinking, p. 145 electronic cigarettes, p. 143 Screening, Brief Intervention, and Referral to Treatment (SBIRT), p. 150 substance use disorder (SUD), Table 10.1, p. 143 tobacco use disorder (TUD), p. 142

Conceptual Focus Addiction Coping Motivation You can accomplish with kindness what you cannot by force. Publilius Syrus http://evolve.elsevier.com/Lewis/medsurg/ Substance use is a serious problem affecting society and the health care system. Substance-related disorders involve several types of substances, ranging from widely used and accepted tobacco and alcohol to illegal, brain-altering drugs such as heroin and cocaine. The Diagnostic and Statistical Manual of Mental Disorders V (DSM-V) outlines criteria used to identify the presence of substance use disorder (SUD)1 (Table 10.1). Whether SUD is mild, moderate, or severe depends on the person’s pattern of use and the functional impact of use on the person’s daily life. Knowing the severity of substance use allows the health care team to tailor treatment according to a patient’s needs. For example, a person who binge drinks may not have alcohol SUD but is at increased risk for it. On the other hand, a person who uses heroin or

cocaine is likely to have severe SUD because these substances are highly addictive. Many patients with substance use problems receive acute care for problems associated with substance use. SUD does not exist in isolation. There are many interrelated concepts depending on the patient situation. Every drug associated with SUD harms some tissue or organ. Substance use causes specific health problems, such as liver damage related to alcohol use or lung cancer related to smoking. Other problems result from injuries associated with substance use, such as falls or motor vehicle accidents. Common health problems related to substance use are outlined in Table 10.2. This chapter focuses on the role of the medical-surgical nurse in identifying and managing the patient with SUD in the acute care setting. A hospitalized patient who uses substances can develop withdrawal when substance use abruptly stops. You need to be able to recognize substance use and its effects on health problems and manage withdrawal. The health care setting offers an opportunity for screening and providing teaching about substance use. It is your responsibility to motivate the patient to change behavior and refer the patient to programs that offer treatment.

Drugs Associated with Substance Use Disorder Nicotine You are most likely to encounter people with tobacco use disorder (TUD). People with TUD are dependent on the drug nicotine due to using tobacco products. Several products contain nicotine, including smoked tobacco (cigarettes, cigars, pipes), smokeless tobacco (chew, snuff, dip), and some electronic cigarettes. Cigarette smoking is the main form of tobacco use in the United States.

TABLE 10.1 Criteria for Substance Use Disorder The following criteria (clustered in 4 groups) can be used to identify substance use disorder (SUD). The severity of SUD can be classified as mild (2-3 criteria), moderate (4-5 criteria), or severe (6 or more criteria).

Impaired Control • Taking more or for longer than intended • Not quitting use despite multiple times of trying to do so • Spending a great deal of time obtaining, using, or recovering from use • Craving the substance

Social Impairment • Missing school, work, or other responsibilities due to use • Continuing use despite problems caused or worsened by use • Giving up or reducing important activities because of use

Risky Use • Recurrent use in hazardous situations • Continued use despite causing or worsening problems

Pharmacologic Dependence • Physical tolerance to effects of the substance • Presence of withdrawal symptoms when not using or using less Source: American Psychiatric Association: The diagnostic and statistical manual of mental disorders, ed 5, Arlington, VA, 2013, The Association.

Effects of Use and Complications Nicotine is a central nervous system stimulant. Within seconds of entering the body, nicotine reaches the brain, causing the release of adrenaline and creating feelings of a “high” or a “buzz.” The effects last about 1 to 2 hours before withdrawal symptoms occur, leaving the person feeling tired, irritable, and anxious. The need to have the “high” or “buzz” feelings again makes the person crave more nicotine, leading to addiction. Smoked tobacco is the most harmful method of nicotine use. Smoking harms nearly every organ in the body and reduces the general health of smokers. More than 14 million persons in the United States have a smoking related disease.2 Smoking causes lung disease, cardiovascular disease, and lung and other cancers and is a major factor in many other conditions (Fig. 10.1). Although those who use smokeless tobacco have less risk for lung disease, use can cause serious health problems. Holding tobacco in the mouth is associated with periodontal disease and cancer of the mouth, cheek, tongue, throat, and esophagus. Smokeless tobacco users experience the systemic effects of nicotine on the cardiovascular system, increasing the risk for heart attack and stroke.3 The use of electronic cigarettes, or e-cigs, continues to increase. Ecigs have a similar look and feel of traditional cigarettes. These battery-operated devices turn nicotine and other chemicals, including propylene glycol and flavorings, into an aerosol. Emerging information shows e-cigs can be harmful. E-cigs may affect the respiratory and immune systems. Those containing nicotine may increase the risk for cardiovascular problems and influence brain development in adolescents and pregnant users.4 Other problems, such as poisonings and facial burns from device explosions, have occurred. Although some believe using an e-cig may aid in smoking cessation, no e-cigs are FDA approved. Do not recommend them as a smoking cessation aid.

TABLE 10.2 Health Problems Related to

Substance Use



Health problems related to SUD are discussed in the appropriate chapters throughout the text where they are identified as risk factors for these problems.

Adapted from National Institute on Drug Abuse: Medical consequence of drug abuse. Retrieved from www.drugabuse.gov/relatedtopics/medical-consequences-drug-abuse.

Nursing and Interprofessional Management: Tobacco Use Disorder Tobacco Cessation As a nurse, you have a professional responsibility to help people stop smoking or using tobacco. The Joint Commission mandates that every

health professional must identify tobacco users and provide them with information on ways to stop using tobacco. Patients who receive even brief advice and intervention from you are more likely to quit than those who receive no intervention. With each patient encounter, encourage the patient to quit and offer specific smoking cessation interventions. The Agency for Healthcare Research and Quality has issued clinical practice guidelines for clinicians, including nurses, to use to motivate users to quit5 (Tables 10.3 and 10.4). Use these brief clinical interventions, called the “5 As,” with each patient encounter. These interventions will help you identify tobacco users, encourage them to quit, determine their willingness to quit, assist them in quitting, and arrange for follow-up. A patient teaching guide (Table 10.5) expands on the fourth strategy, Assist, to help you aid the user willing to quit. If a tobacco user is unwilling to quit, using the “5 Rs” may motivate the user to quit in the future.

FIG 10.1 Health effects of smoking. From Samet JM: Tobacco smoking, Thorac Surg Clin 23[2]:103, 2013.

TABLE 10.3 Clinical Practice Guideline

Treating Tobacco Use Disorder

Source: Agency for Healthcare Research and Quality: AHCPR supported clinical practice guideline: Treating tobacco use and dependence— 2008 update, Washington, DC, 2008, U.S. Public Health Service. A variety of smoking cessation products are available to help support users in quitting. These include prescription medicines as well as over-the-counter (OTC) products such as skin patches, lozenges, and gum. Nicotine replacement products are 1 type of smoking cessation product. These products reduce the craving and withdrawal symptoms associated with cessation by supplying the body with smaller amounts of nicotine (Table 10.6).

TABLE 10.4 Inpatient Tobacco Cessation

Interventions Take the following steps for every hospitalized patient: • Ask each patient on admission if he or she uses tobacco and document tobacco use status. • For current tobacco users, list tobacco use status on the admission problem list and as a discharge diagnosis. • Use counseling and medication to help all tobacco users stay abstinent and to treat withdrawal symptoms. • Give advice and assistance on how to quit during hospitalization and stay abstinent after discharge. • Arrange for follow-up about smoking status. Provide supportive contact for at least a month after discharge.

Source: Agency for Healthcare Research and Quality: AHCPR supported clinical practice guideline: Treating tobacco use and dependence: 2008 update, Washington, DC, 2008, U.S. Public Health Service. Because most health care facilities are tobacco-free environments, admitted patients who are addicted to nicotine may experience withdrawal symptoms since they are unable to smoke. These symptoms are the same as for the person who stops using tobacco “cold turkey.” Offering nicotine replacement therapy to every patient who wants to quit will help control withdrawal symptoms during hospitalization and promote continued cessation after discharge. Non-nicotine products also play a role in helping users quit. Varenicline (Chantix) is a drug used to aid smoking cessation. Varenicline is unique in that it has both agonist and antagonist actions. Its agonist activity at 1 subtype of nicotinic receptors provides some nicotine effects to ease withdrawal symptoms. If the person does resume smoking, its antagonist action blocks the effects of nicotine at another subtype of nicotinic receptor, making smoking less enjoyable. Bupropion (Zyban), an antidepressant drug, reduces the urge to smoke, reduces some symptoms of withdrawal, and helps prevent weight gain associated with smoking cessation.

TABLE 10.5 Patient Teaching

Smoking and Tobacco Use Cessation The following interventions are methods that work for quitting tobacco use. Tobacco users have the best chance of quitting if they use more than 1 method.

Develop a Quit Plan • Set a quit date, ideally within 2 weeks. • Talk to your HCP about getting help to quit.

• Tell family, friends, and co-workers about quitting and request understanding and support. • Expect withdrawal symptoms and challenges when quitting. • Before quitting, avoid smoking in places where you spend a lot of time (work, car, home). • Throw away all tobacco products from your home, car, and work. • Have support options in place by your quit date.

Use Approved Nicotine Replacement Systems • Use a nicotine replacement agent unless you are a pregnant or nursing woman (Table 10.6). • Do not use other forms of tobacco when using nicotine replacement systems.

Support and Encouragement • Joining a quit-tobacco support group will increase your chances of stopping permanently. • If you get the urge for tobacco, call someone to help talk you out of it—preferably an ex-user. • Be proud every time you reach a quit milestone and reward yourself. • Do not be afraid to talk about how you feel while quitting, especially fears of not being able to quit for good. Ask your spouse or partner, friends, and co-workers to support you. Selfhelp materials, mobile phone applications, and hot lines are available: • American Lung Association: 800-586-4872; www.lung.org • American Cancer Society: 800-227-2345; www.cancer.org • National Cancer Institute: LiveHelp; www.smokefree.gov

Dealing With Urges to Use Tobacco • Identify situations that may cause you to want to smoke or use other tobacco, such as being around other smokers, being under time pressure, feeling sad or frustrated, and drinking alcohol. • Avoid difficult situations while you are trying to quit. Try to lower your stress level. • Exercise can help, such as walking, jogging, or bicycling. • Distract yourself from thoughts of smoking and the urge to use tobacco by talking to someone, going to a movie, getting busy with a task, or having a game night with friends. • Drink a lot of water. • Keep your hands busy with a pen or toothpick.

Avoiding Relapse Most relapses occur within the first 3 months after quitting. Do not be discouraged if you start using tobacco again. Remember, most people try several times before they finally quit. Explore different ways to break habits. You may have to deal with some of the following triggers that cause relapse. • Change your environment. Get rid of cigarettes, tobacco (in any form), and ashtrays in your home, car, and place of work. Get rid of the smell of cigarettes in your car and home. • Alcohol. Consider limiting or stopping alcohol use while you are quitting tobacco. • Other smokers at home. Encourage housemates to quit with you. Work out a plan to cope with others who smoke and avoid being around them. • Weight gain. Tackle 1 problem at a time. Work on quitting tobacco first. You will not necessarily gain weight, and increased appetite is often temporary. Eat healthy and exercise. • Negative mood or depression. If these symptoms persist, talk to your

HCP. You may need treatment for depression. • Withdrawal symptoms. Your body will go through many changes when you quit tobacco. You may have a dry mouth, cough, or scratchy throat, and you may feel irritable. The nicotine patch or gum may help with cravings (Table 10.6). • Focus on the benefits of quitting: • Your BP and heart rate will lower almost at once. • Your risk for a heart attack declines within 24 hours. The blood will become less likely to clot, making dangerous blood clots less likely. • Within a few weeks, you will be less short of breath, cough less, and have more energy. Your ability to smell and taste should improve. • Your immune system will be stronger, so you will be less likely to be sick. • Quitting will improve your night vision and help preserve your overall vision. Adapted from National Cancer Institute: 18 ways smoking affects your health. Retrieved from www.smokefree.gov/health-effects.

Drug Alert Varenicline (Chantix) and Bupropion (Zyban) • Serious neuropsychiatric symptoms such as changes in behavior, hostility, agitation, depressed mood, suicidal thoughts and behavior, and attempted suicide can occur. • Tell patients to stop taking these drugs and contact the HCP at once if they have any of these manifestations. Along with using a smoking cessation product, users who wish to quit are more likely to succeed if they take part in a tobacco cessation

program. You should be aware of available community resources. Cessation programs may involve hypnosis, acupuncture, behavioral interventions, aversion therapy, group support programs, individual therapy, and self-help options. Many of these programs teach users to avoid high-risk situations for smoking relapse (e.g., those that promote cue-induced craving) and help them develop coping skills, such as cigarette refusal skills, assertiveness, alternative activities, and peer support systems.

Alcohol Of Americans ages 18 and older, 70% consume alcohol. Most people use alcohol in moderation.6 Risky drinking is consuming more alcohol than the amounts in guidelines established by the National Institute on Alcohol Abuse and Alcoholism (Fig. 10.2). Risky drinking can have negative physical, emotional, and social consequences. Alcohol use disorder (AUD), or alcoholism, affects about 6.2% of U.S. adults.6 A higher percent engages in periodic excess alcohol use. Binge drinking is consuming 5 or more alcoholic drinks for males or 4 or more alcoholic drinks for females on the same occasion at least once per month.

TABLE 10.6 Drug Therapy

Smoking Cessation∗



OTC nicotine replacement agents are also available in generic forms. More information and patient instructions are available from the American Lung Association at www.lungusa.org. †

See the Drug Alert for varenicline on p. 145.

FIG 10.2 U.S. standard drink equivalents. The National Institute on Alcohol Abuse and Alcoholism (NIAAA) guidelines for alcohol use state that healthy men younger than 65 should consume no more than 14 standard drinks per week or 4 drinks per drinking occasion. Healthy, nonpregnant women and adults older than 65 should consume no more than 7 standard drinks per week or 3 drinks per drinking occasion. From NIAAA: What’s a standard drink? Retrieved from www.niaaa.nih.gov.

Effects of Use and Complications Alcohol affects almost all cells of the body. It changes levels of neurotransmitters in the central nervous system (CNS), affecting all areas and functions of the CNS. These include centers that control our impulses, mood, and behavior; coordinate motor activity; and promote respiratory and cardiac function. The immediate effects of alcohol depend on a person’s susceptibility to alcohol and the blood alcohol concentration (BAC). For the person who is not dependent on alcohol, the BAC generally predicts alcohol’s effects. The relationship between BAC and behavior

is different in a person who has developed tolerance to alcohol and its effects. The tolerant person is usually able to drink large amounts without obvious impairment and perform complex tasks without problems at BAC levels much higher than levels that would produce obvious impairment in the nontolerant drinker. Women have higher blood alcohol levels than men do after the same amount of alcohol intake. Alcohol use is linked to many health problems (Table 10.7), which are often the reason that people seek health care. Long-term alcohol use can lead to hypertension, heart disease, stroke, liver disease, and digestive problems. Short-term, excess alcohol use increases the risk for injury from motor vehicle crashes, falls, firearms, assault, drowning, and burns. Patients with AUD undergoing surgery have increased in-hospital death rates and longer lengths of stay.

TABLE 10.7 Effects of Chronic Alcohol Use

Body System

Effects Hypertension, atrial fibrillation, cardiomyopathy, stroke, coronary artery Cardiac disease, sudden cardiac death Gastrointestinal Gastritis, gastroesophageal reflux disease (GERD), peptic ulcer, esophagitis, esophageal varices, gastrointestinal bleeding, pancreatitis, oropharyngeal cancer, colorectal cancer Bone marrow depression, anemia, leukopenia, thrombocytopenia, blood Hematologic clotting abnormalities Alcoholic hepatitis, cirrhosis, liver cancer Hepatic Palmar erythema, spider angiomas, rosacea, rhinophyma Integumentary Musculoskeletal Myopathy, osteoporosis, gout Alcoholic dementia, Wernicke-Korsakoff syndrome, impaired cognitive Neurologic function, psychomotor skills, abstract thinking, and memory. Depression, anxiety, attention deficit, labile moods, seizures, insomnia, peripheral neuropathy, chronic headache Nutrition

Diabetes, anorexia, malnutrition, vitamin deficiencies (especially thiamine)

Reproductive

Breast cancer, testicular atrophy, decreased beard growth, decreased libido, decreased sperm count, gynecomastia Diuretic effect from inhibition of antidiuretic hormone

Urinary

Complications may arise from the interaction of alcohol with commonly prescribed or OTC medications. Those that interact with alcohol in an additive manner include antihypertensives, antihistamines, and antianginals. Alcohol taken with aspirin may cause or worsen GI bleeding. Alcohol taken with acetaminophen may increase the risk for liver damage. Taking a CNS depressant with alcohol can increase, or potentiate, the effect of both. An alcoholdependent person may have cross-tolerance, needing higher doses of CNS depressants to achieve the desired effect.

Nursing and Interprofessional Management: Alcohol Use Disorder Alcohol Toxicity Acute alcohol toxicity occurs when a person has a high level of alcohol in the blood, generally after ingesting a large amount of alcohol. This leads to behavior changes and alcohol-induced CNS depression, resulting in respiratory and circulatory failure. Unconsciousness, coma, and death can occur. Other common effects include hypokalemia, hypomagnesemia, and hypoglycemia. Obtain as accurate a health history as possible and assess for injuries, diseases, and hypoglycemia. No antidote for alcohol is available. Implement supportive care measures to maintain airway, breathing, and circulation (the ABCs) until the alcohol metabolizes. Frequently monitor vital signs and level of consciousness. Treat alcohol-induced hypotension with IV fluids. Patients with hypoglycemia may receive glucose-containing IV solutions. IV thiamine may be given before or with IV glucose solutions to prevent Wernicke-Korsakoff syndrome, which can cause seizures and brain damage.7 Many patients have low serum magnesium levels and other signs of malnutrition, so HCPs often add multivitamins and magnesium to the IV fluids. Agitation and anxiety are common. Stay with the patient as much as possible, orienting as necessary. Assess the patient for increasing

belligerence and a potential for violence. Since the patient is at risk for injury because of lack of coordination and impaired judgment, use protective measures.

Alcohol Withdrawal Syndrome Alcohol withdrawal syndrome (AWS) can develop in a hospitalized patient when the use of alcohol abruptly stops. The onset of AWS is variable depending on the quantity, frequency, pattern, and duration of alcohol use. The early signs usually develop within a few hours after the last drink. They peak after 24 to 48 hours and then disappear unless the withdrawal progresses to alcohol withdrawal delirium. Alcohol withdrawal delirium is a serious complication that can occur from 2 to 3 days after the last drink and last 2 to 3 days. The greater the patient’s dependence on alcohol, the greater the risk for alcohol withdrawal delirium. Death may result from multiorgan dysfunction, dysrhythmias, or peripheral vascular collapse.8 Management begins with identifying at-risk persons. Use a symptom assessment tool, such as the Clinical Institute Withdrawal Assessment of Alcohol Scale, Revised (CIWA-Ar), to determine treatment7 (Table 10.8). Table 10.9 presents the clinical manifestations and suggested treatment for AWS. A nursing care plan (eNursing Care Plan 10.1) for a patient with AWS is available on the website at http://evolve.elsevier.com/Lewis/medsurg.

Check Your Practice A 34-yr-old male patient was admitted for multiple trauma following a car accident. His girlfriend tells you that he always drinks too much and she knew he would get in trouble someday. • What signs and symptoms would alert you to the presence of AWS? • What measures would you use to protect his safety?

• How would you involve members of the interprofessional team in planning patient care?

Use of Other Substances Stimulants Amphetamine-related stimulants are highly addictive substances. While the use of crack cocaine and methamphetamine is illegal, amphetamines have a role in treating narcolepsy, obesity, and attention deficit disorder. Though most people responsibly use prescribed stimulants, prescription stimulants are often misused. All stimulants increase cardiac activity and excite the CNS by increasing levels of norepinephrine, serotonin, and dopamine. People use these drugs to produce feelings of euphoria, increase alertness, and boost their energy. Health problems associated with using stimulants are outlined in Table 10.2.

TABLE 10.8 Clinical Institute Withdrawal

Assessment of Alcohol Scale, Revised (CIWA-Ar ) CIWA-Ar Categories Agitation

Score Range in Each Category 0–7

Anxiety

0–7

Auditory disturbances

0–7

Headache

0–7

Clouding of sensorium

0–4

Paroxysmal sweats

0–7

Tactile disturbances

0–7

Tremor

0–7

Visual disturbances

0–7

Source: University of Maryland School of Medicine. Available at

www.umem.org/files/uploads/1104212257_CIWA-Ar.pdf.

TABLE 10.9 Manifestations and Treatment of

Alcohol Withdrawal

Nursing and Interprofessional Management: Stimulant Use Toxicity Patients with stimulant toxicity present with sympathetic overdrive (increased stimulation of the sympathetic nervous system). The patient has restlessness, agitation, delirium, impaired judgment, and paranoia with psychotic symptoms. Physical effects include hypertension, tachycardia, fever, pupil dilation, seizures, confusion, and diaphoresis. Death may occur from stroke, dysrhythmias, or myocardial infarction.1

TABLE 10.10 Emergency Management

Stimulant Toxicity

The emergency management depends on the clinical manifestations at the time of treatment (Table 10.10). A specific antidote for stimulant toxicity is not available. Treatment focuses on supportive care measures.

Withdrawal Stimulant withdrawal is usually not an emergency. Abrupt cessation can lead to a “crash.” The patient may be depressed and experience fatigue, disturbed sleep, vivid dreams, general aching, irritability, increased appetite, and mood swings.9 Craving for the drug is intense during the first hours to days of drug cessation and may continue for weeks. Supportive care includes providing a safe, quiet environment and allowing the patient to sleep and eat as desired. If a patient has severe depression, initiate suicide precautions and refer for further treatment.

Depressants Commonly used depressants include sedative-hypnotics and opioids.

Depressants have a rapid development of tolerance and dependence. Their use is associated with many medical emergencies involving toxicity and withdrawal. The majority of drug overdose deaths involve an opioid, either alone or in combination with another depressant (e.g., opioid and benzodiazepine).10 Common health problems resulting from depressant use are outlined in Table 10.2.

Sedative-Hypnotics Common sedative-hypnotic agents include barbiturates, benzodiazepines, and barbiturate-like drugs. Sedative-hypnotic drugs depress the CNS, causing sedation at low doses and sleep at high doses. Their use produces a euphoria and intoxication that resembles that of alcohol. Tolerance develops rapidly to the effects of these drugs, requiring higher doses to achieve euphoria. However, tolerance may not develop to the brainstem-depressant effects. As a result, an increased dose may trigger hypotension and respiratory depression, resulting in death.

Opioids Opioids include substances directly derived from the opium poppy (e.g., morphine), semisynthetics (e.g., heroin, hydromorphone), and synthetic compounds (e.g., fentanyl). Persons dependent on opioids include those who use illegal drugs sold on the street and those who misuse prescription opioids. Opioids act on opiate receptors and neurotransmitter systems in the CNS, causing sedation and analgesia. The person taking an opioid experiences euphoria, mood changes, mental clouding, drowsiness, and pain reduction. While this makes prescription opioids useful in treating a number of medical conditions, their pleasurable effects promote misuse. Misusing oxycodone or fentanyl can result in the same harmful consequences as abusing heroin.

Nursing and Interprofessional

Management: Depressant Use Toxicity Overdoses can occur when a person purposefully misuses a depressant or takes 1 prescribed for someone else. Unintentional overdose often occurs, especially when depressants are used with alcohol or other drugs. Depressant toxicity can cause death from respiratory and CNS depression. The priority of care is always the patient’s ABCs. Supporting respiratory and cardiovascular function and continuous monitoring of neurologic status is critical until the patient is stable. The emergency management depends on the substance used and the clinical manifestations (Table 10.11).

TABLE 10.11 Emergency Management

Depressant Toxicity

Sedative-Hypnotics On occasion, a patient with a benzodiazepine overdose may receive

flumazenil, a specific benzodiazepine antagonist. Because flumazenil may have a shorter duration of action than some benzodiazepines, repeated doses may be needed until the benzodiazepine is metabolized. Place the patient on safety precautions as flumazenil can cause seizures. There are no antagonists for barbiturates or other sedative-hypnotic drugs. The patient receives supportive care, including passive rewarming, hydration, and vasopressors, along with treatments to promote drug elimination. If the airway can be maintained, activated charcoal is an option. Dialysis can be used in certain situations.

Opioids Overdose in the inpatient setting may occur when a patient inadvertently receives an incorrect dose, or when opioids are aggressively dosed, given to patients with new kidney or liver impairment, or given with drugs that potentiate respiratory depression.11 Treatment includes supporting respiratory function and giving the opioid antagonist naloxone. Naloxone reverses respiratory depression and other manifestations of toxicity. Monitor the patient closely because naloxone has a shorter duration of action than most opioids. Repeated doses or IV infusion of naloxone may be needed until the opioid is metabolized. Overdose in the community setting can occur when a person deliberately misuses an illegal or prescription opioid, takes an opioid in combination with other depressants, or takes an opioid prescribed for someone else. In many areas, naloxone is publicly available. This allows police, first responders, family members, and friends to give someone naloxone in emergencies, thus reversing the effects of an overdose sooner. As a result, you may see more patients requiring postreversal care.

Withdrawal Sedative-Hypnotics Withdrawal from sedative-hypnotics can be life threatening. The

manifestations and treatment are similar to those of AWS. Early, the patient may have tremors, anxiety, insomnia, fever, orthostatic hypotension, and disorientation. Since the patient may experience delirium, seizures, and respiratory and cardiac arrest within 24 hours after the last dose, closely monitor the patient. Treatment consists of giving a long-acting benzodiazepine in a tapered dose. IV diazepam is an option for severe manifestations. Supportive care includes implementing patient safety and comfort measures, frequently assessing neurologic status and vital signs, and providing reassurance and orientation.

Opioids Opioid withdrawal symptoms depend on the opioid used, route of administration, and duration of use. It is usually not life threatening but can be extremely uncomfortable. Manifestations include intense drug craving, diaphoresis, gastrointestinal distress, restlessness, fever, insomnia, watery eyes, tremors, muscle aches, runny nose, and anxiety.1 With shorter acting drugs, withdrawal may begin 4 to 6 hours after the last dose, peak in 36 to 72 hours, and last 7 to 10 days. With longer acting drugs, manifestations may begin 24 to 48 hours after last dose and peak in 3 to 4 days.11 Treatment focuses on relieving symptoms and often requires drug therapy. Substituting a long-acting opioid (e.g., methadone, buprenorphine) at low doses or α2-adrenergic agonists (e.g., clonidine) decreases withdrawal symptoms. Other therapies include medications for GI distress (e.g., loperamide, ondansetron), acetaminophen or nonsteroidal antiinflammatory agents for muscle aches and fever, and antihistamines for acute anxiety and sleep disturbances.

Inhalants Persons with inhalant use disorder inhale hydrocarbon-based fumes, such as those found in glues or paints, to change their mental state.1

Inhalants are rapidly absorbed and reach the CNS quickly. Most are depressants with effects like those of alcohol. They cause a brief period of euphoria, followed by drowsiness and lightheadedness. Long-term use can result in neurologic problems, including damage to parts of the brain that control cognition, movement, vision, and hearing (Table 10.2). The patient with inhalant toxicity may have lethargy, dizziness, slurred speech, blurry vision, tremors, and impaired coordination.1 The effects usually resolve within minutes to a few hours. Inhalant toxicity is managed with supportive care. However, in some cases, users need emergency treatment for dysrhythmias, heart failure, or CNS hyperactivity (e.g., seizures). Using some inhalants (e.g., toluene) can result in nephrotoxicity; so, you must monitor renal function. Withdrawal is rare as most inhaled substances have a very short duration. Any manifestations that may occur require supportive care.

Cannabis The use of cannabis, also called marijuana or weed, continues to increase in the United States. Cannabis is available in forms that can be smoked, vaporized, or ingested. The main ingredient is tetrahydrocannabinol (THC). At low to moderate doses, THC produces euphoria, reduced anxiety, and improved appetite. Adverse effects include impaired memory, impaired motor coordination, altered judgment, and, in high doses, paranoia and psychosis. Longterm use is associated with a wide range of effects, particularly on cardiopulmonary and mental health (Table 10.2). Legalizing cannabis for recreational and medical use is controversial. Sales for recreational use continue to grow. More than half of the states have legalized its use for specific medical reasons. If an HCP in 1 of those states determines a patient has a disorder that qualifies for medical cannabis use, the HCP can give the patient an authorization for use. This form allows the patient to buy cannabis at special dispensaries or have a limited number of cannabis plants. THC-based medications, dronabinol (Marinol) and nabilone

(Cesamet), are available to control nausea and vomiting from cancer chemotherapy. Dronabinol is also used to stimulate appetite in patients with acquired immunodeficiency syndrome (AIDS). Illegal synthetic cannabinoid drugs (e.g., K2, Spice) have some of the same properties as THC. They contain varying amounts of different ingredients. The result is that these products have unpredictable effects and are more toxic. Sometimes, death has occurred with 1 use. Patients with acute marijuana toxicity can present with acute psychotic episodes, especially if the patient used a synthetic derivative. Cannabis can induce tachycardia and hypertension, triggering dysrhythmias and myocardial infarction. Support the patient’s ABCs. Panic and flashbacks are managed by maintaining a quiet environment and reassuring the patient. Benzodiazepines give symptom relief. 12 Withdrawal can occur in a hospitalized patient who uses cannabis. The patient may have irritability, insomnia, anorexia, cramping, mild agitation, and nausea.13 This peaks about 48 hours after cessation and may be more severe in women. There is no specific drug therapy for treating withdrawal. Supportive care includes measures to promote sleep, safety, and patient comfort, including analgesics and hydration.

Caffeine Caffeine is the most widely used psychoactive substance in the world. It is very weak when compared with the other stimulants. Most people use it to promote wakefulness. Other uses include promoting motor activity and treating headaches. Its use is safe in most people. Problems from high doses of caffeine have occurred in association with specialized drinks. A large caffeine intake can cause cardiac dysrhythmias, hypertension, disturbed sleep, seizures, and anxiety. Treatment consists of seizure control with benzodiazepines and supportive care until the effects wear off. In a hospitalized patient, caffeine withdrawal can result in muscle pain or stiffness, drowsiness, irritability, and headaches after general anesthesia or during restrictions on usual caffeine intake.1

Nursing Management: Substance Use Nursing Assessment You need to be able to determine if patients use substances in a way that places them at risk or if SUD is present. Screening is a simple, effective way to identify patients who need further assessment. Use the Screening, Brief Intervention, and Referral to Treatment (SBIRT) approach (Fig. 10.3). SBIRT consists of 3 parts: (1) screening to quickly identify and assess the severity of any substance use problems, (2) providing a brief intervention or teaching patients about the consequences of substance use, and (3) referring those who screen positive for further treatment.14 Screening is the first part of SBIRT. Use screening tools to identify those who may have problems with substance use. As a baseline, ask every patient about the use of all substances, including prescribed medications, OTC medications, caffeine, tobacco, and recreational drugs. Use simple 1 or 2 question screening tests to detect alcohol, tobacco, and/or other substance use problems (Table 10.12). If a patient has a positive screen, follow up with a detailed assessment to identify specific problems. A screening tool for AUD, the Alcohol Use Disorders Identification Test, is shown in Table 10.13. A score of 8 points or more in men or 7 or more in women is concerning. Another useful tool is the Drug Abuse Screening Test (DAST-10), shown in Table 10.14.

FIG 10.3 Screening, Brief Intervention, and Referral to Treatment approach. From Substance Abuse and Mental Health Services Administration [SAMHSA]: Systems-level implementation of screening, brief intervention, and referral to treatment, Technical Assistance Publication [TAP] Series 33. HHS Publication No. 13-4741, Rockville, MD, 2013, SAMHSA. Retrieved from www.integration.samhsa.gov/SBIRT/tap33.pdf.

TABLE 10.12 Brief Screening Tools for Substance

Use

Single Question Tests Use 1 of the following questions to screen for the presence of alcohol, drug, or tobacco use. • How often in the past year have you had 5 (men) or 4 (women) or more drinks in a day? • How many times in the past year have you used illegal drugs or prescription medications for nonmedical reasons? • In the past year, how often have you used tobacco products?

2-Question Tests Use the following 2 questions to screen for alcohol or drug use. • In the past year, have you ever drunk or used drugs more than you meant to? • Have you felt you wanted or needed to cut down on your drinking or drug use in the past year? Adapted from Strobbe S: Prevention and screening, brief intervention, and referral to treatment for substance use in primary care, Prim Care Clin Office Pract 41:185, 2014. If there is any sign of substance use, figure out when the patient last used the substance. Knowing this information will let you know when to expect the onset of withdrawal and help you anticipate drug interactions. Assess for factors that influence the onset of withdrawal, including the substance used, dose taken, method of intake, and length of time the patient has used the substance. You may discover that the patient is dealing with polysubstance use, or the use of more than 1 substance. Alert the HCP as these patients need care tailored to the combination of substances used. You may find problems associated with substance use during your physical assessment. Assess the patient’s general appearance and nutritional status. Examine the abdomen, skin, and cardiovascular, respiratory, and neurologic systems. The presence of a mental health disorder, such as anxiety, bipolar disorder, or depression, increases the risk for SUD. Serum and urine drug screens can identify the type and amounts of drugs present in the body. A complete blood count, serum electrolytes, blood urea nitrogen, creatinine, and liver function tests evaluate for electrolyte imbalances and cardiac, kidney, or liver dysfunction. During your assessment, look for patient behaviors such as denial, avoidance, underreporting or minimizing substance use, or giving inaccurate information. Behaviors and physical manifestations

suggesting substance use are outlined in Table 10.15. However, these behaviors are not all inclusive.

Nursing Diagnoses Nursing diagnoses for the patient with substance use disorder include: • Substance abuse, drug, alcohol and/or tobacco • Risk for injury • Acute confusion • Altered perception

Planning Nursing care focuses on the priority problems of reducing the risk for injury and managing acute confusion. The overall goals are that the patient with a substance use problem will (1) have normal physiologic functioning, (2) acknowledge a substance use problem, (3) explain the psychologic and physiologic effects of substance use, (4) abstain from substance use, and (5) cooperate with a proposed treatment plan.

TABLE 10.13 Alcohol Use Disorders

Identification Test (AUDIT)

Scoring for AUDIT: Questions 1 through 8 are scored 0, 1, 2, 3, or 4. Questions 9 and 10 are scored 0, 2, or 4 only. The minimum score (nondrinkers) is 0 and the maximum possible score is 40. A score of 9 or more indicates hazardous or harmful alcohol consumption.

Source: Babor TF, Higgins-Biddle JC, Saunders JB, Monteiro M: The alcohol use disorders identification test, ed 2, Geneva, Switzerland, 2001, WHO Press.

TABLE 10.14 Drug Abuse Screening Test (DAST-

10)

© 1982 by Harvey A. Skinner, PhD, and the Centre for Addiction and Mental Health, Toronto, Canada. You may reproduce this instrument for noncommercial use (clinical, research, training purposes) as long as you credit the author, Dr. Harvey A. Skinner, Dean, Faculty of Health, York University, Toronto, Canada.

TABLE 10.15 Findings Suggesting Substance Use

Physiologic • Fatigue • Insomnia • Headaches • Seizure disorder • Changes in mood

• Anorexia, weight loss • Vague physical complaints • Appearing older than stated age, unkempt appearance • Sexual dysfunction, decreased libido, erectile dysfunction • Failure of standard doses of sedatives to have a therapeutic effect

Behavioral • Overuse of mouthwash or toiletries • Citations for driving while intoxicated or impaired • Leisure activities that involve alcohol and/or other drugs • Trauma secondary to falls, auto accidents, fights, or burns • Financial problems, including those related to spending for substances • Defensive or evasive answers to questions about substance use and its importance in the person’s life • Problems in areas of life function (e.g., frequent job changes; marital conflict, separation, or divorce; work-related accidents, tardiness, absenteeism; legal problems; social isolation, estranged from friends or family)

Nursing Implementation Health Promotion Your role in health promotion includes prevention and early detection of substance use. Prevention measures include abstaining from harmful substances and limiting alcohol use. These measures decrease the risk for substance-related injury or illness. You can help prevent substance use problems by (1) teaching about the effects and negative outcomes of substance use and (2) providing support. Through screening, you have an opportunity to prevent patients from becoming dependent on alcohol and drugs. You can do this by using brief interventional techniques and helping patients access

appropriate care through referral to treatment if they show risky behaviors or are already dependent.

Acute Intervention The immediate result of overconsumption is acute toxicity or overdose. The patient may also present with trauma or injuries. The priority of care is supporting the patient’s ABCs, especially respiratory status. In addition to treating injuries, provide supportive care until detoxification can occur. Nursing care includes frequently assessing neurologic status and vital signs, giving IV fluids to prevent dehydration, orienting to time and place, and implementing patient safety measures. Sometimes, uncertainty exists as to what substances are involved. If the patient used multiple substances, a complex clinical picture can result. For example, a patient presents with toxicity and the health care team does not know what substances are involved. Although blood and urine tests will help identify the substances, treatment is started while waiting for the test results. The patient in this situation would usually receive naloxone. If the substance used is a barbiturate or another CNS depressant, naloxone will not help the patient, but it will not hurt the patient either. If the patient does not respond to a total dose of 10 mg of naloxone, it is unlikely opioids are involved. Once acute health issues are resolved, provide a brief intervention to teach patients about the consequences of substance use and support behavioral change. When patients have a substance use problem, it is critical to motivate the patient to engage in long-term treatment. You are in a unique position to facilitate behavior change. When a patient seeks care for health problems related to substance use or when hospitalization interferes with the usual pattern of use, the patient’s awareness of any substance use problem increases. Intervention at this time can promote behavior change. Take an active role in performing motivational interviewing and providing counseling aimed at cessation. (Motivational interviewing is discussed in Chapter 4.) Discuss the risks associated with substance use and provide feedback and advice. If the patient agrees, assist with referral to counseling or

behavioral therapy.

Gerontologic Considerations: Substance Use Substance use in older adults is a fast-growing and often hard to recognize problem. Older adults do not fit the image of users. For example, older users are less likely to binge drink and use different substances than younger users. The effects of alcohol and drugs can be mistaken for medical conditions common among older adults (e.g., hypertension, dementia). So, we may attribute substance use problems to another cause and not offer treatment. Some use alcohol or drugs to cope with grief and loss issues, such as the death of a spouse.15 Because of the higher rate of coexisting medical problems, older adults are at greater risk for medical problems associated with substance use. Common problems include liver damage and cardiovascular, GI, and endocrine problems. Substance use may cause confusion, delirium, memory loss, and neuromuscular impairment. Physiologic changes may lead to toxicity at levels that may not have been a problem at a younger age. Withdrawal symptoms may be more severe than in younger persons.

FIG 10.4 Older adults are often unaware of their substance use problems. © Ned White/iStock/Thinkstock.

It is important to screen older adults for substance use. Family members are important sources of information (Fig. 10.4). Other potential sources include friends, home health aides, meal delivery personnel, and staff members at senior citizen centers and long-term care facilities. It is important for you to discuss drug and alcohol use with older adult patients, including OTC and herbal drug use. Assess the patient’s knowledge of currently used drugs. Common screening questionnaires may not identify an older adult with a substance use problem. The Short Michigan Alcoholism Screening Test–Geriatric version (SMAST-G) is a short-form alcoholism screening instrument for older adults (www.consultgerirn.org) that can identify older adults with potential AUD. Smoking and other tobacco use is another issue. Those who have

smoked for decades may feel unable to stop or believe there is no benefit to stopping at an advanced age. However, smoking contributes to and worsens many chronic illnesses found in the older adult population. Smoking cessation at any age is beneficial. The information about smoking cessation discussed earlier is appropriate for helping older adults with smoking cessation (Tables 10.3 to 10.6). Patient teaching for the older adult includes teaching about the desired effects, possible side effects, and proper use of prescribed and OTC drugs. When you suspect alcohol or substance use, refer the patient for treatment. It is a mistaken belief that older people have little to gain from alcohol and drug dependence treatment. The rewards of treatment can lead to greater quality and quantity of life for older adults.

Case Study Substance Use Disorder

©JPC-PROD/iStock/Thinkstock.

Patient Profile C.M., a 78-yr-old woman, is admitted to the emergency department after falling and injuring her right hip. She has been widowed for 4 years and lives alone. Recently her best friend died. Her only family is a daughter who lives out of town. When contacted by phone, the

daughter tells the nurse that her mother has appeared more disoriented and confused over the past few months when she has talked to her on the phone.

Subjective Data • Describing severe pain in her right hip • Admits she had some wine in the late afternoon to stimulate her appetite • Has experienced several falls in the past 2 months • Reports that she fell after taking a prescribed sleeping pill because she does not sleep well • Speech is hesitant and slurred • Says she smokes about a half pack of cigarettes a day

Objective Data Physical Examination • Oriented to person and place, but not time • BP 162/94, pulse 92, respirations 24 • Severe pain and tenderness in the right hip region • Bilateral hand tremors

Diagnostic Tests • X-ray reveals a subtrochanteric fracture of the right femur requiring surgical repair • Blood alcohol concentration (BAC) 120 mg/dL (0.12%) • Complete blood count: Hemoglobin 10.6 g/dL, hematocrit 33%

Discussion Questions

1. What other information is needed to assess C.M.’s condition? 2. How should you address questions about these areas? 3. What factors may contribute to C.M.’s substance use? 4. Priority Decision: Based on the assessment data given, what are the priority nursing diagnoses? Are there any collaborative problems? 5. Priority Decision: What are the priority nursing interventions during C.M.’s preoperative period? 6. What possible complications and injury risks may occur during C.M.’s postoperative recovery? 7. Safety: To ensure C.M.’s safety, what nursing interventions are necessary after surgery? 8. Delegation Decision: How would you use the unlicensed assistive personnel (UAP) on the postoperative unit to carry out the interventions that you identified in question 5? 9. Collaboration: What referrals are indicated? Answers available at http://evolve.elsevier.com/Lewis/medsurg.

Bridge to Nclex Examination The number of the question corresponds to the same-numbered outcome at the beginning of the chapter.

1. When admitting a patient, the nurse must assess the patient for substance use based on the knowledge that long-term use of addictive substances leads to a. the development of coexisting psychiatric illnesses. b. a higher risk for complications from underlying health problems. c. potentiation of effects of similar drugs taken when the person is drug free. d. increased availability of dopamine, resulting in

decreased sleep requirements. 2. The nurse would suspect cocaine toxicity in the patient who is experiencing a. agitation, dysrhythmias, and seizures. b. blurred vision, restlessness, and irritability. c. diarrhea, nausea and vomiting, and confusion. d. slow, shallow respirations; bradycardia; and hypotension. 3. The most appropriate nursing intervention for a patient who is being treated for an acute exacerbation of chronic obstructive pulmonary disease who is not interested in quitting smoking is to a. accept the patient’s decision and not intervene until the patient expresses a desire to quit. b. ask the patient to identify the risks and benefits of quitting and what barriers to quitting are present. c. realize that some smokers never quit, and trying to assist them increases the patient’s frustration. d. motivate the patient to quit by describing how continued smoking will worsen the breathing problems. 4. While caring for a patient who is experiencing alcohol withdrawal, the nurse should (select all that apply) a. monitor neurologic status on a routine basis. b. provide a quiet, nonstimulating, dimly lit environment. c. pad the side rails and place suction equipment at the bedside. d. orient the patient to environment and person with each contact.

e. give antiseizure drugs and sedatives to relieve withdrawal symptoms. 5. A patient admitted for scheduled surgery has a positive brief screening test result for an alcohol use disorder. Which initial action is most appropriate? a. Notify the health care provider. b. Complete a detailed alcohol use assessment. c. Initiate a referral to a specialty treatment center. d. Provide patient teaching on postoperative health risks. 6. Substance use problems in older adults are usually related to a. use of drugs and alcohol as a social activity. b. continuing the use of illegal drugs started during middle age. c. misuse of prescribed and over-the-counter medications and alcohol. d. a pattern of binge drinking for weeks or months with periods of sobriety. 1. b, 2. a, 3. b, 4. a, c, d, e, 5. b, 6. c For rationales to these answers and even more NCLEX review questions, visit http://evolve.elsevier.com/Lewis/medsurg.

Evolve Website/Resources List http://evolve.elsevier.com/Lewis/medsurg

Review Questions (Online Only) Key Points Answer Keys for Questions

• Rationales for Bridge to NCLEX Examination Questions • Answer Guidelines for Case Study on p. 153 • Answer Guidelines for Managing Care of Multiple Patients Case Study (Section 2) on p. 155 Nursing Care Plan • eNursing Care Plan 10.1: Patient in Alcohol Withdrawal Conceptual Care Map Creator Audio Glossary Content Updates

Case Study Managing Care of Multiple Patients You are assigned to care for the following 5 patients on a medicalsurgical unit. Your team consists of yourself, a new LPN still on orientation, and a UAP.

Patients

Discussion Questions 1. Priority Decision: After receiving report, which patient should you see first? Provide rationale.

2. Collaboration: Which morning task(s) could you delegate to the LPN (select all that apply)? a. Obtain a capillary blood glucose reading on K.C. b. Assess C.L.’s IV site for signs of phlebitis or infiltration. c. Access the hospital’s available translation services for M.S. d. Provide discharge teaching on wound care for K.C. and her daughter. e. Titrate M.L.’s O2 to obtain a pulse oximetry reading of 95% (as ordered by the HCP). 3. Priority and Collaboration: When you and the LPN enter M.S.’s room, you find her sitting up in bed with labored respirations. Although you cannot understand what she is saying, you note that she is unable to say more than a few words without stopping for a breath. Which initial action would be the most appropriate? a. Give M.S.’s cardiac and respiratory medications and reassess her in 30 minutes. b. Ask the LPN to stay with M.S. while you go to the nurse’s station to call the HCP. c. Have the LPN find M.S.’s granddaughter so that she can translate what M.S. is trying to tell you. d. Ask the LPN to obtain an O2 saturation and vital signs while you perform a respiratory assessment.

Case Study Progression M.S.’s assessment reveals bibasilar crackles, 2+ dependent pitting edema, BP 175/84, pulse 116, RR 32, temp 36.8°C, and pulse oximetry 88% on room air. You apply O2 at 4 L/min via nasal cannula and obtain an order from M.S.’s HCP for furosemide 40 mg IV stat. After

giving the diuretic, M.S.’s granddaughter arrives and you discuss her grandmother’s condition. She tells you that her grandmother asked her to bring in potato chips and soda yesterday. She did not think her grandmother should be eating salt, but M.S. insisted that the dietitian said that she could eat them.

4. On further investigation, the dietitian tells you that an interpreter (translator) was not available when she saw M.S. yesterday. Because the dietitian did not understand what the patient was saying, she could not respond to her questions. She planned to visit M.S. today when the granddaughter is present. Being a culturally competent nurse, you realize that M.S. most likely interpreted the dietitian’s silence as a. agreement with what A.Z. was asking. b. demonstrating a lack of respect for A.Z.’s wishes. c. a lack of understanding by the dietitian as to what she was asking. d. a need for the dietitian to get more information before answering her questions. 5. Which assessment findings may suggest elder mistreatment by C.L.’s son with whom she lives (select all that apply)? a. 2 sacral ulcers b. Asking when her son is coming to visit c. Multiple small bruises on her forearms and shins d. Matted hair, poor oral hygiene, overgrown toenails e. C.L. becomes totally silent when her son comes to visit 6. Knowing that C.M.’s confusion and restlessness overnight may indicate acute alcohol withdrawal, you perform a

more thorough assessment. Your assessment reveals a score of 11 on the Clinical Institute Withdrawal Assessment for Alcohol Scale. To prevent alcohol delirium, you plan to give which medication per the HCP’s order? a. morphine b. naloxone c. lorazepam d. IV thiamine 7. Priority Decision: You assess C.M. and find her trying to pull out the IV line and remove the Buck’s traction. What action should you do first? a. Have the UAP stay with C.M. b. Ask C.M.’s daughter to stay with her. c. Obtain a restraint order from the HCP. d. Move C.M. to a room closer to the nurse’s station. 8. Management Decision: The UAP informs you that the LPN is not following C.L.’s fall risk protocol. What is your most appropriate action? a. Notify the unit manager as soon as possible. b. Ask the UAP to explain hospital protocol to the LPN. c. Write up the LPN’s actions so they will be included in her evaluation. d. Talk to the LPN about the importance of following protocol to prevent C.L. from sustaining a fall-related injury. Answers available at http://evolve.elsevier.com/Lewis/medsurg.

References

1. American Psychiatric Association: The diagnostic and statistical manual of mental disorders, 5th ed, Arlington, VA, 2013, The Association. (Classic) 2. Centers for Disease Control and Prevention: Adult cigarette smoking in the U.S. Retrieved from www.cdc.gov/tobacco/data_statistics/fact_sheets/adult_data/cig_smok 3. Centers for Disease Control and Prevention: Health effects of cigarette smoking. Retrieved from www.cdc.gov/tobacco/data_statistics/fact_sheets/health_effects/effects_ Breland A, Soule E, Lopez A, et al: Electronic cigarettes: What are they and what do they do? Ann NY Acad Sci 1394:5, 2017.

5. Agency for Healthcare Research and Quality: Treating tobacco use and dependence: 2008 update. Retrieved from www.ahrq.gov/professionals/cliniciansproviders/guidelinesrecommendations/tobacco/index.html. 6. Alcohol facts and statistics. Retrieved from www.niaaa.nih.gov/alcohol-health/overview-alcoholconsumption/alcohol-facts-and-statistics. Gortney JS, Raub JN, Patel P, et al: Alcohol withdrawal syndrome in medical patients, Cleve Clin J Med 83:67, 2016. Sutton LJ, Jutel A: Alcohol withdrawal syndrome in critically ill patients: Identification, assessment, and management, Crit Care Nurse 36:28, 2016. Rasimas JJ, Sinclair CM: Assessment and management of toxidromes in the critical care unit, Crit Care Clin 33:521, 2017.

10. Centers for Disease Control and Prevention: Understanding the epidemic. Retrieved from www.cdc.gov/drugoverdose/epidemic/index.html. Donroe JH, Holt SR, Tetrault JM: Caring for patients with opioid use

disorder in the hospital, CMAJ 188:17, 2016. Phillips J, Lim F, Hsu R: Synthetic cannabinoid poisoning: A growing health concern, Nursing 46:34, 2016. Bonnet U, Preuss UW: Cannabis withdrawal syndrome: Current insights, Subst Abuse Rehabil 8:9, 2017.

14. SAMSA-HRSA Center for Integrated Health Solutions: SBIRT. Retrieved from www.samhsa.gov/sbirt. Masferrer L, Garre-Olmo J, Caparrós B: Is complicated grief a risk factor for substance use? Addict Research Theory 9:1, 2017. ∗Evidence-based information for clinical practice.

SECTION THREE

Problems Related to Homeostasis and Protection OUTLINE 11. Inflammation and Healing 12. Genetics 13. Immune Responses and Transplantation 14. Infection 15. Cancer 16. Fluid, Electrolyte, and Acid-Base Imbalances

11

Inflammation and Healing Catherine R. Ratliff

LEARNING OUTCOMES 1. Describe the inflammatory response, including vascular and cellular responses and exudate formation. 2. Explain local and systemic manifestations of inflammation and their physiologic bases. 3. Describe the drug therapy, nutrition therapy, and nursing management of inflammation. 4. Distinguish among healing by primary, secondary, and tertiary intention. 5. Describe the factors that delay wound healing and common complications of wound healing. 6. Describe the nursing and interprofessional management of wound healing. 7. Explain the etiology and clinical manifestations of pressure injuries. 8. Apply a patient risk assessment for pressure injuries to measures used to prevent the development of pressure injuries. 9. Discuss nursing and interprofessional management of a patient with pressure injuries.

KEY TERMS adhesions, Table 11.7, p. 163 dehiscence, Table 11.7, p. 163 evisceration, Table 11.7, p. 163 fibroblasts, p. 162 hypertrophic scars, Table 11.7, p. 163 inflammatory response, p. 156 pressure injury, p. 168 regeneration, p. 161 repair, p. 161 shear, p. 168 A kind gesture can reach a wound only compassion can heal. Steve Maraboli http://evolve.elsevier.com/Lewis/medsurg/

Conceptual Focus Health Promotion Inflammation Nutrition Pain Perfusion Sensory Perception Tissue Integrity This chapter focuses on inflammation, wound healing, and pressure injury prevention and management. Maintaining skin and tissue

integrity is a key nursing role. Multiple concepts are closely related to tissue integrity. Adequate nutrition and perfusion are essential so that the body has the necessary factors to promote healing when injury occurs. Impaired mobility and sensory perception increase the risk for injury. When injury does occur, pain and problems regulating temperature and fluid and electrolyte balance are common.

Inflammatory Response The inflammatory response is a sequential reaction to cell injury. It neutralizes and dilutes the inflammatory agent, removes necrotic materials, and establishes an environment suitable for healing and repair. The term inflammation is often incorrectly used as a synonym for infection. Inflammation is always present with infection, but infection is not always present with inflammation. However, a person who is neutropenic may not be able to mount an inflammatory response. An infection involves invasion of tissues or cells by microorganisms, such as bacteria, fungi, and viruses. In contrast, heat, radiation, trauma, chemicals, allergens, and an autoimmune reaction also can cause inflammation. The mechanism of inflammation is basically the same regardless of the injuring agent. The intensity of the response depends on the extent and severity of injury and on the injured person’s reactive capacity. The inflammatory response can be divided into a vascular response, cellular response, formation of exudate, and healing. Fig. 11.1 shows the vascular and cellular response to injury.

FIG 11.1 Vascular and cellular responses to tissue injury.

Vascular Response After cell injury, local arterioles briefly undergo transient vasoconstriction. After release of histamine and other chemicals by the injured cells, the vessels dilate. Chemical mediators cause increased capillary permeability and facilitate fluid movement from capillaries into tissue spaces. At first this inflammatory exudate is made up of

serous fluid. Later, it contains plasma proteins, primarily albumin. These proteins exert oncotic pressure that further draws fluid from blood vessels. Both vasodilation and increased capillary permeability are responsible for redness, heat, and swelling at the site of injury and the surrounding area. As the plasma protein fibrinogen leaves the blood, it is activated to fibrin by the products of the injured cells. Fibrin strengthens a blood clot formed by platelets. In tissues, the clot functions to trap bacteria, prevent their spread, and serve as a framework for the healing process. Platelets release growth factors that start the healing process.

Cellular Response Neutrophils and monocytes move from circulation to the site of injury (Fig. 11.1). Chemotaxis is the directional migration of white blood cells (WBCs) to the site of injury, resulting in an accumulation of neutrophils and monocytes at the site.

Neutrophils Neutrophils are the first WBCs to arrive at the injury site (usually within 6 to 12 hours). They phagocytize (engulf) bacteria, other foreign material, and damaged cells. With their short life span (24 to 48 hours), dead neutrophils soon accumulate. In time, a mixture of dead neutrophils, digested bacteria, and other cell debris accumulates as a creamy substance called pus. To keep up with the demand for neutrophils, the bone marrow releases more neutrophils into circulation. This results in a high WBC count, especially the neutrophil count. Mature neutrophils are called segmented neutrophils. Sometimes the demand for neutrophils increases to the extent that the bone marrow releases immature forms of neutrophils (bands) into circulation. We call an increased number of band neutrophils in circulation a shift to the left. It is common in patients with acute bacterial infections. (See Chapter 29 for a discussion of neutrophils.)

Monocytes Monocytes are the second type of phagocytic cells that migrate from circulating blood. They usually arrive at the site within 3 to 7 days after the onset of inflammation. On entering the tissue spaces, monocytes transform into macrophages. Together with the tissue macrophages, these newly arrived macrophages help in phagocytosis of the inflammatory debris. The macrophage role is important in cleaning the area before healing can occur. Macrophages have a long life span. They can multiply and may stay in the damaged tissues for weeks. These long-lived cells are important in orchestrating the healing process.

TABLE 11.1 Mediators of Inflammation

Mediator Complement components (C3a, C4a, C5a)

Source Anaphylatoxic agents generated from complement pathway activation

Mechanisms of Action Stimulate histamine release and chemotaxis

Cytokines

See

Histamine

Stored in granules of basophils, mast cells, platelets Stored in platelets, mast cells, enterochromaffin cells of GI tract Produced from precursor factor kininogen because of activation of Hageman factor (XII) of clotting system

Causes vasodilation and increased capillary permeability Same as above. Stimulates smooth muscle contraction Cause contraction of smooth muscle and vasodilation. Result in stimulation of pain

Produced from arachidonic acid (Fig. 11.2)

PGs cause vasodilation. LTs stimulate chemotaxis

Serotonin Kinins (e.g., bradykinin) Prostaglandins (PGs) and leukotrienes (LTs)

When particles are too large for a single macrophage, macrophages accumulate and fuse to form a multinucleated giant cell. Collagen encapsulates this giant cell, leading to the formation of a granuloma.

A classic example of this process occurs in tuberculosis of the lung. While the Mycobacterium bacillus is walled off, a chronic state of inflammation exists. The granuloma formed is a cavity of necrotic tissue.

Lymphocytes Lymphocytes arrive later at the site of injury. Their primary role is related to humoral and cell-mediated immunity (see Chapter 13).

Chemical Mediators Mediators of the inflammatory response are outlined in Table 11.1.

Complement System The complement system is an enzyme cascade (C1 to C9) consisting of pathways to mediate inflammation and destroy invading pathogens. Major functions of the complement system are enhanced phagocytosis, increased vascular permeability, chemotaxis, and cellular lysis. All these activities are important mediators of the inflammatory response and healing. Cell lysis occurs when the final components create holes in the cell membranes and cause targeted cell death by membrane rupture. In autoimmune disorders, complement activation and the resulting inflammatory response can damage healthy tissue. Examples of this include rheumatoid arthritis and systemic lupus erythematosus.

Prostaglandins and Leukotrienes When cells are activated by injury, the arachidonic acid in the cell membrane is rapidly converted to produce prostaglandins (PGs), thromboxane, and leukotrienes (Fig. 11.2). PGs are considered proinflammatory. They are potent vasodilators contributing to increased blood flow and edema formation.

FIG 11.2 Pathway of generation of prostaglandins, thromboxane, and leukotrienes. Corticosteroids, nonsteroidal antiinflammatory drugs (NSAIDs), and acetylsalicylic acid (ASA) act to inhibit various steps in this pathway.

Some subtypes of PGs form when platelets are activated and can inhibit platelet and neutrophil aggregation. PGs have a significant role in sensitizing pain receptors to arousal by stimuli that would normally be painless. PGs have a pivotal role as pyrogens when stimulating the temperature-regulating area of the hypothalamus and producing a febrile response (see section on Fever on p. 158). Thromboxane is a powerful vasoconstrictor and platelet-aggregating agent. It causes brief vasoconstriction and skin pallor at the injury site and promotes clot formation. It has a short half-life. The pallor soon gives way to vasodilation and redness, which is caused by PGs and histamine. Leukotrienes form the slow-reacting substance of anaphylaxis (SRSA). SRS-A constricts smooth muscles of the bronchi, causing narrowing of the airway, and increases capillary permeability, leading to airway edema.

Exudate Formation

Exudate consists of fluid and WBCs that move from the circulation to the site of injury. The nature and quantity of exudate depend on the type and severity of the injury and tissues involved (Table 11.2).

Clinical Manifestations The local manifestations of inflammation include redness, heat, pain, swelling, and loss of function (Table 11.3 and Fig. 11.3). Systemic manifestations include an increased WBC count with a shift to the left, malaise, nausea and anorexia, increased pulse and respiratory rate, and fever. Leukocytosis results from the increased release of WBCs from the bone marrow. The causes of other systemic manifestations may be related to complement activation and the release of cytokines (soluble factors secreted by WBCs and other types of cells that act as intercellular and intracellular messengers). Some cytokines (e.g., interleukins [ILs], tumor necrosis factor [TNF]) are important in causing fever and other systemic manifestations of inflammation. An increase in pulse and respiration follows the rise in metabolism because of an increase in body temperature. (Cytokines are discussed in Chapter 13.)

Fever The release of cytokines triggers the onset of fever. Cytokines cause fever by initiating metabolic changes in the temperature-regulating center in the hypothalamus (Fig. 11.4). The synthesis of PGs is the most critical metabolic change. PGs act directly to increase the thermostatic set point. The hypothalamus then activates the autonomic nervous system to stimulate increased muscle tone and shivering and decreased perspiration and blood flow to the periphery. Epinephrine released from the adrenal medulla increases the metabolic rate. The net result is fever.

TABLE 11.2 Types of Inflammatory Exudate

TABLE 11.3 Local Manifestations of Inflammation

Manifestations Cause Increased metabolism at inflammatory site Heat Loss of function

Swelling and pain

Pain

Change in pH. Nerve stimulation by chemicals (e.g., histamine, prostaglandins). Pressure from fluid exudate

Redness

Hyperemia from vasodilation

Swelling

Fluid shift to interstitial spaces. Fluid exudate accumulation

With the physiologic thermostat raised to a higher-than-normal temperature, the body increases heat production and conservation until the temperature reaches that new set point. At this point, the person feels chilled and shivers. The shivering response is the body’s method of raising the body’s temperature to the new set point.1 This seeming paradox is dramatic: the body is hot, yet the person piles on blankets and may go to bed to get warm. When the body temperature reaches the set point, the chills and warmth-seeking behavior cease.

FIG 11.3 Inflammation secondary to postoperative deep wound infection after wrist surgery. From Hayden RJ, Jebson PJL: Wrist arthrodesis, Hand Clin 21[4]:631, 2005.

FIG 11.4 Production of fever. When monocytes/macrophages are activated, they secrete cytokines such as interleukin-1 (IL-1), interleukin-6 (IL-6), and tumor necrosis factor (TNF), which reach the hypothalamic temperature-regulating center. These cytokines promote the synthesis and secretion of prostaglandin E2 (PGE2) in the anterior hypothalamus. PGE2 increases the thermostatic set point, and the autonomic nervous system is stimulated, resulting in shivering, muscle contraction, and peripheral vasoconstriction.

The released cytokines and the fever that they trigger activate the body’s defense mechanisms. Beneficial aspects of fever include increased killing of microorganisms, increased phagocytosis by neutrophils, and increased proliferation of T cells. Higher body temperatures may enhance the activity of interferon, the body’s natural virus-fighting substance (see Chapter 13).

Types of Inflammation The basic types of inflammation are acute, subacute, and chronic. In acute inflammation, the healing occurs in 2 to 3 weeks and usually leaves no residual damage. Neutrophils are the predominant cell type at the site of inflammation. A subacute inflammation has the features of the acute process but lasts longer. For example, infective endocarditis is a smoldering infection with acute inflammation, but it lasts for weeks or months (see Chapter 36). Chronic inflammation lasts for weeks, months, or even years. The injurious agent persists or repeatedly injures tissue. The predominant cell types present at the site of inflammation are lymphocytes and macrophages. Examples of chronic inflammation include rheumatoid arthritis and osteomyelitis. The prolongation and chronicity of any inflammation may be the result of an alteration in the immune response (e.g., autoimmune disease) and can lead to physical deterioration.

Nursing and Interprofessional Management: Inflammation Nursing Implementation Health Promotion The best management of inflammation is the prevention of infection, trauma, surgery, and contact with potentially harmful agents. This is not always possible. A simple mosquito bite causes an inflammatory response. Because occasional injury is inevitable, concerted efforts to minimize inflammation and infection are needed. Adequate nutrition is essential so that the body has the necessary factors to promote healing when injury occurs. A high fluid intake will replace fluid loss from perspiration. There is a 7% increase in metabolism for every 1°F increase in temperature above 100°F (37.8°C), or a 13% increase for every 1°C increase. The increased metabolic rate increases a patient’s need for calories.

Early recognition of inflammation is essential so that appropriate treatment can begin. This may be rest, drug therapy, or specific treatment of the injured site. Immediate treatment may prevent the extension and complications of inflammation.

Acute Care Observation and Vital Signs The ability to recognize the manifestations of inflammation is important. In the immunosuppressed person (e.g., taking corticosteroids, receiving chemotherapy), the classic manifestations of inflammation may be masked. The early symptoms of inflammation may be malaise or “just not feeling well.” Vital signs are important to note with any inflammation, especially when an infectious process is present. With infection, the temperature may rise, and pulse and respiration rates may increase.

Fever An important aspect of fever management is determining its cause. Although many regard fever as harmful, an increase in body temperature is an important host defense mechanism. In the seventeenth century, Thomas Sydenham noted that “fever is a mighty engine which nature brings into the world for the conquest of her enemies.”2 Steps are often taken to lower body temperature to relieve anxiety of the patient and health care professionals. Because mild to moderate fever usually does little harm, imposes no great discomfort, and may help host defense mechanisms, antipyretic drugs are rarely essential to patient welfare. Moderate fevers (up to 103°F [39.4°C]) usually produce few problems in most patients. However, if the patient is very young or very old, is extremely uncomfortable, or has a significant medical problem (e.g., severe heart or lung disease, brain injury), antipyretic use should be considered. Fever in the immunosuppressed patient should be treated immediately with antibiotic therapy because infections can rapidly progress to

septicemia. (Neutropenia is discussed in Chapter 30 on pp. 631.) Fever, especially if greater than 104°F (40°C), can damage body cells, and delirium and seizures can occur. At temperatures greater than 105.8°F (41°C), the hypothalamic temperature control center becomes impaired. Damage can occur to many cells, including those in the brain.

TABLE 11.4 Drug TherapyInflammation and

Healing

Older adults have a blunted febrile response to infection. The body temperature may not rise to the level expected for a younger adult, or there may be a delay in the onset of the rise. The blunted response can delay diagnosis and treatment. By the time fever (as defined for younger adults) is present, the illness may be more severe. Patients who are taking nonsteroidal antiinflammatory drugs (NSAIDs) on a regular basis (e.g., for rheumatoid arthritis) may have a blunted febrile response. Although sponge baths increase evaporative heat loss, they may not decrease the body temperature unless the person received antipyretic

drugs to lower the set point. Otherwise, the body will initiate compensatory mechanisms (e.g., shivering) to restore body heat. The same principle applies to the use of cooling blankets. They are most effective in lowering body temperature after the set point has been lowered. A nursing care plan for the patient with a fever (eNursing Care Plan 11.1) is available on the website for this chapter at http://evolve.elsevier.com/Lewis/medsurg.

Drug Therapy Drugs can decrease the inflammatory response and lower the body temperature (Table 11.4). Aspirin blocks PG synthesis in the hypothalamus and elsewhere in the body. Acetaminophen acts on the heat-regulating center in the hypothalamus. Some NSAIDs (e.g., ibuprofen [Motrin, Advil]) have antipyretic effects. Corticosteroids are antipyretic through the dual actions of preventing cytokine production and PG synthesis. This results in dilation of superficial blood vessels, increased skin temperature, and sweating.

Check Your Practice A 76-yr-old female patient has acute osteomyelitis after a fractured femur. You are checking her temperature every 2 hours and giving acetaminophen when it is higher than 102°F. However, you notice that her temperature is fluctuating from 96° to 103°F. • What should you do? Antipyretics cause a sharp decrease in temperature. They should be given around the clock to prevent acute swings in temperature. Giving them intermittently can induce or perpetuate chills. When the antipyretic wears off, the body may initiate a compensatory involuntary muscular contraction (i.e., chill) to raise the body temperature back up to its previous level. We can prevent this

unpleasant side effect by giving them regularly at 2- to 4-hour intervals. Antihistamine drugs may be used to inhibit the action of histamine. Antihistamines are discussed in Chapters 13 and 26.

Rice Rest, ice, compression, and elevation (RICE) is a key concept in treating soft tissue injuries and related inflammation. Rest Rest helps the body use its nutrients and O2 for the healing process. The repair process is facilitated by allowing fibrin and collagen to form across the wound edges with little disruption. Cold and heat Cold application is usually appropriate at the time of the initial trauma. Use promotes vasoconstriction and decreases swelling, pain, and congestion from increased metabolism in the area of inflammation. Heat may be used later (e.g., after 24 to 48 hours) to promote healing by increasing the circulation to the inflamed site and subsequent removal of debris. Heat is used to localize the inflammatory agents. Warm, moist heat may help debride the wound site if necrotic material is present. Compression and immobilization Compression counters the vasodilation effects and development of edema. Compression by direct pressure over a laceration occludes blood vessels and stops bleeding. Compression bandages support injured joints when tendons and muscles are unable to provide support on their own. Assess distal pulses and capillary refill before and after application of compression to evaluate whether compression has compromised circulation (e.g., pale color of skin, loss of feeling). Immobilization of the inflamed or injured area promotes healing by decreasing the tissues’ metabolic needs. Immobilization with a cast or splint supports fractured bones and prevents further tissue injury

from sharp bone fragments that could sever nerves or blood vessels, causing hemorrhage. As with compression, evaluate the patient’s circulation after application and at regular intervals. Swelling can occur within the closed space of a cast and compromise circulation. Elevation Elevating the injured extremity above the level of the heart reduces the edema at the inflammatory site by increasing venous and lymphatic return. Elevation helps reduce pain associated with blood engorgement at the injury site. Elevation may be contraindicated in patients with significantly reduced arterial circulation.

TABLE 11.5 Regenerative Ability of Different

Types of Tissues

Healing Process The last phase of the inflammatory response is healing. Healing includes 2 major components: regeneration and repair.

Regeneration Regeneration is the replacement of lost cells and tissues with cells of the same type. The ability of cells to regenerate depends on the cell type (Table 11.5).

Repair Repair is healing, with connective tissue replacing lost cells. Repair is the more common type of healing and usually results in scar formation. Repair is a more complex process than regeneration. Most injuries heal by connective tissue repair. Repair healing occurs by primary, secondary, or tertiary intention (Fig. 11.5).

Primary Intention Primary intention healing takes place when wound margins are neatly approximated, as in a surgical incision or a paper cut. A continuum of processes is associated with primary healing (Table 11.6). These processes include 3 phases.

Initial Phase In the initial (inflammatory) phase, the edges of the incision are aligned and sutured (or stapled) in place. The incision area fills with blood from the cut blood vessels, blood clots form, and platelets release growth factors to begin the healing process. This forms a matrix for WBC migration. An acute inflammatory reaction occurs. The area of injury is composed of fibrin clots, erythrocytes, neutrophils (dead and dying), and other debris. Macrophages ingest and digest cellular debris, fibrin fragments, and red blood cells (RBCs). Extracellular enzymes derived from macrophages and neutrophils help digest fibrin. As the wound debris is removed, the fibrin clot serves as a meshwork for future capillary growth and migration of epithelial cells.

Granulation Phase The granulation phase is the second step. The components of granulation tissue include proliferating fibroblasts; proliferating capillary sprouts (angioblasts); various WBCs; exudate; and loose, semifluid, ground substance.

FIG 11.5 Types of wound healing. A, Primary intention. B, Secondary intention. C, Tertiary intention.

TABLE 11.6 Phases in Primary Intention Healing

Phase Initial

Duration 3 to 5 days

Granulation

5 days to 4 weeks

Maturation and scar contraction

7 days to several months

Description Approximation of incision edges. Migration of epithelial cells. Clot serving as meshwork for starting capillary growth Migration of fibroblasts. Secretion of collagen. Abundance of capillary buds. Wound fragile Remodeling of collagen. Strengthening of scar

Fibroblasts are immature connective tissue cells that migrate into the healing site and secrete collagen. In time, the collagen is organized and restructured to strengthen the healing site. At this stage, it is called fibrous or scar tissue. During the granulation phase, the wound is pink and vascular. Numerous red granules (young budding capillaries) are present. At this point, the wound is friable, at risk for dehiscence (Fig. 11.6), and resistant to infection. Surface epithelium at the wound edges begins to regenerate. In a few days, a thin layer of epithelium migrates across the wound surface in a 1-cell-thick layer until it contacts cells spreading from the opposite direction. The epithelium thickens and begins to mature, and the wound now closely resembles the adjacent skin. In a superficial wound, re-epithelialization may take 3 to 5 days.

FIG 11.6 Dehiscence after a cholecystectomy. From Bale S, Jones V: Wound care nursing: A patient-centered approach, ed 2, St Louis, 2006, Mosby.

Maturation Phase and Scar Contraction The maturation phase, during which scar contraction occurs, overlaps with the granulation phase. It may begin 7 days after the injury and continue for several months or years. This is the reason abdominal surgery discharge instructions limit lifting for up to 6 weeks. Collagen fibers are further organized, and the remodeling process occurs. Fibroblasts disappear as the wound becomes stronger. The active movement of the myofibroblasts causes contraction of the healing area, helping to close the defect and bring the skin edges closer together. A mature scar is then formed. In contrast to granulation tissue, a mature scar is virtually avascular and pale. The scar may be more painful at this phase than in the granulation phase.

Secondary Intention Wounds that occur from trauma, injury, and infection have large amounts of exudate and wide, irregular wound margins with extensive tissue loss. These wounds may have edges that cannot be approximated (brought together). The inflammatory reaction may be greater than in primary healing. This results in more debris, cells, and exudate. We may have to clear the debris away (debride) before healing can take place. The process of healing by secondary intention is essentially the same as healing by primary intention. The major differences are the greater defect and the gaping wound edges. Healing and granulation take place from the edges inward and from the bottom of the wound upward until the wound is filled. There is more granulation tissue, and the result is a much larger scar.

Tertiary Intention Tertiary intention (delayed primary intention) healing occurs with delayed suturing of a wound in which 2 layers of granulation tissue are sutured together. This occurs when a contaminated wound is left open and sutured closed after the infection is controlled. It also occurs when a primary wound becomes infected, is opened, allowed to granulate, and then sutured. Tertiary intention usually results in a larger and deeper scar than primary or secondary intention.

Wound Classification A wound is a break or opening into the skin. Wounds often occur because of accidents or injuries. Types of wounds can range from minor scrapes to deep wounds involving bones, blood vessels, and nerves. Identifying the cause of a wound is essential to classifying the wound properly. Wounds can be classified by their cause (surgical or nonsurgical; acute or chronic) or the depth of tissue affected (superficial, partial thickness, or full thickness). A superficial wound involves only the epidermis. Partial-thickness wounds extend into the

dermis. Full-thickness wounds have the deepest layer of tissue destruction. They involve the subcutaneous tissue and sometimes extend into the fascia and underlying structures, including muscle, tendon, or bone. A skin tear is a wound caused by shear, friction, and/or blunt force resulting in separation of skin layers. A skin tear can be partial thickness or full thickness. This type of wound is common, especially in older adults and critically or chronically ill adults.3

Complications of Healing Certain factors can interfere with wound healing and lead to complications (Table 11.7).

TABLE 11.7 Complications of Wound Healing

Adhesions • Bands of scar tissue that form between or around organs • May occur in the abdominal cavity or between the lungs and the pleura • Those in the abdomen may cause an intestinal obstruction.

Contractions • Wound contraction is a normal part of healing. • Complications occur when excessive contraction results in deformity. • Shortening of muscle or scar tissue, especially over joints, results from excessive fibrous tissue formation.

Dehiscence

• Separation and disruption of previously joined wound edges (Fig. 11.6) • Usually occurs when a primary healing site bursts open • May be caused by: • Infection causing an inflammatory process • Granulation tissue not strong enough to withstand forces imposed on wound • Obesity, because adipose tissue has less blood supply and may slow healing • Pocket of fluid (seroma, hematoma) developing between tissue layers and preventing the edges of the wound from coming together

Evisceration • Occurs when wound edges separate to the extent that intestines protrude through wound • Usually needs immediate surgical treatment

Excess Granulation Tissue (“Proud Flesh”) • Excess granulation tissue may protrude above surface of healing wound. • If the tissue is cauterized or cut off, healing continues in normal manner.

Fistula Formation • An abnormal passage between organs or a hollow organ and skin (abdominal or perianal fistula)

Infection (Fig. 11.3)

• ↑ Risk for infection when wound contains necrotic tissue or blood supply is ↓, patient’s immune function is ↓ (e.g., from immunosuppressive drugs), undernutrition, multiple stressors, and hyperglycemia in diabetes.

Hemorrhage • Abnormal internal or external blood loss may be caused by suture failure, clotting abnormalities, dislodged clot, infection, or erosion of a blood vessel by a foreign object (tubing, drains) or infection process.

Hypertrophic Scars • Inappropriately large, raised red and hard scars (Fig. 11.7) • Occur when an overabundance of collagen is made during healing

Keloid Formation • Great protrusion of scar tissue that extends beyond wound edges and may form tumor-like masses of scar tissue (Fig. 11.8) • Permanent without any tendency to subside • Patients often have tenderness, pain, and hyperparesthesia, especially in early stages. • Thought to be a hereditary condition occurring most often in dark-skinned people.

FIG 11.7 Hypertrophic scarring. Reproduced with kind permission from Dr. C. Lawrence, Wound Healing Research Unit, Cardiff. In Bale S, Jones V, eds: Wound care nursing: A patient-centered approach, ed 2, St Louis, 2006, Mosby.

FIG 11.8 Keloid scarring. Reproduced with kind permission from Dr. C. Lawrence, Wound Healing Research Unit, Cardiff. In Bale S, Jones V, editors: Wound care nursing: A patient-centered approach, ed 2, St Louis, 2006, Mosby.

Nursing and Interprofessional Management: Wound Healing Nursing Assessment The first step in wound care is to carefully assess and document the characteristics of the wound and surrounding area. This includes the location, size (longest length and widest width), depth, undermining and tunneling, wound margin (e.g., normal, macerated, erythema), and wound base (e.g., eschar, slough, exudate). There are several ways to measure a wound. One way is shown in Fig. 11.9. Record the consistency, color, and odor of any drainage and report if abnormal for the situation. Staphylococcus and Pseudomonas are common organisms that cause purulent, draining wounds.

Thoroughly assess the wound on admission, or first clinic visit, and on a regular basis thereafter. In healthy people, wounds heal at a normal, predictable rate. Assess for factors that may delay wound healing and contribute to chronic nonhealing wounds (Table 11.8). If deterioration in the wound occurs, you need to assess and document changes more often.4 Chronic wounds are those that do not heal within the normal time (around 3 months). If a wound does not heal as expected, assess and identify factors that may delay healing. Refer the patient to an HCP specializing in wound management. Time does not heal all wounds. While caring for patients during the healing process, you need to continually assess for complications (e.g., infection) associated with healing (Table 11.7).

FIG 11.9 Wound measurements are made in centimeters. The first measurement is oriented from head to toe, the second is from side to side, and the third is the depth (if any). If there is any tunneling (when cotton-tipped applicator is placed in wound, there is movement) or undermining (when cotton-tipped applicator is placed in wound, there is a “lip” around the wound), this is charted in respect to a clock, with 12 o’clock being toward the patient’s head. This wound would be charted as a full-thickness, red wound, 7 × 5 × 3 cm, with a 3-cm tunnel at 7 o’clock and 2 cm undermining from 3 o’clock to 5 o’clock. Courtesy Robert B. Babiak, RN, BSN, CWOCN, San Antonio, TX.

Nursing Implementation The type of wound management and dressings needed depend on the type, extent, and characteristics of the wound and the phase of

healing. The purposes of wound management include (1) protecting a clean wound from trauma so that it can heal normally, (2) cleaning a wound to remove any dirt and debris from the wound bed, and (3) treating infection to prepare the wound for healing.

Clean Wounds Superficial skin injuries may only need cleansing. Material used to close wounds include adhesive strips (e.g., Steri-Strips, butterflies), sutures (stitches), staples, and tissue adhesives (fibrin sealants). We use adhesive strips instead of sutures for some injuries because they decrease scarring and it is easier to care for them. Sutures are used to close wounds because suture material provides the mechanical support needed to sustain closure. A wide variety of suturing materials are available. Tissue adhesives are a biologic adhesive that can be applied alone or with sutures or tape. A dressing material that keeps the wound surface clean and slightly moist is best to promote epithelialization. For wounds that heal by primary intention, it is common to cover the wound or incision with a dry, sterile dressing. It is removed as soon as the drainage stops or in 2 to 3 days. Medicated sprays that form a transparent film on the skin may be used for dressings on a clean incision or injury. Transparent film or adhesive semipermeable dressings (e.g., OpSite, Tegaderm) are occlusive dressings that are permeable to oxygen. The wound is then usually covered with a sterile dressing. Sometimes an HCP will leave a surgical wound uncovered or remove the dressing within 48 hours after surgery.5 Examples of types of wound dressings are described in Table 11.9.

TABLE 11.8 Factors Delaying Wound Healing

TABLE 11.9 Types of Wound Dressings

For more information, see www.woundsource.com/productcategory/dressings. Clean wounds that are granulating and re-epithelializing should be kept slightly moist and protected from further trauma until they heal naturally.6 Do not let a wound that has the potential to heal dry out. Dryness is an enemy of wound healing. “Airing out” a wound is a great mistake. Wounds need a moist environment to heal. Unnecessary manipulation during dressing changes may destroy new granulation tissue and break down fibrin formation. Topical antimicrobials and antibactericidals (e.g., povidone-iodine [Betadine], Dakin’s solution [sodium hypochlorite]), should be used with caution in wound care because they can damage the new epithelium of healing tissue and delay healing. They should never be

used in a clean granulating wound. Sometimes drains are inserted into the wound to help remove fluid. The Jackson-Pratt drain is a suction drainage device consisting of a flexible plastic bulb connected to an internal plastic drainage tube (Fig. 11.10).

Contaminated Wounds If the wound is contaminated, it must be converted into a clean wound before healing can occur normally. Debridement of a wound that has debris or dead tissue may be needed. Another option is absorptive dressings. They can be used to absorb exudate and clean the wound surface. These dressings work by drawing excess drainage from the wound surface. The amount of wound secretions determines the number of dressing changes. In hydrocolloid dressings, such as DuoDerm, the inner part of the dressing interacts with the exudate, forming a hydrated gel over the wound. When the dressing is removed, the gel separates and stays over the wound. The wound must be cleansed gently to prevent damage to newly formed tissue. We can leave these dressings in place for up to 7 days or until leakage occurs around the dressing. Debridement is done to remove dead tissue.7 The debridement method used depends on the amount of debris and the condition of the wound tissue (Table 11.10).

Negative-Pressure Wound Therapy Negative-pressure wound therapy (NPWT) is used to treat acute and chronic wounds. A vacuum source creates continuous or intermittent negative pressure inside the wound to remove fluid, exudates, and infectious materials to prepare the wound for healing and closure. We do not know exactly how NPWT promotes healing. It is thought that NPWT pulls excess fluid from the wound, reduces bacterial load, and encourages blood flow into the wound base. NPWT systems consist of a vacuum pump, drainage tubing, a foam or gauze wound dressing, and an adhesive film dressing

Nursing Management Wound Care In general, the registered nurse (RN) manages wound care for complex or nonhealing wounds. Wound, ostomy, and continence (WOC) nurses may treat and manage pressure injuries, traumatic and draining wounds, surgical incisions, and tubes and fistulas. State nurse practice acts vary in the wound care actions allowed by licensed practical/vocational nurses (LPNs/VNs). In general, the role of the RN includes: • Assess all patients at risk for pressure injury at time of first hospital and/or home visit or whenever the patient’s condition changes. Thereafter, assess at regular intervals based on care setting (every 24 hours for acute care or every visit in home care). • Assess patients for factors that may delay wound healing and develop a plan of care to address these factors. • Assess and document initial wound appearance, including wound size, depth, color, and drainage. • Develop a plan of care to prevent the development of pressure injuries. • Plan nursing actions to aid with wound healing, including wound care, positioning, and nutritional interventions. • Choose dressings and therapies for wound treatment (in conjunction with the HCP and/or wound care specialist). • Implement wound care for complex or new wounds, including negative-pressure wound therapy and hyperbaric O2 therapy. • Evaluate whether wound care is effective in promoting wound healing. • Provide teaching to patient and caregivers about home wound care and pressure injury prevention. • Oversee LPN/VN:

• Perform sterile dressing changes on acute and chronic wounds. • Apply ordered topical antimicrobials and antibactericidals to wounds. • Apply prescribed dressings or medications for wound debridement. • Collect and record data about wound appearance. • Collaborate with dietitian to: • Assess and monitor patient’s nutritional status. • Outline diet to support proper wound healing. that covers and seals the wound.8 In NPWT, the wound is cleansed and a gauze or foam dressing is cut to the dimensions of the wound. A large occlusive dressing is applied, with a small hole made over the gauze or foam dressing where the tubing is attached (Fig. 11.11). The tubing is connected to a pump, which creates a negative pressure in the wound bed.

FIG 11.10 Jackson-Pratt drainage device. From Perry AG, Potter PA, Elkin MK: Nursing interventions and clinical skills, ed 5, St Louis, 2012, Mosby.

TABLE 11.10 Types of Debridement

FIG 11.11 Negative-pressure wound therapy in woman with history of IV drug abuse. A, The completely destroyed femoral artery was reconstructed with a homograft. B, A black open-pore polyurethane foam was directly applied to the vascular reconstruction and negative pressure applied to wound. C, Wound site 16 days after surgery. D, Healed wound at 28 months without reinfection. Reprinted from Mayer D, Hasse B, Koelliker J, et al: Long-term results of vascular graft and artery preserving treatment with negative pressure wound therapy in Szilagyi grade III infections justify a paradigm shift, Ann Surg 254:754, 2011. © Southeastern Surgical Congress.

Monitor the patient’s serum protein levels and fluid and electrolyte balance because of losses from the wound. Also, monitor the patient’s coagulation studies (platelet count, prothrombin time [PT], partial thromboplastin time [PTT]).

Hyperbaric Oxygen Therapy Hyperbaric O2 therapy (HBOT) is the delivery of O2 at increased atmospheric pressures. It can be given topically by creating a chamber around the injured limb. It also can be given systemically with the

patient in an enclosed chamber, receiving 100% O2 at 1.5 to 3 times the normal atmospheric pressure. HBOT allows O2 to diffuse into the serum, rather than RBCs, and be transported to the tissues. By increasing the O2 content in the serum, HBOT moves the O2 past narrowed arteries and capillaries where RBCs cannot go. In addition, high O2 levels stimulate angiogenesis (production of new blood vessels), kill anaerobic bacteria, and increase the killing power of WBCs and certain antibiotics (e.g., fluoroquinolones, aminoglycosides). HBOT accelerates granulation tissue formation and wound healing. Most systemic treatments last from 90 to 120 minutes. The number of treatments is highly variable (from 10 to 60), depending on the condition being treated.

Drug Therapy Platelet-derived growth factor is released from the platelets and stimulates cell proliferation and migration. Becaplermin (Regranex), a recombinant human platelet–derived growth factor gel, actively stimulates wound healing. It is used to treat foot injuries in patients with diabetes (see Chapter 48). Becaplermin should be used only when the wound is free of dead tissue and infection. It should not be used if cancer is suspected in the wound.

Nutritional Therapy Special nutritional measures promote wound healing. A high fluid intake is needed to replace fluid loss from perspiration and exudate formation. An increased metabolic rate intensifies water loss. Persons at risk for wound healing problems are those with malabsorption problems (e.g., Crohn’s disease, GI surgery, liver disease), deficient intake or high energy demands (e.g., cancer, major trauma or surgery, sepsis, fever), and diabetes. Undernutrition puts a person at risk for poor healing. A diet high in protein, carbohydrate, and vitamins with moderate fat intake is

necessary to promote healing. Protein is needed to correct the negative nitrogen balance resulting from the increased metabolic rate. It is also needed for the synthesis of immune factors, WBCs, fibroblasts, and collagen, which are the building blocks for healing. Carbohydrates are needed to meet the increased metabolic energy required for healing. If there is a carbohydrate deficit, the body will break down protein for the needed energy. Fats help in the synthesis of fatty acids and triglycerides, which are part of the cellular membrane.9 Vitamin C is needed for capillary synthesis and collagen production by fibroblasts. The B-complex vitamins are necessary as coenzymes for many metabolic reactions. If a vitamin B deficiency develops, a disruption of protein, fat, and carbohydrate metabolism will occur. Vitamin A aids in epithelialization. It increases collagen synthesis and tensile strength of the healing wound. If the patient is unable to eat, enteral feedings and supplements should be the first choice if the GI tract is functional. Parenteral nutrition is indicated when enteral feedings are contraindicated or not tolerated. (Enteral and parenteral nutrition are discussed in Chapter 39.)

Infection Prevention and Control You and the patient must scrupulously follow aseptic procedures, including hand washing, for keeping the wound free from infection. Do not allow the patient to touch a recently injured area. The patient’s environment should be as free as possible from contamination from items introduced by roommates and visitors. Some patients may receive prophylactic antibiotics. If an infection develops, a culture and sensitivity test is done to determine the organism and the most effective antibiotic for that specific organism. Obtain the culture before the first dose of antibiotic is given. We can obtain cultures by needle aspiration, tissue culture, or swab technique. HCPs perform needle and tissue punch biopsies. As a nurse, you can obtain cultures using the swab technique. This is done using Levine’s technique, which involves rotating a culture swab over a cleansed 1-cm2 area near the center of the wound. Use

enough pressure to extract wound fluid from deep tissue layers. Take a culture of the clean tissue because exudate and necrotic tissue will not provide an accurate sample.10 The sample must be sent to the laboratory within 1 hour.

Psychologic Implications The patient may be distressed at the thought or sight of an incision or wound because of fear of scarring or disfigurement. Drainage and odor from a wound often cause alarm. The patient needs to understand the healing process and normal changes that occur as the wound heals. When changing a dressing, avoid inappropriate facial expressions that may alert the patient to problems with the wound or raise doubts about your ability to care for it. Wrinkling your nose may convey disgust to the patient. Be careful not to focus on the wound to the extent that you are not treating the patient as a total person.

Patient Teaching Because patients are being discharged earlier after surgery and many have surgery as outpatients, it is important that the patient and caregiver know how to care for the wound and perform dressing changes. Wound healing may not be complete for 4 to 6 weeks or longer. Emphasize the importance of adequate rest and good nutrition throughout this time. Physical and emotional stress should be minimal. Observing the wound for complications, such as contractures, adhesions, and secondary infection, is important. Teach the patient and caregiver the signs and symptoms of infection. Have them note changes in the wound color and amount of drainage. Teach the patient to notify the HCP of any signs of abnormal wound healing. Drugs may be given for a time after recovery from the acute infection. Review drug-specific side effects and adverse effects with the patient and caregiver, as well as methods to prevent side effects (e.g., taking with food). Teach the patient to contact the HCP if any of these effects occur. Discuss the need to complete the entire course of therapy. For example, a patient who needed to take an antibiotic for

10 days decides to stop taking the drug after 5 days because of absent symptoms. However, the organism was not entirely eliminated. It becomes resistant to the antibiotic, and the patient develops a more severe infection.

Pressure Injuries Etiology and Pathophysiology A pressure injury is localized damage to the skin and/or underlying soft tissue. It usually occurs over a bony prominence or is related to a medical or other device. The injury occurs because of intense and/or prolonged pressure or pressure in combination with shear. The most common site for pressure injuries is the sacrum, with heels being second.

TABLE 11.11 Risk Factors for Pressure Injuries • Advanced age • Anemia • Contractures • Critically ill, cared for in critical care setting • Diabetes • Fever • Friction (rubbing of surfaces together) • Hip fracture • Immobility • Incontinence • Long and/or extensive surgical procedure • Low diastolic blood pressure (HIV Infection

Mechanism of Action More than one drug combined into a single tablet. Drugs may be from the same or different classes. Examples Atripla (tenofovir DF + emtricitabine + efavirenz) Biktarvy (tenofovir AF + emtricitabine + bictegravir) Combivir (lamivudine + zidovudine) Complera (tenofovir DF + emtricitabine + rilpivirine) Delstrigo (tenofovir DF + lamivudine + doravarine) Descovy (tenofovir AF + emtricitabine) Epzicom (abacavir + lamivudine) Evotaz (atazanavir + cobicistat†) Genvoya (tenofovir AF + emtricitabine + elvitegravir + cobicistat†) Juluca (dolutegravir + rilpivirine) Odefsey (tenofovir AF + emtricitabine + rilpivirine) Prezcobix (darunavir + cobicistat†) Temixys (tenofovir DF + lamivudine) Triumeq (abacavir + lamivudine + dolutegravir) Trizivir (abacavir + lamivudine + zidovudine) Truvada (tenofovir DF + emtricitabine) Stribild (tenofovir DF + emtricitabine + elvitegravir + cobicistat†) Symtuza (tenofovir AF + emtricitabine + darunavir + cobicistat†)

AF, Alafenamide. DF, disoproxil fumarate. † Cobicistat is a pharmacologic booster that enhances the potency of some HIV antiretrovirals. It has no direct effects against HIV.

Drug Therapy for Opportunistic Diseases Management of HIV is complicated by the many opportunistic diseases that can develop as the immune system deteriorates (Table 14.11). Prevention is the preferred approach to opportunistic diseases. Several opportunistic diseases associated with HIV can be delayed or prevented with adequate ART, vaccines (including hepatitis B, influenza, pneumococcal), and disease-specific prevention measures.24 Although it is usually not possible to eradicate opportunistic diseases once they occur, prophylactic medications can significantly decrease morbidity and mortality rates. Advances in the prevention, diagnosis, and treatment of opportunistic diseases have contributed significantly to increased life expectancy.

Preventing Transmission of HIV Preexposure prophylaxis (PrEP) is a comprehensive HIV prevention strategy to reduce the risk for sexually acquired HIV infection in adults at high risk.25 PrEP should be used in conjunction with other proven prevention interventions such as condoms, risk reduction counseling, and regular HIV testing. Currently, certain antiretrovirals are approved for both treatment of HIV in persons living with HIV, as well as prevention of HIV infection in persons without HIV infection. Various formulations have been studied for PrEP. The first medications approved for PrEP were tenofovir disoproxil fumarate (Tenofovir DF) in combination with emtricitabine. Other medications, including injectable options, will soon be available. As PrEP, these medications reduce the risk for HIV infection in uninfected people who are at significant risk for acquiring HIV. Tenofovir and emtricitabine are also used in combination with other antiretroviral agents for the treatment of HIV-infected people.

Nursing Management: HIV Infection Nursing Assessment Nursing assessment of people not known to have HIV infection should focus on behaviors that put the person at risk for HIV and other sexually transmitted and blood-borne infections. Assess patients for risky behaviors on a regular basis. Do not assume that someone is without risk because he or she is too old, too young, heterosexual, or married. Assess risk by asking some basic questions: (1) Have you ever had a blood transfusion or used clotting factors? If so, was it before 1985? (2) Have you ever shared drug-using equipment with another person? (3) Have you ever had a sexual experience in which your penis, vagina, rectum, or mouth came into contact with another person’s penis, vagina, rectum, or mouth? (4) Have you ever had a sexually transmitted infection? (5) Have you ever had sexual contact with someone known to have HIV? These questions provide the minimum information needed to initiate a risk assessment. Follow up a positive response to any of these questions with an in-depth exploration of issues related to the identified risk. A person who has HIV infection needs specific, ongoing assessment. Subjective and objective data are outlined in Table 14.15. Repeated nursing assessments over time are essential because people’s circumstances change. Early recognition and treatment can slow the progression of HIV infection and prevent new infections. A complete history and thorough systems review can help identify and address problems in a timely manner.

Nursing Diagnoses Nursing diagnoses for the patient with HIV disease may include: • Risk for infection • Lack of knowledge • Difficulty coping

• Impaired nutritional status

Planning Nursing interventions can help the patient (1) adhere to drug regimens; (2) adopt a healthy lifestyle that includes avoiding exposure to other sexually transmitted infections and blood-borne diseases; (3) protect others from HIV; (4) maintain or develop healthy and supportive relationships; (5) maintain activities and productivity; (6) explore spiritual issues; (7) come to terms with issues related to disease, disability, and death; and (8) cope with symptoms caused by HIV and its treatments.

Nursing Implementation The complexity of HIV disease is related to its chronic nature. As with most chronic and infectious diseases, primary prevention and health promotion are the most effective health care strategies. When prevention fails, disease results. Table 14.15 shows a summary of nursing goals, assessments, and interventions throughout the course of HIV infection.

Health Promotion Even with recent successes in HIV treatment, prevention is key in controlling the epidemic. In addition, health promotion encourages early detection of the disease so that, if primary prevention has failed, early intervention can be initiated.

TABLE 14.15 Nursing AssessmentHIV-Infected

Patient

Subjective Data Important Health Information

Past health history: Route of infection. Hepatitis, other sexually transmitted infections, tuberculosis. Frequent viral, fungal, and/or bacterial infections Medications: Use of immunosuppressive drugs

Functional Health Patterns Health perception–health management: Perception of illness. Alcohol and drug use. Malaise Nutritional-metabolic: Weight loss, anorexia, nausea, vomiting. Lesions, bleeding, or ulcerations of lips, mouth, gums, tongue, or throat. Sensitivity to acidic, salty, or spicy foods. Difficulty swallowing, abdominal cramping. Skin rashes, lesions, or color changes Elimination: Persistent diarrhea, change in character of stools. Painful urination, low back pain Activity-exercise: Chronic fatigue, muscle weakness, difficulty walking. Cough, shortness of breath Sleep-rest: Insomnia, night sweats, fatigue Cognitive-perceptual: Headaches, stiff neck, chest pain, rectal pain, retrosternal pain. Blurred vision, photophobia, diplopia, loss of vision. Hearing impairment. Confusion, forgetfulness, attention deficit, changes in mental status, memory loss, personality changes. Paresthesias, hypersensitivity in feet, pruritus Role-relationship: Support system(s), career or job, financial resources Sexuality-reproductive: Lesions on genitalia or anus (internal or external), pruritus or burning in vagina, penis, or anus. Painful sexual intercourse, rectal pain or bleeding, changes in menstruation, vaginal or penile discharge. Use of birth control measures, pregnancies, desire for future children Coping–stress tolerance: Stress levels, previous losses, coping patterns, self-concept; social withdrawal

Objective Data General Lethargy, persistent fever, lymphadenopathy, peripheral wasting, fat deposits in truncal areas and upper back

Eyes Presence of exudates, retinal lesions or hemorrhage, papilledema

Integumentary Decreased skin turgor, dry skin, diaphoresis. Pallor, cyanosis. Lesions, eruptions, discolorations, bruises of skin or mucous membranes. Vaginal or perianal excoriation. Alopecia. Delayed wound healing

Respiratory Tachypnea, dyspnea, intercostal retractions. Crackles, wheezing, productive or nonproductive cough

Cardiovascular Pericardial friction rub, murmur, bradycardia, tachycardia

Gastrointestinal Mouth lesions, including blisters (HSV), white-gray patches (Candida infection), painless white lesions on the side of the tongue (hairy leukoplakia), discolorations (Kaposi sarcoma).

Gingivitis, tooth decay or loosening. Redness or white patchy lesions of throat. Vomiting, diarrhea, incontinence, rectal lesions, hyperactive bowel sounds, abdominal masses, hepatosplenomegaly

Musculoskeletal Muscle wasting, weakness

Neurologic Ataxia, tremors, lack of coordination. Sensory loss, slurred speech, aphasia. Memory loss, peripheral neuropathy, apathy, agitation, depression, inappropriate behavior. Decreasing levels of consciousness, seizures, paralysis, coma

Reproductive Genital lesions or discharge, abdominal tenderness secondary to pelvic inflammatory disease (PID)

Possible Diagnostic Findings Positive HIV antibody/antigen assay. Detectable viral load. ↓ CD4 cell count, ↓ WBC count, lymphopenia, anemia, thrombocytopenia. Electrolyte imbalances, abnormal liver function tests. ↑ cholesterol, triglycerides, and blood glucose

Ethical/Legal Dilemmas Individual vs. Public Health Protection

Situation A nurse in a community clinic is having a follow-up visit with V.T., a 38-yr-old woman who was diagnosed with HIV infection during her annual examination 2 weeks ago. During the visit, V.T. discloses that her partner verbally and physically abuses her. V.T. says she had not yet told her partner about the HIV diagnosis because she is afraid that he will hurt her. She has not used any protection during sex with him since she learned of her test results because she suspects he infected her.

Ethical/Legal Points for Consideration • You face a conflict between preventing further harm to V.T. (possible increase in intimate partner violence), providing care to her partner (his need for an HIV test, diagnosis, and treatment), and protecting the public health (potential spread of HIV infection to her partner or from her partner to others in the community). Patient teaching and support are essential because your primary obligation is to the patient. • Because relevant law varies from state to state, your first step is to be familiar with your state law concerning mandated reporting for domestic partner abuse and infectious diseases. • Federal laws about protection of privacy in HIV testing apply everywhere. • In many states, reporting domestic abuse is mandatory only when the reporter actually witnesses the abuse or when the immediate effects of the abuse (e.g., wounds, contusions, broken bones) are witnessed.1 • You should be familiar with crisis counseling services for V.T. and offer her the following advice: Collect and stash a set of car keys or taxi money in a safe place, keep a bag packed and hidden or even stored in a locker somewhere accessible, develop a code phrase to use with a friend or family member to call for help, keep a cell phone charged, and have money hidden in a safe place.

Discussion Questions 1. Within the parameters of your state’s requirements for reportable conditions, how can you protect the patient’s confidentiality to prevent further intimate partner violence? 2. What services does your state offer to notify a partner without disclosing the source patient’s name? How would V.T. access those services in your state? 3. How can you protect the partner from possible infection while also protecting V.T. from further violence? 4. How can you best address the issue of intimate partner violence? What resources would V.T. have in your community? 5. Discuss the benefits of universal, voluntary testing in light of V.T.’s case.

Reference National Coalition Against Domestic Violence. Retrieved from www.ncadv.com.

Prevention of HIV Infection HIV infection is preventable. Avoiding or modifying risky behaviors is the most effective prevention tool. Nursing interventions to prevent disease transmission are based on an assessment of the person’s risk behaviors. Provide culturally sensitive, language-appropriate, and age-specific teaching and behavior change counseling. Nurses who are comfortable with and know how to talk about sensitive topics such as sexuality and drug use are best prepared to provide prevention education.

Promoting Population Health

Prevention and Early Detection of HIV • Increase safer sexual practices, including condom use • Decrease equipment sharing among IV drug users • Increase clinician skills to assess for risk factors for HIV infection, recommend HIV testing, and provide counseling for behavior change • Make voluntary HIV testing a routine part of health care • Increase access to new HIV testing technologies, especially rapid testing • Increase access to HIV testing facilities in traditional health care settings and alternative sites, such as drug and alcohol treatment facilities and community-based organizations • Increase risk assessment and individualized behavior change messages to people with HIV to prevent new infections • Decrease perinatal HIV infection by offering voluntary HIV testing as a part of routine prenatal care • Provide counseling and appropriate HIV therapy to those who are infected A wide variety of activities can reduce the risk for HIV infection.26 Help people choose the methods that best fit their needs and circumstances. Prevention techniques are divided into safe sexual activities (those that eliminate risk) and risk-reducing sexual activities (those that decrease, but do not eliminate, risk). The goal is to develop safer, healthier, and less risky behaviors. The more consistently and correctly one uses prevention methods, the more effective they are in preventing HIV infection. It is a good idea to use a combination of prevention methods (e.g., using condoms, decreasing the number of sex partners) to increase the prevention effect. Decreasing risks related to sexual intercourse

Safe sexual activities eliminate the risk for exposure to HIV in semen and vaginal secretions. Abstaining from all sexual activity is an effective way to achieve this goal, but there are safe options for those who cannot or do not wish to abstain. Limiting sexual behavior to activities in which the mouth, penis, vagina, or rectum does not come into contact with a partner’s mouth, penis, vagina, or rectum eliminates contact with blood, semen, or vaginal secretions. Safe activities include masturbation, mutual masturbation (“hand job”), and other activities that meet the “no contact” requirements. Insertive sex between partners who are not infected with HIV and not at risk of becoming infected with HIV is considered safe. Risk-reducing sexual activities decrease the risk of contact with HIV through the use of barriers. Barriers should be used when engaging in insertive sexual activity (oral, vaginal, anal) with a partner who has HIV or whose HIV status is not known. The most commonly used barrier is the male condom. Male condoms offer protection during anal, vaginal, and oral intercourse. Female condoms are an alternative to male condoms. Squares of latex (known as dental dams) can be used as a barrier during oral sexual activity. Decreasing risks related to drug use Drug use, including alcohol and tobacco, can cause immunosuppression, poor nutrition, and a host of psychosocial problems. However, drug use does not cause HIV infection. The major risk for HIV related to using drugs involves sharing equipment or having unsafe sexual experiences while under the influence of drugs. Basic risk reduction rules are (1) do not use drugs; (2) if you use drugs, do not share equipment; and (3) do not have sexual intercourse when under the influence of any drug, including alcohol, that impairs decision making.27 The safest method is to abstain from drugs, but this may not be a practical option for users who are not prepared to quit or have no access to drug treatment services. The risk for HIV infection for these persons is eliminated if they do not share equipment. Injecting equipment (“works”) includes needles, syringes, cookers (spoons or

bottle caps used to mix the drug), cotton, and rinse water. Blood can contaminate equipment used to snort (straws) or smoke (pipes) drugs and should not be shared.

Evidence-Based Practice Condom Use and HIV As a nurse in an HIV clinic, you are counseling M.J., a 27-yr-old gay man and his partner. M.J. is on antiretroviral therapy (ART). His viral load is very low, and his CD4 cell count is normal. He tells you that since the drugs are working, he and his partner (who is HIVnegative) are considering not using condoms in the future.

Making Clinical Decisions Best Available Evidence. One of the best ways to prevent HIV transmission from an infected person to an uninfected person continues to be the consistent and correct use of latex condoms. Those with HIV who take ART and get and keep an undetectable viral load (95%

Base excess

±2.0 mEq/L

Decreases above sea level and with increasing age.

In both types of alkalosis, symptoms usually result from an accompanying electrolyte abnormality rather than the alkalosis. Hypocalcemia occurs due to increased calcium binding with albumin, lowering the amount of ionized, active calcium. Therefore muscle cramping and symptoms of CNS excitability, including tingling and numbness of the fingers and tetany, occur. If left untreated, respiratory alkalosis can be life-thereatening.13

Blood Gas Values Arterial blood gas (ABG) values give objective information about a patient’s acid-base status, the underlying cause of an imbalance, and the body’s ability to regulate pH. Knowing the patient’s clinical situation and the extent of renal and respiratory compensation allows you to identify acid-base disorders and the patient’s ability to compensate. Blood gas analysis also shows the partial pressure of arterial O2 (PaO2) and O2 saturation. Table 16.14 lists normal blood

gas values. These values help you evaluate the patient’s overall oxygenation status and identify hypoxemia. Table 16.15 shows ROME, a quick memory device for understanding acid-base imbalances.

TABLE 16.15 ROMEMemory Device for Acid-Base

Imbalances For acid-base imbalances, use this quick memory device (mnemonic). In Respiratory conditions, the pH and the PaCO2 go in Opposite directions. • In respiratory alkalosis, the pH is ↑ and the PaCO2 is ↓. • In respiratory acidosis, the pH is ↓ and the PaCO2 is ↑. In Metabolic conditions, the pH and the HCO3− go in the same direction (Equal). The PaCO2 may also go in the same direction. • In metabolic alkalosis, pH and HCO3− are ↑ and the PaCO2 is ↑ or normal. • In metabolic acidosis, pH and HCO3− are ↓ and the PaCO2 is ↓ or normal. To interpret the results of an ABG, perform the following 5 steps: 1. Look at each of the values. If the pH is between 7.35 and 7.45, and the CO2, HCO3−, and PaO2 are within normal limits, the ABGs are normal. If any value is out of normal, then continue. 2. Look at the pH first. Values less than 7.35 indicate acidosis and values greater than 7.45 indicate alkalosis. A normal pH means there is normal acid-base status, compensation is occurring, or a mixed disorder is present. 3. Use ROME (Table 16.15) to figure out if the origin is respiratory or metabolic. Remember respiratory opposite and metabolic equal.

4. Once the metabolic or respiratory origin is determined, look at the remaining value, either the CO2 or HCO3−, to figure the level of compensation. If the value is moving in the opposite direction, the body is trying to compensate. If the remaining value moving to compensate is abnormal and the pH is higher or lower than normal, partial compensation has occurred. If the pH is within normal limits, full compensation has occurred. 5. Assess the PaO2 and O2 saturation. If these values are abnormal, hypoxemia is present. Table 16.16 explains how to analyze ABG results. The laboratory findings section of Table 16.11 shows ABG findings of the 4 major acid-base imbalances. See Chapter 25 for further discussion of ABGs.

Assessment of Fluid, Electrolyte, and Acid-Base Imbalances Assessing patients for fluid, electrolyte, and acid-base imbalances is an important part of your nursing practice. In addition to assessing for the manifestations discussed earlier in this chapter, obtain subjective and objective data from any patient with suspected fluid, electrolyte, or acid-base imbalances.

Subjective Data Important Health Information Past Health History Question the patient about any history of problems involving the kidneys, heart, GI system, or lungs that could affect the present fluid, electrolyte, and acid-base balance. Ask about specific diseases such as diabetes, diabetes insipidus, COPD, renal failure, ulcerative colitis, and Crohn’s disease. Assess for any prior fluid, electrolyte, or acidbase disorders.

Medications Assess the patient’s current and past use of medications. The ingredients in many drugs, especially over-the-counter drugs, are often hidden sources of sodium, potassium, calcium, magnesium, and other electrolytes. Many prescription drugs, including diuretics, corticosteroids, and electrolyte supplements, can cause fluid and electrolyte imbalances.

TABLE 16.16 Applying Arterial Blood Gas (ABG)

Analysis

Surgery or Other Treatments Ask the patient about past or present renal dialysis, kidney surgery, or bowel surgery resulting in a temporary or permanent external collecting system, such as an ileostomy.

Functional Health Patterns Health Perception–Health Management Pattern

If the patient currently has a problem related to fluid, electrolyte, and acid-base balance, obtain a careful description of the illness, including onset, course, and treatment. Ask the patient about any recent changes in body weight.

Nutritional-Metabolic Pattern Ask the patient about diet and any special dietary practices. Weight reduction diets, fad diets, or any eating disorders, such as anorexia or bulimia, can lead to fluid and electrolyte problems. If the patient is on a special diet, such as low sodium or high potassium, assess the ability to adhere to the dietary prescription.

Elimination Pattern Make note of the patient’s usual bowel and bladder habits. Carefully document any deviations from the expected elimination pattern, such as diarrhea, oliguria, polyuria, or incontinence.

Activity-Exercise Pattern Ask about the patient’s exercise pattern and any excess perspiration. Determine if the patient is exposed to extremely high temperatures during leisure or work activity. Ask the patient what he or she does to replace fluid and electrolytes lost through excess perspiration. Assess the patient’s activity level to determine any functional problems that could lead to lack of ability to obtain food or fluids.

Cognitive-Perceptual Pattern Ask about any changes in sensations, such as numbness, tingling, or muscle weakness, which could indicate a fluid and electrolyte problem. Ask the patient and caregiver if there have been any changes in mentation or alertness, such as confusion, memory impairment, or lethargy.

Objective Data

Physical Examination Perform a complete physical examination because fluid, electrolyte, and acid-base balance affects all body systems. As you assess each system, check for manifestations that you would expect with an imbalance. Common abnormal assessment findings of major body systems offer clues to possible imbalances (Table 16.17).

TABLE 16.17 Assessment AbnormalitiesFluid and

Electrolyte Imbalances

Laboratory Values Assessing serum electrolyte values is a good starting point for evaluating fluid and electrolyte balance (Table 16.1). Serum electrolytes can also provide important information about a patient’s acid-base balance. Changes in the serum HCO3− (often reported as total CO2 or CO2 content on an electrolyte panel) indicate metabolic acidosis (low HCO3− level) or alkalosis (high HCO3− level).

Safety Alert Managing Critical Test Results • Promptly report critical laboratory values to the HCP. • Assess the patient and take appropriate actions (e.g., ECG monitoring). Remember that serum electrolyte values often provide limited information. They reflect the concentration of that electrolyte in ECF but not necessarily in ICF. For example, most potassium is found in the cells. Changes in serum potassium values may be the result of a true deficit or excess of potassium or reflect the movement of potassium into or out of the cell during acid-base imbalances. An abnormal serum sodium level may reflect a sodium problem or, more likely, a water problem. Other useful laboratory tests include serum and urine osmolality, serum glucose, blood urea nitrogen, serum creatinine, venous blood gas sampling, urine specific gravity, and urine electrolytes.

Oral Fluid and Electrolyte Replacement In all cases of fluid, electrolyte, and acid-base imbalances, the primary treatment involves correcting the underlying cause. Oral rehydration

solutions containing water, potassium, sodium, and glucose may be used to correct mild fluid and electrolyte deficits. Glucose not only provides calories but also promotes sodium and water absorption in the small intestine. Commercial oral rehydration solutions are now available for home use. Avoid cola drinks because they do not contain adequate electrolyte replacement, and the sugar content may lead to osmotic diuresis.

IV. Fluid and Electrolyte Replacement IV fluid and electrolyte therapy are necessary to treat many different fluid and electrolyte imbalances. Many patients need maintenance IV fluid therapy when they cannot take oral fluids (e.g., during and after surgery). Other patients need corrective or replacement therapy for losses that are ongoing or have already occurred. The amount and type of solution is determined by the normal daily maintenance requirements and by imbalances identified by laboratory results. We classify IV replacement solutions by their concentration or tonicity (Table 16.18). Tonicity is a key factor in determining the appropriate solution to correct imbalances.

Solutions Hypotonic A hypotonic solution has a lower osmolality when compared to plasma.14 Infusing a hypotonic solution dilutes ECF, lowering serum osmolality. Osmosis then produces a movement of water from ECF to interstitial spaces and cells, causing cells to swell. After achieving equilibrium, ICF and ECF have the same osmolality. Hypotonic solutions (e.g., 0.45% NaCl) are useful in treating patients with hypernatremia. They are a good maintenance fluid because normal daily losses are hypotonic. They are not good for replacement because they can deplete ECF and lower BP. Because hypotonic solutions have the potential to cause cellular swelling, monitor patients for changes in mentation that may indicate cerebral edema.

Although 5% dextrose in water is technically an isotonic solution, the dextrose quickly metabolizes. The net result is the administration of hypotonic free water with equal expansion of ECF and ICF. One liter of a 5% dextrose solution provides 50 g of dextrose, or 170 calories. While this amount of dextrose is not enough to meet caloric requirements, it helps prevent ketosis associated with starvation.

Isotonic An isotonic solution has an osmolality similar to plasma.14 Because of this similarity, giving an isotonic solution expands only ECF and the fluid does not move into cells. This makes isotonic solutions the ideal fluid replacement for patients with ECF volume deficits. Examples of isotonic solutions include 0.9% NaCl and lactated Ringer’s solution. Isotonic saline (0.9% NaCl), or normal saline, has a sodium concentration (154 mEq/L) slightly higher than that of plasma (135 to 145 mEq/L) and a chloride concentration (154 mEq/L) significantly higher than the plasma chloride level (96 to 106 mEq/L). Therefore giving too much isotonic saline has the potential to increase sodium and chloride levels. Isotonic saline is used when a patient has had both fluid and sodium losses (e.g., diarrhea, vomiting). Lactated Ringer’s solution contains sodium, potassium, chloride, calcium, and lactate (the precursor of bicarbonate) in about the same concentrations as ECF. This makes it the ideal fluid in certain situations, such as surgery, burns, or GI fluid losses. Patients with liver dysfunction, hyperkalemia, and severe hypovolemia should not receive lactated Ringer’s because they have a decreased ability to convert the lactate to bicarbonate.

Hypertonic A hypertonic solution has a higher osmolality than plasma.14 The higher osmotic pressure draws water out of the cells into ECF. It is useful in the treatment of hyponatremia and trauma patients with head injury. Those receiving hypertonic solutions need frequent monitoring of BP, lung sounds, and serum sodium levels because of the risk for intravascular fluid volume excess.

TABLE 16.18 Common Crystalloid Solutions

Although concentrated dextrose and water solutions (10% dextrose or greater) are hypertonic solutions, once the dextrose is metabolized, the net result is the administration of water. This free water ultimately expands ECF and ICF. The primary use of these solutions is providing calories as part of parenteral nutrition (see Chapter 39). You may give solutions containing 10% dextrose or less through a peripheral line. You must use a central line to give solutions with dextrose concentrations greater than 10%.

IV. Additives Additives in basic IV solutions replace specific losses. KCl, CaCl2, MgSO4, and HCO3− are common additives. The use of each was described earlier in the discussion of the specific electrolyte deficiencies. Many premixed IV solutions containing specific additives are available. Using these solutions reduces error as the solution contains the correct amount of the electrolyte in the proper volume and type of IV solution.

Colloids Colloid solutions contain large molecules that increase oncotic pressure and pull fluid into the blood vessels. Because this action restores blood volume, colloids are also called volume expanders or plasma expanders. Colloids include human plasma products (albumin, fresh frozen plasma, blood) and semisynthetic solutions (dextran, starches). Albumin is available in 5% and 25% solutions. The 5% solution has an albumin concentration similar to that of plasma and results in plasma volume expansion equal to the volume infused. This makes it ideal for treating hypovolemic patients. In contrast, 25% albumin solution is hypertonic and draws fluid from the interstitial space. This makes it useful in treating patients with burns, hepatic failure, and ascites. Dextran solutions are synthetic complex sugar solutions. There are 2 types: low-molecular-weight dextran (dextran 40) and high-

molecular-weight dextran (dextran 70). Because dextran metabolizes slowly, it stays in the vascular system for a prolonged period. It pulls fluid into the intravascular space, expanding it by more volume than what is infused. Hydroxyethyl starches (e.g., Hespan) are synthetic colloids that work similarly to dextran to expand plasma volume. Colloids can lead to circulatory overload because they pull fluid into ECF. Monitor vital signs and urine output frequently and assess for signs and symptoms of fluid volume excess. All colloids affect blood coagulation, with dextran and starches having the strongest anticoagulation effect.14 Monitor coagulation times and implement any necessary precautions. Fatal anaphylactic reactions have occurred with Hespan and dextran. Monitor the patient closely for a hypersensitivity reaction and stop an infusion at once if a reaction occurs. If the patient has lost blood, whole blood or packed RBCs are given. Packed RBCs have the advantage of giving the patient primarily RBCs rather than RBCs and fluid volume. Although packed RBCs have a decreased plasma volume, they increase the oncotic pressure and pull fluid into the intravascular space. The use of whole blood, with its added fluid volume, may cause circulatory overload, particularly in patients who are susceptible to complications from excess circulating volume (e.g., heart failure). To prevent fluid volume excess, loop diuretics may be given with blood and colloids. See Chapter 30 for more information on giving blood and blood products.

Nursing Management IV Therapy • Assess patient for manifestations of fluid and electrolyte imbalances. • Determine if ordered IV therapies are appropriate. • Choose and insert appropriate IV catheters and infusion devices.

• Give IV fluids and medications. • Monitor for adverse reactions to IV fluids or medications. • Assess for manifestations of fluid overload or hypovolemia and initiate appropriate changes in IV fluids. • Evaluate if IV therapies are addressing patient’s fluid and electrolyte needs. • Collaborate with the pharmacist to: • Determine appropriateness of IV therapies and need for dose adjustments. • Prepare IV infusions and medications. • Screen for potential problems, such as compatibility issues. • Monitor response to therapy.

Central Venous Access Devices Central venous access devices (CVADs) are catheters placed in large blood vessels (e.g., subclavian vein, jugular vein) of people who need frequent or special access to the vascular system. There are 3 main types of CVADs: centrally inserted catheters, peripherally inserted central catheters (PICCs), and implanted ports. Advantages of CVADs include immediate access to the central venous system, a reduced need for multiple venipunctures, and decreased risk for extravasation injury. CVADs permit frequent, continuous, rapid, or intermittent administration of fluids and medications. They allow for the administration of drugs that are potential vesicants (agents that can cause tissue damage), blood and blood products, and parenteral nutrition. CVADs can provide a means to perform hemodynamic monitoring and obtain venous blood samples. They are useful with patients who have limited peripheral vascular access or who have a projected need for long-term vascular access. CVADs also can be used to inject radiopaque contrast media. Table 16.19 gives examples of when CVADs are used. The major disadvantages of CVADs are an increased risk for

systemic infection and the invasiveness of the procedure. Extravasation (leakage of fluid) can still occur if there is displacement of or damage to the device.

Centrally Inserted Catheters The tip of centrally inserted catheters (also called central venous catheters [CVCs]) rests in the distal end of the superior vena cava near its junction with the right atrium (Fig. 16.18). The other end of the catheter exits through a separate incision on the chest or abdominal wall. Nontunneled catheters are usually placed in the subclavian or internal jugular vein, more rarely in the femoral vein. They are best for patients with short-term needs in an acute care setting. Surgically placed tunneled catheters (e.g., Hickman, Broviac, Groshong) are suitable for long-term needs. Tunneling of the catheter through subcutaneous tissue and the synthetic cuff used to anchor the catheter provide stability and decrease infection risk. After the site heals, the catheter does not need a dressing, making it easier for the patient to maintain the site at home. CVCs are available with single-, double-, or triple-lumens. Multilumen catheters are useful in the critically ill patient because each lumen can be used simultaneously to provide a different therapy. For example, incompatible drugs infuse in separate lumens without mixing while a third lumen gives access for blood sampling.

TABLE 16.19 Common Indications for Central

Venous Access Devices (CVADs)

FIG. 16.18 Tunneled central venous catheter. Note tip of the catheter in the superior vena cava.

Peripherally Inserted Central Catheters Peripherally inserted central catheters (PICCs) are CVCs inserted into a vein in the arm. The basilic vein is best because of its large diameter (Fig. 16.19). The cephalic, median cubital, or brachial veins are other options. Single-, double-, or triple-lumens are available. Double lumens are preferred because they allow for simultaneous uses. PICCs are used with patients who need vascular access for 1 week to 6 months, but they can be in place for longer periods.

FIG. 16.19 Peripherally inserted central catheter (PICC) can be inserted using the basilic or cephalic vein.

Advantages of a PICC over a CVC are lower infection rate, fewer insertion-related complications, decreased cost, and ability to insert at the bedside or in an outpatient area. PICCs, however, are associated with an increased risk for deep vein thrombosis and phlebitis (Table 16.20). If phlebitis occurs, it usually happens within 7 to 10 days after

insertion. Do not use the arm with the PICC to take a BP reading or draw blood. When the BP cuff is inflated, the PICC can touch the vein wall, increasing the risk for vein damage and thrombosis.

Implanted Infusion Ports An implanted infusion port consists of a surgically implanted CVC connected to a reservoir or port (Fig. 16.20, A). The catheter tip lies in the desired vein. The port lies in a surgically created subcutaneous pocket on the upper chest or arm. It consists of a titanium or plastic reservoir covered with a self-sealing silicone septum. You access the port by using a special noncoring needle with a deflected tip. This prevents damage to the septum that could make the port useless (Fig. 16.20, B). Drugs are placed in the reservoir either by a direct injection or through injection into an established IV line. The reservoir then slowly releases the medicine into the bloodstream. Implanted ports are good for long-term therapy and have a low risk for infection. The hidden port offers the patient cosmetic advantages and overall has less maintenance than other types of CVADs. Monitor accessed ports for infiltration that can occur if the needle is not in place or dislodges.

Midline Catheters Midline catheters technically are peripheral catheters because they do not enter a central vein. However, their use and care are similar to a PICC. A specially trained nurse can insert a midline catheter. A catheter can be from 3 to 8 inches long and have single or double lumens. They are inserted in the antecubital area through either the basilic or cephalic vein, often under ultrasound guidance. The basilic vein is best since it has a larger diameter. The tip rests right below the axilla, staying below the shoulder joint to reduce the risk for vein irritation from moving the shoulder. These lines can stay in place for up to 4 weeks.

TABLE 16.20 Complications of Central Venous

Access Devices (CVADs)

Complications CVADs always have a potential for complications. Careful monitoring and assessment will help you to identify potential complications early. Table 16.19 lists common complications, potential causes, manifestations, and interventions.

Nursing Management: Central Venous

Access Devices Nursing management of CVADs includes assessment, dressing changes and cleansing, injection cap changes, and maintenance of catheter patency. The exact frequency and procedures for these requirements vary by type of CVAD and facility, so it is important to follow your facility’s policies and procedures. The following section discusses some general guidelines. Catheter and insertion site assessment includes inspecting the site for redness, edema, warmth, drainage, tenderness, or pain. Observing the catheter for misplacement or slippage is important. Perform a comprehensive pain assessment, particularly noting any reports of chest or neck discomfort, arm pain, or pain at the insertion site. Do not use a newly placed CVAD until the tip position is verified with a chest x-ray.

Check Your Practice You are taking care of a 74-yr-old patient with a left triple-lumen subclavian catheter. When you are changing the transparent dressing, you note some redness at the site with a small amount of yellow, foulsmelling drainage. • What should you do? Before manipulating a catheter for any reason, perform hand hygiene. Perform dressing changes and cleanse the catheter insertion site using strict sterile technique. Typical dressings include transparent semipermeable dressings or gauze and tape. If the site is bleeding, a gauze dressing may be preferable. Otherwise, transparent dressings are best. They allow observation of the site without having to remove the dressing. Transparent dressings may be left in place for up to 1 week. Change any dressing at once if it becomes damp, loose, or soiled.

Cleanse the skin around the catheter insertion site according to facility policy. A chlorhexidine-based preparation is the cleansing agent of choice. Its effects last longer than either povidone-iodine or alcohol, offering improved killing of bacteria.15 When using chlorhexidine, cleansing the skin with friction is critical to preventing infection. When applying a new dressing, allow the area to air dry completely. Secure the lumen ports to the skin above the dressing site. Document the date and time of the dressing change and initial the dressing.

FIG. 16.20 A, Cross section of implantable port displaying access of the port with the Huber-point needle. Note the deflected point of the Huber-point needle, which prevents coring of the port’s septum. B, 2 Huber-point needles used to enter the implanted port. The 90-degree needle is used for top-entry ports for continuous infusion.

Disinfect catheter hubs, needleless connectors, and injection ports before accessing the catheter. Use an alcoholic chlorhexidine preparation, 70% alcohol, or povidone-iodine. Change injection caps at regular intervals according to facility policy, or if they have damage from excess punctures. Use strict sterile technique. Teach the patient to turn the head to the opposite side of the insertion site during cap change. If you cannot clamp the catheter, have the patient lie flat in bed and perform the Valsalva maneuver whenever the catheter is open to air to prevent an air embolism. Flushing is one of the most effective ways to maintain catheter patency. It also keeps incompatible drugs or fluids from mixing. Use a normal saline solution in a syringe that has a barrel capacity of 10 mL or more to avoid excess pressure on the catheter. If you feel resistance, do not apply force. This could result in a ruptured catheter or create an embolism if a thrombus is present. Because of the risk for contamination and infection, use solution from prefilled syringes or single-dose vials rather than multiple-dose vials when flushing catheters. If you are not using a positive-pressure valve cap, clamp any unused lines after flushing. Use the push-pause technique when flushing all catheters. Pushpause creates turbulence within the catheter lumen, promoting the removal of debris that adheres to the catheter lumen and decreasing the chance of occlusion. This technique involves injecting saline with a rapid alternating push-pause motion, instilling 1 to 2 mL with each push on the syringe plunger. If you are using a negative-pressure cap or neutral pressure cap, clamp the catheter while maintaining positive pressure while instilling the last 1 mL of saline. This prevents reflux of blood back into the catheter. If a positive-pressure valve cap is present, it works to prevent the reflux of blood and resultant catheter lumen occlusion. Remove the syringe before clamping the catheter to allow the positive pressure valve to work correctly.

CVAD Removal Removing a CVAD is done according to agency policy and the nurse’s scope of practice. In many agencies, nurses with demonstrated

competency can remove PICCs and nontunneled central venous catheters. The procedure involves removing any sutures and then gently withdrawing the catheter. Have the patient perform the Valsalva maneuver as the last 5 to 10 cm of the catheter is withdrawn. Immediately apply pressure to the site with sterile gauze to prevent air from entering and to control bleeding. Inspect the catheter tip to determine that it is intact. After bleeding has stopped, apply an antiseptic ointment and sterile dressing to the site.

Case Study Fluid and Electrolyte Imbalance

© Kevin Peterson/Photodisc/Thinkstock.

Patient Profile S.S., a 63-yr-old white woman with acute lymphocytic leukemia, has been receiving chemotherapy on an outpatient basis. She completed her third treatment 5 days ago and has had nausea and vomiting for 2 days despite using ondansetron (Zofran). S.S.’s daughter brings her to the hospital, where she is admitted to the medical unit. As the admitting nurse, you perform a thorough assessment.

Subjective Data • Reports lethargy, weakness, dizziness, and dry mouth • States she has been too nauseated to eat or drink anything for 2 days

Objective Data • Heart rate 110 beats/min, pulse thready • BP 100/65 • Weight loss of 5 lb since she received her chemotherapy treatment 5 days ago • Dry oral mucous membranes

Discussion Questions 1. Based on her manifestations, what fluid imbalance does S.S. have? 2. What additional assessment data should you obtain? 3. What are her risk factors for fluid and electrolyte imbalances? 4. You draw blood for a serum chemistry evaluation. What electrolyte imbalances are likely and why? 5. S.S. is at risk for which acid-base imbalance? Describe the changes that would occur in S.S.’s ABGs with this acid-base imbalance. How would the body compensate? 6. Priority Decision: What are the priority nursing interventions for S.S.? 7. Collaboration: Who should be the primary members of the interprofessional team in caring for S.S.? What is the interprofessional team’s priority at this time for S.S.? 8. The provider orders dextrose 5% in 0.45% saline to infuse at 100 mL/hr. What type of solution is this, and how will it help S.S.’s fluid imbalance?

9. Evidence-Based Practice: S.S. has a double-lumen PICC in her left arm. One lumen is connected to the IV infusion; the other is unused. What is the recommended practice for maintaining the patency of the unused lumen? 10. Quality Improvement: What outcomes will indicate that interprofessional care was effective? Answers available at http://evolve.elsevier.com/Lewis/medsurg.

Case Study Managing Care of Multiple Patients You and another RN are assigned to care for the following 3 patients in the intensive care unit. There is also an unlicensed assistive personnel (UAP) on duty.

Patients (©

G.N., a 65-yr-old black man, was admitted to the ICU after falling into a lit gas grill. He has partial-thickness burns on his face, neck, and upper trunk. He has undergone surgical repair of right tibia and left hip fractures and debridement of a severely lacerated right leg. His voice is slightly hoarse, and he is coughing up sooty sputum. He is receiving O at 4 L/min via nasal 2

cannula, and his O2 saturation is 93%. His WBC count is 26,400/µL (26.4 × 109/L) with 80% neutrophils (10% bands). Stockphoto/Thinkstock.) J.N., a 65-yr-old black man, was transferred to the ICU from the clinical unit last evening with acute respiratory failure. He was diagnosed 2 days ago with AIDS and Pneumocystis jiroveci pneumonia (PCP). Prior to this hospital admission he was started on oral trimethoprim/sulfamethoxazole (Bactrim) and combination antiretroviral therapy. However, his respiratory distress worsened, and he was transferred to the ICU for intubation and mechanical ventilation. He is now receiving IV Bactrim.



iStock.com/Cecilie_Arcurs.) S.S., a 63-yr-old white woman with acute lymphocytic leukemia, has been receiving chemotherapy on an outpatient basis. She completed her third treatment 5 days ago and has been experiencing nausea and vomiting for 2 days despite using ondansetron (Zofran). She was initially admitted to the clinical unit but was transferred to the ICU for close monitoring after becoming severely hypotensive overnight. Her most recent blood pressure was 98/50, HR 82 and regular, O2 saturation 95% on 2 L via nasal cannula, RR 22 and regular.

(© Kevin Peterson/Photodisc/Thinkstock.)

Discussion Questions 1. Priority Decision: After receiving report, which patient should you see first? Provide your rationale. 2. Collaboration: Which morning tasks should you delegate to the UAP (select all that apply)? a. Take BP readings on S.S. b. Perform respiratory assessment on G.N. c. Document strict intake and output on S.S. d. Provide oral care around the endotracheal tube for J.N. e. Titrate S.S.’s IV infusion rate based on her BP reading. 3. Priority Decision and Collaboration: When you enter J.N.’s room, the ventilator alarms are going off. The UAP had just finished providing oral care, and she tells you that J.N. has become increasingly agitated within the last 5 minutes. Which

initial action would be most appropriate? a. Suction J.N.’s endotracheal tube. b. Have the UAP stay with J.N. while you obtain IV sedation for him. c. Ask the UAP to describe exactly what she did when she was providing oral care. d. Assess the ventilator to identify what alarm is going off and to make sure all connections are secure.

Case Study Progression J.N.’s ventilator tubing became disconnected. You quickly reconnect his tubing, and as he settles down his oxygenation improves. You ask the UAP to obtain vital signs on your other patients while you begin a more thorough assessment of J.N. 4. During your assessment of J.N., you note gray-white patches on the inside of his mouth. You recognize these as most likely caused by a. Candida albicans. b. poor oral hygiene. c. Coccidioides immitis. d. irritation from recent mouth care. 5. G.N.’s family asks you why surgery was performed on his leg wound. Your response is based on the knowledge that debridement (select all that apply) a. is used to remove infected tissue. b. is used to remove nonviable tissue. c. prepares the wound bed for healing. d. can be accomplished only in surgery. e. is necessary in any burn wound involving the skin. 6. S.S.’s morning laboratory results reveal a serum potassium level of 2.8 mEq/L. You notify the health care provider and obtain an order for IV potassium. During infusion of the potassium replacement, you prioritize assessment of S.S.’s a. bowel function.

b. cardiac rhythm. c. muscle strength. d. level of consciousness. 7. Priority Decision: As the day continues, you find that you are getting busy. Which nursing task should be your priority? a. Changing the sterile dressings on G.N.’s leg wounds b. Performing routine suctioning of J.N.’s endotracheal tube c. Starting a 500-mL fluid bolus to S.S., whose most recent BP is 76/42 d. Calling the hospital chaplain to speak with S.S., who is upset over her condition 8. Priority Decision: Which medication should you administer first? a. Daily subcutaneous enoxaparin to G.N. b. IV Bactrim, ordered twice daily, to J.N. c. IV proton pump inhibitor, ordered twice daily, to S.S. d. As needed IV morphine to G.N., who reports pain at a level 9 (1 to 10 scale) 9. Management Decision: While sitting at the computer charting your patients’ morning assessments, you overhear the UAP telling a nursing student that J.N. deserves what he got because HIV is God’s way of punishing those who sin. Your most appropriate response would be to a. report the UAP’s actions to the supervisor. b. ask the UAP to keep her opinions to herself. c. ignore the conversation because it does not affect patient care. d. talk to the UAP and student about keeping personal feelings separate from patient care. Answers available at http://evolve.elsevier.com/Lewis/medsurg.

Bridge to Nclex Examination

The number of the question corresponds to the same-numbered outcome at the beginning of the chapter.

1. During the postoperative care of a 76-year-old patient, the nurse monitors the patient’s intake and output carefully, knowing that the patient is at risk for fluid and electrolyte imbalances primarily because a. older adults have an impaired thirst mechanism and need reminding to drink fluids. b. water accounts for a greater percentage of body weight in the older adult than in younger adults. c. older adults are more likely than younger adults to lose extracellular fluid during surgical procedures. d. small losses of fluid are significant because body fluids account for 45% to 50% of body weight in older adults. 2. During administration of a hypertonic IV solution, the mechanism involved in equalizing the fluid concentration between ECF and the cells is a. osmosis. b. diffusion. c. active transport. d. facilitated diffusion. 3a. An older woman is admitted to the medical unit with GI bleeding. Assessment findings that indicate fluid volume deficit include (select all that apply) a. weight loss. b. dry oral mucosa. c. full bounding pulse. d. engorged neck veins.

e. decreased central venous pressure. 3b. The nursing care for a patient with hyponatremia and fluid volume excess includes a. fluid restriction. b. administration of hypotonic IV fluids. c. administration of a cation-exchange resin. d. placement of an indwelling urinary catheter. 3c. The nurse should be alert for which manifestations in a patient receiving a loop diuretic? a. Restlessness and agitation b. Paresthesias and irritability c. Weak, irregular pulse and poor muscle tone d. Increased blood pressure and muscle spasms 3d. Which patient is at greatest risk for developing hypermagnesemia? a. 83-year-old man with lung cancer and hypertension b. 65-year-old woman with hypertension taking βadrenergic blockers c. 42-year-old woman with systemic lupus erythematosus and renal failure d. 50-year-old man with benign prostatic hyperplasia and a urinary tract infection 3e. It is important for the nurse to assess for which manifestation(s) in a patient who has just undergone a total thyroidectomy (select all that apply)? a. Confusion b. Weight gain

c. Depressed reflexes d. Circumoral numbness e. Positive Chvostek’s sign 3f. The nurse expects the long-term treatment of a patient with hyperphosphatemia from renal failure will include a. fluid restriction. b. calcium supplements. c. magnesium supplements. d. increased intake of dairy products. 4. The lungs act as an acid-base buffer by a. increasing respiratory rate and depth when CO2 levels in the blood are high, reducing acid load. b. increasing respiratory rate and depth when CO2 levels in the blood are low, reducing base load. c. decreasing respiratory rate and depth when CO2 levels in the blood are high, reducing acid load. d. decreasing respiratory rate and depth when CO2 levels in the blood are low, increasing acid load. 5. A patient has the following arterial blood gas results: pH 7.52, PaCO2 30 mm Hg, HCO3− 24 mEq/L. The nurse determines that these results indicate a. metabolic acidosis. b. metabolic alkalosis. c. respiratory acidosis. d. respiratory alkalosis. 6. The typical fluid replacement for the patient with a fluid

volume deficit is a. dextran. b. 0.45% saline. c. lactated Ringer’s solution. d. 5% dextrose in 0.45% saline. 7. The nurse is unable to flush a central venous access device and suspects occlusion. The best nursing intervention would be to a. apply warm moist compresses to the insertion site. b. try to force 10 mL of normal saline into the device. c. place the patient on the left side with the head down. d. have the patient change positions, raise arm, and cough. 1. d, 2. a, 3a. a, b, e, 3b. a, 3c. c, 3d. c, 3e. a, d, e, 3f. b, 4. a, 5. d, 6. c, 7. d For rationales to these answers and even more NCLEX review questions, visit http://evolve.elsevier.com/Lewis/medsurg.

Evolve Website/Resources List http://evolve.elsevier.com/Lewis/medsurg

Review Questions (Online Only) Key Points Answer Keys for Questions • Answer Guidelines for Case Study on p. 295 • Rationales for Bridge to NCLEX Examination Questions • Answer Guidelines for Managing Care of Multiple Patients Case Study (Section 3) on p. 298 Student Case Study

• Patient With Hyponatremia/Fluid Volume Imbalance Conceptual Care Map Creator Audio Glossary Fluids and Electrolytes Tutorial Content Updates

References 1. Henderson R: Osmolality, osmolarity, and fluid homeostasis. Retrieved from www.patient.info/doctor/osmolality-osmolarity-and-fluidhomeostasis. 2. Reddi AS: Fluid, electrolyte and acid-base disorders, ed 2, New York, 2018, Springer. Oates LL, Price CI: Clinical assessments and care interventions to promote oral hydration amongst older patients: A narrative systematic review, BMC Nurs 16:4, 2017.

4. Hew-Butler T, Weisz K: Focus the secret stories of sodium: hypernatremia, Clin Lab Sci 29:3, 2016. Hoorn EJ, Zietse R: Diagnosis and treatment of hyponatremia: compilation of the guidelines, J Am Soc Nephrol 28:1340, 2017.

6. Rafiq MF: Hyponatremia still remains largely undiagnosed and untreated, Anaesth Pain Intensive Care 21:1, 2017. Douglas M, Rizzolo D, Kruger D: Hyperkalemia in adults: Review of a common electrolyte imbalance, Clin Rev 3:40, 2017.

8. Pincus M: Management of digoxin toxicity, Austr Prescr 39:1, 2016. 9. Body JJ, Niepel D, Tonini G: Hypercalcemia and hypocalcemia: Finding the balance, Support Care

Cancer 25:5, 2017. 10. Walker M: Fluid and electrolyte imbalance: interpretation and assessment, J Infusion Nurs 39:6, 2016. 11. Boyle SM, Goldfarb S: Phosphate deficiency and the phosphate-depletion syndrome: Pathophysiology, diagnosis, and treatment, New York, 2017, Springer. 12. Hiner A: Electrolyte series: magnesium, Nursing2018 Crit Care 13:15, 2018. 13. Perkins A: Alkalosis in brief, Nursing Made Incredibly Easy 14:13, 2016. 14. Naisbitt C, Buckley H, Kishen R: Crystalloids, colloids, blood products, and blood substitutes, Anaesth Intensive Care 17:308, 2016. Septimus EJ, Moody J: Prevention of device-related healthcareassociated infections, F1000Res 14:5, 2016. ∗Evidence-based information for clinical practice.

SECTION FOUR

Perioperative Care OUTLINE 17. Preoperative Care 18. Intraoperative Care 19. Postoperative Care

17

Preoperative Care Janice A. Neil

LEARNING OUTCOMES 1. Distinguish the common purposes and settings of surgery. 2. Apply knowledge of the purpose and components of a preoperative nursing assessment. 3. Interpret the significance of data related to the preoperative patient’s health status and operative risk. 4. Analyze the components and purpose of the patient’s informed consent for surgery. 5. Examine the nursing role in the physical, psychological, and educational preparation of the surgical patient. 6. Prioritize the nursing responsibilities related to day-of-surgery preparation for the surgical patient. 7. Discern the purposes and types of common preoperative medications. 8. Apply knowledge of the special considerations of preoperative preparation for the older adult surgical patient.

KEY TERMS

ambulatory surgery, p. 300 elective surgery, p. 300 emergency surgery, p. 300 informed consent, p. 307 same-day admission, p. 300 surgery, p. 299 From caring comes courage. Lao Tzu http://evolve.elsevier.com/Lewis/medsurg/

Conceptual Focus Anxiety Patient Education Safety Surgery is the art and science of treating diseases, injuries, and deformities by operation and instrumentation. The total surgical episode is called the perioperative period. This period includes the time before surgery (preoperative period), the time spent during the actual surgical procedure (intraoperative period), and the period after the surgery is over (postoperative period). The surgical experience involves an interprofessional team, including the patient, surgeon, anesthesia care provider (ACP), nurse, and other health care team members. Preparing patients for surgery is an important nursing role. This chapter discusses preoperative care that applies to all surgical patients. Preparation measures for specific surgical procedures (e.g., abdominal, thoracic, or orthopedic surgery) are discussed in the appropriate chapters of this book. Surgery is performed for many reasons. These include:

• Diagnosis: Determine the presence and extent of a pathologic condition (e.g., lymph node biopsy, bronchoscopy). • Cure: Eliminate or repair a pathologic condition (e.g., removal of ruptured appendix or benign ovarian cyst). • Palliation: Alleviate symptoms without cure (e.g., cutting a nerve root [rhizotomy] to reduce pain, creating a colostomy to bypass an inoperable bowel obstruction). • Prevention: Reduce risk of developing a condition (e.g., removal of a mole before it becomes malignant, removal of the colon in a patient with familial polyposis to prevent cancer). • Cosmetic improvement: Alter physical appearance (e.g., repairing a burn scar, breast reconstruction after a mastectomy). • Exploration: Determine the nature or extent of a disease (e.g., laparotomy). With the use of advanced diagnostic tests, exploration is less common because we can identify many problems noninvasively. Surgical procedures are usually described by combining specific suffixes with a body part or organ (Table 17.1).

TABLE 17.1 Suffixes Describing Surgical

Procedures Suffix -ectomy

Meaning Excision or removal of

Example Appendectomy

-lysis

Destruction of

Electrolysis

-orrhaphy

Repair or suture of

Herniorrhaphy

-oscopy

Looking into

Endoscopy

-ostomy

Creation of opening into

Colostomy

-otomy

Cutting into or incision of

Tracheotomy

-plasty

Repair or reconstruction of

Mammoplasty

Surgical Settings Surgery may be a carefully planned event (elective surgery) or may arise with unexpected urgency (emergency surgery). Both elective and emergency surgeries are done in a variety of settings. The type of surgery, potential complications, and the patient’s health status influence the setting where a patient can safely undergo a surgical procedure For inpatient surgery, patients who are going to be admitted to the hospital are usually admitted on the day of surgery (same-day admission). Patients who are in the hospital before surgery are usually there because of acute or chronic medical conditions. Most surgical procedures are performed as ambulatory surgery (also called same-day or outpatient surgery). Many of these surgeries use minimally invasive techniques (e.g., laparoscopic techniques). Ambulatory surgery often occurs in endoscopy clinics, physicians’ offices, freestanding surgical clinics, and outpatient surgery units in hospitals. These procedures can involve the use of general, regional, or local anesthetic. Patients require less than a 24-hour stay after surgery. Many go home with a caregiver within hours of surgery. Patients and HCPs often prefer ambulatory surgery. Generally, it requires fewer laboratory tests and medications and reduces the patient’s risk for health care–associated infections. Patients like the convenience of recovering at home. HCPs prefer the flexibility in scheduling. The costs are usually less for the patient and the insurer. You play an essential role in preparing the patient for surgery, caring for the patient during surgery, and aiding the patient’s recovery after surgery. To perform these functions effectively, first know the reason the patient is undergoing surgery and any comorbidities. Second, identify the individual patient’s response to the stress of surgery. Third, know the results of preoperative diagnostic tests. Last, identify potential risks and complications associated with the surgical procedure and any special considerations that should be addressed in the plan of care. The nurse caring for the patient before surgery is likely to be different from the nurse in the operating room

(OR), postanesthesia care unit (PACU), surgical intensive care unit (SICU), or surgical unit. Communication and documentation of important preoperative assessment findings are essential for quality care.

Patient Interview One of the most important nursing actions is the preoperative interview. The nurse who works in the physician’s office, ambulatory surgery center, or hospital may do the interview. The preoperative interview can occur in advance or on the day of surgery. The primary purposes of the patient interview are to (1) obtain the patient’s health information, including drug and food allergies; (2) provide and clarify information about the planned surgery, including anesthesia; and (3) assess the patient’s emotional state and readiness for surgery, including his or her expectations about the surgical outcomes. The interview gives the patient and caregiver an opportunity to ask questions about the surgery, anesthesia, and postoperative care. Often patients ask about taking their routine drugs, such as insulin, anticoagulants, or heart medications, and if they will have pain. By being aware of the patient’s and caregiver’s needs, you can provide the information and support needed during the perioperative period.

Nursing Assessment of Preoperative Patient The overall goal of the preoperative assessment is to identify risk factors and plan care to ensure patient safety throughout the surgical experience. To achieve this, you will need to do the following: • Establish baseline data for comparison in the intraoperative and postoperative period. • Determine the patient’s psychologic status to reinforce the use

of coping strategies during the surgical experience. • Determine physiologic factors directly or indirectly related to the surgical procedure that may contribute to operative risk factors. • Participate in the identification and documentation of the surgical site according to agency protocol. • Identify prescription drugs, over-the-counter (OTC) drugs, and herbs taken by the patient that may result in drug interactions affecting the surgical outcome. • Review the results of all preoperative diagnostic studies in the patient’s record and share this information with the appropriate HCPs. • Identify cultural and ethnic factors that may affect the surgical experience. • Determine if the patient received adequate information from the surgeon to make an informed decision to have surgery and that the consent form is signed and witnessed.

Subjective Data Psychosocial Assessment Surgery is a stressful event, even when the procedure is minor. The psychologic and physiologic reactions to surgery may elicit the stress response (e.g., elevated BP and heart rate). The stress response enables the body to meet the demands in the perioperative period. If stressors or the responses to the stressors are excessive, the stress response can be magnified and may affect recovery. Many factors influence the patient’s reaction to stress, including age, past experiences with illness and pain, current health, and socioeconomic status. The use of common language and avoidance of medical jargon are essential. Use words and language that are familiar to the patient to help the patient understand the surgery. Familiar language also helps reduce anxiety. Your role in psychologically preparing the patient for surgery is to assess the patient for potential or actual stressors that could negatively

affect surgery (Table 17.2). Communicate all concerns to the appropriate surgical team member, especially if the concern requires intervention later in the surgical experience. Because many patients are admitted directly into the preoperative area from their homes, you must be skilled in assessing important psychologic factors in a short time. The most common psychologic factors are anxiety, fear, and hope.

TABLE 17.2 Psychosocial Assessment of

Preoperative Patient

Situational Changes • Define current degree of personal control, decision making, and independence • Determine the presence of hope and anticipation of positive results • Consider the impact of surgery and hospitalization and possible effects on lifestyle • Identify support systems, including family, other caregivers, and religious and spiritual groups

Concerns With the Unknown • Identify degree of anxiety and fears related to the surgery (e.g., pain) • Identify expectations of surgery, changes in current health status, effects on daily living, and sexual activity (if appropriate)

Concerns With Body Image • Identify current roles or relationships and view of self

• Determine perceived or potential changes in roles or relationships and their impact on body image

Past Experiences • Review previous surgical experiences, hospitalizations, and treatments • Determine responses to those experiences (positive and/or negative) • Identify current perceptions of surgical procedure in relation to the above and information from others (e.g., a friend’s view of a personal surgical experience)

Lack of Knowledge • Determine the amount and type of information the patient wants • Assess understanding of surgical procedure, including preparation, care, interventions, preoperative activities, restrictions, and expected outcomes • Review the accuracy of information the patient has received from others, including health care team, family, friends, and media

Anxiety Most people are anxious when facing surgery because of the unknown. This is normal and is an inborn survival mechanism. However, a high anxiety level can impair cognition, decision making, and coping abilities. Anxiety can arise from lack of knowledge. This can range from not knowing what to expect to uncertainty about the outcome and may result from past experiences or stories heard through friends or the media. You can decrease some anxiety for the patient by giving information about what to expect. This is often done through classes or Web-based or audiovisual teaching materials before surgery.

Inform the surgeon if the patient needs more information or has excessive anxiety. Patients may have anxiety when surgery conflicts with their religious or cultural beliefs. Identify, record, and communicate patient decisions about the possibility of blood transfusions. For example, Jehovah’s Witnesses may choose to refuse blood or blood products.1

Common Fears Patients fear surgery for many reasons. The most common fear is the risk for death or permanent disability resulting from surgery. Sometimes the fear comes after hearing or reading about the risks during the informed consent process. Other fears are related to pain, change in body image, or results of diagnostic procedures.

Evidence-Based Practice Music and Preoperative Anxiety You are taking care of D.G., a 67-yr-old woman scheduled for a renal mass biopsy to rule out metastatic disease. She was admitted early this morning to the preoperative unit. Unfortunately, an emergency surgery has resulted in at least a 4-hour delay of her procedure. You note that she has a high level of anxiety.

Making Clinical Decisions Best Available Evidence. Complementary and alternative therapies include a variety of interventions, such as mental imagery, aromatherapy, acupuncture, and music. Music intervention in the preoperative period, including listening to pre-recorded music or individually tailored music given by a trained therapist, can help reduce anxiety. While sedatives and antianxiety drugs are often given before surgery, these drugs can have negative side effects, especially in the older adult. Clinician Expertise. Anxiety can increase BP and pulse rate and

may lengthen postoperative recovery. Excessive anxiety can even result in surgery being canceled. Patient Preference and Values. D.G. tells you that she cannot relax and would like “a strong pill” to help her calm down. D.G.’s family mentioned to you earlier that she enjoys listening to classical music at home.

Implications for Practice 1. What information would you share with D.G. related to the use of drugs to reduce her anxiety? 2. How would you respond to D.G. when she asks how music could possibly help in reducing her anxiety?

Reference for Evidence Bradt J, Dileo C, Shim M. Music interventions for preoperative anxiety. Cochrane Database Syst Rev. 2013;6:CD006908 (Classic). Fear of death can be extremely harmful. Notify the HCP if the patient has a strong fear of death. A patient’s strong fear of impending death may prompt the HCP to delay the surgery because the emotional state influences the stress response and thus the surgical outcome. Fear of pain and discomfort during and after surgery is common. If the fear is extreme, notify the ACP or the surgeon. Reassure the patient that drugs are available for anesthesia and analgesia during surgery. For pain after surgery, tell patients to ask for pain medication before pain becomes severe. Teach the patient how to use a pain intensity scale (e.g., 0 to 10, FACES). See Chapter 8 for more on pain scales. The patient may receive drugs that provide an amnesic effect so that the patient will not remember what occurs during surgery. Tell the patient that helps decrease anxiety after surgery. Fear of mutilation or an altered body image can occur whether the surgery is radical, such as amputation, or minor, such as a breast

biopsy. Even a small scar on the body can upset some, and others fear keloid development (overgrowth of a scar). Listen to and assess the patient’s concern about this fear with an accepting attitude. Fear of anesthesia may arise from the unknown, personal experience, or tales of others’ bad experiences. These concerns can also result from information about the risks of anesthesia (e.g., brain damage, paralysis). Many patients fear losing control while under anesthesia. If you identify any of these fears, inform the ACP at once so that he or she can talk further with the patient. Fear of disruption of life functioning may be present in varying degrees. It can range from fear of permanent disability to concern about not being able to engage in activities of daily living for a few weeks. You may find concerns about loss of role function, separation from family, and how the family will manage. Financial concerns include dealing with an expected loss of income and the costs of surgery. If you find any of these fears, a consult with the patient’s caregiver, a social worker, a spiritual advisor, or a psychologist may be appropriate. Financial advisors at the hospital may be able to give information about financial support.

Check Your Practice Your 19-yr-old male patient is in the holding area. He is scheduled for an orchiectomy for testicular cancer. He is visibly sweating and agitated. When you ask him how he is doing, he responds, “I am scared. Wouldn’t you be?” • What can you do to reduce his fear?

Hope Although many psychologic factors related to surgery seem to be negative, hope is a positive attribute. Hope may be the patient’s strongest method of coping. To deny or minimize hope may negate

the positive mental attitude necessary for a quick and full recovery. Some patients hopefully anticipate surgery. These can be the surgeries that repair (e.g., plastic surgery for burn scars), rebuild (e.g., total joint replacement to reduce pain and improve function), or save and extend life (e.g., repair of aneurysm, organ transplant). Assess and support the presence of hope and the patient’s anticipation of positive results.

Past Health History Ask the patient about any previous health problems and surgeries. Determine if the patient understands the need for surgery. For example, the patient scheduled for a total knee replacement may say that increasing pain and immobility are the reasons for the surgery. Record the reason for any past hospitalizations, including previous surgeries and the dates. Identify any problems with previous surgeries. For example, the patient may have had a wound infection or a reaction to a drug. Ask women about their menstrual and obstetric history. This includes the date of their last menstrual period, the number of pregnancies, and any history of cesarean section. When obtaining a family health history, ask the patient and caregiver about any inherited traits, since they may contribute to the surgical outcome. Record any family history of heart and endocrine diseases. For example, if a patient reports a parent with hypertension, sudden cardiac death, or myocardial infarction, this should alert you to the possibility that the patient may have a similar predisposition or condition. Obtain information about the patient’s family history of adverse reactions to or problems with anesthesia. For example, malignant hyperthermia has a genetic predisposition. If present, measures will be taken to decrease complications associated with this condition (see Chapter 18).

Medications Document all current medication use, including OTC drugs and herbs. Many surgery centers ask patients to bring their medications with them when reporting for surgery. This helps to accurately assess

and document the name and dosage of medications. The interaction of the patient’s current drugs and anesthetics can increase or decrease the desired physiologic effect of anesthetics. Consider the effects of opioids and prescribed drugs for chronic health conditions (e.g., heart disease, hypertension, depression, seizure disorder, diabetes). For example, certain antidepressants can potentiate the effect of opioid agents used for anesthesia or pain control. Antihypertensive drugs may predispose the patient to shock from the combined effect of the drug and the vasodilator effect of some anesthetic agents. Insulin or oral hypoglycemic drugs may need adjustments during the perioperative period because of increased body metabolism, decreased oral intake, stress, and anesthesia. Antiplatelet drugs (e.g., aspirin, clopidogrel [Plavix]) and nonsteroidal antiinflammatory drugs (NSAIDs) inhibit platelet aggregation and may contribute to postoperative bleeding. HCPs may have patients withhold medications before surgery. Specific timeframes for withholding medications depend on the medication and the patient. Patients on long-term anticoagulation therapy (e.g., warfarin [Coumadin], rivaroxaban [Xarelto], dabigatran [Pradaxa], apixaban [Eliquis]) present a unique challenge. The options for these patients include (1) continuing therapy, (2) withholding therapy for a time before and after surgery, or (3) withholding the therapy and starting subcutaneous or IV heparin therapy during the perioperative period. The management strategy selected is based on the patient history and the nature of the surgery.2 Ask about the use of herbs and dietary supplements because their use is so common. Many patients do not think to include supplements in their list of medications. They believe that herbal and dietary supplements are “natural” and do not pose a surgical risk.3 Excess use of vitamins and herbs can cause harmful effects in patients undergoing surgery. In those taking anticoagulants or antiplatelets, herbal supplements can produce excess postoperative bleeding that may require a return to the OR.3 The Complementary & Alternative Therapies box lists the effects of specific herbs that are of concern during the perioperative period.

Complementary & Alternative Therapies Herbal Products and Surgery Use the following as a guide for patient teaching: • Notify your HCP of all vitamins, herbs, and dietary supplements that you are taking. • Avoid astragalus and ginseng, since they can increase BP before and during surgery. • Avoid garlic, vitamin E, ginkgo, and fish oils because they can increase bleeding. • Avoid kava and valerian because they can cause excessive sedation. • In general, stop taking all herbs 2 to 3 weeks before any surgical procedure. Consult your HCP for specific instructions. • Take multivitamins until the day before surgery. Taking them on the day of surgery on an empty stomach may contribute to nausea and vomiting after surgery. Ask the patient about any substance use. The most likely used substances include tobacco, alcohol, opioids, marijuana, cocaine, and amphetamines. Ask questions about use in a frank manner. Stress that substance use may affect the type and amount of anesthesia the patient will need. When patients become aware of the potential interactions of these substances with anesthetics, most patients respond honestly about using them. Chronic alcohol use can place the patient at risk because of lung, GI, or liver damage. Decreased liver function prolongs the metabolism of anesthetic agents, alters nutritional status, and increases the potential for postoperative complications. Alcohol withdrawal can occur during lengthy surgery or in the postoperative period. Proper planning and management are needed to avoid this life-threatening event (see Chapter 10).

Record and share all findings of the drug history with the perioperative health care team. The ACP will decide the best schedule and dose of the patient’s routine drugs before and after surgery. Ensure that you identify all the patient’s drugs, implement any changes in the medication plan, and monitor the patient for potential interactions and complications.

Allergies Ask the patient about drug intolerances and drug allergies. Drug intolerance usually results in side effects that are unpleasant for the patient but are not life threatening. These effects can include nausea, constipation, diarrhea, or idiosyncratic (opposite than expected) reactions. A true drug allergy produces hives and/or an anaphylactic reaction, causing cardiopulmonary compromise (e.g., hypotension, tachycardia, bronchospasm). Being aware of drug intolerances and drug allergies helps the health care team maintain patient comfort and safety. Record all drug intolerances and allergies and, if needed, place an allergy identification band on the patient on the day of surgery.

Safety Alert Allergies • Some local anesthetic agents contain bisulfite preservatives. • Notify the ACP if the patient reports an allergy to sulfurcontaining drugs. Ask about nondrug allergies, specifically food and environmental (e.g., latex, pollen, animals) allergies. The patient with a history of any allergic reactions has a greater potential for hypersensitivity reactions to drugs given during anesthesia. Screen all patients for latex allergies by gathering data about:

• Risk factors • Contact dermatitis • Contact urticaria (e.g., hives) • Aerosol reactions • History of reactions that suggest an allergy to latex Risk factors for latex allergy include long-term, multiple exposures to latex products, such as those experienced by health care and rubber industry workers. Other risk factors include a history of hay fever, asthma, and allergies to certain foods (e.g., eggs, avocados, bananas, chestnuts, potatoes, peaches).4 Latex allergies are discussed in Chapter 13.

Review of Systems The last part of the patient history is the body systems review. Ask specific questions to confirm the presence or absence of any diseases. Current health problems can alert you to areas that you will need to examine in the preoperative physical examination. The combined review of systems and patient history provide essential data to determine the specific preoperative tests that the patient needs.

Cardiovascular System Evaluate cardiovascular (CV) function to determine preexisting disease or problems (e.g., coronary artery disease, prosthetic heart valve). In reviewing the CV system, you may find a history of hypertension, angina, dysrhythmias, heart failure, or myocardial infarction (MI). Ask about the patient’s current treatment for any CV condition (e.g., drugs) and the level of functioning. A cardiology consult is often needed before surgery if the patient has a significant CV history (e.g., recent MI, valvular heart disease, implantable cardioverter-defibrillator). If indicated, the patient should have a 12-lead electrocardiogram (ECG) and coagulation studies and the results should be on the chart before surgery. The CV assessment provides data on what other

measures the patient needs. For example, the patient who is on diuretic therapy needs to have a serum potassium level drawn before surgery. If the patient has hypertension, the ACP may give vasoactive drugs to maintain adequate BP during surgery. The patient with a prosthetic heart valve may receive antibiotic prophylaxis before surgery to decrease the risk for infective endocarditis (see Chapter 36). Venous thromboembolism (VTE), a condition that includes deep vein thrombosis and pulmonary embolism, is a concern for any surgical patient. Patients at high risk for VTE include those with a history of previous thrombosis, blood-clotting disorders, cancer, varicosities, obesity, tobacco use, heart failure, or chronic obstructive pulmonary disease (COPD).5 People are also at risk for developing a VTE because of immobility and positioning during the operative procedure. Intermittent pneumatic compression devices (IPCs) may be applied in the preoperative holding area.

Respiratory System Ask the patient about any recent or chronic respiratory disease or infections. Elective surgery may be postponed if the person has an upper respiratory tract infection. Upper airway infections may increase the risk for bronchospasm, laryngospasm, decreased O2 saturation, and problems with respiratory secretions. Report a patient’s history of dyspnea at rest or with exertion, coughing (dry or productive), or hemoptysis (coughing blood) to the ACP and surgeon. If a patient has a history of asthma, ask about the use of inhaled or oral corticosteroids and bronchodilators, as well as the frequency and triggers of asthma attacks. The patient with a history of COPD is at high risk for pulmonary complications, including hypoxemia and atelectasis. Gather information about the patient’s tobacco use. The HCP and you should encourage the patient to stop smoking at least 6 weeks before surgery. Smoking increases the risk for pulmonary complications during and after surgery. Report conditions likely to affect respiratory function such as sleep apnea, obesity, and spinal, chest, and airway deformities. For example, patients are often asked to

bring their sleep apnea devices with them to the hospital or surgical center. Depending on the patient’s history and physical examination, baseline pulmonary function tests and arterial blood gases may be done before surgery.

Neurologic System Evaluation of neurologic functioning includes assessing the patient’s ability to respond to questions, follow commands, and maintain orderly thought patterns. Changes in the patient’s hearing and vision may affect responses and the ability to follow directions throughout the perioperative assessment and evaluation. Record the patient’s ability to pay attention, concentrate, and respond appropriately to establish a baseline for postoperative comparison. If you note deficits in cognitive function, determine the extent of the problems and whether they can be corrected before surgery. If the problems cannot be corrected, it is important to involve a legal guardian or person with durable power of attorney for health care to aid the patient and provide informed consent for surgery. Preoperative assessment of the older person’s baseline cognitive function is especially crucial for comparison during and after surgery. The older adult may have intact mental abilities before surgery but is more prone to adverse outcomes during and after surgery than the younger adult. This is due to the added stressors of the surgical procedure, dehydration, hypothermia, and anesthesia and adjunctive drugs. These factors may contribute to the development of emergence delirium, a condition that may be falsely labeled as senility or dementia. In the review of the neurologic system, obtain about any history of strokes, transient ischemic attacks, or spinal cord injury. Ask about neurologic diseases, such as myasthenia gravis, Parkinson’s disease, and multiple sclerosis, and any treatments used.

Genitourinary System Assess for a history of renal or urinary tract diseases, such as chronic kidney disease or repeated urinary tract infections. Record the present

disease state and current treatment. Renal dysfunction is associated with several problems, including fluid and electrolyte imbalances, coagulopathies, increased risk for infection, and impaired wound healing. Because the kidneys metabolize and excrete many drugs, a decrease in renal function can lead to an altered response to drugs and unpredictable drug elimination. Renal function tests (e.g., serum creatinine, blood urea nitrogen [BUN]) are often done before surgery. Record and share with the perioperative team if the patient has problems voiding (e.g., incontinence, hesitancy). Older male patients may have an enlarged prostate that can interfere with the insertion of a bladder catheter or impair voiding after surgery. For a woman of childbearing age, determine if she is pregnant or thinks she could be pregnant. Most agencies perform a pregnancy test for all women of childbearing age before surgery.6 Immediately tell the surgeon if the patient states that she may be pregnant. Maternal and fetal exposure to anesthetics should be avoided during the first trimester.

Hepatic System The liver is involved in glucose homeostasis, fat metabolism, protein synthesis, drug and hormone metabolism, and bilirubin formation and excretion. The liver detoxifies many anesthetics and adjunctive drugs. The patient with hepatic dysfunction may have an increased perioperative risk for clotting abnormalities and adverse responses to drugs. Consider the presence of liver disease if there is a history of jaundice, hepatitis, alcohol abuse, or obesity.

Integumentary System Ask about a history of skin problems. Assess the current condition of the skin, especially at the incision site, for rashes, breakdown, or other skin conditions. A patient with a history of pressure injuries may need extra padding during surgery. Skin problems can affect wound healing. Body art such as tattoos and piercings are increasingly common. When possible, select pigment-free areas for injections, IV sites, and

laboratory draws.

Musculoskeletal System Note any musculoskeletal and mobility problems, especially in the older adult. If the patient has arthritis, identify all affected joints. Mobility restrictions may influence intraoperative and postoperative positioning and ambulation. Spinal anesthesia may be difficult if the patient cannot flex the lumbar spine enough to allow easy needle insertion. If the neck is affected, intubation and airway management may be difficult. Any mobility aids (e.g., cane, walker) should be with the patient on the day of surgery.

Endocrine System The patient with diabetes is especially at risk for adverse effects of anesthesia and surgery. Hypoglycemia, hyperglycemia, delayed wound healing, and infection are common complications of diabetes during the perioperative period. Clarify with the surgeon or ACP whether the patient should take the usual dose of insulin or oral hypoglycemic agents on the day of surgery. ACPs may vary the usual insulin dose based on the patient’s status and history of glucose control. Measure serum or capillary glucose levels the morning of surgery to establish baseline levels. Assess the patient’s glucose levels regularly and, if necessary, manage according to agency protocol. Determine if the patient has a history of thyroid dysfunction. Hyperthyroidism or hypothyroidism can place the patient at surgical risk because of changes in metabolic rate. If the patient takes a thyroid replacement drug, check with the ACP about administering the drug on the day of surgery. If the patient has a history of thyroid dysfunction, laboratory tests may be done to determine current levels of thyroid function. The patient with Addison’s disease needs special consideration during surgery. Addisonian crisis or shock can occur if a patient abruptly stops taking replacement corticosteroids. The patient may need additional IV corticosteroid therapy from the stress of surgery7 (see Chapter 49).

Immune System Note if the patient has a history of a compromised immune system or takes immunosuppressive drugs. Corticosteroids used in immunosuppressive doses may be tapered before surgery. Impairment of the immune system can lead to delayed wound healing and increased risk for infections.8 Elective surgery may be cancelled if the patient has an acute infection (e.g., sinusitis, influenza). Patients with active chronic infections such as hepatitis B or C, acquired immunodeficiency syndrome, or tuberculosis may have surgery if needed. However, when preparing the patient for surgery, remember to take infection control precautions for the protection of the patient and staff. Infection control guidelines are discussed in Chapter 14.

Fluid and Electrolyte Status Ask the patient about any recent conditions that increase the risk for fluid and electrolyte imbalances, such as vomiting, diarrhea, or completing a bowel prep. Identify drugs that change fluid and electrolyte status, such as diuretics. Serum electrolyte levels are often assessed before surgery. Many patients may have restricted fluids for a specific period of time before surgery. They could develop dehydration if surgery is delayed. A patient with or at risk for dehydration may need more fluids and electrolytes before or during surgery. Complete a preoperative fluid balance history for all patients. This is especially critical for older adults. Their reduced adaptive capacity leaves a narrow margin of safety between overhydration and underhydration.

Nutritional Status Nutritional problems include overnutrition and undernutrition, both of which need considerable time to correct. However, knowing that a patient has a nutritional problem can help the health care team provide more customized care. For example, if the patient is thin, place more padding than usual on the OR table. Notify the team if a

patient is severely obese (body mass index [BMI] greater than 40 kg/m2) to allow time to obtain special equipment needed for the patient’s care (e.g., longer instruments for abdominal surgery). Obesity stresses the heart and lung systems and makes access to the surgical site and anesthesia administration more difficult.9 It predisposes the patient to wound dehiscence, wound infection, and incisional herniation after surgery. Adipose tissue is less vascular than other types of tissue. The patient may be slower to recover from anesthesia because adipose tissue absorbs and stores inhalation agents, so they leave the body more slowly. See Chapter 40 for the special needs of obese patients undergoing surgery. Nutritional problems impair the ability to recover from surgery. Remember that the obese patient or the very thin patient can be protein and vitamin deficient. If the problem is severe, surgery may be postponed. Protein and vitamins A, C, and B complex deficiencies are particularly important because these substances are essential for wound healing.10 Patients who are malnourished may receive supplemental nutrition during the perioperative period. The older adult is often at risk for malnutrition and fluid volume deficits.

TABLE 17.3 American Society of

Anesthesiologists’ (ASA) Physical Classification System Rating P1 (ASA I)

Definition Normal healthy person

P2 (ASA II)

Patient with mild systemic disease

P3 (ASA III)

Patient with severe systemic disease

P4 (ASA IV)

Patient with severe systemic disease that is a constant threat to life

P5 (ASA V)

Moribund patient who is not expected to survive without surgery

P6 (ASA VI)

Declared brain-dead patient whose organs are being removed for donor purposes

Source: American Society of Anesthesiologists: ASA physical status classification system, 2014. Retrieved from www.asahq.org/resources/clinical-information/asa-physical-statusclassification-system. Identify patients who consume large quantities of coffee or caffeinated soft drinks. In many cases, withholding caffeinated beverages before surgery or for some time after surgery can lead to severe withdrawal headaches.11 These headaches can be confused with spinal headaches if the preoperative data are not recorded. Giving caffeinated beverages after surgery, when possible, may prevent these headaches.

Objective Data Physical Examination The Joint Commission requires that all patients admitted to the OR have a documented history and physical examination (H&P) in their chart.12 This may be done in advance of surgery or on the day of surgery. Any qualified HCP, including advanced practice nurses, physicians, physician assistants, or ACPs, may perform the H&P. Findings from the H&P enable the ACP to assign the patient a physical status rating for anesthesia administration (Table 17.3). This rating is an indicator of the patient’s perioperative risk and may influence perioperative decisions. It uses a scale of P1 to P6. A rating of P6 is reserved for a brain-dead patient undergoing organ procurement. Patients undergoing surgery in ambulatory or outpatient settings generally have ratings of P1, P2, or P3. Other designations can be added to the ASA status (e.g., “E” to designate an “emergent” procedure). Complete a physical examination of the patient before surgery (Table 17.4). Review the documentation already present in the patient’s chart, including the H&P, to better proceed with your examination. Record all findings and share any relevant findings at once with the surgeon or ACP.

TABLE 17.4 Health Assessment and Physical

Examination of Preoperative Patient∗

Cardiovascular System • Identify acute or chronic problems. Note presence of angina, hypertension, heart failure, recent myocardial infarction. • Identify any drugs (e.g., aspirin) or herbs (e.g., ginkgo) that may affect coagulation. • Identify patients with prosthetic heart valves, pacemakers, or implantable cardioverter-defibrillators. • Assess for edema (including dependent areas), noting location and severity. • Inspect neck veins for distention. • Obtain bilateral baseline BPs. • Assess capillary refill and pulses for rate, rhythm, and quality: apical, radial, and pedal.

Gastrointestinal System • Determine patterns of food and fluid intake and any recent changes in weight. • Review usual pattern of bowel movements, including date of last bowel movement. • Assess for presence of dentures and bridges (loose dentures or teeth may be dislodged during intubation). • Weigh patient. • Auscultate abdomen for presence of bowel sounds.

Genitourinary System

• Identify any infection or preexisting disease. • Determine ability to void. • Note color, amount, and characteristics of urine. • Determine pregnancy status (if appropriate).

Hepatic System • Review any substance use, especially alcohol and IV drug use. • Inspect skin color and sclera of eyes for any signs of jaundice.

Immune System • Note any immunodeficiency or autoimmune disorders. • Assess for use of corticosteroids or other immunosuppressant drugs.

Integumentary System • Determine skin status. Note any current or previous skin problems (e.g., pressure injuries, eczema, bruising). • Inspect skin for rashes, boils, or infection, especially around the planned surgical site. • Inspect mucous membranes and skin turgor for signs of dehydration. • Assess skin moisture and temperature.

Musculoskeletal System • Examine skin around bone pressure points. • Assess for limitations in joint range of motion and muscle strength.

• Assess for joint or muscle pain. • Assess mobility, gait, and balance.

Neurologic System • Determine orientation to person, place, and time. • Assess baseline mental status. Note any confusion, disorderly thinking, or inability to follow commands. • Identify any history of strokes, transient ischemic attacks, or neurologic diseases (e.g., Parkinson’s disease, multiple sclerosis).

Respiratory System • Identify acute or chronic problems. Note presence of infection, chronic obstructive pulmonary disease, or asthma. • Note use of continuous positive airway pressure (CPAP) machine. • Assess tobacco history, including date/time of last cigarette and number of pack-years. • Determine baseline O2 saturation and respiratory rate and rhythm. • Observe for cough, dyspnea, and use of accessory muscles of respiration. • Auscultate lungs for normal and adventitious breath sounds.



See specific body system chapters for more detailed assessments and related laboratory studies.

TABLE 17.5 Common Preoperative Diagnostic

Studies Test ABGs, pulse oximetry

Assessment Respiratory and metabolic function, oxygenation status

Blood glucose

Metabolic status, diabetes

Blood urea nitrogen, creatinine

Renal function

Chest x-ray

Lung disorders, cardiac enlargement, heart failure

CBC: RBCs, Hgb, Hct, WBCs

Anemia, immune status, infection

Electrocardiogram

Heart disease, dysrhythmias

Electrolytes

Metabolic status, renal function, diuretic side effects

hCG

Pregnancy status

Liver function tests

Liver status

PT, PTT, INR, platelet count

Coagulation status

Pulmonary function studies

Pulmonary status

Serum albumin

Nutritional status

Type and crossmatch

Blood available for replacement (elective surgery patients may have own blood available) Renal status, hydration, urinary tract infection

Urinalysis

CBC, Complete blood count; hCG, human chorionic gonadotropin; Hct, hematocrit; Hgb, hemoglobin; INR, international normalized ratio; PT, prothrombin time; PTT, partial thromboplastin time.

Diagnostic Studies Obtain and assess the results of diagnostic studies ordered before surgery (Table 17.5). For example, a patient taking an antiplatelet drug (e.g., aspirin) may have a coagulation profile done or a patient on diuretic therapy may have a potassium level checked. A woman of childbearing age may receive a pregnancy test. An ECG is done for many who take drugs for dysrhythmias or have high blood pressure. Patients with diabetes undergo blood glucose monitoring. In many settings, patients are tested for methicillin-resistant Staphylococcus

aureus. Those with positive results are prescribed antibiotics for several days before surgery.13 Ideally, preoperative tests are ordered based on the patient’s H&P. However, many agencies and insurers have protocols for preoperative tests, which may not include all those in Table 17.5. In addition, some tests may be done days before surgery. Ensure that all laboratory and diagnostic reports are in the patient’s chart. Missing reports may result in a delay or cancellation of the surgery.

Nursing Management: Preoperative Patient Base the preoperative nursing interventions on the nursing assessment, depending on the patient’s specific needs. The pending surgery and routines of the surgery setting guide the patient’s physical preparation. Preoperative teaching may be minimal or extensive. The Association of periOperative Registered Nurses (AORN) provides standards and recommended practices to guide nursing interventions in all perioperative settings.5

Preoperative Teaching The patient has a right to know what to expect and how to take part effectively during the surgical experience. Preoperative teaching increases patient satisfaction and can reduce postoperative fear, anxiety, and stress.14 Teaching may decrease the development of complications, length of hospitalization, and recovery time after discharge. In most surgical settings, patients often arrive only a short time before their surgery. Preoperative teaching for these patients generally occurs in the surgeon’s office or a preadmission surgical clinic and is reinforced on the day of surgery. After ambulatory surgery, the patient usually goes home several hours after recovery, depending on the patient’s progress and procedure-specific needs. Teaching must

include information that focuses on the patient’s safety. Give written materials for patients and caregivers to use for review and reinforcement at home. Discharge teaching is required for all patients (see Chapter 19). When delivering teaching, find a balance between explaining so much that the patient is overwhelmed and telling so little that the patient is unprepared. If you observe and listen carefully to the patient, you can usually figure out how much information is enough. Remember that anxiety and fear may limit learning ability. Assess what the patient wants to know and give priority to those concerns. Generally, preoperative teaching includes 3 types of information: sensory, process, and procedural. Different patients, with varying cultures, backgrounds, and experience, may want different types of information. See Table 4.6 for factors affecting patient teaching. With sensory information, patients find out what they will see, hear, smell, and feel during the surgery. For example, you may tell them that the OR will be cold, but they can ask for a warm blanket; the lights in the OR are bright; or many unfamiliar sounds and specific smells will be present. Patients wanting process information may not want specific details but just the general flow of what is going to happen. This information would include the patient’s transfer to the holding area, visits by the nurse and the ACP before transfer to the OR, and waking up in the PACU. With procedural information, patients desire details that are more specific. For example, this information would include saying an IV line will be started while the patient is in the holding area and the surgeon will mark the operative area with an indelible marker to verify the surgical site.5 Share the preoperative teaching given to the patient with the nurses providing postoperative care to evaluate learning and avoid duplication of teaching. Because there is limited time for teaching, a team approach is often used. For example, teaching may start in the outpatient setting. Your responsibility is to assess the patient’s understanding of this teaching and fill in the gaps at this point in the

surgical process. Record all teaching in the patient’s chart. A guide for preoperative patient and caregiver teaching is outlined in Table 17.6. See Chapter 4 for more on patient and caregiver teaching.

General Surgery Information Unless it is contraindicated (e.g., after craniotomy, tonsillectomy), all patients should receive instruction about deep breathing, coughing, and early ambulation postoperatively. This is essential because patients may not want to do these activities after surgery unless they know the reason for them and practice them before surgery. Tell patients and caregivers if tubes, drains, monitoring devices, or special equipment will be used after surgery. Explain that these devices help you to safely care for the patient. Examples of specific teaching may include how to use incentive spirometers or patient-controlled analgesia pumps. Patients should have a clear understanding of how to rate their pain and how their pain will be managed10 (see Chapter 8).

TABLE 17.6 Patient & Caregiver

TeachingPreoperative Preparation Include the following information in the preoperative teaching plan for the patient and caregiver.

Sensory Information • Preoperative holding area may be noisy • Drugs and cleaning solutions may be odorous • Operating room (OR) can be cold. Forced air warming devices may be used. Warm blankets are available • Talking may be heard but may be distorted because of masks. Ask questions if something is not understood • OR bed will be narrow. A safety strap will be applied over the

thighs • Lights in the OR may be bright • Monitoring machines may be heard (e.g., beeping noises) when awake

Procedural Information • What to bring and what type of clothing to wear to the surgery center • Any changes in time of surgery • Fluid and food restrictions • Physical preparation needed (e.g., shower, bowel, or skin preparation) • Purpose of frequent vital signs assessment • Pain control and other comfort measures • Why turning, deep breathing, and coughing after surgery are important. Do practice sessions • Insertion of IV lines • Procedure for anesthesia administration • Surgical site may be marked with indelible ink or marker

Process Information Information About General Flow of Surgery • Admission area • Preoperative holding area, OR, and postanesthesia care unit (PACU) • Caregivers can usually stay in preoperative holding area until surgery • Caregivers will be able to see patient after discharge from the PACU or possibly in PACU once the patient is awake

• Identification of any technology that may be present on awakening, such as monitors, central lines, intermittent pneumatic compression devices

Where Caregivers Can Wait During Surgery • Encourage caregivers to ask questions and express any concerns • OR staff will update caregivers during surgery and when surgery is over • Surgeon will usually talk with caregivers after surgery The patient should also receive surgery-specific information. For example, a patient having a total joint replacement may have an immobilizer after surgery. Tell a patient having open heart surgery about waking up in the intensive care unit.

Ambulatory Surgery Information The ambulatory surgery patient or the patient admitted to the hospital the day of surgery needs to receive information before admission. Some ambulatory surgical centers telephone patients several days before the procedure to obtain health information, give instructions, and answer questions. Each center has policies and procedures for communicating this information. In addition to specifics on the procedure, patients need information on day-of-surgery events such as arrival time, registration, parking, what to wear, what to bring, and the need to have a responsible adult present for transportation home after surgery. Traditionally, we tell patients having elective surgery to have nothing by mouth (NPO) starting at midnight on the night before surgery. Evidence-based guidelines for healthy patients of all ages undergoing elective surgery (except women in labor) from the American Society of Anesthesiologists are less strict15 (Table 17.7). Restricting fluids and food is designed to reduce the risk for pulmonary aspiration and nausea and vomiting. Protocols may vary

for patients having local anesthesia or surgery scheduled late in the day. Follow the NPO protocol of each surgical setting. The patient who has not followed the NPO instructions may have surgery delayed or cancelled. It is critical that the patient understands the reason for and follows all restrictions.

TABLE 17.7 Preoperative Fasting

Recommendations

Liquid and Food Intake Clear liquids (e.g., water, clear tea, black coffee, carbonated beverages, fruit juice without pulp)

Minimum Fasting Period (hr) 2

Breast milk

4

Nonhuman milk, including infant formula

6

Light meal (e.g., toast and clear liquids)

6

Regular meal (may include fried or fatty food, meat)

8 or more

Source: Practice guidelines for preoperative fasting and the use of pharmacologic agents to reduce the risk of pulmonary aspiration: Application to healthy patients undergoing elective procedures, Anesthesiology 126:376, 2017.

Legal Preparation for Surgery Legal preparation for surgery consists of checking that all required forms have been correctly signed and are present in the patient’s chart and that the patient and caregiver clearly understand what is going to happen. Standard consent forms include those for the surgical procedure and blood transfusions. Other forms may include advance directives and durable power of attorney for health care (see Chapter 9).

Consent for Surgery

Before nonemergency surgery can be legally performed, the patient must voluntarily sign an informed consent form in the presence of a witness. Informed consent is an active, shared decision-making process between the HCP and recipient of care. Three conditions must be met for consent to be valid. First, there must be adequate disclosure of the (1) diagnosis; (2) nature and purpose of the proposed treatment; (3) risks and consequences of the proposed treatment; (4) probability of a successful outcome; (5) availability, benefits, and risks of alternative treatments; and (6) prognosis if treatment is not instituted. Second, the patient must show a clear understanding of the information before receiving sedating preoperative drugs. If a patient is sedated prior to signing the consent, surgery may be cancelled or delayed. Third, the recipient of care must give consent voluntarily. The patient must not be persuaded or coerced in any way by anyone to undergo the procedure. The surgeon is ultimately responsible for obtaining the patient’s consent for surgical treatment. You may be asked to witness the patient’s signature on the consent form. At this time, you must be a patient advocate, verifying that the patient understands the information in the consent and the implications of consent, and that consent for surgery is truly voluntary. If the patient is unclear about the surgical plans, contact the surgeon about the patient’s need for more information. The patient should be aware that consent, even when signed, can be withdrawn at any time. If the patient is a minor, unconscious, or mentally incompetent to sign the permit, a legally appointed representative or responsible family member may give written permission. An emancipated minor is one who is younger than the legal age of consent but is recognized as having the legal capacity to provide consent.10 Procedures for obtaining consent vary among states and agencies. Follow your state’s nurse practice act and agency policies that apply to a specific situation.

Ethical/Legal Dilemmas Informed Consent

Situation J.S., a 72-yr-old woman, is waiting in the preoperative holding area. You are discussing her impending surgery when you realize that this competent adult does not fully understand her surgery and was not informed of the alternatives to this surgery. Although she has previously signed a consent form, your assessment is that she was not fully informed about her treatment options or does not recall them.

Ethical/Legal Points for Consideration • Informed consent requires that patients have complete information about the proposed treatment, as well as alternative treatments, risks and benefits of each treatment option, and possible consequences of the surgical procedure. The person (usually the surgeon) performing the procedure usually has this responsibility. • An opportunity to have questions answered about the various treatment options and their possible outcomes is a crucial element of informed consent. • A patient can revoke the consent at any time, even at the very last minute. It is essential that you report any circumstance that suggests that the patient does not understand the information or is revoking the informed consent to the person who obtained the consent. • In most states, the registered nurse’s legal role is to witness the signing of the document. This means that as a nurse, you attest to the fact that the patient’s signature was valid.

Discussion Questions 1. What do you think you should do next?

2. What is your role as a patient advocate in the informed consent process? 3. What should you do if the patient states that she does not want to know about the surgical procedure or alternatives to surgery? A true medical emergency may override the need to obtain consent.10 The next of kin may give consent when immediate medical treatment is necessary to preserve life or prevent serious impairment to life or limb and the patient is incapable of giving consent. If reaching the next of kin is not possible, the HCP may begin treatment without written consent. A note in the chart must document the medical necessity of the procedure. In the case of an emergency in which consent cannot be obtained, you will usually need to complete an event report because it is an occurrence that is inconsistent with routine agency practices.

Day-of-Surgery Preparation Nursing Role Day-of-surgery preparation varies a great deal depending on whether the patient is an inpatient or an ambulatory surgical patient. Your responsibilities immediately before surgery include final preoperative teaching, assessment, and communication of pertinent findings. In addition, ensure that all preoperative orders are done and that the chart is complete and goes with the patient to the OR. It is especially important to verify the presence of a signed informed consent form, results of laboratory and diagnostic studies, an H&P, a record of any consultations, baseline vital signs, proper skin preparation, and completed nursing notes. The surgical site is identified and marked with an indelible marker by the surgeon and documented to show that the patient agrees.5

FIG. 17.1 The nurse performs a safety check by verifying that the patient has an identification band (wristband) as part of the preoperative preparations before she goes to surgery. Courtesy Susan R. Volk, RN, MSN, CCRN, CPAN, Staff Development Specialist, Christiana Care Health System, Newark, DE.

Hospitals often require that a patient wear a hospital gown with no underclothes. Surgical centers may allow the patient to wear underwear, depending on the procedure. The patient should remove any cosmetics, since observation of skin color is important. Remove nail polish and artificial nails so you can assess capillary refill and pulse oximetry. Place an identification band on the patient and, if applicable, an allergy band (Fig. 17.1). Return all patient valuables to a

caregiver or secure according to agency policy. All prostheses, including dentures, contact lenses, and glasses, are generally removed to prevent loss or damage. If electrocautery devices will be used during surgery, jewelry in piercings must be removed as a safety measure. Leave hearing aids in place to allow the patient to better follow instructions. Return glasses to the patient as soon as possible after surgery. Encourage the patient to void before you give preoperative drugs and before transfer to the OR. An empty bladder prevents involuntary elimination under anesthesia and reduces the risk for urinary retention during the early postoperative recovery. Many preoperative drugs interfere with balance and increase the risk for a fall during ambulation. Carefully assess each patient for responses to drugs given and adjust the plan of care as needed.

Check Your Practice You are caring for an older female patient who received a dose of alprazolam (Xanax) for preoperative anxiety. One hour later, she requests to use the bathroom. You ask her if she can walk and she replies “yes.” When helping her to stand, she becomes dizzy and almost falls. You return her to bed. • Instead of trying to help this patient ambulate to the bathroom, what should have you done?

TABLE 17.8 Drug TherapyCommonly Used

Preoperative Medications

Preoperative Medications Preoperative medications are used for a variety of reasons (Table 17.8). A patient may receive a single drug or a combination of drugs. Benzodiazepines are used for their sedative and amnesic properties. Anticholinergics are sometimes given to reduce secretions. Opioids may be given to decrease pain and anesthetic requirements during surgery. Antiemetics can decrease nausea and vomiting. Other drugs that may be given before surgery include antibiotics, eyedrops, and routine prescription drugs. Antibiotics may be given throughout the perioperative period for patients with a history of prosthetic heart valve to prevent infective endocarditis and for patients with previous joint replacement. They also may be given when wound contamination is a potential risk (e.g., GI surgery). Antibiotics are most often given IV. We often give a single or first dose within 30 to 60 minutes of the surgical incision.

Informatics in Practice Computer-Based Timing for Antibiotic Administration • A patient who receives the appropriate preoperative antibiotic

has a decreased risk for a health care–associated infection. • Using a computer to time antibiotic administration can decrease the incidence of wound infections. • Computer-based timing systems aid with quality of care by tracking patient outcomes. • You can look at the time patients received antibiotics and compare the rate of wound infections for those who did and did not receive timely treatment. People with known hypertension or coronary artery disease may receive β-adrenergic blockers (β-blockers) to control BP or reduce the chances of MI and cardiac arrest.16 Those with diabetes are carefully monitored and may receive insulin in the preoperative period.10 Eyedrops are often given prior for the patient undergoing cataract and other eye surgery. Many times, the patient will need multiple sets of eyedrops given at 5-minute intervals. It is important to give these drugs as ordered and on time to adequately prepare the eye for surgery. Patients may or may not receive drugs they routinely take on the day of surgery. To aid patient teaching and remove confusion about which drugs patients are taking, carefully check written preoperative orders and clarify the orders with the surgeon and/or ACP if there is any question. Preoperative drugs may be given by mouth (PO), IV, or subcutaneously. Provide PO drugs with a small sip of water 60 to 90 minutes before the patient goes to the OR unless otherwise ordered. Subcutaneous injections (e.g., insulin) and IV drugs are usually given to the patient after arrival in the preoperative holding area. Teach the patient about the expected effects of the drugs (e.g., drowsiness).

Safety Alert Preoperative Checklist

• Use a preoperative checklist (Table 17.9) to make sure you have completed all required preparations. • This is especially important to do before the patient receives any sedating drugs.

Transportation to the Operating Room For inpatients, transport staff move the patient by stretcher to the OR. Help the patient in moving from the bed to the stretcher and raise the side rails. Ensure that the completed chart and any needed equipment goes with the patient. In many agencies, the caregiver may go with the patient to the holding area. In an ambulatory surgical center, the patient may go to the OR by stretcher or wheelchair. If no sedatives have been given, the patient may even walk with someone to the OR. In all cases, it is important to ensure patient safety during transport. Record the method of transportation and the person who transports the patient to the OR. Provide the hand-off communication to the nurse receiving the patient. This allows each of you to ensure you have shared all pertinent information about the patient. To avoid adverse events related to miscommunication, AORN recommends the use of the Situation-Background-Assessment-Recommendation (SBAR) model for the hand-off process in this setting5 (see Table 1.4). Show the caregiver where to wait for the patient during surgery. Many hospitals have a surgical waiting room where OR staff communicate the patient’s status to the caregiver(s) and let them know when the surgery is complete. The surgeon can find the caregiver in this room after surgery to discuss the outcome. Some hospitals give pagers to caregivers so that they may eat or do errands during the surgery.

TABLE 17.9 Preoperative Checklist

Preoperative Data Height _____ Weight _____ Isolation Y or N Type _____ Allergies noted on chart Y or N Vital signs (baseline) T _____ P _____ R _____ BP _____ Pulse Ox _____ Chart Review H&P on chart H&P within 30 days? Y or N Signed and witnessed informed consent form on chart Y or N Signed consent for blood administration Y or NA Blood type and crossmatch Y or NA Diagnostic Results Hgb/Hct _____ /_____ NA PT/INR/PTT _____ /_____ /_____ NA CXR _____ NA ECG _____ NA hCG _____ Negative _____ Positive ______NA Other labs: Final Chart Review Additional forms attached:

Initials

Culturally Competent Care: Preoperative Patient Include cultural considerations when assessing and implementing care for the patient’s preoperative needs. For example, culture often determines one’s expression of pain, family expectations, and ability to verbally express needs. One’s culture may require that the family be included in any decision making. For example, many older Hispanic women may defer to their family for the decision whether to have surgery. Respect these decisions. If the patient or caregiver does not speak English, you must use a qualified interpreter (translates orally) or translator (interprets written text) communication system.17 See more on culturally competent care in Chapter 2.

Gerontologic Considerations: Preoperative Patient Many patients older than 65 years of age undergo surgery. Surgery on older adults requires careful evaluation. Frequently performed procedures in older adults include cataract extraction, coronary and vascular procedures, prostate surgery, cholecystectomy, and joint repair or replacement. Communication is important. The patient’s primary HCP is usually not the surgeon. Often several HCPs are involved in the patient’s care. Be particularly alert when assessing and caring for the older adult surgical patient. An event that has little effect on a younger adult may be overwhelming to the older patient. Hospitalization may represent a physical decline and loss of health, mobility, and independence. The older adult may view the hospital as a place to die or as a steppingstone to a nursing home. Help to decrease anxieties and fears while maintaining the self-esteem of the older adult during the surgical experience. The risks associated with anesthesia and surgery increase in the older patient. In general, the older the patient, the greater are the risks for complications after surgery. In planning care, consider the patient’s physiologic status, not only the chronologic age. The surgical risk in the older adult relates to normal physiologic aging and changes that compromise organ function, reduce reserve capacity, and limit the body’s ability to adapt to stress. This decreased ability to cope with stress, often compounded by the burden of one or more chronic illnesses, and the surgery itself increase the risk for complications. Confirm and document the patient’s goals and treatment preferences. In those with advance directives, discuss any new risks associated with the surgical procedure. Make sure the approach for treating any potential problems is consistent with the patient’s preferences.18 Older adults may have some sensory deficits. Bright lights may bother those with eye problems. They can have reduced vision and hearing. Thought processes and cognitive abilities may be slowed or

impaired. Assess and record baseline sensory and cognitive function. Physical reactions are often slowed because of mobility and balance problems. Because of these changes, the older adult may need more time to complete preoperative testing and understand preoperative instructions. These changes also require you to pay more attention to promote patient safety and prevent injury. When older adults live in a long-term care or assisted living facility, you may need to coordinate transportation from these facilities so that timely arrival allows for surgery preparation. A legal representative of the patient must be present to provide consent for surgery if the patient cannot sign for himself or herself. Finally, determine the presence of or need for caregiver support for the older adult undergoing surgery. With the increase in outpatient surgical procedures and shorter length of stays after surgery, caregiver support is critical in the continuity of care for this population.

Case Study Preoperative Patient

© Ryan McVay/Photodisc/Thinkstock.

Patient Profile F.D., a 72-yr-old Hispanic retired librarian, is admitted to the hospital with compromised circulation of the right lower leg and a necrotic right foot. She has diabetes and takes insulin to maintain appropriate blood glucose levels. She has been NPO since midnight. It is now 10

AM

on the morning of the surgery.

Subjective Data • History of type 2 diabetes for 30 years; states, “My blood sugar is hard to control” and “I just started taking insulin” • History of hypertension and peripheral vascular disease • History of stage 2 chronic kidney disease • History of macular degeneration in right eye; reports poor vision • Surgical history: cesarean section at age 30, cholecystectomy at age 65; reports poor wound healing after last surgery • States her Social Security checks barely cover her living expenses • States she often runs out of her drugs and cannot always afford to refill them right away • Reports chronic burning pain in both legs and has trouble sleeping at night • Lives alone but has family who want her to move in with them after surgery • Uses herbs to control blood glucose levels and often skips her insulin

Objective Data Physical Examination • Alert, cognitively intact, anxious, older woman with numbness and lack of feeling in right leg • Weight 190 lb, height 5 ft 3 in • BP 180/94, pulse 84 and slightly irregular • Wears glasses for close work and reading

Diagnostic Studies

• Admission serum blood glucose level 272 mg/dL (15.2 mmol/L), glycosylated hemoglobin (Hb A1C) 14% • Morning capillary blood glucose level 198 mg/dL (11 mmol/L) • Doppler pulses for right lower leg weak, absent in right foot • Doppler pulses in left lower leg present, weak in left foot • Serum creatinine 2.0 mg/dL (176 mmol/L)

Interprofessional Care • Scheduled for a below-the-knee amputation of the right leg at 1 PM today

Discussion Questions 1. What factors may influence F.D.’s response to hospitalization and surgery? 2. Priority Decision: Given F.D.’s history, what priority preoperative nursing assessments would you want to complete and why? 3. What potential perioperative complications may you expect for F.D.? 4. Priority Decision: What priority topics would you include in F.D.’s preoperative teaching plan? 5. Priority Decision: Based on the assessment data presented, identify the priority nursing diagnoses and related interventions. Are there any collaborative problems? 6. Collaboration: Identify appropriate interventions that could be delegated to unlicensed assistive personnel (UAP). 7. Safety: To ensure F.D.’s safety, what preoperative nursing interventions are essential? 8. Evidence-Based Practice: F.D. asks you why she received insulin this morning when she has not eaten anything since midnight. How would you respond to her?

Answers available at http://evolve.elsevier.com/Lewis/medsurg.

Bridge to NCLEX Examination The number of the question corresponds to the same-numbered outcome at the beginning of the chapter.

1. An overweight patient (BMI 28.1 kg/m2) is scheduled for a laparoscopic cholecystectomy at an outpatient surgery setting. The nurse knows that a. surgery will involve multiple small incisions. b. this setting is not appropriate for this procedure. c. surgery will involve removing a part of the liver. d. the patient will need special preparation because of obesity. 2. The patient tells the nurse in the preoperative setting that she has noticed she has a reaction when wearing rubber gloves. What is the most appropriate action? a. Notify the surgeon so that the surgery can be cancelled. b. Ask additional questions to assess for a possible latex allergy. c. Notify the OR staff at once so they can use latex-free supplies. d. No action is needed because the patient’s rubber sensitivity has no bearing on surgery. 3. A 59-yr-old man scheduled for a herniorrhaphy in 2 days reports that he takes ginkgo daily. What is the priority intervention? a. Inform the surgeon, since the procedure may have to be

rescheduled. b. Notify the anesthesia care provider, since this herb interferes with anesthetics. c. Ask the patient if he has noticed any side effects from taking this herbal supplement. d. Tell the patient to continue to take the herbal supplement up to the day before surgery. 4. A 17-yr-old patient with a leg fracture who is scheduled for surgery is an emancipated minor. She has a statement from the court for verification. Which intervention is most appropriate? a. Witness the permit after the surgeon obtains consent. b. Call a parent or legal guardian to sign the permit since the patient is under 18. c. Notify the hospital attorney that an emancipated minor is consenting for surgery. d. Obtain verbal consent since written consent is not necessary for emancipated minors. 5. A priority nursing intervention to aid a preoperative patient in coping with fear of postoperative pain would be to a. inform the patient that pain medication will be available. b. teach the patient to use guided imagery to help manage pain. c. describe the type of pain expected with the patient’s particular surgery. d. explain the pain management plan, including the use of a pain rating scale.

6. A patient is scheduled for surgery requiring general anesthesia at an ambulatory surgical center. The nurse asks him when he ate last. He replies that he had a light breakfast a couple of hours before coming to the surgery center. What should the nurse do first? a. Tell the patient to come back tomorrow, since he ate a meal. b. Have the patient void before giving any preoperative medications. c. Proceed with the preoperative checklist, including site identification. d. Notify the anesthesia care provider of when and what the patient last ate. 7. A patient who normally takes 40 units of glargine insulin (long acting) at bedtime asks the nurse what to do about her dose the night before surgery. The best response would be to have her a. skip her insulin altogether the night before surgery. b. get instructions from her surgeon or HCP on any insulin adjustments. c. take her usual dose at bedtime and eat a light breakfast in the morning. d. eat a moderate meal before bedtime and then take half her usual insulin dose. 8. Preoperative considerations for older adults include (select all that apply) a. using only large-print educational materials. b. speaking louder for patients with hearing aids.

c. recognizing that sensory deficits may be present. d. providing warm blankets to prevent hypothermia. e. teaching important information early in the morning. 1. a, 2. b, 3. a, 4. a, 5. d, 6. d, 7. b, 8. c, d For rationales to these answers and even more NCLEX review questions, visit http://evolve.elsevier.com/Lewis/medsurg.

Evolve Website/Resources List http://evolve.elsevier.com/Lewis/medsurg

• Review Questions (Online Only) • Key Points • Answer Keys for Review Questions • Rationales for Bridge to NCLEX Examination Questions • Answer Guidelines for Case Study on p. 311 • Conceptual Care Map Creator • Audio Glossary • Content Updates

References 1. Jehovah’s Witnesses: Why don’t Jehovah’s Witnesses accept blood transfusions? Retrieved from www.jw.org/en/jehovahs-witnesses/faq/jehovahswitnesses-why-no-blood-transfusions/. Ebner M, Birschmann I, Peter A, et al: Point-of-care testing for emergency assessment of coagulation in patients treated with direct oral anticoagulants, Critical Care 21:32, 2017.

3. Society of Gastroenterology Nurses and Associates:

Patient safety issues with use of herbal supplements. Retrieved from www.sgna.org/Practice/GI-NurseSedation/Patient-Care-Safety. 4. American College of Allergy, Asthma, and Immunology: Latex allergy. Retrieved from https://acaai.org/allergies/types/latex-allergy. 5. Association of periOperative Registered Nurses: Guidelines for perioperative practice. Denver, 2017, AORN. Bock M, Fritsch G, Hepner D: Preoperative laboratory testing, Anesthesiol Clin 34:43, 2016. Troy HK, Stikkelbroeck NM, Smans LC, et al: Adrenal crisis: Still a deadly event in the 21st century, AJM 129:339, 2016.

8. Wound Care Centers: How diabetes affects wound healing. Retrieved from www.woundcarecenters.org/article/living-withwounds/how-diabetes-affects-wound-healing. Prabhaker A, Helander E, Chopra N, et al: Preoperative assessment for ambulatory surgery, Curr Pain Headache Rep 21:43, 2017.

10. Rotruck JC: Alexander’s care of the patient in surgery, ed 16, St Louis, 2018, Elsevier. Martin VT, Vij B: Diet and headache, Headache 56:1543, 2016.

12. The Joint Commission: History and physical content. Retrieved from www.jointcommission.org/standards_information/jcfaqdetails.aspx? StandardsFaqId=1851&ProgramId=46. Torres EG, Lindmair JM, Langan JW, et al: Is preoperative nasal povidone-iodine as efficient and cost-effective as standard MRSA screening protocol in total joint arthroplasty? J Arthroplasty 31:215, 2016. Wilson RA, Watt-Watson J, Hodnett E, et al: A randomized controlled trial of an individualized preoperative education intervention for

symptom management after total knee arthroplasty, Orthopaedic Nursing 35:20, 2016. Practice guidelines for preoperative fasting and the use of pharmacologic agents to reduce the risk of pulmonary aspiration: Application to healthy patients undergoing elective procedures, Anesthesiology 126:376, 2017.

16. Smeltz A, Kumar P: Angiotensin axis blocking drugs in the perioperative period, Anesthesiol News, 2016. Retrieved from www.anesthesiologynews.com/ReviewArticles/Article/02-16/Angiotensin-Axis-Blocking-DrugsIn-the-Perioperative-Period/35357/ses=ogst. 17. The Joint Commission: Standard FAQ details. Retrieved from www.jointcommission.org/standards_information/jcfaqdetails.aspx? StandardsFaqId=1490&ProgramId=46. Mohanty S, Rosenthal RA, Russell MM, et al: Optimal perioperative management of the geriatric patient: A best practices guideline from the American College of Surgeons NSQIP and the American Geriatrics Society, JACS 222:930, 2016 ∗Evidence-based information for clinical practice.

18

Intraoperative Care Mark Karasin

LEARNING OUTCOMES 1. Distinguish various areas of perioperative department and appropriate attire. 2. Outline the roles and responsibilities of interprofessional surgical team members. 3. Prioritize needs of patients undergoing surgery. 4. Analyze role of a perioperative nurse in the management of patients undergoing surgery. 5. Apply basic principles of infection prevention and aseptic technique in the operating room. 6. Recognize operating room safety measures related to patients, equipment, and anesthesia. 7. Distinguish various anesthesia techniques and common anesthesia drugs.

KEY TERMS anesthesia care provider (ACP), p. 315 anesthesiology, p. 315

epidural block, p. 325 general anesthesia, p. 320 local anesthesia, p. 324 malignant hyperthermia (MH), p. 325 nurse anesthetist, p. 315 regional anesthesia, p. 324 spinal anesthesia, p. 324 Unless someone like you cares a whole awful lot, nothing is going to get better, it’s not. Dr. Seuss http://evolve.elsevier.com/Lewis/medsurg/

Conceptual Focus Gas Exchange Pain Perfusion Safety Tissue Integrity Historically, surgery took place in the traditional environment of the hospital operating room (OR). Now, many surgical procedures are done as ambulatory surgery (outpatient surgery). In addition, the use of minimally invasive surgery (MIS) is rapidly increasing. More procedures use endoscopes, robotics, and other advanced technologies that lead to decreased blood loss, incision size, pain, recovery time, and hospital length of stay. Hybrid ORs, which allow for MIS, such as endovascular procedures, and the traditional open incision approach within the same room, are becoming more common. This chapter discusses the basics of intraoperative care that apply to

all surgical patients regardless of where or how the surgery is done.

Physical Environment of the Operating Room Department Layout The surgery department is a controlled environment designed to minimize the spread of pathogens and allow a smooth flow of patients, staff, and equipment needed to give safe surgical patient care. The department is divided into 3 distinct zones: (1) unrestricted, (2) semirestricted, and (3) restricted (Fig. 18.1). The unrestricted zone is where people in street clothes interact with those in scrub attire. These areas typically include the points of entry for patients (e.g., holding area), staff (e.g., locker rooms), and information (e.g., nursing station or control desk). The semirestricted zone includes the surrounding support areas and corridors. Only authorized staff are allowed access to semirestricted areas. All staff in the semirestricted area should wear clean surgical attire. This includes scrub attire that was laundered in an accredited laundry facility, long-sleeved jacket, shoes dedicated for surgery use or shoe covers, surgical head cover and mask that covers all head and facial hair, and any appropriate personal protective equipment (e.g., face shield). The restricted zone is found within the semirestricted area. It includes the surgical suite (OR) where the invasive procedure takes place and the sterile core (Fig. 18.2). Masks should be worn and traffic minimized whenever sterile supplies are open in the restricted area.1 The physical layout is designed to reduce cross-contamination. The flow of clean and sterile supplies and equipment is separate from contaminated supplies, equipment, and waste by space, time, and traffic patterns. Staff members move supplies from clean areas, such as the sterile core, through the OR for surgery, and on to the instrument decontamination and sterilization area (e.g., central processing department [CPD]).

FIG. 18.1 Perioperative department layout.

FIG. 18.2 Typical OR. © iStock.com/windslegend.

Holding Area The holding area, often called the preoperative holding area, is an unrestricted zone where patient identification and assessment take place. The size can range from a large centralize area that handles many patients to a small designated area right outside of the OR. In some settings, the holding area is called the admission, observation, and discharge (AOD) unit. An AOD unit is designed to allow early morning admission for outpatient surgery, same-day admission, and inpatient holding before surgery. The patient is identified and assessed before and after surgery, before being discharged home or transferred to an inpatient room. The AOD unit is important in outpatient surgery and prevents unnecessary overnight stays in the inpatient setting.

Operating Room The traditional OR is a unique setting separate from other clinical units. This restricted zone is controlled geographically, environmentally, and aseptically (Fig. 18.1). It is best to have the OR next to the postanesthesia care unit (PACU) and the surgical intensive care unit. This allows for quick transport of the patient after surgery and close proximity to anesthesia staff if complications occur. We use several methods to prevent the transmission of infection in the OR. Filters and controlled airflow in the ventilating systems provide dust control. Positive air pressure in the rooms prevents air from entering the OR from the halls and corridors. ORs are kept within a narrow range of temperature and humidity to prevent bacteria growth. ORs follow strict protocols for cleaning between cases and terminal cleaning at the end of the day. The use of ultraviolet lighting reduces the number of microorganisms in the air.2 Using OR furniture that is adjustable, easy to clean, and easy to move promotes safety and comfort. All equipment is checked frequently to ensure proper functioning and electrical safety. The lighting is designed to give a low- to high-intensity range for a precise view of the surgical site. A communication system offers a way to deliver routine and emergency messages.3

Surgical Team Registered Nurse The perioperative nurse is a registered nurse (RN) who collaborates with the rest of the surgical team and implements the patient’s plan of care during perioperative period. Depending on the size of the OR department, this role may include three domains: (1) preoperative RN, (2) OR RN, and (3) PACU RN. As an OR RN, you are the patient’s advocate during surgery. This includes (1) maintaining the patient’s safety, dignity, and confidentiality; (2) communicating with the patient, the surgical team, and other departments (e.g., CPD, PACU, laboratory); and (3) providing nursing care discussed in the Nursing

Management section of this chapter.

TABLE 18.1 Intraoperative Nursing Activities

Circulating, Nonsterile Activities • Helps prepare room, ensuring that supplies and equipment are available, in working order, and sterile • Maintains aseptic technique in all required activities • Monitors practices of aseptic technique in self and others • Checks mechanical and electrical equipment and environmental factors • Conducts a preprocedure verification process • Assesses patient’s physical and emotional status • Confirms and implements facility protocols and safety measures • Plans and coordinates intraoperative nursing care • Checks chart and relates pertinent data to team members • Helps with applying monitoring devices and insertion of invasive lines and other devices • Assists with and ensures patient safety in transferring and positioning patient • Aids with anesthesia induction • Monitors draping • Takes part in surgical time-out • Records intraoperative care • Prepares, records, labels, and sends blood, pathology, and any anatomic specimens to proper locations • Measures blood, urine output, and other fluid loss • Confirms, dispenses, and records drugs used, including local anesthetics • Coordinates all intraoperative activities with team members and other staff and departments • Works with scrubbed personnel to keep correct count of sponges, needles, instruments, and medical devices • Facilitates patient transfer to PACU • Gives hand-off report to PACU nurse with information relevant to care of patient Scrubbed, Sterile Activities • Helps prepare the OR • Completes surgical hand antisepsis and gowns and gloves self and other members of surgical team • Prepares instrument table and arranges sterile equipment for functional use • Assists with draping • Takes part in surgical time-out procedure • Passes instruments to surgeon and assistants by anticipating their needs • Keeps correct count of sponges, needles, instruments, and medical devices that could be retained in the patient • Monitors practices of aseptic technique in self and others • Keeps track of irrigation solutions used for calculation of blood loss • Accepts, verifies, and reports drugs used by surgeon and/or ACP, including local anesthetics

During surgery, the OR RN assumes functions that involve either sterile or unsterile activities (Table 18.1). The scrub nurse (sterile) follows the designated surgical hand antisepsis and glove and gown sterile attire and prepares and manages the sterile field and instrumentation. The circulating nurse stays in the unsterile field, facilitates the progress of the procedure, and keeps documentation.4 Examples of nursing activities that occur during each phase of the surgical experience are outlined in Table 18.2. After meeting specific criteria (e.g., 2 years of experience), perioperative RNs can obtain OR certification (CNOR). CNOR certification is an objective measure (written test) that validates a nurse has essential knowledge and skills in perioperative nursing.5

Licensed Practical/Vocational Nurse and Surgical Technologist Depending on the state’s nurse practice act, an LPN/VN or a surgical technologist may fill the role of the circulating or scrub nurse. Surgical technologists attend an associate degree program or a vocational, hospital, or military training program. The Association of Surgical Technologists sets the standards for education, provides continuing education opportunities, and offers certification for surgical technologists.6 If the circulating nurse is not an RN, the LPN/VN or surgical technologist must always have access to an RN. As an OR RN, you take on responsibility for supervising an LPN/VN or surgical technologist performing delegated nursing tasks.7

Surgeon and Assistant The surgeon is the physician who does the surgical procedure. The surgeon is primarily responsible for: • Preoperative medical history and physical assessment, directing preoperative testing, and postoperative management

Obtaining informed consent • Leading the surgical team and directing the course of a procedure The surgeon’s assistant can be another physician, registered nurse first assistant (RNFA), physician’s assistant, surgical resident or fellow, medical student, or a certified surgical first assistant. The assistant usually holds retractors to expose surgical areas and helps with hemostasis and suturing. In some agencies, especially in educational settings, the assistant may perform some portions of the surgery under the surgeon’s direct supervision.

Registered Nurse First Assistant The registered nurse first assistant (RNFA) works with the surgeon to achieve an optimal surgical outcome for the patient. The Association of periOperative Registered Nurses (AORN) states that you must have formal education for this role and work collaboratively with the surgeon, patient, and surgical team.8 CNOR nurses or nurse practitioners can complete RNFA program to assume this expanded role. RNFAs can obtain certification (C-RNFA).

Anesthesia Care Provider Anesthesiology is a medical specialty that focuses on clinical management of the patient in the perioperative period, pain management, critical care, trauma, airway management, and cardiopulmonary resuscitation. The anesthesia care provider (ACP) is the person responsible for administering anesthetic agents and managing vital life functions (e.g., breathing, BP) during the perioperative period.9 This can be an anesthesiologist, nurse anesthetist, or anesthesiologist assistant (AA). A nurse anesthetist is a master’s or a doctorate prepared RN who has graduated from an accredited nurse anesthesia program and completed a national certification examination to become a certified

registered nurse anesthetist (CRNA). The CRNA’s scope of practice includes:10 • Performing and documenting a preanesthetic assessment and evaluation • Developing and implementing a plan for delivering anesthesia • Choosing, obtaining, and administering anesthesia, adjuvant drugs, and fluids • Choosing, applying, and inserting appropriate monitoring devices • Managing a patient’s airway and pulmonary status • Managing emergence and recovery from anesthesia • Releasing or discharging patients from a PACU • Ordering, starting, or modifying pain relief therapy • Responding to emergency situations by providing airway management

TABLE 18.2 Common Perioperative Nursing

Activities

An AA is a master’s-prepared health professional who serves under the direction of an anesthesiologist. AAs have completed an accredited program and passed a national certification examination. They take part in all types of anesthesia. This includes giving drugs, obtaining vascular access, applying and interpreting monitors, maintaining airways, and helping with preoperative assessment.

Nursing Management: Patient Before Surgery The preoperative assessment of the surgical patient provides baseline data for intraoperative and postoperative care and is used to plan intraoperative care. Preoperative care of the patient is discussed in Chapter 17. Provide physical and emotional comfort for the patient and caregivers along with teaching about the upcoming surgery. This is particularly important in the same-day surgery settings, where caregivers must assume greater responsibility for postoperative care.

Psychosocial Assessment Knowing about the activities that occur when a patient moves into the OR allows you to provide teaching and comfort, especially to the anxious patient. You can usually answer general questions about surgery and anesthesia, such as, “When will I go to sleep?” “Who will be in the room?” “When will my surgeon arrive?” “How much of my body will be exposed?” “Will I be cold?” “When will I wake up?” Refer specific questions about the details of the surgery and anesthesia to the surgeon or ACP. For patients who do not speak English, use a qualified interpreter (see Table 2.10). Separation from caregivers just before surgery can produce anxiety for the patient. Allowing the caregiver to wait with the patient in the holding area until we transfer the patient to the OR can reduce anxiety.

Physical Assessment Perform a thorough physical assessment during the preoperative preparation of the patient (see Chapter 17).

Chart Review Required chart data vary with agencies, patient conditions, and surgical procedures. Tables 17.2 and 17.4 provide examples of data we obtain during the preoperative assessment. This information gives an understanding of past and present medical history and an opportunity to anticipate and prepare for potential needs during surgery, such as obtaining equipment or drugs. You can discuss any abnormal findings or concerns for infection and other complications with the surgeon or ACP.

Check Your Practice Your patient has arrived in the holding area. As you review the chart, you realize the patient has not signed the consent for blood. You see the patient has Alzheimer’s disease and is not mentally competent to give consent. • How would you proceed?

Admitting the Patient Agency policy guides the protocol you follow when admitting the patient to the holding area and OR. A general routine includes initial greeting, proper identification, and offer of human contact and warmth. The admitting process continues with reassessment of the patient and time for last-minute questions. Determine if any other tasks need to be done. Complete the chart review for the previously mentioned data and note any problems or changes. Ask the patient about

valuables, prostheses, and last intake of food and fluid. Confirm that any ordered preoperative drugs were given. Provide a pillow or adjust the patient’s position if requested. Most agencies require the patient’s hair to be covered just before transfer to the OR suite to reduce potential shedding. You may offer complementary and alternative therapies, such as aromatherapy, music therapy, guided imagery, and distraction (see the Complementary & Alternative Therapies box). These therapies may decrease anxiety, promote relaxation, and reduce pain.11 Some agencies start these therapies before the patient is admitted to the OR. In others, such as ambulatory settings, they may start after the patient arrives in the holding area.

Complementary & Alternative Therapies Music Therapy Music is an ancient healing tool recognized in the writings of Plato.

Scientific Evidence Strong evidence supports using music therapy to reduce stress and anxiety and enhance mood.

Nursing Implications • To be effective, the music used must be appropriate for the situation. Music can have many different physiologic effects. • Listening to calming music can result in slower, deeper breathing and a decrease in heart rate and BP. Both indicate relaxation. • Music with a faster pace can energize a person and promote mental alertness. • Music therapy is safe in combination with other treatment approaches. Source: Daniel E: Music used as anti-anxiety intervention for patients

during outpatient procedures: a review of the literature, Complement Ther Clin Pract 22:21, 2016.

Nursing Management: Patient During Surgery Patient care in the surgical setting is dynamic and depends on the knowledge, skills, and judgment of the RN.4 The circulating nurse is responsible for implementing the intraoperative plan of care and serving as the patient’s advocate. The circulating nurse focuses on the whole patient. This involves ongoing assessment, reassessment, and adjusting the care plan to promote the best surgical outcomes.

Room Preparation Before transferring the patient into the OR, prepare the room to ensure privacy, prevention of infection, and safety. Individualized preparation is essential to achieve the expected patient outcomes. When a patient is severely obese, extra staff and special equipment may be needed to safely position and transfer the patient to and from the OR bed. During surgery, special equipment (e.g., extra-long instrumentation, bariatric OR bed) may be used.

Check Your Practice You are assigned to observe in the OR. A severely obese patient is admitted to the holding area. The circulating nurse tells you that the team will address the unique needs of the patient for a safe surgical experience. • What special considerations are needed for this patient? All people entering the OR wear surgical attire (Fig. 18.3). All

electrical and mechanical equipment is checked for proper functioning. Each surgical item is opened and placed on the instrument table using aseptic technique. Sponges, needles, instruments, and small medical devices (e.g., surgical clip cartridges, universal adapters) are counted according to strict processes to ensure accurate retrieval at the end of the procedure. Any retained surgical supplies, devices, or instruments are sentinel events (never events) or serious reportable events (SREs) that can result in negative outcomes for the patient.1,4 (Sentinel events and SREs are discussed in Chapter 1.)

FIG. 18.3 All surgical personnel wear surgical attire. © iStock.com/Ridofranz.

During room preparation and the surgical procedure, the scrub person does surgical hand antisepsis, dons sterile gown and gloves, and touches only items in the sterile field. The circulating nurse stays in the unsterile field and does those activities that involve contact with

all unsterile items and the patient. This coordinated effort allows for smooth functioning throughout the procedure.

Transferring Patient The patient is moved into the OR after the preoperative assessment is complete and the surgical suite is ready. Always maintain privacy during transfers through public areas by covering the patient with a gown and/or blanket. Each time a patient is transferred between beds, the wheels of each must be locked. Enough staff members using ergonomic tools for safe patient handling and movement should be available to lift, guide, and prevent accidental falling or injury to staff and the patient. Once the patient is on the OR bed, ensure that there is always someone on both sides of the patient until a safety strap is secured to prevent falls. The monitor leads (e.g., ECG leads), BP cuff, and pulse oximeter are usually applied after the patient is safe on the OR bed.

Scrubbing, Gowning, and Gloving Surgical hand antisepsis is required of all sterile members of the surgical team (scrub nurse, surgeon, assistant). When wet scrubbing is the chosen method for surgical hand antisepsis, your finger nails are cleaned first, followed by scrubbing each plane of individual fingers, palms, and forearms in the distal to proximal fashion. The hands should always be held away from surgical attire and higher than the elbows. This prevents contamination from clothing or detergent suds and water from draining from the unclean area above the elbows to the clean and previously scrubbed areas of the hands and fingers. Waterless, alcohol-based agents are replacing soap and water in many agencies. When using an alcohol-based surgical hand-scrub product, prewash hands and forearms with soap and dry completely before applying the alcohol-based product. After applying the alcohol-based product, rub hands and forearms thoroughly until dry before donning sterile attire.1,4 Once surgical hand antisepsis is completed, the team members

enter the OR to put on sterile gowns and 2 pairs of gloves. This protects patients and themselves from the transmission of microorganisms.1,4 Because the gowns and gloves are sterile, those who have scrubbed can manipulate and organize all sterile items for use during the procedure.

Basic Aseptic Technique Aseptic technique is practiced in the OR to prevent infection. This is done through the creation and maintenance of a sterile field. The center of the sterile field is the site of the surgical incision. Items used in the sterile field, including surgical instruments and equipment, have been sterilized by appropriate sterilization methods. Team members must understand specific principles to practice aseptic technique (Table 18.3). If these principles are not followed, the patient’s safety is compromised and the risk for infection is increased.1,4 The surgical team is also responsible for following the guidelines established by the U.S. Occupational Safety and Health Administration (OSHA) and the AORN to protect the patient and the team from exposure to blood-borne pathogens.12 These guidelines emphasize (1) standard and transmission-based precautions, (2) engineering and work practice controls, and (3) the use of personal protective equipment, such as gloves, gowns, caps, face shields, masks, and protective eyewear. This is especially important in the OR because of the high potential for exposure to blood-borne pathogens.

Assisting Anesthesia Care Provider While you check the OR to complete the final preparations, the ACP prepares the patient for receiving anesthesia. You need to understand the effects of the anesthetic agents and know the location of all emergency drugs and equipment.

TABLE 18.3 Principles of Aseptic Technique in

Operating Room

• All materials that enter the sterile field must be sterile. • If a sterile item comes in contact with an unsterile item, it is contaminated. • Contaminated items are removed at once from the sterile field. If the unsterile item is small (e.g., unopened suture), once it is removed, the area is marked off (i.e., covered with a sterile drape). If the entire field is contaminated, it should be set up again with all new materials. • The surgical team working in the operative field must wear sterile gowns and gloves. Once dressed for procedure, they must recognize that the only parts of the gown considered sterile are the front from chest to table level and sleeves to 2 inches above elbow. • A wide margin of safety is maintained between sterile and unsterile fields. • Tables are sterile only at tabletop level. Items extending beneath this level are contaminated. • The edges of a sterile package are contaminated once the package has been opened. If a sterile package (e.g., package of sutures) is placed on the sterile field, that entire package stays sterile even when opened. • Microorganisms travel on airborne particles and will enter the sterile field with excessive air movements and currents. • Microorganisms travel by capillary action through moist fabrics, resulting in contamination. • Microorganisms on the patient’s and team members’ hair, skin, and respiratory tracts must be confined by proper attire.

If you are the circulating nurse, you may be involved in placing monitoring devices used during the procedure (e.g., ECG leads). If the patient is having general anesthesia, stay at the patient’s side to ensure safety and aid the ACP. These responsibilities may include measuring BP and helping maintain the patient’s airway. During the procedure, you are a vital communication link for the ACP to other departments, such as the laboratory or blood bank.

Positioning Patient The surgical team carefully plans the patient’s positioning and monitors the patient throughout the procedure. Positioning is a critical part of every procedure and usually follows induction of anesthesia. The ACP says when to begin positioning. The patient’s position should allow for accessibility to the operative site,

administering and monitoring of anesthetic agents, and maintaining the patient’s airway. We use a variety of surgical positions, including supine, prone, lateral, lithotomy, or sitting. The supine is the most common position. It allows operating on most body systems, including the abdomen, heart, chest, or head. The prone position is often used in spine surgery (e.g., laminectomy). The lithotomy position is used for various gynecological, genitourinary, and colon procedures. With any position, take great care to prevent injury to the patient. Take care to (1) provide correct musculoskeletal alignment; (2) prevent undue pressure on nerves, skin over bony prominences, earlobes, and eyes; (3) provide for adequate thoracic excursion; (4) prevent occlusion of arteries and veins; (5) provide modesty in exposure; and (6) recognize and respect individual needs, such as previously assessed pains or deformities. It is your responsibility to secure the extremities, provide adequate padding and support, and have physical or mechanical help to avoid unnecessary straining of the staff and patient. Because anesthesia blocks the sensory nerve impulses, the patient will not feel pain, discomfort, or stress placed on nerves, muscles, bones, and skin. General anesthesia causes peripheral vessels to dilate. Position changes affect where the pooling of blood occurs. If the head of the OR bed is raised, the lower torso will have increased blood volume and the upper torso may become compromised. Hypovolemia and cardiovascular disease can further compromise the patient’s status. Improper positioning can potentially result in muscle strain, joint damage, pressure injuries, nerve damage, and other untoward effects.

Electrosurgery and Smoke Care must be taken to correctly place the grounding pad and all electrosurgical equipment to prevent injury from burns or fire. When an electrosurgical unit is in use, the patient must be properly grounded to prevent unintended injury (Fig. 18.4). Excess hair, adipose tissue, bony prominences, fluid (edema), adhesive failure, and

scar tissue can compromise safety. Fire in the OR can have devastating consequences for the patient. Fortunately, we can prevent surgical fires with awareness of the hazards and emphasis on safe practices.13

Preparing Surgical Site The purpose of skin preparation, or “prepping,” is to reduce the number of microorganisms available to migrate to the surgical wound. The circulating nurse, surgeon, or surgical assistant completes the task of prepping before surgery.

FIG. 18.4 A well-vascularized muscle mass is the best site for grounding. Courtesy Covidien, Mansfield, MA.

The skin is prepared by mechanically scrubbing or cleansing the surgical site with an antimicrobial agent specific to the procedure.

Follow manufacturer’s instructions for proper application of the prepping agent. The principle of scrubbing from the clean area (site of the incision) to the dirty area (distal to the incision) is always followed. Antiseptic agents used for skin preparation may contain alcohol and therefore are flammable. Skin injury can occur if these agents pool under the patient. Care must be taken to ensure that these agents are properly confined and allowed to fully dry. After the skin is prepped and the fumes are allowed to dispel to reduce the risk for fire, the sterile members of the surgical team drape the area. Only the site to be incised is left exposed.

Safety Considerations All surgical procedures put the patient at risk for injury. These injuries include infections, physical trauma from positioning or equipment used, or physiologic effects of surgery itself. Although technical skills, such as operating equipment or proper instrument handling, are a critical part of OR RN competency, there is strong research supporting that nontechnical skills (NTS) also have a high impact on outcomes. These include proper and clear communication, teamwork, situational awareness (e.g., anticipatory cognitive skills), and stress and fatigue management.14 Considering the importance of NTS skills, especially in crisis events, some agencies use special training programs to develop these skills. There are standard approaches, such as a variety of communication tools, that promote safe patient care and minimize the potential negative effects of human factors.

Communication Many team members care for patients as they move through the perioperative continuum. Chances for error arise whenever team members share information. The Joint Commission requires that all health care providers use a standardized approach to hand-off communication. As a RN, use SBAR (see Table 1.4) to ensure that a complete and accurate hand-off is done every time patient care is

transferred to another provider (e.g. change of shift, surgeon to nurse, OR RN to PACU RN).

Surgical Care Improvement Project The Surgical Care Improvement Project (SCIP) is a national quality partnership of organizations focused on improving surgical care by significantly reducing the number of complications from surgery.2 Specific SCIP measures include (1) a prophylactic antibiotic started within 30 to 60 minutes before the surgical incision to decrease risk for infection, (2) applying a warming blanket to prevent unintended hypothermia, and (3) applying intermittent pneumatic compression devices (IPCs) to minimize the risk for VTE.

Time Out and Surgical Checklist The National Patient Safety Goals (NPSGs) require a preprocedure verification process. This includes verification of relevant documentation (e.g., history and physical examination, signed consent forms, nursing and preanesthetic assessment) and the results of any diagnostic studies (e.g., x-rays, biopsy reports). Any needed blood products, implants, devices, and special equipment must be available. The Universal Protocol, one of the NPSGs, is followed to prevent wrong site, wrong procedure, and wrong surgery. Wrong surgical procedure and surgery on the wrong body part or wrong patient are sentinel events (never events) or SREs (described in Chapter 1). The AORN has a position statement about correct site surgery and guidelines for implementing the Universal Protocol.15 The surgeon marks the procedure site. If possible, the marking is done with the patient’s involvement.3 A patient safety checklist for ORs is the cornerstone of a major focus to make surgery safer. Using the World Health Organization (WHO) Surgical Safety Checklist has improved compliance with standards and decreased complications from surgery (Fig. 18.5). In addition, OR staff complete a fire risk assessment to identify and reduce the potential for a fire.

Safety Alert Surgical Time-Out • Before anesthesia induction, ask the patient to confirm name, birthdate, procedure and site, and consent. • All members of the surgical team stop what they are doing just before the procedure starts to verify patient identification, procedure, and surgical site.

Nursing Management: Patient After Surgery Through constant observation of the surgical process, the ACP anticipates the end of the procedure. The ACP gives proper types and doses of anesthetic agents so that their effects will be minimal at the end of the surgery. This allows greater physiologic control of the patient during the transfer to the PACU. The ACP and you or another member of the surgical team go with the patient to the PACU. The hand-off, including the patient’s status and the procedure done, is communicated to the nurse receiving the patient in the PACU to promote safe, ongoing care.

Anesthesia The American Society of Anesthesiologists (ASA) defines anesthesia according to the effect that it has on the patient’s sensorium and pain perception. These definitions include minimal sedation (e.g., anxiolysis), moderate sedation/analgesia, deep sedation/analgesia, and general anesthesia. The science of providing anesthesia continues to evolve. For example, noninvasive electroencephalogram-based technology allows ACPs to track the level of patient awareness (i.e.,

awareness monitoring) during surgery and adjust anesthesia as needed.

FIG. 18.5 WHO Surgical Safety Checklist.

The anesthetic technique and agents are chosen by the ACP in collaboration with the surgeon and patient. The ACP has ultimate responsibility for the choice of anesthesia. Contributing factors include the patient’s current physical and mental status, age, allergies, pain history, expertise of the ACP, and factors related to the procedure (e.g., length, site, discharge plans). An absolute contraindication to any anesthetic technique or agent is patient refusal. The ACP obtains anesthesia consent, writes orders for preoperative and postoperative drugs, and assigns the patient an anesthesia classification. The ASA physical status classification system is based on the patient’s physiologic status. It uses a scale of P1 to P6 (see Table 17.3). An intraoperative complication is more likely to develop with a higher classification number.

Anesthesia Techniques Types of anesthesia techniques include moderate to deep sedation, monitored anesthesia care (MAC), general anesthesia, and local and regional anesthesia (Table 18.4).

Moderate to Deep Sedation Moderate to deep sedation is used for procedures done outside of the OR (e.g., reduction of dislocated joints in the emergency department). The presence of an ACP is not needed. Trained RNs who are allowed by agency protocols and state nurse practice acts can provide this type of anesthesia.16 It is given by the nurse under the direct supervision of a physician.

Monitored Anesthesia Care Monitored anesthesia care (MAC) is used for diagnostic or therapeutic procedures done in or outside of the OR (e.g., endoscopy clinic). It includes varying levels of sedation, analgesia, and anxiolysis. A critical part of MAC is the assessment and management of any physiologic problems that may develop. The provider of MAC must be an ACP since it may be necessary to change to general anesthesia during the procedure.

General Anesthesia The goals of anesthesiology include the (1) control of excessive biologic responses induced by a variety of stressors and (2) protection of patients from stress-induced complications. To this end, total intravenous anesthesia (TIVA) and newer inhalation agents have a fast onset, fast elimination, and fewer undesirable side effects than earlier agents. These factors promote early discharge from the PACU and ambulatory surgery centers. General anesthesia is the technique of choice for patients who are having surgical procedures that are of significant duration, need

skeletal muscle relaxation, require uncomfortable operative positions because of the location of the incision site, or require control of ventilation. Other reasons include patient refusal of local or regional techniques, contraindications to other techniques, and uncooperative patients. Patients may be uncooperative due to intoxication, emotional lability, head injury, impaired cognition, or inability to remain immobile for any length of time. Phases of general anesthesia are outlined in Table 18.5.

TABLE 18.4 Anesthesia Techniques and Effects

Source: American Society of Anesthesiologists: Distinguishing monitored anesthesia care (“MAC”) from moderate sedation/analgesia (conscious sedation), Schaumburg, Ill, 2013, The Society.

TABLE 18.5 Phases of General Anesthesia

General anesthesia may be induced by IV or inhalation and maintained by either or a combination of the two (Table 18.6). A balanced technique, using adjunctive drugs to complement the induction, is the most common approach used for general anesthesia.

IV. Agents All routine general anesthetics begin with an IV induction agent, whether it is a hypnotic, an anxiolytic, or a dissociative agent. When used during the initial period of anesthesia, these agents induce sleep with a rapid onset of action. A single dose lasts only a few minutes. This is long enough for placement of a laryngeal mask airway (LMA) or an endotracheal (ET) tube. Once this is done, the ACP gives the inhalation and IV agent(s). Recent advances in IV hypnotics (e.g., dexmedetomidine

[Precedex]) and opioids (e.g., remifentanil [Ultiva]) have led to the more frequent use of TIVA. However, the patient may still need advanced airway management (e.g., LMA, ET tube) to receive oxygen/air mixtures.

Inhalation Agents Inhalation agents are the cornerstone of general anesthesia. They may be volatile liquids or gases. Volatile liquids are given through a specially designed vaporizer after being mixed with oxygen as a carrier gas. This gas mixture is then delivered to the patient through the anesthesia circuit. Waste gases are removed using negative evacuation pressure venting to the outside of the agency.

TABLE 18.6 Drug TherapyGeneral Anesthesia

Inhalation agents enter the body through the alveoli in the lungs. Ease of administration and rapid excretion by ventilation make them desirable agents. One undesirable trait is the irritating effect some inhalation agents (e.g., desflurane [Suprane]) have on the respiratory tract. Complications include coughing, laryngospasm, and increased secretions. Once the patient has been induced with an IV agent, the choice for delivering inhalation agents is usually through an ET tube or LMA. The ET tube allows control of ventilation and protects the airway from

aspiration. LMAs are currently an important option for patients with difficult airways, but they do not provide access to the trachea or airway protection with the same certainty as ETs. Complications of ET tube or LMA use are primarily related to insertion and removal. These include failure to intubate, damage to teeth and lips, laryngospasm, laryngeal edema, sore throat, and hoarseness caused by injury or irritation of the vocal cords or surrounding tissues.

Adjuncts to General Anesthesia General anesthesia is rarely limited to a single agent. Drugs added to an inhalation anesthetic (other than an IV induction drug) are termed adjuncts. Adjuncts are added to the anesthetic regimen to achieve unconsciousness, analgesia, amnesia, muscle relaxation, or autonomic nervous system control. They include opioids, benzodiazepines, neuromuscular blocking agents (muscle relaxants), and antiemetics (Table 18.7). It is important to know that we often give these drugs in combination and they may have synergistic or antagonistic effects. You may see deeper levels of sedation or more drug-related side effects beyond those seen with inhalation anesthetics alone. If needed, drugs are available to reverse the effects of some of these adjuncts.

TABLE 18.7 Drug TherapyAdjuncts to General

Anesthesia

Dissociative Anesthesia Dissociative anesthesia interrupts associative brain pathways while blocking sensory pathways. The patient may appear catatonic, is amnesic, and has profound analgesia that lasts into the postoperative period. Ketamine (Ketalar) (given IV or IM) is a common dissociative anesthetic. It is a potent analgesic and amnesic. Ketamine is given to asthmatic patients because it promotes bronchodilation. In trauma

patients, it increases heart rate and helps maintain cardiac output. Because ketamine is a phenyl cyclohexyl piperidine (PCP) derivative, the drug may cause hallucinations and nightmares, limiting its usefulness. Concurrent use of midazolam (Versed) can reduce or eliminate the hallucinations. Providing a quiet, unhurried environment in the PACU is especially important for all patients receiving dissociative anesthesia.

Local and Regional Anesthesia Local anesthesia interrupts the generation of nerve impulses by changing the flow of sodium into nerve cells. The result is autonomic nervous system blockade, anesthesia, and skeletal muscle flaccidity or paralysis. Local anesthetics are topical, ophthalmic, nebulized, or injected. A local anesthetic is applied to a specific area of the body by the surgeon or ACP. It does not involve sedation or loss of consciousness. Regional anesthesia (or block) using a local anesthetic is always injected. It involves a central nerve (e.g., spinal) or group of nerves (e.g., plexus) that innervate a site remote to the point of injection. Administration of a local or regional anesthetic may involve concurrent use of MAC or moderate to deep sedation (Table 18.4), either preinjection or intraoperatively. Regional blocks are used as preoperative analgesia, during surgery to manage surgical pain, and after surgery to control pain. Indwelling catheters that deliver local anesthetic to the surgical site through a pump implanted during surgery can give continuous pain relief up to 72 hours after surgery. Advantages of local and regional anesthesia include rapid recovery and discharge with continued postoperative analgesia without any accompanying cognitive dysfunction. They can be safely used in patients who have co-morbidities that prevent the use of general anesthesia. Disadvantages include the potential for technical problems, discomfort at the injection site, and the inability to precisely match the agent’s duration of action to the duration of the procedure. Another disadvantage is the risk for inadvertent vascular injection leading to

local anesthetic systemic toxicity (LAST). LAST first presents as confusion, metallic taste, oral numbness, and dizziness.17 Without treatment, seizures, coma, and dysrhythmias may occur. The topical applications of creams, ointments, aerosols, and liquids are standard methods to administer local anesthesia. The drug is applied directly to the skin, mucous membranes, or open surface. Eutectic mixture of local anesthetics (EMLA cream, a combination of prilocaine and lidocaine) is an example. It is applied to the site 30 to 60 minutes before a procedure. The success of injected local anesthetics may be limited by prolonged duration of procedure or infection at the injection site that interferes with drug absorption. In ambulatory or outpatient procedures, you may aid the ACP in administering a peripheral or regional block. You must be familiar with the drugs, including the methods of administration and adverse and toxic effects. Initial assessment of the patient should include the patient’s history with the use of local anesthetics and any adverse events associated with their use by the patient or blood relatives. Many patients report “allergies” to local anesthetics. Although true allergies to local anesthetics occur, they are rare. Allergies are likely to be a result of additives or preservatives in the preparation. Some local anesthetics are combined with epinephrine to provide localized vasoconstriction. This decreases absorption and extends the action of the agent. However, if the local anesthetic is absorbed in the tissues or inadvertently injected IV and enters the general circulation, the patient may have tachycardia, hypertension, and a general feeling of panic. Examples of common regional nerve blocks include brachial plexus block; IV regional anesthesia (IVRA) or Bier block anesthesia; and femoral, axillary, cervical, sciatic, ankle, and retrobulbar blocks. For IVRA or Bier block, the patient has a double-cuff tourniquet applied as a safety measure. You can promote the success of regional anesthesia by properly positioning the patient, monitoring vital signs during block delivery, applying oxygen therapy, and using supporting devices (at the direction of the ACP) that contribute to the anesthesia (e.g.,

ultrasound imaging, nerve stimulator, tourniquets). When a patient is receiving regional anesthesia, airway equipment, emergency drugs, and a cardiac monitor/defibrillator should be available to provide advanced airway and cardiopulmonary support if needed.

Spinal and Epidural Anesthesia Spinal anesthesia and epidural anesthesia are also types of regional anesthesia. Spinal anesthesia involves the injection of a local anesthetic into the cerebrospinal fluid in the subarachnoid space, usually below the level of L2 (Fig. 18.6, A). The local anesthetic mixes with cerebrospinal fluid. Depending on the extent of its spread, various levels of anesthesia are achieved. Because the local anesthetic is given directly into the cerebrospinal fluid, a spinal anesthetic produces an autonomic, sensory, and motor blockade. Patients develop vasodilation and may become hypotensive from the autonomic block. They feel no pain because of the sensory block. They cannot move because of the motor block. The duration of action of the spinal anesthetic depends on the drug used and the dose given. A spinal anesthetic may be used for procedures involving the extremities (e.g., joint replacements) and lower gastrointestinal, prostate, and gynecologic surgeries.

FIG. 18.6 Location of needle point and injected anesthetic relative to dura and spinal cord. A, Spinal anesthesia. B, Single-injection epidural. C, Epidural catheter. (Interspaces most often used are L2-3, L4-5, L34.)

An epidural block involves injection of a local anesthetic into the epidural space via a thoracic or lumbar approach (Fig. 18.6, B). The anesthetic agent does not enter the cerebrospinal fluid but binds to nerve roots as they enter and exit the spinal cord. With the use of a low concentration of local anesthetic, sensory pathways are blocked but motor fibers are still intact. In higher doses, sensory and motor fibers are blocked. Epidural anesthesia may be the sole anesthetic for a surgical procedure. In addition, a catheter may be placed to allow for intraoperative use and continued analgesia in the postoperative period (Fig. 18.6, C). For postoperative analgesia, lower doses of epidural local anesthetic, usually in combination with an opioid, are used. Epidural anesthesia is often used for analgesia or in combination

with MAC or general anesthesia, in obstetrics, vascular procedures involving the lower extremities, lung resections, and renal and midabdominal surgeries. The desirable effects of vasodilation and analgesia contribute to better surgical outcomes. With spinal or epidural anesthesia, the patient can stay fully conscious, receive MAC, or choose general anesthesia. The onset of spinal anesthesia is more rapid than that of epidural anesthesia. Both may be extended in duration using indwelling catheters, thus allowing for more doses of anesthetic. With either anesthesia, closely observe the patient for manifestations of autonomic nervous system blockade. These include hypotension, bradycardia, nausea, and vomiting. There is less autonomic nervous system blockade with epidural anesthesia than with spinal anesthesia. Should “too high” a block be present, the patient may have tingling in the arms and hands or inadequate breathing and apnea. Other complications include postdural puncture headache, back pain, isolated nerve injury, and meningitis.

Gerontologic Considerations: Patient During Surgery Although anesthetic agents have become safer and more predictable, the aging process affects the absorption, distribution, and metabolism of drugs. This results in changes in their onset, peak, and duration independent of the route of administration. Because of this, anesthetic drugs need to be carefully titrated when given to older adults. Physiologic changes in aging may also change the patient’s response to blood and fluid loss and replacement, hypothermia, pain, and tolerance of the procedure and positioning. Carefully monitor the older adult’s response to all anesthetic agents. Postoperative delirium is a common complication in this population and associated with adverse surgical outcomes.18 Assess the postoperative recovery from anesthesia before the patient is transferred out of the PACU. Some older adults may have a hard time communicating and following directions because of problems with hearing or vision.

These factors increase the need for clear and concise communication in the OR, especially when preoperative sedation is combined with already existing sensory deficits. Because of decreased ability to perceive discomfort or pressure on vulnerable areas and a loss of skin elasticity, the older adult’s skin is at risk for injury from tape, electrodes, warming and cooling blankets, and certain types of dressings. Pooling of solutions used to prepare the skin in dependent areas can quickly create skin burns or abrasions. Care and vigilance are needed in preparing and positioning the older patient. The older adult often has osteoporosis and/or osteoarthritis. Misalignment, pressure, or other insults to arthritic joints desensitized from an anesthetic may create long-term injury and disability. Older adults are at a greater risk for perioperative hypothermia. Consider using warming devices and carefully monitor them when used.

Perioperative Crisis Events Although the incidence of crisis events has significantly decreased with scientific advancements, there is an inherent risk with surgery for an adverse outcome, which may be of critical nature. Some events may be expected (e.g., cardiac arrest in an unstable patient, massive blood loss during trauma surgery). Others may occur without warning (e.g., air embolism, hypoxia), demanding immediate intervention by all members of the OR team. More rare events include anaphylactic reactions and malignant hyperthermia.

Anaphylactic Reactions Anaphylaxis is the most severe form of an allergic reaction, manifesting with life-threatening pulmonary and circulatory complications. ACPs give patients a variety of drugs, including anesthetics, antibiotics, and blood products. Anesthetic agents, antibiotics, and latex cause many allergic reactions. Vigilance and rapid intervention are essential. Anesthesia may mask the initial manifestations of anaphylaxis. An

anaphylactic reaction causes hypotension, tachycardia, bronchospasm, and pulmonary edema. Anaphylaxis is discussed in Chapter 13. Latex allergy has become a concern in the surgical setting. Gloves, catheters, and many devices contain natural rubber latex. Latex allergy protocols should be set up in each agency to provide a latexsafe environment for susceptible patients.19 Latex allergies are discussed in Chapter 13.

Malignant Hyperthermia Malignant hyperthermia (MH) is a rare disorder characterized by hyperthermia with skeletal muscle rigidity. It can result in death. MH occurs in susceptible people when they are exposed to certain anesthetic agents. Succinylcholine (Anectine), especially when given with volatile inhalation agents, is the primary trigger of MH. Other factors include stress, trauma, and heat. When MH does occur, it is usually during general anesthesia. It may occur in the recovery period, too.20 MH is an autosomal dominant trait. It is variable in its genetic manifestation, so predictions based on family history are important but not reliable. The fundamental defect is hypermetabolism of skeletal muscle resulting from altered control of intracellular calcium. This leads to muscle contracture, hyperthermia, hypoxemia, lactic acidosis, and hemodynamic and cardiac problems. Tachycardia, tachypnea, hypercarbia, and ventricular dysrhythmias may occur but are nonspecific to MH. MH is diagnosed after ruling out other causes of the hypermetabolism. The rise in body temperature is not an early sign of MH. Unless promptly detected and treated, MH can result in cardiac arrest and death. The definitive treatment of MH is prompt administration of dantrolene (Dantrium, Ryanodex).20 Dantrolene slows metabolism, reduces muscle contraction, and mediates the catabolic processes associated with MH. To prevent MH, take a careful family history and be alert to the development of MH perioperatively. The patient known or suspected

to be at risk for this disorder can receive anesthesia with minimal risks if proper precautions are taken. Patients with MH need to be aware of the condition so that family members may be genetically tested.

Case Study Intraoperative Patient

© shironosov/iStock/Thinkstock.

Patient Profile G.S., a 63-yr-old retired accountant, was admitted to the hospital for severe pain from acute cholecystitis. G.S.’s medical history includes hypertension and type 2 diabetes. His pain has been managed with hydromorphone (Dilaudid) using patient-controlled analgesia. Intractable nausea and vomiting required the placement of a NG

tube. He is scheduled for a laparoscopic cholecystectomy. The surgery will be done under general anesthesia.

Subjective Data • G.S. is awake and able to identify himself, his birth date, procedure, and surgical site • Rates pain as a 4 on a 0- to 10 scale on arrival to the holding area

Objective Data • Admitted to the holding area with an NG tube in place and one peripheral IV catheter • Capillary blood glucose 1 hour ago was 125 mg/dL • Oxygen saturation 96% on room air

Interprofessional Care • Vital signs per holding area routine • 0.9 normal saline solution at 100 mL/hr • Titrate O2 therapy to keep O2 saturation >90% • NG tube connected to low, intermittent suction

Discussion Questions 1. What are the potential intraoperative problems that you may expect with G.S.? 2. Priority Decision: What priority nursing interventions would be appropriate to prevent these complications from occurring? 3. Collaboration: What are the interprofessional team’s priorities for G.S.? 4. Evidence-Based Practice: G.S. tells you that he is cold despite a

blanket in place. Why is it important that G.S. stays warm? 5. Safety: Identify 2 areas of risk for injury to G.S. What actions can be taken to ensure patient safety? Answers available at http://evolve.elsevier.com/Lewis/medsurg.

Bridge to Nclex Examination The number of the question corresponds to the same-numbered outcome at the beginning of the chapter.

1. Proper attire for the semirestricted area of the surgery department is a. street clothing. b. surgical attire and head cover. c. scrub attire, head cover, shoe covers. d. street clothing with the addition of shoe covers. 2. Activities that the nurse might perform in the role of a scrub nurse during surgery include (select all that apply) a. checking electrical equipment. b. preparing the instrument table. c. assisting with draping the patient. d. passing instruments to the surgeon and assistants. e. documenting activities occurring in the operating room. 3. The nurse is caring for a patient undergoing surgery for a knee replacement. What is critical to the patient’s safety during the procedure (select all that apply)? a. Universal protocol is followed. b. The ACP is an anesthesiologist.

c. The patient has adequate health insurance. d. The patient’s family is in the surgery waiting area. e. The patient’s allergies are conveyed to the surgical team. 4. The nurse’s primary responsibility for the care of the patient undergoing surgery is a. developing an individualized plan of nursing care for the patient. b. carrying out specific tasks related to surgical policies and procedures. c. ensuring that the patient has been assessed for safe administration of anesthesia. d. performing a preoperative history and physical assessment to identify patient needs. 5. When scrubbing at the scrub sink, the nurse should a. scrub from elbows to hands. b. scrub without mechanical friction. c. scrub for a minimum of 10 minutes. d. hold the hands higher than the elbows. 6. When positioning a patient in preparation for surgery, the nurse understands that injury to the patient can occur because of (select all that apply) a. loss of pain perception. b. incorrect musculoskeletal alignment. c. vasoconstriction of the peripheral vessels. d. hypovolemia contributing to decreased perfusion. e. inability to sense pressure over bony prominences. 7. IV induction for general anesthesia is the method of choice

for most patients because a. the patient is not intubated. b. the agents are nonexplosive. c. induction is rapid and controlled. d. emergence is longer but with fewer complications. 1. c, 2. b, c, d, 3. a, e, 4. a, 5. d, 6. a, b, d, e, 7. c For rationales to these answers and even more NCLEX review questions, visit http://evolve.elsevier.com/Lewis/medsurg.

Evolve Website/Resources List http://evolve.elsevier.com/Lewis/medsurg

Review Questions (Online Only) Key Points Answer Keys for Questions • Rationales for Bridge to NCLEX Examination Questions • Answer Guidelines for Case Study on p. 326 Conceptual Care Map Creator Audio Glossary Content Updates

References Association of periOperative Registered Nurses: 2018 Guidelines for perioperative practice. Denver, 2018, AORN.

2. The Joint Commission: Surgical care improvement project core measure set. Retrieved from www.jointcommission.org/assets/1/6/Surgical%20Care%20Improvem

3. The Joint Commission: National patient safety goals. Retrieved from www.jointcommission.org/standards_information/npsgs.aspx 4. Rothrock JC: Alexander’s care of the patient in surgery, ed 16, St Louis, 2018, Mosby. 5. Competency and Credentialing Institute: CNOR certification. Retrieved from www.ccinstitute.org/cnor/about. 6. Association of Surgical Technologists: About the profession. Retrieved from www.ast.org/AboutUs/About_AST. Association of periOperative Registered Nurses: AORN position statement on allied health care providers and support personnel in the perioperative practice setting. Retrieved from www.aorn.org//media/aorn/guidelines/position-statements/posstat-personnel-alliedhealth-care.pdf. Association of periOperative Registered Nurses: AORN position statement on RN first assistants. Retrieved from www.aorn.org//media/aorn/guidelines/position-statements/posstat-rnfa.pdf.

9. American Society of Anesthesiologists: Types of careers in anesthesia. Retrieved from https://www.asahq.org/education-and-career/careerresources/anesthesia-as-a-career/types-of-careers-inanesthesia. 10. American Association of Nurse Anesthetists. Scope of nurse anesthesia practice. Retrieved from www.aana.com/docs/default-source/practice-aana-comweb-documents-(all)/scope-of-nurse-anesthesiapractice.pdf?sfvrsn=250049b1_2. Hudson BF, Ogden J: Exploring the impact of intraoperative interventions for pain and anxiety management during local anesthetic surgery: A systematic review and meta-analysis, J

PeriAnesthesia Nurs 31:118, 2016.

12. Occupational Safety and Health Administration: Occupational safety and health standards, toxic and hazardous substances: Bloodborne pathogens. Retrieved from www.osha.gov/pls/oshaweb/owadisp.show_document? p_id=10051&p_table=STANDARDS. 13. Spruce L: Back to basics: Surgical fire prevention, AORN J 104:217, 2017. 14. Sanchez JA, Barach P, Johnson J: Surgical patient care: Improving safety, quality and value, New York, 2017, Springer. Association of periOperative Registered Nurses: Prevention of sentinel events. Retrieved from www.aorn.org/education/staffdevelopment/prevention-of-sentinel-events .

16. American Association of Nurse Anesthetists: Non anesthesia provider procedural sedation and analgesia. Retrieved from www.aana.com/docs/defaultsource/practice-aana-com-web-documents-(all)/nonanesthesia-provider-procedural-sedation-andanalgesia.pdf?sfvrsn=670049b1_2. 17. Wadlund DL: Local anesthetic systemic toxicity, AORN J 106:367, 2017. Mohanty S, Rosenthal R, Russell M, et al: Optimal perioperative management of the geriatric patient: A best practices guideline from the American College of Surgeons NSQIP and the American Geriatrics Society, JACS 222:930, 2016.

19. Seifert P: Crisis management of anaphylaxis in the OR, AORN J 105:219, 2017. 20. Malignant Hyperthermia Association of the United States: Emergency treatment for an acute MH event. Retrieved from www.mhaus.org/healthcare-

professionals/managing-a-crisis. ∗Evidence-based information for clinical practice.

19

Postoperative Care Diane M. Rudolphi

LEARNING OUTCOMES 1. Prioritize nursing responsibilities related to managing patients in the postanesthesia care unit (PACU). 2. Prioritize nursing responsibilities to maintain patient safety and prevent postoperative complications in the PACU and clinical unit. 3. Apply data from the initial nursing assessment to the management of the patient after transfer from the PACU to the clinical unit. 4. Select nursing interventions to manage potential problems during the postoperative period. 5. Distinguish discharge criteria from Phase I and Phase II postanesthesia care.

KEY TERMS airway obstruction, p. 332 atelectasis, p. 332 delayed emergence, p. 337 emergence delirium, p. 337

patient-controlled analgesia (PCA), p. 338 postoperative ileus (POI), p. 340 Three things in human life are important. The first is to be kind. The second is to be kind. And the third is to be kind. Henry James http://evolve.elsevier.com/Lewis/medsurg/

Conceptual Focus Gas Exchange Fluids and Electrolytes Infection Pain Perfusion Safety Tissue Integrity The postoperative period begins immediately after surgery and continues until the patient is discharged from medical care. This chapter focuses on the multiple concepts central to postoperative nursing. Nursing plays a vital role in supporting ventilation and perfusion, maintaining fluid and electrolyte balance, promoting comfort, reducing infection, and promoting safety. Specific surgical procedures and related postoperative care are discussed in the appropriate chapters of this text.

Postoperative Care of Surgical Patient The patient’s immediate recovery period is managed in a postanesthesia care unit (PACU). It is usually next to the operating room (OR). This location limits transportation of the patient right after

surgery and gives ready access to anesthesia and OR staff. The goals of PACU care are to maintain patient safety during recovery from anesthesia and identify actual and potential patient problems that may occur because of anesthesia and surgery and intervene appropriately.

Postanesthesia Care Unit Admission The patient’s admission to the PACU is a joint effort among the anesthesia care provider (ACP), OR nurse, and PACU nurse. This collaboration fosters a smooth transfer of care to the PACU and helps determine which phase we assign the patient.

PACU Progression There are 3 phases of postanesthesia care. During each phase, we provide different levels of care depending on the patient’s needs1 (Table 19.1). How patients move through the phases of care is determined by their condition and the type of anesthesia they received. If a patient assigned to Phase I care on admission to the PACU is stable and recovering well, the patient may rapidly progress through Phase I to either Phase II care or an inpatient unit. This accelerated progress is called rapid postanesthesia care unit progression (RPP). Another accelerated system of care is fast-tracking, which involves admitting ambulatory surgery patients directly to Phase II care. Although RPP and fast-tracking can result in time and cost savings, the patient’s safety is the primary factor determining where and at what level we provide postoperative care.

TABLE 19.1 Phases of Postanesthesia Care

Phase I • Care during the immediate postanesthesia period

• ECG and more intense monitoring (e.g., arterial BP monitoring, mechanical ventilation) Goal: Prepare patient for transfer to Phase II level of care, an inpatient unit, or intensive care setting

Phase II • Ambulatory surgery patients • Fast-tracking (i.e., patients who have bypassed Phase I level of care) Goal: Prepare patient for transfer to extended observation, home, or extended care facility

Extended Observation • Extended care or observation after transfer/discharge from Phase I or Phase II levels of care Goal: Prepare patient for self-care

Blended Levels of Care • Various levels of care offered in the same environment Source: American Society of PeriAnesthesia Nurses: 2015-2017 Perianesthesia nursing standards, practice recommendations and interpretive statements, Cherry Hill, NJ, 2015, The Society.

Phase I Initial Assessment On admission of the patient to the PACU, the ACP gives you a postanesthesia hand-off report (Table 19.2). Hand-off reports should be standardized and interactive, allowing you to ask questions and clarify information.2 The ACP should stay in the PACU until you

accept responsibility for the care of the patient. Potential problems in the postoperative period are shown in Fig. 19.1. Table 19.3 describes key parts of a PACU assessment. Begin your initial assessment by evaluating the patient’s airway, breathing, and circulation (ABC) status. Residual neuromuscular blockade, opioid use, and patient characteristics such as sleepdisordered breathing (e.g., obstructive sleep apnea [OSA], abnormal airway anatomy) affect oxygenation and ventilation. Be alert for signs of inadequate oxygenation and ventilation (Table 19.4). Any sign of respiratory distress needs prompt intervention. Pulse oximetry monitoring is a noninvasive means of assessing oxygenation and can provide an early warning of hypoxemia. Transcutaneous carbon dioxide (PtcCO2) and end-tidal CO2 (PetCO2) (capnography) monitoring are used to detect respiratory depression in high-risk patients.3 Volumetric capnography and acoustic respiratory rate monitoring can help you detect respiratory distress early.4 Pulse oximetry, capnography, PtcCO2, and PetCO2 are discussed in Chapter 25. Note and assess changes in ECG findings from the preoperative baseline. Measure the BP and compare it with baseline readings. Invasive monitoring (e.g., arterial BP) may be needed. Assess body temperature, peripheral pulses, capillary refill, and skin condition (e.g., color, moisture). Any signs of inadequate tissue perfusion need prompt intervention. Focus the initial neurologic assessment on level of consciousness; orientation; sensory and motor status; and size, equality, and reactivity of the pupils. The patient may be awake, drowsy but arousable, or asleep. Because hearing is the first sense to return in the unconscious patient, explain all activities to the patient from the time of admission to the PACU. If the patient received a regional anesthetic (e.g., spinal, epidural), sensory and motor blockade may still be present and you should assess dermatome levels (Fig. 19.2). During recovery from regional anesthesia, sensory and motor function first returns distal to the site where the anesthetic was given. This means the areas near the site of injections are the last to recover.

TABLE 19.2 PACU Hand-Off Report

General Information • Patient name and age • Surgeon and anesthesia care provider • Surgical procedure • Presence of tubes, drains, catheters, and IV lines • Type of anesthesia (e.g., general, regional, monitored anesthesia care) • Use of any reversal agents • Airway status (artificial airway and/or interventions to maintain adequate oxygenation) • Pain management interventions • NPO status and postoperative orders that need started

Patient History • Indication for surgery • Medical history, medications, allergies • Preoperative or baseline vital signs, laboratory and diagnostic findings • Level of consciousness, orientation • Specific patient characteristics (e.g., hearing loss, vision impairment, mobility limitations) • Patient preferences (e.g., cultural, personal beliefs/restrictions) • Patient emotional status on arrival to OR

Intraoperative Management

• Anesthetic agents • Other drugs received preoperatively or intraoperatively • Last dose of opioid administration/pain management plan • Total fluid replacements, including blood transfusions • Total fluid losses (e.g., blood, nasogastric drainage) • Urine output

Intraoperative Course • Unexpected anesthetic events or reactions • Unexpected surgical events • Most recent vital signs and monitoring trends • Results of laboratory tests and x-rays

Safety Alert Regional Anesthesia • Monitor for complications of regional anesthesia. • Be alert for respiratory distress, hypotension, dysrhythmias, changes in heart rate, bleeding or hematoma at site, headache, neurologic deficit or prolonged block, urinary retention, nausea, and pruritis. • Implement treatment protocols and notify the health care provider (HCP) as needed. Assess the urinary system by measuring intake and output and determining fluid balance. Intraoperative fluid totals are part of the ACP report. Note the presence of all IV lines; all irrigation solutions and infusions; and all output devices, including catheters and wound drains. Assess the surgical site. Note the condition of any dressings

and the type and amount of any drainage. Implement orders related to incision care. The rest of this chapter discusses the nursing management of select problems. You can apply this information to patients in both the PACU and clinical unit.

FIG. 19.1 Potential problems in the postoperative period.

TABLE 19.3 Initial PACU Assessment

Airway • Patency

• Oral or nasal airway • Laryngeal mask airway • Endotracheal tube with ventilator settings

Breathing • Respiratory rate and quality • Auscultated breath sounds • Pulse oximetry • Capnography or other technology-supported monitoring if indicated • Supplemental O2

Circulation • ECG monitoring: rate and rhythm • BP: noninvasive or arterial line • Hemodynamic pressure readings (if applicable) • Temperature • Capillary refill • Color, temperature, moisture of skin • Apical and peripheral pulses

Neurologic • Level of consciousness • Orientation • Sensory and motor status • Pupil size and reaction

Surgical Site • Dressings and visible incisions • Drains: type, patency, and drainage • IV assessment: location and condition of sites, solutions infusing

Genitourinary • Urine output

Gastrointestinal • Nausea, vomiting • Intake (fluids, irrigations) • Output (vomitus) • Bowel sounds

Pain • Incision • Other

Patient Safety Needs • Patient position • Fall risk assessment

TABLE 19.4 Signs of Inadequate Oxygenation

Cardiovascular System • Hypertension • Hypotension • Tachycardia • Bradycardia • Dysrhythmias • Delayed capillary refill • Weak peripheral pulses • Decreased O2 saturation

Central Nervous System • Restlessness • Agitation • Confusion • Muscle twitching • Seizures • Coma

Integumentary System • Flushed, cool, or moist skin • Cyanosis

Renal System • Urine output 90%

• Pain controlled or acceptable • Nausea and vomiting controlled • Report given

Ambulatory Surgery Discharge Criteria (Phase II or Extended Observation) • All PACU discharge criteria (Phase I) met • No IV opioid drugs for last 30 minutes • Voided if appropriate to surgical procedure or orders • Able to ambulate if not contraindicated • Responsible adult present to accompany and drive patient home • Written discharge instructions given and patient and caregiver understanding confirmed

TABLE 19.9 Postoperative SBAR Hand-Off

Communication

Situation Patient _____________________________ Date of birth ________________ Transferring to Room # ___________ Surgeon _______________________ ACP ________________________ Type of Anesthesia _________________ Procedure ______________________________________________________ Surgical site(s) __________________________________________________ Past medical history _____________________________________________ Code status ____________________ Isolation precautions _____________ Background Allergies _______________________________________________________ Medications received in PACU ____________________________________ IV site/fluids ____________________________________________________ Dressings and/or drains __________________________________________ Significant OR events ____________________________________________ Assessment PACU vital signs T _____ P _____ RR _____ BP ______ O2 Sat _________

O2 source ________________ FIO2 _________________________________ Pain rating at discharge __________________________________________ Method of pain management _____________________________________ Last dose of pain medication _____________________________________ Mental status ___________________________________________________ Nausea/vomiting at discharge _____________________________________ Intake __________________________ Output ________________________ Laboratory tests ________________________________________________ Recovery comments ____________________________________________ Recommendations Equipment needed ______________________________________________ Orders to be completed __________________________________________ Family __________________________________________________________ Other notes ____________________________________________________ Transferring RN _____________ Phone # for questions _______________ Receiving RN ___________________________________________________

TABLE 19.10 Nursing Assessment

Care of Patient on Admission to Clinical Unit 1. Record time of patient’s return to unit and assess airway, breathing, and circulation. 2. Obtain baseline vital signs, including O2 saturation. 3. Assess neurologic status, including level of consciousness and movement of extremities. 4. Assess level of pain: • Last dose and type of pain control • Current pain rating 5. Assess wound, dressing, and drainage tubes: • Type and amount of drainage • Tubing connected to gravity or suction drainage (per orders) 6. Assess color, temperature, and appearance of skin. 7. Position for airway maintenance, comfort, and safety (bed in low position, side rails up). 8. Check IV infusion: • Type of solution

• Amount of fluid remaining • Patency and flow rate • Condition of insertion site and size of catheter 9. Assess urinary status: • Time of voiding • Presence of catheter, patency, and total output • Bladder distention or urge to void 10. Assess for any nausea or vomiting. • Availability of emesis basin and tissues 11. Position call bell within reach, and orient patient to use of call bell. 12. Determine emotional state and provide support as needed. 13. Check for presence of caregiver. • Patient and caregiver oriented to immediate environment 14. Check and carry out postoperative orders.

Ambulatory Surgery Phase II and Extended Observation Advances in minimally invasive and noninvasive procedures, anesthesia, and analgesia have resulted in an increase in ambulatory surgical procedures. Ambulatory surgery patients include those patients receiving Phase II and extended observation postoperative care (Table 19.1). PONV and pain are common problems after ambulatory surgery. These can lead to delirium, prolonged PACU stay, delayed discharge, readmission, delayed resumption of usual activities, and decreased patient satisfaction.

Ambulatory Surgery Discharge The patient leaving an ambulatory surgery setting must be hemodynamically stable, mobile, alert, and able to provide a degree of self-care when discharged to home (Table 19.8). PONV and pain must

be under control. Overall, the patient must be stable and near the level of preoperative functioning for discharge from the unit. The patient may not drive and must be accompanied by an adult at the time of discharge. Carefully assess the patient’s readiness for discharge and home care needs. Determine availability of caregivers (e.g., family, friends) and access to (1) a pharmacy for prescriptions, (2) a phone in the case of an emergency, and (3) follow-up care.

Informatics in Practice Discharge Teaching • When discharging a patient who needs a complex dressing change and the written instructions are not adequate, consider using a video. This may be available on the hospital’s television system or the Internet (e.g., YouTube). • If using a video from the Internet, check to ensure that the procedure is properly performed. • The patient and caregiver can view the video or pictures at home as a reference when performing the procedure. • Have the patient and/or caregiver provide teach back information and/or demonstration.

Planning for Discharge and Follow-up Care Preparation for the patient’s discharge is an ongoing process that begins before surgery. Include the patient and caregiver in discharge planning and provide them with the information and support to make informed decisions about ongoing care. The informed patient is prepared as events unfold and gradually assumes more responsibility for self-care during the postoperative period. As discharge approaches, be sure that the patient and caregiver(s) have the following information:

• Symptoms to report (e.g., fever, increased incisional drainage, unrelieved incisional pain, discomfort in other parts of the body) • When and how to take prescribed drugs and possible side effects • Care of incision and any dressings, including bathing recommendations • Activities allowed and prohibited, when various activities can be resumed safely (e.g., driving, return to work, sexual intercourse, leisure activities) • Dietary restrictions or modifications • Where and when to return for follow-up appointment • Answers to any questions or concerns Common reasons patients seek help after discharge include unrelieved pain, need for advice about drugs, and wound issues (e.g., drainage). Attention to complete discharge instructions may prevent needless distress for the patient and caregiver. Standardized, preprinted discharge instructions that are surgery specific and easy to read ensure that information is complete. Record the discharge teaching in the chart. For the patient, the postoperative phase of care continues and extends into the recuperative period. Assessment and evaluation of the patient after discharge may be done with a follow-up call or by a visit from a home health nurse, who can address any specific questions and concerns. Increasingly, patients are discharged from the hospital with many care needs. They may be transferred to transitional care facilities, to long-term care facilities, or directly to their homes. When discharged directly to home, the patient is expected to continue self-care, with help from caregivers or home health care personnel (e.g., nurses, physical therapists). The care may include dressing changes, wound care, catheter or drain care, home antibiotics, or continued physical therapy. Working together with the discharge planner or case manager, ensure the patient’s safe transition from hospital-based care to community- or home-based care.

Gerontologic Considerations: Postoperative Patient The older surgical patient deserves special consideration. The older adult has decreased respiratory function, including decreased ability to cough and decreased thoracic compliance. These changes lead to an increase in the work of breathing and a decreased ability to eliminate drugs. Carefully monitor reactions to anesthetic drugs. Pneumonia is a common complication in older adults. Altered vascular function in the older adult is due to atherosclerosis and decreased elasticity in the blood vessels. Cardiac function is often compromised with limited compensatory responses to changes in BP and volume. Circulating blood volume decreases. Hypertension is common. Cardiovascular status needs to be monitored closely throughout surgery and the postoperative period. Drug toxicity is a potential problem in the older adult. Renal perfusion normally decreases, along with a reduced ability to remove drugs that the kidneys excrete. Decreased liver function leads to reduced drug metabolism and increased drug activity. Carefully assess renal and liver function to prevent drug overdose and toxicity. Observing for changes in mental status is an important part of postoperative care in older adults. Factors such as age, history of alcohol abuse, poor baseline cognition, hypoxia, metabolic imbalances, hypotension, and polypharmacy can contribute to postoperative delirium. Anesthetics, especially anticholinergic and benzodiazepine drugs, increase the risk for delirium. Pain control in the older patient is challenging because of possible preexisting cognitive deficits, impaired communication, and physiologic changes that affect drug metabolism. Patients may hesitate to ask for pain medication because they believe pain is inevitable with surgery. Some older patients may fear addiction or be nervous about using PCA machines. Thoroughly assess pain in a surgical patient who does not report any pain. Encourage the use of analgesics. Explain to the patient and caregiver that untreated pain has a negative effect on recovery.

Case Study Postoperative Patient

© BananaStock/BananaStock/Thinkstock.

Patient Profile E.G., a 74-yr-old retired college professor, has just undergone surgery for a fractured hip. He fell off a ladder while painting his house. E.G.’s medical history includes type 2 diabetes and COPD. The surgery, done while he was under general anesthesia, lasted 3 hours.

Subjective Data • Active walker in his home community • Smokes 1 pack of cigarettes per day × 58 years • Always had problems sleeping • Difficulty hearing, wears hearing aid • Upset with injury and its impact on life • Is a widower and has no relatives nearby or friends to assist with care • Reports pain is 8 on a 0 to 10 scale on arrival to PACU

Objective Data • Admitted to PACU with abduction pillow between his legs, one peripheral IV catheter, a self-suction drain from the hip dressing, an indwelling urinary catheter • O2 saturation 91% on 40% O2 face mask

Interprofessional Care Postoperative Orders • Vital signs per PACU routine • Capillary blood glucose level on arrival and every 4 hours. Call for blood glucose level 250 mg/dL. Follow agency guidelines for management of hypoglycemia. • 0.45 normal saline at 100 mL/hr

• Morphine via patient-controlled analgesia 1 mg q10min (20 mg max in 4 hr) for pain • Advance diet as tolerated • Incentive spirometry q1hr × 10 while awake • O2 therapy to keep O2 saturation >90% • Respiratory: albuterol 2.5 mg via nebulizer every 4 hours PRN for wheezing • Neurovascular checks q1hr × 4 hr • Empty and measure self-suction drain every shift • Strict intake and output

Discussion Questions 1. What are the potential postanesthesia problems you may expect with E.G.? 2. Priority Decision: What priority nursing interventions would be appropriate to prevent these problems from occurring? 3. Collaboration: Which interventions could you delegate to unlicensed assistive personnel (UAP)? 4. What factors predispose E.G. to the following problems: atelectasis, SSI, and VTE? 5. How would you determine E.G. is sufficiently recovered from general anesthesia to be discharged to the clinical unit? 6. What potential postoperative problems on the clinical unit might you expect? 7. What are risk factors for his developing postoperative delirium? What are the signs and symptoms of delirium? 8. Why is drug toxicity a potential problem for E.G.? 9. Priority Decision: Based on the assessment data, identify 3 priority nursing diagnoses. Are there any collaborative problems? 10. Evidence-Based Practice: E.G. tells you he does not want the “catheter” out because he does not want anyone to help him to

the bathroom. How would you respond to this request? 11. Patient-Centered Care: What teaching will you provide so that E.G. can successfully self-manage his care? 12. Collaboration: What referrals may be indicated based on E.G.’s medical history? 13. Safety: Identify 2 areas of risk for injury to E.G. What actions can you take to ensure patient safety? 14. Quality Improvement: What outcomes would indicate that interprofessional care with respiratory therapy was effective? Answers available at http://evolve.elsevier.com/Lewis/medsurg.

Case Study Managing Care of Multiple Patients You have been called into work at 10:00 AM to cover patients for a nurse who had a family emergency. You take over care for the following 3 patients on a surgical unit. You have 1 UAP available who is assigned to help you. Two other RNs are on the unit.

Patients

Discussion Questions 1. Priority Decision: After receiving report, which patient should you see first? Provide a rationale for your decision. 2. Collaboration: Which tasks should you delegate to the UAP? (select all that apply) a. Explain discharge instructions to G.S. b. Obtain noon vital signs on E.G. and F.D. c. Measure capillary blood glucose levels on F.D. and G.S. d. Confirm E.G.’s understanding of how to use the PCA pump.

e. Remind E.G. and G.S. to use their incentive spirometers every hour. 3. Priority Decision and Collaboration: When you enter F.D.’s room, you find her somewhat withdrawn and lethargic. Her face is cool and slightly clammy. What initial action would be most appropriate? a. Give 1 ampule of D50 IV stat. b. Increase F.D.’s IV rate to 150 mL/hr. c. Obtain a stat capillary blood glucose level. d. Ask the UAP to give F.D. a glass of orange juice.

Case Study Progression F.D.’s capillary blood glucose reading was 52 mg/dL. You notify her HCP and give 1 ampule of D50 IV dextrose as ordered. You then change her IV infusion to D5 ½NS. You check her capillary blood glucose within 15 minutes and then monitor her blood glucose levels each hour. 4. A preoperative checklist for F.D. is used to ensure completion of (select all that apply) a. removal of nail polish and jewelry. b. signed and witnessed informed consent. c. patient understanding of sensory information. d. identification of surgical site with surgical skin marker. e. notification of family of where to wait during the surgery. 5. F.D. tells you that she is afraid they may amputate the wrong leg. She tells you she has read stories of that happening at other hospitals. Your best response to F.D. would be to a. ask her if she would like a sedative to calm her fears. b. reassure her that it has never happened in this hospital. c. explain the “time-out” procedure for preventing such

errors. d. offer to go to the operating room with her to ensure the correct leg is amputated. 6. Priority Decision: The laboratory calls to report that E.G.’s aPTT (activated partial thromboplastin time) is 84 seconds. You assess him and find that the hip dressing is saturated with serosanguinous drainage. The next dose of heparin is due at 2100 this evening; the last dose was at 0900 this morning. His blood pressure is 92/54 with a heart rate of 110 bpm. Respiratory rate is 30 breaths/min, and O2 saturation is 98% on 2 L of O2. The nursing priority for this patient would be to a. notify physical therapy that his session today will have to be postponed until evening. b. notify the previous RN that a medication error occurred with the patient’s heparin dose at 0900. c. send an order to the laboratory for stat CBC and type and screen for 4 units of packed red blood cells. d. notify the provider of the aPTT result and anticipate orders for reversal agent, such as protamine. 7. Collaboration: Which instructions should you give to the UAP who will be helping E.G. with ADLs? (Select all that apply.) a. Use a soft toothbrush for oral care. b. Provide an emery board for nail care. c. Avoid overinflating blood pressure cuffs. d. Use an electric razor to shave the patient. e. Offer mouthwash with alcohol for rinsing. 8. Management Decision: When providing discharge instructions to G.S., he tells you that the UAP told him that he could do whatever activity he was comfortable doing—to let pain guide his progress. Your initial reaction to this statement should be to a. ask the UAP to clarify what was said to G.S. b. report the UAP’s actions to the nurse manager. c. teach G.S. about the reason for activity restrictions. d. clarify the discharge instructions with the health care provider.

Answers available at http://evolve.elsevier.com/Lewis/medsurg.

Bridge to Nclex Examination The number of the question corresponds to the same-numbered outcome at the beginning of the chapter.

1. What are the priority interventions the nurse performs when admitting a patient to the PACU? a. Assess the surgical site, noting presence and character of drainage. b. Assess the amount of urine output and the presence of bladder distention. c. Assess for airway patency and quality of respirations and obtain vital signs. d. Review results of intraoperative laboratory values and medications received. 2. A patient is admitted to the PACU after major abdominal surgery. During the initial assessment the patient tells the nurse he thinks he is going to “throw up.” A priority nursing intervention is to a. increase the rate of the IV fluids. b. give antiemetic medication as ordered. c. obtain vital signs, including O2 saturation. d. position patient in lateral recovery position. 3. After admitting a postoperative patient to the clinical unit, which assessment data require the most immediate attention? a. O2 saturation of 85%

b. Respiratory rate of 13/min c. Temperature of 100.4°F (38°C) d. Blood pressure of 90/60 mm Hg 4. A 70-kg postoperative patient has an average urine output of 25 mL/hr during the first 8 hours. The priority nursing intervention(s) given this assessment would be to a. notify the surgeon and expect obtaining blood work to evaluate renal function. b. perform a straight catheterization to measure the amount of urine in the bladder. c. continue to monitor the patient because this is a normal finding during this time period. d. evaluate the patient’s fluid volume status since surgery and obtain a bladder ultrasound. 5. Discharge criteria for the Phase II patient include (select all that apply) a. no nausea or vomiting. b. ability to drive self home. c. no respiratory depression. d. written discharge instructions understood. e. opioid pain medication given 45 minutes ago. 1. c, 2. d, 3. a, 4. d, 5. c, d, e For rationales to these answers and even more NCLEX review questions, visit http://evolve.elsevier.com/Lewis/medsurg.

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Review Questions (Online Only) Key Points Answer Keys for Questions • Rationales for Bridge to NCLEX Examination Questions • Answer Guidelines for Case Study on p. 345 • Answer Guidelines for Managing Care of Multiple Patients Case Study (Section 4) on p. 347 Student Case Study • Patient Undergoing Surgery Nursing Care Plan • eNursing Care Plan 19.1: Postoperative Patient Conceptual Care Map Creator Audio Glossary Content Updates

References 1. Schick L, Windle P: Perianesthesia nursing core curriculum: Preprocedure, phase i and phase II PACU nursing, ed 3, St Louis, 2016, Elsevier. 2. Odom-Forren J: Drain’s perianesthesia nursing: A critical care approach, ed 7, St Louis, 2018, Elsevier. Smallwood CD, Walsh BK: Noninvasive monitoring of oxygen and ventilation, Respir Care 62:6, 2017. Patino M, Kalin M, Griffin A, et al: Comparison of postoperative respiratory monitoring by acoustic and transthoracic impedance technologies in pediatric patients at risk of respiratory depression, Anesthes Analg 124:6, 2017.

Gillies M, Sander M, Shaw A, et al: Current research priorities in perioperative intensive care medicine, Intensive Care Med 43:9, 2017. Auffret V, Becerra Munoz V, Loirat A, et al: Transcatheter aortic valve implantation versus surgical aortic valve replacement in lower surgical risk patients with chronic obstructive pulmonary disease, Am J Cardiol 120:10, 2017. Feng B, Lin J, Jin J et al: Thirty–day postoperative complications following primary total knee replacement arthroplasty: A retrospective study of incidence and risk factors at a single center in China, Chin Med J 130:21, 2017. Misal U, Joshi S, Shaikh M: Delayed recovery from anesthesia: A postgraduate educational review, Anesth Essays Res 10:2, 2016. Takagi H, Ando T, Umemoto T: Perioperative depression or anxiety and postoperative mortality in cardiac surgery: A systematic review and meta-analysis, Heart Vessels 32:12, 2017. Oh E, Fong, T, Hsheih T, et al: Delirium in older persons advances in diagnosis and treatment, JAMA 318:12, 2017. Singh K, Bohl D, Ahn J, et al: Multimodal analgesia versus intravenous patient-controlled analgesia for minimally invasive transforaminal lumbar interbody fusion procedures, Spine 42:15, 2017.

12. Polomano R, Fillman M, Giordano N et al: Multimodal analgesia for acute postoperative and trauma-related pain, AJN 117:3, 2017. 13. The Joint Commission: Specifications manual for national hospital inpatient quality measures. Retrieved from www.jointcommission.org/specifications_manual_for_national_hospi Ziolkowski N, Rogers A, Xiong W, et al: The impact of operative time and hypothermia in acute burn surgery, Burns 43:1673, 2017. Venara A, Neunlist M, Slim K et al: Postoperative ileus: Pathophysiology, incidence, and prevention, J Visc Surg 153:6, 2016. Cao X, White, P, Ma, H: An update on the management of

postoperative nausea and vomiting, J Anesthes 31:617, 2017.

17. Rothrock J: Alexander’s care of the patient in surgery, ed 15, 2015, St Louis. 18. Berrios-Torres S, Umscheid C, Bratzler D, et al: Centers for Disease Control and Prevention guidelines for the prevention of surgical site infection, JAMA Surg 152:784, 2017 ∗Evidence-based information for clinical practice.

SECTION FIVE

Problems Related to Altered Sensory Input OUTLINE 20. Assessment and Management: Visual Problems 21. Assessment and Management: Auditory Problems 22. Assessment: Integumentary System 23. Integumentary Problems 24. Burns

20

Assessment and Management Visual Problems Jonel L. Gomez

LEARNING OUTCOMES 1. Describe the structures and functions of the visual system. 2. Explain the physiologic processes involved in normal vision. 3. Obtain significant subjective and objective assessment data related to the visual system. 4. Perform a physical assessment of the visual system using the appropriate techniques. 5. Distinguish normal from common abnormal findings of a physical assessment of the visual system. 6. Link the age-related changes in the visual system to differences in assessment findings. 7. Describe the purpose, significance of results, and nursing responsibilities related to diagnostic studies of the visual system. 8. Compare and contrast the types of refractive errors and appropriate corrections. 9. Describe the common causes and assistive measures for severe visual impairment. 10. Discuss nursing measures that promote eye health.

11. Explain the pathophysiology, clinical manifestations, and interprofessional and nursing management of the patient with ocular disorders. 12. Discuss the general preoperative and postoperative care of patients undergoing surgery of the eye.

KEY TERMS age-related macular degeneration (AMD), p. 369 astigmatism, p. 359 cataract, p. 364 conjunctivitis, p. 362 enucleation, p. 373 glaucoma, p. 369 hordeolum, p. 361 hyperopia, p. 358 keratitis, p. 362 myopia, p. 358 presbyopia, p. 358 retinal detachment, p. 367 retinopathy, p. 367 strabismus, p. 363 Be the beacon of light in someone’s darkness. Randi Fine http://evolve.elsevier.com/Lewis/medsurg/

Conceptual Focus Coping Functional Ability Infection Sensory Perception

Visual System For people to be as independent as possible and take part in fulfilling activities, it is important that the visual system is as functional as possible. The impact of poor vision or blindness can be devastating to activities of daily living (ADLs) and independence. The psychosocial consequences can include decreased quality of life, social isolation, depression, and loss of self-esteem. Vision loss also takes a huge toll on caregivers. This makes our being involved in vision-loss prevention, detection, and treatment strategies important.

Structures and Functions of Visual System The visual system is part of the central nervous system (CNS). It consists of 2 main parts, the eyes, which contain the image receptors, and the brain. The brain functions to process and interpret the information transmitted from the receptors into images. Anatomically, the visual system is made up of the orbit, the ocular adnexa (external tissues and structures surrounding the eye), the eye, and the visual pathway (optic nerve, optic chiasm, lateral geniculate nucleus, and visual cortex). The entire visual system is important for visual function.

Periocular Structures

Orbit The orbits, or eye sockets, are the bony structures that house the eyeballs. Seven bones form the orbit: frontal, zygoma, maxilla, ethmoid, sphenoid, lacrimal, and palatine (Fig. 20.1). The average orbit is 35 mm high and 40 mm wide. In addition to the eye, the orbits contain the associated muscles, nerves, blood vessels, and fat.1 Within the orbit are 3 main orbital openings, or fissures, the optic canal, the superior orbital fissure, and the inferior orbital fissure. They are all important conduits for arteries, veins, and nerves. The optic canal is located at the top of the socket. It provides an entry point for the optic nerve (CN II). The superior orbital fissure is a small slit in the posterior orbit. It is the main entry point for several other cranial nerves to enter the orbit from the brain. These include the oculomotor nerve (CN III), trochlear nerve (CN IV), trigeminal nerve (CN V), and abducens nerve (CN VI). The inferior orbital fissure is in the floor of the orbit. It holds the zygomatic branch of the maxillary nerve.

FIG. 20.1 Bones that form the orbit, or eye socket. From Lampignano J, Kendrick L: Bontrager’s textbook of radiographic positioning and related anatomy, ed 9, St Louis, 2018, Mosby.

There are 6 extraocular muscles: (1) superior and inferior rectus muscles, (2) medial and lateral rectus muscles, and (3) superior and inferior oblique muscles. They emerge from the apex of the orbit and attach to the eye to stabilize and move it (Fig. 20.2). Neuromuscular coordination produces simultaneous movement of the eyes in the same direction.

Ocular Adnexa The ocular adnexa include the eyebrows, eyelids, eyelashes, and lacrimal system. Eyebrows, eyelids, and eyelashes are vital in protecting the eye. They are a physical barrier to dust and foreign particles. Blinking protects the eye from injury, distributes tears over

the anterior surface of the eyeball, and supplies necessary nourishment to surface cells. The upper and lower eyelids join at the medial and lateral canthi. Eyelid skin is the thinnest skin in the human body, measuring less than 1 mm thick. The upper eyelids contain the levator palpebrae superioris muscle, innervated by the superior division of CN III. This muscle elevates and retracts the upper eyelid. The eyelids close through the action of the orbicularis muscle, which is innervated by CN VII.

Lacrimal System The lacrimal system includes the structures needed for tear production and drainage. The main lacrimal gland and accessory lacrimal glands make tears. The lacrimal glands, in the superotemporal orbit, are exocrine glands. They make and secrete the aqueous layer of tear film and are responsible for reflex tear production. The tear film moistens the eye and supplies oxygen to the cornea. The accessory lacrimal glands, the glands of Wolfring and glands of Krause, are found within the conjunctiva of the upper eyelid. They are responsible for baseline tear production. Tears pass over the surface of the eye and then enter the nasolacrimal system. The nasolacrimal drainage system includes the puncta, canaliculi, lacrimal sac, and nasolacrimal duct (Fig. 20.3).

Eyeball The eyeball, or globe, is composed of 3 layers (Fig 20.4). The tough outer layer is composed of the cornea, conjunctiva, and sclera. The middle layer consists of the uveal tract (iris, choroid and ciliary body), and the innermost layer, the retina. The anterior cavity is divided into the anterior and posterior chambers. The anterior chamber lies between the iris and posterior surface of the cornea. The posterior chamber lies between the anterior surface of the lens and posterior surface of the iris. The posterior cavity lies in the large space behind the lens and in front of the retina.

FIG. 20.2 The 6 extraocular muscles. From Drake R, Vogl AW, Mitchell AWM: Gray’s anatomy for students, ed 3, Philadelphia, 2015, Churchill Livingstone.

External Ocular Structures The conjunctiva is a transparent mucous membrane that covers the inner surfaces of the eyelids and extends over the sclera. Glands in the conjunctiva secrete mucus and tears. Tenon’s capsule, also called the fascia bulbi, is a thin layer of fascia that encases the eyeball behind the conjunctiva. The capsule extends posteriorly, ultimately fusing with the optic nerve.

FIG. 20.3 External eye and lacrimal apparatus. Tears made in the lacrimal gland pass over the surface of the eye and enter the lacrimal canal. From there the tears are carried through the nasolacrimal duct to the nasal cavity. Modified from Patton KT, Thibodeau GA: Anatomy and physiology, ed 8, St Louis, 2013, Mosby.

The cornea allows light to enter the eye. It is transparent and avascular. Its curved shape refracts or bends incoming light rays to help focus them on the retina. The cornea has 6 layers: epithelium, Bowman’s layer, stroma, Descemet’s membrane, Dua’s layer, and endothelium. The sclera, the white part of the eye, is a fibrous connective tissue layer that protects the eye and helps the eye maintain its shape and structure. The sclera extends from the cornea to the optic nerve. We call the junction of the sclera and cornea the limbus.

Middle Ocular Structures The iris gives the eye its color. It has a small round opening in the center, the pupil, which allows light to enter the eye. The pupil constricts by action of the iris sphincter muscle (under parasympathetic control) and dilates by action of the iris dilator muscle (under sympathetic control). This controls the amount of light that enters the eye. The ciliary body contains the ciliary muscle and ciliary processes. It is behind the iris. The ciliary muscle helps us focus by changing the shape of the lens to refract light onto the retina. The ciliary processes make aqueous humor for both the anterior and posterior chamber. The choroid is a highly vascular structure that nourishes the ciliary body, iris, and outer part of the retina. It lies inside and parallel to the sclera.

Internal Structures Aqueous Humor Aqueous humor fills the anterior chamber of the eye. It is a clear watery fluid composed of electrolytes, growth factors, and proteins. It nourishes the nonvascular structures of the anterior chamber, such as the lens. Aqueous humor is made from capillary blood in the ciliary body. It is secreted into the posterior chamber and flows through the pupil to enter the anterior chamber. Aqueous humor exits the eye through the trabecular meshwork and into the canal of Schlemm and venous circulation or through the ciliary muscle. Balanced secretion and excretion of aqueous humor is important. Excess production or decreased outflow can increase intraocular pressure (IOP) above the normal 10 to 21 mm Hg, a condition termed glaucoma.

FIG. 20.4 The human eye. Modified from Patton KT, Thibodeau GA: Anatomy and physiology, ed 8, St Louis, 2013, Mosby.

Lens The lens is a biconvex structure behind the iris. It is kept in place by small fibers collectively called the suspensory ligament, or the zonule. The ligament is a series of microscopic wire-like threads that connect the lens to the ciliary body. The primary function of the lens is to change shape to alter the focal distance of the eye. It works with the cornea to refract, or bend light. The lens shape is changed by action of the ciliary body as part of accommodation, a process that allows a person to focus. An example of accommodation is the ability to focus on near objects, such as when reading.

Vitreous Humor The retina lines the back of the eye, extending from the area of the optic nerve to the ciliary body (Fig. 20.4). Neurons make up most of the retina. Therefore retinal cells are unable to regenerate if destroyed. The retina converts images into a form that the brain can understand and process as vision. The retina has 2 main parts, the peripheral retina and central retina. The central retina contains the macula and fovea. The macula is about 6 mm in diameter. It is responsible for the central visual field. The fovea is at the center of the macula. This area provides the sharpest visual acuity, which we need for activities in which detail is important, like reading and driving. The retina contains light-sensitive structures called photoreceptor cells. There are 2 types of photoreceptors, rods and cones. Rods and cones convert light to neural signals, which the nervous system translates into vision. Rods are mostly found in the peripheral retina. They are responsible for most of our peripheral vision and night vision. Rods only perceive light and dark and do not contribute to color vision. Cones are in the central retina, condensed mostly in the fovea. They are responsible for central vision and color vision. There are 3 types of cone cells, red, green, and blue. They all work together to create the full color spectrum. The retina receives oxygen and nutrients from the choroid and the retinal vasculature. The central retinal artery carries blood and nutrients into the retina. The central retinal vein carries blood away from the retina.

Optic Nerve The optic nerve, or CN II, transmits visual information from the retina to the brain. The optic nerve begins at the optic disc, which is the region of the retina where the optic nerve and vessels leave the retina. Because there are no photoreceptor cells over the optic disc, there is an anatomic blind spot in this area. In the center of the optic disc is a white, cup-shaped area called the optic cup.

Visual Pathway For light to reach the retina, it must pass through many structures: the cornea, aqueous humor, lens, and vitreous humor. These structures must be clear for light to reach the retina and stimulate the photoreceptor cells. Once the image travels through the refractive media, it is focused on the retina (Fig. 20.5). From the retina, the impulses travel through the optic nerve to the optic chiasm, where the nasal fibers of each eye cross over to the other side. Fibers from the left field of both eyes form the left optic tract and travel to the left occipital cortex. The fibers from the right field of both eyes form the right optic tract and travel to the right occipital cortex.

Gerontologic Considerations: Effects of Aging on the Visual System Every structure of the visual system is subject to changes as a person ages. While many of these changes are relatively benign, others may result in severely compromised visual acuity in the older adult. Agerelated changes in the visual system and differences in assessment findings are shown in Table 20.1.

FIG. 20.5 The visual pathway. Fibers from the nasal portion of each retina cross over to the opposite side of the optic chiasma, ending in the lateral geniculate body of the opposite side. Location of a lesion in the visual pathway determines the resulting visual defect.

Assessment of Visual System Assessment of the visual system may be as simple as determining a patient’s visual acuity or as complex as collecting complete subjective and objective data pertinent to the visual system. The patient in a clinic or office setting is often seeking routine eye care or a change in

the prescription of eyewear. However, the patient may have some underlying concerns that he or she does not mention or even recognize. To perform an appropriate visual evaluation, assess what is necessary for the specific patient. While many of these assessments are within your scope of practice, some require special training.

Case Study Patient Introduction

© Jack Hollingsworth/Photodisc/Thinkstock.

F.M. is an 81-yr-old Hispanic woman who comes to the emergency department with visual changes. F.M. states that her vision “looks like everything is covered with a spider web.” She reports seeing periodic light flashes and small white spots “floating” in the air.

Discussion Questions 1. What are the possible causes of F.M.’s vision problems? 2. What type of assessment would be most appropriate for F.M.: comprehensive, focused, or emergency? 3. What assessment questions will you ask her? You will learn more about F.M. and her condition as you read through this assessment chapter. (See p. 354 for more information on F.M.) Answers available at http://evolve.elsevier.com/Lewis/medsurg.

TABLE 20.1 Gerontologic Assessment

DifferencesVisual System

Subjective Data Important Health Information Past Health History Take information about the patient’s past health history, including the

ocular and nonocular history. The patient’s nonocular history can be significant in assessing and treating an eye condition. Ask the patient about systemic diseases that may have ocular manifestations. These include diabetes, hypertension, cancer, rheumatoid arthritis, syphilis and other sexually transmitted infections (STIs), acquired immunodeficiency syndrome (AIDS), muscular dystrophy, myasthenia gravis, multiple sclerosis, inflammatory bowel disease, and hypothyroidism or hyperthyroidism. Include any history of stroke or neurologic problems as these have the potential to result in visual field defects. Obtain a history of tests for visual acuity, including the date of the last examination and change in glasses or contact lenses. Ask the patient about a history of strabismus, amblyopia, cataracts, retinal detachment, refractive surgery, or glaucoma. Note any trauma to the eye, its treatment, and sequelae. Obtain information about allergies. Allergies often cause eye symptoms, such as itching, burning, watering, drainage, and blurred vision.

FIG. 20.6 Arcus senilis, or age-related degeneration of the cornea. From Kanski JJ: Clinical ophthalmology: A synopsis, ed 2, New York, 2009, Butterworth-Heinemann.

Medications Obtain a complete medication history, including dosage and frequency of over-the-counter (OTC) medicines, eyedrops, herbal therapies, and dietary supplements. Many of these drugs have ocular effects. For example, many cold preparations contain a form of epinephrine (e.g., pseudoephedrine) that can dilate the pupil. Note the use of any antihistamine or decongestant, since these drugs can cause ocular dryness. Ask whether the patient uses any prescription drugs, such as corticosteroids, thyroid medications, or oral hypoglycemics and insulin. Long-term use of corticosteroid preparations can contribute to the development of glaucoma or cataracts.2 Note whether the patient is taking any β-blockers, since β-blockers used to treat glaucoma can potentiate their effects. Hydroxychloroquine, which is used to treat rheumatoid arthritis and other autoimmune diseases, has the potential to result in retinal toxicity. It is important that these patients have annual comprehensive eye examinations.

Surgery or Other Treatments Obtain a comprehensive history of both ocular and nonocular surgeries. Include laser-based surgery and invasive treatments, such as retinal injections.

Functional Health Patterns The focus of the functional health pattern assessment depends on the presence or absence of vision loss and whether the loss is permanent or temporary. Table 20.2 lists suggested health history questions related to the functional health patterns.

Health Perception–Health Management Pattern Patient characteristics, such as gender, ethnicity, and age, are important in assessing eye problems. Men are more likely than women to have color blindness. The leading cause of blindness among blacks is glaucoma.3

The patient’s visual health can affect activities at home or at work. It is important to know how the patient perceives the current health problem. As outlined in Table 20.2, guide the patient in describing the current problem. Assess the patient’s ability to perform self-care, especially any eye care related to the patient’s eye problem. The patient may not recognize the importance of eye-safety practices, like wearing protective eyewear during potentially hazardous activities or avoiding noxious fumes and other eye irritants. Ask about the use of sunglasses in bright light. Prolonged exposure to ultraviolet (UV) light can affect the retina. Ask about night driving habits and any problems encountered. Today, millions of people wear contact lenses, but many do not care for them properly. The type of contact lenses used and the patient’s wearing and care habits may provide an opportunity for teaching.

TABLE 20.2 Health HistoryVisual System

Health Perception–Health Management • Describe the change in your vision. Describe how this affects your daily life. • Do you wear protective eyewear (sunglasses, safety goggles, hats)?∗ • Do you wear contact lenses? If so, how do you take care of them? • If you use eyedrops, how do you instill them? • Do you have any allergies that cause eye symptoms?∗ • Do you have a family history of cataracts, glaucoma, or macular degeneration?∗

Nutritional-Metabolic • Do you take any nutritional supplements?∗

• Does your visual problem affect your ability to obtain and prepare food?∗

Elimination • Do you have to strain to void or defecate?∗

Activity-Exercise • Are your activities limited in any way by your eye problem?∗ • Do you take part in any leisure activities that have the potential for eye injury?∗

Sleep-Rest • Is your vision affected by the amount of sleep you get?∗ • Does your eye problem affect your sleeping patterns?∗

Cognitive-Perceptual • Does your eye problem affect your ability to read?∗ • Do you have any eye pain?∗ • Do you have any eye itching, burning, or foreign body sensation? ∗

Self-Perception–Self-Concept • How does your eye problem make you feel about yourself?

Role-Relationship • Do you have any problems at work or home because of your eyes?∗ • Have you made any changes in your social activities because of your eyes?∗

Sexuality-Reproductive • Has your eye problem caused a change in your sex life?∗ • For women: Are you pregnant? Do you use birth control pills?∗ • For men: Do you use any erectile dysfunction drugs? Any vision problems with their use?∗

Coping–Stress Tolerance • Do you feel able to cope with your eye problem?∗ • How do you feel that your eye problem has affected your life, and how do you cope with these changes?∗

Value-Belief • Do you have any conflicts about the treatment of your eye problem?∗



If yes, describe.

Hereditary systemic diseases (e.g., sickle cell anemia) can significantly affect eye health. In addition, many refractive errors and

other eye problems are hereditary. Ask whether the patient has a family history of arteriosclerosis, diabetes, thyroid disease, hypertension, arthritis, or cancer. Determine whether the patient has a family history of eye problems, including cataracts, tumors, glaucoma, refractive errors (especially myopia, hyperopia), and retinal degenerative conditions (e.g., macular degeneration, retinal detachment).

Genetic Risk Alert Glaucoma • Certain types of glaucoma have a strong genetic link. We have discovered many different glaucoma genes. • The risk for developing glaucoma is higher in people with a positive family history.

Age-Related Macular Degeneration (AMD) • Some cases of AMD have a genetic link. Multiple genes may be associated with AMD.

Nutritional-Metabolic Pattern High doses of vitamins containing antioxidant, carotenoids, and omega-3 fatty acids (vitamins C and E, beta-carotene, zinc) may be important to ocular health. Some patients with age-related macular degeneration (AMD) may benefit from supplements of these vitamins.

Elimination Pattern Straining to defecate (Valsalva maneuver) can raise IOP. After patients have eye surgery, many HCPs do not want them to strain. Assess the patient’s usual pattern of elimination and determine whether there is

the potential for constipation in the patient who has had eye surgery.

Activity-Exercise Pattern The patient’s usual level of activity or exercise may be affected by reduced vision, symptoms accompanying an eye problem, or activity restrictions after surgery. Ask about leisure activities during which the patient may incur an eye injury. For example, gardening, woodworking, and other craft activities can result in corneal or conjunctival foreign bodies or even penetrating injuries of the globe. Sports activities, such as racquetball, baseball, and tennis, carry risks for blunt trauma to the eyes. People should wear protection goggles for these sports.

Sleep-Rest Pattern In the otherwise healthy person, lack of sleep may cause ocular irritation, especially if the patient wears contact lenses. Painful eye problems, such as corneal abrasions, may disrupt normal sleep patterns.

Cognitive-Perceptual Pattern Assess for other cognitive or perceptual problems. For example, the functional ability of a patient with a visual deficit will be further compromised if the patient also has hearing problems. The patient who cannot see to read may find it harder to follow discharge instructions if he or she also has trouble hearing or remembering verbal instructions. Eye pain is always an important symptom to assess. If eye pain is present, ask the patient about treatment and response.

Self-Perception–Self-Concept Pattern The loss of independence that can follow a partial or complete loss of vision, even if the condition is temporary, can have devastating effects on the patient’s self-concept. Evaluate the potential effect of vision loss on the patient’s self-image. For instance, disabling glare from a

cataract may prevent nighttime driving. In today’s highly mobile society, losing the ability to drive can represent a significant loss of independence and self-esteem.

Role-Relationship Pattern Eye problems can negatively affect the patient’s ability to take part in roles and responsibilities in the home, work, and social environments. For example, with decreased visual acuity, the patient may no longer adequately function at work. Many occupations place workers in conditions in which eye injury may occur. For example, factory workers may be at risk from flying metal debris. Eye-safety practices, such as the use of goggles or safety glasses, are now a legal requirement in some workplaces. The patient with diabetes may not be able to see well enough to self-administer insulin. This patient may resent dependence on a caregiver who takes over this function. Sensitively ask if the problem has affected the patient’s preferred roles and responsibilities.

Sexuality-Reproductive Pattern The patient with severe vision loss may develop such a poor selfimage that the ability to be sexually intimate is lost. Assure the patient that low vision or blindness does not affect a person’s ability to be sexually expressive. Often touch is more important than vision.

Coping–Stress Tolerance Pattern The patient with temporary or permanent visual problems may have emotional stress. Assess the patient’s coping strategies and availability of support systems.

Value-Belief Pattern Be sensitive to each patient’s individual values and spiritual beliefs as these may guide decisions about eye care. It can be hard to understand why a patient refuses treatment that has potential benefit or wants treatment that may have limited potential benefit.

Case Study Subjective Data

© Jack Hollingsworth/Photodisc/Thinkstock.

A focused subjective assessment of F.M. revealed the following information: • PMH: Extraocular extraction of cataract on right eye (OD) with implantation of intraocular lens 2 mo ago. Type 2 diabetes, hypothyroidism, and hypertension. • Medications: Glucophage 500 mg twice daily, levothyroxine 100 mcg daily, metoprolol 50 mg daily. • Health Perception–Health Management: States she used antibiotic and corticosteroid eyedrops after surgery as directed and followed-up with surgeon. Recovery was uneventful. Eyedrops were stopped 2 wk ago. Does not have allergies. Had excellent eyesight until today. • Elimination: Has had problems moving bowels with increased straining. Trying prune juice to help. • Activity-Exercise: Walks in the mall at least ½ mile 3 times a week. No resistance or isotonic exercises. • Cognitive-Perceptual: Denies eye pain, itching, or tearing. Having difficulty reading. • Coping–Stress Tolerance: Afraid she is having a stroke.

Discussion Questions 1. Which subjective assessment findings are of most concern to you? 2. What should be included in the physical assessment? For what would you be looking? 3. How will you individualize the assessment based on her age, ethnic/cultural background, and condition? You will learn more about the physical assessment of the visual system in the next section.

(See p. 358 for more information on F.M.) Answers available at http://evolve.elsevier.com/Lewis/medsurg.

Objective Data Physical Examination Physical examination of the visual system includes inspecting the ocular structures and determining the status of their respective functions. Physiologic functional assessment includes (1) assessing the patient’s visual acuity, ability to judge closeness and distance, and extraocular muscle function; (2) evaluating visual fields; (3) checking pupil function; and (4) measuring IOP. Assessment of ocular structures should include examining the ocular adnexa, external eye, and internal structures. Some structures, such as the retina, blood vessels, and optic disc, must be assessed with an ophthalmoscope.

TABLE 20.3 Normal Physical Assessment of

Visual System • Visual acuity 20/20 OU. No diplopia • External eye structures symmetric and without lesions or deformities • Lacrimal apparatus nontender and without drainage • Conjunctiva clear. Sclera white • PERRLA (pupils equal, round, reactive to light and accommodation) • Lens clear • EOMs intact (extraocular movements intact) • Optic disc margins sharp • Retinal vessels without hemorrhages or spots

Normal physical assessment of the visual system is outlined in Table 20.3. Assessment techniques related to vision are described in Table 20.4. Table 20.5 shows select assessment abnormalities. A focused assessment is used to evaluate the status of previously identified visual problems and to monitor for signs of new problems. A focused assessment of the visual system is shown in the box above.

Focused Assessment Visual System Use this checklist to make sure the key assessment steps have been done.

Subjective Ask the patient about any of the following and note responses.

Changes in vision (e.g., acuity, blurred)

Y

N

Eye redness, itching, discomfort

Y

N

Drainage from eyes

Y

N

Objective: Physical Examination Inspect Eyes for any discoloration or drainage



Conjunctiva and sclera for color and vascularity



Lens for clarity



Eyelid for ptosis



Assess Vision based on patient looking at nurse or Snellen chart



Extraocular movements (EOMs)



Peripheral vision PERRLA

✓ ✓

PERRLA, Pupils equal, round, reactive to light and accommodation.

Initial Observation Your initial observation of the patient can provide information that will help focus the assessment. A patient dressed in clothing with unusual color combinations may have a color-vision deficit. Note an unusual head position. The patient with diplopia may hold the head in a skewed position to try to see a single image. The patient with a corneal abrasion or photophobia will cover the eyes with the hands to try to block out room light. Make a crude estimate of depth perception by extending a hand for the patient to shake. During the initial observation, observe the patient’s overall facial and eye appearance. The eyes should be symmetric and normally placed on the face. The globes should not have a bulging or sunken appearance.

TABLE 20.4 Nursing AssessmentAssessment

Techniques: Visual System

Assessing Functional Status Visual acuity Always record the patient’s visual acuity for medical and legal reasons. When doing a physical examination of the eyes, assess the right eye first and then the left eye. Use the abbreviations right eye “OD,” left eye “OS,” and both eyes “OU.” Record the patient’s visual acuity before the patient receives any eye care. To assess visual acuity, position the person on a mark exactly 20 ft (6 m) from the Snellen eye chart. If the person wears glasses or contacts, leave them on. Using an occlude, cover one eye at a time during the test. Ask the person to read down the lines of the chart to the smallest line of letters and numbers possible. Record the result using the numeric fraction at the end of the last successful line read. Indicate whether any letters were missed and if corrective lenses were worn (e.g., “Right eye, 20/30-2, with contacts”). Next ask the patient to cover the other eye and repeat the process. Normal visual acuity is 20/20. The first number indicates the distance the person is standing or sitting from the chart. The second number gives the distance at which

a normal eye can read the particular line. Legal blindness is defined as the best-corrected vision in the better eye of 20/200 or less.

TABLE 20.5 Assessment AbnormalitiesVisual

System

If the patient reports near vision difficulty or is 40 years of age or older, use a hand-held vision screener with varying print sizes (e.g., a

Jaeger chart). Hold the card at 14 in (35 cm) from the eye in good light to assess near vision. Examine each eye separately, with glasses on if worn. A normal result is “14/14” in each eye, read without hesitancy and without the patient moving the card. If you must assess near visual acuity without access to a Jaeger eye chart, you can still make an accurate assessment using newsprint or the label on a container. Record the acuity as “reads newspaper headline at X inches.” If the patient is unable to read any of the lines on both the near and distant visual acuity charts, the next step is to assess whether they can see hand motion and light perception. Extraocular muscle functions Assess the corneal light reflex to evaluate for weakness or imbalance of the extraocular muscles. In a darkened room, ask the patient to look straight ahead while shining a penlight directly on the cornea. The light reflection should be in the center of both corneas as the patient faces the light source. To assess eye movement, hold a finger or an object within 10 to 12 inches of the patient’s nose. Ask the patient to follow with eyes only the movement of the object or finger in the 6 cardinal positions of gaze. This test can indicate weakness or paralysis in the extraocular muscles and cranial nerves (CN III, CN IV, and CN VI). Pupil function and intraocular pressure Pupil function is determined by inspecting the pupils and their reactions to light. The normal finding is often abbreviated as PERRL (pupils are equal [in size], round, and reactive to light). The pupils should react to light directly (pupil constricts when a light shines into the eye) and consensually (pupil constricts when a light shines into the opposite eye). In a small number of people, the pupils are normally unequal in size (anisocoria). To test for accommodation, ask the person to focus on a distant object. This process dilates the eyes. Then have the person shift the focus to a near object (e.g., your finger held about 3 inches from the person’s nose). A normal response is constriction of the eyes and

convergence (inward movement of both eyes toward each other). When accommodation is assessed with the pupillary light reflex, a normal response is PERRLA (pupils are equal, round, and reactive to light and accommodation). IOP (Table 20.4) is measured by a variety of methods, including tonometry. Normal IOP ranges from 10 to 21 mm Hg.

Assessing Structures We assess the visual system structures primarily by inspection. The visual system is unique because we can inspect not only the external structures but also many of the internal structures. The iris, lens, vitreous, retina, and optic nerve can be seen directly through the clear cornea and pupil opening. This direct inspection requires special observation equipment, such as the slit lamp microscope or ophthalmoscope. These permit examination of the conjunctiva, sclera, cornea, anterior chamber, iris, lens, vitreous, and retina under magnification. The ophthalmoscope is a hand-held instrument with a light source and magnifying lenses that is held close to the patient’s eye to visualize the posterior part of the eye. Little pain or discomfort is associated with these examinations. Eyebrows, eyelashes, and eyelids All structures should be present and symmetric, without deformities, redness, or swelling. Eyelashes extend outward from the lid margins. In normal closing, the upper and lower eyelid margins just touch. The lacrimal puncta should be open and positioned properly against the globe. Conjunctiva and sclera The conjunctiva and sclera are easily examined at the same time. Assess the color, smoothness, and presence of lesions or foreign bodies. The conjunctiva covering the sclera is normally clear, with fine blood vessels visible. These blood vessels are more common in the periphery. The sclera is normally white. A slight yellow cast may be found in

some dark-skinned people, such as blacks and Native Americans, or in the older adult from lipid deposition. A pale blue cast caused by scleral thinning can be normal in older adults. Cornea The cornea should be clear, transparent, and shiny. The iris should appear flat and not bulge toward the cornea. The area between the cornea and iris should be clear, with no blood or purulent material visible in the anterior chamber. Iris Both irises should be of similar color and shape. However, a color difference between the irises occurs normally in a small number of people. Retina and optic nerve We can get vital information about the vascular system and CNS through direct visualization with an ophthalmoscope. It is used to magnify the retina and optic nerves and bring them into crisp focus (Fig. 20.7). Skilled use of this instrument takes practice. Examine the optic nerve or disc for size, color, and abnormalities. The optic disc is creamy yellow with distinct margins. A central depression in the disc, called the physiologic cup, may be seen. This area is the exit site for the optic nerve. The cup should be less than half the diameter of the disc. Normally, no hemorrhages or exudates are present in the fundus (retinal background). Careful inspection of the fundus can reveal retinal holes, tears, detachments, or lesions. Small hemorrhages can be associated with diabetes or hypertension and can appear in various shapes, such as dots or flames. Finally, examine the macula for shape and appearance. This area is normally devoid of any blood vessels.

FIG. 20.7 Magnified view of retina through the ophthalmoscope. From Newell FW: Ophthalmology: Principles and concepts, ed 7, St Louis, 1992, Mosby.

Special Assessment Techniques Color Vision Testing the patient’s ability to distinguish colors is an important part of the overall assessment. Some occupations require accurate color discrimination. The Ishihara color test determines the patient’s ability

to distinguish a pattern of color in a series of color plates.

Stereopsis Stereoscopic vision allows a patient to see objects in 3 dimensions. An event that causes a patient to have monocular vision (e.g., enucleation, patching) results in the loss of stereoscopic vision. Without stereopsis, the person’s ability to judge distances or the height of a step is impaired. This can have profound consequences if the person trips over a step when walking or follows too closely behind another vehicle when driving.

Case Study Objective Data: Physical Examination and Diagnostic Studies

© Jack Hollingsworth/Photodisc/Thinkstock.

Physical examination findings of F.M. were as follows: • PERRL. No abnormalities noted on visual examination of external eye structures. EOMs intact and symmetric.

The HCP performs an ophthalmoscopic examination and finds a partial retinal detachment. Ultrasonography confirms the diagnosis.

Discussion Questions 1. Are these the diagnostic studies that you expected to be ordered? 2. Which diagnostic study results are of most concern to you? Answers available at http://evolve.elsevier.com/Lewis/medsurg.

Diagnostic Studies of Visual System Diagnostic studies of the visual system provide vital information in monitoring the patient’s condition and planning appropriate interventions. These studies are considered objective data. Table 20.6 presents common diagnostic studies of the visual system.

Visual Problems Refractive Errors Refraction is the eye’s ability to bend light rays so that they fall on the retina. In the normal eye, parallel light rays are focused through the lens into a sharp image on the retina. When the light does not focus properly, it is called a refractive error. This defect prevents light rays from converging into a single focus on the retina. Defects are a result of irregularities of the corneal curvature, focusing power of the lens, or length of the eye. Refractive errors are the most common visual problem. Blurred vision is the major symptom. In some cases, the patient may have eye discomfort, eyestrain, or headaches. Most refractive errors can be corrected using eyeglasses or contact lenses, refractive eye laser surgery, or surgical implantation of an artificial lens. Myopia (nearsightedness) is an inability to accommodate for objects

at a distance. It causes light rays to be focused in front of the retina. This means the person can see near objects but objects in the distance are blurry. Myopia may occur because of excessive light refraction by the cornea or lens or because of an abnormally long eye. Myopia is the most common refractive error. About 30% of Americans have this disorder.4 There is strong evidence that many people inherit myopia, or at least the tendency to develop myopia.4

TABLE 20.6 Diagnostic StudiesVisual System

Hyperopia (farsightedness) is an inability to accommodate for near objects. It causes the light rays to focus behind the retina and requires the person to use accommodation to focus the light rays on the retina for near objects. The person with hyperopia can see distant objects clearly. This type of error occurs when the cornea or lens does not have adequate focusing power or when the eyeball is too short. Presbyopia is the loss of accommodation associated with age. One usually begins to notice this condition in the early to mid-40s. As the eye ages, the lens becomes larger, firmer, and less elastic. These changes, which progress with aging, result in an inability to focus on

near objects. Astigmatism is an uneven or irregular curvature of the cornea. The irregularity causes the incoming light rays to be bent unequally. Thus, the light rays do not come to a single point of focus on the retina, which results in visual distortion. Astigmatism can occur in conjunction with any of the other refractive errors. Aphakia is the absence of the lens. Rarely, the lens may be absent congenitally, or it may be removed during cataract surgery. A lens that is traumatically injured is removed and replaced with an intraocular lens (IOL) implant. The absence of the lens results in a significant refractive error. Without the focusing ability of the lens, images are projected behind the retina.

Nonsurgical Corrections Corrective Glasses The right corrective lenses can enhance vision in those with myopia, hyperopia, presbyopia, and astigmatism. Glasses for presbyopia are often called “reading glasses” because they are usually worn only for close work. Presbyopic correction may be combined with a correction for another refractive error, such as myopia or astigmatism. In these combined glasses, the presbyopic correction is in the lower part of the spectacle lens. A traditional bifocal or trifocal has visible lines. However, most lenses today that correct vision at various distances do not have visible lines. The prescription varies throughout the lens, allowing distance focusing in the top two thirds and near focus in the bottom one third of the lens.

Contact Lenses Contact lenses are another way to correct refractive errors. Contact lenses are made from various plastic and silicone substances. They are highly permeable to oxygen and have a high water content. These features allow for increased wearing time with greater comfort. If the oxygen supply to the cornea is decreased, it becomes swollen, visual acuity decreases, and the patient has severe discomfort.

In general, you need to know whether the patient wears contact lenses, the pattern of wear (daily versus extended), and care practices. Shining a light obliquely on the eyeball can help visualize a contact lens. Contact lenses are associated with microbial keratitis, a severe sight-threatening complication. Risk factors for keratitis include poor hand cleaning, poor lens case hygiene, and inadequate lens cleaning. Teach the patient the importance of following recommended cleaning practices and reporting redness, sensitivity, vision problems, and pain to the eye care provider. Teach the patient to remove contact lenses at once if any of these problems occur.

Surgical Therapy Surgery can eliminate or reduce the need for eyeglasses or contact lenses and correct refractive errors by changing the focus of the eye. Surgical management for refractive errors includes laser surgery and IOL implantation.

Laser Laser-assisted in situ keratomileusis (LASIK) may be considered for patients with low to moderately high amounts of myopia or hyperopia, with or without astigmatism. The procedure first involves using a laser or surgical blade to create a flap in the cornea. The flap is folded back, exposing the middle section (stroma) of the cornea. Pulses from a computer-controlled laser vaporize a part of the stroma. The flap is then repositioned, adhering on its own without sutures in a few minutes.5 Photorefractive keratectomy (PRK) is indicated for low to moderate amounts of myopia or hyperopia, with or without astigmatism. It is a good option for a patient with insufficient corneal thickness for a LASIK flap. In PRK, the epithelium is removed and the laser sculpts the cornea to correct the refractive error. Laser-assisted subepithelial keratomileusis (LASEK) is similar to PRK, except that the epithelium is replaced after surgery.

Implant

Refractive intraocular lens (refractive IOL) implantation is an option for patients with a high degree of myopia or hyperopia. Like cataract surgery, it involves removing the patient’s natural lens and implanting an IOL. The IOL implant used is a special lens designed to correct the patient’s refractive error. Refractive IOLs can correct both myopia and presbyopia. Phakic intraocular lenses (phakic IOLs) are sometimes called implantable contact lenses. They are implanted into the eye without removing the eye’s natural lens. They are used for patients with high degrees of myopia or hyperopia. Unlike refractive IOLs, the phakic IOL is placed in front of the eye’s natural lens. Leaving the natural lens preserves the eye’s ability to focus for reading vision.

Promoting Health Equity Visual Problems • Glaucoma has an increased incidence and severity among blacks compared with whites. • Hispanic Americans have an increased incidence of diabetic retinopathy. • Whites have a higher incidence of macular degeneration than Hispanics, blacks, and Asian Americans.

Visual Impairment Visual impairment describes vision that cannot be fully corrected by corrective lenses, medical treatment, or surgery. The term visual impairment includes conditions ranging from low vision to the absence of all vision (total blindness). Many terms are used when people refer to visual impairment, including: • Low vision refers to impaired vision that cannot be improved

by conventional eyeglasses, contact lenses, medications, or surgery in which some good usable vision remains. • Severe visual impairment describes visual impairment in people who are unable to read ordinary newsprint even with correction. People with a severe visual impairment may or may not be legally blind. • Legal blindness refers to central visual acuity of 20/200 or less in the better eye with correction or a peripheral visual field of 20 degrees or less.6 Most blindness in the United States is the result of common eye diseases, including cataracts, glaucoma, age-related macular degeneration, and diabetic retinopathy.

Nursing Management: Visual Impairment Nursing Assessment It is important to assess how long the patient has had a visual impairment. Recent loss of vision has different implications for nursing care. Determine how the patient’s visual impairment affects normal functioning. Ask the patient about the level of difficulty involved in doing certain tasks. For example, how hard is it for the patient to read, write a check, move from one room to the next, or view the television? Other questions can help determine the personal meaning that the patient attaches to the visual impairment. Ask how the vision loss has affected specific aspects of the patient’s life, whether the patient has lost a job, or what activities the patient does not engage in because of the visual impairment. Determine the patient’s emotional reactions, coping strategies, and support systems. The patient may attach many negative meanings to the impairment because of societal views of blindness. For example, the patient may view the impairment as punishment or view

themselves as useless and burdensome.

Planning The overall goals are that the patient with impaired vision will (1) make a successful adjustment to the impairment, (2) discuss feelings related to the loss, (3) identify personal strengths and support systems, and (4) use appropriate coping strategies. If the patient has been functioning at an appropriate or acceptable level, the goal is to maintain the current level of function.

Nursing Implementation Health Promotion Encourage the patient with preventable causes of further visual impairment to seek appropriate health care. For example, the patient with vision loss from glaucoma may be able to prevent further visual loss by with prescribed therapies and eye examinations.

Acute Care Provide emotional support and direct care to the patient with recent visual impairment. Allow the patient to express fear, anger, and grief. Help the patient identify positive coping strategies. Caregivers are intimately involved in the experiences that occur with vision loss. With the patient’s knowledge and permission, include caregivers in discussions and encourage them to express their concerns. Many people are uncomfortable around a person with visual impairment because they are not sure what behaviors are appropriate. Being sensitive to the patient’s feelings without being overly worried or smothering the patient’s independence is vital in creating a therapeutic nursing presence. Always communicate in a normal conversational tone and manner with the patient and address the patient, not the caregiver. Common courtesy dictates introducing yourself and any other people who approach the patient. It is important to say good-bye when leaving the patient’s presence.

Making eye contact with the patient achieves several goals. It ensures that you are speaking while facing the patient so that the patient has no difficulty hearing. Your head position confirms that you are attentive to the patient. In addition, establishing eye contact ensures that you can observe the patient’s facial expressions and reactions. Help the patient using a sighted-guide technique. Stand slightly in front and to one side of the patient and offer an elbow for the patient to hold. Serve as the sighted guide, walking slightly ahead of the patient with the patient holding the back of your arm. As you walk, describe the environment to help orient the patient. For example, “We’re going through an open doorway and approaching 2 steps down.” Help the patient sit by placing one of his or her hands on the seat of the chair.

Ambulatory Care In working with the patient who is visually impaired, remember that a person classified as legally blind may have some useful vision. Rehabilitation after partial or total loss of vision can foster independence, self-esteem, and productivity. Know what services and devices are available and make appropriate referrals. For the legally blind patient the primary resource for services is the state agency for rehabilitation of the blind. Legally blind persons are often eligible for federal and state assistance and income tax benefits. A list of agencies that serve the partially sighted or blind patient is available from the American Foundation for the Blind (www.afb.org). Braille or audio books for reading and a cane or guide dog for ambulation are examples of vision substitution techniques. These are usually best for the patient with no functional vision. For most patients who have some remaining vision, vision enhancement techniques can help in learning to ambulate, read printed material, and perform ADLs.

Optical Devices for Vision Enhancement A wide range of newer technologies are available to help people with low vision. These devices include desktop video magnification/closed

circuit units, electronic hand-held magnifiers, text-to-speech scanners (material read aloud to you), E-readers, and computer tablets (material read aloud, magnification, image zooming, brighter screen, voice recognition). Many of these devices require some training by an assistive technology professional. Encourage patients to practice with the technologic device to ensure they can use it successfully.

Nonoptical Methods for Vision Enhancement Approach magnification is a simple way to enhance the patient’s residual vision. Recommend that the patient sit closer to the television or hold books closer to the eyes. Contrast enhancement techniques include watching television in black and white, using a black felt-tip marker, and using contrasting colors (e.g., a red stripe at the edge of steps or curbs). Increased lighting can be provided by halogen lamps, direct sunlight, or gooseneck lamps that are aimed directly at the reading material or other near objects. Large type is often helpful, especially when used with other vision enhancements.

Non–24-Hour Sleep/Wake Disorder A common problem that can occur in blind people, especially those who are totally blind, is non–24-hour sleep/wake disorder (Non-24). It is a circadian rhythm sleep disorder in which a person’s biologic clock does not synchronize to a 24-hour day.7 It is caused by lack of light input to the circadian clock. People with Non-24 have problems falling asleep or staying asleep at night. During the day, they may have an uncontrollable urge to sleep. This can result in severe sleep issues, including insomnia, excessive sleepiness, changing patterns of when a person sleeps, and social and work consequences. Taking melatonin can shift the circadian clock earlier (an advance) or later (a delay). Tasimelteon (Hetlioz), a melatonin receptor agonist, also can be used for treatment. It works by targeting receptors in the brain that control the timing of the sleep/wake cycle.

Evaluation The overall expected outcomes are that the patient with visual impairment will: • Follow treatment plan to prevent further loss of vision • Be able to use adaptive coping strategies • Maintain self-esteem and take part in social interactions • Function safely within her or his own environment

Promoting Population Health Responsible Eye Care • Regular hand washing prevents the spread of disease from one eye to the other. • Seeking appropriate health care can lead to early detection of disease and prevent further loss of vision in patients with certain types of partial vision loss. • Wearing sunglasses and practicing proper nutrition may help prevent cataract development and age-related macular degeneration. • Wearing eye protection during potentially hazardous work, hobby, and sport activities reduces the risk for eye injuries.

Gerontologic Considerations: Visual Impairment The older adult is at an increased risk for vision loss caused by eye disease. They may have other deficits, such as cognitive impairment or limited mobility, that further affect the ability to function in usual ways. Societal devaluation of older adults may compound the selfesteem or isolation issues associated with visual impairment.

Financial resources may be inadequate to secure vision services or assistive devices. The older patient may become increasingly confused or disoriented when visually compromised. The combination of decreased vision and confusion increases the risk for falls, which can have serious consequences. Decreased vision may compromise the older patient’s ability to function, resulting in concerns about independence and a diminished self-image. Decreased manual dexterity may make instilling prescribed eyedrops hard. Those with low vision are more likely to make medication errors that are potentially dangerous, such as taking too much insulin or mistaking one drug for another.

Eye Trauma Although the eyes are well protected by the bony orbit and fat pads, everyday activities can result in eye trauma. The most common eye injuries in the United States are due to falls and fights. Injuries at home may be caused by cleaning, gardening, power tool use, and home repair work. Sport- and work-related injuries are other causes of eye trauma.8

Check Your Practice You are working in your garden when your neighbor comes running into your yard. She is screaming and waving her arms. Her husband was using a chain saw to cut down a tree when a piece of wood chip flew into his eye. When you go to your neighbor’s yard, the husband is on the ground crying in pain and you assess that the wood chip is embedded in his eye. • What should you do next? Table 20.7 outlines the emergency management of the patient with an eye injury. Chemical burns can be devastating to the eye and need

immediate attention. Alkaline chemicals with a pH greater than 7 are the most harmful. They can penetrate the eye and damage the inner components. Acidic chemicals with a pH of less than 7 are unable to penetrate the eye but can damage the cornea. Both types of injury have the potential to result in blindness. A Morgan lens may be used to provide continuous irrigation of an injured eye. It consists of a sterile plastic device resembling a contact lens that floats over the eye (never physically touches it) and allows copious irrigation of the eye. The device is connected to tubing that delivers irrigating solution. The Morgan lens provides relief for chemical or thermal burns and removes nonembedded foreign materials in the eye. Trauma is often a preventable cause of visual impairment. Many eye injuries could be prevented by wearing protective eyewear. Your role in individual and community education is extremely important in reducing the incidence of eye trauma.

Extraocular Disorders Inflammation and Infection One of the most common eye conditions is inflammation or infection of the external eye. Many external irritants or microorganisms can affect the eye, conjunctiva, and avascular cornea. An external hordeolum (or a sty) is an infection of the meibomian glands in the lid margin (Fig. 20.8). The most common bacterial infective agent is Staphylococcus aureus. A red, swollen, circumscribed, and acutely tender area develops rapidly. Have the patient apply warm, moist compresses at least 4 times a day until it improves. This may be the only treatment needed. If it tends to recur, teach the patient to do lid scrubs daily. On occasion, antibiotic ointments or drops may be needed. A chalazion is a chronic inflammatory granuloma of the meibomian glands in the lid. It may evolve from a hordeolum or occur in response to the material released into the lid when a blocked gland ruptures.

The chalazion usually appears on the upper lid as a swollen, tender, reddened area that may be painful. Initial treatment is like that for a hordeolum. If warm, moist compresses are ineffective in promoting spontaneous drainage, the HCP may drain the lesion or inject it with corticosteroids.

TABLE 20.7 Emergency ManagementEye Injury

FIG. 20.8 Hordeolum (sty) on the upper eyelid caused by staphylococcal infection. Courtesy Stephen J. Laquis, MD, FACS Ophthalmic Facial Plastic Surgery Specialists, Fort Myers, FL.

Blepharitis is a common chronic bilateral inflammation of the lid margins. The lids are red rimmed with many scales or crusts on the lid margins and lashes. The patient mainly has itching but may also have burning, irritation, and photophobia. If a staphylococcal infection caused blepharitis, an eye antibiotic ointment must be used. Often blepharitis is caused by both staphylococcal and seborrheal microorganisms. The treatment must be more vigorous to avoid hordeolum, keratitis (inflammation of the cornea), and other eye infections. Emphasize thorough cleaning practices of the skin and scalp. Gentle cleansing of the lid margins with baby shampoo or lid scrubs can effectively soften and remove crusting.

Conjunctivitis Conjunctivitis is an infection or inflammation of the conjunctiva. Infections may be bacterial or viral. Conjunctival inflammation may result from exposure to allergens or chemical irritants. Careful hand washing and use of individual or disposable towels help prevent spreading the condition.

Bacterial Infections Acute bacterial conjunctivitis (pinkeye) is a common infection. Although it occurs in every age group, epidemics are common among children. S. aureus is the most common cause. The patient with bacterial conjunctivitis may have discomfort, pruritus, redness, and a mucopurulent drainage. Although it typically occurs initially in one eye, it generally spreads to the unaffected eye. It is usually selflimiting, but treatment with antibiotic drops shortens the course of the disorder. Teach patients the importance of hand washing and avoiding contact with an infected person.

Viral Infections Many different viruses cause conjunctival infections. The patient with viral conjunctivitis may have tearing, foreign body sensation, redness, and mild photophobia. This condition is usually mild and selflimiting. However, it can be severe, with increased discomfort and subconjunctival hemorrhaging. Adenovirus conjunctivitis may be contracted in contaminated swimming pools and through direct contact with an infected patient. Epidemic keratoconjunctivitis (EKC) is the most serious ocular adenoviral disease. EKC is spread by direct contact. In the medical setting, contaminated hands and instruments can be the source of spread. The patient may have tearing, redness, photophobia, and foreign body sensation. In most patients, the disease involves only one eye. Treatment is primarily palliative and includes ice packs and dark glasses. Therapy for severe cases can include mild topical corticosteroids to temporarily relieve symptoms and topical antibiotic ointment. Teach the patient the importance of good hygiene practices to avoid spreading the disease.

Chlamydial Infections Trachoma is a chronic conjunctivitis caused by Chlamydia trachomatis (serotypes A through C). It is a major cause of blindness worldwide. Trachoma is most often seen in underdeveloped countries. It is transmitted mainly by the hands and by flies. Adult inclusion

conjunctivitis (AIC) is caused by C. trachomatis (serotypes D through K). AIC is becoming more prevalent in the United States because of the increase in sexually transmitted chlamydial infection.9 Manifestations of both trachoma and AIC are mucopurulent eye discharge, irritation, redness, and lid swelling. For unknown reasons, AIC does not carry the long-term consequences of trachoma. Antibiotic therapy is usually effective for trachoma and AIC. Patients with AIC have a high risk for concurrent chlamydial genital infection and STIs that may need treatment.

Allergic Conjunctivitis Conjunctivitis caused by exposure to an allergen can be mild and transitory, or it can be severe enough to cause significant swelling. The defining symptom of allergic conjunctivitis is itching. The patient may have burning, redness, and tearing. The patient may develop allergic conjunctivitis in response to pollens, animal dander, ocular solutions, and medications. Teach the patient to avoid known allergens if possible. Artificial tears can be effective in diluting the allergen and washing it from the eye. Topical medications include antihistamines and corticosteroids.

Keratitis Keratitis is an inflammation or infection of the cornea. It is caused by a variety of microorganisms or by other factors. The condition may involve the conjunctiva and/or the cornea. When it involves both, the disorder is termed keratoconjunctivitis.

Bacterial Infections The cornea can become infected by a variety of bacteria. Risk factors include mechanical or chemical corneal epithelial damage, contact lens wear, nutritional deficiencies, immunosuppressed states, and contaminated products (e.g., lens care solutions and cases, topical medications, cosmetics). Treatment includes topical antibiotics. In some cases, the patient may need subconjunctival antibiotic injection

or, in severe cases, IV antibiotics.

Viral Infections Herpes simplex virus (HSV) keratitis is the most common infectious cause of corneal blindness in the Western hemisphere. It is a growing problem, especially with immunosuppressed patients. The corneal ulcer has a characteristic dendritic (tree-branching) appearance. Pain and photophobia are common. Current treatment for HSK includes acyclovir, ganciclovir, trifluorothymidine, penciclovir, and valacyclovir.10 Therapy may also involve corneal debridement. Topical corticosteroids are usually contraindicated because they contribute to a longer course and possible deeper ulceration of the cornea. The varicella-zoster virus (VZV) causes both chickenpox and herpes zoster ophthalmicus (HZO). HZO may occur by reactivation of an endogenous infection that has persisted in a latent form after an earlier attack of varicella or by contact with a patient with chickenpox or herpes zoster. It occurs most often in the older adult and immunosuppressed patient. Care of the patient with acute HZO may include analgesics for pain, topical corticosteroids to reduce inflammation, antiviral agents to reduce viral replication, mydriatic agents to dilate the pupil and relieve pain, and topical antibiotics to combat secondary infection. The patient may apply warm compresses and povidone-iodine gel to the affected skin.

Other Causes of Keratitis Keratitis may be caused by fungi, such as Aspergillus, Candida, and Fusarium species. This is especially true in the case of eye trauma in an outdoor setting where fungi are prevalent in the soil and moist organic matter. Acanthamoeba keratitis is caused by a parasite that is associated with contact lens wear, usually from contaminated lens care solutions or cases. Homemade saline solution is particularly susceptible to Acanthamoeba contamination. Teach the patient who wears contact lenses about good lens care practices. The treatment of Acanthamoeba

keratitis is difficult since the organism is resistant to most drugs. Antifungal agents (e.g., ketoconazole) may be given. If antimicrobial therapy fails, the patient may need a corneal transplant. Exposure keratitis occurs when the eyelids cannot adequately close. The patient with exophthalmos (protruding eyeball) from thyroid eye disease or masses posterior to the globe is susceptible to exposure keratitis (Fig. 20.9).

Corneal Ulcer Tissue loss caused by a corneal infection produces a corneal ulcer (infectious keratitis) (Fig. 20.10). The infection can be due to bacteria, viruses, or fungi. Corneal ulcers are often painful. The patient may feel as if there is a foreign body in the eye. Other symptoms can include tearing, purulent or watery discharge, redness, and photophobia. Treatment is aggressive to avoid permanent vision loss. Antibiotic, antiviral, or antifungal eyedrops may be given as often as every hour for the first 24 hours. An untreated corneal ulcer can result in corneal scarring and perforation, or hole in the cornea. A corneal transplant may be needed.

FIG. 20.9 Exophthalmos. Courtesy Stephen J. Laquis, MD, FACS Ophthalmic Facial Plastic Surgery Specialists, Fort Myers, FL.

FIG. 20.10 Corneal ulcer. Infection associated with poor contact lens care. Courtesy Cory J. Bosanko, OD, FAAO, Eye Centers of Tennessee, Crossville, TN.

Nursing Management: Inflammation and Infection Assess ocular changes, such as edema, redness, decreased visual acuity, feelings that a foreign body is present, or discomfort. Record the findings in the patient’s record. Consider the psychosocial aspects of the patient’s condition, especially when vision is impaired. The patient’s primary need is for information about prescribed care and how to perform that care. Careful asepsis and frequent, thorough hand washing are essential to prevent spreading organisms from one eye to the other, to other patients, to caregivers, and to health care team members. Teach the patient and caregivers how to avoid sources

of ocular irritation or infection and to respond appropriately if an eye problem occurs. The patient with infective disorders that may have a sexual mode of transmission needs specific information about those disorders. Apply warm or cool compresses as needed. Darkening the room and giving an analgesic are other comfort measures. If the patient’s visual acuity is decreased, modify the environment and activities for safety. Suggest alternative ways to perform daily activities and selfcare. The patient may need eyedrops as often as every hour. If the patient receives 2 or more different drops, stagger the eye drops to promote maximum absorption. For example, if 2 different eyedrops are ordered hourly, give 1 drop on the hour and 1 drop on the half hour (unless otherwise prescribed). The patient who needs to instill eyedrops frequently may have sleep deprivation. Review the proper technique for eye drop instillation. Review the use and care of lenses and lens care products. Teach the patient who wears contact lenses and develops infections to discard all opened or used lens care products and cosmetics. This will decrease the risk for reinfection from contaminated products.

Dry Eye Disorders Keratoconjunctivitis sicca (dry eyes) is a common problem, especially in older adults and people with certain systemic autoimmune diseases, such as scleroderma, systemic lupus erythematosus, and Sjögren’s. It is caused by a decrease in the quality or quantity of the tear film. Patients with dry eyes report irritation or “sand in my eye.” The sensation typically worsens through the day. Treatment is aimed at the underlying cause. With decreased tear secretion, the patient may use artificial tears or ointments. Cyclosporine ophthalmic emulsion (Restasis) helps to increase the eyes’ natural ability to make tears. In severe cases, closure of the lacrimal puncta may be done.

Strabismus Strabismus is a condition in which a person cannot consistently focus both eyes simultaneously on the same object. One eye may deviate in (esotropia), out (exotropia), up (hypertropia), or down (hypotropia). Strabismus in an adult may be caused by thyroid disease, neuromuscular problems of the eye muscles, retinal detachment repair, or cerebral lesions. The primary problem is double vision.

Corneal Disorders Corneal Scars Any wound (e.g., trauma, infection) to the cornea can cause it to become scarred and opacified, thus decreasing the normal transparency. The treatment is a corneal transplant.

Keratoconus Keratoconus is a noninflammatory, usually bilateral disease with a familial tendency. Keratoconus usually appears during adolescence and slowly progresses between ages 20 and 60 years. The anterior cornea thins and protrudes forward, taking on a cone shape. The only symptom is blurred vision. The astigmatism may be corrected with glasses or rigid contact lenses. Intacs inserts are generally used to delay the need for a corneal transplant when contact lenses or glasses no longer help a patient achieve adequate vision. They are clear plastic lenses surgically inserted on the cornea perimeter to reduce astigmatism and myopia. Sometimes, the cornea can perforate as central corneal thinning progresses. In these cases, a corneal transplant is done before the cornea can perforate.

Corneal Transplant Around 46,000 corneal transplants are done in the United States each

year. The surgery is one of the fastest and safest of all tissue or organ transplant surgeries.11 Indications for corneal transplants (keratoplasty) are corneal scarring and keratoconus. Types include penetrating (full thickness) corneal transplant and lamellar corneal transplant. Penetrating (full thickness) cornea transplant involves transplanting all the layers of the cornea using a donor cornea. In this procedure, the HCP removes the full thickness of the patient’s cornea and replaces it with a donor cornea that is sutured into place (Fig. 20.11). Vision may not be restored for up to 12 months. During a lamellar cornea transplant, only some layers of the cornea are replaced with the transplant. This can include the deepest layer, called the endothelium (posterior lamellar cornea transplant). Versions of this procedure include Descemet’s stripping endothelial keratoplasty (DSEK) or Descemet’s membrane endothelial keratoplasty (DMEK). Lamellar transplants may be better than full penetrating transplants when the disease process is limited to only part of the cornea.

FIG. 20.11 Sutures on a donated cornea after penetrating keratoplasty (corneal transplant). Courtesy Cory J. Bosanko, OD, FAAO, Eye Centers of Tennessee, Crossville, TN.

The time between the donor’s death and the removal of the tissue should be as short as possible. Eye banks test donors for human immunodeficiency virus (HIV) and hepatitis B and C. The tissue is preserved in a special nutritive solution. Improved methods of tissue procurement and preservation, postoperative topical corticosteroids, and careful follow-up have decreased graft rejection. Matching the blood type of the donor and recipient improves the success rate.

Intraocular Disorders Cataract A cataract is an opacity within the lens. The patient may have a cataract in one or both eyes. If cataracts are present in both eyes, one may affect the patient’s vision more than the other. Cataract removal is the most common surgery in the United States.12

Etiology and Pathophysiology Although most cataracts are age related (senile cataracts), they can be associated with other factors. These include blunt or penetrating trauma, smoking, alcohol use, radiation or UV light exposure, certain drugs (e.g., steroids), and ocular inflammation. The rate of cataract development varies from patient to patient. The patient with diabetes tends to develop cataracts at a younger age.13 In senile cataract formation, altered metabolic processes within the lens cause an accumulation of water and changes in the lens fiber structure. These changes affect lens transparency, causing vision changes.

Clinical Manifestations and Diagnostic Studies The patient with cataracts may have a decrease in vision, abnormal color perception, and glare. Glare is due to light scatter caused by the lens opacities. It may be significantly worse at night when the pupil dilates. The visual decline is gradual. Diagnosis is based on decreased visual acuity or other visual problem. The opacity is directly observable by ophthalmoscopic or slit lamp microscopic examination. A totally opaque lens creates the appearance of a white pupil. Table 20.6 lists other diagnostic studies that may be helpful in evaluating a cataract.

Interprofessional Care The presence of a cataract does not necessarily indicate a need for surgery. For many patients the diagnosis is made long before they decide to have surgery. Interprofessional care for cataracts is outlined in Table 20.8.

Nonsurgical Therapy Currently, no treatment is available to “cure” cataracts other than surgical removal. Often changing the patient’s eyewear prescription can improve visual acuity, at least temporarily. Other visual aids, such as strong reading glasses or magnifiers, may help the patient with

near vision. Increasing the amount of light to read or do other nearvision tasks is useful. The patient may be willing to adjust his or her lifestyle to adjust to visual decline. For example, if glare makes it hard to drive at night, a patient may choose to drive only during daylight hours or to have a someone else drive at night. Sometimes, informing and reassuring the patient about the disease process makes the patient comfortable about choosing nonsurgical measures, at least temporarily.

Surgical Therapy When palliative measures no longer provide an acceptable level of visual function, the patient is a candidate for surgery. The patient’s occupational needs and lifestyle changes are also factors affecting the decision to have surgery. In some instances, factors other than the patient’s visual needs may influence the need for surgery. Lensinduced problems, such as increased IOP, may require lens removal. Opacities may prevent the HCP from getting a clear view of the retina in the patient with diabetic retinopathy or other sight-threatening pathologic conditions. In those cases, the cataract is removed to allow visualization of the retina and adequate management of the problem.

TABLE 20.8 Interprofessional CareCataract

Diagnostic Assessment • History and physical examination • Visual acuity measurement • Ophthalmoscopy (direct and indirect) • Slit lamp microscopy • Glare testing, potential acuity testing in selected patients • Keratometry and A-scan ultrasound (if surgery is planned) • Other tests (e.g., visual field perimetry) to determine cause of visual loss

Management Nonsurgical • Change in glasses prescription • Strong reading glasses or magnifiers • Increased lighting • Lifestyle adjustment

Acute Care: Surgical Therapy Preoperative • Mydriatic, cycloplegic agents • Nonsteroidal antiinflammatory drugs • Topical antibiotics • Antianxiety medications

Surgery • Removal of lens • Phacoemulsification • Extracapsular extraction • Correction of surgical aphakia • Intraocular lens implantation (most frequent type of correction) • Contact lenses

Postoperative • Topical antibiotic • Topical corticosteroid or other antiinflammatory agent • Mild analgesia, if necessary

• Eye patch or shield and activity as prescribed Preoperative Phase Before surgery, obtain an appropriate history and physical examination. Because most patients have local anesthesia, they do not need extensive preoperative physical assessment. However, most patients with cataracts are older adults who may have several medical problems that should be evaluated and controlled before surgery. Most patients are admitted on an outpatient basis. The patient normally presents several hours before surgery to allow time for preoperative procedures. The patient receives a nonsteroidal antiinflammatory eyedrop to reduce inflammation and dilating drops. One type of drug used for dilation is a mydriatic, an α-adrenergic agonist that produces pupillary dilation by contracting the iris dilator muscle. Another type of drug is a cycloplegic, such as tropicamide (Mydriacyl), which are anticholinergic agents. They block the effects of acetylcholine on the ciliary body muscles. This produces paralysis of accommodation (cycloplegia), and on the iris sphincter muscle, pupillary dilation (mydriasis). The patient may receive antianxiety medication before surgery.

FIG. 20.12 Intraocular lens implant after cataract surgery. Courtesy Cory J. Bosanko, OD, FAAO, Eye Centers of Tennessee, Crossville, TN.

Drug Alert Cycloplegics and Mydriatics • Teach the patient to wear dark glasses to minimize photophobia. • Monitor for signs of systemic toxicity (e.g., tachycardia, CNS effects). Intraoperative Phase The most common form of cataract surgery is phacoemulsification. In this procedure, a very small incision is made in the surface of the eye in or near the cornea. A thin ultrasound probe is inserted into the eye and ultrasonic vibrations are used to dissolve the clouded lens into fragments. These pieces are then suctioned out through the same

ultrasound probe. The small incisions are self-sealing and usually do not need sutures. An extracapsular cataract extraction procedure is used for very advanced cataracts where the lens is too dense to dissolve into fragments. This technique requires a larger incision so that the cataract can be removed in one piece without being fragmented inside the eye. Sutures are needed to close the larger wound, and visual recovery is often slower. Most patients have an IOL implanted at the time of cataract extraction surgery (Fig. 20.12). The lens of choice is a posterior chamber lens that is placed in the capsular bag behind the iris. At the end of the procedure, other drugs, such as antibiotics and corticosteroids, may be given. Postoperative Phase Unless complications occur, the patient is usually ready to go home as soon as the effects of sedative agents have worn off. Postoperative medications usually include antibiotic drops to prevent infection and corticosteroid drops to decrease the inflammatory response. The eyedrops are gradually reduced in frequency and then stopped when the eye has healed. Recommendations for activity restrictions and nighttime eye shielding vary based on the HCP’s preference. Many prefer that the patient avoid activities that increase the IOP, such as bending or stooping, coughing, or lifting. During each postoperative examination, the HCP measures the patient’s visual acuity, checks anterior chamber depth, assesses corneal clarity, and measures IOP. Even on the operative day, the patient’s uncorrected visual acuity in the operative eye may be good. However, it is not unusual if the patient’s visual acuity is reduced right after surgery. Multifocal IOL can correct for both near and far vision. Some patients may still need glasses or contact lenses to achieve their best visual acuity.

Nursing Management: Cataracts Nursing Assessment Assess the patient’s distance and near visual acuity. If the patient is going to have surgery, especially note the visual acuity in the patient’s unoperated eye. Use this information to determine how visually compromised the patient may be while the operative eye is healing. Assess the psychosocial impact of the visual disability and the level of knowledge about the disease process and therapeutic options. After surgery, assess the patient’s level of comfort and ability to follow the discharge plan.

Planning Preoperatively, the overall goals are that the patient with a cataract will (1) make informed decisions about therapeutic options and (2) have minimal anxiety. Postoperatively, the overall goals are that the patient with a cataract will (1) understand and follow discharge instructions, (2) maintain an acceptable level of physical and emotional comfort, and (3) remain free of infection and other complications.

Nursing Implementation Health Promotion There are no proven measures to prevent cataract development. However, it is wise to suggest that the patient wear sunglasses, avoid unnecessary radiation, and maintain appropriate intake of antioxidant vitamins (e.g., vitamins C, E) and good nutrition. Provide information about vision enhancement techniques for the patient who chooses not to have surgery.

Acute Care Before surgery, the patient with cataracts needs accurate information

about the disease process and treatment options, since cataract surgery is considered an elective procedure. Be available to the patient and caregiver to help them make an informed decision about treatment. For the patient having surgery, provide information, support, and reassurance about the surgical and postoperative experience to reduce anxiety. Photophobia is common when receiving pupil dilation medications. Therefore decreasing the room lighting is helpful. These medications produce transient stinging and burning. After cataract surgery the patient usually has little or no pain but may have some scratchiness or blurriness in the operative eye. Mild analgesics are usually enough to relieve any pain. If the pain is intense, the patient should notify the HCP because this may indicate hemorrhage, infection, or increased IOP. A nursing care plan for the patient after eye surgery (eNursing Care Plan 20.1) is available on the website for this chapter.

Ambulatory Care Patients with cataracts who have surgery remain in the surgical facility for only a few hours. The patient and caregiver are responsible for almost all postoperative care. Give them written and verbal instructions before discharge. Include the caregiver in the instructions because some patients may have difficulty with self-care activities, especially if the vision in the unoperated eye is poor. Table 20.9 outlines patient and caregiver teaching after eye surgery. Most patients have little visual impairment after surgery. IOL implants provide immediate visual improvement. Many patients achieve a usable level of visual acuity within a few days after surgery.

TABLE 20.9 Patient & Caregiver TeachingAfter

Eye Surgery Include the following information in the teaching plan for the patient and caregiver after eye surgery:

• Proper hygiene and eye care techniques to ensure that medications, dressings, and/or surgical wound is not contaminated during eye care • Signs and symptoms of infection (e.g., increased or purulent drainage, increased redness, any decrease in visual acuity) and when and how to report these to allow for early recognition and treatment of possible infection • Importance of following restrictions on head positioning, bending, coughing, and Valsalva maneuver to optimize visual outcomes and prevent increased IOP • How to instill eye medications using aseptic techniques and adherence with prescribed eye medication routine to prevent infection • How to take pain medication and report pain not relieved by medication • Importance of continued follow-up as recommended to maximize potential visual outcomes A few patients may have significant visual impairment after surgery. These include patients who do not have an IOL implanted at the time of surgery, those who need several weeks to achieve a usable level of visual acuity after surgery, or those with poor vision in their unoperated eye. For those patients, the time between surgery and receiving glasses or contacts can be a period of significant visual disability. Suggest ways the patient and caregiver can modify activities and the environment to maintain an adequate level of safe functioning. Suggestions may include getting help with steps, removing area rugs and other potential obstacles, preparing meals for freezing before surgery, or obtaining audio books for diversion until visual acuity improves. If a patch is used, tell patients that they will not have depth perception until the patch is removed. This makes special measures to avoid falls or other injuries necessary. The patient with significant visual impairment in the unoperated eye needs more help while the

operative eye is patched. Some patients may need 1 or 2 weeks for the visual acuity in the operated eye to reach an adequate level for most visual needs. These patients need special assistance until the vision improves.

Evaluation The overall expected outcomes are that the patient after cataract surgery will: • Have improved vision • Be better able to take care of self • Have minimal to no pain • Be optimistic about expected outcomes

Gerontologic Considerations: Cataracts Most patients with cataracts are older. When the older patient is visually impaired, even temporarily, the patient may have a loss of independence, lack of control over her or his life, and a significant change in self-perception. Societal devaluation of the older adult complicates these experiences. The older patient often needs emotional support and encouragement, as well as specific suggestions to allow a maximum level of independent function. Assure the older patient that cataract surgery can be done safely and comfortably with minimal sedation.

Retinopathy Retinopathy is a process of microvascular damage to the retina. It can develop slowly or rapidly and lead to blurred vision and progressive vision loss. Retinopathy occurs most often in adults with diabetes or hypertension. Diabetic retinopathy is a common complication of diabetes, especially in patients with long-standing uncontrolled disease.13 Nonproliferative

retinopathy is the most common form of diabetic retinopathy. It is characterized by capillary microaneurysms, retinal swelling, and hard exudates. Macular edema represents a worsening of the retinopathy as plasma leaks from macular blood vessels. As capillary walls weaken, they can rupture, leading to intraretinal “dot or blot” hemorrhaging (Fig. 20.13). A severe loss in central vision can result. As the disease advances, proliferative retinopathy may occur. New blood vessels grow, but they are abnormal, fragile, and predisposed to leak, thus causing severe vision loss. (Diagnosis and treatment of diabetic retinopathy are discussed in Chapter 48.) Hypertensive retinopathy is caused by blockages in retinal blood vessels from hypertension. (Hypertension is discussed in Chapter 32.) These changes may not initially affect a person’s vision. On a routine eye examination, retinal hemorrhages, anoxic cotton-wool spots, and macular swelling can be seen. Sustained, severe hypertension can cause sudden visual loss from swelling of the optic disc and nerve (papilledema). Treatment, which may be an emergency, focuses on lowering the BP. Normal vision is usually restored by treating hypertension.

Retinal Detachment A retinal detachment is a separation of the sensory retina and the underlying pigment epithelium, with fluid accumulation between the 2 layers. In the patient with no other risk factors who has had a retinal detachment in one eye, the risk for detachment in the second eye is as high as 25%.14 Most patients with an untreated, symptomatic retinal detachment become blind in the involved eye.

Etiology and Pathophysiology Retinal detachment has many causes. The most common is a retinal break. Retinal breaks are an interruption in the full thickness of the retinal tissue. They can be classified as tears or holes. Retinal holes are atrophic retinal breaks that occur spontaneously. Retinal tears can

occur as the vitreous humor shrinks during aging and pulls on the retina. The retina tears when the traction force exceeds the strength of the retina. Once the retina has a break, liquid vitreous can enter the subretinal space between the sensory layer and the retinal pigment epithelium layer, causing a rhegmatogenous retinal detachment. Risk factors for retinal detachment are listed in Table 20.10.

FIG. 20.13 Diabetic retinopathy. Intraretinal dot or blot hemorrhages. Courtesy Cory J. Bosanko, OD, FAAO, Eye Centers of Tennessee, Crossville, TN.

Clinical Manifestations and Diagnostic Studies Patients with a detaching retina describe symptoms that include photopsia (light flashes), floaters, and a “cobweb,” “hairnet,” or ring in the field of vision. Once the retina has detached, the patient describes a painless loss of peripheral or central vision, “like a curtain” coming across the field of vision.

The area of visual loss corresponds inversely to the area of detachment. For example, if the retinal detachment involves the superior retina, the defect is seen in the inferior visual field. If the detachment is small or develops slowly, the patient may not be aware of a visual problem. Visual acuity measurements should be the first diagnostic procedure with any report of vision loss (Table 20.11). The HCP can see a retinal detachment using direct and indirect ophthalmoscopy or slit lamp microscopy in conjunction with a special lens to view the far periphery of the retina. Ultrasound may be useful in finding a retinal detachment if the retina cannot be directly visualized (e.g., when the cornea, lens, or vitreous is hazy or opaque).

TABLE 20.10 Risk Factors for Retinal Detachment • Age • Cataract surgery • Eye trauma • Family or personal history of retinal detachment • Severe myopia Source: National Eye Institute, National Institutes of Health: Retinal detachment. Retrieved from www.nei.nih.gov/health/retinaldetach.

TABLE 20.11 Interprofessional CareRetinal

Detachment

Diagnostic Assessment • History and physical examination

• Visual acuity measurement • Ophthalmoscopy (direct and indirect) • Slit lamp microscopy • Ultrasound if cornea, lens, or vitreous is hazy or opaque

Management Preoperative • Mydriatic, cycloplegic agents • Photocoagulation of retinal break that has not progressed to detachment

Surgery • Laser photocoagulation • Cryopexy • Scleral buckling procedure • Vitrectomy • Intravitreal bubble

Postoperative • Topical antibiotic • Topical corticosteroid • Analgesia • Mydriatics • Positioning and activity as prescribed

Interprofessional Care Some retinal breaks are not likely to progress to detachment. In these

situations, the HCP simply monitors the patient and teaches the patient to seek immediate evaluation if warning signs and symptoms of impending detachment occur. The goals of treatment are to reattach the retina and seal any retinal breaks. Several techniques are used to meet these goals.

Surgical Therapy Laser Photocoagulation and Cryopexy These techniques seal retinal breaks by creating an inflammatory reaction that causes a chorioretinal adhesion or scar. Laser photocoagulation involves using an intense, precisely focused light beam to create an inflammatory reaction. The light is directed at the area of the retinal break. Cryopexy involves freezing (cryotherapy) the retinal break by placing a probe on the ocular surface at the location of the break. The probe is activated with compressed nitrous oxide gas that temporarily freezes the break. The freeze thaw reaction creates scarring in the area that will seal the break. For retinal breaks accompanied by significant detachment, photocoagulation or cryopexy may be used intraoperatively in conjunction with scleral buckling. Tears or holes without accompanying retinal detachment may be treated prophylactically with laser photocoagulation or cryopexy if there is a high risk for progression to a retinal detachment. When used alone, laser photocoagulation and cryopexy therapy are outpatient procedures. They usually require topical anesthesia. The patient may have minimal adverse symptoms during or after the procedure.

Scleral Buckling Scleral buckling is an extraocular surgical procedure that involves placing a band around the globe to move the pigment epithelium, choroid, and sclera toward the detached retina. A silicone implant is sutured against the sclera, causing the sclera to buckle inward. An encircling band may be placed over the implant if there are multiple retinal breaks, if suspected breaks cannot be found, or if there is

widespread inward traction on the retina (Fig. 20.14). If present, subretinal fluid may be drained using a small-gauge needle. This promotes contact between the retina and buckled sclera. Scleral buckling is usually done as an outpatient procedure.

Intraocular Procedures Intraocular procedures are used on occasion. Pneumatic retinopexy is the intravitreal injection of a gas to form a temporary bubble in the vitreous that closes retinal breaks and provides apposition of the separated retinal layers. Because the intravitreal bubble is temporary, this technique is combined with laser photocoagulation or cryopexy. The patient with an intravitreal bubble must position the head so that the bubble is in contact with the retinal break. The patient may need to maintain this position as much as possible for up to several weeks. Vitrectomy (surgical removal of the vitreous) may relieve traction on the retina, especially when the traction results from proliferative diabetic retinopathy. Vitrectomy may be combined with scleral buckling to provide a dual effect in relieving traction.

Postoperative Considerations Visual prognosis varies, depending on the extent, length, and area of detachment. After surgery, the patient may be on bed rest and need special positioning to maintain proper position of an intravitreal bubble. The level of activity restriction after retinal detachment surgery varies. Verify the prescribed level of activity with the HCP and help the patient plan for any help needed related to activity restrictions. The patient may need multiple topical medications, including antibiotics, antiinflammatory agents, or dilating agents. Give prescribed pain medications and teach the patient to take the medication as prescribed after discharge. In most cases, retinal detachment is an urgent situation, and the patient is suddenly confronted with the need for surgery. The patient needs emotional support, especially during the immediate preoperative period when preparations for surgery can lead to more

anxiety. The patient may go home within a few hours of surgery or may remain in the hospital for several days, depending on the surgeon and type of repair. Discharge planning and teaching are important and should begin early. Patient and caregiver teaching after eye surgery is discussed in Table 20.11. Because the patient is at increased risk for retinal detachment in the other eye, teach the patient the signs and symptoms of retinal detachment. Promote the use of proper protective eyewear to help avoid damage related to trauma.

FIG. 20.14 Retinal break with detachment and surgical repair by scleral buckling technique.

Age-Related Macular Degeneration Age-related macular degeneration (AMD) is the most common cause of irreversible central vision loss in people over age 60 in the United States. AMD is classified as dry (nonexudative) or wet (exudative). Dry AMD is the more common form, accounting for 90% of all cases. Those with dry AMD often notice that close vision tasks become harder. In dry AMD, the macular cells start to atrophy. This leads to a slowly progressive and painless vision loss. Wet AMD is the more severe form. It accounts for most cases of AMD-related blindness. Wet AMD has a more rapid onset of vision loss. With wet AMD there is the development of abnormal blood vessels in or near the macula. Many patients with wet AMD have dry AMD first.

Etiology and Pathophysiology AMD is related to retinal aging. Genetic factors also play a major role, and family history is a major risk factor for AMD.15 Other risk factors include light-colored irises, high C-reactive protein levels, smoking, and hypertension. Dry AMD starts with the abnormal accumulation of yellowish extracellular deposits called drusen in the retinal pigment epithelium. Over time atrophy and degeneration of macular cells occur. In wet AMD, vascular endothelial growth factor (VEGF) promotes the growth of new blood vessels in an abnormal location in the retinal epithelium. As the new blood vessels grow, they leak fluid and can bleed, causing scar tissue to gradually form.

Clinical Manifestations and Diagnostic Studies Acute vision loss may occur from either the dry or wet forms of AMD.

The patient may have blurred and darkened vision, scotomas (blind spots in the visual field), and metamorphopsia (distortion of vision). If only one eye is affected, the patient may not notice early changes in vision. In addition to visual acuity measurement, the primary diagnostic procedure is ophthalmoscopy. The HCP looks for drusen and other fundus changes associated with AMD. The Amsler grid test may help define the involved area. It provides a baseline for future comparison (Fig. 20.15). Fundus photography and IV angiography with fluorescein and/or indocyanine green dyes may help to further determine the extent and type of AMD. Retinal anatomy can be analyzed using optical coherence tomography (OCT) or scanning laser ophthalmoscopy.

Interprofessional Care Visual prognosis varies greatly. Limited treatment options for patients with wet AMD include medications that are injected directly into the vitreous cavity. Ranibizumab (Lucentis), bevacizumab (Avastin), aflibercept (Eylea), and pegaptanib (Macugen) inhibit VEGF. This helps slow vision loss by stopping new vessels from forming.15 Side effects can include blurred vision, eye irritation, eye pain, and photosensitivity. Injections are given at 4- to 6-week intervals, depending on treatment response. Disease stability is determined by OCT, which looks at pathology in the macula. The findings determine the need for continued intravitreal injections.

FIG. 20.15 Amsler grid. A, Normal grid. B, Abnormal grid as seen by person with macular degeneration.

Photodynamic therapy (PDT) uses verteporfin (Visudyne) IV and a “cold” laser to excite the dye. The PDT procedure is used in wet AMD to damage the abnormal blood vessels. Verteporfin is a photosensitizing drug that becomes active when exposed to the lowlevel laser light wave. Until the drug is completely excreted by the body, it can be activated by exposure to sunlight or other highintensity light, such as halogen. Have patients avoid direct exposure to sunlight and other intense forms of light for 5 days after treatment. Exposure of the skin to sunlight could activate the drug in that area, causing a chemical burn. Nutritional factors may play a role in the progression of AMD. Dietary supplements of vitamin C, vitamin E, beta-carotene, and zinc decrease the progression of AMD. Lutein/zeaxanthin supplements may help some patients. Teach the patient to eat dark green, leafy vegetables containing lutein (e.g., kale and spinach) and fatty fish at least twice a week.16 Smoking cessation may help in halting the progression of dry AMD to a more advanced stage. The management of the patient with visual impairment discussed on p. 359 is appropriate for the patient with AMD. Many patients with low-vision assistive devices can continue reading and keep a license to drive during the daytime and at lowered speeds. The permanent loss

of central vision has significant psychosocial implications for nursing care. Avoid giving the impression that “nothing can be done” about the problem when caring for the patient with AMD. Although therapy may not recover lost vision, much can be done to augment the remaining vision.

Glaucoma Glaucoma is a group of disorders characterized by increased IOP and its’ consequences, optic nerve atrophy, and peripheral visual field loss. Glaucoma is the second leading cause of permanent blindness in the United States and the leading cause of blindness among blacks.3,17 Many people with glaucoma are unaware of their condition. The incidence of glaucoma increases with age. Blindness from glaucoma is largely preventable with early detection and proper treatment. Genetic factors play a role in some types of glaucoma.17

Etiology and Pathophysiology A proper balance between the rate of aqueous production (inflow) and the rate of aqueous reabsorption (outflow) is essential to maintain the IOP within normal limits. We call the place where the outflow occurs the angle because it is the angle where the iris meets the cornea. When the rate of inflow is greater than the rate of outflow, IOP can increase above the normal limits. If IOP stays increased, permanent vision loss may occur. Primary open-angle glaucoma (POAG) is the most common type of glaucoma. In POAG the outflow of aqueous humor is decreased in the trabecular meshwork. The drainage channels become clogged, like a clogged kitchen sink. Damage to the optic nerve can then result. Angle-closure glaucoma (ACG) is due to a reduction in the outflow of aqueous humor that results from angle closure. Usually, this is caused by the lens bulging forward because of the aging process. Angle closure may also occur because of pupil dilation in the patient with anatomically narrow angles. Acute angle-closure glaucoma (AACG)

may be precipitated by situations in which the pupil stays partially dilated long enough to cause an acute and significant rise in the IOP. This may occur because of drug-induced mydriasis, emotional excitement, or darkness. Drug-induced mydriasis may occur from topical eye preparations or many systemic medications (both prescription and OTC). Check medication records before giving medications to the patient with ACG. Teach the patient not to take any mydriatic medications.

Clinical Manifestations POAG develops slowly and without symptoms of pain or pressure. The patient usually does not notice the gradual visual field loss until peripheral vision has been severely compromised. Eventually, the patient with untreated glaucoma has “tunnel vision,” with only a small center visual field. All peripheral vision is absent. AACG causes definite symptoms, including sudden, severe pain in or around the eye. The patient often has nausea and vomiting. Visual symptoms include seeing colored halos around lights, blurred vision, and ocular redness. Manifestations of subacute or chronic ACG appear more gradually. The patient who had a previous, unrecognized episode of subacute ACG may report blurred vision, seeing colored halos around lights, ocular redness, or eye or brow pain.

Diagnostic Studies IOP is usually increased in glaucoma (normal is 10 to 21 mm Hg). In the patient with increased pressures, the measurements are repeated over time to verify the elevation. In POAG, IOP is usually between 22and 32-mm Hg. In AACG, IOP may be more than 50 mm Hg. In POAG, slit lamp microscopy reveals a normal angle. In ACG, there may be a markedly narrow or flat anterior chamber angle, an edematous cornea, a fixed and moderately dilated pupil, and ciliary injection (hyperemia of the ciliary blood vessels produces a red color). Measures of peripheral and central vision provide more diagnostic

information. While central acuity may remain 20/20 even in the presence of severe peripheral visual field loss, visual field perimetry may reveal subtle changes in the peripheral vision early in the disease process, long before actual scotomas develop. In ACG, central visual acuity is reduced if the patient has corneal edema, and the visual fields may be markedly decreased. As glaucoma progresses, optic disc cupping may be one of the first signs of chronic POAG. The optic disc becomes wider, deeper, and paler (light gray or white), which is visible with direct or indirect ophthalmoscopy (Fig. 20.16).

Interprofessional Care The primary focus of glaucoma therapy is to keep the IOP low enough to prevent the patient from developing optic nerve damage. Therapy varies with the type of glaucoma. The diagnostic and interprofessional care of glaucoma is outlined in Table 20.12.

Chronic Open-Angle Glaucoma Drug therapy is the initial treatment in POAG (Table 20.13). The patient must understand that continued treatment and supervision are needed because the drugs control, but do not cure, glaucoma. Many patients with glaucoma have systemic illnesses or take systemic medications that may affect their therapy. The patient using a βadrenergic blocking glaucoma agent may have an additive effect if a systemic β-adrenergic blocking drug is also being taken. All βadrenergic blocking glaucoma agents are contraindicated in the patient with bradycardia, heart block greater than first-degree heart block, cardiogenic shock, and heart failure. The noncardioselective βadrenergic blocking glaucoma agents are contraindicated in the patient with chronic obstructive pulmonary disease (COPD) or asthma. The hyperosmolar agents may precipitate heart failure or pulmonary edema in the susceptible patient. The patient on high-dose aspirin therapy should not take carbonic anhydrase inhibitors. The αadrenergic agonists can cause tachycardia or hypertension. This may have profound consequences in the older patient.

FIG. 20.16 A, In the normal eye the optic cup is pink with little cupping. B, In glaucoma the optic cup is bleached and optic cupping is present. (Note the appearance of the retinal vessels, which travel over

the edge of the optic cup and appear to dip into it.)

TABLE 20.12 Interprofessional CareGlaucoma

Diagnostic Assessment • History and physical examination • Visual acuity measurement • Tonometry • Ophthalmoscopy (direct and indirect) • Slit lamp microscopy • Gonioscopy • Visual field perimetry

Management Chronic Open-Angle Glaucoma Drug Therapy (Table 20.13) • β-Adrenergic blockers • α-Adrenergic agonists • Cholinergic agents (miotics) • Carbonic anhydrase inhibitors

Surgical Therapy • Argon laser trabeculoplasty (ALT) • Trabeculectomy with or without filtering implant

Acute Angle-Closure Glaucoma

• Topical cholinergic agent • Hyperosmotic agent • Laser peripheral iridotomy • Surgical iridectomy

TABLE 20.13 Drug TherapyAcute and Chronic

Glaucoma

ALT, Argon laser trabeculoplasty; Nd:YAG, neodymium-doped yttrium aluminum garnet

(laser).

Argon laser trabeculoplasty (ALT) is a noninvasive way to lower IOP when medications are not successful or when the patient either cannot or will not use the drug therapy as recommended. ALT is an outpatient procedure that uses topical anesthetic. The laser stimulates scarring and contraction of the trabecular meshwork, which opens the outflow channels. ALT reduces IOP most of the time. The patient uses topical corticosteroids for 3 to 5 days after the procedure. The most common complication is an acute rise in IOP. The HCP examines the patient at 1 week and again at 4 to 6 weeks after surgery. Filtration surgery, also called a trabeculectomy, may be used if medical management and laser therapy are not successful.

Acute Angle-Closure Glaucoma AACG is an ocular emergency that needs immediate intervention. Miotics (Table 20.13) and oral or IV hyperosmotic agents, including glycerin liquid (Ophthalgan), isosorbide solution (Ismotic), and mannitol solution (Osmitrol), are usually successful in immediately lowering IOP. A laser peripheral iridotomy or surgical iridectomy is necessary for long-term treatment and prevention of more episodes. These procedures allow the aqueous humor to flow through a newly created opening in the iris and into normal outflow channels. A procedure may be done on the other eye as a precaution because many patients often have an acute attack in the other eye.

Drug Alert Miotics • Warn patients about decreased visual acuity, especially in dim light.

Nursing Management: Glaucoma Nursing Assessment Because glaucoma is a chronic condition requiring long-term management, assess the patient’s ability to understand and adhere to the therapy plan. Assess the patient’s psychologic reaction to the diagnosis of a potentially sight-threatening chronic disorder. Include the patient’s caregiver in the assessment process because the chronic nature of this disorder affects them too. For example, caregivers may become the eyedrop administrator if the patient is unwilling or unable.

Nursing Diagnoses Nursing diagnoses for the patient with glaucoma include: • Risk for injury • Acute pain

Planning The overall goals are that the patient with glaucoma will (1) have no progression of visual impairment, (2) follow the treatment plan, and (3) have no complications.

Nursing Implementation Health Promotion Loss of vision because of glaucoma is a preventable problem. Teach the patient and caregiver about the risk for glaucoma and that it increases with age. Stress the importance of early detection and treatment in preventing visual impairment. A comprehensive eye examination is important in identifying people with glaucoma or those at risk for developing glaucoma. The current recommendation is for an eye examination every 2 to 4 years for people between ages 40

and 64 years, and every 1 to 2 years for people age 65 years or older. Blacks in every age category should have one more often because of the increased incidence and more aggressive course of glaucoma.17

Acute Care Acute nursing interventions are directed primarily toward the patient with AACG and the surgical patient. The patient with AACG needs medication immediately to lower the IOP. Most surgeries for glaucoma are outpatient procedures. Provide care to relieve any discomfort related to the procedure. Patient and caregiver teaching after eye surgery is discussed in Table 20.9.

Ambulatory Care Because of the chronic nature of glaucoma, teach the patient to follow the therapy plan and follow-up recommendations prescribed by the HCP. Provide accurate information about the disease process and treatment options, including the reason for each option. In addition, the patient needs information about the purpose, frequency, and technique for administering antiglaucoma drugs. Encourage adherence by helping the patient set up a medication administration schedule and advocating a change in therapy if the patient reports unacceptable side effects.

Evaluation The overall expected outcomes are that the patient with glaucoma will: • Have no further loss of vision • Adhere to the recommended therapy • Safely function within own environment • Have relief from pain associated with the disease and surgery

Intraocular Inflammation and Infection

The term uveitis is used to describe inflammation of the uveal tract, retina, vitreous body, or optic nerve. Inflammation may be caused by bacteria, viruses, fungi, or parasites. Cytomegalovirus retinitis (CMV retinitis) is an opportunistic infection that occurs in patients with acquired immunodeficiency syndrome (AIDS) and in other immunosuppressed patients. The cause of sterile intraocular inflammation includes autoimmune disorders, AIDS, cancer, or disorders associated with systemic diseases, such as inflammatory bowel disease. Pain and photophobia are common symptoms. Endophthalmitis is an extensive intraocular inflammation of the vitreous cavity. Bacteria, viruses, fungi, or parasites can induce this serious inflammatory response. The mechanism of infection may be endogenous, in which the infecting agent arrives at the eye through the bloodstream, or exogenous, in which the infecting agent is introduced through a surgical wound or a penetrating injury. Although rare, endophthalmitis is a devastating complication of intraocular surgery or penetrating ocular injury. It can lead to irreversible blindness within hours or days. Manifestations include ocular pain, photophobia, decreased visual acuity, headaches, reddened and swollen conjunctiva, and corneal edema. Treatment depends on the underlying cause. Intraocular infections require antimicrobial agents. They may be delivered topically, subconjunctivally, intravitreally, systemically, or in some combination. Inflammatory responses require antiinflammatory medications (e.g., corticosteroids). The patient with intraocular inflammation is usually uncomfortable and may be noticeably anxious and frightened. Provide accurate information and emotional support to the patient and caregiver. In severe cases, enucleation may be needed. When the patient has lost visual function or even the entire eye, the patient will grieve the loss. Your role includes helping the patient through the grieving process.

Ocular Tumors Benign and cancerous tumors can occur in many areas of the eye,

including the conjunctiva, retina, and orbit.18 Eyelid cancers include basal cell and squamous cell cancers (see Chapter 23). Uveal melanoma is a cancer of the iris, choroid, or ciliary body. It more often occurs in light-skinned people with light eye color, who are over age 60, and have chronic UV exposure.19 Uveal melanoma can arise from preexisting nevi in the eye. Tumors may be asymptomatic or associated with vision loss. This depends on their size and location and presence of hemorrhage and retinal detachment. As with other cancers, cancer stage and cell type are important variables in the prognosis. Diagnostic testing may include ultrasound, MRI, and fine-needle aspiration biopsy. Uveal melanoma often appears as a dome-shaped, well-circumscribed, solid brown to golden pigment in the iris, choroid, or ciliary body (Fig. 20.17). Depending on the status of the involved eye, treatment options can include enucleation, radiation therapy (brachytherapy), external beam radiation, transpupillary photocoagulation, eye wall resection, and eye removal. Many patients do not lose their eye. Some may have good vision after treatment in the affected eye.

Enucleation Enucleation is the removal of the eye. The primary reason for enucleation is a blind, painful eye. This may result from glaucoma, infection, or trauma. Enucleation may be used to treat ocular cancer. The surgical procedure includes severing the extraocular muscles close to their insertion on the globe, inserting an implant to maintain the intraorbital anatomy, and suturing the ends of the muscles over the implant. The conjunctiva covers the joined muscles, and a clear conformer is placed over the conjunctiva until the permanent prosthesis is fitted. A pressure dressing helps prevent bleeding.

FIG. 20.17 Uveal melanoma. A large tumor in the choroid, the most common location in the eye for melanoma. Courtesy Cory J. Bosanko, OD, FAAO, Eye Centers of Tennessee, Crossville, TN.

After surgery, observe the patient for signs of complications, including excess bleeding or swelling, increased pain, displacement of the implant, and fever. Patient teaching should include the instillation of topical ointments or drops and wound cleansing. Teach the patient how to insert the conformer into the socket in case it falls out. The loss of an eye is often devastating, even when enucleation occurs after a lengthy period of painful blindness. Recognize the patient’s emotional response and provide support to the patient and caregivers. About 6 weeks after surgery, the wound is sufficiently healed for the permanent prosthesis. An ocularist fits the prosthesis and designs it to match the remaining eye. Teach the patient how to remove, cleanse, and insert the prosthesis. Special polishing is needed periodically to remove dried protein secretions.

Ocular Manifestations of Systemic

Diseases Many systemic diseases have significant ocular manifestations. Ocular signs and symptoms may be the first finding or complaint in the patient with a systemic disease. One example is the patient with undiagnosed diabetes who seeks eye care for blurred vision. A careful history and examination can reveal that the underlying cause of the blurred vision is lens swelling from hyperglycemia. Another example is the patient who seeks care for a conjunctival lesion. AIDS may be diagnosed based on the presence of a conjunctival Kaposi sarcoma (KS).

Case Study Glaucoma and Diabetic Retinopathy

© Kevin Peterson/Stockbyte/Thinkstock.

Patient Profile J.K. is a 68-yr-old black woman with a history of osteoarthritis and type 2 diabetes for the past 15 years. She now has diabetic

retinopathy. She returns to the eye clinic with her daughter for continued care of primary open-angle glaucoma (POAG) and reexamination for changes in diabetic retinopathy. Her current drug therapy for POAG includes topical timolol maleate 0.5% extended (Timoptic-XE) once daily in both eyes (OU) and latanoprost (Xalatan) 0.005% OU daily at bedtime. At her last examination, she had microaneurysms and hard exudates of the retina.

Subjective Data • She can no longer read the newspaper and reports that medication labels are difficult to read. • States she is not always successful in getting the eyedrops instilled because her hands are gnarled and painful from osteoarthritis.

Objective Data • Distant and near visual acuity are stable at 20/60 (OD) and 20/50 (OS). This is a reduction from 20/40 (OU) at her last visit. • Intraocular pressure (IOP) stable at 20 mm Hg (OU). • There is a new scotoma on visual field testing in the OS. • Fluorescein angiography reveals diabetic macular edema OU.

Interprofessional Care • Brimonidine 0.15% (OS) 15 min before and immediately after argon laser trabeculoplasty (ALT) • Argon laser (OU) to seal leaking microaneurysms from macular edema • Check IOP 1 hr after ALT • Continue previous glaucoma drop regimen • Follow-up examination for in 2 wk for possible ALT of OD

Discussion Questions 1. Explain the cause of the new scotoma. 2. Why is ALT an appropriate therapy for J.K.? 3. What is the purpose of the eyedrops before and immediately after ALT? 4. What is the cause of the vision loss from diabetic retinopathy? 5. Priority Decision: Based on the assessment data, what are the priority nursing diagnoses? Are there any collaborative problems? 6. Priority Decision: What are the priority nursing interventions for J.K.? 7. Patient-Centered Care: What are the priority topics that should be discussed in discharge teaching with J.K.? 8. Evidence-Based Practice: J.K. wants to know if her glaucoma is related to her diabetes. How would you respond to her question? Answers available at http://evolve.elsevier.com/Lewis/medsurg.

Bridge to Nclex Examination The number of the question corresponds to the same-numbered outcome at the beginning of the chapter.

1. In a patient who has a hemorrhage in the posterior cavity of the eye, the nurse knows that blood is accumulating a. in the aqueous humor. b. between the lens and retina. c. between the cornea and lens. d. in the space between the iris and lens. 2. Increased intraocular pressure may occur because of

a. edema of the corneal stroma. b. dilation of the retinal arterioles. c. blockage of the lacrimal canals and ducts. d. increased aqueous humor production by the ciliary process. 3. Ask patients using eyedrops to treat their glaucoma about a. use of corrective lenses. b. their usual sleep pattern. c. a history of heart or lung disease. d. sensitivity to opioids or depressants. 4. Always assess the patient with an eye problem for a. visual acuity. b. pupillary reactions. c. intraocular pressure. d. confrontation visual fields. 5. When examining the patient’s eyes, which finding would be of most concern to the nurse? a. Intraocular pressure of 16 mm/Hg b. Slightly yellowish cast of the sclera c. Outward turning of the lower lid margin d. Small, white nodule on the upper lid margin 6. Presbyopia occurs in older people because a. the eyeball elongates. b. the lens becomes inflexible. c. the corneal curvature becomes irregular. d. light rays are focusing in front of the retina.

7. Before injecting fluorescein for angiography, it is important for the nurse to (select all that apply) a. obtain an emesis basin. b. ask if the patient is fatigued. c. administer a topical anesthetic. d. inform patient that skin may turn yellow. e. assess for allergies to iodine-based contrast media. 8. A patient says she was diagnosed with astigmatism. When she asks what that is, what is the best explanation the nurse can give to the patient? a. “It happens because the lens of the eye is absent.” b. “People with astigmatism have abnormally long eyeballs.” c. “The cornea of the eye is uneven or irregular with astigmatism.” d. “Astigmatism occurs because the eye muscles weaken with age.” 9. Which intervention would be part of the plan of care for a patient who has new vision loss? a. Allow the patient to express feelings of grief and anger. b. Have the UAP perform all self-care activities for the patient. c. Address any family present first when discussing care concerns. d. Speak loudly and clearly, addressing the patient with each contact. 10. Which patient behaviors would the nurse promote for

healthy eyes (select all that apply)? a. Protective sunglasses when bicycling b. Taking part in a smoking cessation program c. Supplementing diet intake of vitamin C and betacarotene d. Washing hands thoroughly before putting in or taking out contact lenses e. A woman avoiding pregnancy for 4 weeks after receiving MMR immunization 11. The most important intervention for the patient with epidemic keratoconjunctivitis is a. cleansing the affected area with baby shampoo. b. monitoring spread of infection to the opposing eye. c. regular instillation of artificial tears to the affected eye. d. teaching the patient and caregivers good hygiene techniques. 12. What should be included in the discharge teaching for the patient who had cataract surgery (select all that apply)? a. Eye discomfort is often relieved with mild analgesics. b. A decline in visual acuity is common for the first week. c. Stay on bed rest and limit activity for the first few days. d. Notify the provider if an increase in redness or drainage occurs. e. Following activity restrictions is essential to reduce intraocular pressure. 1. b, 2. d, 3. c, 4. a, 5. d, 6. b, 7. a, d, 8. c, 9. a, 10. a, b, c, d, 11. d, 12. a, d, e For rationales to these answers and even more NCLEX review

questions, visit http://evolve.elsevier.com/Lewis/medsurg.

Evolve Website/Resources List http://evolve.elsevier.com/Lewis/medsurg

Review Questions (Online Only) Key Points Answer Keys for Questions • Rationales for Bridge to NCLEX Examination Questions • Answer Guidelines for Case Study on pp. 351, 354, 358, and 373 Student Case Study • Patient Undergoing Cataract Surgery eNursing Care Plan • eNursing Care Plan 20.1: Patient After Eye Surgery Conceptual Care Map Creator Audio Glossary Supporting Media • Animations • Cataract Removal • LASIK • Myringotomy • Scleral Buckling Content Updates

References 1. Lampignano J, Kendrick L: Bontrager’s textbook of radiographic positioning and related anatomy, ed 9, St Louis, 2018, Elsevier. Martin E, Patrianakos T, Giovingo M: Medication induced glaucoma, Disease-a-Month 63:54, 2017.

3. National Eye Institute: Statistics and data. Retrieved from www.nei.nih.gov/eyedata. 4. American Optometric Association: Myopia. Retrieved from www.aoa.org/patients-and-public/eyeand-vision-problems/glossary-of-eye-and-visionconditions/myopia?sso=y. 5. US Food and Drug Administration: LASIK. Retrieved from www.fda.gov/medicaldevices/productsandmedicalprocedures/surgerya 6. American Optometric Association: Low vision. Retrieved from www.aoa.org/patients-and-public/caringfor-your-vision/low-vision. Salva MA, Hartley S, Léger D, et al : Non-24-hour sleep–wake rhythm disorder in the totally blind: Diagnosis and management., Front Neurol 8:686, 2017.

8. American Academy of Ophthalmology: Preventing eye injuries. Retrieved from www.aao.org/eyehealth/diseases/preventing-injuries. Satpathy G, Behera HS, Ahmed NH: Chlamydial eye infections: Current perspectives, Indian J Ophthalmol 65:97, 2017. Azher TN, Yin XT, Tajfirouz D, et al: Herpes simplex keratitis: Challenges in diagnosis and clinical management, Clin Ophthalmol 11:185, 2017.

11. Saving Sight: Important information about saving sight. Retrieved from www.saving-sight.org/cornea-

donation-facts. 12. Date RC, Al-Mohtaseb ZN: Advances in preoperative testing for cataract surgery, Internat Ophthalmol Clin 57:99, 2017. 13. American Diabetes Association: Standards of medical care in diabetes—2018, Diabetes Care 1:S105, 2018. 14. Schachat AP, Sadda SR, Hinton DR, et al: Ryan’s retina: Principles and practice, ed 6, St Louis, 2018, Elsevier. 15. American Macular Degeneration Foundation: About macular degeneration. Retrieved from www.macular.org/about-macular-degeneration. Carneiro Â, Andrade JP: Nutritional and lifestyle interventions for age-related macular degeneration: A review, Oxid Med Cell Longev, 2017.

17. Glaucoma Research Foundation: Glaucoma. Retrieved from www.glaucoma.org/glaucoma/. 18. International Society of Ocular Oncology: Eye tumors. Retrieved from www.isoo.org/tumors. Pandiani C, Béranger GE, Leclerc J, et al : Focus on cutaneous and uveal melanoma specificities, Genes Dev 31:724, 2017. ∗Evidence-based information for clinical practice.

21

Assessment and Management Auditory Problems Mariann M. Harding

LEARNING OUTCOMES 1. Describe the structures and functions of the auditory system. 2. Obtain significant subjective and objective assessment data related to the auditory system from a patient. 3. Perform a physical assessment of the auditory system using the appropriate techniques. 4. Distinguish normal from common abnormal findings of a physical assessment of the auditory system. 5. Link the age-related changes in the auditory system to differences in assessment findings. 6. Describe the purpose, significance of results, and nursing responsibilities related to diagnostic studies of the auditory system. 7. Explain the pathophysiology, clinical manifestations, and nursing and interprofessional management of common ear problems. 8. Compare the common causes, management, and rehabilitative potential of conductive and sensorineural hearing loss. 9. Explain the use, care, and patient teaching related to assistive

devices for ear problems. 10. Describe measures used to assist the patient in adapting to decreased hearing.

KEY TERMS acoustic neuroma, p. 387 benign paroxysmal positional vertigo (BPPV), p. 387 external otitis, p. 383 Ménière’s disease, p. 386 nystagmus, p. 378 otosclerosis, p. 385 presbycusis, p. 378 tinnitus, p. 378 vertigo, p. 378 Kindness is a language which the deaf can hear and the blind can see. Mark Twain http://evolve.elsevier.com/Lewis/medsurg/

Conceptual Focus Coping Functional Ability Infection Sensory Perception

Auditory System Hearing is a complex process that allows us to interact with the environment. It is the basis for social interaction and communication. Having a hearing impairment can lead to major challenges that can negatively affect well-being. In the adult, difficulties with related concepts, including functional ability and cognition, may be present with hearing loss. This chapter presents an overview of auditory function and discusses care when problems occur.

Structures and Functions of Auditory System The auditory system is composed of the peripheral auditory system and central auditory system. The peripheral auditory system includes the structures of the ear itself: external, middle, and inner ear (Fig. 21.1). This system is involved with the reception and perception of sound. The inner ear functions in hearing and balance. The central auditory system integrates and assigns meaning to what one hears. This system includes the vestibulocochlear nerve (cranial nerve [CN] VIII) and auditory cortex of the brain. The brain and its pathways transmit and process sound and sensations that maintain a person’s equilibrium. The role of the external and middle part of the ear is to conduct and amplify sound waves from the environment. This part of sound conduction is termed air conduction. Problems in these two parts of the ear may cause conductive hearing loss, resulting in a decrease in sound intensity and/or a distortion in sound.1 Disturbances in equilibrium can impair coordination, balance, and orientation. Damage to or an abnormality of the inner ear or along the nerve pathways results in sensorineural hearing loss. In addition to causing distortion or faintness of sound, sensorineural hearing loss may affect the ability to understand speech or cause complete hearing loss. Impairment within the auditory pathways of the brain causes

central hearing loss. This type of hearing loss causes difficulty in understanding the meaning of words the person heard. Types of hearing loss are discussed later in this chapter on pp. 387-389.

External Ear The external ear consists of the auricle (pinna), external auditory canal, and tympanic membrane (TM). The auricle is composed of cartilage and connective tissue covered with epithelium, which also lines the external auditory canal (Fig. 21.1). The external auditory canal is a slightly S-shaped tube about 1 inch (2.5 cm) in length in the adult. The lining of the proximal one third of the canal contains fine hairs (cilia), sebaceous (oil) glands, and ceruminous (wax) glands. The oil and wax lubricate the ear canal, keep it free from debris, and kill bacteria. Thin epithelium lines the distal two thirds of the canal. It is over bone and very sensitive. The function of the external ear and canal is to collect and transmit sound waves to the TM, or eardrum. The TM is a shiny, translucent, pearl-gray membrane. It is made up of epithelial cells, connective tissue, and mucous membrane. It serves as a partition and transmits sounds between the external auditory canal and middle ear.

Middle Ear The middle ear cavity is an air space in the temporal bone. Mucous membrane lines the middle ear and is continuous from the nasal pharynx via the eustachian (auditory) tube. The eustachian tube equalizes atmospheric air pressure between the middle ear and throat. This allows the TM to move freely. It is normally closed, opening only with yawning, swallowing, and chewing. Blockage of the tube can occur with allergies, nasopharyngeal infections, or enlarged adenoids. A tube that stays open is called patulous. When this occurs, autophony, or hearing your own voice, may be present. The middle ear contains the ossicles, the 3 smallest bones in the body: malleus, incus, and stapes. Vibrations of the TM cause the ossicles to move and transmit sound waves to the oval window. The superior

part of the middle ear is the epitympanum, or the attic. It also communicates with air cells within the mastoid bone. The mastoid is the posterior part of the temporal bone. The facial nerve (CN VII) traverses above the oval window of the middle ear. The thin, bony covering of the facial nerve can become damaged by chronic ear infection, skull fracture, or trauma during ear surgery. Problems may occur related to voluntary facial movements, eyelid closure, and taste discrimination. Permanent damage to the facial nerve can result.

Inner Ear The inner ear consists of 3 spaces in the temporal bone, assembled in a system called the bony labyrinth. The space is filled with watery fluid called perilymph. Within the perilymph is the membranous labyrinth. It follows the shape of the bony labyrinth and holds a thicker fluid called endolymph. The inner ear holds the functional organs for hearing and balance. The receptor organ for hearing is the cochlea, a coiled structure that contains the organ of Corti. Its tiny hair cells respond to stimulation of select portions of the basilar membrane according to pitch. This stimulus is converted into an electrochemical impulse. It is transmitted by the acoustic part of the vestibulocochlear nerve (CN VIII) to the temporal lobe of the brain to process and interpret the sound.

FIG. 21.1 External, middle, and inner ear. Modified from Patton KT, Thibodeau GA: Anatomy and physiology, ed 8, St Louis, 2013, Mosby.

Three semicircular canals and the vestibule make up the organ of balance. The semicircular canals sit at right angles to each other. Structures in each canal and the vestibule generate nerve impulses in response to our movements. The vestibule is beside the oval window between the semicircular canals and the cochlea. Nerves from receptors in the vestibule join those from the semicircular canals to form the vestibular nerve, which joins with the cochlear nerve to form the vestibulocochlear nerve, or CN VIII.

Transmission of Sound Sound waves travel by air (air conduction) and are picked up by the auricles and auditory canal. Sound waves strike the TM, causing it to vibrate. The central part of the TM is connected to the malleus, which then starts to vibrate. The malleus transmits the vibration to the incus and then the stapes. As the stapes moves back and forth, it pushes the membrane of the oval window in and out. Movement of the oval window makes waves in the perilymph. Once sound waves are transmitted to the liquid medium of the

inner ear, the vibration is picked up by the tiny sensory hair cells of the cochlea, which initiate nerve impulses. These impulses are carried by nerve fibers to the main branch of the acoustic portion of CN VIII and then to the brain. The bones of the skull can also transmit sound directly to the inner ear (bone conduction).

Gerontologic Considerations: Effects of Aging on Auditory System Presbycusis, or hearing loss due to aging, is the third most common health issue in older adults, after arthritis and heart disease.2 Sound transmission is diminished by calcification of the ossicles. Tinnitus, or ringing in the ears, may accompany the hearing loss that results from the aging process. Cerumen glands atrophy, causing cerumen (earwax) to be much drier. The hair in the ear becomes thicker and coarser, entrapping the hard, dry cerumen in the canal. Accumulation of dry cerumen in the external canal can interfere with the transmission of sound. A decline in balance results from atrophy of vestibular structures in the inner ear, slowing of motor responses, and musculoskeletal limitations. Age-related changes in the auditory system and differences in assessment findings are outlined in Table 21.1.

Case Study Patient Introduction

© iStock.com/EyeMark.

R.S. is a 57-yr-old woman who comes to the emergency department with extreme dizziness. R.S. states that she is so dizzy she “can’t do anything but lie down.” She also reports feeling like her right ear is

“plugged” and is having ringing in that ear.

Discussion Questions 1. What are the possible causes of R.M.’s hearing and balance problems? 2. Is her condition stable or an emergency? 3. What assessment questions will you ask her? You will learn more about R.S. and her condition as you read this chapter. (See p. 380 for more information on R.S.) Answers available at http://evolve.elsevier.com/Lewis/medsurg.

Assessment of Auditory System Assessment of the auditory system should include assessment of hearing and equilibrium because the auditory and vestibular (balance) systems are closely related. It is often hard to separate symptoms related to these two systems. Help the patient describe symptoms and problems to determine the source of the problems. Health history questions to ask a patient with an auditory problem are listed in Table 21.2. Problems with balance may manifest as vertigo or nystagmus. Vertigo is a sense that the person or objects around the person are moving or spinning. It is usually stimulated by head movement. Dizziness is a sensation of being off-balance that occurs when standing or walking. Nystagmus is an abnormal eye movement that may be seen as a twitching of the eyeball or described by the patient as a blurring of vision with head or eye movement. At first, try to determine symptoms that are related to balance and separate them from those related to hearing loss or tinnitus. The symptoms can be combined later in the assessment to help make a diagnosis and care plan for the patient.

Subjective Data Important Health Information Past Health History Many ear problems result from childhood illnesses or problems of adjacent organs. This makes a careful assessment of past health problems is important. Ask the patient about previous ear problems, especially during childhood. Record the (1) frequency of acute middle ear infections (otitis media); (2) surgical procedures (e.g., myringotomy); (3) perforations of the eardrum; (4) drainage; and (5) history of mumps, measles, or scarlet fever. Assess for systemic conditions, including hypertension, rheumatoid arthritis, and inflammatory bowel disease, that are associated with hearing loss.3 Document head injury because it may result in hearing loss. Information about food and environmental allergies is important because they can cause the eustachian tube to become edematous and prevent aeration of the middle ear.

TABLE 21.1 Gerontologic Assessment

DifferencesAuditory System

Record symptoms such as vertigo, tinnitus, and hearing loss in the patient’s words. Ask for specific details of the sensations and situations that may cause them or make them worse. Information about family members with hearing loss and type of hearing loss is important. Some congenital hearing loss is hereditary. The age of onset of presbycusis also follows a familial pattern.

Medications Obtain information about present or past use of ototoxic drugs (cause damage to CN VIII). These include aspirin, some antibiotics (aminoglycosides, erythromycin, vancomycin), loop diuretics, nonsteroidal antiinflammatory drugs (NSAIDs), antimalarial agents, and certain chemotherapy drugs (e.g., bleomycin, cyclophosphamide, cisplatin). Ask about hearing and balance problems, such as hearing loss, tinnitus, and vertigo, in patients receiving these drugs. For many, the hearing loss may be reversible if treatment is stopped. Chemicals used in industry (e.g., toluene, carbon disulfide, mercury) may damage the inner ear.

Surgery or Other Treatments Document previous hospitalizations for ear surgery, including myringotomy (ventilation holes placed in the TM with or without tubes), tympanoplasty (surgical repair of TM), tonsillectomy, and adenoidectomy. Record the use of and satisfaction with a hearing aid. Note any problems with impacted cerumen.

Functional Health Patterns Hearing and balance problems can affect all aspects of a person’s life. To assess the impact of hearing loss, ask health history questions based on a functional health patterns approach (Table 21.2).

Health Perception–Health Management Pattern Note the onset of hearing loss, whether sudden or gradual, and who noted the onset (e.g., patient, family, significant others). Gradual

hearing losses are often noted by those who communicate with the patient. Sudden losses and those worsened by other condition are often reported by the patient. Assess the patient for personal measures used to preserve hearing. The use of protective ear covers or earplugs is good practice for people in high-noise environments. Document if the patient is a swimmer and the frequency and duration of swimming and use of ear protection. Note the type of water (pool, lake, ocean) in which the swimming takes place to help identify contact with contaminated water. Assess for the placement of any item in the ear, including hearing aids, which can cause trauma to the canal and TM.

Nutritional-Metabolic Pattern Alcohol, sodium, and dietary supplements affect the amount of endolymph in the inner ear system. Patients with Ménière’s disease may notice some improvement in their symptoms with alcohol restriction and a low-sodium diet. Note changes in symptoms with food intake. Ask the patient about any ear pain (otalgia) or discomfort associated with chewing or swallowing. These symptoms are often associated with middle ear problems.

TABLE 21.2 Health HistoryAuditory System

Health Perception–Health Management Hearing • Have you had a change in your hearing?∗ If yes, how does this change affect your daily life? • Do you use any devices to improve your hearing (e.g., hearing aid, special volume control, headphones for television or stereo)?∗ • How do you protect your hearing? • Do you have any allergies that result in ear problems?∗

Equilibrium • When did the dizziness or spinning sensation first occur? • Does this sensation occur when you first stand up, when you are lying down, or both? • Have you ever fallen because of the dizziness?∗ • Can you drive or walk alone? If no, elaborate. • Are there any times of the day when your symptoms are worse?∗

Tinnitus • How long have you experienced ringing in your ears? Has it changed?∗ Describe the ringing (e.g., buzzing, ringing, roaring). Do you also have a feeling of fullness or pressure?∗ • When does it bother you the most? • What things have you tried that help or have not helped? • What medications are you taking?

Nutritional-Metabolic • Do you notice any differences in symptoms with changes in diet? ∗

• Does your ear problem cause nausea that interferes with your food intake?∗ • Does chewing or swallowing cause you any ear discomfort?∗

Elimination • Does straining during a bowel movement cause ear pain?∗

Activity-Exercise • Do you need help with certain activities (e.g., lifting, bending, climbing stairs, driving, speaking) because of symptoms?∗

Sleep-Rest • Is your sleep disturbed by noises or ringing in the ears or by a sensation of spinning?∗

Cognitive-Perceptual • Do you experience ear pain?∗ What relieves the pain? What makes it worse? Does the pain affect your hearing or balance? • Have you noticed any problem with communicating or understanding what people are saying?∗

Self-Perception–Self-Concept • Have changes in your hearing affected how you feel about yourself or your feeling of independence?∗

Role-Relationship • What effect has your ear problem had on your work, family, or social life? • Are you able to recognize the effects of your ear problems on your life?∗

Sexuality-Reproductive

• Has your ear problem caused a change in your sex life?∗

Coping–Stress Tolerance • Do you consider your ear problem a source of stress?∗ • How do you cope when you are experiencing symptoms?

Value-Belief • Do you have a conflict between what your health care provider would like you to do and what you believe you should do?



If yes, describe.

Assessment of clenching or grinding of the teeth helps distinguish problems of the ear from referred pain of the temporomandibular joint (TMJ). Ask about dental problems and dentures.

Elimination Pattern Elimination patterns are of interest in the patient with perilymph fistula and after surgical procedures. Frequent constipation or straining with bowel or bladder elimination may interfere with healing or repair of a perilymph fistula. After middle ear surgery (stapedectomy) the patient needs to prevent increased intracranial (and consequent inner ear) pressure associated with straining during bowel movements. Stool softeners may be needed after surgery for the patient who reports chronic problems with constipation.

Activity-Exercise Pattern A review of the patient’s activity-exercise pattern is essential when assessing for balance problems. Ask the patient about the onset,

duration, and frequency of symptoms. Identify activities that relieve or worsen symptoms and how they relate to the time of the day. For example, patients with Ménière’s disease are less able to compensate for environmental input as the day progresses.

Sleep-Rest Pattern Ask the patient with chronic tinnitus about sleep problems. Find out if the patient has tried anything to minimize the tinnitus (e.g., having fan on, using white noise devices). Assess for snoring. It can be caused by swelling or hypertrophy of tissue in the nasopharynx. This excess tissue can impair eustachian tube function and cause the sensation of ear fullness or pain.

Cognitive-Perceptual Pattern Pain is associated with some ear problems, particularly those involving the middle ear and auditory canal. If pain is present, ask the patient to describe the pain, presence of drainage (otorrhea), history of teeth grinding, and treatments used for relief. Note the effect on the pain level when you move the auricle or palpate the tragus. Note the patient’s ability to pay attention and follow directions. Problems with these tasks may be an early indicator of hearing loss. The patient may not recognize a gradual hearing loss. Ask caregivers if they have noted any change in the patient’s hearing.

Self-Perception–Self-Concept Pattern Ask the patient to describe how the ear problem has affected his or her personal life and feelings about himself or herself. Hearing loss and chronic vertigo are particularly distressing for the patient. Hearing loss can result in embarrassing social situations that affect the patient’s self-concept. People may think a patient with chronic vertigo is intoxicated. Sensitively question the patient about such situations. Clarify the symptom history with the patient and consider an evaluation with a hearing specialist.

Role-Relationship Pattern Ask the patient about the effect that an ear problem or vertigo has had on family life, work responsibilities, and social relationships. Hearing loss can result in strained relationships and misunderstandings. Ask about employment or contact with environments that have excessive noise levels, such as work with jet engines and machinery and electronically amplified music. Document the use of preventive devices worn in noisy environments. Many jobs rely on the ability to hear accurately and respond appropriately. If a hearing loss is present, gather detailed information on the effect this has on the patient’s job. The unpredictability of vertigo attacks can have devastating effects on all aspects of life. Ordinary activities, such as driving, cooking, and work, that require balance all have an element of danger.

Sexuality-Reproductive Pattern Determine whether hearing loss or vertigo has interfered with having a satisfactory sex life. Although intimacy does not depend on the ability to hear, hearing loss can interfere with establishing or maintaining a relationship.

Coping–Stress Tolerance Pattern Ask the patient about his or her usual coping style, stress management strategies, and available support. If the patient seems unable to manage the situation, outside intervention may be needed. Denial is a common response to a hearing problem and should be assessed.

Value-Belief Pattern Ask the patient about any conflicts produced by the problem or treatment related to values or beliefs. Make every effort to resolve the problem so that the patient does not have added stress. Ask about the use of home remedies such as hot oil in the ear.

Case Study Subjective Data

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A focused subjective assessment of R.S. revealed the following information: • PMH: History of mild osteoarthritis. Hysterectomy 5 years ago. Last saw health care provider 6 months ago. • Medications: Multivitamin 1 PO daily, ASA 81 mg PO daily, ibuprofen 200 mg PO every 6 hours as needed. • Health Perception–Health Management: She says last night she felt like she had the start of a cold. The symptoms were present this morning when she woke up. She tried to clear her ear by blowing her nose and could not use that ear to talk on the phone. Had excellent hearing until today. Denies any syncope. Does not have allergies. • Nutritional-Metabolic: States she is nauseous but has not vomited. Has only had a few sips of water since the symptoms started. • Activity-Exercise: Dizziness worse when standing. It is still present when lying down but is less. Her husband drove her to the emergency room since she was unable to drive. Normally walks 1 to 2 miles 5 times a week and attends yoga class 2 times a week. • Cognitive-Perceptual: Denies any ear pain, headache. • Coping–Stress Tolerance: Concerned she is having a stroke.

Discussion Questions 1. Which subjective assessment findings concern you most? 2. Based on the subjective assessment findings, what should you include in the physical assessment? For what would you be looking? You will learn more about the physical assessment of the auditory

system in the next section. (See p. 381 for more information on R.S.) Answers available at http://evolve.elsevier.com/Lewis/medsurg.

Objective Data Physical Examination During the interview to obtain a health history, obtain objective data about the patient’s ability to hear. Look for cues that a patient cannot hear (Table 21.3). Record these observations. This is important because the patient is often unaware of hearing loss or does not admit to changes in hearing until moderate losses have occurred. A normal assessment of the auditory system is shown in Table 21.4. Age-related changes of the auditory system and differences in assessment findings are found in Table 21.1.

TABLE 21.3 Indicators of Possible Hearing Loss • Does not respond to or understand oral communication • Has excessively loud or soft speech • Answers questions inappropriately • Tilts head, leans forward when listening • Constantly needs to clarify conversation • States other people mumble all the time • Increases the volume of radio or TV • Difficulty hearing over the phone

TABLE 21.4 Normal Physical Assessment of

Auditory System

• Ears symmetric in location and shape • Auricles and tragus nontender, without lesions • Canal clear, tympanic membrane intact, landmarks and light reflex intact • Able to hear low whisper at 30 cm. Weber test results, no lateralization. Rinne test results AC > BC AC, Air conduction; BC, bone conduction. A focused assessment is used to evaluate the status of previously identified auditory problems and monitor for signs of new problems. A focused assessment of the auditory system is presented in the box below.

Focused Assessment Auditory System Use this checklist to make sure the key assessment steps have been done.

Subjective Ask the patient about any of the following and note responses.

Changes in hearing

Y

N

Ear pain

Y

N

Ear drainage

Y

N

Tinnitus

Y

N

Objective: Physical Examination Inspect Alignment and position of ears on head



Size, shape, symmetry, color, and skin intactness External auditory meatus for discharge or lesions

✓ ✓

Assess Hearing based on ability to respond to conversation, respond to a whisper, or hear a ticking watch



External Ear Inspect and palpate the external ear before examining the external canal and tympanum. Observe the auricle, preauricular area, and mastoid area for symmetry, color of skin, swelling, redness, and lesions. Then palpate the auricle and mastoid areas for tenderness and nodules. Grasping the auricle or pressing on the tragus may cause pain, especially if the external ear or canal is inflamed.

External Auditory Canal and Tympanum Before inserting an otoscope, inspect the canal opening for patency, palpate the tragus, and gently move the auricle to check for discomfort. Select a speculum slightly smaller than the size of the ear canal. Tip the patient’s head to the opposite shoulder. Grasp the top of the auricle and gently pull up and backward to straighten the canal. Hold the otoscope while stabilizing it with your fingers on the patient’s cheek, and then insert it slowly. A pneumatic otoscope creates negative pressure to pull at the TM and is helpful in confirming TM retraction or fluid behind the membrane. A tight seal of the speculum is essential during this step of the examination. Observe the canal for size and shape and the color, amount, and type of cerumen. Be careful when clearing the canal of cerumen. Damage can occur to the middle ear if the TM is perforated.

FIG. 21.2 Normal tympanic membrane. From Jarvis C: Physical examination and health assessment, ed 7, St Louis, 2015, Elsevier.

Inspect the TM for color, fluid behind the membrane, landmarks, contour, and intactness (Fig. 21.2). The TM is normally pearl gray, white, or pink; shiny; and translucent. The handle (manubrium) of the malleus and its short process (umbo) should be visible through the membrane. The position and dome (concave) shape of the TM cause the light from the otoscope to reflect in a cone shape with crisp edges. If the TM is bulging or retracted, the edges of the light reflex will be fuzzy (diffuse) and may spread over the TM. The middle and inner ear cannot be examined with the otoscope. Table 21.5 summarizes assessment abnormalities of the auditory system.

Case Study Objective Data: Physical Examination

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Physical examination findings of R.S. were as follows: • Neurologic and otoscopic examinations normal

• Unable to hear whisper on the right at 30 cm • Vision normal. PERRLA without nystagmus • Gait unsteady. No motor weakness • Skin pale, warm, and dry • Heart rate 84 beats/min, temperature 97.4° F (36.3° C)

Discussion Questions 1. What physical assessment findings concern you most? 2. What diagnostic studies might you expect to be ordered? As you continue to read this chapter, consider diagnostic studies that you would expect being performed for R.S. (See p. 382 for more information on R.S.) Answers available at http://evolve.elsevier.com/Lewis/medsurg.

TABLE 21.5 Assessment AbnormalitiesAuditory

System

Diagnostic Studies of Auditory System Table 21.6 describes common diagnostic studies used to assess the auditory system.

Audiometry Audiometry is beneficial as a screening test for hearing acuity and as a diagnostic test to determine the degree and type of hearing loss. The most common test performed by the audiologist is pure-tone audiometry. The audiometer produces pure tones at varying intensities to which the patient can respond. Sound is characterized by the number of vibrations or cycles that occur each second. Hertz (Hz) is the unit of measurement used to classify the frequency of a tone. The higher the frequency is, the higher the pitch. Hearing loss can affect certain sound frequencies. The specific pattern produced on the audiogram by these losses can help in diagnosing the type of hearing loss. The intensity or strength of a

sound wave is expressed in terms of decibels (dB), ranging from 0 to 110 dB. The intensity of a sound needed to make any frequency barely audible to the average normal ear is 0 dB. Threshold refers to the signal level at which pure tones are detected (pure-tone thresholds) or the signal level at which the patient correctly hears 50% of the signals (speech detection thresholds). Normal speech is around 40 to 65 dB; a soft whisper is 20 dB. Normally, a child and a young adult can hear frequencies from about 16 to 20,000 Hz, but hearing is most sensitive between 500 and 4000 Hz. This is similar to normal speech frequencies. A 40- to 45-dB loss in these frequencies causes moderate difficulty in hearing normal speech. A hearing aid may be helpful because it makes sound information louder but not clearer. A hearing aid may not be helpful to the patient who has problems with discrimination of sounds or sound information because the consonants are still not heard well enough to make speech understandable.

Specialized Tests More sophisticated tests are available to determine the cause of certain hearing losses (Table 21.6). CT scan and MRI can detect lesions such as a tumor of the auditory nerve.

Case Study Objective Data: Diagnostic Studies

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The Weber’s test shows lateralization to the left. An audiogram confirms low-frequency, sensorineural hearing loss with normal speech discrimination. An MRI of the head is normal.

Discussion Questions 1. Are these the diagnostic studies that you expected to be ordered? 2. Which diagnostic study results are of most concern to you? (See p. 393 for more information on R.S.) Answers available at http://evolve.elsevier.com/Lewis/medsurg.

TABLE 21.6 Diagnostic StudiesAuditory System

Auditory Problems: External Ear and Canal External Otitis The skin of the external ear and canal is subject to the same problems as skin anywhere on the body. External otitis involves inflammation or infection of the epithelium of the auricle and ear canal. Swimming may change the flora of the external canal because of chemicals and contaminated water. This can result in an infection often referred to as “swimmer’s ear.” Trauma from picking the ear or using sharp objects (e.g., hairpins) often causes the initial break in the skin. Piercing of cartilage in the upper part of the auricle also places the patient at higher risk for infection. Infections and skin conditions may cause external otitis. Bacteria or fungi may be the cause. Pseudomonas aeruginosa is the most common bacterial cause. Fungi, especially Candida albicans and Aspergillus, thrive in warm, moist climates. The warm, dark environment of the ear canal provides a good growth medium for microorganisms. Malignant external otitis is a serious infection caused by P. aeruginosa. It occurs mainly in older patients with diabetes. The infection, which can spread from the external ear to the parotid gland and temporal bone (osteomyelitis), is usually treated with antibiotics. Ear pain (otalgia) is one of the first signs of external otitis. Even in mild cases, the patient may have significant discomfort with chewing, moving the auricle, or pressing on the tragus. Swelling of the ear canal can muffle hearing. There may be serosanguineous (blood-tinged fluid) or purulent (white to green thick fluid) drainage. Fever occurs when the infection spreads to surrounding tissue.

Nursing and Interprofessional Management: External Otitis

External otitis is diagnosed by otoscopic examination of the ear canal. Take care to avoid pain when pulling on the pinna to straighten out the canal or when inserting the otoscope speculum. The eardrum may be hard to see due to swelling in the canal. Culture and sensitivity studies of the drainage may be done. Moist heat, mild analgesics, and topical anesthetic drops usually control the pain. Topical treatments may include antibiotics for infection and corticosteroids for inflammation. If the surrounding tissue is involved, systemic antibiotics are used. Improvement should occur in 48 hours. The patient needs to adhere to the prescribed therapy for 7 to 14 days for complete resolution.

TABLE 21.7 Patient & Caregiver

TeachingPrevention of External Otitis Include the following instructions when teaching the patient and caregiver: 1. Do not put anything in your ear canal unless requested by your health care provider. 2. Report itching if it becomes a problem. 3. Earwax is normal. • It lubricates and protects the canal. • Report chronic excess cerumen if it impairs your hearing. 4. Keep your ears as dry as possible. • Use earplugs if you are prone to swimmer’s ear. • Turn your head to each side for 30 seconds at a time to help water run out of the ears. • Do not dry with cotton-tipped applicators. • A hair dryer set to low and held at least 6 inches from the ear can speed water evaporation. Wash hands before and after applying eardrops (otic drops). The drops should be at room temperature. Cold drops can cause vertigo

due to stimulation of the semicircular canals, and heated drops can burn the tympanum. The tip of the dropper should not touch the ear during application to prevent contamination of the entire bottle of drops. Position the ear so that the drops can run into the canal. The patient should stay in this position for 2 minutes to allow the drops to spread. Sometimes you can place the drops onto a wick of cotton, then place the wick in the canal. Tell the patient not to push the cotton farther into the ear. Careful handling and disposal of material saturated with drainage are important. Teach the patient ways to reduce the risk for external otitis (Table 21.7).

Cerumen and Foreign Bodies in External Ear Canal Impacted cerumen (earwax) can cause discomfort and decreased hearing. Other symptoms include tinnitus and vertigo. Remove an impaction by irrigating the canal with body-temperature solutions to soften the earwax. Special syringes may be used. These vary from a simple bulb syringe to special irrigating equipment. Place the patient in a sitting position with an emesis basin under the ear. Pull the auricle up and back, and direct the flow of solution above or below the impaction. Do not completely occlude the ear canal with the syringe tip. If irrigation does not remove the wax, use mild lubricant drops to soften the earwax. The HCP may need to remove severe impactions. Attempts to remove a foreign object from the ear may result in pushing it farther into the canal. Vegetable matter in the ear tends to swell. This can create a secondary inflammation, making removal more difficult. Mineral oil or lidocaine drops can be used to kill an insect before removal under microscope guidance. The HCP should remove impacted objects. Cleanse ears with a washcloth and finger. Avoid using cottontipped applicators. Penetration of the middle ear by a cotton-tipped applicator can cause serious injury to the TM and ossicles. Their use

can also cause earwax to become impacted against the TM and impair hearing.

Trauma Trauma to the external ear can cause injury to the subcutaneous tissue and result in a hematoma. If a hematoma is not aspirated, inflammation of the membranes of the ear cartilage (perichondritis) can result. Blows to the ear can cause conductive hearing loss if the ossicles in the middle ear are damaged or the TM is perforated. Head trauma that injures the temporal lobe of the cerebral cortex can impair the ability to understand the meaning of sounds.

Malignancy of External Ear Skin cancers are the only common cancers of the ear. Precancerous actinic keratoses, rough sandpaper-like lesions on the upper border of the auricle, are associated with chronic sun exposure. They are often treated with liquid nitrogen. Cancers in the external ear canal include basal cell carcinoma in the pinna and squamous cell carcinoma in the ear canal. If left untreated, they can invade underlying tissue. Teach the patient about the dangers of sun exposure and the importance of using hats and sunscreen when outdoors. See Chapter 23 for more about skin cancer.

Middle Ear and Mastoid Otitis Media Acute Otitis Media Acute otitis media is an infection of the tympanum, ossicles, and space of the middle ear. Swelling of the auditory tube from colds or allergies can trap bacteria, causing a middle ear infection. Pressure from the inflammation pushes on the TM, causing it to become red, bulging,

and painful. Acute otitis media is usually a childhood disease. In children the auditory tube that normally drains fluid and mucus from the middle ear is shorter and narrower, and its position is flatter than in adults. Infection can be due to viruses or bacteria. Pain, fever, malaise, drainage, and reduced hearing are signs and symptoms of infection. Referred pain from the TMJ, teeth, gums, sinuses, or throat can also cause ear pain. Oral antibiotics and eardrops are used if an infection is present. Surgical intervention is reserved for the patient who does not respond to medical treatment. A myringotomy involves an incision in the tympanum to release the increased pressure and exudate from the middle ear. A tympanostomy tube may be used short- or long-term for ventilation of the ear. Prompt treatment of an episode of acute otitis media can help prevent spontaneous perforation of the TM. If allergies are a causative factor, the patient may receive antihistamines and a nasal corticosteroid spray.

Otitis Media With Effusion Otitis media with effusion is an inflammation of the middle ear with a collection of fluid in the middle ear space. The fluid may be thin, mucoid, or purulent. If the auditory tube does not open and allow equalization of atmospheric pressure, negative pressure within the middle ear pulls fluid from surrounding tissues. This problem commonly follows upper respiratory tract or chronic sinus infections, barotrauma (caused by pressure change), or otitis media.

FIG. 21.3 Perforation of the tympanic membrane (TM). From Flint P, Haughey B, Lund V, Niparko JK, eds: Cummings otolaryngology: Head and neck surgery, ed 5, St Louis, 2010, Mosby.

Symptoms include a feeling of fullness of the ear, a “plugged” feeling or popping, and decreased hearing. The patient does not have pain, fever, or discharge from the ear. It is common to have otitis media with effusion for weeks to months after an episode of acute otitis media. It usually resolves without treatment but may recur.

Chronic Otitis Media and Mastoiditis Repeated attacks of otitis media may lead to chronic otitis media, especially in adults who have a history of recurrent otitis media in

childhood. Because the mucous membrane of the middle ear is continuous with the air cells of the mastoid bone, both can be involved in the chronic infectious process. Chronic otitis media is characterized by a purulent exudate and inflammation that can involve the ossicles, auditory tube, and mastoid bone. It is often painless. Hearing loss, nausea, and episodes of dizziness can occur. Hearing loss is a complication from inflammatory destruction of the ossicles, a TM perforation, or accumulation of fluid in the middle ear space. A mass of epithelial cells and cholesterol in the middle ear (cholesteatoma) may develop. The cholesteatoma enlarges and can destroy the adjacent bones. Unless removed surgically, it can cause extensive damage to the ossicles and impair hearing. Otoscopic examination of the TM may reveal changes in color and mobility or a perforation (Fig. 21.3). Culture and sensitivity tests of the drainage are necessary to identify the organisms involved so the patient may receive the appropriate antibiotic therapy. The audiogram may show a hearing loss as great as 50 to 60 dB if the ossicles have been damaged or separated. Sinus x-rays, MRI, or a CT scan of the temporal bone can assess for bone destruction and the presence of a mass.

Nursing and Interprofessional Management: Chronic Otitis Media The goals of treatment are to clear the middle ear of infection, repair any perforations, and preserve hearing (Table 21.8). Otic and systemic (oral and IV) antibiotic therapy is started based on the culture and sensitivity results. In many cases of chronic otitis media, antibiotic resistance is present. The patient may need to have frequent evacuation of drainage and debris in an outpatient setting.

TABLE 21.8 Interprofessional CareChronic

Otitis Media

Diagnostic Assessment • History and physical examination • Otoscopic examination • Culture and sensitivity of middle ear drainage • Mastoid x-ray

Management • Ear irrigations • Otic, oral, or parenteral antibiotics • Analgesics • Antiemetics • Surgery • Tympanoplasty • Mastoidectomy

TABLE 21.9 Patient & Caregiver TeachingAfter

Ear Surgery Include the following information in the teaching plan for the patient and caregiver after ear surgery. 1. Sleep on your back or the unoperated ear for 1 week. 2. Avoid air travel and sun exposure for 6 weeks. 3. If you need to cough or sneeze, keep your mouth open. 4. Blow your nose gently, without blocking either nostril. 5. Do not shampoo your hair for 5 days. Wear a shower cap when bathing.

6. No swimming. Keep your ear dry for 6 weeks. 7. You may resume strenuous activity and contact sports in 1 month. 8. Change your ear dressing daily as prescribed. 9. Report excess drainage or severe dizziness to the health care provider. Often chronic TM perforations do not heal with conservative treatment, and surgery is necessary. Tympanoplasty (myringoplasty) involves reconstruction of the TM and/or the ossicles. A mastoidectomy is often performed with a tympanoplasty to remove infected portions of the mastoid bone. Removal of tissue stops at the middle ear structures that appear capable of conducting sound. Sudden pressure changes in the ear and postoperative infections can disrupt healing or cause facial nerve paralysis. Expect impaired hearing during the postoperative period if there is packing in the ear. A cotton ball dressing is used if an incision was made through the external auditory canal. Teach the patient to change the cotton packing as needed (Table 21.9). If a postauricular (behind the ear) incision was used and a drain is in place, place a dressing over that area. Then, place a soft outer dressing over the top of that dressing. This will prevent putting pressure on the auricle. Monitor the tightness of the outer dressing to prevent tissue necrosis and assess the amount and type of drainage. Keep the suture line dry.

Otosclerosis Otosclerosis is a hereditary autosomal dominant disease. It is the most common cause of hearing loss in young adults. Spongy bone develops from the bony labyrinth, preventing movement of the footplate of the stapes in the oval window. This reduces the transmission of vibrations to the inner ear fluids and results in conductive hearing loss. Although otosclerosis is typically bilateral, one ear may show faster progression of hearing loss. The patient is often unaware of the problem until the loss becomes so severe that

communication is difficult.

TABLE 21.10 Interprofessional CareOtosclerosis

Diagnostic Assessment • History and physical examination • Otoscopic examination • Rinne test • Weber test • Audiometry • Tympanometry

Management • Hearing aid • Surgery (stapedectomy or stapes prosthesis) • Drug therapy • Calcium carbonate • Sodium fluoride with vitamin D Otoscopic examination may reveal a reddish blush of the tympanum (Schwartz’s sign) caused by the vascular and bony changes within the middle ear. Tuning fork tests (e.g., Rinne) and an audiogram show good hearing by bone conduction with poor hearing by air conduction (air-bone gap) (Table 21.6). Usually a difference of at least 20 to 25 dB between air and bone conduction levels of hearing occurs with otosclerosis. The hearing loss associated with otosclerosis may be stabilized by giving oral sodium fluoride with vitamin D and calcium carbonate. These medications slow bone resorption and promote the calcification of bony lesions. Amplifying sound with a hearing aid can be effective

because inner ear function is normal. Interprofessional care of otosclerosis is outlined in Table 21.10. Microdrill or laser surgical treatment involves opening the footplate (stapedotomy) or replacing the stapes with a metal or Teflon substitute (prosthesis). These procedures are usually done with the patient under conscious sedation. The ear with poorer hearing is repaired first. The other ear may be operated on within a year. Immediately after surgery the patient often reports a significant improvement in hearing in the operative ear. Because blood and fluid accumulates in the middle ear during the postoperative period, the hearing level decreases initially, but it improves gradually with healing. Nursing management of the patient undergoing surgery to correct otosclerosis is like that of the patient having a tympanoplasty. Place a cotton ball in the ear canal and cover the ear with a small dressing. The patient may have dizziness, nausea, and vomiting because of stimulation of the labyrinth during surgery. Disturbing the perilymph fluid can cause nystagmus. Teach the patient to avoid sudden movements that may bring on or worsen vertigo and actions that increase inner ear pressure, such as coughing, sneezing, lifting, bending, and straining during bowel movements.

Inner Ear Problems Three manifestations that indicate disease of the inner ear are vertigo, sensorineural hearing loss, and tinnitus. Symptoms of vertigo arise from the vestibular labyrinth, while hearing loss and tinnitus arise from the auditory labyrinth. There is an overlap between manifestations of inner ear problems and central nervous system (CNS) disorders.

Ménière’s Disease Ménière’s disease is a progressive disorder leading to an accumulation of endolymph in the membranous labyrinth. Although

it usually affects only one ear, it can affect both. The cause is unknown. Genetic and environmental factors may play a role. Symptoms usually begin between 30 and 60 years of age. Women are more likely to be affected.4 The excess fluid and resulting pressure lead to hearing and balance problems, including episodic vertigo, tinnitus, and ear pressure or fullness. Progressive hearing loss occurs over time. The patient has significant disability because of sudden, severe attacks of vertigo with nausea, vomiting, and sweating. A sense of fullness in the ear, increasing tinnitus, and muffled hearing may precede an attack. The patient may have the feeling of being pulled to the ground (“drop attacks”). Some patients report feeling like they are whirling in space. Attacks may last hours or days and may occur several times a year. The clinical course of the disease is highly variable.

Nursing and Interprofessional Management: Ménière’s Disease Interprofessional care of Ménière’s disease (Table 21.11) includes diagnostic tests to rule out other causes of the symptoms, including CNS disease. Results that suggest Ménière’s disease include lowfrequency sensorineural hearing loss on audiogram, 2 or more spontaneous episodes of vertigo, and abnormal vestibular tests.5 A glycerol test may aid in diagnosis. The patient receives an oral dose of glycerol, followed by serial audiograms over 3 hours. Improvement in hearing or speech discrimination supports a diagnosis of Ménière’s disease. This is attributed to the osmotic effect of glycerol pulling fluid from the inner ear. No cure exists for Ménière’s disease. Treatments aim to reduce the number and severity of vertigo attacks. During an acute attack, corticosteroids, antihistamines (e.g., diphenhydramine), anticholinergics (e.g., atropine), and benzodiazepines (e.g., lorazepam [Ativan]) can decrease the abnormal sensation and lessen nausea and vomiting.4 Acute vertigo is treated symptomatically with bed rest,

sedation, and antiemetics (e.g., prochlorperazine) or antivertigo drugs (e.g., meclizine) for motion sickness. Management between attacks may include diuretics, corticosteroids, a low-sodium diet, and stress reduction. Over time, most patients respond to the medications but must learn to live with the unpredictability of the attacks and the loss of hearing. Frequent and incapacitating attacks are indications for surgical intervention. Decompression of the endolymphatic sac and shunting can reduce the pressure on the cochlear hair cells and prevent further damage and hearing loss. If relief is not achieved, a vestibular nerve section (cutting the nerve) may be done. When involvement is unilateral, surgical ablation of the labyrinth, resulting in the loss of vestibular and hearing cochlear function, is an option. Some patients with severe attacks of vertigo have shown improvement with the injection of gentamicin through the TM. This results in inner ear damage and a reduction in endolymph production.

TABLE 21.11 Interprofessional CareMénière’s

Disease

Diagnostic Assessment • History and physical examination • Studies (including speech discrimination, tone decay) • Vestibular tests (including caloric test, positional test) • Electronystagmography • Glycerol test

Management Acute Care Drug Therapy

• Anticholinergics • Antihistamines • Antiemetics • Benzodiazepines • Corticosteroids

Surgical Therapy • Endolymphatic sac decompression • Endolymphatic shunt • Labyrinthectomy • Vestibular nerve section

Ambulatory Care • Diuretics • Corticosteroids • Dietary restriction of sodium, caffeine, nicotine, and alcohol • Stress reduction techniques Plan nursing interventions to minimize vertigo and provide patient safety. During an acute attack, keep the patient in a quiet, darkened room in a comfortable position. Teach the patient to avoid sudden head movements and position changes and to close the eyes until vertigo stops. Avoid fluorescent or flickering lights and television as they may worsen symptoms. Make an emesis basin available because vomiting is common. To minimize the risk for falling, keep the side rails up and the bed in a low position when the patient is in bed. Teach the patient to call for help when getting out of bed. Give medications and fluids parenterally. Monitor intake and output. When the attack subsides, help the patient with ambulation because unsteadiness may remain.

Discharge teaching should emphasize ways to protect the patient from injury between attacks. Review with the patient the need to sit or lie down at the onset of any dizziness. Discuss home safety and measures to decrease fall risk. Teach the need to avoid swimming under water, using ladders, and being on high places until vertigo is under control. Encourage the patient to practice any balance therapy exercises daily.

Benign Paroxysmal Positional Vertigo Benign paroxysmal positional vertigo (BPPV) is a common cause of vertigo. About 50% of the cases of vertigo may be due to BPPV. In BPPV, free-floating debris in the semicircular canal causes vertigo with specific head movements, such as getting out of bed, rolling over in bed, and sitting up from lying down. The debris (“ear rocks”) is composed of small crystals of calcium carbonate that come from the utricle in the inner ear. The utricle may have been injured by head trauma, infection, or degeneration from the aging process. However, for many patients, we do not know the cause. Symptoms of BPPV include nystagmus, vertigo, light-headedness, loss of balance, and nausea. There is no hearing loss, and symptoms tend to be intermittent. The symptoms of BPPV may be confused with those of Ménière’s disease. Diagnosis is based on the results of auditory and vestibular tests. Although BPPV is bothersome, it is rarely serious unless a person falls. The Epley maneuver, or canalith repositioning procedure, is effective in providing symptom relief for many patients. This maneuver moves ear debris from areas in the inner ear that cause symptoms and into less sensitive areas where they do not cause these problems. It does not change the presence of debris but changes the location. A trained HCP can teach the patient how to perform the maneuver (Fig. 21.4).

Acoustic Neuroma

An acoustic neuroma is a unilateral benign tumor that occurs where the vestibulocochlear nerve (CN VIII) enters the internal auditory canal. Early diagnosis is important because the tumor can compress the trigeminal and facial nerves and arteries within the internal auditory canal. Symptoms usually begin between 40 and 60 years of age. Early symptoms are associated with CN VIII compression and destruction. They include unilateral, progressive, sensorineural hearing loss; reduced touch sensation in the posterior ear canal; unilateral tinnitus; and mild, intermittent vertigo. Diagnostic tests include neurologic, audiometric, and vestibular tests; CT scans; and MRI. Surgery to remove small tumors can preserve hearing and vestibular function. Large tumors (larger than 3 cm) and the surgery to remove them can leave the patient with permanent hearing loss and facial paralysis. Stereotactic radiosurgery may slow tumor growth and preserve the facial nerve. Teach the patient to report any clear, colorless discharge from the nose. This may be cerebrospinal fluid (CSF), which increases the risk for infection. Follow-up care after surgery is important to monitor hearing and for tumor recurrence.

Hearing Loss and Deafness Hearing disorders are a common cause of disability. Age is the strongest predictor of hearing impairment. In the United States, about 25% of those 65 to 74 and 50% of those 75 and older have hearing loss.6 Causes of hearing loss are shown in Fig. 21.5.

Types of Hearing Loss Conductive Hearing Loss Conductive hearing loss occurs when conditions in the outer or middle ear impair the transmission of sound through air to the inner ear. Common causes of conductive hearing loss in adults include impacted cerumen, otitis media with effusion, TM perforation, otosclerosis, and

narrowing of the external auditory canal.1 The audiogram shows better hearing through bone than through air (air-bone gap). The patient often speaks softly because hearing his or her own voice (which is conducted by bone) seems loud. This patient hears better in a noisy environment. The first step is to identify and treat the cause if possible. If correction of the cause is not possible, a hearing aid may help if the loss is greater than 40 to 50 dB.

FIG. 21.4 Epley maneuver.

FIG. 21.5 Causes of hearing loss.

Sensorineural Hearing Loss Sensorineural hearing loss is caused by impairment of function of the inner ear or the vestibulocochlear nerve (CN VIII). Congenital and hereditary factors, noise exposure, aging (presbycusis), Ménière’s disease, trauma, and ototoxicity can cause sensorineural hearing loss. The main problems are the ability to hear sound but not to understand speech and the lack of understanding of the problem by others. The

ability to hear high-pitched sounds (including consonants) diminishes. Sounds become muffled and hard to understand. An audiogram shows a loss in decibel levels of the 4000-Hz range and eventually the 2000-Hz range. A hearing aid may help some patients, but it only makes sounds and speech louder, not clearer.

Mixed Hearing Loss Mixed hearing loss occurs due to a combination of conductive and sensorineural causes. Careful evaluation is needed if corrective surgery for conductive loss is planned because the sensorineural hearing loss will still be present.

Central and Functional Hearing Loss Central hearing loss involves an inability to interpret sound, including speech, because of a problem in the brain (CNS). A careful history is helpful because there are usually cases of deafness in the family. Refer the patient to a qualified hearing and speech service if indicated. An emotional or a psychologic factor can cause functional hearing loss. The patient does not seem to hear or respond to pure-tone subjective hearing tests, but no physical reason for hearing loss can be found. Psychologic counseling may help.

Genetic Link Heredity hearing loss is labeled non-syndromic or syndromic. Most persons have non-syndromic hearing impairment, in which hearing loss is the only primary problem. GJB2 gene mutations are one of the most common causes of non-syndromic hearing loss. These result in changes in the production of the protein Connexin 26, which has a role in the cochlear function. Other genetic mutations increase the risk for ototoxicity or result in malformations of structures in the middle and/or inner ear. Syndromic hearing impairment is associated with other clinical abnormalities, such as malformations of the external ear or problems involving other organs. There are more than 400 syndromes that include hearing loss.

Classification of Hearing Loss Hearing loss can be classified by the decibel level or loss as recorded on the audiogram. Normal hearing is in the 0- to 15-dB range. Most people with a hearing loss of 90 decibels or greater have been deaf since birth (congenitally deaf). Table 21.12 describes the levels of hearing loss.

Clinical Manifestations Common early signs of hearing loss are answering questions inappropriately and not responding when not looking at the speaker (Table 21.3). Other behaviors that suggest hearing loss include straining to hear, cupping the hand around the ear, reading lips, and an increased sensitivity to slight increases in noise level. Often the patient is unaware of minimal hearing loss. Family and friends who get tired of repeating or talking loudly are often the first to notice the hearing loss. Pressure exerted by significant others is a significant factor in whether the patient seeks help for hearing impairment. Sudden hearing loss, or sudden deafness, occurs as an unexplained, rapid loss of hearing (usually in one ear) either at once or over several days. It is a medical emergency, and the patient should see an HCP at once.

Tinnitus and Hearing Loss Tinnitus is the perception of sound in the ears where no external source is present. It is “ringing in the ears” or “head noise” (see www.ata.org). Tinnitus is sometimes the first symptom of hearing loss, especially in older adults. It may be soft or loud, high pitched or low pitched. Often, tinnitus occurs because of noise exposure. It also can be a drug side effect. More than 200 drugs are known to cause tinnitus.

Nursing and Interprofessional

Management: Hearing Loss and Deafness Deafness is often called the “unseen handicap” because you may not realize the difficulty in communication with a deaf person until you begin a conversation with that person. You need to confirm a deaf person’s understanding of health teaching. Descriptive visual aids can be helpful. If the significantly hearing-impaired person uses sign language to communicate, the Americans with Disabilities Act requires providing an interpreter when presenting significant information, such as for patient consent or discharge teaching.7

TABLE 21.12 Classification of Hearing Loss

Decibel (dB) Loss 0–15

Meaning Normal hearing

16–25

Slight hearing loss

26–40

Mild impairment

41–55

Moderate impairment

56–70

Moderately severe impairment

71–90

Severe impairment

>90

Profound deafness

Interference in communication and interaction with others can be the source of many problems for the patient and caregiver. Often the patient refuses to admit or may be unaware of impaired hearing. Irritability is common because the patient must concentrate so hard to understand speech. The loss of clarity of speech in the patient with sensorineural hearing loss is most frustrating. The patient may hear what is said but not understand it. Withdrawal, depression, and accelerated cognitive decline are often associated with advancing

hearing loss.8

Check Your Practice Your newly assigned 68-yr-old female patient is being discharged today following a hip replacement. Before going to her room, you prepared the materials and information for her discharge. You sit down by her bed and start talking with her. She shakes her head and says, “No, no.” You are perplexed until she flashes a bracelet that says I am deaf. • How will you proceed?

Health Promotion Environmental Noise Control Noise is the most preventable cause of hearing loss. Fig. 21.6 lists the levels of environmental noise generated by common indoor and outdoor sounds. Sudden severe loud noise (acoustic trauma) and chronic exposure to loud noise (noise-induced hearing loss) can damage hearing. Acoustic trauma causes hearing loss by destroying the hair cells of the organ of Corti. Sensorineural hearing loss from increased and prolonged environmental noise, such as amplified sound, is occurring in young adults at an increasing rate. Amplified music (e.g., on smartphones) should not exceed 50% of maximum volume. Ear protection should be worn when firing a gun and during other recreational pursuits with high noise levels. Health teaching about avoiding continued exposure to noise levels greater than 70 dB is essential. In work environments known to have high noise levels (more than 85 dB), people should wear ear protection. Occupational Safety and Health Administration (OSHA) standards mandate ear protection for workers in environments where the noise levels consistently exceed 85 dB. Periodic audiometric screening should be part of the health

maintenance policies of industry. This provides baseline data on hearing to measure subsequent hearing loss. Employees should take part in hearing conservation programs in work environments. Such programs should include noise exposure analysis, provision for control of noise exposure (hearing protectors), measurements of hearing, and employee-employer notification and education. Encourage young adults to keep amplified music at a reasonable level and limit their exposure time. Hearing loss caused by noise is not reversible

Promoting Population Health Promoting Healthy Hearing • Wear ear protection during recreational and work activities involving high noise levels. • Monitor your audio level and how long you use personal listening devices. • Avoid exposure to excessively loud noise whenever possible. • Undergo audiometric screening to detect hearing loss before it progresses. • Avoid injury from cotton-tipped applicators and other cleaning materials.

FIG. 21.6 Range of common environmental sounds.

Immunizations Various viruses can cause deafness because of fetal damage and malformations affecting the ear. Promote childhood and adult immunizations, including the measles, mumps, and rubella (MMR) vaccine. Rubella infection during the first 8 weeks of pregnancy is associated with a high incidence of congenital rubella syndrome, which causes sensorineural deafness. Women of childbearing age should be tested for antibodies to these viral diseases. Women should avoid pregnancy for at least 3 months after being immunized. Immunization must be delayed if a woman is pregnant. Women who

are susceptible to rubella can be vaccinated safely during the postpartum period.

Ototoxic Substances Monitor the patient who is receiving ototoxic drugs or exposed to ototoxic agents for signs and symptoms of ototoxicity, including tinnitus, diminished hearing, and balance problems. If these symptoms develop, stopping the drug may prevent further damage and allow the symptoms to disappear.

Assistive Devices and Techniques Hearing Aids The patient with a suspected hearing loss should have a hearing assessment by a qualified audiologist. If a hearing aid is needed, it should be fitted by an audiologist or a speech and hearing specialist. Many types of hearing aids are available, each with advantages and disadvantages (Table 21.13). The conventional hearing aid serves as a simple amplifier. For the patient with bilateral hearing impairment, binaural hearing aids offer the best sound lateralization and speech discrimination. The goal of hearing aid therapy is improved hearing with consistent use. Patients who are motivated and optimistic about using a hearing aid are more successful users. Determine the patient’s readiness for hearing aid therapy, including acknowledgment of a hearing problem, the patient’s feelings about wearing a hearing aid, the degree to which the hearing loss affects life, and any difficulties the patient has manipulating small objects such as putting a battery in a hearing aid. Initially, use of a hearing aid should be restricted to quiet situations in the home. The patient must first adjust to voices (including the patient’s own voice) and household sounds. The patient should try increasing and decreasing the volume as situations require. As the patient adjusts to the increase in sounds and background noise, they can progress to situations in which several people will be talking at once. Next, the environment is expanded to the outdoors and then a

shopping mall or grocery store. Adjustment to different environments occurs gradually, depending on the patient. When a hearing aid is not being worn, it should be placed in a dry, cool area where it will not be inadvertently damaged or lost. The battery should be disconnected or removed when not in use. Battery life averages 1 week, depending on the hearing aid, battery, and amount of use. Advise patients to buy only a month’s supply at a time. Ear molds should be cleaned weekly or as needed. Toothpicks or pipe cleaners can easily clear a clogged ear tip.

TABLE 21.13 Types of Hearing Aids

An implantable hearing device or aid is available to patients who cannot or will not use traditional hearing aids or cochlear implants.

Implanted hearing devices amplify sound and transmit the sound vibrations through the ear. The device does not have visible external components. There are 2 types of implantable hearing devices: fully implantable and partially implantable. Fully implantable devices are placed surgically, and nothing is visible externally. Partially implanted devices have an internal device that is implanted surgically and an external device that is worn behind or in the ear.

Speech Reading Speech reading, or lip reading, can be helpful in increasing communication. It allows for about 40% understanding of the spoken word. The patient uses visual cues associated with speech, such as gestures and facial expressions, to help clarify the spoken message. In speech reading, many words look alike to the patient (e.g., rabbit, woman). Help the patient by using and teaching verbal and nonverbal communication techniques as described in Table 21.14.

TABLE 21.14 Communicating With Patients With

Hearing Impairment

Nonverbal Aids • Draw attention with hand movements. • Have speaker’s face in good light. • Avoid light behind the speaker. • Maintain eye contact. • Avoid covering mouth or face with hands. • Avoid chewing, eating, smoking while talking. • Remove background noise. • Move close to better ear.

Verbal Aids

• Speak normally and slowly. Do not shout. • Do not exaggerate facial expressions. • Do not overenunciate. • Use simple sentences. • Rephrase sentence. Use different words. • Write name or difficult words. • Speak in normal voice directly into better ear.

Sign Language Sign language is a form of communication for people with profound hearing impairment. It involves gestures and facial features such as eyebrow motion and lip-mouth movements. Sign language is not universal. American Sign Language (ASL) is used in the United States and the English-speaking parts of Canada.

FIG. 21.7 Cochlear implant.

Cochlear Implant A cochlear implant may be used for some people with severe to profound sensorineural hearing loss in one or both ears.9 The implant bypasses damaged or missing portions of the ear and directly activates cranial nerve VIII. The ideal candidate is one who has become deaf after acquiring speech and language. The system consists of (1) an external microphone placed behind the ear, (2) a speech processor, (3) a transmitter implanted under the skin that changes

sounds into electrical impulses, and (4) electrodes placed within the cochlea that stimulate the auditory nerves in the ear (Fig. 21.7). The electrodes are inserted as far as possible into the cochlea. Cochlear implants send information that covers the entire range of sound frequencies. For patients with conductive and mixed hearing loss, the cochlear Baha system may be surgically implanted. The system works through direct bone conduction and integrates with the skull bone over time. Extensive training and rehabilitation are essential to receive the most benefit from these implants. Besides providing sound to a person who heard none, cochlear implants improve lip-reading ability, allow self-monitoring of the loudness of speech, improve the sense of security, and decrease feelings of isolation.

Assistive Listening Devices Many devices are available to help the hearing-impaired person. Direct amplification devices, amplified telephone receivers, alerting systems that flash when activated by sound, an infrared system for amplifying the sound of the television, and a combination FM receiver and hearing aid may be options based on patient needs. People with profound deafness may be aided by text-telephone alerting systems that flash when activated by sound, closed captioning on television, and a specially trained dog. The dogs are trained to alert their owners to specific sounds within the environment, thus increasing the person’s safety and independence.

TABLE 21.15 Classification of Presbycusis

Gerontologic Considerations: Hearing Loss Presbycusis, hearing loss associated with aging, includes the loss of peripheral auditory sensitivity, a decline in word recognition ability, and associated psychologic and communication issues. Because consonants (high-frequency sounds) help us recognize spoken words, the older person with presbycusis has a decreased ability to understand speech. Vowels are heard, but one cannot distinguish consonants in the high-frequency range. This may lead to confusion and embarrassment because of the difference in what was said and what was heard. Degenerative changes in the inner ear cause presbycusis. Noise exposure is thought to be a common factor. Table 21.15 describes the classification of specific causes and associated hearing changes of presbycusis. Often a person may have more than one type of presbycusis. The prognosis for hearing depends on the cause of the loss. Sound amplification with the right device is often helpful in improving the understanding of speech. In other situations, an audiologic rehabilitation program can be valuable. The older adult is often reluctant to use a hearing aid for sound amplification. Reasons cited most often include cost, appearance, insufficient knowledge about hearing aids, amplification of competing noise, and unrealistic expectations. Most hearing aids and batteries are small, and neuromuscular changes such as stiff fingers, enlarged joints, and decreased sensory perception often make the care and handling of a hearing aid frustrating for an older person. Some older adults may also tend to accept their losses as part of getting older and

believe there is no need for improvement.

Case Study Ménière’s Disease

© iStock.com/EyeMark.

Patient Profile While R.S. is in the emergency department, she starts violently vomiting. She tells you that any movement is making her feel like she

is “spinning like crazy.” The HCP decides to admit her under observation with plans to administer an intratympanic injection of dexamethasone.

Objective Data • Skin pale, extremely diaphoretic • Heart rate 112 beats/min, respirations 22 breaths/min, BP 100/64

Interprofessional Care • 1000 mg sodium diet as tolerated • Ondansetron 2 mg IV now • Lorazepam 1 mg IV every 6 hours • Meclizine 25 mg PO every 6 hours • Electronystagmogram and glycerol test • Dextrose 5% with 0.45% NaCl at 75 mL/hr

Discussion Questions 1. Explain the etiology of Ménière’s disease. 2. What clinical manifestations of Ménière’s disease does R.S. exhibit? 3. Give the rationale for each treatment measure ordered. 4. Priority Decision: Based on the assessment data, what are the priority nursing diagnoses? 5. Priority Decision: What are the priority nursing interventions for R.S.? 6. Delegation Decision: Identify interventions for R.S. that can be delegated to unlicensed assistive personnel (UAP). 7. Safety: Identify an area of risk for injury to R.S. What actions will you take to ensure patient safety? 8. Patient-Centered Care: What teaching will you provide so R.S.

can successfully self-manage her condition after discharge? 9. Quality Improvement: What outcomes would indicate interprofessional care was effective? Answers available at http://evolve.elsevier.com/Lewis/medsurg.

Bridge to Nclex Examination The number of the question corresponds to the same-numbered outcome at the beginning of the chapter.

1. In a patient with vertigo, the parts of the ear most likely involved are the (select all that apply) a. cochlea. b. ossicles. c. vestibule. d. semicircular canals. e. tympanic membrane. 2. A patient reports tinnitus and balance problems. The medication that may be responsible is a. digoxin. b. warfarin. c. furosemide. d. acetaminophen. 3. What assessment technique should the nurse use to assess an adult patient’s tympanic membrane? a. Have the patient tilt the head toward the nurse. b. Stabilize the otoscope with your fingers on the patient’s cheek.

c. Pull the auricle down and back to straighten the auditory canal. d. Use a speculum slightly larger than the size of the patient’s ear canal. 4. A normal finding the nurse would expect when assessing hearing would be a. absent cone of light. b. bluish purple tympanic membrane. c. fluid level at hairline in the tympanum. d. midline tone heard equally in both ears. 5. Common age-related changes in the auditory system include (select all that apply) a. drier cerumen. b. tinnitus in both ears. c. auditory nerve degeneration. d. atrophy of the tympanic membrane. e. greater ability to hear high-pitched sounds. 6. The nurse teaches a patient scheduled for an electronystagmography that the test involves a. measuring ear drum movement in response to pressure. b. recording eye movements associated with ear irrigation. c. placing an electrode on the eardrum and assessing for dizziness. d. wearing headphones and determining which sounds can be heard. 7. Care of the patient experiencing an acute attack of Ménière’s disease includes (select all that apply)

a. giving antiemetics as needed. b. implementing fall precautions. c. keeping the room dark and quiet. d. placing the patient on NPO status. e. ambulating in the hall independently. 8. The patient who has a conductive hearing loss a. hears better in a noisy environment. b. hears sound but does not understand speech. c. often speaks loudly because his or her own voice seems low. d. has clearer sound with a hearing aid if the loss is less than 30 dB. 9. Teach the patient who is newly fitted with bilateral hearing aids to (select all that apply) a. replace the batteries monthly. b. clean the ear molds weekly or as needed. c. clean ears with cotton-tipped applicators daily. d. disconnect or remove the batteries when not in use. e. initially restrict usage to quiet listening in the home. 10. Which strategies would best aid the nurse communicate with a patient who has a hearing loss (select all that apply)? a. Overenunciate speech. b. Speak normally and slowly. c. Exaggerate facial expressions. d. Raise the voice to a higher pitch. e. Write out names or difficult words. 1. c, d, 2. c, 3. b, 4. d, 5. a, b, c, d, 6. b, 7. a, b, c, 8. a, 9. b, d, e, 10. b, e

For rationales to these answers and even more NCLEX review questions, visit http://evolve.elsevier.com/Lewis/medsurg.

Evolve Website/Resources List http://evolve.elsevier.com/Lewis/medsurg

Review Questions (Online Only) Key Points Answer Keys for Questions • Rationales for Bridge to NCLEX Examination Questions • Answer Guidelines for Case Study on pp. 378, 380, 381, 382, and 393 Conceptual Care Map Creator Audio Glossary Content Updates

References 1. Eggermont J: Hearing loss: Causes, prevention, and treatment, Cambridge, 2017, Academic Press. 2. Hearing Loss Association of America Retrieved from http://hearingloss.org. 3. Popelka G, Moore B, Fay R, Popper A, eds: Hearing aids, Switzerland, 2016, Springer International Publishing. 4. Patel H, Isildak H: Ménière’s disease, Oper Tech Otolaryngol Head Neck Surg 27:184, 2016. 5. Pullen R: Navigating the challenges of Ménière’s disease, Nursing 47:38, 2017.

6. Quick statistics about hearing. Retrieved from www.nidcd.nih.gov/health/statistics/quick-statisticshearing. 7. Communicating with people who are deaf or hard of hearing in hospital settings. Retrieved from www.ada.gov/hospcombr.htm. 8. Tremblay KL: Why is hearing loss a public health concern, Hear J 70:14, 2017. 9. National Institute on Deafness and Other Communication Disorders: Cochlear implants. Retrieved from www.nidcd.nih.gov. Evidence-based information for clinical practice.

22

Assessment Integumentary System Mariann M. Harding

LEARNING OUTCOMES 1. Describe the structures and functions of the integumentary system. 2. Link the age-related changes in the integumentary system to differences in assessment findings. 3. Obtain significant subjective and objective data related to the integumentary system from a patient. 4. Compare the critical components for describing primary and secondary lesions. 5. Perform a physical assessment of the integumentary system using appropriate techniques. 6. Specify the structural and assessment differences in light- and dark-skinned persons. 7. Distinguish normal from common abnormal findings of a physical assessment of the integumentary system. 8. Describe the purpose, significance of results, and nursing responsibilities related to diagnostic studies of the integumentary system.

KEY TERMS alopecia, Table 22.8, p. 404 dermis, p. 396 epidermis, p. 395 erythema, Table 22.8, p. 404 hirsutism, Table 22.8, p. 404 intertriginous, p. 401 keloid, p. 404 keratinocytes, p. 395 melanocytes, p. 395 mole (nevus), Table 22.8, p. 404 pruritus, p. 401 sebaceous glands, p. 397 The greatest gift you can give another is the purity of your attention. Richard Moss http://evolve.elsevier.com/Lewis/medsurg/

Conceptual Focus Health Promotion Tissue Integrity The integumentary system is the largest organ of the body. It is composed of the skin, hair, nails, and certain glands. The skin has 2 major layers: epidermis (outer layer) and dermis (inner layer). The subcutaneous tissue (layer) lies under the dermis (Fig. 22.1). The skin is as complex as any organ, but, unlike the others, it is readily visible.

Being able to see and touch the skin helps you assess your patients. You can see abnormalities, understand their significance, and intervene early.

Structures and Functions of Skin and Appendages Structures Epidermis The epidermis, the outer layer of the skin, is relatively thin, ranging from 0.05 mm on the eyelids to 0.1 mm on the soles.1 There are no lymphatic or vascular structures in the epidermis. It is supported by passive circulation from the dermis. The epidermis is divided into 5 distinct but interrelated layers. Two of the layers are the stratum corneum (the surface layer) and the stratum germinativum (deepest, basal layer) (Fig. 22.1). Most epithelial cells are keratinocytes (90%). The remaining cells are melanocytes, Langerhans’ cells, and Merkel cells. Keratinocytes form in the basal layer. Initially, they are undifferentiated and shaped like columns. As they mature (keratinize), they move to the surface, where they flatten and die to form the outer skin layer (stratum corneum). Keratinocytes make a fibrous protein, keratin, which is vital to the skin’s protective barrier function. The upward movement of keratinocytes from the basal layer to the outermost levels of the stratum corneum takes about 14 days. The keratinocytes stay there for another 14 days, allowing the epidermis to regenerate every 28 days. Thus each month you have a new layer of skin. Many skin problems result from changes in this cell cycle. If dead cells slough off too rapidly, the skin appears thin and eroded. If new cells form faster than you shed old cells, the skin becomes scaly and thickened. Failure of the epidermis to function normally occurs with skin cancer and psoriasis (discussed in Chapter 23).

Melanocytes are found in the deep, basal layer. They contain melanin, a pigment that gives color to the skin and hair and protects the body from damaging ultraviolet (UV) sunlight. Sunlight and hormones stimulate the melanosome (within the melanocyte) to increase the production of melanin. People of all races have similar numbers of melanocytes. In darker skin, the melanosomes are larger and more numerous, thus producing more melanin.2 This increased melanin forms a natural sun shield for dark skin and results in a decreased incidence of skin cancer. The distribution of melanocytes varies from one area of the body to another. For example, the face has more melanocytes than the abdomen.

FIG. 22.1 Microscopic view of the skin in longitudinal section. From Jarvis C: Physical examination and health assessment, ed 6, St Louis, 2012, Saunders.

Langerhans’ cells are a type of dendritic cell (discussed in Chapter 13 on p. 191). They are immunocompetent cells that recognize antigens. When they are depleted, the skin cannot initiate an immune response. The Langerhans’ cells in bioengineered skin grafts have been removed to prevent graft rejection. In skin diseases such as psoriasis and sarcoidosis, there are decreased numbers of Langerhans’ cells. Merkel cells are found in the basal layer and are involved in the sensation of light touch. We use them when feeling the texture of an object and figuring out what it is. The basement membrane zone is between the epidermis and dermis. This structure provides for the (1) exchange of fluids between the epidermis and dermis and (2) structural support for the epidermis.

The basement membrane helps to secure the two layers together. Inflammation and separation of the epidermal and dermal layers result in the blisters seen with problems such as burns, full-thickness wounds, and mechanical trauma.

Dermis The dermis is the connective tissue below the epidermis. Dermal thickness ranges from 0.3 mm on the eyelid to 3.0 mm on the back.1 The dermis is very vascular, containing many blood vessels. It also contains nerves, lymphatic vessels, hair follicles, sebaceous glands, and specialized cells such as mast cells and macrophages that protect the body from external stimuli. The dermis is made of 3 types of connective tissue: collagen, elastic fibers, and reticular fibers. Collagen forms the greatest part of the dermis. It gives the skin toughness and strength. The primary cell type in the dermis is the fibroblast, which makes collagen and elastin. Collagen is critical in wound healing. The dermis has 2 layers: upper thin papillary layer and a deeper, thicker reticular layer. The papillary layer is arranged haphazardly in ridges, or papillae, which extend into the outer epidermal layer. These elevated surface ridges form fingerprints and footprints. The reticular layer forms the bulk of the dermis. It is made up of thick collagen bundles arranged parallel to the skin’s surface.

Subcutaneous Tissue The subcutaneous tissue lies below the dermis. It is made of loose connective tissue and fat cells that provide insulation, cushioning, temperature regulation, and energy storage. The subcutaneous tissue attaches the skin to underlying tissues, such as muscle and bone. The distribution pattern of subcutaneous tissue varies with gender, heredity, age, and nutritional status.

Skin Appendages Skin appendages include the hair, nails, and glands (sebaceous,

apocrine, and eccrine). These appendages are epidermal extensions that have their roots in the dermis. These structures receive nutrients, electrolytes, and fluids from the dermis. Hair and nails form from specialized keratin. Systemic diseases can affect the condition and health of both hair and nails. Hair grows on most of the body except for the lips, palms of the hands, interdigital spaces, portions of the genitalia, and soles of the feet. The density and pattern of distribution varies depending on age, sex, and race. Hair color is a result of heredity and determined by the type and amount of melanin in the hair shaft. Hair grows about 1 cm per month. People lose about 100 hairs each day.3 Baldness, or alopecia, results when we do not replace lost hair.

FIG. 22.2 Structure of a nail. From Patton KT, Thibodeau GA, Douglas M: Essentials of anatomy and physiology, St Louis, 2014, Mosby.

Nails are made of heavily keratinized cells. The part of the nail that you can see is the nail body. The rest is the nail root. A fold of skin hides most of the nail root. The cuticle borders this skinfold. Nail growth begins in the nail root. The part of the nail root you can see is the lunula. This white, crescent-shaped area is the site of mitosis and nail growth (Fig. 22.2). Under the nail is an area of epidermis called the nail bed. The nail bed has many blood vessels. Nails grow slowly, but continuously. Fingernails grow much faster than toenails, at a rate

of 0.5 to 2 mm per week.1 It takes 3 to 6 months to replace a fingernail. A toenail may take 12 months or longer to replace. Nail color ranges from pink to yellow or brown depending on skin color. Color and texture variations in nails may be normal or represent an abnormal condition. Pigmented longitudinal bands (melanonychia striata) occur in the nail bed in 90% or more of people with dark skin4 (Fig. 22.3). There are 2 major types of glands in the skin: sebaceous and sweat (apocrine and eccrine) glands. Sebaceous glands secrete sebum, which is emptied into the hair follicles. Sebum waterproofs and lubricates the skin and promotes the absorption of fat-soluble substances. Sebum is somewhat bacteriostatic and fungistatic. These glands depend on sex hormones, particularly testosterone, to regulate sebum secretion and production. Actual production varies depending on age, sex, and testosterone and estrogen levels. Sebaceous glands are present on all areas of the skin except the palms and soles and dorsum of the feet. These glands are most abundant on the face, scalp, upper chest, and back. The apocrine sweat glands are mainly found in the axillary, genital, and breast areas. They are always connected to a hair follicle. These glands enlarge and become active at puberty because of reproductive hormones. They secrete a thick milky substance that is naturally odorless. Odor occurs when skin surface bacteria alter the secretions. The eccrine sweat glands are found on most of the body, except the lips, ear canals, nail beds, labia minora, glans penis, and prepuce. One square inch of skin has about 3000 eccrine sweat glands. Their main function is to cool the body by evaporation, excrete waste products, and moisturize surface cells. Sweat is a transparent watery solution composed of salts, ammonia, urea, and other wastes. In extreme situations, the body can make 2 to 4 L of sweat per hour or up to 12 liters in 24 hours. Heat, certain mental stimuli, and ingestion of hot, spicy foods stimulate sweat secretion.

FIG. 22.3 Pigmented nail bands normally seen with dark skin color. From Ball J, Dains J, Flynn J, et al: Seidel’s guide to physical examination, ed 8, St Louis, 2014, Mosby.

Functions of Integumentary System The skin’s main function is to protect the underlying body tissues by serving as a barrier to the external environment. The skin acts as a barrier against invasion by bacteria and viruses and prevents excess water loss. The fat in the subcutaneous layer insulates the body and provides protection from trauma. Melanin screens and absorbs UV radiation. The skin with its nerve endings and special receptors collects sensory information from environmental stimuli. These highly specialized nerve endings give information to the brain related to pain, heat and cold, touch, pressure, and vibration. The skin controls heat regulation by responding to changes in internal and external temperature with vasoconstriction or vasodilation. The skin’s excretory function and heat regulation are related. We lose between 600 and 900 mL of water daily through

insensible water loss (invisible vaporization from the lungs and skin), which helps regulate body temperature. Sebum and sweat lubricate the skin surface. Endogenous synthesis of vitamin D, which is critical to calcium and phosphorus balance, occurs in the epidermis. Vitamin D is made in the epidermis when UV light acts on vitamin D precursor cells.

Gerontologic Considerations: Effects of Aging on Integumentary System Many skin changes are associated with aging. Depending on a person’s view of self, the normal, visible effects of aging on the skin and hair may have a profound psychologic effect. Having a youthful look may affect a person’s self-image. The appearance of the signs of aging can be a threat to self-concept. Other changes in skin structure related to normal changes with aging can pose serious risk. Agerelated changes of the integumentary system and differences in assessment findings are listed in Table 22.1. Chronic UV exposure is the major contributor to the photoaging and wrinkling of skin.5 Sun damage to the skin is cumulative (Fig. 22.4). The wrinkling of sun-exposed areas such as the face and hands is more marked than that of a sun-shielded area, such as the buttocks. A photoaged person is more susceptible to skin cancers because UV exposure decreases the ability to repair cellular damage. Chronic UV exposure from tanning beds causes the same damage as UV from the sun. Other factors that influence skin aging include diabetes, smoking, and alcohol use.

TABLE 22.1 Gerontologic Assessment

DifferencesIntegumentary System

The junction between the dermis and epidermis flattens. This causes the two layers to lose their tight bond. Skin tears and other trauma become common as the epidermis slides separately from the dermis. Collagen fibers stiffen, elastic fibers degenerate, and the amount of subcutaneous tissue decreases. These changes, with the added effects of gravity, lead to wrinkling. Fewer free fatty acids in the epidermis results in dry, scaly, itchy skin. Dryness, combined with trauma caused by scratching, increases the risk for fissures (cracks) in the skin and secondary infections. Decreased subcutaneous fat increases the risk for traumatic injury, hypothermia, and skin shearing, which may lead to pressure ulcers.

FIG. 22.4 Photoaging. Irregular pigmentation and keratoses occur on sun-damaged skin on forehead. From Gawkrodger D, Ardern-Jones MR: Dermatology, ed 5, Edinburgh, 2012, Churchill Livingstone.

Fewer melanocytes are present, and with decreased levels of melanin, hair color fades. Hormonal and vitamin deficiencies can cause dry, thin hair and alopecia. The growth rate of the hair and nails decreases because of atrophy. The nail plate thins, and nails become brittle and more prone to splitting and yellowing. Nails, especially the toenails, may thicken with age. With aging, the apocrine and eccrine sweat glands atrophy, causing dry skin and decreased body odor. Benign neoplasms related to the aging process can occur. These growths include seborrheic keratoses, vascular lesions such as cherry angiomas, and skin tags. Actinic keratoses appear on areas of chronic sun exposure, especially in the person who has a fair complexion and light eyes (blue, green, or hazel). These premalignant cutaneous lesions place a person at increased risk for squamous cell and basal cell carcinomas.

Assessment of Integumentary System The general skin assessment begins with your first contact with the

patient and continues throughout the examination. As you are meeting your patient for the first time, take a moment to note the overall condition of the patient’s skin and hair. You will assess specific areas of the skin when examining other body systems, unless the chief complaint is a skin problem. Record a general statement about the skin’s physical condition (Table 22.2). In addition, ask the health history questions presented in Table 22.3 when you note a skin problem.

Case Study Patient Introduction

© iStockphoto/Thinkstock.

D.A. is a 74-yr-old woman who comes to the medical clinic with concerns related to various “spots” on her face. She says they have been there for a while and she thought they were just “age spots.” She became concerned after her friend was diagnosed with a malignant melanoma.

Discussion Questions 1. Which type of assessment should you perform: comprehensive, focused, or emergency?

2. What are the possible causes of D.A.’s facial lesions? 3. What questions would you ask D.A. to determine the possible causes? You will learn more about D.A. and her condition as you read this chapter. (See p. 401 for more information on D.A.) Answers available at http://evolve.elsevier.com/Lewis/medsurg.

TABLE 22.2 Normal Physical Assessment of

Integumentary System

Subjective Data Perform the interview using a sensitive and nonjudgmental attitude. The problem may be the result of poor hygiene or unhealthful behaviors. Some problems are highly visible and affect the patient’s body image and self-concept. A thorough health history yields information about possible causes and the effect of the problem on the person’s life.

Important Health Information Past Health History Past health history reveals previous trauma, surgery, or disease that involves the skin. Many diseases have skin manifestations (Table 22.4). Determine if the patient has noticed any problems such as

jaundice (liver disease), delayed wound healing (diabetes), cyanosis (respiratory, cardiovascular disorder), or pallor (anemia). Obtain specific information related to food sensitivities, pet or drug allergies, and skin reactions to insect bites and stings. Note any history of chronic or unprotected exposure to UV light, including tanning bed use and radiation treatments.

Medications A thorough medication history is important. Ask the patient about skin-related problems that occurred because of taking a medication. Many hormones, antibiotics, corticosteroids, and antimetabolites have side effects that manifest in the skin. Medications may contain fragrances and preservatives that can cause skin reactions. Document the use of medications specifically used to treat a primary skin problem, such as acne, or a secondary skin problem, such as itching. Record the drug’s name, length of use, method of application, and effectiveness.

Surgery or Other Treatments Determine if any surgical procedures, including cosmetic surgery, were done on the skin. Record any biopsy results. Note any treatments specific for a skin problem (e.g., phototherapy) or for a health problem (e.g., radiation therapy). Document any treatments undergone primarily for cosmetic purposes, such as tanning booth use, laser resurfacing, or cosmetic “peels.”

Functional Health Patterns Health Perception–Health Management Pattern Ask the patient about health practices, such as self-care habits related to daily hygiene. Document the frequency of use and sun protection factor (SPF) of sunscreen products. Assess the use of personal care products (e.g., shampoos, moisturizing agents, cosmetics), including brand name, quantity, and frequency. Record a description of any

current skin problem, including onset, symptoms, course, and treatment. Note any medications used for treating hair loss. Obtain information about the family history of any skin diseases, including congenital and familial diseases (e.g., alopecia, psoriasis) and systemic diseases with skin manifestations (e.g., diabetes, thyroid disease, cardiovascular diseases, immune disorders). Note any family and personal history of skin cancer, particularly melanoma.

TABLE 22.3 Health HistoryIntegumentary

System

Health Perception–Health Management • Describe your daily hygiene practices. • What skin products are you now using? • Describe any current skin condition, including onset, course, and treatment (if any).

Nutritional-Metabolic • Describe any changes in the condition of your skin, hair, nails, and mucous membranes. • Have you noticed any recent changes in the way sores or wounds heal?∗ • Have you had any weight loss or dietary changes?∗

Elimination • Have you noticed recent changes in your skin related to excess sweating, dryness, or swelling?∗

Activity-Exercise • Do your leisure or work activities involve using any chemicals that might irritate your skin?∗ • Do you do anything to protect yourself from the sun?∗

Sleep-Rest • Does your skin condition keep you awake or awaken you from sleep?∗

Cognitive-Perceptual • Do you have any unusual sensations of heat, cold, or touch?∗ • Do you have any pain associated with your skin condition?∗ • Do you have any joint pain?∗

Self-Perception–Self-Concept • How does your skin condition make you feel about yourself?

Role-Relationship • Has your skin condition changed your relationships with others?∗ • Have you changed your lifestyle because of your skin condition?∗

Sexuality-Reproductive • Has your skin condition changed your intimate relationships

with others?∗ • Has your birth control method (if used) caused a skin problem?∗

Coping–Stress Tolerance • Are you aware of any situation or stressor that changes your skin condition?∗ • Do you think that stress plays a role in your skin condition?∗ • How do you handle stress?

Value-Belief • Are there any cultural beliefs that influence your thinking or feelings about your skin condition?∗ • Are there any treatment options that you would be opposed to using?



If yes, describe.

Genetic Risk Alert • The primary risk factor leading to skin cancer and melanoma is environmental exposure to UV radiation. UV radiation damages DNA, causing an error in the genetic code and resulting in abnormal skin cells.6 • Inherited genetic factors can increase skin cancer risk. A person has an increased risk for developing melanoma if they have a first-degree relative (e.g., parent, full sibling) who had a melanoma.

• People with a fair complexion (light-colored skin that easily freckles, red or blond hair, and blue or light-colored eyes) have an increased risk for skin cancer.

TABLE 22.4 Diseases With Skin Manifestations

Nutritional-Metabolic Pattern Ask the patient about the condition of skin, hair, nails, and mucous membranes and whether they notice any changes related to diet. A diet history reveals the adequacy of nutrients essential to healthy skin and wound healing such as vitamins A, D, E, and C; dietary fat; and protein. Note any food allergies that cause a skin reaction. Ask obese patients if they have areas of chafing or a rash in intertriginous areas, where skin surfaces overlap and rub on each other (e.g., below the breasts, axillae, and groin). Skin in these areas is predisposed to skin tags (acrochordons) and candidiasis (yeast), intertrigo (bacteria, fungi, yeast), and erythrasma (bacteria) infections. Note any excess or absent sweating. Ask the patient about poor or delayed wound healing.

Elimination Pattern Ask the patient about skin conditions, such as dehydration, edema, and pruritus (itching), which can indicate changes in fluid balance. If urinary or fecal incontinence is a problem, ask about the condition of the skin in the anal and perineal areas.

Activity-Exercise Pattern Obtain information about environmental hazards in relation to hobbies and recreational activities, including exposure to known carcinogens, chemical irritants, and allergens. Ask the patient if any changes occur in the skin during exercise or other activities.

Sleep-Rest Pattern

Ask the patient about changes in sleep patterns caused by a skin condition. For example, pruritus can be distressing and interfere with normal sleep. Poor sleep and resulting tiredness can be reflected in a patient’s face by dark circles under the eyes and a decreased firmness in the facial skin.

Cognitive-Perceptual Pattern Determine the patient’s perception of the sensations of heat, cold, pain, and touch. Note any discomfort associated with a skin condition, especially when observed in intact skin, or any reports of unusual skin sensations. Patients with neuropathy may describe numbness, tingling, or crawling sensations in their arms or legs. Ask about joint pain. Assess the mobility of the joints, since the patient’s skin condition may cause changes in mobility.

Self-Perception–Self-Concept Pattern Assess any feelings related to the patient’s skin condition such as sadness, anxiety, despair, or altered body image. These feelings can occur with classic signs of aging or visible skin problems such as acne, rosacea, and psoriasis, which alter physical appearance.

Role-Relationship Pattern Determine how the patient’s skin condition affects relationships with family members, peers, and work associates. Ask the patient about the effect of environmental factors on the skin, such as occupational exposure to irritants, sun, and unusually cold or unhygienic conditions. Contact dermatitis caused by allergens and irritants is a common problem associated with occupation.

Sexuality-Reproductive Pattern Tactfully assess the effect of the patient’s skin condition on sexual activity. Note the reproductive status of the female patient relative to possible therapeutic interventions. For example, isotretinoin, used to treat acne, and topical fluorouracil, used to treat actinic keratoses, are

teratogenic drugs that may cause abnormal fetal development. Pregnant women or women who could become pregnant should not use them.

Coping–Stress Tolerance Pattern Assess the role that stress may play in creating or worsening the skin condition. Ask the patient what coping strategies are used to manage the skin condition.

Value-Belief Pattern Ask about cultural or religious beliefs that could influence the patient’s self-image as related to the skin condition. Assess values and beliefs that may influence or limit the choice of treatment options.

Case Study Subjective Data

© iStockphoto/Thinkstock.

A focused subjective assessment of D.A. reveals the following: • PMH: Negative except for an appendectomy at age 16. • Medications: None at present. NKA. • Health Perception–Health Management: Washes her face with a skin cleanser in the morning and nighttime. After cleansing, she applies a moisturizer with SPF 15. She has used these facial products for the past 3 years since she first started noticing small age spots appearing. Before that, she just used soap and water.

• Nutritional: D.A. reports that her skin seems to be drier as she ages but otherwise no changes besides the “age spots” or “whatever they are.” Denies any changes in the way cuts or sores heal. No weight loss. Does not take any supplemental vitamins or minerals. • Elimination: Although skin is a little dry, D.A. does not perceive it to be excessively dry. Denies excess sweating or any swelling. • Activity-Exercise: Loves to garden and go for walks outdoors. Reports a history of frequent, sometimes severe, sunburns as a child. No use of sunscreen growing up but does remember her mother making her wear T-shirts over her bathing suits to help prevent sunburn. Has used sunscreen for the past 20 years when outdoors. Reapplies as needed. • Cognitive-Perceptual: Denies any pain or discomfort associated with skin lesions. • Coping–Stress Tolerance: Fearful that she might have skin cancer.

Discussion Questions 1. Which subjective assessment findings are of most concern to you? 2. What should you include in the physical assessment? What specific characteristics of the skin lesions would you be looking for? You will learn more about the physical examination of the skin in the next section. (See p. 406 for more information on D.A.) Answers available at http://evolve.elsevier.com/Lewis/medsurg.

Objective Data Physical Examination A physical examination of the skin begins with a systematic, general

inspection and then a more specific assessment of problem areas. A normal range of differences exists in the skin, hair, and nails. Your assessment should note normal skin changes related to age, genetic factors, and environmental exposures from other changes. Look for changes in the color of the skin, turgor, temperature, dryness, thickness, and vascularity. General principles when assessing the skin are: • Have a private examination room of moderate temperature with good lighting; a room with exposure to daylight is preferred. • Ensure that the patient is comfortable and in a dressing gown that allows easy access to all skin areas. • Perform a general inspection and then a lesion-specific examination. • Use the metric system when taking measurements. • Use the right terminology when reporting or documenting.

Clinical Photography Photographs are an adjunct to documentation and promote communication among the interprofessional team. They are used to assess and monitor skin conditions and determine if the condition has improved or declined with treatment. They can be used to track moles and precancerous lesions and detect any changes early. Follow clinical agency protocol for obtaining a patient’s consent to photograph lesions.

Inspection Inspect the skin for general color and pigmentation, vascularity, bruising, and lesions or discolorations. The critical factor in assessment of skin color is change. A skin color that is normal for one patient can be a sign of a pathologic condition in another patient. The skin color depends on the amount of melanin (brown), carotene (yellow), oxyhemoglobin (red), and reduced hemoglobin (bluish red)

present at a particular time. The most reliable areas to assess erythema, cyanosis, pallor, and jaundice are the areas of least pigmentation, such as the sclera, conjunctivae, nail beds, lips, and buccal mucosa. The true skin color is best seen in photo-protected areas such as the buttocks. Activity, sun (UV) exposure, emotions, cigarette smoking, and edema, as well as respiratory, renal, cardiovascular, and hepatic disorders, can all directly affect skin color. In your general inspection, note the presence of body art such as piercings and tattoos. The nose, ears, eyebrows, lips, navel, and nipples are common sites of piercing. Examine tattoos and needletrack marks and note the location and characteristics of the surrounding skin area. Tattoo pigments deposited in the skin may cause itching, pain, and sensitivity for several weeks after the tattoo is placed. Examine the skin for problems related to vascularity, including bruising and vascular and purpuric lesions such as angioma (benign tumor of blood or lymph vessels), petechiae (tiny, flat, purplish red pinpoint lesions on skin), ecchymosis (bruise larger than petechiae), or purpura (purple colored spots and patches characterized by ecchymosis or other small hemorrhages). Note the reaction to direct pressure on the lesion. If a lesion blanches on direct pressure and then refills, the redness is due to dilated blood vessels. If the discoloration stays, it is the result of subcutaneous or intradermal bleeding or a nonvascular lesion. Note any pattern of bruising such as discoloration in the shape of the hand or fingers or bruises at different stages of resolution. These may indicate other health problems or abuse and need further investigation. Record the color, size, height, distribution, location, and shape of any lesions. Lesions may be primary or secondary lesions. Primary skin lesions develop on previously unaltered skin. The common characteristics of primary skin lesions are shown in Table 22.5. Secondary skin lesions are lesions that change with time or occur because of scratching or infection. Secondary skin lesions are shown in Table 22.6. Skin lesions are usually described in terms related to the lesions’

configuration (solitary or pattern in relation to other lesions) and distribution (arrangement of lesions over an area of skin) (Table 22.7). Note any unusual odors. Skin sites with lesions, such as rashes, may be colonized with yeast or bacteria, which can be associated with distinctive odors in areas where skin rubs together (Fig. 22.5). Inspect all body hair. Note the distribution, texture, and quantity of hair. Changes in the normal distribution of body hair and growth may indicate an endocrine or vascular disorder. Carefully inspect the nails, including nail shape, thickness, curvature, and surface. Note any grooves, pitting, ridges, or detachment from nail bed. Changes in nail smoothness or thickness can occur with anemia, psoriasis, thyroid problems, decreased vascular circulation, and some infections.

Palpation Palpate the skin to obtain information about temperature, turgor, moisture, and texture. Use the back of your hand to gauge skin temperature. The skin should be warm, not hot. Skin temperature increases when blood flow to the dermis increases. A localized temperature increase occurs with burns and local inflammation. A generalized increase occurs when a person has a fever. A decreased body temperature may occur when shock or other circulatory problems, chilling, or infection are present.

TABLE 22.5 Primary Skin Lesions

Turgor refers to the elasticity of the skin. Assess turgor by gently pinching an area of skin under the clavicle or on the back of the hand. Skin with good turgor should move easily when lifted and immediately return to its original position when released. In patients with dehydration and aging, a loss of turgor occurs and can cause

tenting of the skin.

TABLE 22.6 Secondary Skin Lesions

Skin moisture (dampness or dryness of the skin) increases in areas where skin rubs together. Skin moisture varies with environmental temperature, muscular activity, body weight, and body temperature. The skin should be intact with no flaking, scaling, or cracking. Skin generally becomes drier with increasing age.

TABLE 22.7 Lesion Distribution Terminology

Term Annular

Description Circular, begins in center and spreads to periphery (e.g., tinea corporis [ringworm])

Asymmetric Unilateral distribution Merging together (e.g., urticaria [hives]) Confluent Discrete

Distinct individual lesions that are separate (e.g., acne)

Gyrate

Twisted, coiled spiral, snakelike

Grouped

Clusters of lesions (e.g., vesicles of contact dermatitis)

Localized

Clearly defined, limited areas of involvement (confined to one area)

Polycyclic

Annular lesions grow together (e.g., psoriasis)

Solitary

Single lesion

Symmetric Zosteriform

Bilateral distribution Linear arrangement along a dermatome area (e.g., herpes zoster)

Texture refers to the fineness or coarseness of the skin. The skin should feel smooth and firm with the surface evenly thin in most areas. Thickened callus areas are normal on the soles and palms and relate to weight bearing. Increased skin thickness is often work related and the result of excess pressure. Excess calluses on the soles of patients with neuropathy or diabetes predispose them to developing lesions. Use a focused assessment to evaluate the status of previously identified skin problems and to monitor for signs of new problems. A focused assessment of the skin is presented in the following box. Assessment abnormalities of the skin are described in Table 22.8.

Focused Assessment Integumentary System Use this checklist to make sure the key assessment steps have been done.

Subjective Ask the patient about any of the following and note responses.

Hair loss (unusual or rapid)

Y

N

Changes in skin (e.g., lesions, bruising)

Y

N

Nail discoloration

Y

N

Objective: Diagnostic Check the following for results and critical values.

Biopsy results



Albumin



Objective: Physical Examination Inspect Skin for color, integrity, scars, lesions, signs of breakdown



Facial and body hair for distribution, color, quantity, hygiene



Nails for shape, contour, color, thickness, cleanliness



Dressings, if present



Palpate Skin for temperature, texture, moisture, thickness, turgor, mobility

FIG. 22.5 Intertrigo. Rash in body folds with Candida infection. From Graham-Brown R, Bourke J, Cunliffe T: Dermatology: Fundamentals of practice, Edinburgh, 2008, Mosby.



Assessment of Dark Skin The structures of dark skin are no different from those of lighter skin, but they are often harder to assess (Table 22.9). Color is easiest to assess in areas where the epidermis is thin, and pigmentation is not influenced by sun exposure, such as the lips, mucous membranes, nail beds, and protected areas (e.g., buttocks). Palmar and plantar surfaces are lighter than other skin areas in darker skinned persons. Rashes are often harder to see and may have to be palpated. Wrinkling is less apparent in those with dark skin. Persons with dark skin are predisposed to certain skin and hair conditions. Keloid is an overgrowth of collagenous tissue at the site of a skin injury (e.g., ear piercing) (Fig. 22.6). Vitiligo is total loss of pigment in the affected area (Fig. 22.7). In dermatosis papulosa nigra, the person has small, pigmented wart-like papules, often on the face (Fig. 22.8). Nevus of Ota is a slate-gray or blue-gray birthmark found on the forehead and face around the eye area. It may involve the sclera. Traction alopecia may be the result of trauma from hair rollers or from tight braiding of the hair (Fig. 22.9). The hair loss may be temporary or permanent. Pseudofolliculitis is an inflammatory response to ingrown hairs that occurs after shaving too closely in the beard area. The ingrown hairs result in pustules and papules.

TABLE 22.8 Assessment

AbnormalitiesIntegumentary System Finding Alopecia

Angioma

Description Loss of hair (localized or general)

Tumor consisting of blood or lymph vessels Yellow discoloration of skin, no

Possible Etiology and Significance Heredity, friction, rubbing, traction, trauma, stress, infection, inflammation, chemotherapy, pregnancy, emotional shock, tinea capitis, immunologic factors Normal increase in incidence with aging, liver disease, pregnancy, varicose veins Vegetables containing carotene (e.g.,

Carotenemia (carotenosis)

yellowing of sclerae, most noticeable on palms and soles

carrots, squash), hypothyroidism

Comedo (acne lesion)

Enlarged hair follicle plugged with sebum, bacteria, and skin cells; can be open (blackhead) or closed (whitehead) Slightly bluish gray or dark purple discoloration of the skin and mucous membranes caused by excess amounts of reduced hemoglobin in capillaries Sac containing fluid or semisolid material Large, bruise-like lesion caused by collection of extravascular blood in dermis and subcutaneous tissue Redness occurring in patches of variable size and shape

Heredity, certain drugs, hormonal changes with puberty and pregnancy

Cyanosis

Cyst Ecchymosis Erythema

Hematoma

Extravasation of blood of enough size to cause visible swelling Male distribution of hair in women

Cardiorespiratory problems, vasoconstriction, asphyxiation, anemia, leukemia, and cancers Obstruction of a duct or gland, parasitic infection Trauma, bleeding disorders Heat, certain drugs, alcohol, ultraviolet rays, any problem that causes dilation of blood vessels in the skin Trauma, bleeding disorders

Abnormality of ovaries or adrenal glands, decrease in estrogen level, familial trait Loss of pigmentation resulting in Chemical agents, nutritional factors, Hypopigmentation lighter patches than the normal skin burns, inflammation, infection Dermatitis of overlying surfaces of the Moisture, irritation, obesity; may be Intertrigo skin (Fig. 22.5) complicated by Candida infection Yellow (in white patients) or yellowish Liver disease, red blood cell Jaundice brown (in dark-skinned patients) hemolysis, pancreatic cancer, discoloration of the skin, best seen in common bile duct obstruction the sclera, secondary to increased bilirubin in the blood Hypertrophied scar beyond wound Predisposition more common in Keloid margins (Fig. 22.6) dark-skinned persons Thickening of the skin with Repeated scratching, rubbing, and Lichenification accentuated normal skin markings irritation usually because of pruritus or neurosis Benign overgrowth of melanocytes Defects of development; excess Mole (nevus) numbers and large, irregular moles; often familial Pinpoint, discrete deposits of blood ) have different effects on the skin. UVA light is responsible for tanning, UVB for sunburn. The damage caused by UV rays is cumulative. It results in degenerative changes in the dermis and premature aging (e.g., loss of elasticity, thinning, wrinkling, abnormal dryness). Prolonged and repeated sun exposure increases risk for actinic keratosis, basal and squamous cell cancers, and melanoma. Patient teaching on sun protection is important. People often do not understand the serious risks of sun exposure. Following sun safety guidelines beginning early in life can help avoid the damaging effects of the sun and prevent the formation of skin cancer later in life. Fairskinned persons and those with light-colored eyes should be especially cautious about excess sun exposure. They have less melanin and thus less natural protection. Teach the patient ways to avoid the damaging effects of the sun. This includes wearing protective clothing, including sunglasses, a large-brimmed hat, and a darker colored, long-sleeved shirt of a tightly woven fabric or carrying an umbrella. The greatest risk is with midday sun, between the hours of 10:00 am and 2:00 pm, regardless of the latitude. This is when 80% of UV rays occur. Even on overcast

days, serious sunburn can occur because up to 80% of the sun’s UV rays can penetrate the clouds. Warn people of the dangers of tanning booths and sun lamps, which emit UVA. Tanning booths increase the risk for sunburn, cataracts, and skin cancer.1 Sunscreens can filter both UVA and UVB wavelengths. The two types of topical sunscreens are chemical and physical. Chemical sunscreens are light creams or lotions designed to absorb or filter UV light, resulting in decreased UV light penetration. Physical sunscreens are thick, opaque, heavy creams that reflect UV radiation. Regular sunscreen use decreases the risk for developing melanoma. The U.S. Food and Drug Administration (FDA) rates sunscreen products on their sun protection factor (SPF). The SPF measures the effectiveness of a sunscreen in filtering and absorbing UV radiation. All sunscreen labels in the United States must say which rays they protect against. Products labeled with “broad spectrum” block both UVA and UVB.2 Sunscreens with broad spectrum labeling must have an SPF of at least 15. Sunscreens with an SPF of 15 or more filter 92% of the UVB rays and make sunburn unlikely when applied appropriately. People need to select the right sunscreen for their needs. The general recommendation is that everyone should use daily sunscreen with a minimum SPF of 15. Teach patients to look for the term broad spectrum on sunscreen packaging. Those who have a history of skin cancer or problems with sun sensitivity should use a product with an SPF of at least 30. Sunscreens should be applied 20 to 30 minutes before going outdoors, even in cloudy weather. The SPF value of all sunscreens decreases with time. Sunscreen should be reapplied every 2 hours. You should apply 1 ounce per total body application. The ears, toes, and lips also need sunscreen. Sunscreens are not “waterproof” and must be reapplied after swimming.

TABLE 23.1 Wavelengths of Sun and Effects on

Skin

TABLE 23.2 Drug TherapyDrugs That May Cause

Photosensitivity Categories Antidepressants

Examples amitriptyline, doxepin, venlafaxine

Antidysrhythmics

quinidine, amiodarone (Cordarone)

Antihistamines

Antifungals

diphenhydramine, chlorpheniramine, clemastine, cetirizine (Zyrtec) tetracycline, sulfamethoxazole, azithromycin (Zithromax), ciprofloxacin (Cipro) griseofulvin, ketoconazole

Antipsychotics

chlorpromazine, haloperidol

Chemotherapy

methotrexate, dacarbazine, fluorouracil

Diuretics

furosemide (Lasix), hydrochlorothiazide

Hypoglycemics

tolbutamide, glipizide (Glucotrol), glyburide

Nonsteroidal antiinflammatory drugs

diclofenac (Voltaren), piroxicam (Feldene), sulindac

Antimicrobials

Evidence-Based Practice Tanning Booths and Skin Cancer You are a nurse working in a dermatology clinic. D.F., a 30-yr-old woman with fair skin and blue eyes, is completing her health history before her annual skin screening. She says she regularly visits an indoor tanning salon every other week. She tells you that being tan

makes her feel “healthier and prettier.”

Making Clinical Decisions Best Available Evidence. There is a strong link between exposure to UVA from indoor tanning booth use and increased risk for skin cancer (melanoma and nonmelanoma). Melanoma causes less than 5% of skin cancers yet accounts for almost 75% of skin cancer deaths. Melanoma risk increases with the number of years, hours, and sessions of indoor tanning independent of outdoor exposure. Clinician Expertise. You note that D.F. has the following skin cancer risk factors: fair skin, blue eyes, frequent use of tanning booths. Patient Preferences and Values. After listening, D.F. tells you that she will consider reducing the frequency of her visits—going only when she has an important event to attend.

Implications for Nursing Practice 1. How would you respond to D.F. given the information that she has provided to you? 2. What resources can help address her view that a “tan looks healthy?” 3. What sun safety guidelines should she follow when outdoors to prevent skin cancer?

Reference for Evidence Gershenwald J.E, Halpern A.C, Sondak V.K. Melanoma prevention: avoiding indoor tanning and minimizing overexposure to the sun. JAMA. 2016;316(18):1913. Tripp M.K, Watson M, Balk S.J, et al. State of the science on prevention and screening to reduce melanoma incidence and mortality. CA Can J Clin. 2016;66:460.

Certain drugs potentiate the sun’s effects, even with brief exposure. The chemicals in these drugs absorb light when exposed to natural sunlight and release energy that harms cells and tissues. Common photosensitizing drugs are shown in Table 23.2-anchor>. The manifestations of drug-induced photosensitivity (Fig. 23.1-anchor>) are like those of a sunburn. These include swelling, erythema, vesicles, and papular, plaquelike lesions. Assess the photosensitivity of each individual drug. Teach patients who are taking these drugs about their photosensitizing effect and the need to protect the skin from photosensitivity reactions by using sunscreen products. Teach patients to self-examine their skin monthly. They should have a periodic professional assessment of areas that are hard to see. The cornerstone of skin examination is the ABCDE rule. Examine skin lesions for Asymmetry, Border irregularity, Color change and variation, Diameter of 6 mm or more, and Evolving in appearance (Fig. 23.2anchor>). Emphasize that a persistent skin lesion that does not heal and lesions once flat and now raised, once small and recently growing, or changing in appearance are warning signs. Patients should consult their HCP at once if any lesions or moles show any clinical signs (ABCDEs).

Skin Cancer Skin cancer is the most commonly diagnosed cancer.3 Skin cancers are either nonmelanoma or melanoma. The fact that skin lesions are so visible increases the chance of early detection and diagnosis. This can often lead to a highly favorable prognosis.

FIG. 23.1 Intense eruption in areas exposed to sunlight after patient started on hydrochlorothiazide. From Habif TP: Clinical dermatology: A color guide to diagnosis and therapy, ed 5, St Louis, 2011, Mosby.

FIG. 23.2 The ABCDEs of melanoma. A, Asymmetry: one half unlike the other half. B, Border irregularity: edges are ragged, notched, or blurred. C, Color: varied pigmentation; shades of tan, brown, and black. D, Diameter: greater than 6 mm (diameter of a pencil eraser). E, (not pictured) Evolving; changing appearance (change in shape, size, color, or other characteristic noted over time). From The Skin Cancer Foundation, New York, NY.

Risk Factors Risk factors for skin cancer include (1) having fair skin, blond or red hair with blue eye color; (2) history of outdoor sunbathing; (3) living near the equator or at high altitudes; (4) family or personal history of skin cancer; (5) having an outdoor occupation; (6) spending a lot of time in outdoor recreation activities; and (7) indoor tanning.4 The Fitzpatrick Classification of Skin Type can help you determine a person’s skin complexion and how likely the person is to get skin cancer (Table 23.3-anchor>). Patients treated with oral methoxsalen (psoralen) and psoralen plus ultraviolet A radiation (PUVA) have a higher risk.

TABLE 23.3 Fitzpatrick Classification of Skin

Type Skin Type

Skin Color

Characteristics Always burns, never tans

III

White, freckles, very fair. Red or blond hair. Blue eyes White, fair. Red or blond hair. Blue, hazel, or green eyes Cream white, fair. Any eye or hair color

IV

Brown, typical Mediterranean skin

V

Deep brown, Middle Eastern skin types

VI

Black

I II

Usually burns, tans with difficulty Sometimes mild burn, gradually tan Rarely burns, tans with ease Very rarely burns, tans very easily Never burns, tans very easily

Promoting Health Equity Skin Problems • Blacks, Asians, and Hispanics have a lower incidence of skin cancer than whites. • Melanoma can occur in dark-skinned persons but often goes unrecognized until the advanced stages. • Blacks and Asians are more likely to develop a keloid at the site of an injury. • Skin cancer outcomes are poorer for ethnic minorities, those of low socioeconomic status, and the uninsured. Dark-skinned persons are less susceptible to skin cancer because of their increased melanin, which acts like a sunscreen. However, there is still a risk, and they need to wear sunscreen. They often have melanomas on areas with less melanin, such as the palms, soles,

mucous membranes, and under the nails. Since it is common for people with dark skin to have pigmented, longitudinal bands on their nails, assess and follow any nail discoloration.

Nonmelanoma Skin Cancer Nonmelanoma skin cancers (basal cell and squamous cell cancers) are the most common forms of skin cancer. More than 5.4 million new cases are diagnosed each year.3 Nonmelanoma skin cancers do not develop from melanocytes. They develop in the basement membrane of the skin. Although there are few deaths from nonmelanoma skin cancer, they have the potential for severe local destruction, permanent disfigurement, and disability. Nonmelanoma skin cancers usually develop in sun-exposed areas, such as the face, head, neck, back of the hands, and arms. The most common causative factor is sun exposure. There are some differences between basal and squamous cell cancers. Squamous cell cancers usually occur on the head and neck where there is the highest degree of UV radiation. Basal cell cancers do not follow that pattern and may occur in sun-protected areas.

Actinic Keratosis Actinic keratosis (AK), also known as solar keratosis, is the most common precancerous skin lesion. They affect most of the older white population. Sun exposure is a key factor. AKs appear most often on skin that has been exposed to the sun or to artificial UV light. They may spontaneously resolve if a person reduces exposure to sunlight. The clinical appearance of AK can be highly varied. The typical lesion is an irregularly shaped, flat, slightly erythematous papule with indistinct borders and an overlying hard keratotic scale or horn (Table 23.4-anchor>). Because AK is impossible to distinguish from squamous cell cancer, treatment should be aggressive. Nonsurgical procedures are the first-line treatment. Any lesion that persists should be evaluated for a biopsy.

TABLE 23.4 Premalignant and Malignant

Conditions of the Skin

Basal Cell Carcinoma Basal cell carcinoma (BCC) is a locally invasive cancer arising from epidermal basal cells. It is the most common type of skin cancer but the least deadly. BCC usually occurs in middle-aged to older adults. Most BCCs occur in the head and neck area (e.g., sun-exposed), followed by the trunk and extremities.5 Manifestations are described in Table 23.4. Some BCCs are pigmented, with curled borders and an opaque appearance. They may be hard to distinguish from melanoma. A tissue biopsy is needed to confirm the diagnosis. BCCs rarely metastasize (Fig. 23.3-anchor>). However, untreated BCC may result in massive tissue destruction. Treatment depends on the tumor location and histologic type, size, history of recurrence, and patient characteristics (Table 23.4).

Squamous Cell Carcinoma Squamous cell carcinoma (SCC) is a cancer arising from keratinizing epidermal cells. SCC can be aggressive and has the potential to metastasize. It may lead to death if not treated early and correctly. SCC often occurs at the base of an actinic keratosis or another lesion. The main risk factors are sun exposure and immunosuppression after organ transplantation.6 Pipe, cigar, and cigarette smoking contribute to the formation of SCC on the mouth and lips. The manifestations of SCC are described in Table 23.4. A biopsy should always be done when a lesion is suspected to be SCC.

Melanoma Melanoma is a tumor arising from melanocytes, the cells that make melanin. It causes most skin cancer deaths. Unlike most cancers whose incidence is stable or decreasing, the incidence of melanoma is steadily rising.1 More than 87,000 new cases are diagnosed every year in the United States and almost 10,000 people will die from the

disease.3 Melanoma can metastasize to any organ, including the brain and heart. A combination of environmental and genetic factors is likely involved in the development of melanoma. UV radiation from the sun is the main cause of melanoma. Artificial sources of UV radiation, such as sunlamps and tanning booths, also play a role. UV radiation damages the deoxyribonucleic acid (DNA) in skin cells, causing “misspellings” (mutations) in their genetic code. This alters the cells. Although anyone can develop melanoma, the risk is greatest for people who have red or blond hair, blue or light-colored eyes, and light-colored skin that freckles easily. These people have less melanin and thus less protection from UV radiation. The use of immunosuppressive drugs and a history of dysplastic nevi also increase risk.

FIG. 23.3 Basal cell carcinoma. Rolled, well-defined border and central erosion. From Goldman L, Schafer A: Goldman-Cecil medicine, ed 25, Philadelphia, 2016, Saunders.

A person may have a genetic predisposition toward getting melanoma. Of those with melanoma, 5% to 10% have a first-degree relative (e.g., parent, full sibling) who had melanoma.4 This risk increases significantly if multiple relatives have had melanoma. Mutated genes have been found in some families who have a high familial incidence of melanoma. Cutaneous melanoma begins in the skin. There are 4 subtypes of melanoma: (1) superficial spreading melanoma, (2) nodular melanoma, (3) lentigo maligna melanoma, and (4) acral lentiginous melanoma.

Clinical Manifestations Melanoma often occurs on the lower legs in women and on the trunk and head in men. About one fourth of melanomas occur in existing nevi or moles. About 20% occur in dysplastic nevi. Rarely, it occurs in the mouth, intestines, and eyes. The cornerstone of skin examination is the ABCDE rule (Fig. 23.2). Because most melanoma cells continue to produce melanin, melanoma tumors are often deep brown or black (Table 23.4). Lesions showing any sudden or progressive change in the ABCDE rule need evaluated.

Interprofessional Care One of the first steps in diagnosing a suspicious lesion is dermoscopic examination. Dermoscopy can help the HCP decide if a lesion should be biopsied. Biopsy is a critical tool for determining the type of lesion. A biopsy should be done using an excisional biopsy technique. Shave biopsy, shave excision, or electrocauterization should not be done because these techniques do not measure the depth of the lesion. The most important prognostic factor is tumor thickness at the time of diagnosis. We use 2 methods to determine thickness. The Breslow measurement indicates the depth of the tumor in millimeters (Fig. 23.4anchor>). The Clark level indicates the depth of invasion of the tumor; the higher the number, the deeper the melanoma.

Treatment depends on the site of the original tumor and the stage of the cancer. Melanoma staging (stages 0 to IV) is based on tumor size (thickness), nodal involvement, and metastasis. In stage 0, melanoma is confined to one place (in situ) in the epidermis. Melanoma is nearly 100% curable by excision if diagnosed at stage 0. Unfortunately, those with deep tumors or disease that has already spread to lymph nodes often develop metastases. The 5-year survival rate for those with advanced disease is less than 10%.7 The initial treatment of melanoma is wide surgical excision. Melanoma that has spread to the lymph nodes or nearby sites usually requires additional (adjuvant) therapy with combinations of immunotherapy, targeted therapy, chemotherapy, and/or radiation therapy. Immunotherapy can include cytokines (α-interferon, interleukin-2), PD-1 inhibitors, and CTLA-4 inhibitors. Cytokines enhance the production of many immune system cells, including T cells and B cells. Drugs that block PD-1 or CTLA-4 boost the immune response against melanoma cells.7 PD-1 inhibitors include nivolumab (Opdivo) and pembrolizumab (Keytruda). They block PD-1, a protein on T cells that keeps T cells from attacking other cells in the body. Ipilimumab (Yervoy) blocks the action of CTLA-4, another protein that normally suppresses the action of T cells.

FIG. 23.4 A, Breslow measurement of tumor thickness. B, Clark level, showing tumor invasion.

From Habif TP: Clinical dermatology: A color guide to diagnosis and therapy, ed 6, St Louis, 2016, Mosby.

FIG. 23.5 Dysplastic nevus. Irregular border and color. From Graham-Brown R, Bourke J, Cunliffe T: Dermatology: Fundamentals of practice, Edinburgh, 2008, Mosby.

Targeted therapy for melanoma includes BRAF and MEK inhibitors. About half of all melanomas have mutations in the BRAF gene, which makes an altered BRAF protein that signals melanoma cells to proliferate. Vemurafenib (Zelboraf), dabrafenib (Tafinlar), trametinib (Mekinist), and cobimetinib (Cotellic) are drugs that target BRAF mutations.7 Chemotherapy is not as effective for melanoma as it is for most other cancers. It is usually used only with advanced disease. Drugs used includes dacarbazine, temozolomide, cisplatin, paclitaxel, carboplatin, and vincristine.3 Radiation therapy has a role in treating

lymph node and brain metastases.

Atypical or Dysplastic Nevus Dysplastic nevi (DN), or atypical moles, are nevi that are larger than usual (greater than 5 mm across) with irregular borders and various shades of color (Fig. 23.5-anchor>). DN may have the same ABCDE characteristics as melanoma, but they are less pronounced. About 5% of the white population have DN.8 Those with DN have an increased risk for developing melanoma in a mole or elsewhere on the body. The more DN a person has, the higher the risk. Those with 10 or more DN have 12 times the risk for developing melanoma.

Check Your Practice You are working in an HCP office, and your next patient is a 78-yrold white man. He is worried about the many “brown” spots on his face and arms. He tells you that they probably happened because he worked outside in construction most of his life. • How do you distinguish among an age spot (lentigo), normal mole, and melanoma? • What risk factors would you assess for in a patient with a suspected cancerous lesion?

Skin Infections and Infestations Bacterial Infections The skin provides an ideal environment for bacterial growth with an abundant supply of nutrients, water, and warm temperature. Bacterial infection occurs when the balance between the host and microorganisms is changed. This can occur as a primary infection after a break in the skin. Or, a secondary infection can occur in already

damaged skin or as a sign of a systemic disease (Table 23.5-anchor>). Predisposing factors include the presence of excess moisture, obesity, having atopic dermatitis, systemic corticosteroid and antibiotic use, and having a chronic disease, such as diabetes. Staphylococcus aureus and group A β-hemolytic streptococci are the major types of bacteria responsible for primary and secondary skin infections. Streptococci cause impetigo, erysipelas, cellulitis, and lymphangitis. S. aureus causes impetigo, folliculitis, cellulitis, and furuncles (Fig. 23.6-anchor>). When an infection is present, the resulting drainage is infectious. Good skin hygiene and infection control practices are necessary to prevent the spread of the infection.

Viral Infections Like viral infections anywhere in the body, viral infections of the skin are hard to treat. When a virus infects a cell, a skin lesion may develop. Lesions can also result from an inflammatory response to viral infections. Herpes simplex, herpes zoster (Fig. 23.7-anchor>), and warts (Fig. 23.8-anchor>) are the most common viral infections affecting the skin (Table 23.6-anchor>).

TABLE 23.5 Common Bacterial Infections of the

Skin

MRSA, Methicillin-resistant S. aureus.

FIG. 23.6 Cellulitis with characteristic redness, tenderness, and edema. From Habif TP: Clinical dermatology: A color guide to diagnosis and therapy, ed 5, St Louis, 2011, Mosby.

FIG. 23.7 Herpes zoster (shingles) on the anterior chest, classic dermatomal distribution. From James WD, Berger T, Elston DMD: Andrews’ diseases of the skin, ed 11, Philadelphia, 2011, Saunders.

FIG. 23.8 Plantar wart. A, Keratotic lesion. B, After excision. From Swartz MH: Textbook of physical diagnosis: History and examination, ed 6, Philadelphia, 2010, Saunders.

Infestations and Insect Bites There are many opportunities for exposure to infestations (harboring insects or worms) and insect bites (Table 23.7-anchor>). In many instances, an allergy to the venom plays a key role in the reaction. In other cases, the clinical manifestations are a reaction to the eggs, feces, or body parts of the invading organism. Some people react with a severe hypersensitivity (anaphylaxis), which can be life threatening. Anaphylaxis is discussed in Chapter 13. Preventing insect bites by avoidance or using repellents is somewhat effective. Meticulous hygiene related to personal articles, clothing, bedding, and examination and care of pets, as well as careful choice of sexual partners, can reduce the incidence of infestations. Prompt, routine skin inspection is necessary in geographic areas where there is a risk for tick bite. Lyme disease, which is caused by a tick, is discussed in Chapter 64.

Fungal Infections Because of the large number of fungi that are present everywhere, exposure to some pathologic varieties may occur. Skin, hair, and nails can become infected with fungi, including candidiasis and tinea

unguium. Common fungal infections of the skin are described in Table 23.8-anchor>. Most infections are harmless in healthy adults, but they can cause embarrassment and distress. Fungal infections are easy to diagnose. A microscopic examination showing the appearance of hyphae (threadlike structures) in a skin scraping mounted in 10% to 20% potassium hydroxide (KOH) indicates a fungal infection. A Wood’s light examination of hair infected with certain fungi will fluoresce blue to green.

Allergic Skin Problems Patients often seek treatment for irritant or allergic dermatitis, two common types of contact dermatitis. Irritant contact dermatitis results from direct chemical injury to the skin. Allergic contact dermatitis is an antigen-specific, type IV delayed hypersensitivity response. The pathophysiology of allergic and contact dermatitis is discussed in Chapter 13. Skin problems associated with allergies and hypersensitivity reactions may present a challenge to the clinician (Table 23.9-anchor>). A careful family history and discussion of exposure to possible offending agents can provide valuable data. Patch testing can help determine possible causative agents (see Fig. 22.10). The best treatment of allergic dermatitis is to avoid known irritants. The extreme pruritus and its potential for chronicity make it a frustrating problem for you and the patient, especially if we cannot determine the offending agent.

Cutaneous Drug Reactions Stevens Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are rare, life-threatening diseases. They are violent immune responses that often occur as a severe adverse reaction to either a medication or, more rarely, an infection. The result is the acute destruction of the epithelium of the skin and mucous membranes. SJS, SJS-TEN overlap, and TEN represent a spectrum of disease severity. SJS involves less than 10% of total body surface area, TEN involves more than 30% of

total body surface area, and SJS-TEN overlap involves 10% to 29% of total body surface area.8 SJS/TEN typically occur 4 to 21 days after starting use of the offending drug. Systemic symptoms, including fever, cough, headache, anorexia, myalgia, and nausea, precede skin and mucous membrane findings by 1 to 3 days. Skin involvement starts as an erythematous, macular rash with purpuric centers. Over a period of hours to days, the rash merges to form blisters with sheet-like epidermal detachment (Fig. 23.9-anchor>). The lesions usually start on the palms, soles, and trunk, then spread to the face and extremities. They are extremely painful. Most people have mucosal lesions in the eye, mouth, and genital areas.

TABLE 23.6 Common Viral Infections of the Skin

TABLE 23.7 Common Infestations and Insect

Bites

TABLE 23.8 Common Fungal Infections of the

Skin and Nails

TABLE 23.9 Common Allergic Conditions of the

Skin

Identifying and stopping the offending drug(s) is the most important action in caring for a patient with SJS/TEN. The most common drugs involved include sulfonamides, carbamazepine, nonsteroidal antiinflammatory drugs, lamotrigine, allopurinol, phenytoin, and phenobarbital.8 Immunotherapy may play a role in slowing disease progression and promoting skin repair. The patient receives supportive care, often in an intensive care unit. Interventions focus on airway management, preserving renal function, maintaining fluid and electrolyte balance, and pain control. Fluid replacement is given to maintain urine output. Proper wound care helps prevent infection and promote healing. Dressing with petrolatum gauze or other nonadhesive material provides a barrier and offers moisture to help the skin repair. Because of painful oral lesions, most patients need parenteral or enteral nutrition to meet nutrition and caloric demands. Apply eyedrops, lubricating ointment, and antibiotic drops to those with conjunctivitis.

Benign Skin Problems Although the list of benign skin problems is extensive, some of the most commonly seen and distressing ones include acne vulgaris (Fig. 23.10-anchor>), psoriasis, and seborrheic keratoses. Benign problems are outlined in Table 23.10-anchor>. Psoriasis is a chronic autoimmune disease. It is fairly common, affecting about 7.5 million Americans.9 Men and women develop psoriasis at equal rates. The rate is highest in whites (3.6%).10 It usually develops in those 15 to 35 years old. One third of people with psoriasis have at least one relative with the disease. It is associated with metabolic syndrome, heart disease, and type 2 diabetes. Up to 40% of people with psoriasis also have psoriatic arthritis. Psoriatic arthritis is discussed in Chapter 64. The diagnosis of plaque psoriasis, the most common form, is based on the skin’s appearance (Fig. 23.11-anchor>). Lesions are distinct and appear as red, scaling papules that merge to form plaques. The affected area is normally rounded, with adherent silver scales that bleed easily when removed. Plaques are common on the knees, elbows, scalp, hands, feet, and lower back.9 They are often pruritic and may be painful. Clinical presentation varies. While most have mild disease, some have psoriasis on much of their skin surface. Treatment is tailored to meet a person’s needs. This varies depending on the location of lesions, severity, patient preferences, and comorbidities. Goals range from improved quality of life to complete disease resolution. Psoriasis for most is more emotionally than physically disabling. It erodes the self-image. The person may be selfconscious and withdraws from social contacts.8 Quality of life can diminish as people avoid activities. Depression is common.

FIG. 23.9 Toxic epidermal necrolysis. From Ferri’s clinical advisor 2018. Dabiri, Ganary, MD, PhD; Rüenger, Thomas M., MD, PhD. Published January 1, 2018. Pages 1282.e21282.e3. © 2018.

FIG. 23.10 Acne vulgaris. Papules and pustules. From James WD, Berger T, Elston DMD: Andrews’ diseases of the skin, ed 11, Philadelphia, 2011, Saunders.

Drug Alert Isotretinoin (Accutane) • Used to treat acne (Table 23.10) • Can cause serious damage to fetus

• Contraindicated in women who are pregnant or want to become pregnant • Cannot donate blood during treatment and for 1 month after treatment ends • May cause depression and suicidal ideation

Interprofessional Care: Skin Problems Diagnostic Studies A careful history is of prime importance in diagnosing skin problems. The HCP must be skilled at detecting any evidence that could lead to the cause of many different skin problems. After a careful history and physical examination, inspect individual lesions. The history, physical examination, and diagnostic test results guide therapy.

Interprofessional Therapy Many different treatment methods are used in dermatology. Advances in this field have brought relief to many previously chronic, untreatable conditions. Many of the specific therapeutic treatments require specialized equipment. They are usually used by a dermatologist or specially trained nurse.

Phototherapy Ultraviolet light (UVL) therapy is a part of treating many skin problems, including psoriasis, cutaneous T-cell lymphoma, atopic dermatitis, vitiligo, and pruritus. Light sources available include broadband UVB, narrowband UVB, and long-wave UV (UVA1). One form of phototherapy combines the use of the photosensitizing drug methoxsalen with UVA light (PUVA). With PUVA, patients receive methoxsalen and then are exposed to UVA. Treatments are generally given 2 to 3 times a week. Side effects include nausea, itching, and erythema. Taking methoxsalen with food and milk may reduce nausea. Caution patients about the hazards of

using methoxsalen and concurrent exposure to UV rays from sunlight or artificial UVL during therapy. Because of the risk for cataracts, patients receiving PUVA need to wear prescription goggles that block 100% of UVL. Teach patients to wear the eyewear for 24 hours after taking the medication when outdoors or near a bright window because UVA penetrates glass. Perform frequent skin assessments on all patients receiving phototherapy. The immunosuppressive effects of PUVA increase the risk for SCC, BCC, and melanoma. Photodynamic therapy is a special type of phototherapy used to treat actinic keratosis and some skin cancers. This therapy uses a photosensitizing agent in a different way than other phototherapy treatments. The patient receives the photosensitizing agent IV or topically, depending on the area treated. Time is allowed for the drug to be absorbed by the target cells. Light is then applied to the area, causing the drug to react with oxygen. This starts a reaction that kills the cells.11

Check Your Practice You are working in a dermatology clinic preparing a 64-yr-old woman for phototherapy to treat multiple actinic keratoses on her nose and both cheeks. She says the first lesion appeared a few years ago. She then started to worry about all the time she spent in her garden without sunscreen. She thought the lesions were just “age spots” and was unconcerned until a few started to grow and periodically bleed. • What teaching will you do to get her ready for the procedure and to take care of herself after the procedure?

Radiation Therapy The use of radiation therapy to treat BCC and SCC varies. The best candidates are those with lesions in challenging locations, such as the ear, nose, scalp, neck, and shin; those who may have trouble with

wound healing; or those with medical comorbidities who cannot undergo surgery.12 Use is limited in those with melanoma to palliative pain control or treating brain metastases.

TABLE 23.10 Common Benign Conditions of the

Skin

PUVA, Psoralen ultraviolet A; UVA, ultraviolet A; UVB, ultraviolet B.

FIG. 23.11 Psoriasis. Characteristic inflammation and scaling. From Habif TP: Clinical dermatology: A color guide to diagnosis and therapy, ed 5, St Louis, 2011, Mosby.

Radiation therapy requires multiple visits to a radiology

department. It can produce permanent hair loss (alopecia) of the irradiated areas. Other adverse effects, depending on anatomic location and dose of radiation delivered, include telangiectasia, atrophy, hyperpigmentation, depigmentation, ulceration, hearing loss, ocular damage, atrophy, and mucositis. Careful shielding is necessary to prevent ocular lens damage if the irradiated area is around the eyes. See Chapter 15 for more on radiation therapy. Total-body skin irradiation is one treatment for cutaneous T-cell lymphoma. Treatment follows a lengthy course and causes premature aging of the skin. Patients have varying degrees of permanent alopecia and radiation dermatitis with a transient loss of sweat gland function.

Laser Technology Laser treatment is expanding rapidly as an efficient surgical tool for many types of skin problems (Table 23.11-anchor>). Depending on the type of laser and the wavelength, lasers serve a wide variety of functions. Lasers can make measurable, repeatable, consistent zones of tissue damage. They can cut, coagulate, and vaporize tissue to some degree. Laser light does not accumulate in body cells and cannot cause cumulative cellular changes or damage. With less damage to surrounding tissue, there is a decreased risk for scarring. The surgical use of laser energy requires a focusing device to produce a small, high-density spot of energy. Several types of lasers are available. The CO2 laser, the most common, has many applications as a vaporizing and cutting tool for most tissues. The argon laser emits light that is primarily absorbed by hemoglobin. It helps in the treatment of vascular and other pigmented lesions. Other, less common lasers include copper and gold vapors and neodymium:yttrium-aluminum-garnet (Nd:YAG). Those who work with laser equipment must be familiar with facility policies and procedures on laser safety.

Drug Therapy

Antibiotics Several topical and systemic antibiotics are used to treat skin problems. Sometimes they are used concurrently. Many common systemic antibiotics are not used topically because of the danger of allergic contact dermatitis. Common OTC topical antibiotics include bacitracin-neomycin-polymyxin (Neosporin), bacitracin, and polymyxin B. Some HCPs do not recommend Neosporin because of the risk for allergic contact dermatitis. Prescription topical antibiotics include (1) mupirocin (for superficial Staphylococcus infections such as impetigo), (2) gentamicin (used for Staphylococcus and many gramnegative organisms), and (3) erythromycin (used for gram-positive cocci [staphylococci and streptococci] and gram-negative cocci and bacilli). Metronidazole is a common therapy for rosacea. Topical erythromycin and clindamycin are options for acne vulgaris.

TABLE 23.11 Skin Conditions Treated by Laser • Acne scars • Hair removal • Hemangiomas • Leg veins • Pigment discoloration in epidermis • Pigmented nevi • Port wine stain • Psoriasis • Resurfacing of skin • Rosacea • Skin lesions • Tattoo removal • Vascular lesions • Warts

• Wrinkles Systemic infections require systemic antibiotics. They have a role in treating acne vulgaris and bacterial infections, such as erysipelas, cellulitis, abscesses, and certain wound infections. Frequently used oral drugs include penicillin, erythromycin, doxycycline, clindamycin, and linezolid. Vancomycin is the drug of choice for severe infections.13 Give patients drug-specific instructions on the proper technique of taking or applying antibiotics.

Corticosteroids Corticosteroids are effective in treating a wide variety of skin problems. They can be used topically, intralesionally, or systemically. Topical corticosteroids have local antiinflammatory and antipruritic effects. Since corticosteroids may alter the manifestations, try to diagnose a skin problem before applying a corticosteroid preparation. The potency of a preparation depends on the concentration of active drug. With prolonged use, high-potency corticosteroids can cause adrenal suppression, especially if a large surface area is covered and occlusive dressings are used. Other side effects include skin atrophy from impaired cell mitosis, capillary fragility, rosacea eruptions, severe exacerbations of acne vulgaris, and bruising. In general, atrophy does not occur until a corticosteroid has been in use for 2 to 3 weeks. If drug use is stopped at the first sign of atrophy, recovery usually occurs in several weeks. Rebound dermatitis can occur when therapy is stopped. Tapering the use of high-potency topical corticosteroids when improvement is noted reduces the risk. Low-potency corticosteroids such as hydrocortisone act more slowly. However, they can be used for a longer time without producing serious side effects. Low-potency corticosteroids are safe to use on the face and areas where skin may touch or rub together, such as the axillae and groin. The most potent delivery system for a topical corticosteroid is an ointment form. Apply creams and ointments in thin layers and slowly massage into the site 1 to 3 times a day.

Intralesional corticosteroids are injected directly into or just beneath the lesion. This method provides a reservoir of medication with an effect lasting several weeks to months. Intralesional injection is common in the treatment of psoriasis, alopecia areata (patchy hair loss), cystic acne, hypertrophic scars, and keloids. Triamcinolone acetonide (Kenalog) is the most common drug used for intralesional injection. Systemic corticosteroids can have remarkable results in the treatment of skin conditions. However, they often have undesirable systemic effects (see Chapter 49). Corticosteroids are helpful in shortterm therapy for acute conditions such as contact dermatitis caused by poison ivy. Long-term therapy is reserved for those with severe disease such as bullous (blistering) disorders.

Antihistamines Oral antihistamines are helpful in treating urticaria, angioedema, and pruritus that can occur in problems such as atopic dermatitis, allergic dermatitis, and other allergic cutaneous reactions. Several antihistamines may be tried before getting an acceptable effect. Antihistamines with sedative effects, such as hydroxyzine and diphenhydramine, may be better for pruritic conditions because the tranquilizing and sedative effects offer symptomatic relief. Warn the patient about sedative effects, a problem when driving or using heavy machinery. Antihistamines, such as loratadine (Claritin), fexofenadine (Allegra), and cetirizine (Zyrtec), bind to peripheral histamine receptors, giving antihistamine action without sedation. They are not effective for controlling pruritus. Use any antihistamines with caution in older adults because of their long half-life and anticholinergic effects.

Topical Fluorouracil Fluorouracil is a topical cytotoxic agent with selective toxicity for sundamaged cells. It is used to treat precancerous lesions (especially AK) and some skin cancers. Patient adherence is a consideration in the use of fluorouracil. The medication produces erythema, burning, and

pruritus within 3 to 5 days. Painful, eroded areas over the damaged skin occur within 1 to 3 weeks, depending on skin thickness at the site. Reduce redness and pruritus by applying a low-potency topical corticosteroid 20 minutes after. There are 5 strengths (0.5%, 1%, 2%, 4%, and 5%). Treatment must continue with applications 1 or 2 times a day for 2 to 4 weeks. Healing may take up to 4 weeks after the medication is stopped.8 Adherence to therapy depends on your teaching. Tell the patient that they will look worse before they look better. Teach about the effect of the medication. Because fluorouracil is a photosensitizing drug, tell the patient to avoid sunlight during treatment. After treatment, skin should be smooth and free of AK. AK may recur in treated areas, and multiple courses of therapy may be necessary over the years for those with severely sun-damaged skin.

Immunomodulators Topical immunomodulators, such as pimecrolimus (Elidel) and tacrolimus (Protopic), are used to treat atopic dermatitis, psoriasis, and rosacea.14 They work by suppressing an overreactive immune system. The side effects are minimal and may include a transient burning or feeling of heat at the application site. Use may increase the risk for skin cancer and precancerous lesions. The topical immunomodulator imiquimod (Aldara) is used to treat external genital warts, AK, and superficial BCC. It stimulates the production of α-interferon and other cytokines to enhance cellmediated immunity. It boosts the immune response only where applied and is safe for transplant patients. Most patients using this cream experience skin reactions, including redness, swelling, blistering, peeling, itching, and burning. Dosing varies depending on the type of lesion treated and the strength of medication prescribed.8

Diagnostic and Surgical Therapy Skin Scraping

Scraping with a scalpel blade can yield a sample of surface cells (stratum corneum) for microscopic inspection and diagnosis. The most common tests of skin scrapings are mineral oil examination for scabies and 10% to 20% potassium hydroxide (KOH) for fungus.

Electrodessication and Electrocoagulation Electrical energy can be converted to heat with the tip of an electrode. The heat burns and destroys tissue. The major uses of these therapies are coagulation of bleeding vessels to obtain hemostasis and destruction of small telangiectasias (dilation of groups of superficial capillaries and venules). Electrodessication usually involves more superficial destruction. It uses a monopolar electrode. Electrocoagulation uses a bipolar electrode. It has a deeper effect, with better hemostasis, but an increased chance of scarring. While minor electrosurgery on patients with a pacemaker poses minimal risk, the electrical energy can affect both pacemakers and internal defibrillators.

Curettage Curettage is the removal and scooping away of tissue using an instrument called a curette. A curette looks like a small spoon with very sharp edges. Although a curette is not usually strong enough to cut normal skin, it can remove many types of small, soft skin tumors and superficial lesions, such as warts, AK, seborrheic keratosis, and small BCCs and SCCs. The area to be curetted is anesthetized before the procedure. The HCP removes the lesion and then cauterizes the skin. The removed tissue is usually sent for biopsy. A dressing may be applied, and you will need to teach the patient wound care. A small scar and hypopigmentation can result.

Punch Biopsy Punch biopsy is a common procedure used to obtain a tissue sample for histologic study or to remove small lesions (Fig. 23.12-anchor>). The procedure is simple. The HCP marks the biopsy area and then

anesthetizes it so that the anesthetic will not obscure the landmarks. The HCP rotates the punch into the skin and removes a small cylinder of skin. Hemostasis is achieved with pressure or absorbable gelatin (Gelfoam) packing. Sites of 4 mm or larger are usually closed with sutures. Punch biopsies are not done below the knee if other sites are available. Circulatory changes can make evaluating the tissue sample more difficult.

FIG. 23.12 Punch biopsy. A, Removal of skin for diagnostic purposes.

B, Specimen obtained. From Graham-Brown R, Bourke J, Cunliffe T: Dermatology: Fundamentals of practice, Edinburgh, 2008, Mosby.

Cryosurgery Cryosurgery is the use of subfreezing temperatures to destroy epidermal lesions. Cryosurgery is used to treat common and genital warts, cutaneous tags, thin seborrheic keratoses, lentigines, AK, BCC, and SCC. Topical liquid nitrogen is the agent most commonly used for cryosurgery.12 Damage occurs in treated tissue because of intracellular ice formation. It causes the cell to rupture during thaw, leading to cell death and necrosis. The degree of damage depends on the rate of cooling and the minimum temperature achieved. Liquid nitrogen is applied topically (directly onto the lesion) with a direct spray or contact probe. Tell patients that they will feel a painful, stinging cold sensation. The lesion first becomes swollen and red, and it may blister. A scab forms and falls off in 1 to 3 weeks. The skin lesion sloughs along with the scab. Growth of new skin follows. The size of an affected area may limit the use of cryotherapy. Other disadvantages include the potential for harming adjacent healthy tissue and the low temperature of liquid nitrogen destroying melanocytes, leaving an area of hypopigmentation resembling a scar.

Excision Excision is an option if the lesion involves the dermis. Complete closure of the excised area usually results in a good cosmetic result. A specific type of excision is Mohs surgery, which is the microscopically controlled removal of a skin cancer. In this procedure, the HCP removes tissue sections in thin horizontal layers. All the specimen’s margins are examined to see if any cancer cells remain (Fig. 23.13-anchor>). Any residual tumor not removed by the first surgical excision is removed in serial excisions performed the same day. Benefits of Mohs surgery are that it preserves normal tissue, produces the smallest possible wound, and can completely remove the cancer. Although it can be a lengthy procedure, it is done in an

outpatient setting using local anesthesia.

FIG. 23.13 A, Removal of melanoma by Mohs surgery. B, After

plastic surgery using a skin flap to repair defect. Courtesy Peter Bonner, Placitas, NM.

Nursing Management: Skin Problems Ambulatory Care Skin problems are not usually a primary reason for hospitalization. Nevertheless, many hospitalized patients have skin problems that need nursing intervention and patient education. Nursing interventions for skin conditions fall into broad categories. They apply to many problems in both inpatient and outpatient settings. A nursing care plan for the patient with chronic skin lesions (eNursing Care Plan 23.1) is available on the website for this chapter. In your general teaching with the patient, stress the duration of the treatment and the need to follow package directions. Skin problems may be slow to resolve. Tell the patient to follow package directions when using OTC drugs. If the package insert says its use should not exceed 7 days, patients should heed this warning. Teach the patient to stop self-care and seek the help of an HCP if any systemic signs of inflammation or extensions of the skin problem (e.g., an increasing number of lesions, increased erythema, increased swelling) develop.

Wet Compresses For superficial skin problems that involve inflammation, itching, and infection, wet compresses are commonly used. They are appropriate for damaged, oozing skin. Wet compresses are a good way to remove crusts and scabs that are adhering to the wound surface. They provide comfort and treatment of conditions such as poison ivy, insect bites, and skin infections. It is important to understand how to do a wet compress correctly. Unless there is a concern about water quality, tap water at room temperature is the best choice. If drinkable water is not available, use filtered, bottled, or sterile water. Depending on the problem, additives may be used. Common solutions include (1) saline, (2) Burow’s

solution (Domeboro powder [aluminum acetate; calcium acetate]), (3) acetic acid (vinegar), and (4) silver nitrate.8 The temperature of the fluid should be tepid. However, when an antiinflammatory effect is desired, the fluid should be cool. The material you select for the compress should be 4 to 8 layers thick and slightly larger than the area that you are treating. Use gauze or any clean material (e.g., thin cotton sheeting, thermal underwear, tube socks). Ingenuity is sometimes needed when covering oddshaped body parts. Do not use gauze sponges with fillers (abdominal pads). They will retain too much solution, and fibers can be left in the wound if the skin is open. Place the prescribed compress material into fresh solution and squeeze out excess fluid. Your goal is a wet compress—not damp but not dripping. Wet compresses are applied continuously or intermittently. When used continuously, remove the compress and replace with a new one as needed. Do not add solution to a compress. This can change the fluid’s concentration and damage the skin. They can be placed intermittently, for 10 to 30 minutes, several times a day. Careful monitoring of the skin is important. If the skin appears macerated (softens and turns white), stop the compresses for 2 to 3 days. Change and wash daily any material used repeatedly throughout the day. Protect the patient from discomfort and chilling. A water-resistant pad will help protect the mattress, linens, and furniture.

Baths Baths are an appropriate intervention when large areas of the body need treatment. Baths may be relaxing and will help decrease itching. Agents such as colloidal oatmeal (Aveeno) and sodium bicarbonate can be added directly to bath water. Fill the tub with tepid water to cover the affected areas. Depending on the severity of the problem and the patient’s discomfort, have the patient soak for 15 to 20 minutes 3 or 4 times a day. Stress to the patient not to rub the skin dry with a towel but gently pat to prevent increased irritation and inflammation. Avoid adding oils as their use increases the risk for falls. To sustain the hydrating effect, apply cream, ointment emollients

(moisturizers), or other prescribed topical agents after the bath. This helps seal the moisture in the hydrated cells and increases the absorption of any topical agents.

Hygienic Practices The patient’s skin type, lifestyle, culture, age, and gender influence hygienic practices. The normal acidity of the skin and perspiration protect against bacterial overgrowth. Most soaps are alkaline and neutralize the skin surface, leading to a loss of protection. Using mild, moisturizing soaps and lipid-free cleansers and avoiding hot water and vigorous scrubbing can noticeably decrease local skin irritation and inflammation. Skin piercings in which jewelry has been inserted can be cared for with antibacterial soaps that do not contain sulfites. In general, skin and hair must be washed often enough to remove excess oil and excretions and to prevent odor. Older persons should avoid harsh soaps and shampoos and frequent bathing because of the dryness of their skin and scalp. Using moisturizers right after a bath or shower (while the skin is still damp) seals in the moisture.

Topical Medications Topical medications are commonly used to treat skin problems. The effectiveness of topical therapy depends on which base the medication is prepared in. Table 23.12-anchor> summarizes the common agents used as bases for topical preparations and their therapeutic considerations. The base selected depends on the properties needed. Creams are very versatile and most commonly prescribed. Ointments are more lubricating than creams and offer enhanced potency of the active ingredient. They may be too occlusive for conditions with lots of exudate or in body creases. Gels work well on the scalp, where other compounds may mat the hair, and for acute exudative conditions such as poison ivy. Lotions are also fine for the scalp but may cause stinging and drying when used in skinfolds. Pastes are good for protecting the skin but are messy. A limited number of foams are available.

TABLE 23.12 Drug TherapyCommon Bases for

Topical Medications Agent Cream Gel

Therapeutic Considerations Emulsions of oil and water. Most common base for topical medications. Lubrication and protection Nongreasy combination of propylene glycol and water. May contain alcohol

Emulsions of water, alcohol, and/or oil. Cooling and drying. Some leave residual powder film after evaporation of water. Useful in subacute pruritic eruptions Ointment Oil with differing amounts of water added in suspension. Lubrication and prevention of dehydration. Petrolatum most common Mixture of powder and ointment, used when drying effect necessary because moisture Paste is absorbed Promotion of dryness. Lubricates skinfold areas to prevent irritation. Base for Powder antifungal preparations. Protect patient from inhaling Lotion

Apply topical medications as directed. Proper administration will yield best results and avoid waste. Some are very costly. As a rule, apply topical medication in a thin film to clean skin and spread evenly in a downward motion in the direction of hair growth. Thick creams will spread easier if the skin is still damp. If you are using a secondary dressing, you can apply the medication directly onto a dressing. Teach the patient and caregiver proper dosing, application technique, expected results, and common reactions. Occlusion with a plastic wrap is an effective way to increase the absorption of topical corticosteroids or simple emollients. The plastic wrap traps perspiration against the outer layer of the epidermis. Applying preparations to moist skin increases absorption 10-fold. Use tape or stretch wraps to keep the plastic wrap in place. For conditions on the feet or lower legs, the patient can wear socks over the plastic wrap. Wraps applied multiple times daily are kept in place for 2 to 8 hours. Some patients choose to use the occlusion technique at bedtime. Occlusion is not appropriate in areas prone to infection, such as skin creases.

Control of Pruritus Many conditions cause pruritus (itching). This includes dry skin, almost any physical or chemical stimulus to the skin (such as drugs or insects), and any scaling skin disorder. The itch sensation is carried by the same nonmyelinated nerve fibers as pain and temperature. The patient will have pain rather than an itch if the epidermis is damaged or absent. It is important to figure out if itching preceded a skin lesion. Itching can lead to scratching that results in an excoriated and inflamed lesion. Certain circumstances make itching worse. Teach the patient ways to help break the itch/scratch cycle. A cool environment may cause vasoconstriction and decrease itching. Hydration, wet compresses, and moisturizers (including antipruritic lotions) are normally helpful. Apply wet compresses for 30 to 60 minutes, pat the skin dry, and apply a lubricant or medication. Topical and injectable corticosteroids are sometimes used. Topically applied menthol, camphor, or phenol numb itch receptors. Systemic antihistamines may give relief. The main side effect of most antihistamines is sedation. This may be desirable because pruritus is often worse at night and can interfere with sleep. Adequate rest increases the patient’s ability to tolerate itching, thereby decreasing skin damage from the resultant scratching. Have the patient avoid anything that causes vasodilation, such as heat or rubbing. Dry skin lowers the itch threshold and increases the itch sensation. Lichenification is a thickening of epidermis with exaggerated markings resembling a washboard. It is caused by chronic scratching or rubbing of the skin. Lichenification is often associated with atopic dermatoses and other pruritic conditions. Although any area of the body may be affected, the hands, forearms, shins, and nape of the neck are common sites. Scratching may become a habit. Persistent scratching can cause excoriations. Treating the cause of the itching is the key to preventing lichenification.

Prevention of Spread Although most skin problems are not contagious, infection control

precautions indicate wearing gloves when working with any open wounds or lesions with drainage. Not all infected drainage is purulent. Careful hand washing and properly disposing of soiled dressings are the best means of preventing the spread of infections or infestations. The most common contagious lesions include impetigo, streptococcal infections, staphylococcal infections (e.g., methicillinresistant S. aureus [MRSA]), fungal infections, primary chancre, scabies, and pediculosis.

Prevention of Secondary Infections Open skin lesions are susceptible to invasion by other viral, bacterial, or fungal organisms. Meticulous hygiene, hand washing, and dressing changes are important to minimize the potential for secondary infections. Warn the patient about scratching lesions, which can cause excoriations and create a portal of entry for pathogens. Trim the patient’s nails short to minimize trauma from scratching.

Specific Skin Care You are often in a position to teach patients skin care after simple surgical procedures, such as skin biopsy, excision, and cryosurgery. In general, your teaching should include dressing changes, use of topical antibiotics, and the signs and symptoms of infection. After a skin procedure, cleanse any oozing wound with a saline solution twice daily or as ordered by the HCP. Potable (safe, drinking water) is a safe alternative in some situations. Apply antibiotic or plain petrolatum ointment with a secondary dressing that is both absorbent and nonadherent. Wounds that are kept moist and covered heal more rapidly and with less scarring. The initial crust that forms should be left undisturbed as a protective coating for the damaged skin beneath it. Healing crusts that have been moisturized and protected will separate naturally from healed epidermis. A sutured wound may be covered with a variety of dressings. Sutures are generally removed in 4 to 14 days, depending on the placement site. Sometimes alternating sutures are removed after the

third day. Incision lines may need daily cleansing, usually with plain water. If necessary, a topical antibiotic is applied and the wound either is covered with a dry dressing or left open to air. The patient may have some swelling and discomfort in the first 24 hours. Intermittent application of cold (ice packs) over the surgical dressing may reduce edema. Mild analgesics, such as acetaminophen, should control discomfort. Teach the patient how to distinguish normal inflammation from an infection. A slight red border during the first few days after a procedure is normal. Signs and symptoms of infection include redness that persists longer than a week or extends beyond a 1-cm border, a fever above 101° F, increased pain, pronounced swelling, and purulent drainage. If these occur, they should be reported to the HCP at once.

Nursing Management Skin Conditions • Assess patient’s skin for acute and chronic skin problems. • Assess patient’s risk factors for skin problems. • Document skin condition and risk factor assessment and develop a plan of care. • Determine whether patient is taking drugs that increase photosensitivity. • Teach about risks associated with sun exposure and methods for decreasing exposure to the sun. • Administer prescribed therapies such as dressings and oral or topical medications. • Teach about therapies used for skin disorders, including dressings, baths, and oral or topical medications used on an outpatient basis. • Evaluate treatment for effectiveness and any adverse effects.

Psychologic Effects of Chronic Skin Problems Emotional stress can occur for those who suffer from chronic skin problems, such as psoriasis, atopic dermatitis, or acne. The sequelae of chronic skin problems could result in social and employment problems with subsequent financial implications, a poor self-image, problems with sexuality, and increasing and progressive frustration. The usual lack of systemic illness coupled with the visibility of the skin lesions often presents a real problem to the patient. Help the patient follow the prescribed regimen. Allow the patient to verbalize the “Why me?” question, even though there is no ready answer. Refer the patient to dermatology support groups. Many are listed on the American Academy of Dermatology website (www.aad.org). These groups are extremely helpful with patient support and education. The location of lesions and scars is the determining factor with respect to their cosmetic implications. Facial scars are the most damaging psychologically because they are so visible. Creative use of cosmetics can do much to mask lesions and scarring. Consider individual sensitivity to product ingredients when selecting cosmetics. Oil-free, hypoallergenic cosmetics are available and may be beneficial for the allergic patient. Rehabilitative cosmetics are available to help camouflage and deemphasize such lesions as vitiligo (loss of pigmentation), melasma (tan to brown patches on the face), or healed postoperative wound sites. These commercially available products are opaque, smudge resistant, and water resistant.

Cosmetic Procedures A vast array of cosmetic procedures is available, including chemical peels, toxin injections, fillers, laser surgery, breast enlargement and reduction (see Chapter 51), face-lift, eyelid-lift, and liposuction. Common cosmetic topical procedures are outlined in Table 23.13anchor>. Other types of cosmetic procedures include the injection of botulinum toxin (Botox), deoxycholic acid (Kybella), calcium hydroxylapatite (Radiesse), collagen (Zyplast), and hyaluronic acid

fillers (e.g., Restylane, Perlane, Juvéderm).15 Transitory side effects may occur, such as mild redness, pain, swelling, and bruising. Uncommon side effects from cosmetic procedures include allergic reaction, infection, grayish skin discoloration, or lumps at the injection sites. Tell the patient that the procedure will need repeating at prescribed intervals to maintain the desired appearance. The reasons for undergoing these procedures are as varied as the techniques. The most common reason that people incur the discomfort and financial expense (most are not covered by health insurance) of a cosmetic procedure is to improve their body image. If they feel better about themselves after having cosmetic procedures, they often act more confident and self-assured. Often social position and economic considerations are part of the decision. Increased longevity is providing a larger population to whom cosmetic procedures are appealing. Regardless of the patient’s reasons for seeking a cosmetic procedure, maintain a supportive, nonjudgmental attitude. If the patient wishes to change or enhance a body feature perceived as unattractive and has realistic expectations about the outcome, you should support this decision.

Elective Surgery Laser Surgery Laser surgery is used to treat congenital and acquired vascular lesions (cherry angiomas, spider leg veins, hemangiomas, port wine stains, and tattoo removal) and for skin resurfacing and hair removal. Lasers can reduce scarring and fine wrinkles around the lips or eyes and remove facial lesions (Table 23.11). Swelling, redness, and bruising are common after treatment. The treated areas usually are kept moist with ointment or occlusive dressings for the first few days. The patient must protect treated skin from the sun.

TABLE 23.13 Common Cosmetic Topical

Procedures

FIG. 23.14 Face-lift. A, Preoperative. B, Postoperative. From Cuzalina A, Copty TV, Khan H: Current therapy in oral and maxillofacial surgery, St Louis, 2012, Elsevier.

Face-Lift A face-lift (rhytidectomy) is the lifting and repositioning of the lower two thirds of the face and neck to improve appearance (Fig. 23.14anchor>). Indications for this procedure include: • Redundant soft tissue or scarring resulting from disease (e.g., acne scarring) • Asymmetric redundancy of soft tissues (e.g., facial palsy) • Redundant soft tissue resulting from trauma • Preauricular lesions • Redundant soft tissues resulting from solar elastosis (sagging of the skin from sun damage), changes in body weight, and the effects of gravity • Restoration of body image The surgical approach and lines of incisions vary according to the desired correction and the position of the hairline. Eyelid-lifts (blepharoplasty) can remove redundant tissue and possibly improve the field of vision. Preventing hematoma formation is the most important postoperative consideration. Ice packs are usually applied for the first 24 to 48 hours to reduce swelling and decrease the possibility of hematoma formation. Usually the pain is minimal. Antibiotics are used at the HCP’s discretion. Complications can occur if the person smokes or is involved in vigorous exercise.

Liposuction Liposuction is a technique for removing subcutaneous fat to improve facial and body contours. Although not a substitute for diet and exercise, it can be successful in removing areas of fat from almost any body area that is resistant to other techniques. Liposuction is relatively free of complications. Possible contraindications include the use of anticoagulants, uncontrolled hypertension, diabetes, and poor cardiovascular status. Those under

40 years of age with good skin elasticity are the best candidates. However, patients over 40 can be treated successfully. The procedure is usually done on an outpatient basis under local anesthesia. One or more sessions may be needed, depending on the size of the area. The HCP inserts a blunt-tipped cannula through a small incision and pushes into the fat to break it loose from the fibrous stroma. Multiple repeated thrusts disrupt the fat and create tunnels. The loosened fat is removed with a powerful suction. Afterward, firm pressure is applied to the wounds until drainage stops.16 It may take several months for the results to be evident.

Nursing Management: Cosmetic Surgery Many cosmetic surgical procedures are done in well-equipped daysurgery units or in dermatologist or plastic surgeon in-office surgery suites.

Preoperative Management A major consideration before surgery relates to informed consent and realistic expectations of what cosmetic surgery can accomplish. Although the HCP should provide this information, reinforce it and answer questions and concerns. For instance, a face-lift has little or no effect on deep wrinkling of the forehead and temples, deep nasolabial grooves, or vertical lip wrinkles. Before-and-after treatment photographs of similar cases are often useful in helping the patient to set realistic expectations. Your teaching plan should include the timeframe for healing. Explain the oozing, crusting stage of an abrasive procedure so the patient can plan time off from work if necessary. Since wound healing may not be complete for 1 year, the patient should not expect complete results at once. The final result is affected by the patient’s age, general state of health, and skin type and the extent (severity) of

the condition being treated. Efforts should be made to correct or control any existing health problem before the procedure.

Postoperative Management Most cosmetic procedures are not extremely painful. Usually, mild analgesics are enough to keep the patient comfortable. Although infection is not a common problem after cosmetic surgery, assess the sites for signs of infection. Teach the patient signs and symptoms of infection. Stress that it is important to report them at once so that treatment can be started. If the surgery involved a change in the skin’s circulation, as in a face-lift, carefully monitor for adequate circulation. Warm, pink skin that blanches on pressure shows that adequate circulation is present in the surgical area. Supportive, compressive dressings and ice packs may be necessary early in the postoperative period.

Skin Grafts Uses Skin grafts may be necessary to protect underlying structures or to reconstruct areas for cosmetic or functional purposes. They may be used to facilitate rapid closure and minimize complications. Ideally, wounds heal by primary intention. However, large wounds, surgically created wounds, trauma, and chronic wounds can result in extensive tissue destruction, making healing by primary intention impossible. In these cases, skin grafting may be necessary to close the defect. Improved surgical techniques make it possible to graft skin, bone, cartilage, fat, fascia, muscles, and nerves. For cosmetically pleasing results, the color, thickness, texture, and hair-growing nature of skin used for grafting should match the recipient site. See Chapter 24 for a discussion of skin grafting for patients with burn injuries.

Types

The two types of traditional skin grafts are free grafts and skin flaps. Free grafts are classified according to how they supply blood to the grafted skin. One method is to transfer the graft (epidermis and part or all the dermis) to the recipient site from the donor site. The autograft (from the patient’s own body) or isograft (from an identical twin) revascularizes and becomes fixed to the new site. The other method of free skin grafting is by reconstructive microsurgery. With the use of an operating microscope, the HCP establishes circulation immediately in the graft by connecting blood vessels in the skin flap to vessels in the recipient site. Skin flaps involve moving a section of skin and subcutaneous tissue from one part of the body to another without terminating the vascular attachment (pedicle). Skin flaps are used to cover wounds with a poor vascular bed, provide padding when needed, and cover wounds over cartilage and bone. The patient may need intermediate flap placement if the recipient site is far removed from the donor site. For instance, a skin flap from the thigh to the head would require an intermediate graft. The flap is advanced to the recipient site when circulation is well established at the intermediate site. The patient’s needs and the type of defect determine the type of flap and the route of transfer. Soft tissue expansion is a technique for providing skin (1) for resurfacing of a defect, such as a burn scar; (2) for removal of a disfiguring mark (e.g., a tattoo); or (3) as a preliminary step in breast reconstruction. A subcutaneous tissue expander of a proper size and shape is placed under the skin, usually as an outpatient procedure. Weekly expansion with saline solution can be done in a health care setting or by the patient at home. This expansion procedure is repeated until the skin reaches the size needed for the repair. This may take from several weeks to 3 to 4 months. Once enough skin is available, the old incision is opened, the expander is removed, and the soft tissue is ready to be used as an advancement flap. The tissue expander next to a defect has the primary tissue characteristics, such as color and texture. Engineered skin substitutes (e.g., Apligraf, Dermagraft, Integra) are gaining popularity. There are several available, each with its own

indications and benefits. Some are two-layered membranes with both dermal and epidermal components. Others are only one layer. The skin is engineered from neonatal foreskins and cadavers. Skin substitutes do not contain structures such as blood vessels, hair follicles, sweat glands, or cells such as melanocytes, Langerhans cells, macrophages, and lymphocytes.17 Engineered skin grafts have an extended shelf life. Some are cryopreserved, others shipped overnight as they are needed. Advantages include ready availability, the avoidance of a donor site, application in outpatient settings, minimal scarring, and less pain.

Case Study Melanoma and Dysplastic Nevi

© Dimedrol68/iStock/Think stock.

Patient Profile G.L. is a 48-yr-old white, fair-skinned man who is a long-distance truck driver. In his leisure time, he enjoys swimming. He comes to the clinic because of a changing lesion on his left arm.

Subjective Data • History of a basal cell cancer (BCC) on his left ear in the last 4 years

• Father treated for metastatic melanoma in the last 2 years • First noted the lesion 1 month ago when it started changing size • Anxious that removing the lesion will require extensive, disfiguring surgery

Objective Data Physical Examination • Has a 4-mm lesion, deep brown, scalloped with vaguely defined borders • 5 dysplastic nevi found on back

Diagnostic Studies • Excisional biopsy confirmed superficial spreading melanoma. • Sentinel node biopsy results were negative. • Diagnostic tests indicate melanoma stage I.

Discussion Questions 1. What risk factors for melanoma does he have? 2. What are the usual clinical manifestations associated with melanoma? 3. What is the prognosis for a patient with this stage of melanoma? 4. What treatment options are available for him? 5. Priority Decision: Based on the assessment data presented, what are the priority nursing diagnoses? 6. Patient-Centered Care: How would you help G.L. deal with his anxiety over the treatment outcomes? 7. Priority Decision: What is the priority of care for G.L.? 8. Safety: What would you include in his patient teaching plan to address future sun exposure?

9. Evidence-Based Practice: G.L. wants to know whether regularly applying sunscreen will reduce his risk for developing a second melanoma. How would you reply? Answers available at http://evolve.elsevier.com/Lewis/medsurg.

Bridge To Nclex Examination The number of the question corresponds to the same-numbered outcome at the beginning of the chapter.

1. Which safe sun practices would the nurse include in the teaching plan for a patient who has photosensitivity (select all that apply)? a. Wear protective clothing. b. Apply sunscreen liberally and often. c. Emphasize the short-term use of a tanning booth. d. Avoid exposure to the sun, especially during midday. e. Wear any sunscreen as long as it is bought at a drugstore. 2. When teaching a patient with melanoma about this disorder, the nurse recognizes that the patient’s prognosis is most dependent on a. the thickness of the lesion. b. the degree of asymmetry in the lesion. c. the amount of ulceration in the lesion. d. how much the lesion has spread superficially. 3. The nurse determines that a patient with which disorder is most at risk for spreading the disease?

a. Tinea pedis b. Impetigo on the face c. Candidiasis of the nails d. Psoriasis on the palms and soles 4. A mother and her two children have been diagnosed with pediculosis corporis at a health care center. An appropriate measure to treat this condition is a. applying pyrethrins to the body. b. topical application of griseofulvin. c. moist compresses applied frequently. d. administration of systemic antibiotics. 5. A common site for the lesions associated with atopic dermatitis is the a. buttocks. b. temporal area. c. antecubital space. d. plantar surface of the feet. 6. During the assessment of a patient, you note an area of red, sharply defined plaques covered with silvery scales that are mildly itchy on the patient’s knees and elbows. You would describe this finding as a. lentigo. b. psoriasis. c. actinic keratosis. d. seborrheic keratosis. 7. In teaching a patient who is using topical corticosteroids to treat acute dermatitis, the nurse should tell the patient that

(select all that apply) a. the cream form is the most efficient system of delivery. b. short-term use of topical corticosteroids usually does not cause systemic side effects. c. use a glove to apply small amounts of creams or ointments to prevent further infection. d. abruptly stopping the use of topical corticosteroids may cause the dermatitis to reappear. e. systemic side effects from topical corticosteroids are likely if the patient is malnourished. 8. Important patient teaching after a chemical peel includes a. avoidance of sun exposure. b. application of firm bandages. c. limitation of vigorous exercise. d. use of moist heat to relieve discomfort. 1. a, b, d, 2. a, 3. b, 4. a, 5. c, 6. b, 7. b, d, 8. a. For rationales to these answers and even more NCLEX review questions, visit http://evolve.elsevier.com/Lewis/medsurg.

Evolve Website/Resource List http://evolve.elsevier.com/Lewis/medsurg

Review Questions (Online Only) Key Points Answer Keys for Questions • Rationales for Bridge to NCLEX Examination Questions • Answer Guidelines for Case Study on p. 429

Nursing Care Plan • eNursing Care Plan 23.1: Patient With Chronic Skin Lesions Conceptual Care Map Creator Audio Glossary Supporting Media • Animation • Mohs Surgery Content Updates

References Tripp MK, Watson M, Balk SJ, et al: State of the science on prevention and screening to reduce melanoma incidence and mortality, CA Can J Clin 66:460, 2016.

2. US Food and Drug Administration: Sunscreen Innovation Act. Retrieved from www.fda.gov/drugs/guidancecomplianceregulatoryinformation/ucm4 3. American Cancer Society: Skin cancer facts. Retrieved from www.cancer.org/cancer/skin-cancer.html. 4. Canavan T, Cantrell W: Recognizing melanoma: Diagnosis and treatment options, TNP 41:24, 2016. Verkouteren JA, Ramdas KH, Wakkee M, et al: Epidemiology of basal cell carcinoma: Scholarly review, Br J Dermatol 177:359, 2017. Green AC, Olsen CM: Cutaneous squamous cell carcinoma: An epidemiological review, Br J Dermatol 177:373, 2017. Coit DG, Thompson JA, Algazi A, et al: Melanoma, version 2.2016, NCCN clinical practice guidelines in oncology, JCCN 14:450, 2016.

8. Habif TP: Clinical dermatology, ed 6, St Louis, 2016,

Saunders. 9. American Academy of Dermatology: Psoriasis. Retrieved from www.aad.org/public/diseases/scalyskin/psoriasis. Cantrell W: Psoriasis and psoriatic therapies, TNP 42:35, 2017. Abrahamse H, Hamblin MR: New photosensitizers for photodynamic therapy, Biochem J 473:347, 2016. Stegman L: Electronic brachytherapy for nonmelanoma skin cancer, Oncology Times 39:38, 2017. Russo A, Concia E, Cristini F, et al: Current and future trends in antibiotic therapy of acute bacterial skin and skin-structure infections, Clin Microbiol Infect 22:S27, 2016.

14. Luger TA, McDonald I, Steinhoff M: Clinical and basic immunodermatology, New York, 2017, Springer. Costa CR, Kordestani R, Small KH, et al: Advances and refinement in hyaluronic acid facial fillers, PRS 138:233, 2016. Chia CT, Neinstein RM, Theodorou SJ: Evidence-based medicine: Liposuction, PRS 139:267, 2017.

17. Bryant R, Nix D: Acute and chronic wound, ed 5, St Louis, 2016, Mosby. Evidence-based information for clinical practice.

24

Burns Cecilia Bidigare

LEARNING OUTCOMES 1. Relate the causes of burns to the prevention strategies for burn injuries. 2. Distinguish between partial-thickness and full-thickness burns. 3. Apply tools used to determine the severity of burns. 4. Compare the pathophysiology, clinical manifestations, complications, and interprofessional care throughout the 3 burn phases. 5. Compare the fluid and electrolyte shifts during the emergent and acute burn phases. 6. Outline the nutritional needs of the burn patient throughout the 3 burn phases. 7. Compare the various burn wound care techniques and surgical options for partial-thickness and full-thickness burn wounds. 8. Prioritize nursing interventions in the management of the burn patient’s physiologic and psychosocial needs. 9. Examine the various physiologic and psychosocial aspects of burn rehabilitation. 10. Develop a plan of care to prepare the burn patient and caregiver for discharge.

KEY TERMS burn, p. 431 carboxyhemoglobin, p. 433 chemical burns, p. 432 contracture, p. 448 cultured epithelial autograft (CEA), p. 447 debridement, p. 442 electrical burns, p. 433 escharotomy, p. 439 excision and grafting, p. 446 full-thickness burns, p. 434 partial-thickness burns, p. 434 smoke and inhalation injuries, p. 432 thermal burns, p. 432 Every life deserves a certain amount of dignity, no matter how poor or damaged the shell that carries it. Rick Bragg http://evolve.elsevier.com/Lewis/medsurg/

Conceptual Focus Coping Fluids and Electrolytes Infection Nutrition Pain Perfusion

Tissue Integrity The focus of this chapter is the care of patients who have a burn injury. A burn is an injury to the skin or other tissues of the body caused by heat, chemicals, electric current, or radiation. The resulting effects on tissue integrity are influenced by the temperature and type of burning agent, duration of contact, and type of tissue that is injured. The location of the injury, associated injuries, and age and general health of the patient influence the seriousness of the injury. The patient with a burn injury may have a multitude of problems. There may be difficulty maintaining an airway and adequate circulation, affecting perfusion. Fluid and electrolyte imbalances are common. We must give attention to preventing malnutrition and infection. The patient often has fear, anger, guilt, and depression. The patient may have body image concerns, especially with facial and hand burns; anxiety about future therapy and surgery; and frustrations with ongoing pain. An estimated 486,000 Americans seek medical care each year for burns.1 Around 40,000 people are hospitalized, 60% receiving care in specialized burn centers. About 3275 Americans die annually as a direct result of their injuries. The highest fatality rates occur in children ages 4 years and younger and adults over age 65. Worldwide, over 11 million people need medical attention annually for burn injuries and about 180,000 die.2 Although burn incidence in the United States has decreased over the past 20 years, international burn injuries still occur too often, mainly to those living in low- and middle-income counties. Most burn accidents are preventable. The focus of burn prevention has shifted from blaming victims to educating people in vulnerable communities to identify hazards and provide first aid. Coordinated national prevention programs in higher income countries have focused on child-resistant lighters, tap water anti-scald devices, stricter building codes, having smoke detectors, and fire and burn safety education curriculums for schools.3 As a nurse, you can advocate for and teach about burn risk-reduction strategies in the home and at work (Tables 24.1 and 24.2).

TABLE 24.1 Common Sources of Burn Injury

Home Hazards Bathroom and Kitchen • Hot water heaters set at 120°F (60°C) or higher • Microwaved food • Steam, hot grease or liquids from cooking

General Household • Carelessness with cigarettes, matches, candles • Heat lamps • Fireplaces (e.g., gas, wood) • Flammables (e.g., starter fluid, gasoline, kerosene) • Frayed or defective wiring • Multiple extension cords per outlet • Open space heaters • Outdoor grills (e.g., propane, charcoal) • Radiators (e.g., home, automobile)

Occupational Hazards • Cement • Chemicals • Combustible fuels • Electricity from power lines • Fertilizers, pesticides • Hot metals

• Sparks from live electric sources • Steam pipes • Tar

TABLE 24.2 Promoting Population

HealthStrategies to Reduce Burn Injury

Chemical • Store chemicals safely in approved containers and label clearly. • Ensure safety of workers handling chemicals (education, protective eyewear, gloves, masks, clothing).

Electrical • Avoid or repair frayed wiring. • Avoid outdoor activities during electrical (i.e., lightning) storms. • Ensure electrical power source is shut off before beginning repairs. • Wear protective eyewear and gloves when making electrical repairs.

Flame or Contact • Never smoke in bed. • Use “child-resistant” lighters. • Hold regular home fire exit drills. • Never leave hot oil unattended while cooking. • Never use gasoline or other flammable liquids to start a fire. • Never leave candles unattended or near open windows or

curtains. • Consider a flame-retardant smoking apron for older or “at-risk” people. • Exercise caution when microwaving food and beverages as they can get very hot.

Inhalation • Install smoke and carbon monoxide detectors and change batteries annually (if appropriate).

Scald • Use “anti-scald” devices with showerhead or faucet fixtures. • Lower hot water temperature to the “lowest point” or 120°F (49°C). • After running bath water, check temperature with back of hand or bath thermometer. • Supervise bathing with small children, older adults, or anyone with impaired physical movement, physical sensation, or judgment.

Types of Burn Injury Thermal Burns Thermal burns, caused by flame, flash, scald, or contact with hot objects, are the most common type of burn injury (Fig. 24.1). The severity of the injury depends on the temperature of the burning agent and duration of contact time. Scald injuries often occur in bathrooms and kitchens. Flash, flame, or contact burns can occur while cooking, smoking, or burning leaves in the backyard.

Chemical Burns Chemical burns are the result of contact with acids, alkalis, and organic compounds. In addition to skin damage, eyes can be injured if splashed. Acids are found in the home and at work. They include hydrochloric, oxalic, and hydrofluoric acid. Alkali burns can be more difficult to manage than acid burns since alkalis adhere to tissue, causing protein hydrolysis and melting. Alkalis are found in cement, oven and drain cleaners, and heavy industrial cleansers.4 Organic compounds, including phenols (chemical disinfectants) and petroleum products (creosote and gasoline), produce contact burns and systemic toxicity.

Smoke and Inhalation Injury Smoke and inhalation injuries from breathing noxious chemicals or hot air can damage the respiratory tract. Three types of smoke and inhalation injuries can occur: upper airway injury, lower airway injury, and metabolic asphyxiation. Smoke inhalation injuries are a major predictor of mortality in burn patients. Rapid initial and ongoing assessment is critical. Airway compromise and pulmonary edema can quickly develop within hours of injury.5

FIG. 24.1 Types of burn injury. A, Superficial, partial-thickness scald

burn to thigh. B, Deep, partial-thickness flame burn to hand. C, Fullthickness flame burn to posterior chest and arm. Courtesy Judy Knighton, Toronto, Canada.

Metabolic Asphyxiation Most deaths at a fire scene are the result of inhaling certain smoke elements, primarily carbon monoxide (CO) or hydrogen cyanide. Oxygen delivery to or consumption by tissues is impaired, resulting in hypoxia. Death may occur if carboxyhemoglobin (i.e., hemoglobin combined with CO) blood levels are greater than 20%. CO and hydrogen cyanide poisoning may occur in the absence of burn injury to the skin.

Upper Airway Injury Upper airway injury results from an inhalation injury to the mouth, oropharynx, and/or larynx. The injury may be caused by thermal burns or the inhalation of hot air, steam, or smoke. Mucosal burns of the oropharynx and larynx are manifested by redness, blistering, and edema (Table 24.3). The swelling can be massive and the onset rapid. Burns to the neck and chest may make breathing more difficult because of the burn eschar, which becomes tight and constricting. Edema from facial and neck burns can be lethal, as can internal pressure from edema narrowing the airway. Obstruction can occur quickly, presenting a true airway emergency.

Lower Airway Injury An inhalation injury to the trachea, bronchioles, and alveoli is usually caused by breathing in toxic chemicals or smoke. Tissue damage is related to the duration of exposure to toxic fumes or smoke. Manifestations of lower airway lung injury are outlined in Table 24.3. Carefully assess the patient for facial burns, singed nasal hair, hoarseness, painful swallowing, darkened oral and nasal membranes, carbonaceous sputum, history of being burned in an enclosed space, and clothing burns around the neck and chest. Pulmonary edema may

not appear until 12 to 48 hours after the burn. Then it may manifest as acute respiratory distress syndrome (ARDS) (see Chapter 67).

Electrical Burns Electrical burns result from intense heat generated from an electric current. Direct damage to nerves and vessels, causing tissue anoxia and death, can occur. The severity of an electrical injury depends on the amount of voltage, tissue resistance, current pathways, surface area in contact with the current, and length of time that the current flow was sustained (Fig. 24.2). Tissue densities offer various amounts of resistance to electric current. For example, fat and bone offer the most resistance. Nerves and blood vessels offer the least resistance. Current that passes through vital organs (e.g., brain, heart, kidneys) produces more life-threatening sequelae than that which passes through other tissues. In addition, electric sparks may ignite the patient’s clothing, causing a flash injury.

TABLE 24.3 Manifestations of Burn-Related Lung

Injury

Upper Airway • Blisters, edema • Copious secretions • Difficulty swallowing • Hoarseness • Stridor • Substernal and intercostal retractions • Total airway obstruction

Lower Airway

• High degree of suspicion if patient was trapped in a fire in an enclosed space or clothing caught fire • Altered mental status • Carbonaceous sputum • Dyspnea • Facial burns or singed nasal or facial hair • Hoarseness • Wheezing As with inhalation injury, perform a rapid assessment of the patient with an electrical injury. Transfer to a burn center is indicated. The severity of an electrical injury can be hard to determine since most of the damage is below the skin. Determining the electric current contact points and history of the injury may help reveal the likely path of the current and potential areas of injury. Contact with electric current can cause muscle contractions strong enough to fracture the long bones and vertebrae. Another reason to suspect long bone or spinal fractures is a fall resulting from the electrical injury. For this reason, consider cervical spine injury for all patients with electrical burns. Continue cervical spine immobilization during transport and diagnostic testing until injury is ruled out. Electrical injury puts the patient at risk for dysrhythmias or cardiac arrest, severe metabolic acidosis, and myoglobinuria.6 The electric shock can cause immediate heart standstill or ventricular fibrillation. Delayed dysrhythmias or arrest can occur without warning during the first 24 hours after injury. Whenever massive muscle and blood vessel damage occurs, myoglobin from injured muscle and hemoglobin from damaged red blood cells (RBCs) are released into the circulation. The myoglobin travels to the kidneys and can block the renal tubules. This can result in acute tubular necrosis (ATN) and acute kidney injury (see Chapter 46).

FIG. 24.2 Electrical injury produces heat coagulation of blood supply

and contact area as electric current passes through the skin. A, Back and buttock (arrows). B, Leg (arrow). Courtesy Judy Knighton, Toronto, Canada.

Cold Thermal Injury Cold thermal injury, or frostbite, is discussed in Chapter 68.

Classification of Burn Injury The treatment of burns is related to the severity of the injury.7 Severity is determined by (1) depth of burn, (2) extent of burn calculated in percent of total body surface area (TBSA), (3) location of burn, and (4) age of the patient, preburn medical history, and circumstances or complicating factors. The American Burn Association (ABA) uses referral criteria to determine which burn injuries should be treated in burn centers (Table 24.4).8 Patients with minor burn injuries can be managed in community hospitals.

TABLE 24.4 Burn Center Referral Criteria Burn injuries that should be referred to a burn center include the following: 1. Partial thickness burns greater than 10% total body surface area (TBSA) 2. Burns that involve the face, hands, feet, genitalia, perineum, or major joints 3. Third-degree burns in any age-group 4. Electrical burns, including lightning injury 5. Chemical burns 6. Inhalation injury 7. Injury in patients with preexisting medical disorders that could complicate management, prolong recovery, or affect mortality 8. Any patient with burns and concomitant trauma (e.g., fractures)

in which the burn injury poses the greatest risk for morbidity or mortality. In such cases, if the trauma poses the greater immediate risk, the patient may be initially stabilized in a trauma center before being transferred to a burn unit. Physician judgment will be necessary in such situations and should be in concert with the regional medical control plan and triage protocols 9. Burned children in hospitals without qualified personnel or equipment for the care of children 10. Burn injury in patients who will need special social, emotional, or rehabilitative intervention Source: American Burn Association: Guidelines for the operation of burn centers. Retrieved from http://ameriburn.org/wpcontent/uploads/2017/05/burncenterreferralcriteria.pdf.

Depth of Burn Burn injury involves the destruction of the integumentary system. Table 24.5 compares the various burn classifications according to the depth of the burn injury. One system defines an injury by degrees as first, second, third, or fourth degree. The ABA recommends a more precise definition and classifies burns according to depth of skin destruction: partial-thickness burns and full-thickness burns (Fig. 24.3). If significant damage occurs to the dermis (i.e., a full-thickness burn), not enough skin cells remain to regenerate new skin. A permanent, alternative source of skin must be found.

Extent of Burn Two common tools for determining the TBSA affected or the extent of a burn wound are the Lund-Browder chart (Fig. 24.4, A) and the Rule of Nines (Fig. 24.4, B). First-degree burns, equivalent to a sunburn, are not included when calculating TBSA. The Lund-Browder chart is considered more accurate because it considers the patient’s age in

proportion to relative body-area size. The Rule of Nines is often used for initial assessment of a burn patient because it is easy to remember. For irregular- or odd-shaped burns, the patient’s hand (including the fingers) is 1% TBSA. Other tools include the Sage Burn Diagram, a free, Web-based tool for estimating TBSA burned (www.sagediagram.com). There are mobile applications (e.g., 3D Burn Report, Mersey Burns) that can estimate the percent of burn and fluid resuscitation needs.9

Location of Burn The location of the burn injury influences the severity. Burns to the face and neck and circumferential burns to the chest or back may interfere with breathing because of obstruction from edema or leathery, devitalized burn tissue (eschar). These burns may indicate possible smoke or inhalation injury. Burns to the hands, feet, joints, and eyes are of concern because they make self-care difficult and may jeopardize future function. Burns to the hands and feet are challenging to manage because of superficial vascular and nerve supply systems that must be protected while the burn wounds are healing. Burns of the ears and nose are at risk for infection as the skin is very thin and the underlying cartilage may be exposed. Burns to the buttocks or perineum are at high risk for infection from urine or feces contamination. Circumferential burns to the extremities can cause circulation problems distal to the burn, with possible nerve damage to the affected extremity. Patients may develop compartment syndrome (see Chapter 62) from deep damage to muscles.

TABLE 24.5 Classification of Burn Injury Depth

Patient Risk Factors Any patient with preexisting heart, lung, or kidney disease has a poorer prognosis for recovery because of the increased demands placed on the body by a burn injury. The patient with diabetes or peripheral vascular disease is at high risk for delayed healing, especially with foot and leg burns.10 General physical weakness from any chronic disease, including alcohol or drug use and malnutrition, makes it challenging for the patient to fully recover from a burn injury. The burn patient who has fractures, head injuries, or other trauma has a more difficult recovery.

FIG. 24.3 Cross section of skin showing the depth of burn and structures involved.

Prehospital and Emergency Care At the scene of the injury, priority is given to removing the person from the source of the burn and stopping the burning process. Rescuers must protect themselves from being injured. In the case of electrical and chemical injuries, initial care involves removing the patient from contact with the electrical or chemical source. Small thermal burns (10% or less of TBSA) should be covered with a clean, cool, tap water–dampened towel for the patient’s comfort and protection until medical care is available. Cooling of the injured area

(if small) within 1 minute helps minimize the depth of the injury. If the burn is large (greater than 10% TBSA) or an electrical or inhalation burn is suspected, and the patient is unresponsive, first focus your attention on CAB: • Circulation: Check for presence of pulses and elevate the burned limb(s) above the heart to decrease pain and swelling. • Airway: Check for patency, soot around nares and on the tongue, singed nasal hair, darkened oral or nasal membranes. • Breathing: Check for adequacy of ventilation. If the patient is responsive, your priorities would follow the order of the ABCs: airway, breathing, and circulation. To prevent hypothermia, cool large burns for no more than 10 minutes. Do not immerse the burned body part in cool water because it may cause extensive heat loss. Never cover a burn with ice, since this can cause hypothermia and vasoconstriction of blood vessels, thus further reducing blood flow to the injury. Gently remove as much burned clothing as possible to prevent further tissue damage. Leave adherent clothing in place until the patient is transferred to a hospital. Wrap the patient in a dry, clean sheet or blanket to prevent further contamination of the wound and provide warmth. Chemical burns are best treated by quickly removing any chemical particles or powder from the skin. Remove all clothing containing the chemical because the burning process continues while the chemical is in contact with the skin. Flush the affected area with copious amounts of water to irrigate the skin from 20 minutes to 2 hours after exposure. Tap water is acceptable for flushing eyes exposed to chemicals. Tissue destruction may continue for up to 72 hours after contact with some chemicals.

FIG. 24.4 A, Lund-Browder chart. By convention, areas of partialthickness injury are colored in blue and areas of full-thickness injury in red. Superficial partial-thickness burns are not calculated. B, Rule of Nines chart.

Watch patients with inhalation injuries closely for signs of respiratory distress. These patients need to be treated quickly and efficiently if they are to survive. If CO poisoning is suspected, treat the patient with 100% humidified O2. Patients who have both burns and an inhalation injury must be transferred to the nearest burn center. Always remember that the burn patient may have sustained other injuries that could take priority over the burn itself. Persons involved in the prehospital phase of burn care must fully share the circumstances of the injury to emergency department (ED) staff. This is especially important if the patient was trapped in a closed space, exposed to hazardous chemicals or electricity, or had a possible traumatic injury (e.g., fall). Prehospital and emergency care are outlined in tables that describe thermal burns (Table 24.6), inhalation injury (Table 24.7), electrical burns (Table 24.8), and chemical burns (Table 24.9).

Phases of Burn Management Burn management can be organized chronologically into 3 phases: emergent (resuscitative), acute (wound healing), and rehabilitative

(restorative). Overlap in care does exist. For example, the emergent phase begins at the time of the burn injury, and care often begins prehospital or in the ED. Wound care is the primary focus of the acute phase, but wound care takes place in both the emergent and rehabilitation phases. Planning for rehabilitation begins on the day of the burn injury or admission to the burn center. Formal rehabilitation begins as soon as functional assessments can be done.

Emergent Phase The emergent (resuscitative) phase is the time needed to resolve the immediate, life-threatening problems resulting from the burn injury. This phase usually lasts up to 72 hours from the time the burn occurred. The main concerns are the onset of hypovolemic shock and edema formation. The emergent phase ends when fluid mobilization and diuresis begin.

Pathophysiology Fluid and Electrolyte Shifts The greatest initial threat to a patient with a major burn is hypovolemic shock (Fig. 24.5). It is caused by a massive shift of fluids out of the blood vessels because of increased capillary permeability and can begin as early as 20 minutes after the burn. As the capillary walls become more permeable, water, sodium, and plasma proteins (especially albumin) move into the interstitial spaces and other surrounding tissue. The colloidal osmotic pressure decreases with progressive loss of protein from the vascular space. This results in more fluid shifting out of the vascular space into the interstitial spaces (Fig. 24.6).

TABLE 24.6 Emergency ManagementBurns

TBSA, Total body surface area.

TABLE 24.7 Emergency ManagementInhalation

Injury

CO, Carbon monoxide; TBSA, total body surface area.

TABLE 24.8 Emergency ManagementElectrical

Burns

NaHCO3, Sodium bicarbonate; TBSA, total body surface area.

TABLE 24.9 Emergency ManagementChemical

Burns

TBSA, Total body surface area.

FIG. 24.5 At the time of major burn injury, there is increased capillary permeability. All fluid components of the blood begin to leak into the interstitium, causing edema and a decreased blood volume. Hematocrit increases, and the blood becomes more viscous. The combination of decreased blood volume and increased viscosity produces increased peripheral resistance. Burn shock, a type of hypovolemic shock, rapidly ensues and, if not corrected, can result in death.

FIG. 24.6 A, Facial edema before fluid resuscitation. B, Facial edema after 24 hours. Courtesy Judy Knighton, Toronto, Canada.

Fluid moves to areas that normally have minimal to no fluid, a phenomenon termed third spacing. Examples of third spacing in burn injury are exudate and blister formation, as well as edema in unburned areas. Other sources of fluid loss are insensible losses by evaporation from large, denuded body surfaces and the lungs. The normal insensible loss of 30 to 50 mL/hr is higher in the severely burned patient. The net result of the fluid shifts and losses is termed intravascular volume depletion. Signs of hypovolemic shock include decreased BP and increased heart rate. If hypovolemic shock is not corrected, refractory shock and death may result. (Shock is discussed in Chapter 66.) The circulatory system is affected by the hemolysis of RBCs from

circulating factors (e.g., oxygen free radicals) released at the time of the burn and the direct insult of the burn injury. Thrombosis in the capillaries of burned tissue causes loss of more circulating RBCs. A high hematocrit is often caused by hemoconcentration due to fluid loss. After fluid balance is restored, the hematocrit levels return to normal. Major electrolyte shifts of sodium and potassium occur during this phase. A potassium shift develops first because injured cells and hemolyzed RBCs release potassium into the circulation. Sodium rapidly moves to the interstitial spaces and stays there until edema formation ends (Fig. 24.7). Toward the end of the emergent phase, capillary membrane permeability is restored if fluid replacement is adequate. Interstitial fluid gradually returns to the vascular space (Fig. 24.7). Diuresis occurs, and the urine has a low specific gravity.

Inflammation and Healing Burn injury to tissues and vessels causes coagulation necrosis. Neutrophils and monocytes accumulate at the site of injury. Fibroblasts and newly formed collagen fibrils appear and begin wound repair within the first 6 to 12 hours after injury. (The inflammatory response is discussed in Chapter 11.)

Immunologic Changes A burn injury challenges the body’s immune system. The skin barrier to invading organisms is destroyed. Bone marrow depression occurs and circulating levels of immunoglobulins decrease. Defects occur in the function of white blood cells (WBCs). The inflammatory cytokine cascade, triggered by tissue damage, impairs the function of lymphocytes, monocytes, and neutrophils. Thus the patient is at a greater risk for infection.

Clinical Manifestations The patient with severe burns is likely to be in shock from

hypovolemia. Often the areas of full-thickness and deep partialthickness burns are at first painless because the nerve endings have been destroyed. Superficial to moderate partial-thickness burns are very painful. Blisters, filled with fluid and protein, are common in partial-thickness burns. The patient with a larger burn may develop a paralytic ileus, with absent or decreased bowel sounds. Shivering may occur because of chilling that is caused by heat loss, anxiety, or pain.

FIG. 24.7 The effects of burn shock are shown above the purple line. As the capillary seal is lost, interstitial edema develops. Cellular integrity is altered, with sodium (Na) moving into the cell in abnormal amounts and potassium (K) leaving the cell. The shifts after the

resolution of burn shock are shown below the blue line. The water and sodium move back into the circulating volume through the capillary. Albumin stays in the interstitium. Potassium is transported into the cell and sodium is transported out as the cellular integrity returns.

The patient may be alert and able to answer questions shortly after admission or until intubated (if there is respiratory compromise). Patients are often frightened and need your calm reassurances. Give simple explanations of what to expect as you provide care. Unconsciousness or altered mental status in a burn patient usually results from hypoxia associated with smoke inhalation. Other possibilities include head trauma, substance use, or excess amounts of sedation or pain medication.

Complications The three major organ systems most susceptible to complications during the emergent phase of burn injury are the cardiovascular, respiratory, and urinary systems.

Cardiovascular System Cardiovascular complications include dysrhythmias and hypovolemic shock. These, if untreated, may progress to irreversible shock. Circulation to the extremities can be severely impaired by deep circumferential burns and subsequent edema formation, which act like a tourniquet. If untreated, ischemia, paresthesia, and necrosis can occur. An escharotomy (an incision through the full-thickness eschar) is often done to restore circulation to compromised extremities or improve chest expansion (Fig. 24.8). Initially, blood viscosity increases because of the fluid loss. Microcirculation is impaired because of the damage to skin structures that contain small capillary systems. This results in a phenomenon termed sludging. Sludging is corrected by adequate fluid replacement. Burn patients are at an increased risk for venous thromboembolism (VTE) if 1 or more of the following conditions are present: advanced age, obesity, extensive or lower extremity burns, concomitant lower

extremity trauma, and prolonged immobility. VTE prophylaxis with anticoagulant drugs should be started, unless contraindicated.11

Respiratory System The respiratory system is vulnerable to 2 types of injury: (1) upper airway burns and (2) lower airway injury (Table 24.3). Upper airway distress may occur with or without smoke inhalation, and airway injury at either level may occur in the absence of burn injury to the skin. (Smoke and inhalation injuries are discussed earlier in this chapter on pp. 432-433.)

FIG. 24.8 Escharotomies of the anterior and lateral chest and arm (indicated by arrows). Courtesy Judy Knighton, Toronto, Canada.

The patient may need a fiberoptic bronchoscopy and carboxyhemoglobin blood levels to confirm a suspected inhalation injury. Look in the prehospital and ED notes to see if the patient was exposed to smoke or fumes. Examine any sputum for carbon. Watch

for signs of respiratory distress, such as increased agitation, anxiety, restlessness, or a change in the rate or character of the patient’s breathing, as symptoms may not be present at first. In general, there is no correlation between the percentage TBSA burn (% TBSA) and the severity of inhalation injury. In a patient with inhalation injury, a chest x-ray may appear normal on admission, but changes can occur over the next 24 to 48 hours. Arterial blood gas (ABG) values may be within the normal range on admission and change over time.

Other Cardiopulmonary Problems Patients with preexisting heart disease (e.g., myocardial infarction) or lung disease (e.g., chronic obstructive pulmonary disease [COPD]) are at an increased risk for complications. If fluid replacement is too vigorous, watch for early signs of heart failure or pulmonary edema. Invasive measures (e.g., hemodynamic monitoring) may be needed to monitor fluid resuscitation. Patients with preexisting lung disease are more likely to develop a respiratory infection. Pneumonia, a common complication of major burns, is the leading cause of death in patients with an inhalation injury.12

Urinary System The most common complication of the urinary system in the emergent phase is ATN. If your patient becomes hypovolemic, blood flow to the kidneys is decreased, causing renal ischemia. If this continues, acute kidney injury may develop. With full-thickness and major electrical burns, myoglobin (from muscle cell breakdown) and hemoglobin (from RBC breakdown) are released into the bloodstream and block renal tubules. Carefully monitor the adequacy of fluid replacement because this can reverse the obstruction of the tubules.

Nursing and Interprofessional

Management: Emergent Phase In the emergent phase, the patient’s survival depends on rapid and thorough assessment and appropriate interventions. Usually the HCP and you make an initial assessment of the depth and extent of the burn and coordinate the actions of others on the health care team. In a community hospital, determine whether the patient needs inpatient or outpatient care. In the case of inpatient care, decide whether the patient stays at the hospital or must be transferred to a burn center (Table 24.4). Care mainly focuses on airway management, fluid therapy, and wound care (Table 24.10). Patients can improve or worsen, unpredictably. Although physical therapy (PT) and occupational therapy (OT) are important in both the acute and rehabilitation phases, proper positioning and splinting begin on the day of admission. Emotional support and teaching of patients and caregivers begin on admission. A nursing care plan for the patient with burn injury (eNursing Care Plan 24.1) is available on the website for this chapter.

Informatics in Practice Staff Training Using Gaming • Preparing burn center staff for a mass casualty incident involving burn victims is essential. • Interactive, video game–based training modules simulate real-life emergency events surrounding a mass casualty burn incident. • Critical skills for triage and initial resuscitation (emergent phase) for multiple victims can be practiced.13

Airway Management Airway management often involves early endotracheal (preferably

orotracheal) intubation.14 Early intubation removes the need for emergency tracheostomy after respiratory problems have become apparent. In general, the patient with burns to the face and neck needs intubation within 1 to 2 hours after injury. Intubation is discussed in Chapter 65. After intubation, the patient is placed on ventilatory support, with settings based on ABG results. Extubation may occur when the edema resolves. This is usually 3 to 6 days after burn injury unless severe inhalation injury exists. Chest escharotomy may be needed to relieve respiratory distress with circumferential, full-thickness burns of the neck and chest (Fig. 24.8). A fiberoptic bronchoscopy should be done to assess the lower airway within 6 to 12 hours after injury if smoke inhalation is suspected. When intubation is not done, treatment of inhalation injury includes giving 100% humidified O2. Place the patient in a high Fowler’s position, unless contraindicated (e.g., spinal injury). Encourage deep breathing and coughing every hour. Reposition the patient every 1 to 2 hours. Provide suctioning and chest physiotherapy. If severe respiratory distress (e.g., hoarseness, shortness of breath) develops, intubation and mechanical ventilation are started. Positive end-expiratory pressure (PEEP) may be used to prevent collapse of the alveoli and progressive respiratory failure (see Chapters 65 and 67). Bronchodilators may be given to treat severe bronchospasm. CO poisoning is treated by giving 100% O2 until carboxyhemoglobin levels return to normal.

Safety Alert Pulse CO Oximetry Monitoring • Standard pulse oximetry (SpO2) does not distinguish oxyhemoglobin from carboxyhemoglobin.

• A patient with CO poisoning will have normal SpO2 readings despite high carboxyhemoglobin levels. • For patients with suspected or confirmed CO poisoning, use a pulse CO oximetry (SpCO) device.

Fluid Therapy Obtaining IV access is critical for fluid resuscitation and drug administration. At least 2 large-bore IVs must be in place for patients with burns that are 15% TBSA or more. It is critical to obtain IV access that can handle large volumes of fluid. For patients with burns greater than 30% TBSA, consider a central line for fluid and drug administration and blood sampling (central lines are discussed in Chapter 16). An arterial line is often placed if frequent ABGs or invasive BP monitoring is needed. Assess the extent of the burn wound using a standardized tool (Fig. 24.4). Then use a standardized formula to estimate the patient’s fluid resuscitation needs. Fluid replacement is achieved with crystalloid solutions (usually lactated Ringer’s), colloids (albumin), or a combination of the two. IV saline is usually started during the prehospital phase.

TABLE 24.10 Interprofessional CareBurn Injury

The Parkland (Baxter) formula for fluid replacement is the most common formula used (Table 24.11 or www.mdcalc.com/parklandformula-for-burns). Remember that all formulas are estimates. Fluids are titrated based on the patient’s response (e.g., hourly urine output, vital signs). Patients with an electrical injury have greater than normal fluid needs. They generally require an osmotic diuretic (mannitol [Osmitrol]) to increase their urine output and overcome high levels of hemoglobin and myoglobin in the urine. Too much fluid and overestimation of TBSA contribute to over-resuscitation of fluids or “fluid creep.”15 For the first 24 hours, the recommendation is 2 to 4 mL lactated Ringer’s/kg/%TBSA burned.16 Colloidal solutions (e.g., 5% albumin) may be given. However, they are often not started until 12 to 24 hours postburn when capillary permeability returns to normal or near normal. After this time, the plasma stays in the vascular space and expands the circulating volume. The replacement volume is calculated based on the patient’s body weight and TBSA burned (e.g.,

0.3 to 0.5 mL/kg/%TBSA burned). Assess for the adequacy of fluid resuscitation hourly using clinical parameters. Urine output, the most often used parameter, and cardiac parameters are defined as follows: • Urine output: 0.5 to 1 mL/kg/hr; 75 to 100 mL/hr for electrical burn patient with evidence of hemoglobinuria or myoglobinuria. • Cardiac parameters: Mean arterial pressure (MAP) greater than 65 mm Hg, systolic BP greater than 90 mm Hg, heart rate less than 120 beats/min. MAP and BP are best measured by an arterial line. Manual BP measurement is often invalid because of edema and vasoconstriction.

Check Your Practice You are admitting a new burn patient who weighs 72 kg and has 45% TBSA burn. • Outline the patient’s fluid requirements over the first 24 hours.

TABLE 24.11 Fluid Resuscitation Formulas

Parkland (Baxter)∗ 4 mL lactated Ringer’s solution per kilogram (kg) of body weight per percent of total body surface area (% TBSA) burned = Total fluid requirements for first 24 hr after burn

Application 1⁄2 of total in first 8 hr 1⁄4 of total in second 8 hr 1⁄4 of total in third 8 hr

Example For a 70-kg patient with a 50% TBSA burn:

1⁄2 of total in first 8 hr = 7000 mL (875 mL/hr) 1⁄4 of total in second 8 hr = 3500 mL (437 mL/hr) 1⁄4 of total in third 8 hr = 3500 mL (437 mL/hr)

American Burn Association Consensus Fluid Resuscitation 2–4 mL lactated Ringer’s solution per kilogram (kg) of body weight per percent of total body surface area (% TBSA) burned = Total fluid requirements for first 24 hr after burn

Wound Care Once a patent airway, effective circulation, and adequate fluid replacement have been achieved, priority is given to care of the burn wound. Partial-thickness burn wounds appear pink to cherry-red and are wet and shiny with serous exudate. These wounds may or may not have intact blisters; are painful when touched; and have only minor, localized sensation because nerve endings may have been destroyed in the burned dermis. You can perform cleansing and gentle debridement (using scissors and forceps) on a shower cart (Fig. 24.9), in a regular shower, or on a patient’s bed or stretcher. Extensive, surgical debridement is done in the operating room (OR) (Fig. 24.10). During debridement, necrotic

skin is removed. Releasing escharotomies and fasciotomies are done in the emergent phase, usually in burn centers by physicians. Patients find the first wound care to be both physically and mentally demanding. Provide emotional support and begin to build trust during this activity. A once-daily shower and dressing change in the morning, with an evening dressing change in the patient’s room, are part of the routine in many burn centers. Others opt to shower the patient on admission and then perform all other dressing changes in the patient’s room. Some of the newer antimicrobial dressings can be left in place from 3 to 14 days, reducing the frequency of dressing changes. Infection can cause further tissue injury and possible sepsis. The source of infection in burn wounds is likely the patient’s own flora, mostly from the skin, respiratory, and gastrointestinal (GI) systems. Two approaches to burn wound treatment are (1) the open method and (2) the use of multiple dressing changes (closed method). In the open method the patient’s burn is covered with a topical antimicrobial and has no dressing over the wound. This approach is usually limited to the care of facial burns. In the multiple dressing change, or closed method, sterile gauze dressings are impregnated with or laid over a topical antimicrobial (Fig. 24.11). These dressings are changed from every 12 hours to once every 14 days depending on the product. Most burn centers use the closed technique.

FIG. 24.9 Shower cart. Showering presents an opportunity for PT and wound care. Courtesy Judy Knighton, Toronto, Canada.

FIG. 24.10 Surgical debridement of full-thickness burns is necessary to prepare the wound for grafting. Courtesy Judy Knighton, Toronto, Canada.

FIG. 24.11 Application of silver sulfadiazine cream to salinemoistened gauze. Courtesy Judy Knighton, Toronto, Canada.

When the patient’s open burn wounds are exposed, always wear personal protective equipment (PPE) (e.g., disposable hats, masks, gowns, gloves). When removing contaminated dressings and washing wounds, use nonsterile, disposable gloves. Use sterile gloves when applying ointments and sterile dressings. In addition, prevent shivering by keeping the room warm (around 85°F [29.4°C]). Before leaving one patient, remove your PPE and wash your hands. Don new PPE before you treat another patient.

TABLE 24.12 Skin Grafts Used for Burn Injury

Permanent skin coverage is the primary goal for burn wound care. There is rarely enough unburned skin in the major (greater than 50% TBSA) burn patient for immediate skin grafting. In this situation, temporary wound closure methods are needed. Allograft (homograft) skin (from skin donor cadavers) is used, along with newer biosynthetic options. Treatment approaches vary among burn centers (Table 24.12).

Other Care Measures Certain parts of the body (e.g., face, eyes, hands, arms, ears, perineum) need vigilant nursing care. The face is highly vascular and can become very swollen. It is often covered with ointments and gauze but not wrapped to limit pressure on delicate facial structures. An eye exam should occur soon after admission for all patients with facial burns. Periorbital edema can temporarily prevent eye opening and is often frightening for the patient. Always check that the patient’s eyelashes are not turned inward toward the eyeball. Provide assurance that the swelling is not permanent. Instill methylcellulose drops or artificial tears into the eyes for moisture and comfort. Apply antibiotic eye ointment for corneal burns or edema as ordered. Keep the ears free from pressure because of their poor vascularization and tendency to become infected. Do not use pillows for the patient with ear burns. The pressure on the cartilage may cause

chondritis. Also, the ear may stick to the pillowcase, causing pain and bleeding. Raise the patient’s head using a rolled towel placed under the shoulders, being careful to avoid pressure necrosis. Follow the same strategy for the patient with neck burns to hyperextend the neck and prevent neck contracture. Extend burned hands and arms and raise them on pillows or plastic-covered foam wedges to reduce edema. Ask the physical therapist (PT) and the HCP if splints should be applied to burned hands and feet to keep them in positions of function. Remove the splints often and inspect the skin and bony prominences to avoid areas of pressure from inappropriate or prolonged application. Elastic wraps may reduce edema. Keep your patient’s perineum as clean and dry as possible after each voiding or bowel movement. In addition to monitoring hourly urine outputs, an indwelling catheter prevents urine contamination of the perineal area. Regular once- or twice-daily perineal care is essential. Assess the need for an indwelling urinary catheter daily. Remove when it is no longer needed to limit the risk for a urinary tract infection. If your patient has frequent, loose stools, consider using a fecal diversion device. Perform laboratory tests to monitor fluid and electrolyte balance. Draw ABGs to assess adequacy of ventilation and oxygenation in patients with suspected or confirmed inhalation or electrical injury. Work with PT to perform range-of-motion (ROM) exercises during dressing changes and throughout the day. Movement aids the shift of the interstitial fluid back into the vascular bed. Active and passive exercise also maintains function and prevents skin and joint contractures. It may reassure the patient that movement is still possible.

Drug Therapy Analgesics and Sedatives Promote the use of analgesics for the patient’s comfort. Early in the postburn period, IV pain medications should be given because (1)

onset of action is fastest with this route; (2) oral drugs have a slower onset of action and are not as effective when GI function is slowed or impaired because of shock or paralytic ileus; and (3) IM injections are not absorbed well in burned or edematous areas, causing pooling of drugs in the tissues. Consequently, when fluid mobilization starts, the patient could be inadvertently overdosed from the interstitial accumulation of previous IM drugs. Common drugs used for pain control are listed in Table 24.13. Opioids are the drug of choice for severe pain. When given appropriately, these drugs should provide adequate pain relief. Evaluate the pain management plan often since the patient’s needs may change and tolerance to drugs may develop over time. Remember that the patient’s pain level may not directly correlate with the extent and depth of burn. Analgesic needs vary from one patient to another. Consider a multimodal approach to pain control. Sedatives/hypnotics and antidepressants can be given with analgesics to control the anxiety, insomnia, or depression that patients may have (Table 24.13).

Tetanus Immunization All burn patients routinely receive tetanus toxoid because of the risk for anaerobic burn wound contamination. If the patient has not received an active immunization within 10 years before the burn injury, tetanus immunoglobulin should be considered. (Tetanus immunization is discussed in Table 68.6.)

TABLE 24.13 Drug TherapyBurns

Antimicrobial Agents After the wound is cleansed, topical antimicrobial agents may be applied (Fig. 24.11) and covered with a light dressing. Systemic antibiotics are not routinely used to control burn wound flora because the burn eschar has little or no blood supply, so little antibiotic is delivered to the wound. In addition, the routine use of systemic antibiotics increases the chance of developing multidrug-resistant organisms. Some topical burn agents penetrate the eschar and inhibit bacterial invasion of the wound. Silver-impregnated dressings can be left in place from 3 to 14 days, depending on the patient’s clinical situation and the product. Silver sulfadiazine (Silvadene) and mafenide acetate (Sulfamylon) creams are also used.17

Safety Alert Drug Allergy Check • Check the patient for any allergies to sulfa since many burn antimicrobial creams contain sulfa. Sepsis is a leading cause of death in the patient with major burns and may lead to multiple organ dysfunction syndrome (see Chapter 66). Systemic antibiotic therapy is started when the diagnosis of sepsis is made or when some other source of infection is identified (e.g., pneumonia). Fungal infections may develop in the patient’s mucous membranes (mouth and genitalia) because of systemic antibiotic therapy and low resistance. The offending organism is usually Candida albicans. Oral infection is treated with nystatin (Mycostatin) mouthwash. When a normal diet is resumed, yogurt or Lactobacillus (Lactinex) may be given to reintroduce the normal intestinal flora that was destroyed by antibiotic therapy.

Venous Thromboembolism Prophylaxis Burn patients are at risk for VTE. If there are no contraindications, it is recommended that low-molecular-weight heparin (enoxaparin) or low-dose unfractionated heparin be started as soon as it is considered safe. For burn patients who have a high bleeding risk, VTE prophylaxis with intermittent pneumatic compression devices and/or graduated compression stockings is used until the bleeding risk decreases and heparin can be started (Table 24.13). (VTE prophylaxis is discussed in Chapter 37.)

Nutritional Therapy Once fluid replacement needs have been addressed, nutrition takes priority in the initial emergent phase. Early and aggressive nutritional support within several hours of the burn injury can decrease

complications and mortality, optimize burn wound healing, and minimize the negative effects of hypermetabolism and catabolism.18 Nonintubated patients with a burn of less than 20% TBSA will usually be able to eat enough to meet their nutritional needs. Intubated patients and those with larger burns need more support. Enteral feedings have almost entirely replaced parenteral feeding. Early enteral feeding, usually with smaller bore tubes, preserves GI function, increases intestinal blood flow, and promotes optimal conditions for wound healing. In general, begin the feedings slowly at a rate of 20 to 40 mL/hr and increase to the goal rate within 24 to 48 hours. If a large nasogastric tube is used, gastric residuals should be checked to rule out delayed gastric emptying. Assess bowel sounds every 8 hours. A hypermetabolic state proportional to the size of the wound occurs after a major burn injury. Resting metabolic expenditure may be increased by 50% to 100% above normal in patients with major burns. Core temperature is increased. Catecholamines, which stimulate catabolism and heat production, are increased. Massive catabolism can occur and is characterized by protein breakdown and increased gluconeogenesis. Failure to supply adequate calories and protein leads to malnutrition and delayed healing. Calorie-containing nutritional supplements are often given to meet the caloric needs.19 Protein powder can be added to food and liquids. Supplemental vitamins may be started in the emergent phase, with iron supplements often given in the acute phase (Table 24.13).

Acute Phase The acute phase of burn care begins with the mobilization of extracellular fluid and subsequent diuresis. It ends when partialthickness wounds are healed or full-thickness burns are covered by skin grafts. This may take weeks or months.

Pathophysiology A healing burn injury causes many pathophysiologic changes in the body. Diuresis from fluid mobilization occurs, and the patient is less edematous. Bowel sounds return. The depth of the burn wounds may be more apparent as they “declare” themselves as partial or full thickness. The patient may now become more aware of the enormity of the situation and will benefit from emotional support and information. Some healing begins as WBCs surround the burn wound and phagocytosis occurs. Necrotic tissue begins to slough. Fibroblasts lay down matrices of the collagen precursors that eventually form granulation tissue. A partial-thickness burn will heal, from both the wound edges and the dermal bed below, if kept free from infection and desiccation (dryness). However, full-thickness burn wounds, unless extremely small, must have the burn eschar surgically removed (excised) and skin grafts applied to heal. In some cases, healing time and length of hospitalization are decreased by early excision and grafting.

Clinical Manifestations Partial-thickness wounds form eschar, which begins separating soon after injury. Once the eschar is removed, re-epithelialization begins at the wound margins and appears as red or pink scar tissue. Epithelial buds, from the hair follicles and glands in the dermal bed, eventually close the wound. Healing is spontaneous and usually occurs within 10 to 21 days. Margins of full-thickness eschar take longer to separate. As a result, full-thickness burn wounds require surgical debridement and skin grafting to heal.

Laboratory Values Because the body is trying to reestablish fluid and electrolyte balance in the initial acute phase, it is important to follow serum electrolyte

levels closely.

Sodium Hyponatremia can develop from excess GI suction and diarrhea. Manifestations include headache, irritability, confusion, vomiting, seizures, and even coma. The patient may develop, dilutional hyponatremia, called water intoxication, from excess water intake. To avoid this condition, offer the patient fluids other than water, such as juice or nutritional supplements. Hypernatremia may occur after successful fluid resuscitation if large amounts of hypertonic solutions were used. Hypernatremia also may be caused by tube feedings or inappropriate fluid administration. Manifestations include changes in mental status, ranging from drowsiness, restlessness, confusion, and lethargy to seizures and coma. Sodium restrictions may be applied to IV fluids and enteral or oral feedings until levels return to safe limits.

Potassium Hyperkalemia may occur if the patient has renal failure, adrenocortical insufficiency, or massive deep muscle injury (e.g., electrical burn). Large amounts of potassium are released from damaged cells. Dysrhythmias and arrest can occur with high potassium levels. The patient may have confusion, tetany, muscle cramps, paresthesias, and weakness. Hypokalemia occurs with vomiting, diarrhea, prolonged GI suction, and IV therapy without potassium supplementation. Potassium is also lost through the patient’s burn wounds. Besides dysrhythmias, the patient may have muscle weakness, paresthesia, decreased GI motility, and decreased reflexes (see Chapter 16).

Complications Infection A burn injury destroys the body’s first line of defense, the skin. The burn wound is now colonized with the person’s own organisms that

were on the skin before the burn. The WBCs have functional defects, and the patient is immunosuppressed for many months after the burn injury. If the levels of bacteria between the eschar and viable wound bed rise to greater than 105 per gram of tissue, the patient has a burn wound infection. Infection can convert partial-thickness burns to fullthickness wounds. Wound infections may be treated with systemic and local antibiotics based on wound culture and sensitivity results. Localized inflammation, induration, and sometimes pus can be seen at the burn wound margins. Watch for signs and symptoms of infection, including hypothermia or hyperthermia, increased heart and respiratory rate, decreased BP, and decreased urine output. The patient may have mild confusion, chills, malaise, and loss of appetite. The WBC count is between 10,000/µL (10 × 109/L) and 20,000/µL (20 × 109/L). The causative organisms of sepsis are usually gram-negative bacteria (e.g., Pseudomonas, Proteus), putting the patient at further risk for septic shock. If sepsis is suspected, obtain cultures from all possible sources, including the burn wound, blood, urine, sputum, oropharynx and perineal regions, and IV site. A lactate level is collected. Treatment begins with a bolus of normal saline IV and antibiotics.20 Antibiotic therapy may be continued or changed based on the culture and sensitivity results. At this stage, the patient’s condition is considered critical. Close monitoring of vital signs and mental status is needed.

Cardiovascular and Respiratory Systems The same cardiovascular and respiratory complications present in the emergent phase continue into the acute phase of care. In addition, new problems might arise, requiring prompt intervention.

Neurologic System Neurologically, the patient probably has no physical symptoms, unless severe hypoxia from respiratory injuries or complications from

electrical injuries occur. Probable causes of neurologic complications include electrolyte imbalance, stress, cerebral edema, sepsis, sleep problems, and the use of analgesics and antianxiety drugs. Some patients may have certain behaviors that are not completely understood. The patient may become extremely disoriented, withdraw or become combative, hallucinate, or have frequent nightmare-like episodes. Delirium is more acute at night and occurs more often in the older patient. Start appropriate nursing interventions to prevent delirium and use a screening tool to diagnose delirium (see Table 59.18). Orient and reassure a patient who is confused or agitated. This state is usually transient, lasting from a day or two to several weeks, but complications and sequelae can last for years and be serious.

Musculoskeletal System The musculoskeletal system is particularly prone to complications during the acute phase. The involvement of both PT and OT is vitally important. As the burns begin to heal and scar tissue forms, the skin is less supple and pliant. ROM may be limited, and skin and joint contractures can occur. Because of pain, the patient prefers a flexed position for comfort. Have the patient stretch and move the burned body parts as much as possible. Consult with PT or OT about proper positioning and splinting to prevent or reduce contracture formation.

Gastrointestinal System The GI system may develop complications during this phase. Sepsis can cause paralytic ileus. Diarrhea may result from the use of enteral feedings or antibiotics. Constipation can occur as a side effect of opioids, decreased mobility, and a low-fiber diet. Curling’s ulcer is a type of gastroduodenal ulcer characterized by diffuse superficial lesions (including mucosal erosion). It is caused by a generalized stress response to decreased blood flow to the GI tract. The patient has increased gastric acid secretion. Aim to prevent Curling’s ulcer by feeding the patient as soon as possible after the burn injury. Antacids, H2-histamine blockers (e.g.,

ranitidine), and proton pump inhibitors (e.g., omeprazole) are used prophylactically to neutralize stomach acids and inhibit histamine and the secretion of hydrochloric acid (Table 24.13). Patients with major burns may have occult blood in their stools during the acute phase and require close monitoring for bleeding.

Endocrine System Watch for transient increases in the patient’s blood glucose levels because of stress-mediated cortisol and catecholamine release. There is an increased mobilization of glycogen stores and gluconeogenesis. Subsequently, glucose is produced, along with an increase in insulin production. However, insulin’s effectiveness is decreased because of relative insulin insensitivity. This results in a high blood glucose level. Hyperglycemia also may be caused by the increased caloric intake needed to meet some patients’ metabolic requirements. When hyperglycemia occurs, check blood glucose levels and give insulin as ordered. Point-of-care testing of glucose can be done, but serum glucose testing is more accurate. As the patient’s metabolic demands are met and less stress is placed on the entire system, this stressinduced condition is reversed.

Nursing and Interprofessional Management: Acute Phase The major therapeutic interventions in the acute phase are (1) wound care, (2) excision and grafting, (3) pain management, (4) PT and OT, and (5) nutritional therapy.

Wound Care The goals of wound care are to (1) prevent infection by cleansing and debriding the area of necrotic tissue that would promote bacterial growth and (2) promote wound re-epithelialization and/or successful skin grafting.

Wound care consists of ongoing observation, assessment, cleansing, debridement, and dressing reapplication. Nonsurgical debridement, dressing changes, topical antimicrobial therapy, graft care, and donor site care are done as often as needed, depending on the topical cream or dressing ordered. Enzymatic debriding agents made of natural ingredients, such as collagenase, may be used for enzymatic debridement of burn wounds, which speeds up the removal of dead tissue from the healthy wound bed. Cleanse wounds with soap and water or normal saline-moistened gauze to gently remove the old antimicrobial agent and any loose necrotic tissue, scabs, or dried blood. During the debridement phase, cover the wound with topical antimicrobial creams (e.g., silver sulfadiazine) or silver-impregnated dressings. When the partialthickness burn wounds have been fully debrided, a protective, coarse or fine-meshed, greasy-based (paraffin, petrolatum) gauze dressing is applied to protect the re-epithelializing keratinocytes as they resurface and close the open wound bed. If grafting is done, protect the skin graft (discussed later) with the same greasy gauze dressings next to the graft, followed by salinemoistened middle dressing and dry gauze outer dressings. With facial grafts, the unmeshed sheet graft is left open, so it is possible for blebs (serosanguineous exudate) to form between the graft and recipient bed. Blebs prevent the graft from permanently attaching to the wound bed. The evacuation of blebs is best done by aspiration with a tuberculin syringe and only by those trained in this specialized skill. (Dressings are discussed in Table 11.9.)

Excision and Grafting Management of full-thickness burn wounds involves early removal (surgical excision) of the necrotic tissue, followed by application of split-thickness autograft skin.21 This approach has improved the management and survival rate of burn patients. In the past, patients with major burns had low rates of survival because healing and wound coverage took so long that the patient usually died of sepsis or

malnutrition. Many patients, especially those with major burns, are taken to the OR for wound excision on day 1 or 2 (emergent phase). The wounds are covered with a biologic dressing or allograft for temporary coverage until permanent grafting can occur (Table 24.12). During the procedure of excision and grafting, devitalized tissue (eschar) is excised down to the subcutaneous tissue or fascia, depending on the degree of injury. Surgical excision can result in massive blood loss. To decrease surgical blood loss, topical application of epinephrine or thrombin, injection of saline and epinephrine, application of extremity tourniquets, or application of a fibrin sealant (Artiss) is used. Once hemostasis has been achieved, a graft is then placed on clean, viable tissue to achieve good adherence. Whenever possible, the freshly excised wound is covered with autograft (the person’s own) skin (Table 24.12). Recently, fibrin sealant has been used to attach skin grafts to the wound bed. Grafts also can be stapled or sutured into place (Fig. 24.12, A). Negative pressure wound therapy dressings are often placed on top of skin grafts to optimize adherence of the graft to the excised wound bed.22 A temporary allograft can be used to test the suitability of the recipient site to accept a graft. The allograft is then removed several days later in the OR and an autograft applied. With early excision, function is restored, and scar tissue formation is minimized. Clots between the graft and wound keep the graft from adhering to the wound. Outer occlusive dressings apply just enough pressure to promote adherence of the graft to the wound bed and help control bleeding. Protect the grafted area from shearing, friction, and pressure. Facial, neck, and hand burns require skilled nursing care to identify and manage clots quickly for the best functional and aesthetic outcomes. Donor skin is taken from the patient for grafting by means of a dermatome, which removes a thin split-thickness layer of skin from an unburned site (Fig. 24.12, B). The donor skin can be meshed to allow for greater wound coverage, or it may be applied as an unmeshed sheet for a better cosmetic result when grafting the face, neck, and

hands. The donor site now becomes a new open wound. The goals of donor site care are to promote rapid, moist wound healing; decrease pain at the site; and prevent infection. The choices of dressings for donor sites include transparent dressings (e.g., OpSite), xenograft, silver sulfadiazine, silver-impregnated dressings, calcium alginate, and hydrophilic foam dressings (Fig. 24.12, C). Nursing care of the donor site is specific to the dressing used. Several of the newer dressings decrease healing time, which allows earlier reharvesting of skin at the same site. The average healing time for a donor site is 10 to 14 days (Fig. 24.12, D).

Cultured Epithelial Autografts In the patient with large body burns, only a limited amount of unburned skin may be available as donor sites for grafting, and some of that skin may not be suitable for harvesting. Cultured epithelial autograft (CEA) is a method of getting permanent skin from a person with limited skin available for harvesting. CEA is grown from biopsy samples obtained from the patient’s unburned skin. This procedure is done in suitable patients in some burn centers as soon as possible. The specimens are sent to a commercial laboratory, where the biopsied keratinocytes are grown in a culture medium containing epidermal growth factor. After about 18 to 25 days, the keratinocytes have expanded up to 10,000 times and form sheets that we can use as skin grafts. The cultured skin is returned to the burn center, where it is placed on the patient’s excised burn wounds (Fig. 24.13, A). CEA grafts generally form a seamless, smooth replacement skin tissue (Fig. 24.13, B). Problems related to CEA include a poor graft take because of thin epidermal skin, graft loss during healing, infection, and contracture development.

FIG. 24.12 A, Freshly applied split-thickness sheet skin graft to the hand. B, Split-thickness skin graft is harvested from a patient’s thigh using a dermatome. C, Donor site is covered with a hydrophilic foam dressing after harvesting. D, Healed donor site. Courtesy Judy Knighton, Toronto, Canada.

FIG. 24.13 Patient with cultured epithelial autograft (CEA). A, Intraoperative application of CEA. B, Appearance of healed CEA.

Dermal Substitutes Dermal substitutes act as a synthetic dermis and are covered by skin graft.23 The Integra artificial skin dermal regeneration template is an example of a skin replacement system. As with CEA, it is used in the treatment of life-threatening full-thickness or deep partial-thickness burn wounds when a conventional autograft is not available or advisable, as in older or high anesthetic-risk patients. It also has been successfully used in reconstructive burn surgery procedures. It must be applied within a few days postburn for greatest success. Integra artificial skin has a bilayer membrane composed of acellular dermis and silicone. The wound is excised, the bilayer membrane is placed dermal layer down, and the wound is wrapped with dressings in the OR. The dermal layer functions as a biodegradable template that induces organized regeneration of new dermis by the body. The silicone layer stays intact for 3 weeks as the dermal layer degrades, and epidermal autografts become available. At this point, the silicone is removed during a second surgery and replaced by the patient’s own epidermal autografts. Another dermal replacement is AlloDerm, a cryopreserved allogenic dermis. Human allograft dermis, harvested from cadavers, is decellularized to make it immunogenic and then freeze-dried. Once thawed, AlloDerm is rehydrated in normal saline immediately before placement on a freshly excised wound.

Pain Management Many aspects of burn care cause pain. Eliminating all pain is difficult, but most patients will have acceptable levels of relative comfort if they receive adequate analgesia. To provide effective pain management, you must understand both the physiologic and psychologic aspects of pain. Pain management is discussed in Chapter 8. Burn patients have 2 kinds of pain: (1) continuous, background pain that might be present throughout the day and night; and (2) treatmentinduced pain associated with dressing changes, ambulation, and

rehabilitation activities. The first line of pain treatment is drugs (Table 24.13). With background pain, frequent IV administration of an opioid (e.g., hydromorphone [Dilaudid]) provides a steady, therapeutic level of the drug. If tolerating food, slow-release, twice-daily opioids (e.g., morphine [MS Contin]) can be used. Patient-controlled analgesia (PCA) is used in some burn centers, with varying degrees of success. Anxiolytics (e.g., lorazepam [Ativan], midazolam) and adjuvant analgesics (e.g., gabapentin [Neurontin], pregabalin [Lyrica]), can enhance opioids. The use of these drugs can help reduce the opioid dosage and undesirable side effects. Breakthrough doses of analgesia must be available regardless of the regimen used. Additional doses of opioids are usually given. For treatment-induced pain, premedicate with an analgesic, and possibly an anxiolytic, via the IV or oral route. For patients with an IV, a shortacting analgesic is often used.

Check Your Practice Your patient with a burn injury is ordered fentanyl (Sublimaze) before a dressing change. The patient has multiple IV lines, and you are not sure which line to use to insert the drug. You know that mixing up IV lines can lead to serious drug errors. • How would you determine which IV line to use to give the drug? Some pain can be managed using nondrug strategies. Relaxation breathing, guided imagery, hypnosis, biofeedback, computerized gaming, and music therapy can help patients cope with pain (see Chapter 6).24 Remember, the more control the patient has in managing pain, the more successful the chosen strategies will be. Active participation in asking for time-outs and scheduling treatments and rest periods can help the patient manage feelings of anticipatory pain.

Physical and Occupational Therapy Continuous PT throughout burn recovery is imperative if the patient is to regain and maintain muscle strength and optimal joint function. A good time for exercise is during dressing changes, when bulky dressings are removed and patients are medicated for pain. Passive and active ROM should be performed on all joints. PT and OT may join the nurse and patient during dressing changes. Ensure that the patient with neck burns continues to sleep without pillows or with the head hanging slightly over the top of the mattress to encourage hyperextension. Maintain the OT schedule for wearing custom-fitted splints, which are designed to keep joints in functional position. Check the splints often to ensure an optimal fit, with no undue pressure that may lead to skin breakdown or nerve damage.

Nutritional Therapy The goal of nutritional therapy during the acute burn phase is to provide adequate calories and protein to promote healing. When the wounds are still open, the burn patient is in a hypermetabolic and catabolic state. The patient may benefit from an antioxidant protocol, which includes selenium, vitamin E, acetylcysteine, ascorbic acid, zinc, and a multivitamin. Meeting daily caloric requirements is crucial and should start within the first 1 to 2 days postburn. The daily estimated caloric needs must be regularly calculated by a dietitian and readjusted as the patient’s condition changes (e.g., wound healing improves, sepsis develops). Monitor laboratory values (e.g., albumin, prealbumin, total protein, transferrin) on a regular basis. If the patient is on mechanical ventilation or unable to eat enough calories by mouth, a small-bore feeding tube is placed, and enteral feedings are started. When the patient is extubated, contact the speech pathologist for a swallowing assessment before an oral diet is started. Encourage the patient to eat high-protein, high-carbohydrate foods to meet caloric goals. Ask caregivers to bring in favorite foods from

home. Appetite is usually reduced, and you will need to reinforce whatever steps are taken to achieve adequate intake. Ideally, weight loss should not be more than 10% of preburn weight. Record the patient’s daily caloric intake using calorie count sheets, which are reviewed by the dietitian. Weigh your patient weekly to evaluate progress.

Rehabilitation Phase The formal rehabilitation phase begins when the patient’s wounds have nearly healed and they are engaging in some level of self-care. This may happen as early as 2 weeks or as long as 7 to 8 months after a major burn injury. Goals for the patient now are to (1) work toward resuming a functional role in society and (2) rehabilitate from any functional and cosmetic postburn reconstructive surgery that may be needed.

Pathophysiologic Changes and Clinical Manifestations Burn wounds heal by either spontaneous re-epithelialization or skin grafting. Layers of keratinocytes begin rebuilding the tissue structure destroyed by the burn injury. Collagen fibers, present in the new scar tissue, help with healing and add strength to weakened areas. The new skin appears flat and pink. In about 4 to 6 weeks, the area becomes raised and hyperemic. If adequate ROM is not started, the new tissue will shorten, causing a contracture. Mature healing is reached in about 12 months, when suppleness has returned and the pink or red color has faded to a slightly lighter hue than the surrounding unburned tissue. Tell patients who have more heavily pigmented skin that it will take longer for it to regain its color because many of the melanocytes have been destroyed. Often, the skin does not regain its original color, though this is impossible to predict. Provide teaching and emotional support to help the patient with grieving about these changes to his or

her body. Cosmetic camouflage, the implantation of pigment within the skin, can help even out unequal skin tones and improve the patient’s overall appearance and self-image. Scarring has 2 characteristics: discoloration and contour. The discoloration of scars fades somewhat with time. However, scar tissue tends to develop altered contours. That is, it is no longer flat or slightly raised but becomes elevated and enlarged above the original burned area. Some burn care providers think that pressure can eventually help keep a scar flat. Gentle pressure is maintained on the healed burn with custom-fitted pressure garments and clear, thermoplastic face masks. Pressure garments and masks should never be worn over unhealed wounds. Once a wearing schedule has been set, they are removed only for short periods while bathing. Pressure garments are worn up to 23 hours a day for as long as 12 to 18 months. The patient typically reports discomfort from itching where healing is occurring. Teach your patient about the application of water-based moisturizers and selective, short-term use of oral antihistamines (e.g., hydroxyzine [Atarax]) to help reduce the itching. Massage, cooling, emollients, gabapentin, antidepressants, and anesthetic creams also may help.25 As “old” epithelium is replaced by new cells, flaking occurs. The newly formed skin is extremely sensitive to trauma. Blisters and skin tears are likely to develop from slight pressure or friction. These newly healed areas can be hypersensitive or hyposensitive to cold, heat, and touch. Grafted areas are more likely to be hyposensitive until peripheral nerve regeneration occurs. Have patients protect healed burn areas from direct sunlight for about 3 months to prevent hyperpigmentation and sunburn injury. Tell them to always wear sunscreen when outside.

Complications The most common complications during the rehabilitation phase are skin and joint contractures and hypertrophic scarring.26 A joint

contracture (an abnormal condition of a joint characterized by flexion and fixation) develops because of the shortening of scar tissue in the flexor tissues of a joint. Areas that are most susceptible to skin and joint contractures include the anterior and lateral neck areas, axillae, antecubital fossae, fingers, groin areas, popliteal fossae, knees, and ankles (Fig. 24.14). Some areas encompass major joints. Not only does the skin over these areas develop contractures, but the underlying tissues, such as the ligaments and tendons, tend to shorten during the healing process. Carefully watch the patient for these potential problems. Encourage proper positioning, splinting, and exercise to minimize this complication. Tell the patient to continue with these strategies until the skin matures at around 1-year post healing. Rehabilitative therapy is aimed at the extension of body parts because the flexors are stronger than the extensors. Burned legs first may be wrapped with elastic (e.g., tensor, ACE) bandages to assist with circulation to leggraft and donor sites before ambulation. Burned arms can be wrapped with a layer of tubular elastic gauze (e.g., Tubigrip). This interim pressure prevents blister formation, promotes venous return, and decreases pain and itchiness. Once the skin is completely healed and less fragile, custom-fitted pressure garments replace the elastic bandages and tubular gauze.

FIG. 24.14 Neck contracture. Courtesy Linda Bucher, RN, PhD, CEN, CNE, Staff Nurse, Virtua Memorial Hospital, Mt. Holly, NJ.

Nursing and Interprofessional Management: Rehabilitation Phase During the rehabilitation phase, encourage both the patient and caregiver to take part in care. Since the patient may go home with unhealed wounds, teach your patient and caregiver the skills for wound care. Before discharge, have them show you the proper dressing change. In addition, make sure they know when to contact the burn team (e.g., signs of infection, increased pain) and the need to keep outpatient visits to ensure good wound healing.

If needed, arrange home care nursing to assist with care. The newly discharged patient will need to know how to gently remove the dressings in the shower once daily, if a nonadherent, greasy gauze dressing is used or twice daily if a topical, antimicrobial cream is ordered. Teach that showering, not bathing, with mild soap and warm water keeps the wounds clean. Give advice on scar management, moisturizing, and sun protection. Suggest using water-based creams that penetrate the dermis (e.g., Vaseline Intensive Rescue) on healed areas to keep the skin supple and moisturized. This will decrease itching and flaking. Sometimes antihistamines are used at bedtime if itching persists. Base ongoing pain management and nutritional needs on individual patient status. Continue to encourage the patient to perform the PT and OT routines. Encourage and reassure the patient to maintain morale, particularly once the patient realizes that recovery can be slow. Rehabilitation may have to be a primary focus for at least the next 6 to 12 months. Postburn reconstructive surgery is often done after a major burn. The need for further surgery is reviewed at the outpatient burn clinic appointments after discharge.

Gerontologic Considerations: Burns The older patient presents many challenges for the burn team.27 The normal aging process puts the patient at risk for injury because of unsteady gait, limited eyesight, and decreased hearing. As people age, skin becomes drier and more wrinkled. Older adults have thinning of the dermal layer, a loss of elastic fibers, a reduction in subcutaneous adipose tissue, and a decrease in vascularity. As a result, the thinner dermis, with reduced blood flow, sustains deeper burns with poorer rates of healing. Once injured, the older adult has more complications in the emergent and acute phases of burn resuscitation because of preexisting co-morbidities. For example, older patients with diabetes, heart failure, or COPD have morbidity and mortality rates exceeding

those of healthy, younger patients. In older patients, pneumonia is a frequent complication, burn wounds and donor sites take longer to heal, and surgical procedures are not well tolerated. Weaning from a ventilator can be a challenge. Although usually self-limiting, delirium, if it develops, may be distressing.28 It usually takes longer for these patients to rehabilitate to the point at which they can safely return home. For some, a return home to independent living may not be possible. As the population ages, developing strategies to prevent burn injuries in older adults is a priority.

Emotional/Psychologic Needs of Patients and Caregivers Patients and caregivers have many emotional/psychologic needs during the often lengthy, unpredictable, and complex course of care. You have an important supportive and counseling role as patients struggle to get their lives back on track. To manage the enormous range of emotional responses that the burn patient may have, assess the circumstances of the burn (e.g., cause, people involved), family relationships, and previous ways of coping with stress. At any time, the patient may have a variety of emotions, such as fear, anxiety, anger, guilt, and depression (Table 24.14). Burn survivors often have thoughts and feelings that are frightening and disturbing, such as guilt about the burn incident, reliving the burn experience, fear of dying, concern about future therapy and surgery, frustrations with ongoing discomfort and treatment, and hopelessness about the future. During recovery, as more independence is expected from the patient, new fears may occur: “Can I really do this?” “Am I a desirable person?” “How can I go outside looking like this?” These challenges confront patients throughout their recovery and often for years to come. A burn injury may adversely affect the person’s self-esteem. Some may fear the loss of relationships because of perceived or actual

physical disfigurement. In a society that values physical beauty, changes in body image can result in psychologic distress. Open and frequent communication among the patient, caregivers, close friends, and burn team members is essential. Because of the tremendous psychologic impact of a burn injury, be particularly sensitive to the patient’s emotions and concerns. Encourage the patient to discuss fears about loss of life as they once knew it, loss of function, temporary or permanent deformity and disfigurement, return to work and home life, and financial burdens resulting from a long and costly hospitalization and rehabilitation.29

TABLE 24.14 Common Emotional Responses

Encourage appropriate independence and an eventual return to preburn activities, such as school or work. Peer counseling and informal interactions with other burn survivors may bring comfort and help to restore confidence. Reassure patients that their feelings during this period of adjustment are a normal reaction to an extraordinary life event. Their frustration and impatience are to be expected as they work to establish a new life. Help patients in

adapting to a realistic, yet positive appraisal of their specific situation, emphasizing what they can do instead of what they cannot do. Caregivers may share some or all these challenges and feelings. At times, they may feel helpless or too exhausted to help their loved one. Continued support from trusted and familiar burn team members is essential. Helping caregivers assist with aspects of the patient’s care helps them to reconnect with their loved one and eases the transition home. Many burn survivors and their caregivers remark on the powerful learning experience of the burn and a renewed appreciation of life, despite the ongoing challenges of a prolonged recovery. You must acknowledge that their feelings are real and common. Most burn survivors speak of a real satisfaction with their postburn life and are more empowered as time goes on. It is important to address individual spiritual and cultural needs because both have a role in treatment decisions and recovery. Pastoral care may be a helpful resource for the patient and caregiver. The need for support, information, and family involvement may vary among cultures. Identify what is important to your patient and caregiver and communicate that information in the patient’s plan of care. Encourage the burn care team to be culturally aware of and sensitive to the patient’s and caregiver’s cultural needs. The difficult issue of sexuality must be met with honesty. Acceptance of any changes in physical appearance is difficult at first for the patient and significant other. The nature of skin injury in itself can cause modifications in processing sexual stimuli.30 Touch is an important part of sexuality, and immature scar tissue may make the sensation of touch unpleasant or may dull it. This may be only transient, but the patient and partner need to know that it is normal and receive anticipatory guidance from the burn team to avoid undue emotional strain. Burn survivors may have preexisting mental health or substance use issues, any of which may have contributed to the burn incident.31 The stress of the burn injury can precipitate a psychologic crisis. Assessment by a psychiatrist who can prescribe appropriate drugs, if needed, and offer counseling is often helpful. Early psychiatric

intervention is essential if the patient has been previously treated for a psychiatric illness or if the injury was a suicide attempt. Many burn patients have posttraumatic stress disorder. A history of mental health issues can influence the length of hospitalization and time needed to prepare for discharge.31 However, it has been noted that distress and trauma symptoms can act as a catalyst for positive posttraumatic growth. Coping styles and social support assist in these positive changes postburn.32 Psychologic care typically begins in the hospital, but links to community resources must be made before discharge to ensure continuity of treatment. A referral to a psychiatrist, psychologist, psychiatric advanced practice nurse (APN), mental health counselor, or social worker should be discussed if concerns are raised at burn clinic follow-up. Caregiver and patient support groups may be beneficial in meeting the patient’s and caregiver’s emotional needs at any phase of the recovery process. Speaking with others who have had burn trauma can be beneficial, both in terms of confirming that the patient’s feelings are normal and in sharing helpful advice. The Phoenix Society (www.phoenix-society.org) is an international, highly respected burn survivors’ support group. For many years the society has offered valuable support and resources (e.g., annual World Burn Congress conference) to burn survivors, caregivers, and burn team staff.

Special Needs of Nurses Warm, trusting, and mutually satisfying relationships often develop between burn patients and nursing staff during hospitalization and the long-term rehabilitation period. Sometimes the bond can be so strong that the patient has difficulty separating from the hospital and staff. The frequency and intensity of family contact can be rewarding as well as draining to you. You may find it difficult to cope with the deformities caused by the burn injury, odors, unpleasant sight of the wound, and reality of the pain that accompanies the burn and its treatment. Do not hesitate to seek help from co-workers, a manager, or

the employee assistance program should you feel the need. In time, you will come to know that the specialized burn care you provide makes a critical difference in helping patients not only survive but also cope with and triumph over an intense and complex injury. Ongoing support services or critical incident stress debriefings led by a psychiatrist, psychologist, psychiatric APN, or social worker may be helpful. Peer support groups (e.g., ABA, International Society for Burn Injuries) can serve a similar purpose by helping you cope with difficult feelings experienced when caring for burn patients. Because burn nursing is physically, psychologically, and intellectually demanding, it has many challenges and inherent rewards. Attention to your own self-care is important to maintain a positive attitude and healthy work-life balance. Time with family and friends and rest and relaxation at home are essential parts of self-care and a balanced life with purpose and meaning.

Case Study Burn Injury

© Comstock/Thinkstock.

Patient Profile G.M., a 52-yr-old married white man, arrives at the ED with burns to

his face, neck, chest, right arm and hand, and right foot. He was burning brush on his farm when the fire went out of control. He has an 18-gauge IV with NSS running at 100 mL/hr, and he is receiving 100% humidified O2 by mask.

Subjective Data • Reports blurry vision and trouble swallowing • States his burns are painful and that he is scared • States he is a “diabetic” and has “high blood pressure”

Objective Data Physical Examination • Is awake, alert, and oriented, but in some distress • Eyes are red, irritated • Voice is hoarse; nasal hair is singed • Face is reddened with blisters noted on the nose and forehead • Right arm, right hand, anterior chest, neck, and right foot have shiny, bright red, wet wounds • Is shivering

Discussion Questions 1. Priority Decision: What are the priorities of care in the prehospital setting and ED? How should his airway, breathing, and circulation be managed? 2. Priority Decision: What factors place G.M. at high risk for an inhalation injury? What priority interventions can be anticipated? 3. Patient-Centered Care: What pain medications might be considered to relieve his pain? 4. Which of the criteria for burn center referral does G.M. meet for

admission to the hospital burn unit? 5. What metabolic disturbances would be expected soon after G.M.’s admission? Explain the physiologic basis for these changes. 6. How might G.M.’s co-morbidities affect his burn care and rehabilitation? 7. Patient-Centered Care: What measures should be taken to support G.M.’s caregivers? 8. Priority Decision: Based on the assessment data presented, what are the priority nursing diagnoses? 9. Evidence-Based Practice: What are the most effective wound care strategies to manage G.M.’s burn wounds? 10. Patient-Centered Care: Prior to discharge what teaching should be provided to G.M. and his family so they can successfully manage his care at home? 11. Safety: To ensure G.M.’s safety at home, what interventions are necessary prior to discharge? 12. Quality Improvement: What outcomes will indicate that interprofessional care was effective? Answers available at http://evolve.elsevier.com/Lewis/medsurg.

Case Study Managing Care of Multiple Patients You are working the day shift on a medical-surgical unit and have been assigned to care for the following 5 patients. You have 1 UAP who is assigned to work with you. There are 15 other patients on the unit being cared for by an additional 3 RNs and 3 UAP.

Patients

Discussion Questions 1. Priority Decision: After receiving report, which patient should you see first? Provide rationale. 2. Collaboration: Which tasks could you delegate to the UAP (select all that apply)? a. Obtain vital signs on F.M. b. Take a blood pressure reading on D.B. c. Perform an admission assessment on G.L. d. Explain planned diagnostic testing to R.S. e. Obtain a 12-lead electrocardiograph on D.A. 3. Priority Decision and Collaboration: When you enter D.B.’s room, he tells you he is not feeling well. He says he has a headache and his legs are “cramping up.” He is also somewhat confused as he is unaware that he is in the hospital. What initial action would be most appropriate? a. Administer acetaminophen for headache relief. b. Have the UAP obtain a STAT capillary blood glucose reading. c. Notify D.B.’s health care provider of his altered level of consciousness. d. Ask the UAP to obtain vital signs on D.B. while you review recent laboratory results.

Case Study Progression D.B.’s vital signs are BP 154/88 mm Hg, heart rate is 112 bpm, respirations are 18 breaths/min, and temperature is 98°F (36.8°C). His most recent laboratory results reveal a serum sodium level of 128 mEq/L (128 mmol/L). You notify his HCP, who orders a normal saline IV to infuse at 100 mL/hr. 4. D.B. complains of thirst and asks for something to drink. Which fluids would be appropriate to give him (select all that apply)? a. Gatorade

b. Tap water c. Cola soda d. Apple juice e. Orange juice 5. In addition to teaching F.M. how to administer postoperative eyedrops, you will also explain a. position and activity restrictions. b. how to change the dressing on her eye. c. the necessity for restricting fluid intake. d. that protective eyewear will no longer be required. 6. When giving report to your UAP regarding your assigned patients, you are asked by the UAP if there is a significant difference between D.A. and G.L.’s skin cancers. You reply based on knowledge that a. basal cell carcinoma is the deadliest form of skin cancer. b. melanoma typically appears as red, rough patches on the skin. c. melanoma can metastasize to any organ, including the brain and heart. d. basal cell carcinoma often occurs during the second and third decades of life. 7. Management Decision: Another RN offers to help you by providing care for F.M. Which observed action by the RN would require your immediate intervention? a. The RN assists F.M. to lie flat on her back. b. The RN gives F.M. oral medication for pain. c. The RN assures F.M. that retinal reattachment is usually successful. d. The RN explains to F.M. that she is at risk for detachment in the other eye. 8. Priority Decision: Which intervention has the highest priority for R.S.? a. Keeping the room dark and quiet. b. Placing an emesis basin at the bedside.

c. Elevating the head of the bed to the height desired. d. Raising the side rails and having the bed in low position. Answers available at http://evolve.elsevier.com/Lewis/medsurg.

Bridge to NCLEX Examination The number of the question corresponds to the same-numbered outcome at the beginning of the chapter.

1. Which prevention strategy would the nurse include when teaching about home fire safety? a. Set hot water temperature at 140°F. b. Use only hardwired smoke detectors. c. Encourage regular home fire exit drills. d. Do not allow older adults to cook unattended. 2. The injury that is least likely to result in a full-thickness burn is a. sunburn. b. scald injury. c. chemical burn. d. electrical injury. 3. When assessing a patient with a partial-thickness burn, the nurse would expect to find (select all that apply) a. blisters. b. exposed fascia. c. exposed muscles. d. intact nerve endings.

e. red, shiny, wet appearance. 4. A patient is admitted to the burn center with burns to his head, neck, and anterior and posterior chest after an explosion in his garage. On assessment, the nurse auscultates wheezes throughout the lung fields. On reassessment, the wheezes are gone, and the breath sounds are greatly decreased. Which action is the most appropriate for the nurse to take next? a. Encourage the patient to cough and auscultate the lungs again. b. Obtain vital signs, oxygen saturation, and a STAT arterial blood gas. c. Document the findings and continue to monitor the patient’s breathing. d. Anticipate the need for endotracheal intubation and notify the provider. 5. Fluid and electrolyte shifts that occur during the early emergent phase of a burn injury include a. adherence of albumin to vascular walls. b. movement of potassium into the vascular space. c. movement of sodium and water into the interstitial space. d. hemolysis of red blood cells from large volumes of rapidly administered fluid. 6. To maintain a positive nitrogen balance in a major burn, the patient must a. eat a high-protein, high-carbohydrate diet. b. increase normal caloric intake by about four times.

c. eat at least 1500 calories/day in small, frequent meals. d. eat a gluten-free diet for the chemical effect on nitrogen balance. 7. A patient has 25% TBSA burn from a car fire. His wounds have been debrided and covered with a silverimpregnated dressing. The nurse’s priority intervention for wound care would be to a. reapply a new dressing without disturbing the wound bed. b. observe the wound for signs of infection during dressing changes. c. apply cool compresses for pain relief in between dressing changes. d. wash the wound aggressively with soap and water three times a day. 8. Pain management for the burn patient is most effective when (select all that apply) a. a pain rating tool is used to monitor the patient’s level of pain. b. painful dressing changes are delayed until the patient’s pain is completely relieved. c. the patient is informed about and has some control over the management of the pain. d. a multimodal approach is used (e.g., sustained-release and short-acting opioids, NSAIDs, adjuvant analgesics). e. nonpharmacologic therapies (e.g., music therapy, distraction) replace opioids in the rehabilitation phase of a burn injury.

9. A therapeutic measure used to prevent hypertrophic scarring during the rehabilitation phase of burn recovery is a. applying pressure garments. b. repositioning the patient every 2 hours. c. performing active ROM at least every 4 hours. d. massaging the new tissue with water-based moisturizers. 10. A patient is recovering from second- and third-degree burns over 30% of his body, and the burn care team is planning for discharge. The first action the nurse should take when meeting with the patient would be to a. arrange a return-to-clinic appointment and prescription for pain medications. b. teach the patient and the caregiver proper wound care to be performed at home. c. review the patient’s current health care status and readiness for discharge to home. d. give the patient written information and websites for information for burn survivors. 1. c, 2. a, 3. a, d, e, 4. d, 5. c, 6. a, 7. b, 8. a, c, d, 9. a, 10. c For rationales to these answers and even more NCLEX review questions, visit http://evolve.elsevier.com/Lewis/medsurg.

Evolve Website/Resources List http://evolve.elsevier.com/Lewis/medsurg

Review Questions (Online Only) Key Points

Answer Keys for Questions • Rationales for Bridge to NCLEX Examination Questions • Answer Guidelines for Case Study on p. 451 • Answer Guidelines for Managing Care of Multiple Patients Case Study (Section 5) on p. 454 Student Case Study • Patient With Burns Nursing Care Plan • eNursing Care Plan 24.1: Patient With a Thermal Burn Injury Conceptual Care Map Creator Audio Glossary Content Updates

References 1. American Burn Association: Burn incidence and treatment in the US: 2016 fact sheet. Retrieved from http://ameriburn.org/who-we-are/media/burn-incidencefact-sheet/. 2. WHO International: Burns fact sheet March 2018. Retrieved from www.who.int/news-room/factsheets/detail/burns. 3. Grant EJ: Burn injuries: Prevention, advocacy, and legislation, Clin Plast Surg 44:451, 2017. 4. Roberts JR, Custalow CB, Thomsen TW: Roberts and Hedges’ clinical procedures in emergency medicine and acute care, ed 7, Philadelphia, 2019, Elsevier.

5. Gupta K, Mehrotra M, Kumar P, et al: Smoke inhalation injury: Pathogenesis, diagnosis, and management, Indian J Crit Care Med 22:180, 2018. 6. Greenhalgh DG: Burn care for general surgeons and general practitioners, Wiesbaden, Germany, 2016, Springer. 7. Understanding burn care. Retrieved from http://understandingburncare.org/burn-severity.html. 8. American Burn Association Burn Center referral criteria. Retrieved from www.ameriburn.org/wpcontent/uploads/2017/05/burncenterreferralcriteria.pdf 9∗. Wallis L, Fleming J, Hasselberg M, et al: A smartphone app and cloud-based consultation system for burn injury, Emerg Care 11:1, 2016. 10∗. Sorg H, Tilkorn D, Hager S, et al: Skin wound healing: An update on the current knowledge and concepts, European Surgical Res 58:81, 2017. 11∗. Pannucci C, Obi A, Timmins B, et al: Venous thromboembolism in patients with thermal injury: A review of risk assessment tools and current knowledge on the effectiveness and risks of mechanical and chemical prophylaxis, Clin Plastic Surg 44:573, 2017. 12∗. Sutton T, Lenk I, Conrad P, et al: Severity of inhalation injury is predictive of alterations in gas exchange and worsened clinical outcomes, J Burn Care Res 38:390, 2017. 13. Alves dos Santos C, Souza-Junior V, Ferreira Lanza F, et al: Serious games in virtual environments for health teaching and learning, Northeast Netw Nurs J 18:702, 2017.

14. Deutsch C, Tan A, Smailes S, et al: The diagnosis and management of inhalation injury: An evidence-based approach, Burns 44:1040-1051, 2018. 15. Cartotto R, Greenhalgh D, Cancio C, et al: Burn state of the science: Fluid resuscitation, J Burn Care Res 38:e596-e604, 2017. 16. Ahuja R, Gibran N, Greenhalgh D, et al: ISBI practice guidelines for burn care, Burns 42:953, 2016. 17. Herndon DN: Total burn care, Edinburgh, 2018, Elsevier. 18. Berger M, Pantet O: Nutrition in burn injury: Any recent changes? Curr Opin Crit Care 22:285, 2016. 19. Clark A, Imran J, Madni T, et al : Nutrition and metabolism in burn patients, Burns Trauma 5:1, 2017. 20. Dellinger R, Schorr C, Levy M: A users guide to the 2016 surviving sepsis guidelines, Crit Care Med 45:381, 2017. 21. Ahuja R, Gibran N, Greenhalgh D, et al: ISBI practice guidelines for burn care, Burns 42:953, 2016. 22. Mushin O, Bogue J, Esquenazi M, et al: Use of a home vacuum-assisted closure device in the burn population is both cost-effective and efficacious, Burns 43:490, 2017. 23. Hussain A: Surgical treatment of acute burns, Wounds UK 14:30, 2018. 24. Najafi Ghezeljeh T, Mohades Ardebili F, Rafii F: The effects of massage and music on pain, anxiety and relaxation in burn patients, Burns 43:1034, 2017. 25. Parnell L: Itching for knowledge about wound and scar pruritus, Wounds 30:17, 2018. 26. Oosterwijk A, Mouton L, Schouten H, et al:

Prevalence of scar contractures after burn: A systematic review, Burns 43:41, 2017. 27. Gregg D, Patil S, Singh K, et al: Clinical outcomes after burns in elderly patients over 70 years: A 17year retrospective analysis, Burns 44:65, 2018. 28. Holmes E, Laughon S, Jones S: Retrospective analysis of neurocognitive impairment in older patients with burn injuries, Psychosomatics 58:386, 2017. 29. Jonathan B, Pius A, Richcane A: Study on acute burn injury survivors and the associated issues, J Acute Dis 3:206, 2016. 30. Kornhaber R, Haik J, Sayers J, et al: People with borderline personality disorder and burns: Some considerations for health professionals, Issues Mental Health Nurs 38:767, 2017. 31. Li F, Coombs D: Mental health history: A contributing factor for poorer outcomes in burn survivors, Burns Trauma 6:1, 2018. 32. Kruithof N, Traa M, Karabatzakis M, et al: Perceived changes in quality of life in trauma patients: A focus group study, J Trauma Nurs 25:177, 2018. ∗Evidence-based information for clinical practice.

SECTION SIX

Problems of Oxygenation: Ventilation OUTLINE 25. Assessment: Respiratory System 26. Upper Respiratory Problems 27. Lower Respiratory Problems 28. Obstructive Pulmonary Diseases

25

Assessment Respiratory System Eugene Mondor

LEARNING OUTCOMES 1. Distinguish the structures and functions of the upper respiratory tract, lower respiratory tract, and chest wall. 2. Describe the process that initiates and controls inspiration and expiration. 3. Describe the process of oxygenation and ventilation. 4. Identify the respiratory defense mechanisms. 5. Describe the significance of arterial blood gas values in relation to respiratory function. 6. Relate the signs and symptoms of inadequate oxygenation to physical assessment findings. 7. Link age-related changes of the respiratory system to key differences in assessment findings. 8. Obtain significant subjective and objective assessment data related to the respiratory system. 9. Perform a physical assessment of the respiratory system using the appropriate techniques. 10. Distinguish normal from common abnormal findings in a

physical assessment of a patient’s respiratory system. 11. Describe the purpose, significance of results, and nursing responsibilities related to diagnostic studies of the respiratory system.

KEY TERMS adventitious breath sounds, p. 467 chemoreceptor, p. 459 compliance, p. 458 crackles, Table 25.6, p. 468 dyspnea, p. 458 elastic recoil, p. 458 fremitus, p. 465 mechanical receptors, p. 459 oxygenation, p. 458 resistance, p. 458 surfactant, p. 457 tidal volume (VT), p. 457 ventilation, p. 458 wheezes, Table 25.6, p. 468 Do your little bit of good where you are; it’s those little bits of good put together that overwhelm the world. Desmond TuTu http://evolve.elsevier.com/Lewis/medsurg/

Conceptual Focus Functional Ability Gas Exchange The primary purpose of the respiratory system is gas exchange. This involves the transfer of oxygen (O2) and carbon dioxide (CO2) between the atmosphere and blood. While adequate perfusion is needed to distribute O2 to the body tissues, adequate oxygenation depends on a healthy, functioning respiratory system.

Structures and Functions of Respiratory System The respiratory system is divided into 2 parts: the upper respiratory tract and the lower respiratory tract (Fig. 25.1).

Upper Respiratory Tract The upper respiratory tract includes the nose, mouth, pharynx, epiglottis, larynx, and trachea. Air enters the respiratory tract through the nose. The nose is made of bone and cartilage. It is divided into 2 nares by the nasal septum. The inside of the nose is shaped into 3 passages by projections called turbinates. The turbinates increase the surface area of the nasal mucosa that warms and moistens the air as it enters the nose. The internal nose opens directly into the sinuses. The nasal cavity connects with the pharynx. It is a tubular passageway that is subdivided into 3 parts: the nasopharynx, oropharynx, and laryngopharynx.

FIG. 25.1 Structures of the respiratory tract. A, Pulmonary functional

unit. B, Ciliated mucous membrane. Redrawn from Price SA, Wilson LM: Pathophysiology: Clinical concepts of disease processes, ed 6, St Louis, 2003, Mosby.

The nose functions to protect the lower airway by warming and humidifying air and filtering small particles before air enters the lungs. The olfactory nerve, found within the mucosa of the upper part of the nasal cavity, is responsible for the sense of smell.1 Air moves through the oropharynx to the laryngopharynx. It then travels through the epiglottis to the larynx before moving into the trachea. The epiglottis is a small flap behind the tongue that closes over the larynx during swallowing. This prevents solids and liquids from entering the lungs. The vocal cords are in the larynx. Air passes through the glottis (the opening between the vocal cords) and into the trachea. The trachea is a cylindrical tube about 5 in (10 to 12 cm) long and 1 in (1.5 to 2.5 cm) in diameter. U-Shaped cartilages keep the trachea open but allow the adjacent esophagus to expand for swallowing. The trachea bifurcates into the right and left mainstem bronchi at a point called the carina. The carina is located at the angle of Louis, which is at the level of the 4th and 5th thoracic vertebrae.2 The carina is highly sensitive. Stimulation of this area during suctioning causes vigorous coughing.

Lower Respiratory Tract Once air passes the carina, it is in the lower respiratory tract. The lower respiratory tract consists of the bronchi, bronchioles, alveolar ducts, and alveoli. Except for the right and left mainstem bronchi, all lower airway structures are found within the lungs. The right lung is divided into 3 lobes (upper, middle, and lower) and the left lung into 2 lobes (upper and lower) (Fig. 25.2).

FIG. 25.2 Landmarks and structures of the chest wall. A, Anterior view. B, Posterior view. Redrawn from Thompson JM, McFarland GK, Hirsch JE, et al: Mosby’s clinical nursing, ed 5, St Louis, 2002, Mosby.

The mainstem bronchi, pulmonary vessels, and nerves enter the lungs through a slit called the hilus. The right mainstem bronchus is shorter, wider, and straighter than the left mainstem bronchus. That is why aspiration is more likely to occur in the right lung than in the left lung. The mainstem bronchi subdivide several times to form the lobar, segmental, and subsegmental bronchi. Further divisions form the bronchioles. The most distant bronchioles are the respiratory bronchioles. The bronchioles are encircled by smooth muscles that constrict and dilate in response to various stimuli. The terms bronchoconstriction and bronchodilation refer to a decrease or increase in the diameter of the airways caused by contraction or relaxation of these muscles. Beyond the bronchioles lie the alveolar ducts and alveoli (Fig. 25.3).

FIG. 25.3 Structures of lower airways. Redrawn from Thompson JM, McFarland GK, Hirsch JE, et al: Mosby’s clinical nursing, ed 5, St Louis, 2002, Mosby.

The trachea and bronchi act as a pathway to conduct gases to and from the alveoli. The volume of air in the trachea and bronchi is called the anatomic dead space (VD).3 This air does not take part in gas exchange. In adults, a normal tidal volume (VT), or volume of air exchanged with each breath, is about 500 mL (in a 150-lb man). Of each 500 mL inhaled, about 150 mL is VD. The alveoli are the terminal part of the respiratory tract (Fig. 25.3). Alveoli are small sacs in the lungs that are the primary site of gas exchange for O2 and CO2. The adult lung has over 300 million alveoli, each 0.3 mm in diameter. The alveoli are interconnected by pores of Kohn.4 They allow movement of air from alveolus to alveolus (Fig. 25.1). Deep breathing promotes air movement through these pores and helps move mucus out of the respiratory bronchioles. Bacteria can also move through these pores, spreading infection to previously uninfected areas. Alveoli have a total volume of about 2500 mL with a

surface area for gas exchange that is about the size of a tennis court. Gases are exchanged across the alveolar-capillary membrane, where the alveoli come in contact with pulmonary capillaries (Fig. 25.4). In conditions such as pulmonary edema, excess fluid fills the interstitial space and alveoli, markedly reducing gas exchange.

Surfactant Because alveoli are unstable, they have a natural tendency to collapse. Alveolar cells secrete surfactant. Surfactant is a lipoprotein that lowers the surface tension in the alveoli.5 It reduces the amount of pressure needed to inflate the alveoli and makes them less likely to collapse. Normally, each person takes a slightly larger breath, termed a sigh, after every 5 or 6 breaths. This sigh stretches the alveoli and promotes surfactant secretion. When there is not enough surfactant, the alveoli collapse. The term atelectasis refers to collapsed, airless alveoli. The postoperative patient is at risk for atelectasis because of the effects of anesthesia, decreased mobility, and pain, which can alter breathing and lung expansion. In acute respiratory distress syndrome (ARDS), lack of surfactant contributes to widespread atelectasis and collapse of lung tissue (see Chapter 67).

FIG. 25.4 Partial pressure of respiratory gases in normal respiration. The pressures are shown in inhaled and exhaled air from the lungs and at the level of the alveoli and pulmonary venous and arterial blood vessels.

Blood Supply The lungs have 2 different types of circulation: pulmonary and bronchial. Pulmonary circulation provides the lungs with blood that takes part in gas exchange. The pulmonary artery receives deoxygenated blood from the right ventricle of the heart and delivers it to pulmonary capillaries that lie directly alongside the alveoli. O2– CO2 exchange occurs at this point. The pulmonary veins return oxygenated blood to the left atrium, which then delivers it to the left ventricle, and into systemic circulation. Venous blood is collected from capillary networks of the body and returned to the right atrium by way of the superior and inferior vena cava. Bronchial circulation starts with the bronchial arteries, which arise from the thoracic aorta. Bronchial circulation does not take part in gas

exchange but provides O2 to the bronchi and other lung tissues. Deoxygenated blood returns from the bronchial circulation through the azygos vein into the superior vena cava.1

Chest Wall The chest wall is shaped, supported, and protected by 24 ribs (12 on each side). The thoracic cage, which consists of the ribs and sternum, protect the lungs and the heart from injury. The mediastinum is the space in the middle of the thoracic cavity. It contains the major organs of the chest, including the heart, aorta, and esophagus. The mediastinum physically separates the right and left lungs into 2 separate compartments. The chest cavity is lined with a membrane called the parietal pleura. The lungs are lined with a membrane called the visceral pleura. The parietal and visceral pleurae join to form one continuous membrane. The visceral pleura does not have any sensory (pain) fibers or nerve endings. The parietal pleura has pain fibers. This is why irritation or inflammation of the parietal pleura can cause pain with each breath. The intrapleural space is the space between the pleural layers. Normally this space contains 20 to 25 mL of fluid. This fluid serves 2 purposes: (1) it provides lubrication, allowing the pleural layers to slide over each other during breathing and (2) it increases unity between the pleural layers. This promotes expansion of the pleurae and lungs during inspiration. Fluid drains from the pleural space via lymphatic circulation. Several pathologic conditions may cause the accumulation of greater amounts of fluid, termed a pleural effusion. Pleural fluid may accumulate because of blockage of lymphatic drainage (e.g., from cancer) or because of an imbalance between intravascular and oncotic fluid pressures, as in heart failure. Purulent pleural fluid with bacterial infection is called empyema. The diaphragm is the major muscle of respiration. During inspiration the diaphragm contracts, moves downward, and increases intrathoracic volume. At the same time, the internal intercostals relax

and the external intercostal muscles contract. This increases the lateral and anteroposterior (AP) dimension of the chest.6 The scalene muscles also contract on inspiration, raising the first and second ribs. This causes the size of the thoracic cavity to increase and intrathoracic pressure to decrease, pulling air into the lungs. The diaphragm is made up of 2 hemidiaphragms, each innervated by the right and left phrenic nerves. The phrenic nerves arise from the spinal cord between C3 and C5, the 3rd and 5th cervical vertebrae. Injury to the phrenic nerve results in hemidiaphragm paralysis on the side of the injury. Complete spinal cord injuries above the level of C3 result in total diaphragm paralysis and dependence on a mechanical ventilator.

Physiology of Respiration Oxygenation Oxygenation refers to the process of obtaining O2 from the atmospheric air and making it available to the organs and tissues of the body. The lungs’ ability to oxygenate arterial blood adequately is evaluated by partial pressure of O2 in arterial blood (PaO2), arterial O2 saturation (SaO2), and patient assessment (Table 25.1). O2 is carried in the blood in 2 forms: dissolved O2 and hemoglobinbound O2. The PaO2 represents the amount of O2 dissolved in the plasma. It is expressed in millimeters of mercury (mm Hg). The SaO2 is the amount of O2 bound to hemoglobin in comparison with the amount of O2 the hemoglobin can carry. The SaO2 is expressed as a percent. For example, if the SaO2 is 90%, this means that 90% of hemoglobin attachments for O2 have O2 bound to them.

TABLE 25.1 Manifestations of Inadequate

Oxygenation

O2 and CO2 move back and forth across the alveolar-capillary membrane by diffusion. The overall direction of movement is from the area of higher concentration to the area of lower concentration. Thus O2 moves from alveolar gas (atmospheric air) into the arterial blood and CO2 from the arterial blood into the alveolar gas. Diffusion continues until equilibrium is reached.

Ventilation Ventilation involves inspiration, or inhalation (movement of air into the lungs), and expiration, or exhalation (movement of air out of the lungs). Air moves in and out of the lungs because intrathoracic pressure changes in relation to pressure at the airway opening. Contraction of the diaphragm and external intercostal and scalene muscles increases chest dimensions, thus decreasing intrathoracic pressure. Gas flows from an area of higher pressure (atmospheric) to one of lower pressure (intrathoracic). When dyspnea (shortness of

breath) occurs, neck and shoulder muscles, as well as other accessory muscles of respiration, can aid the effort. Some conditions (e.g., phrenic nerve paralysis, rib fractures, neuromuscular disease) may limit diaphragm or chest wall movement. This causes the patient to breathe with smaller tidal volumes. As a result, the lungs do not fully inflate and gas exchange may be impaired. In contrast to inspiration, expiration is passive. Elastic recoil is the tendency for the lungs to return to their original size after being stretched or expanded. The elasticity of lung tissue is due to the elastin fibers found in the alveolar walls and surrounding the bronchioles and capillaries. The elastic recoil of the chest wall and lungs allows the chest to passively decrease in size (volume). When intrathoracic pressure rises, air moves out of the lungs. Exacerbations of asthma or chronic obstructive pulmonary disease (COPD) cause expiration to become an active, labored process (see Chapter 28). Abdominal, intercostal, and accessory muscles (e.g., scalene, trapezius) help expel air during labored breathing.

Compliance and Resistance Compliance (distensibility) is a measure of the ease of expansion of the lungs. This is a product of the elasticity of the lungs and elastic recoil of the chest wall.6 When compliance is decreased, it is harder for the lungs to inflate. This occurs with conditions that increase fluid in the lungs (e.g., pulmonary edema, ARDS, pneumonia), make lung tissue less elastic or distensible (e.g., pulmonary fibrosis, sarcoidosis), or restrict lung movement (e.g., pleural effusion). Compliance increases when there is destruction of alveolar walls and loss of tissue elasticity, as in COPD. On the other hand, resistance refers to any obstacle to airflow during inspiration and/or expiration. The main factor affecting airway resistance is changes in the diameter (size) of the airways. For example, a patient with an acute asthma attack has narrowed airways, resulting in increased resistance. The presence of secretions in the bronchi also increases resistance. Secretions can partially occlude airways, making airways narrower. This makes it harder for patients

to get air into their lungs. Giving bronchodilators decreases resistance by increasing the diameter of the bronchi, promoting air entry. Changes in compliance and/or resistance can seriously affect both oxygenation and ventilation.

Control of Respiration Located in the brainstem, the respiratory center (the medulla) responds to chemical and mechanical signals. The medulla sends impulses to the respiratory muscles through the spinal cord and phrenic nerves.

Chemoreceptors A chemoreceptor is a receptor that responds to a change in the chemical composition (PaCO2 and pH) of the fluid around it. Central chemoreceptors are found in the medulla. They respond to changes in the hydrogen ion (H+) concentration.7 An increase in the H+ concentration (acidosis) causes the medulla to increase the respiratory rate and VT. A decrease in H+ concentration (alkalosis) has the opposite effect. Changes in PaCO2 regulate ventilation primarily by their effect on the pH of the cerebrospinal fluid. When the PaCO2 level is increased, more CO2 is available to combine with H2O and form carbonic acid (H2CO3). This lowers the cerebrospinal fluid pH and stimulates an increase in respiratory rate. The opposite process occurs with a decrease in PaCO2 level. Peripheral chemoreceptors are found in the carotid bodies at the bifurcation of the common carotid arteries and in the aortic bodies above and below the aortic arch.8 The peripheral chemoreceptors respond to decreases in PaO2 and pH and to increases in PaCO2. These changes also stimulate the respiratory center. In a healthy person, an increase in PaCO2 or a decrease in pH causes an immediate increase in the respiratory rate. The PaCO2 does not vary more than about 3 mm Hg if lung function is normal. Conditions such as COPD change lung function and may result in

chronically elevated PaCO2 levels. In these instances, the patient is not sensitive to further increases in PaCO2 as a stimulus to breathe and may be maintaining ventilation largely because of a hypoxic drive from the peripheral chemoreceptors (see Chapter 28).

Mechanical Receptors Mechanical receptors are found in the conducting upper airways, chest wall, diaphragm, and capillaries of the alveoli. They are stimulated by a variety of physiologic factors, such as irritants, muscle stretching, and alveolar wall distortion. The 3 major types of mechanical receptors are irritant, stretch, and juxtacapillary (J) receptors.9 Irritant receptors are found in the conducting airways. These receptors are sensitive to inhaled particles and aerosols and, when stimulated, initiate the cough reflex. Signals from stretch receptors, in the smooth muscle of the airways, aid in the control of respiration. As the lungs inflate, stretch receptors activate the inspiratory center to inhibit further lung expansion. This is called the Hering-Breuer reflex, and it prevents overdistention of the lungs. Stimulation of J receptors, found in the capillaries of the alveoli, occurs with increased pulmonary capillary pressure. This causes rapid, shallow respiration (tachypnea) seen in pulmonary edema.

Respiratory Defense Mechanisms Respiratory defense mechanisms are efficient in protecting the lungs from inhaled particles, microorganisms, and toxic gases. The defense mechanisms include air filtration, mucociliary clearance system, cough reflex, reflex bronchoconstriction, and alveolar macrophages.

Filtration of Air Nasal hairs filter inspired air. In addition, the abrupt changes in direction of airflow that occur as air moves through the nasopharynx and larynx increase air turbulence. This causes particles and bacteria to contact the mucosa lining these structures. Most large particles

(greater than 5 µm) are less dangerous because they are removed in the nasopharynx or bronchi and do not reach the alveoli. The velocity of airflow slows greatly after it passes the larynx, facilitating the deposition of smaller particles (1 to 5 µm). They settle out the way that sand does in a river, a process termed sedimentation. Particles less than 1 µm in size are too small to settle in this manner and are deposited in the alveoli. An example of small particles that can build up is coal dust, which can lead to pneumoconiosis (see Chapter 27).

Mucociliary Clearance System Below the larynx, the mucociliary clearance system, also called the mucociliary escalator, is responsible for the movement of mucus. Goblet cells and submucosal glands continually secrete mucus at a rate of about 100 mL/day. This mucus forms a blanket that contains the impacted particles and debris from distal lung areas (Fig. 25.1). Secretory immunoglobulin A (IgA) in the mucus helps protect against bacteria and viruses. Cilia cover the airways from the level of the trachea to the respiratory bronchioles (Fig. 25.1). Each ciliated cell has about 200 cilia. They beat rhythmically about 1000 times per minute in the large airways, moving mucus toward the mouth. We normally swallow the mucus without noticing. The ciliary beat is slower further down the tracheobronchial tree. As a result, we remove particles that penetrate more deeply into the airways less rapidly. Dehydration, smoking, inhalation of high O2 concentrations, infection, and drugs, such as atropine, anesthetics, alcohol, or cocaine, impair ciliary action. Patients with COPD and cystic fibrosis often have repeated lower respiratory tract infections. These conditions are associated with destroyed cilia, resulting in impaired secretion clearance, a chronic productive cough, and chronic colonization by bacteria. These lead to frequent respiratory tract infections.

Cough Reflex

The cough is a protective reflex that clears the airway by a highpressure, high-velocity flow of air. It is a backup for mucociliary clearance, especially when this clearance mechanism is overwhelmed or ineffective. Coughing is effective in removing secretions only above the subsegmental level (large or main airways). Secretions below this level must be moved upward by the mucociliary mechanism before we can remove them by coughing.

Reflex Bronchoconstriction Reflex bronchoconstriction is another defense mechanism. In response to the inhalation of large amounts of irritating substances (e.g., dusts, aerosols), the bronchi constrict to prevent entry of the irritants. A person with hyperreactive airways, such as a person with asthma, may have bronchoconstriction after inhalation of triggers, such as cold air, perfume, or other strong odors.

Alveolar Macrophages Because there are no ciliated cells below the level of the respiratory bronchioles, the primary defense mechanism at the alveolar level is alveolar macrophages. Alveolar macrophages rapidly phagocytize inhaled foreign particles, such as bacteria. The debris is moved to the level of the bronchioles for removal by the cilia or removed from the lungs by the lymphatic system. Particles (e.g., coal dust, silica) that cannot be adequately phagocytized tend to remain in the lungs for indefinite periods and can stimulate inflammatory responses (see Chapter 27). Because alveolar macrophage activity is impaired by cigarette smoke, the smoker who is employed in an occupation with heavy dust exposure (e.g., mining, foundries) is at an especially high risk for lung disease.

Gerontologic Considerations: Effects of Aging on Respiratory System Age-related changes in the respiratory system can be divided into alterations in structure, defense mechanisms, and respiratory control

(Table 25.2). Structural changes include calcification of the costal cartilages, which can interfere with chest expansion. The outward curvature of the spine is marked, especially with osteoporosis, and the lumbar curve flattens. Therefore the chest may appear barrel shaped, and the older person may need to use accessory muscles to breathe. Respiratory muscle strength progressively declines after age 50. Overall, the lungs in the older adult are harder to inflate.

TABLE 25.2 Gerontologic Assessment

DifferencesRespiratory System

Within the lung, the number of functional alveoli decreases and they become less elastic. Small airways in the lung bases close earlier in expiration. Therefore more inspired air is distributed to the lung apices and ventilation is less well matched to perfusion, lowering the PaO2. As a result, older adults have less tolerance for exertion and dyspnea can occur if their activity exceeds their normal exercise. In older adults, respiratory defense mechanisms are less effective because of a decline in both cell-mediated and humoral immunity

(ability to produce antibodies). The alveolar macrophages are less effective at phagocytosis. An older patient has a less forceful cough and fewer and less functional cilia. Mucous membranes tend to be drier. Retained mucus predisposes the older adult to respiratory tract infections. Formation of secretory IgA, an important defense mechanism, is decreased. Swallowing is slower because of transit time in the pharyngeal area, and there is reduced sensation in the pharynx. Consequently, the older adult is at greater risk for aspiration. The aging process alters respiratory control, resulting in a more gradual response to changes in blood O2 or CO2 level. The PaO2 may drop to a slightly lower than normal level, and the PaCO2 may rise to a level slightly higher than normal before the respiratory rate changes. The extent of these changes in people of the same age varies greatly. For example, the older adult who has a significant smoking history, is obese, and has a chronic illness is at greater risk for adverse outcomes.

Assessment of Respiratory System Determining a patient’s needs related to the respiratory system requires an accurate health history and a thorough physical examination. A respiratory assessment can be done as part of a comprehensive physical examination or as a focused respiratory examination. Use judgment in determining whether all or part of the history and physical examination will be completed, based on your immediate assessment of the patient’s degree of respiratory distress. If respiratory distress is severe, only obtain pertinent information and defer a thorough assessment until the patient’s condition stabilizes.

Case Study Patient Introduction

© Fuse/Thinkstock.

F.T. is a 70-yr-old black man who comes to the emergency department (ED) with nausea, fatigue, and increased shortness of breath, which started 3 days ago. He says that he started using his albuterol inhaler every 4 hours 2 days ago, and while it worked initially, it is no longer helping. He can walk only a few feet in his apartment before he becomes short of breath. He sleeps in a recliner in the living room. He has noticed some swelling to his hands and feet and has been having trouble urinating.

Discussion Questions 1. What are the possible causes of F.T.’s shortness of breath? 2. Does F.T. need to be admitted to the hospital or is his condition stable and he can be seen by an HCP in a few hours? 3. What questions would be a priority during the subjective assessment? You will learn more about F.T. and his condition as you read through this assessment chapter. (See p. 464 for more information on F.T.) Answers available at http://evolve.elsevier.com/Lewis/medsurg.

Subjective Data Important Health Information Past Health History It is important to determine the frequency of upper respiratory problems (e.g., colds, sore throats, sinus problems, allergies) and whether seasonal changes influence these problems. Ask about a history of lower respiratory problems, such as asthma, COPD, pneumonia, and tuberculosis (TB). Ask the patient with allergies about possible precipitating factors or triggers, such as medications, pollen, smoke, mold, or pet exposure. Record the characteristics and severity of the allergic reaction, such as

runny nose, wheezing, scratchy throat, or chest tightness. Determine the frequency of asthma exacerbations. Because respiratory symptoms are often manifestations of problems that involve other body systems, it is important to ask about a history of other health problems. For example, the patient with heart problems may have dyspnea (shortness of breath) because of heart failure. The patient with human immunodeficiency virus (HIV) infection may have frequent respiratory tract infections because of compromised immune function.

TABLE 25.3 Health HistoryRespiratory System

Health Perception–Health Management • Describe your daily activities. Have breathing problems prevented you from doing activities that you used to be able to do?∗ Are your breathing problems better, worse, or about the same compared with 6 months ago? • How do your breathing problems affect your self-care abilities? • Have you ever smoked? Do you smoke now? If so, what have you smoked? Cigarettes? Cigars? Pipes? Electronic cigarettes? • If yes, how many cigarettes each day and for how long? Are you interested in stopping smoking? Are there aids we can tell you about that would assist your quitting? Would you be willing to come back for a visit so that we can explore your quitting? If you stopped smoking, did you do so because of your health?∗ How did you stop? • Have you ever used chewing tobacco? • Have you ever smoked street drugs?∗ • Do you get the flu shot yearly? When was your last flu shot? Have you had a Pneumovax vaccination? • What equipment helps you manage your respiratory problems?

How often do you use it? Does it help? Cause problems? • Do you feel that your respiratory problem is getting better or worse?

Nutritional-Metabolic • Have you recently lost weight because of trouble eating related to your respiratory problem? How much weight have you lost? Have you lost this weight voluntarily? • Do any foods affect your breathing?∗ Sputum production?∗

Elimination • Does your breathing problem make it hard for you to get to the toilet?∗ • Are you inactive because of shortness of breath to the point that you have incontinence?∗ Constipation?∗

Activity-Exercise • Are you ever short of breath during exercise?∗ At rest?∗ • Do you get too short of breath to do the things you want to do?∗ • Is your home 1 story? 2 stories? How many steps from the street to your door? • Can you walk up a flight of steps without stopping? • Are you able to maintain your typical activities of daily living? If not, what are you able to do independently? What do you need help with? What have you had to give up? • What do you do when you get short of breath? Does this help? How long does it take you to recover after you have been short of breath?

Sleep-Rest • Do breathing problems cause you to wake up during the night?∗ • Can you lie flat at night? If not, how many pillows do you use? • Do you need to sleep upright in a chair?∗ • Are you or your partner aware of any snoring? • Do you awaken in the morning feeling rested? • Do you ever wake up in the morning with a headache?∗ • Do you fall asleep easily during the day?∗

Cognitive-Perceptual • Do you have any pain associated with breathing?∗ On a scale from 0 to 10, with 0 being “no pain” and 10 being “the worst pain you can imagine,” where would you rate your pain? Does it hurt more on inspiration?∗ Expiration?∗ Or both?∗ • If you are having pain with breathing, describe the pain. • Has the pain gotten better, worse, or stayed about the same over the past 6 months? • Do you ever feel restless, irritable, or confused without a reason?∗ • Do you have difficulty remembering things?∗

Self-Perception–Self-Concept • Describe how your respiratory problems have changed your life. • If you use O2, do you ever go out without bringing it with you? How often does this occur? Why?

Role-Relationship

• Has your respiratory problem caused any problems in your work, family, or social relationships?∗

Sexuality-Reproductive • Has your respiratory problem caused a change in your sexual activity?∗ • Have you and your partner talked about ways to minimize your breathing problems during sexual activity?

Coping–Stress Tolerance • On a daily/weekly basis, how often do you leave your home? • Do you feel under any stress right now? • Does stress influence your breathing?∗ • Do you notice if your emotions have any effect on your respiratory problems? • Are you aware of any respiratory support groups in your area?

Value-Belief • What do you think causes/has caused your respiratory problem(s)? • How are you feeling right now? • Do you think the things you have been told to do for your respiratory problems help? If not, why? • What are you looking for/expecting from the HCP today, in terms of your breathing problem(s)?



If answer is “yes” to any of the above questions, ask the patient to

describe.

Medications Take a thorough medication history, including the names of prescription and over-the-counter (OTC) medications and nonprescription (illicit) substances. Ask about the dose (if known), frequency, length of time taken, any side effects, and the reason for taking the medication. Assess for overuse of short-term bronchodilators as a key indicator of symptom control. Cough is a common side effect of angiotensin-converting enzyme (ACE) inhibitors. Encourage the patient to bring all medication bottles and any inhalers to each visit with an HCP. If the patient is using O2 for a breathing problem, record the fraction of inspired O2 concentration (FIO2), flow rate (liters per minute), method of administration, number of hours used per day, and effectiveness of the therapy. Assess safety practices, including the patient’s cognitive and physical ability related to using O2 and any metered-dose inhalers.

Surgery or Other Treatments Find out if the patient has been hospitalized for a respiratory problem. Note the dates, therapy (including surgery), and status of the problem. Determine if the patient has ever been intubated because of a respiratory problem. Ask about the use of and response to respiratory treatments, such as a nebulizer, humidifier, airway clearance modalities (see Chapter 28), high-frequency chest wall oscillation, postural drainage, and percussion.

Functional Health Patterns Health history questions to ask a patient with a respiratory problem are outlined in Table 25.3.

Health Perception–Health Management Pattern Ask the patient if there has been a perceived change in health status

within the last several days, months, or years. In COPD, lung function declines slowly over many years. The patient may not notice this decline because they have been altering activity to accommodate reduced tolerance. If an upper respiratory tract infection is superimposed on a chronic problem, dyspnea and decreased exercise tolerance may occur very quickly. In asthma, symptoms may occur or worsen during exercise, in the presence of mold, or with changes in temperature or air pollution. Explore common manifestations of respiratory problems (e.g., cough, dyspnea). Describe the course of the patient’s illness, including when it began, type of symptoms, and factors that worsen or relieve these symptoms. Because of the chronic nature of respiratory problems, the patient may relate a change in symptoms (rather than the onset of new symptoms) when describing the present illness. For example, increased shortness of breath or increased purulence of sputum may suggest an acute exacerbation of COPD. If a cough is present, assess its quality. For example, a loosesounding cough occurs with secretions. A dry, hacking cough may mean an airway irritation or obstruction. A harsh, barky cough suggests upper airway obstruction from inhibited vocal cord movement due to subglottic edema. Assess whether the cough is strong enough to clear secretions. Note whether it is productive or nonproductive of secretions. Determine if the cough is acute or chronic (longer than 3 weeks in duration) or if it first began with an upper respiratory tract infection. The pattern and cause of the cough are determined by asking questions such as: What has been the pattern of coughing? Has it been regular or paroxysmal (i.e., sudden, periodic onset) or related to a time of day, the weather, certain activities, talking, or deep breathing? Any change over time? Do you clear your throat a lot? What have you tried to relieve the coughing? Did you try any prescription or OTC drugs? If the patient has a productive cough, evaluate the following characteristics of sputum: amount, color, consistency, and odor. Quantify the amount of sputum per day. Note any recent increases or decreases in the amount. Sputum is normally clear or slightly whitish.

If a patient is a cigarette smoker, the sputum is usually clear to gray with occasional specks of brown. The patient with COPD may have clear, whitish, or slightly yellow sputum, especially in the morning on rising. If the patient reports any change from baseline color, suspect pulmonary complications. Note any changes in consistency of sputum to thick, thin, or frothy and pink tinged. These changes may indicate dehydration, postnasal drip or sinus drainage, or possible pulmonary edema. Normally sputum should be odorless. A foul odor or exceptionally bad breath or taste in the mouth suggests an infectious process. Ask the patient if sputum production increases or decreases with changes in position (e.g., increased with lying down) or activity. When assessing phlegm, determine if the patient has a history of spitting or coughing up blood (hemoptysis). Hemoptysis can range from a slight streaking of blood in the sputum to massive coughing up of blood. The patient may not be able to tell between hemoptysis and hematemesis (vomiting blood). Hemoptysis occurs with a variety of conditions such as pneumonia, TB, lung cancer, and severe bronchiectasis. Assess for a history of any difficulty breathing. For example, wheezes are musical sounds that can be audible. Wheezing indicates some degree of airway obstruction, such as asthma, foreign body aspiration, and emphysema. Assess for any history of family exposure to Mycobacterium tuberculosis.

Genetic Risk Alert • Respiratory problems that have a strong genetic link include cystic fibrosis, COPD from α1-antitrypsin deficiency, and asthma. • If people have a family history of these respiratory problems, they have a greater risk for developing them. • Although cigarette smoking is a major risk factor for COPD, only a minority of cigarette smokers develop symptomatic disease. The risk for COPD related to cigarette smoking is genetically

related. • Determine if there is a family history of any respiratory problems that may have genetic or familial tendencies. Smoking is the most important risk factor for COPD and lung cancer. Ask about cigarette use and find out about the use of any tobacco products. This includes cigars, pipes, chewing tobacco, electronic cigarettes (e-cigarettes), and hookah (instrument for vaporizing and smoking flavored tobacco). Find out about exposure to secondhand smoke. Determine if the patient has tried to quit using tobacco products, including using prescription, OTC, and herbal remedies. Discuss current and past smoking habits. Quantify smoking habits in pack-years. Do this by multiplying the number of cigarettes smoked per day by the number of years smoked. For example, a person who smoked 20 cigarettes per day for 15 years has a 15 pack-year history. Assess if the patient received immunizations for influenza (flu) and pneumococcal pneumonia. Patients should receive an influenza vaccine yearly in the fall. Recommendations for pneumococcal vaccines are shown in Table 27.5. Ask where the patient has lived and traveled. Risk factors for TB include prior residence in China, India, Africa, the former Soviet Republics, Latin America, or any developing country. Other TB risk factors include exposure to people with high rates of TB transmission, such as the homeless, injection drug users, and people with HIV infection. Risk factors for fungal lung infections include those exposed to bird and rodent feces or polluted water, those working closely with the soil, and immunocompromised patients. Ask the patient about the use of equipment to manage respiratory symptoms (e.g., home O2 equipment, inhalers, devices for sleep apnea). Find out the type of equipment used, cleaning of the device, frequency of use, its effect, and any side effects. Have patients show you the use of their inhalers. Many patients do not use these devices correctly (see Chapter 28).

Nutritional-Metabolic Pattern

Weight loss can be a symptom of respiratory disease. Determine if weight loss was intentional, and, if not, if food intake is changed by anorexia (from medications), fatigue (from hypoxemia, increased work of breathing), or feeling full quickly (from lung hyperinflation). Anorexia, weight loss, and chronic malnutrition are common in patients with COPD, lung cancer, TB, and chronic severe infection (bronchiectasis). Assess fluid intake. Dehydration can cause sputum to thicken and obstruct the airway. Rapid weight gain from fluid retention may impair gas exchange.

Elimination Pattern Healthy elimination habits depend on a healthy balance between activity and rest. Activity intolerance secondary to dyspnea could result in incontinence, when unable to reach a toilet when needed. Dyspnea can be the cause of limited mobility, which can cause constipation. Ask the patient with dyspnea about frequency, urgency, and elimination patterns (e.g., day vs night). People with a chronic cough, especially women, may have urinary incontinence during paroxysms of coughing.

TABLE 25.4 Dyspnea Rating ScaleModified Borg

Rating Scale for Perceived Dyspnea Rate 0

Description Nothing at all

0.5

Very, very slight shortness of breath

1

Very mild shortness of breath

2

Mild shortness of breath

3

Mild shortness of breath or breathing difficulty

4

Somewhat severe

5

Strong or hard breathing

6

7

Severe shortness of breath or very hard breathing

8 9

Extremely severe

10

Shortness of breath so severe you need to stop

From Hillegass E: Essentials of cardiopulmonary physical therapy, ed 4, Philadelphia, 2017, Saunders.

Activity-Exercise Pattern Determine if dyspnea limits activity. Assess whether the patient’s residence (e.g., number of steps, levels) poses any problems. Ask the patient about the perceived degree of the dyspnea (Table 25.4). For example, can the patient walk up 1 flight of stairs without stopping because of dyspnea? Is dyspnea associated with any activity better, worse, or about the same in the last few days? Months? Determine if the patient has difficulty breathing in a certain position, or if dyspnea is relieved by assuming a different position (e.g., tripod position in COPD). Discuss whether the patient can carry out activities of daily living without dyspnea or other respiratory symptoms. If unable, record the amount and type of care the patient needs. Immobility and sedentary habits are risk factors for hypoventilation leading to atelectasis or pneumonia.

Sleep-Rest Pattern Determine if the patient wakes up at night because of pulmonary problems. The patient with asthma or COPD may awaken with chest tightness, wheezing, or coughing. This suggests a need for adjunct therapy or other medication changes. The patient with heart disease (e.g., heart failure) may sleep with the head elevated on several pillows to avoid respiratory problems brought on by lying flat (orthopnea). Excess weight interferes with normal ventilation and may cause sleep apnea (see Chapter 7). Extremely obese persons may hypoventilate while awake or asleep. Manifestations of sleep apnea include snoring, insomnia, abrupt awakenings, daytime drowsiness,

and early morning headaches. Night sweats may be a sign of TB.

Cognitive-Perceptual Pattern Because hypoxia can cause neurologic symptoms, ask the patient about apprehension, restlessness, irritability, and memory changes. These can indicate inadequate cerebral oxygenation (Table 25.1). Assess the patient’s cognitive ability to cooperate with treatment. Hypoxemia interferes with the ability to learn and retain information. Failure or inability to take part in needed therapy may result in worsening of respiratory problems. For this reason, teaching may be more effective if the caregiver is present during teaching sessions to provide reinforcement later. Ask about any discomfort or pain with breathing. Explore reports of chest pain carefully to rule out heart involvement. Problems such as pleurisy, fractured ribs, and costochondritis cause chest pain. Careful assessment of the patient having pain with breathing, such as onset, exact location of the pain, and factors that make the pain better or worse, can help establish a diagnosis.

Self-Perception–Self-Concept Pattern Dyspnea limits activity, impairs ability to fulfill normal roles, and often alters self-esteem. A patient may be reluctant to appear in public with a highly visible nasal cannula and O2 equipment. A barrel chest, clubbed fingers, pursed-lip breathing, and frequent expectoration of sputum or throat clearing can be embarrassing and can lead to social isolation. Explore with the patient any body image concerns. Referral to a support group or pulmonary rehabilitation program may be beneficial in developing a support system and coping strategies.

Role-Relationship Pattern Acute and chronic respiratory problems can seriously affect performance in work or other activities. Discuss the impact of medications, O2 therapy, and special routines (e.g., pulmonary hygiene for cystic fibrosis) on the patient’s family, job, and social life.

Review the nature of the patient’s work and frequency and intensity of exposure to fumes, toxins, asbestos, coal, fibers, or silica. Ask whether symptoms are worse in specific situations (e.g., home vs. work environments). Hobbies, such as woodworking (sawdust) or pottery (silica), and animal exposure (allergies) can cause respiratory problems. Because of hyperreactive airways, exposure to fumes, smoke, and other chemicals may trigger an attack in the patient with asthma.

Sexuality-Reproductive Pattern Most patients can continue to have satisfactory sexual relationships despite marked physical limitations. In a tactful manner, ask whether breathing difficulties have caused changes in sexual activity. If so, discuss positions that decrease dyspnea during sexual activity and alternative strategies for sexual fulfillment. For example, patients may need to perform good pulmonary hygiene (bronchodilators, coughing, deep breathing) before intimacy. They may need to use O2 therapy equipment during intercourse just like they would with any strenuous physical activity.

Coping–Stress Tolerance Pattern Dyspnea causes anxiety, and anxiety worsens dyspnea. The result is a vicious cycle—the patient avoids activities that cause dyspnea, becoming more deconditioned and more dyspneic. The outcome is often physical and leads to social isolation. Assess how often the patient leaves home and interacts with others. Referral to a support group or pulmonary rehabilitation program may be helpful. The chronic nature of many respiratory problems, such as COPD and asthma, can cause prolonged stress. Ask about the patient’s coping strategies to manage this stress.

Value-Belief Pattern Determine the patient’s adherence to his or her treatment program. Explore possible reasons for lack of adherence, including conflict with

cultural beliefs, financial constraints (e.g., costs of prescriptions), or failure to understand benefit. Correct misinformation and provide upto-date information about respiratory conditions and medication management. Including the patient and caregiver in the planning of care can improve adherence.

Objective Data Physical Examination Vital signs are important data to collect before examining the respiratory system.

Nose Inspect the nose for patency, inflammation, deformities, symmetry, and discharge. Check each nare for air patency with respiration while briefly occluding the other nare. Tilt the patient’s head backward and push the tip of the nose upward

Case Study Subjective Data

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A focused subjective assessment of F.T. revealed the following information: PMH: COPD, hypertension, heart failure, benign prostatic hyperplasia. No history of allergies. Medications: Metoprolol (Toprol XL) 50 mg daily PO, furosemide 20 mg PO daily, finasteride (Proscar) 5 mg/day PO, Advair inhaler (fluticasone and salmeterol) 2 puffs twice daily, and albuterol inhaler 2 puffs every 4hr PRN. Uses O2 @ 3L/min via nasal cannula at home for the past 10 years. Health Perception–Health Management: States he usually manages his COPD well with the Advair inhaler and occasional use of the albuterol inhaler. He thinks he caught a cold from his granddaughter last week. Increasing difficulty breathing, even with albuterol. Has a history of 30 pack-years of smoking, quitting 5 years ago. Nutritional-Metabolic Pattern: Eating and drinking very little over past 2 to 3 days. Elimination: Voiding small amounts of dark, concentrated urine (mostly at night). Activity-Exercise: At present, cannot walk 100 feet without feeling short of breath. Cannot walk up 1 flight of stairs (21 steps) to get in or out of his apartment without stopping to catch his breath. Sleep-Rest: Difficulty sleeping. Last night he slept upright in his recliner. Cognitive-Perceptual: Denies any pain associated with shortness of breath. Feels slightly irritable because of lack of sleep. Coping–Stress Tolerance: Does not know how he will manage to get groceries or clean his apartment. His daughter lives an hour away and has 3 children in school.

Discussion Questions

1. Of the information provided, which subjective assessment findings are of most concern to you? 2. From the information provided from F.T., what other information would you ask him about his condition (time permitting)? 3. What type of assessment would be most appropriate for F.T.: comprehensive, focused, or emergency? 4. F.T. cannot use his inhaler appropriately while he is talking with you. Is this a good time to teach him about the proper use of his inhaler? 5. What will you include in the physical assessment? What would you think will be priorities in your physical assessment? You will learn about the physical assessment of the respiratory system in the next section. (See p. 467 for more information on F.T.) Answers available at http://evolve.elsevier.com/Lewis/medsurg. gently. With a nasal speculum and a good light, inspect the interior of the nose. The mucous membrane should be pink and moist, with no evidence of edema (bogginess), exudate, or bleeding. Inspect the nasal septum for deviation, perforations, and bleeding. Some septal deviation is normal in an adult. Inspect the turbinates for polyps, which are abnormal, fingerlike projections of swollen nasal mucosa. Polyps may result from long-term irritation of the mucosa (e.g., from allergies). Assess any discharge for color and consistency. Purulent and malodorous discharge could occur with a foreign body. Watery discharge could be related to allergies or from cerebrospinal fluid. Bloody discharge could be from trauma or dryness. Thick mucosal discharge could mean an infection.

Mouth and Pharynx Using a good light source, inspect the interior of the mouth for color, lesions, masses, gum retraction, bleeding, and poor dentition. Inspect the tongue for symmetry and lesions. Observe the pharynx by

pressing a tongue blade gently against the middle of the back of the tongue. If the oropharynx is tight, have the patient yawn, since this usually allows more structures to be visible. The pharynx should be smooth and moist, with no evidence of exudate, ulcerations, swelling, or postnasal drip. Note the color, symmetry, and any enlargement of the tonsils. Stimulate the gag reflex by placing a tongue blade along the side of the pharynx, at the back of the tongue. A normal response (gagging) means that cranial nerves IX (glossopharyngeal) and X (vagus) are intact and that the airway is protected.

Neck Inspect the neck for symmetry and tender or swollen areas. Palpate the lymph nodes while the patient is sitting erect with the neck slightly flexed. Progression of palpation is from the nodes around the ears, to the nodes at the base of the skull, and then to those under the angles of the mandible to the midline. The patient may have small, mobile, nontender nodes (shotty nodes), which are not a sign of a pathologic condition. Tender, hard, or fixed nodes may indicate disease. Describe the location and characteristics of any palpable nodes.

Thorax and Lungs Picture imaginary lines on the chest to help identify abnormalities (Fig. 25.2). Describe abnormalities in terms of their location relative to these lines (e.g., 2 cm lateral from the right midclavicular line). Chest examination is best done in a well-lit, warm room with measures taken to ensure the patient’s privacy. Expose the patient’s chest. Perform all physical assessment maneuvers (inspection, palpation, percussion, auscultation) on either the anterior or the posterior chest first rather than moving from anterior to posterior or vice versa with each maneuver. It is best to begin on the posterior chest, particularly with female patients, since you can obtain more information without interference from breast tissue. If the patient tires or you are interrupted, you will obtain baseline data with the most information from examining the posterior chest.

When assessing the posterior chest, ask the patient to lean forward with arms folded. This position moves the scapulae away from the spine, exposing more of the area you need to examine. When assessing the anterior chest, have the patient sit upright or position the patient supine with the head of the bed elevated to 30 degrees (semiFowler’s position). The patient may need to lean forward for support on the bedside table to facilitate breathing. Inspection First, observe the patient’s appearance and note any evidence of respiratory distress, such as tachypnea or use of accessory muscles. Next, determine the shape and symmetry of the chest. Chest movement should be equal on both sides, and the anterior-posterior (AP) diameter should be less than the side-to-side or transverse diameter. Normal AP ratio is 1:2. An increase in AP diameter (e.g., barrel chest) may be due to normal aging or result from lung hyperinflation. Look for abnormalities in the sternum (e.g., pectus carinatum [a prominent protrusion of the sternum]) and pectus excavatum (an indentation of the lower sternum above the xiphoid process). Note any spinal curvature. Spinal curvatures that affect breathing include kyphosis, scoliosis, and kyphoscoliosis. Observe the respiratory rate, depth, and rhythm. The normal adult respiratory rate is 12 to 20 breaths/min. Inspiration (I) should take half as long as expiration (E) (I/E ratio = 1:2). Observe for abnormal breathing patterns, such as Kussmaul (rapid, deep breathing), CheyneStokes (abnormal respirations characterized by alternating periods of apnea and deep, rapid breathing), or Biot’s (irregular breathing with apnea every 4 to 5 cycles) respirations. Skin color provides clues to respiratory status. Cyanosis, a late sign of hypoxemia, is best seen in light-skinned patients as a bluish tinge to the mucous membranes, lips, and palms of the hands. In dark-skinned persons, cyanosis may be seen as a gray or white discoloration in the conjunctivae or around the mouth. Causes of cyanosis include hypoxemia or decreased cardiac output. Inspect the fingers for evidence of long-standing hypoxemia, known as clubbing. It is an

increase in the angle between the base of the nail and the fingernail to 180 degrees or more. Clubbing usually accompanied by an increase in the depth, bulk, and sponginess of the end of the finger. Palpation Determine tracheal position by gently placing the index fingers on either side of the trachea just above the suprasternal notch and gently pressing backward. Normal tracheal position is midline; deviation to the left or right is abnormal. Tracheal deviation occurs away from the side of a tension pneumothorax or a neck mass, but toward the side of a pneumonectomy or lobar atelectasis. Symmetry of chest expansion and extent of movement are determined at the level of the diaphragm. Place your hands over the lower anterior chest wall along the costal margin and move them inward until the thumbs meet at midline. Ask the patient to breathe deeply. Observe the movement of the thumbs away from each other. Normal expansion is 1 in (2.5 cm). Hand placement on the posterior side of the chest is at the level of the tenth rib. Move the thumbs until they meet over the spine (Fig. 25.5). You can check expansion anteriorly or posteriorly. It is not necessary to check both. Normal chest movement is equal. Unequal expansion occurs when air entry is limited by conditions involving the lung (e.g., atelectasis, pneumothorax) or the chest wall (e.g., incisional pain). Equal but decreased expansion occurs in conditions that produce a hyperinflated or barrel chest or in neuromuscular diseases (e.g., amyotrophic lateral sclerosis, spinal cord lesions). Movement may be absent or unequal over a pleural effusion, an atelectasis, or a pneumothorax. Fremitus is the vibration of the chest wall made by vocalization. You can feel tactile fremitus by placing the palmar surface of your hands against the patient’s chest with the fingers hyperextended. Ask the patient to repeat a phrase, such as “boy-oh-boy,” “toy boat,” or “blue balloons,” in a deeper, louder-than-normal voice. At the same time, move your hands from top to bottom on the patient’s chest (Fig. 25.6). As you palpate, simultaneously compare vibrations (right side

vs. left side, from top to bottom). Tactile fremitus is most intense by the sternum and between the scapulae because these areas are closest to the major bronchi. Fremitus is less intense farther away from these areas.

FIG. 25.5 Estimation of thoracic expansion. A, Exhalation. B, Maximal inhalation.

Note any increase, decrease, or absence of fremitus. Increased fremitus occurs when the lung becomes filled with fluid or is denser. As the patient’s voice moves through a dense tissue or fluid, you can feel that the vibration is increased. This happens with pneumonia, lung tumors, thick bronchial secretions, and above a pleural effusion (the lung is compressed upward). Fremitus is decreased if the hand is farther from the lung (e.g., pleural effusion) or the lung is hyperinflated (e.g., barrel chest). Absent fremitus may occur with

pneumothorax or atelectasis. The anterior of the chest is harder to palpate for fremitus because of the large muscles and breast tissue. Percussion Percussion is used to assess the density or aeration of the lungs. Percussion sounds are described in Table 25.5. (The technique for percussion is described in Chapter 3 and Fig. 3.3.)

FIG. 25.6 Hand position for tactile fremitus. Place the palms of the hands in the position designated as “low’ on the right and left sides of the chest. Compare the intensity of vibrations. Continue for all positions in each sequence.

TABLE 25.5 Percussion Sounds

Sound

Description Sound with medium-intensity pitch and duration heard over areas of “mixed” Dull solid and lung tissue, such as top area of liver, partially consolidated lung tissue (pneumonia), or fluid-filled pleural space Soft, high-pitched sound of short duration heard over very dense tissue where Flat air is not present, such as posterior chest below level of diaphragm Hyperresonance Loud, lower pitched sound than normal resonance heard over hyperinflated lungs, such as in chronic obstructive pulmonary disease and acute asthma Low-pitched sound heard over normal lungs Resonance Drum-like, loud, empty quality sound heard over pneumothorax Tympany

FIG. 25.7 Sequence for auscultation of the chest. A, Anterior sequence. B, Lateral sequence. C, Posterior sequence. Place the stethoscope at each position and listen to at least 1 complete inspiratory and expiratory cycle. Keep in mind that with a female patient the breast tissue will modify the completeness of the anterior examination.

FIG. 25.8 Diagram of percussion areas and sounds on the anterior side of the chest. For percussion, tap the chest at each designated position, moving downward from side to side. Compare percussion sounds at all positions. Redrawn from Thompson JM, McFarland GK, Hirsch JE, et al: Mosby’s clinical nursing, ed 5, St Louis, 2002, Mosby.

The anterior chest is percussed with the patient in a semi-sitting or supine position. Starting above the clavicles, percuss downward, intercostal space by intercostal space (Fig. 25.7). The area over lung tissue should be resonant, except for the area of cardiac dullness (Fig. 25.8). To percuss the posterior chest, have the patient sit leaning forward with arms folded. The posterior chest should be resonant over lung tissue to the level of the diaphragm (Fig. 25.9). Auscultation During chest auscultation, have the patient breathe slowly and a little more deeply than normal through the mouth. Auscultation should proceed from the lung apices to the bases, comparing opposite areas

of the chest. If the patient is in mild respiratory distress or you think the patient will tire easily, start at the bases. Place the stethoscope over lung tissue, not over bony prominences. At each placement of the stethoscope, listen to at least 1 cycle of inspiration and expiration. Visualize the location of normal breath sounds by using a lung model (Fig. 25.10). Lung sounds are heard anteriorly from a line drawn perpendicular from the sternum lateral to the midclavicular line. From the xiphoid process, palpate inferiorly (down) 2 ribs in the midaxillary line and around to the posterior chest. This gives you a fairly accurate and easy way to locate the lung fields. When recording the location of lung sounds, divide the anterior and posterior right lung into thirds (upper, middle, and lower) and the left lung into upper and lower areas. With practice, you will be able to identify which lobes of the lung has particular lung sounds.

FIG. 25.9 Diagram of percussion areas and sounds on the posterior side of the chest. Percussion proceeds from the lung apices to the lung

bases while comparing sounds in opposite areas of the chest. Redrawn from Thompson JM, McFarland GK, Hirsch JE, et al: Mosby’s clinical nursing, ed 5, St Louis, 2002, Mosby.

The 3 normal breath sounds are bronchial, bronchovesicular, and vesicular. Bronchial sounds are loud, high-pitched sounds that resemble air blowing through a hollow pipe. Bronchial sounds have an inspiratory to expiratory (I/E) ratio of 2:3, with a gap between inspiration and expiration. To hear bronchial breath sounds, place the stethoscope next to the trachea in the neck. Bronchovesicular sounds have a medium pitch and intensity. They are best heard anteriorly between the first and second intercostal space and posteriorly between the scapulae. Bronchovesicular sounds have a 1:1 ratio, with inspiration equal to expiration. Vesicular sounds are relatively soft, lowpitched, gentle, rustling sounds. They are heard over all lung areas except the major bronchi. Vesicular sounds have a 3:1 ratio, with inspiration 3 times longer than expiration.

FIG. 25.10 Normal auscultatory sounds. Redrawn from Beare PG, Myers JL: Adult health nursing, ed 3, St Louis, 1998, Mosby.

We classify breath sounds into 2 main categories: normal and abnormal (adventitious). There are a variety of terms that have been inconsistently used to describe abnormal breath sounds. Adventitious breath sounds include crackles (fine and coarse), wheezes, stridor, and pleural friction rub (Table 25.6). A focused assessment is used to evaluate the status of previously identified respiratory problems and

to monitor for signs of new problems. A focused assessment of the respiratory system is shown in the box on this page. As you begin your assessment of lung sounds, first note the air entry, which may be adequate, slightly decreased, or decreased. Absent air entry in any part of the lung is an assessment finding that you should report at once. Next, listen for the breath sounds and the presence of normal and adventitious sounds. Are the normal breath sounds where you would expect to hear them? Focus your assessment on the characteristics of

Case Study Objective Data: Physical Examination

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Physical examination findings of F.T. are as follows: Temperature: 38°C (100.4°F), apical pulse 110 (irregular), respiratory rate 30 (regular, shallow, slightly labored), BP 170/90. Sitting on edge of bed with arms resting on bedside table. Skin color normal for race with no signs of cyanosis. Using accessory muscles in neck and shoulders. Trachea midline. Barrel-shaped chest; chest expansion minimal but equal. Prolonged expiration. Slight clubbing noted. Edema: 3+ pitting edema of both lower legs and feet, bilaterally. Lungs: adequate air entry at apices bilaterally with fine crackles; decreased air entry to right middle lobe and both bases with coarse crackles. Slight expiratory wheeze heard throughout all lung fields. Cough: moist, productive, with yellow-tinged sputum. You decide to check F.T.’s O2 saturation (SpO2). His SpO2 is 87% on room air.

Discussion Questions 1. What physical assessment findings are of most concern to you? 2. Identify 3 interventions that may be implemented immediately. 3. With F.T.’s physical assessment information, what diagnostic studies would you expect to be ordered? (See p. 475 for more information on F.T.) Answers available at http://evolve.elsevier.com/Lewis/medsurg. any abnormal sound, including the location, pitch (e.g., high, low), duration of sound, and whether the sound is heard on inspiration, expiration, or both. Assessment abnormalities of the thorax and lungs are outlined in Table 25.6. A record of the normal physical assessment of the respiratory system is shown in Table 25.7. Chest examination findings in common pulmonary problems are described in Table 25.8. Agerelated changes in the respiratory system and assessment findings are outlined in Table 25.2.

Focused Assessment Respiratory System Use this checklist to make sure the key assessment steps have been done.

Subjective Ask the patient about any of the following and note responses.

Shortness of breath

Y

N

Pain with breathing

Y

N

Cough

Y

N

Sputum production (color, quantity)

Y

N

Wheezing

Y

N

Objective: Physical Examination Observe

Respirations: Rate, quality, and pattern Accessory muscle use Mouth or nose breathing

Inspect Neck for position of trachea Shape, symmetry, and movement of chest wall Skin and nails for integrity and color

Palpate Chest and back for abnormalities (i.e. masses)

Auscultate Lung sounds (anterior and posterior)

Objective: Diagnostic Check the following diagnostic tests for abnormal results.

Arterial blood gases Chest x-ray Hemoglobin Hematocrit

TABLE 25.6 Assessment

AbnormalitiesRespiratory System

Diagnostic Studies of Respiratory System Numerous diagnostic studies are available to assess the respiratory system. Tables 25.9 through 25.17 describe common studies. Select studies are described in more detail here. Two methods are used to assess the efficiency of gas transfer in the lung and tissue oxygenation: (1) pulse oximetry and (2) analysis of arterial blood gases (ABGs) (Table 25.9). These are primarily used to assess for hypoxia. For the patient with normal or near-normal cardiac function, assessing PaO2 or SaO2 is usually enough to determine the level of oxygenation. With either one, we can also use CO2 monitoring to assess for hypercapnia to determine patient’s oxygenation and ventilatory status. The patient with impaired cardiac output or hemodynamic instability (e.g., altered level of consciousness, changes in heart rate and rhythm, low BP) may have inadequate tissue O2 delivery and/or abnormal O2 consumption. For these patients, we can evaluate a mixed venous blood gas.

Oximetry Arterial O2 saturation can be monitored noninvasively and continuously using a pulse oximetry probe on the finger, toe, ear, forehead, or bridge of the nose. The abbreviation SpO2 is used to indicate the O2 saturation of hemoglobin as measured by pulse oximetry. SpO2 and heart rate are displayed on the monitor as digital readings. Normal SpO2 values are 94% to 99% (Table 25.10).

TABLE 25.7 Normal Physical Assessment of the

Respiratory System

In many inpatient areas, SpO2 is assessed with each routine vital sign check. Oximetry is also used during exercise testing and when adjusting flow rates during O2 therapy. Pulse oximetry is especially valuable in perioperative and critical care situations, in which anesthesia, sedation, or decreased consciousness may mask hypoxia. Changes in SpO2 can be detected and treated quickly (Table 25.9). Values obtained by pulse oximetry are less accurate if the SpO2 is less than 70%.10 At this level the oximeter may display a value that is ±4% of the actual value. For example, if the SpO2 reading is 70%, the actual value can range from 66% to 74%. Pulse oximetry is inaccurate if hemoglobin variants (e.g., carboxyhemoglobin, methemoglobin) are present. Other factors that can alter the accuracy of pulse oximetry include motion, low perfusion, anemia, cold extremities, bright fluorescent lights, intravascular dyes, thick acrylic nails, and dark skin color. If there is doubt about the accuracy of the SpO2 reading, obtain an ABG analysis to verify the values.

Arterial Blood Gases ABGs are obtained to determine oxygenation status and acid-base

balance. ABG analysis includes measurement of the PaO2, PaCO2 (the partial pressure of CO2 in arterial blood), acidity (pH), bicarbonate (HCO3−), and SaO2. Normal values for ABGs are shown in Table 25.11. Blood for ABG analysis can be obtained by arterial puncture or from an arterial catheter, which is usually inserted into the radial or femoral artery. Both techniques allow only intermittent analysis, but an arterial catheter permits ABG sampling without repeated arterial punctures. The normal PaO2 decreases with advancing age. It varies in relation to the distance above sea level. At higher altitudes, the barometric pressure is lower, resulting in a lower inspired O2 pressure and a lower PaO2.

TABLE 25.8 Chest Examination Findings in

Respiratory Problems

TABLE 25.9 Diagnostic Studies: Oxygenation

SvO2, venous O2 saturation.

TABLE 25.10 Normal and Critical Values for PaO2

and SpO2

TABLE 25.11 Normal Arterial Blood Gas Values

Laboratory Value

Sea Level BP 760 mm Hg 7.35–7.45

1 Mile Above Sea Level BP 629 mm Hg 7.35–7.45

PaO2†

80–100 mm Hg

65–75 mm Hg

SaO2†

>95%

>95%

PaCO2

35–-45 mm Hg

35–45 mm Hg

HCO3−

22–26 mEq/L (mmol/L)

22–26 mEq/L (mmol/L)

pH

BP, Barometric pressure; HCO3−, bicarbonate; PaO2, partial pressure of O2 in arterial blood; PaCO2, partial pressure of arterial CO2; SaO2, arterial O2 saturation.

TABLE 25.12 Normal Venous Blood Gas Values

PvCO2, Partial pressure of CO2 in venous blood; PvO2, partial pressure of O2 in venous blood; SvO2, venous O2 saturation.

TABLE 25.13 Sputum Studies

TABLE 25.14 Interpreting Tuberculin Skin

Testing

Source: Centers for Disease Control and Prevention: Tuberculosis (TB) fact sheet: Tuberculin skin testing. Retrieved from www.cdc.gov/tb/publications/factsheets/testing/skintesting.htm.

CO2 Monitoring CO2 can be monitored using transcutaneous CO2 (PtCO2) and endtidal CO2 (PetCO2) capnography. Transcutaneous measurement of CO2 is a noninvasive method of estimating arterial pressure of CO2 (PaCO2) using an electrode placed on the skin.11 PetCO2 is the noninvasive measurement of alveolar CO2 during exhalation when CO2 concentration is at its peak. It is used to monitor and assess trends in the patient’s ventilatory status. Expired gases are sampled from the patient’s airway and are analyzed by a CO2 sensor that uses infrared light to measure exhaled CO2. The sensor may be attached to an adaptor on the endotracheal tube or the tracheostomy tube. A nasal cannula with a sidestream capnometer can be used in patients without an artificial airway. Capnography is usually presented as a graph of expiratory CO2 plotted against time.12 In the past, capnography was mainly used during and after surgery and in critical care units. Today’s PetCO2 monitors are portable and practical for use in emergency departments and on inpatient units.

Mixed Venous Blood Gases The pulmonary artery (PA) catheter is a flow-directed catheter. When it is positioned correctly, the tip of the catheter lies in the pulmonary artery. Blood drawn from a PA catheter is called a mixed venous blood gas (SvO2), because (1) it consists of venous blood that has returned to the right side of the heart from all parts of the body and (2) it samples blood just before blood enters the lungs to be oxygenated. Normal SvO2 is 60% to 80%. Other normal mixed venous values are given in Table 25.12. SvO2 can be monitored intermittently by obtaining a blood sample from the PA catheter or continuously via a fiberoptic sensor as part of a specific central line with SpO2 monitoring capability. Changes in SvO2 provide an early warning of a change in cardiac output or tissue O2 delivery. A decrease in SvO2 suggests that less O2 is being

delivered to the tissues or that more O2 is being consumed.

Sputum Studies Observe the patient’s sputum for color, volume, viscosity, and presence or absence of blood. We can obtain a sputum sample by expectoration, tracheal suction, or bronchoscopy. When the patient is unable to expectorate spontaneously, sputum may be collected by inhaling an irritating aerosol, usually hypertonic saline. This is called sputum induction. Specimens may be examined for culture and sensitivity to identify an infecting organism (e.g., Mycobacterium) or to confirm a diagnosis (e.g., cancer). Table 25.13 describes common sputum tests and specific responsibilities when obtaining samples.

TABLE 25.15 Diagnostic StudiesRespiratory

System

FIG. 25.11 Fiberoptic bronchoscope. A, The transbronchoscopic balloon-tipped catheter and the flexible fiberoptic bronchoscope. B, The catheter is introduced into a small airway and the balloon inflated with 1.5 to 2 mL of air to occlude the airway. Bronchoalveolar lavage is done by injecting and withdrawing 30-mL aliquots of sterile saline solution, gently aspirating after each instillation. Specimens are sent to the laboratory for analysis. A, Courtesy Olympus America Inc, Melville, NY.

Skin Tests Skin tests may be done to test for allergic reactions (see Chapter 13) or exposure to TB bacilli or fungi. Skin tests involve the intradermal injection of an antigen. Table 25.14 discusses how to interpret tuberculin skin testing. For example, a positive result on a TB skin test means that the patient has been exposed to the antigen. It does not

mean that the patient has TB. A negative result means either no exposure or a depression of cell-mediated immunity, which occurs in HIV infection. Our responsibilities are similar for all skin tests. First, to prevent a false-negative reaction, be sure that the injection is intradermal and not subcutaneous. After the injection, circle the site(s) and tell the patient not to remove the marks. When charting administration of the antigen, draw a diagram of the forearm and hand, and label the injection site. The diagram is especially helpful when the patient receives more than 1 test. When reading test results, use a good light. If an induration is present, use a marking pen to indicate the periphery on all 4 sides of the induration. As the pen touches the raised area, make a mark. Then determine the diameter of the induration in millimeters. Do not measure reddened, flat areas.

Endoscopy Bronchoscopy Bronchoscopy is a procedure in which the bronchi are visualized through a fiberoptic tube (Fig. 25.11). Bronchoscopy may be used for diagnostic purposes (obtain biopsy specimens) and for treatment (e.g., to remove mucous plugs, foreign bodies). Laser therapy, electrocautery, cryotherapy, and stents may be placed through a bronchoscope to achieve patency of an airway that has been partially or nearly fully obstructed by tumors (Table 25.15). Bronchoscopy can be done in an outpatient procedure room, in a surgical suite, or at the bedside in the critical care unit or on a medical-surgical unit. The patient may be positioned supine, in lowFowler’s, or even be seated. The HCP inserts the bronchoscope through the nose or mouth. Depending on the approach, the nasopharynx or oropharynx is anesthetized with local anesthetic spray. The bronchoscope is coated with water-soluble lubricant and inserted down into the airways. Small amounts (30 mL) of sterile saline may be injected through the scope and withdrawn and

examined for cells, a technique termed bronchoalveolar lavage (BAL). Bronchoscopy can be done through the endotracheal tube of a mechanically ventilated patient.

Lung Biopsy Lung biopsy may be done (1) transbronchially, (2) percutaneously or via transthoracic needle aspiration (TTNA), (3) by video-assisted thoracic surgery (VATS), or (4) as an open lung biopsy (Table 25.15). The purpose of a lung biopsy is to obtain tissue, cells, and/or fluid for evaluation. Specimens can be cultured or examined for cancer cells. Transbronchial biopsy involves passing a forceps or needle through the bronchoscope for a specimen. A combination of transbronchial lung biopsy and BAL is used to distinguish infection and rejection in lung transplant recipients. A percutaneous or TTNA biopsy involves inserting a needle through the chest wall, usually under bedside ultrasound or CT guidance. Because of the risk for a pneumothorax, a chest x-ray is done after TTNA. In VATS, a rigid scope with a lens is passed through a trocar placed into the pleura via 1 or 2 small incisions in the thoracic cavity. The HCP views the lesions in the pleura or peripheral lung on a monitor directly via the scope and can obtain biopsy specimens. A chest tube is kept in place until the lung expands. VATS is much less invasive than open lung biopsy. It is associated with shorter hospital stays and reduced mortality.13 It is ideal for pleural biopsy and resecting lung nodules. An open lung biopsy is used when other procedures cannot diagnose pulmonary disease. With the patient under anesthesia, the chest is opened with a thoracotomy incision and a biopsy specimen is obtained. Postprocedure care is the same as after thoracotomy (see Chapter 27).

Thoracentesis Thoracentesis is the insertion of a large-bore needle through the chest wall into the pleural space to obtain specimens for diagnostic

evaluation, remove pleural fluid, or instill medication (Fig. 25.12). The patient is positioned sitting upright, leaning on an overbed table with feet supported. The skin is cleansed and a local anesthetic (lidocaine) is injected subcutaneously. A percutaneous catheter may be left in to allow further drainage of fluid (Table 25.15).

Pulmonary Function Tests Pulmonary function tests (PFTs) measure lung volumes and airflow. The results of PFTs can diagnose pulmonary disease, monitor disease progression, assess response to bronchodilators, and evaluate disability. Airflow measurement is obtained by trained personnel using a spirometer. The patient inserts a mouthpiece, takes as deep a breath as possible, and exhales as hard, as fast, and for as long as possible. Verbal coaching is given to ensure that the patient continues blowing out until exhalation is complete. Computer software calculates the patient’s percent of predicted values, that is, how well the performance compares with an average based on age, gender, race, and height.14 Normal values are 80% to 120% of the predicted value. Normal values for PFTs are shown in Tables 25.16 and 25.17.

FIG. 25.12 Thoracentesis. A catheter is positioned in the pleural space to remove accumulated fluid.

TABLE 25.16 Lung Volumes and Capacities



Normal values vary with patient’s height, weight, age, race, and gender.

Spirometry may be done before and after giving a bronchodilator to determine the patient’s response. This helps gauge the reversibility of airway obstruction (e.g., asthma). A positive bronchodilator response is an increase of greater than 200 mL or 12% in FEV1 after administering a bronchodilator.

TABLE 25.17 Pulmonary Function Airflow



Normal values vary with patient’s height, age, race, and gender.

Home spirometry may be used to monitor lung function in people with asthma, cystic fibrosis, or COPD, as well as before and after lung transplantation or other thoracic surgeries. A peak flow meter is the hand-held instrument used at home. The person blows through it forcefully and quickly after taking a deep breath. Spirometry changes can warn of early lung transplant rejection or infection. Data from a peak flow meter provide important feedback to patients with asthma so that they can learn to change activities and medications in response to changes in peak expiratory flow rates. More specific pulmonary function parameters can be directly assessed at the bedside in a high-acuity or critical care unit to determine the need for or weaning and extubation from mechanical ventilation (see Table 65.13).

Case Study Objective Data: Diagnostic Studies

© Fuse/Thinkstock.

The HCP orders the following diagnostic studies for F.T.: • Pulse oximetry • Chest x-ray • 12-lead electrocardiogram (ECG) • CBC, basic metabolic panel (electrolytes, BUN, creatinine) • ABGs • Sputum for culture and sensitivity F.T.’s SpO2 is 87% on O2 @ 3/L min via nasal cannula. The chest xray shows a slightly enlarged heart and bilateral consolidation to both lower lobes. The 12-lead ECG reveals sinus tachycardia, rate 110, with no ST segment elevation or depression and no T-wave inversion. The ABGs show compensated respiratory alkalosis with hypoxemia. The WBC is 17,350/µL and potassium 2.9 mEq/L. Sputum results are pending. F.T. is admitted to the medical nursing unit.

Discussion Questions 1. Of the diagnostic test results, is anything abnormal? 2. Which results concern you most? 3. What do you think is the cause of F.T.’s problems? 4. What patient teaching can you do with F.T. as he is waiting to be admitted to the hospital unit? 5. What is the interprofessional team’s top priority for F.T. at this time? You will learn more about the upper and lower respiratory problems and chronic obstructive pulmonary disease (COPD) in the next 3 chapters. Answers available at http://evolve.elsevier.com/Lewis/medsurg.

Bridge to Nclex Examination

The number of the question corresponds to the same-numbered learning outcome identified at the beginning of this chapter.

1. The key anatomic landmark that separates the upper respiratory tract from the lower respiratory tract is the a. carina. b. larynx. c. trachea. d. epiglottis. 2. A patient asks, “How does air get into my lungs?” The nurse bases her answer on knowledge that air moves into the lungs because of a. positive intrathoracic pressure. b. contraction of the accessory abdominal muscles. c. stimulation of the respiratory muscles by the chemoreceptors. d. a decrease in intrathoracic pressure from an increase in thoracic cavity size. 3. The nurse can best determine adequate arterial oxygenation of the blood by assessing a. heart rate. b. hemoglobin level. c. arterial oxygen partial pressure. d. arterial carbon dioxide partial pressure. 4. Defense mechanisms that help protect the lung from inhaled particles and microorganisms include the (select all that apply) a. cough reflex.

b. mucociliary escalator. c. alveolar macrophages. d. reflex bronchoconstriction. e. alveolar capillary membrane. 5. A student nurse asks the RN what can be measured by arterial blood gas (ABG). The RN tells the student that the ABG can measure (select all that apply) a. acid-base balance. b. oxygenation status. c. acidity of the blood. d. bicarbonate (HCO3–). e. compliance and resistance. 6. To detect early signs or symptoms of inadequate oxygenation, the nurse would examine the patient for a. dyspnea and hypotension. b. apprehension and restlessness. c. cyanosis and cool, clammy skin. d. increased urine output and diaphoresis. 7. During the respiratory assessment of an older adult, the nurse would expect to find (select all that apply) a. a vigorous reflex cough. b. increased chest expansion. c. increased residual volume. d. decreased lung sounds at base of lungs. e. increased anteroposterior (AP) chest diameter. 8. When assessing subjective data related to the respiratory

health of a patient with emphysema, the nurse asks about (select all that apply) a. date of last chest x-ray. b. dyspnea during rest or exercise. c. pulmonary function test results. d. ability to sleep through the entire night. e. prescription and over-the-counter medication. 9. When auscultating the chest of an older patient in mild respiratory distress, it is best to a. begin listening at the apices. b. begin listening at the lung bases. c. begin listening on the anterior chest. d. Ask the patient to breathe through the nose with the mouth closed. 10. Which respiratory assessment finding does the nurse interpret as abnormal? a. Inspiratory chest expansion of 1 inch b. Symmetric chest expansion and contraction c. Resonance (to percussion) over the lung bases d. Bronchial breath sounds in the lower lung fields 11. The nurse is preparing the patient for a diagnostic procedure to remove pleural fluid for analysis. The nurse would prepare the patient for which test? a. Thoracentesis b. Bronchoscopy c. Pulmonary angiography d. Sputum culture and sensitivity

1. a, 2. d, 3. c, 4. a, b, c, d, 5. a, b, c, d, 6. b, 7. c, d, e, 8. b, d, e, 9. b, 10. d, 11. a For rationales to these answers and even more NCLEX review questions, visit http://evolve.elsevier.com/Lewis/medsurg.

Evolve Website/Resources List http://evolve.elsevier.com/Lewis/medsurg

Review Questions (Online Only) Key Points Answer Keys for Questions • Rationales for Bridge to NCLEX Examination Questions • Answer Guidelines for Case Study on pp. 460, 464, 467, and 475 Conceptual Care Map Creator Audio Glossary Supporting Media • Animations ○ Inhalation ○ Oxygenation ○ Pulse Oximetry ○ Respiration Cycle ○ Respiratory System Overview • Audio ○ Bronchial Breath Sounds ○ Bronchovesicular Breath Sounds ○ High-Pitched Crackles

○ High-Pitched Wheeze ○ Low-Pitched Crackles ○ Low-Pitched Wheeze ○ Pleural Friction Rub ○ Stridor ○ Vesicular Breath Sounds Content Updates

References 1. Patton KT, Thibodeau GA: Essentials of anatomy and physiology, ed 9, St Louis, 2016, Mosby. 2. Tatco V, Smith D: Carina. Retrieved from https://radiopaedia.org/articles/carina. 3. Meriam-Webster Dictionary: Anatomic dead space. Retrieved from: www.merriamwebster.com/medical/anatomical%20dead%20space. 4. Goel A, Gaillard F: Pores of Kohn. Retrieved from https://radiopaedia.org/articles/pores-of-kohn. 5. Stacy KM: Pulmonary anatomy and physiology. In: Urden LD, Stacy KM, Lough ME (ed): Critical care nursing: Diagnosis and management, ed 8, St Louis, 2018, Mosby. 6. DeWit SC, Stromberg HK, Dallred CV: Medicalsurgical nursing: Concepts and practice, ed 3, St Louis, 2017, Mosby. Whitten C: Don’t withhold oxygen from that CO2 retainer. Retrieved from https://airwayjedi.com/2016/01/09/dont-withhold-oxygen-from-thatco2-retainer/.

8. Rhoades RA, Bell DR: Medical physiology: Principles for

clinical medicine, ed 5, Philadelphia, 2018, WoltersKluwer. 9. Pathway Medicine: J receptors. Retrieved from www.pathwaymedicine.org/j-receptors. 10. Wilson SF, Giddens JF: Health assessment for nursing practice, ed 6, St Louis, 2017, Mosby. Horvath CM, Brutsche MH, Baty F, et al: Transcutaneous versus blood carbon dioxide monitoring during acute noninvasive ventilation in the emergency department, Swiss Med Wkly 146:w14373, 2016.

12. Luehrs P: Continuous end-tidal carbon dioxide monitoring. In Wiegand, DL (ed): AACN procedure manual for high acuity, progressive, and critical care, ed 7, St Louis, 2017, Saunders. 13. Jarrar D: Video-assisted thoracic surgery (VATS). Retrieved from https://emedicine.medscape.com/article/1970013-overview. 14. Mottram CD: Ruppel’s manual of pulmonary function testing, ed 11, St Louis, 2017, Mosby. ∗Evidence-based information for clinical practice.

26

Upper Respiratory Problems Eugene Mondor

LEARNING OUTCOMES 1. Describe the clinical manifestations and nursing and interprofessional management of problems of the nose. 2. Discuss the clinical manifestations and nursing and interprofessional management of problems of the paranasal sinuses. 3. Describe the clinical manifestations and nursing and interprofessional management of problems of the pharynx and larynx. 4. Relate the nursing and interprofessional management of the patient who has a tracheostomy. 5. Identify the steps involved in performing tracheostomy care and suctioning a patient with a tracheostomy. 6. Outline the risk factors for and clinical manifestations of head and neck cancer. 7. Discuss the nursing and interprofessional management of patients requiring surgery for head and neck cancer. 8. Explain essential components of discharge teaching for the patient going home with a permanent tracheostomy after total laryngectomy for cancer.

KEY TERMS allergic rhinitis, p. 480 decannulation, p. 493 deviated septum, p. 477 epistaxis, p. 478 laryngectomy, p. 494 laryngitis, p. 487 nasal polyps, p. 486 pharyngitis, p. 486 rhinoplasty, p. 478 sinusitis, p. 485 surgical cricothyroidotomy, p. 488 tracheostomy, p. 488 You really can change the world if you care enough. Marian Wright Edelman http://evolve.elsevier.com/Lewis/medsurg/

Conceptual Focus Cellular Regulation Functional Ability Gas Exchange Immunity Infection Sensory Perception Disorders of the upper respiratory system, including the nose, sinuses,

pharynx, and larynx, and the care of those undergoing surgery for head and neck cancers are the focus of this chapter. The primary concern with these problems is the impact on ventilation and oxygen (O2) availability. Upper airway problems can negatively affect sleep and impair the ability to obtain and maintain nutrition. Sinus and upper respiratory tract infections, allergies, and oral problems can change the senses of both smell and taste. The patient with head and neck cancer often has depression and changes in body image and sexuality.

Problems Of Nose And Paranasal Sinuses Deviated Septum Deviated septum is a deflection of the normally straight nasal septum. Although up to 80% of adults may have septa that are slightly off center, the diagnosis of deviated septum is generally reserved for those whose septa are severely shifted.1 Trauma to the nose, either at birth or later in life, is the most common cause of deviated septum.2 Deviated septum can interfere with both airflow and sinus drainage through the narrowed passageway. Symptoms vary depending on the degree of deviation. Minor septal deviations can range from asymptomatic to nasal congestion and frequent sinus infections. Manifestations of severe septal deviation include facial pain, nosebleeds (epistaxis), and obstruction to nasal breathing. The diagnosis of deviated septum is made during physical examination with a nasal speculum. The medical management of minor septal deviation focuses on symptom control. For nasal inflammation and congestion, use saline rinses and decongestants to clear nasal passages and analgesics for pain relief. For severe septal deviation, a nasal septoplasty, done under local or general anesthetic, reconstructs and properly aligns the deviated septum.

Nasal Fracture Nasal fracture is the most common facial fracture and the third most common fracture of any bone.3 They often occur from blunt trauma, including fights, automobile accidents, falls, and sports injuries. Using protective sports equipment and safeguarding against falls can prevent many nasal fractures. There is no universally accepted classification system for nasal fractures. We can classify nasal fractures according to the fracture pattern (e.g., impacted, comminuted) or based on direction of injury (e.g., lateral, frontal). Simple fractures may be unilateral or bilateral and typically have little or no displacement. Powerful frontal blows can cause complex fractures, which may involve damage to adjacent facial structures, such as the teeth or eyes. Patients with complex nasal fractures should be evaluated for injury to the cervical spine, orbital bone, or mandible.4 Complications include airway obstruction, nosebleeds, meningeal tears causing cerebrospinal fluid (CSF) leakage, septal hematoma, and cosmetic deformity. Diagnosis of a nasal fracture is based on health history and physical assessment. Although facial deformity with a nasal fracture is common, a nosebleed may be the only manifestation. Other manifestations include localized pain, crepitus on palpation, swelling, difficulty breathing out of the nostrils, and bruising. Assess the patient’s ability to breathe through each side of the nose. Note the presence of edema, bleeding, or hematoma. Periorbital bruising involving both eyes is called raccoon eyes. It suggests a basilar skull fracture (see Chapter 56). Inspect the nose internally for evidence of septal deviation, clear drainage, edema, or bleeding. Clear or pink-tinged persistent drainage after control of bleeding suggests a possible CSF leak. Checking this fluid for glucose at the bedside to help confirm the presence of CSF is not recommended because the result is highly unreliable. If needed, send a specimen to the laboratory to determine the fluid type. Goals of nursing management are to maintain a patent airway, reduce edema and pain, prevent complications, and provide

emotional support. The best way to maintain the airway is to keep the patient sitting upright. Apply ice to the face and nose in 10- to 20minute intervals to help reduce edema and bleeding. Give analgesia as ordered to control pain. Acetaminophen is preferred over nonsteroidal antiinflammatory drugs (NSAIDs) or acetylsalicylic acid (ASA; aspirin) for the first 48 hours to avoid prolonging clotting time and increasing the risk for bleeding. Nasal stuffiness may be relieved with nasal decongestants, saline nasal sprays, and a humidifier. The patient should avoid hot showers and alcohol for the first 48 hours to prevent an increase in swelling. Encourage the patient to quit or decrease smoking to help tissue healing. When a fracture is confirmed, the goals are to realign the fracture using closed or open reduction.5 Simple fractures are often reduced with manual manipulation. With complex nasal fractures, considerable swelling of soft tissues occurs. It may be necessary to wait to repair the fracture until after the edema subsides, which may be 5 to 10 days. Antibiotics should be considered for any nasal fracture with disruption to the mucosa. Surgical options include septoplasty and rhinoplasty. Septoplasty is done to correct a deviated septum. Patients have rhinoplasty for several reasons. Both procedures help maintain a patent airway, restore function of the nose, and help reestablish the patient’s cosmetic appearance. The presence of septal hematoma increases the patient’s risk for deformity and infection, which may require drainage and antibiotic therapy.

Rhinoplasty Rhinoplasty, surgical reconstruction of the nose, is done to improve airway function when trauma or developmental deformities result in nasal obstruction or for cosmetic reasons. When caring for rhinoplasty patients before surgery, assess the patient’s expectations of the surgery. Actual or perceived changes in body image (e.g., deformed or enlarged nose) can affect self-esteem and interactions with others. The HCP can use digital photographs to show patients their projected

appearance after surgery. These images can help patients decide whether to undergo rhinoplasty. Most rhinoplasty is an outpatient procedure using regional or general anesthesia. Nasal tissue is added or removed, and the nose may be lengthened or shortened. Plastic implants are sometimes used to reshape the nose. Incisions are typically inside the nose and hidden. Sonic rhinoplasty incorporates the use of an ultrasonic device to gently aspirate bone, enabling a refined cosmetic result.6 After surgery, nasal packing may be inserted to apply pressure and prevent bleeding or septal hematoma formation. An external plastic splint protects and supports the new shape of the nose during the healing process. If present, nasal packing is usually removed 1 or 2 days after surgery. The splint may be left in place for 1 to 2 weeks.

Nursing Management: Nasal Surgery Before surgery, teach patients to notify the HCP about any medications that they take at home. Aspirin-containing drugs and NSAIDs may need to be stopped for 5 days to 2 weeks preoperatively to reduce the risk for bleeding. Encourage smoking cessation to promote postoperative wound healing. During the immediate postoperative period, nursing interventions include (1) ensuring patency of the airway, (2) continuous assessment of respiratory status, (3) monitoring for airway obstruction, (4) pain management, and (5) observation of the surgical site for edema, bleeding, and signs and symptoms of infection. Teaching is important because the patient must be able to detect complications at home. The patient typically has temporary nasal and/or facial edema and bruising. Cold compresses and elevation of the head can help minimize swelling and discomfort. Teach about activity restrictions aimed at preventing bleeding and injury (no nose blowing, swimming, heavy lifting, strenuous exercise). Sometimes swelling may be slow to resolve, delaying the achievement of a full cosmetic result for up to 1 year.

Epistaxis Epistaxis (nosebleed) most often occurs in adults over age 50. Nosebleeds can be caused by trauma, hypertension, low humidity, upper respiratory tract infections, allergies, sinusitis, foreign bodies, chemical irritants (e.g., street drugs), overuse of decongestant nasal sprays, facial or nasal surgery, anatomic malformation, and tumors.7 Conditions that prolong bleeding time or change platelet counts may predispose a patient to nosebleeds. Bleeding time may be prolonged if the patient takes aspirin, NSAIDs, warfarin, or other anticoagulant drugs. About 90% of nosebleeds occur in the anterior part of the nasal cavity and are easily visualized. Anterior bleeding can be self-treated and usually stops spontaneously. Posterior bleeding occurs more often with older adults secondary to other health problems (e.g., hypertension). Since posterior nosebleeds are closer to the throat, it is often hard to determine how much blood loss has occurred. Posterior bleeding may need medical treatment.

Interprofessional and Nursing Care Use simple first aid measures to control nosebleeds. These include (1) place the patient in a sitting position, leaning slightly forward with head tilted forward; (2) apply direct pressure by squeezing the entire soft lower part of the nose (nostrils) together for 5 to 15 minutes; and (3) reassure and calm the patient. If bleeding does not stop within 15 minutes, seek medical assistance. Medical management involves trying to find the location of the bleed. For anterior bleeds, a pledget (nasal tampon) impregnated with anesthetic solution (lidocaine) and/or vasoconstrictive agents (epinephrine) may be placed into the nasal cavity. Absorbable materials, such as oxidized cellulose (surgical), gelatin foam (Gelfoam), or a gelatin-thrombin combination (Floseal), are another option. Packing for anterior bleeds can stay in place for 48 to 72 hours. Silver nitrate may be used to chemically cauterize a specific bleeding point. Thermal cauterization is reserved for more severe bleeding and

may require the use of local or general anesthesia.8 It may be harder to find the location of a posterior bleed. Posterior bleeds often need packing. Packing with compressed nasal sponges (e.g., Merocel) or epistaxis balloons (e.g., Rapid Rhino) is preferred over the use of traditional Vaseline ribbon gauze because of the ease of placement. Packing is inserted into the nares and advanced along the floor of the nasal cavity. The sponge expands with moisture to fill the nasal cavity and tamponade bleeding. The epistaxis balloon is inflated with air to achieve the same pressure effect (Fig. 26.1). In the absence of a specific nasal device, a size 10F, 12F, or 14F Foley catheter with a 30-mL balloon may be used. A nasal sling (folded 2 × 2–inch gauze pad) may be gently taped under the nares to absorb drainage. If packing does not stop the bleeding, arterial embolization may be needed. Nasal sponges, packing, and balloons can impair respiratory status. Closely monitor the level of consciousness, heart rate and rhythm, respiratory rate, and O2 saturation (SpO2) using pulse oximetry. Observe for any signs of difficulty breathing or swallowing. Because of the increased risk for complications due to location of the injury, all patients with posterior packing should be admitted to a monitored unit for close observation. Nasal packing is painful because sufficient pressure must be applied to stop the bleeding. The patient should receive appropriate analgesia. Nasal packing predisposes patients to infection from bacteria (e.g., Staphylococcus aureus) present in the nasal cavity. Antibiotics effective against staphylococci may be prescribed. Nasal packing for posterior bleeds may be left in place for 2 to 3 days. Before removal, pre-medicate the patient for pain because this procedure is uncomfortable. After packing removal, cleanse the nares gently and lubricate them with water-soluble jelly.

FIG. 26.1 A, Epistaxis balloon. The balloon is inflated after insertion. (Courtesy Boston Medical, Westborough, Mass.) B, Epistaxis balloon in proper position in nares. (From Roberts JR, Hedges JR: Clinical procedures in emergency medicine, ed 5, Philadelphia, 2009, Saunders.) C, Method for placing posterior nasal pack. Catheter is passed through the bleeding side of the nose and pulled out through

the mouth with a hemostat. Strings are tied to the catheter, and the pack is pulled up behind the soft palate and into the nasopharynx. D, Nasal pack in position in the posterior nasopharynx. Dental roll at the nose helps maintain correct position.

Before discharge teach the patient and caregiver about follow-up care. Review how to use saline nasal spray and/or a humidifier. Have the patient sneeze with the mouth open and avoid the use of aspirincontaining products or NSAIDs. Teach the patient to avoid vigorous nose blowing, engaging in strenuous activity, and lifting and straining for 4 to 6 weeks.

Allergic Rhinitis Allergic rhinitis is inflammation of the nasal mucosa, often in response to a specific allergen. Allergic rhinitis can be classified according to the causative allergen (seasonal or perennial) or the frequency of symptoms (episodic, intermittent, or persistent). Episodic refers to symptoms related to sporadic exposure to allergens not typically encountered in the patient’s normal environment, such as exposure to animal dander when visiting another person’s home. Intermittent means that the symptoms are present less than 4 days a week or less than 4 weeks per year. Persistent means that symptoms are present more than 4 days a week and for more than 4 weeks per year. Seasonal rhinitis usually occurs in the spring and fall. It is caused by allergy to pollens from trees, flowers, grasses, or weeds. Attacks may last for several weeks during times when pollen counts are high; then it disappears and often recurs at the same time the next year. Perennial rhinitis occurs year-round from exposure to environmental allergens, such as animal dander, dust mites, cockroaches, fungi, and molds. Both seasonal and perennial rhinitis can be classified as episodic, intermittent, or persistent, depending on the duration and frequency of symptoms. Sensitization to an allergen occurs with initial allergen exposure, which results in the production of antigen-specific immunoglobulin E

(IgE) (see Fig. 13.6). After exposure, mast cells and basophils release histamine, cytokines, prostaglandins, and leukotrienes. These cause the early symptoms of sneezing, itching, rhinorrhea, and congestion.9 4 to 8 hours after exposure, inflammatory cells infiltrate the nasal tissues, causing and maintaining the inflammatory response. Because symptoms of rhinitis are like those of the common cold, the patient may think the condition is a continuous or repeated cold.

Clinical Manifestations Manifestations of allergic rhinitis are sneezing; watery, itchy eyes and nose; decreased sense of smell; and thin, watery nasal discharge that can lead to a more sustained mucus production and nasal congestion. Nasal turbinates appear pale, boggy, and swollen. The turbinates may fill the air space and press against the nasal septum. The posterior ends of the turbinates can become so enlarged that they obstruct sinus aeration or drainage and result in sinusitis. With chronic exposure to allergens, the patient may develop a headache, stuffy nose, nasal congestion, and sinus pressure. Nasal polyps and postnasal drip are the most common causes of cough. The patient may report hoarseness and the need to frequently clear the throat.

Interprofessional and Nursing Care The key step to managing allergic rhinitis is identifying and avoiding triggers of allergic reactions (Table 26.1). Teach the patient to take note when allergic reactions occur and keep a diary of activities that precipitate the reaction. Patients are often more aware of intermittent exposure to an allergen, such as pets, than they are of a more persistent exposure to allergens, such as dust mites, cockroaches, or mold. Identifying triggers is the first step toward avoiding them.

TABLE 26.1 Patient & Caregiver

TeachingAvoiding Allergens in Allergic Rhinitis Include the following instructions when teaching a patient or caregiver about allergic rhinitis:

The goal of drug therapy is to reduce inflammation associated with allergic rhinitis, reduce nasal symptoms, minimize associated complications, and maximize quality of life. Nasal corticosteroid sprays are the first-line and most effective treatment for allergic rhinitis.10 Appropriate oral medication options include H1antihistamines, decongestants, and leukotriene receptor antagonists (LTRAs). Intranasal medications include antihistamines, anticholinergics, corticosteroids, cromolyn, and decongestants (Table 26.2).11

TABLE 26.2 Drug TherapyRhinitis and Sinusitis

PT, prothrombin time; ICP, intracranial pressure; MAOI, monoamine oxidase inhibitor.

Second-generation antihistamines are used before first-generation antihistamines because of their nonsedating effects. Teach patients taking antihistamines to have adequate fluid intake to reduce adverse symptoms. Nasal corticosteroid sprays decrease inflammation with little absorption in the systemic circulation. Therefore systemic side effects are rare. If monotherapy does not relieve symptoms, a 2-drug combination, such as an oral H1-antihistamine and an intranasal corticosteroid, may be helpful.

Drug Alert Antihistamines • First-generation antihistamines (e.g., chlorpheniramine [ChlorTrimeton]) can cause drowsiness and sedation. • Warn patients that operating machinery and driving may be dangerous because of the sedative effect.

Drug Alert Pseudoephedrine (Sudafed) • Large doses may cause tachycardia and palpitations, especially in patients with heart disease. • Overdose in those over 60 years of age may result in central nervous system depression, seizures, and hallucinations. Immunotherapy (allergy shots) may be used when a specific, unavoidable allergen is identified, and drugs are not tolerated or are ineffective in controlling symptoms. Immunotherapy involves controlled exposure to small amounts of the known allergen through frequent (at least weekly) injections with the goal of decreasing sensitivity. Sublingual or intranasal administration of allergen immunotherapy may an option for select patients. Immunotherapy is discussed in Chapter 13.

Acute Viral Rhinopharyngitis Acute viral rhinopharyngitis (nasopharyngitis, common cold) is an infection of the upper respiratory tract. It is the most prevalent infectious disease, with the average adult contracting 1 to 3 colds per year. More than 200 different viruses can cause a common cold. Most are caused by the coronavirus and are mild and self-limiting. Other viruses, such as human respiratory syncytial virus (RSV) and enterovirus, can cause a common cold. The viruses are contagious. They spread by airborne droplets emitted by the infected person while breathing, talking, sneezing, or coughing. Because they can survive on inanimate objects for up to 3 days, transmission also occurs by direct hand contact. Frequency of the infection increases in winter months when people stay indoors and overcrowding is more common. Other factors that increase susceptibility include fatigue, physical and emotional stress, allergies

affecting the nose and throat, and a compromised immune status. Exercise may reduce the number of upper respiratory tract infections. Symptoms typically begin 2 or 3 days after infection. They may include runny nose, watery eyes, nasal congestion, sneezing, cough, sore throat, fever, headache, and fatigue. Patients are contagious 1 to 2 days before symptom onset and remain contagious until symptoms have subsided. Symptoms may last 2 to 14 days, with typical recovery in 7 to 10 days.

Complementary & Alternative Therapies Echinacea

Scientific Evidence • Echinacea may slightly reduce the incidence of the common cold. • Taking echinacea does not appear to reduce the duration of a common cold.

Nursing Implications • Echinacea is considered safe when used on a short-term basis in recommended doses. • Caution patients with autoimmune disorders or a tendency toward allergic reactions about using this herb. Source: Retrieved from www.nccih.nih.gov/health/echinacea/ataglance.htm.

Complementary & Alternative Therapies

Zinc

Scientific Evidence • Zinc is available in 2 forms: oral zinc (e.g., lozenges, tablets, syrup) and intranasal zinc (e.g., swabs, gels). • When given within 24 hrs of onset of symptoms, zinc lozenges may reduce the duration of cold symptoms.

Nursing Implications • Intranasal zinc can cause an irreversible loss of the sense of smell. • Long-term zinc use, especially in high doses, can cause copper deficiency and may increase the risk for urinary tract problems and reduce immune function. • Zinc may interact with drugs, including antibiotics and penicillamine. Source: Retrieved from www.nccih.nih.gov/health/zinc.

Interprofessional and Nursing Care Interventions are directed at relieving symptoms. Rest, oral fluids, antipyretics, and analgesics are recommended. Warm salt water gargles, ice chips, lozenges, or sprays may help ease a sore throat. Petroleum jelly soothes a raw nose. Saline nasal spray reduces nasal congestion. Antihistamine and decongestant therapy reduce postnasal drip and decreases the severity of cough, nasal obstruction, and nasal discharge. Caution patients to use intranasal decongestant sprays for no more than 3 days to prevent rebound congestion from occurring. Cough suppressants, for irritating, bothersome coughs, may be used, but may not be effective. Patients may ask about vitamin C, echinacea, and zinc products. There is inconclusive evidence to support treatment with these therapies.

Complications include acute bronchitis, sinusitis, otitis media, tonsillitis, and pneumonia. Antibiotics have no effect on viruses. They are an option only if complications are present. Refer to an HCP if there is no improvement in symptoms within 10 to 14 days. Teach patients to recognize the manifestations of a secondary bacterial infection, such as a temperature higher than 103° F (39.4° C); tender, swollen glands; severe sinus or ear pain; or significantly worsening symptoms. Green, purulent nasal drainage during the later stages of a cold is not uncommon and not always indicative of bacterial infection. In the patient with lung disease, signs of infection include a change in consistency, color, or volume of the sputum. Because infection can progress rapidly, teach the patient with chronic respiratory disease to immediately report sputum changes, increased shortness of breath, and chest tightness. During the cold season, teach patients with a chronic illness or a compromised immune system to avoid crowded situations and those with obvious cold symptoms. Frequent hand washing and avoiding hand-to-face contact can help prevent direct spread.

Influenza Influenza (flu) is a highly contagious respiratory illness that causes significant morbidity and mortality. Millions of Americans (about 5% to 20% of U.S. population) contract influenza each year. The flu season begins in September and continues through April of each year, peaking between December to February. More than 310,000 people were hospitalized for flu-related complications in 2016.12 Although the exact number of flu-related deaths is not known, it is estimated that influenza is responsible for 3000 - 49,000 deaths annually, depending on the strain.13 Vaccination of high-risk groups may help prevent many of these deaths.

Etiology and Pathophysiology We classify influenza viruses into 4 serotypes (A, B, C, D). Only A and

B cause significant illness in humans. Influenza A is subtyped based on the presence of 2 surface proteins: hemagglutinin (H) and neuraminidase (N). The H antigens enable the virus to enter the cell, and the N antigens facilitate cell-to-cell transmission. As a result, we name influenza A viruses according to their H and N type (e.g., H3N2). Influenza A is the most common and most virulent flu virus. It can infect a variety of animals as well as humans. More than 100 types of influenza A are found in birds (avian flu), pigs (swine flu), horses, seals, and dogs. When the virus mutates (changes), this allows it to infect different species. When a new viral strain reaches humans, people do not have immunity and the virus can spread quickly around the globe, causing a pandemic. For example, type A H1N1 influenza (swine flu) emerged in 2009 and had never been seen in humans before, resulting in a worldwide pandemic. The reemergence of a viral strain that has not circulated for many years can also trigger a pandemic. Epidemics are more localized outbreaks, often occurring yearly, caused by variants of already circulating strains of the influenza virus. Influenza B and C viruses only infect humans. They are not divided into subtypes. Outbreaks of influenza B can cause regional epidemics, but the disease it produces is milder than that caused by influenza A. Influenza C causes mild illness and does not cause epidemics or pandemics. Influenza D only occurs in animals. Influenza is communicable between humans primarily through infected droplets, inhalation of aerosolized particles, and, to a lesser extent, through direct contact with contaminated surfaces. The virus has an incubation period of 1 to 4 days, with peak transmission risk starting 1 day before onset of symptoms and continuing for 5 to 7 days after a person first becomes sick.14

Clinical Manifestations For some patients, it may be hard to tell between the common cold and flu (Table 26.3). The onset of flu is abrupt. There may be chills,

fever, and generalized myalgia, often accompanied by a headache, cough, sore throat, and fatigue. Assessment findings are usually minimal, with normal breath sounds on chest auscultation. In uncomplicated cases, symptoms often subside within 7 days. Common complications include pneumonia, which can be either primary influenza [viral] pneumonia or secondary bacterial pneumonia, and ear or sinus infections. Dyspnea and diffuse crackles are signs of pulmonary complications. Some patients, especially older adults, have weakness or lethargy that may last for weeks. The patient who develops secondary bacterial pneumonia usually has gradual improvement of influenza symptoms, then worsening cough and purulent sputum. Treatment with antibiotics is usually effective if started early.

Diagnostic Studies Influenza is often diagnosed based on the patient’s health history and physical assessment and the knowledge of other cases of influenza in the community.

TABLE 26.3 Comparison of Common Cold and

Influenza Manifestations Common Cold (Viral Rhinitis) and Treatment Appear gradually Symptom onset Rare Fever

Influenza Abrupt onset. Within 3–6 hr

Headache

Uncommon, but may occur

Characteristically high 102–104° F (38.9– 40° C]). Lasts 3–4 days Common (can be severe)

General aches and pains

Slight

Often severe myalgia

Fatigue and weakness

Sometimes. Usually mild

Usual. Starts early and can last up to 2– 3 wks

Exhaustion Stuffy nose

Uncommon Common

Usual at beginning of illness Sometimes

Sneezing

Common

Sometimes

Sore throat

Common

Sometimes

Common. Mild to moderate hacking Chest discomfort, cough cough Complications Sinus congestion. Earache Prevention

Hand washing. Avoid close contact with anyone who has a cold

Treatment

Temporary relief of symptoms: rest, hydration, decongestants, acetaminophen or ibuprofen for headache, aches, and pains

Common

Bronchitis, pneumonia, acute respiratory failure, ARDS. Can be life-threatening Hand washing. Annual vaccination. Antiviral drugs. Avoid close contact with anyone who has the flu Antiviral drugs if given within 24– 48 hrs of onset. Rest, hydration, acetaminophen or ibuprofen for headache, aches, and pains

Adapted from CDC Centers for Disease Control and Prevention. Retrieved from www.cdc.gov/flu/about/qa/coldflu.htm.

TABLE 26.4 Types of Influenza Immunization

Viral cultures, once considered the gold standard for diagnosing influenza, have decreased in popularity with the emergence of other rapid testing methods. We can obtain a viral culture from a throat swab, nasopharyngeal swab, expectorated sputum, ET tube sample, or bronchoscopy (bronchial wash). A viral culture can identify which virus (A, B, or another respiratory virus) and which viral strains are present. Rapid influenza diagnostic tests (RIDTs) can help in the diagnosis by detecting the virus in secretions from the respiratory tract. Depending on the method, the test may be completed in the HCP’s office with results available in as little as 5 minutes. The test can help distinguish influenza from other viral and bacterial infections with similar manifestations that may be serious but are treated differently. RIDTs are best used within the first 48 hours of the onset of symptoms. The main disadvantages of the rapid flu test are that it will miss some cases or occasionally be positive when a person does not actually have the flu. Always evaluate test results considering the patient’s clinical condition.

Interprofessional and Nursing Care The most effective strategy for managing influenza is prevention. Two types of flu vaccines are available: inactivated and live attenuated (Table 26.4). Receiving a flu vaccine results in the production of antibodies against the viruses in the vaccine. The influenza vaccine is changed on a yearly basis, depending on the virus strains the Centers for Disease Control and Prevention (CDC) determines as being most likely to cause illness in the upcoming flu season. The best time to receive the vaccine is in September or October (before flu exposure) because it takes 2 weeks for full protection to occur. However, the vaccine can be given at any time during the flu season.

Safety Alert Influenza Vaccination • Advocate for vaccination of all people older than 6 months of age, especially those at high risk (e.g., health care workers, residents of long-term care facilities). • Give high priority to groups, such as health care workers, who can transmit influenza to high-risk persons. Vaccinating healthy people decreases the incidence and risk for transmitting influenza to those who have less ability to cope with the effects of this illness. Many people do not get receive the vaccination despite the obvious benefits. Current vaccines are highly purified, and reactions are extremely rare. Soreness at the injection site is the most reported adverse effect. Contraindications are a history of severe allergic reactions to previous flu vaccine. Patients with anaphylactic hypersensitivity to eggs should discuss the vaccine with their HCP, as alternatives for vaccinating patients with egg allergies are now available. The primary nursing goals are relief of symptoms and prevention of secondary infection. Unless the patient with influenza is at high risk or complications develop, supportive therapy is often all the patient needs. Rest, hydration, analgesics, and antipyretics can provide symptom relief. Older adults and those with a chronic illness may need hospitalization. There are several antiviral medications we can use to treat shorten the duration of influenza symptoms and reduce the risk for complications. Zanamivir (Relenza), oseltamivir (Tamiflu), and peramivir (Rapivab) are neuraminidase inhibitors that prevent the virus from being released and spreading to other cells. 15 Zanamivir is given using an inhaler, oseltamivir is available as an oral capsule, and peramivir is given IV. The newest drug is baloxavir marboxil

(Xofluza). It is a PA endonuclease inhibitor that works by inhibiting viral replication. Patients receive 1 oral dose. Do not give Xofluza with dairy products or calcium-fortified drinks. Treatment with antiviral medication should be started as soon as possible in hospitalized patients with influenza, those with severe or complicated illness, or those at high risk for complications. For maximum benefit in the treatment of influenza, therapy should begin within 2 days of the onset of symptoms, but it can be started later based on clinical judgment.

Sinusitis Sinusitis affects 1 in every 7 adults. It develops when inflammation or swelling of the mucosa blocks the openings (ostia) in the sinuses, through which mucus drains into the nose (Fig. 26.2). Rhinosinusitis, which may accompany sinusitis, is concurrent inflammation or infection of the nasal mucosa. Nasal polyps, foreign bodies, deviated septa, or tumors can cause obstruction of mucus drainage. Secretions that accumulate behind the blocked ostia provide a rich medium for growth of bacteria, viruses, and fungi, all of which may cause infection. Viral sinusitis may follow an upper respiratory tract infection in which the virus penetrates the mucous membrane and decreases ciliary function. Viral infections usually resolve without treatment in less than 14 days. If symptoms worsen after 3 to 5 days or last for longer than 10 days, a secondary bacterial infection may be present. Only 5% to 10% of patients with viral sinusitis develop a bacterial infection and need antibiotic therapy.

FIG. 26.2 Location of the sinuses.

Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis are the most common causes of bacterial sinusitis.7 Fungal sinusitis is uncommon. It usually occurs in patients who are debilitated or immunocompromised. Sinusitis can be classified as acute, subacute, or chronic.16 Acute sinusitis typically begins within 1 week of an upper respiratory tract infection and lasts less than 4 weeks. Subacute sinusitis is present when symptoms progress over 4 to 12 weeks. Chronic sinusitis (lasting longer than 12 weeks) is a persistent infection usually associated with allergies and nasal polyps. Chronic sinusitis generally results from repeated episodes of acute sinusitis that result in irreversible loss of the normal ciliated epithelium lining the sinus cavity.

Clinical Manifestations Acute sinusitis causes significant pain over the affected sinus, purulent nasal drainage, nasal obstruction, congestion, fever, and malaise. The patient may appear acutely ill. Inspect the nasal mucosa

and palpate the paranasal sinuses for pain. Findings that indicate acute sinusitis include edematous mucosa, discolored purulent nasal drainage, enlarged turbinates, tenderness over the involved frontal and/or maxillary sinuses, and halitosis (bad breath). Recurrent headaches are common and may change in intensity with position changes or when secretions drain. The symptoms of chronic sinusitis are often nonspecific. The patient is rarely febrile. The patient may have facial or dental pain, nasal congestion, and increased drainage. Severe pain and purulent drainage are often absent. Some symptoms mimic those seen with allergies. X-rays or CT scan of the sinuses may help confirm the diagnosis. CT scans may show the sinuses are filled with fluid or a thickened mucous membrane. Nasal endoscopy with a flexible scope may be used to examine the sinuses, obtain a specimen for culture, and restore normal drainage. As many as 50% of patients with moderate to severe asthma have chronic sinusitis. The exact link between these diseases is unclear. Postnasal drip associated with sinusitis may trigger asthma by stimulating bronchoconstriction. Gastroesophageal reflux disease (GERD) and smoking may increase the risk for a person with asthma developing sinusitis. Appropriate treatment of sinusitis often causes a reduction in asthma symptoms.

Interprofessional and Nursing Care If allergies are the precipitating cause of sinusitis, teach the patient ways to reduce sinus inflammation and infection, including environmental control of allergens and appropriate drug therapy (see allergic rhinitis discussed earlier in this chapter). Initial treatment for acute sinusitis focuses on symptom relief. Medications include oral or topical decongestants to promote drainage, intranasal corticosteroids to decrease inflammation, analgesics to relieve pain, and saline nasal spray to relieve congestion. Teach patients using topical decongestants to use the medication for no longer than 4 to 5 days to prevent rebound congestion caused by vasodilation. Saline irrigation of the nasal cavity can rinse nasal

passages, promote drainage, and decrease inflammation. Saline nasal spray is available over the counter. If symptoms worsen or last longer than 1 week, antibiotic therapy may be prescribed. Amoxicillin is the first-line drug of choice. It is taken for 10 to 14 days to prevent the formation of antibiotic-resistant organisms.17 If symptoms do not resolve, the antibiotic should be changed to amoxicillin with clavulanate, a fluoroquinolone, or a 2nd or 3rd generation cephalosporin. With chronic sinusitis, mixed bacterial flora is often present and infections are hard to eliminate. Broad-spectrum antibiotics may be used for 4 to 6 weeks. Patient and caregiver teaching for acute and chronic sinusitis is shown in Table 26.5. Medical therapy may not relieve the symptoms of some patients with persistent, recurrent, or chronic sinus illnesses. These patients may need nasal endoscopic surgery to relieve blockage caused by hypertrophy or septal deviation. This is usually done as an outpatient procedure using local anesthesia. Propel, a self-expanding implant, can be placed directly in the sinus during surgery. Propel helps maintain patency to the sinus cavity after surgery and provide local corticosteroid delivery directly to the sinus lining before dissolving after 30 days.

TABLE 26.5 Patient & Caregiver TeachingAcute or

Chronic Sinusitis Include the following instructions when teaching the patient and caregiver about management of sinusitis: 1. Get plenty of rest to help body fight infection and promote recovery. 2. Keep well hydrated by drinking 6 to 8 glasses of water per day to loosen secretions. 3. Take hot showers. Use a steam inhaler (15-minute vaporization of boiled water), bedside humidifier, or nasal saline spray to

promote secretion drainage. 4. Apply warm, damp towels around nose, cheeks, and eyes to ease facial pain. 5. Sleep with head elevated to help sinuses drain and reduce congestion. 6. Report a temperature of 100.4° F (38° C) or higher, which indicates infection. 7. Follow prescribed medication plan: • Take analgesics to relieve pain. • Take decongestants/expectorants to relieve swelling. • Take antibiotics (as prescribed) for infection. Be sure to take entire prescription and report continued symptoms or a change in symptoms. • Use nasal sprays to relieve congestion. 8. Perform nasal saline washes once or twice a day to wash sinuses. 9. Do not smoke and avoid exposure to smoke (will irritate and will worsen symptoms). 10. If allergies predispose to sinusitis, follow instructions about environmental control, drug therapy, and immunotherapy to reduce the inflammation and prevent sinus infection.

Obstruction of Nose and Sinuses Nasal Polyps Nasal polyps are soft, painless, benign (noncancerous) growths that form slowly in response to repeated inflammation of the sinus or nasal mucosa. They are most common in adults over age 40 and are twice as likely to occur in men than women.18 Polyps, which appear as chronic yellow, gray, or pink semitransparent projections in the naris, can exceed the size of a grape. Small polyps are typically asymptomatic. Manifestations of larger polyps include nasal obstruction, nasal discharge (usually clear mucus), and speech distortion. Topical and systemic corticosteroids

are primary therapies used to shrink nasal polyps. Endoscopic or laser surgery can remove nasal polyps, but recurrence is common.

Foreign Bodies A variety of foreign bodies may potentially lodge in the upper respiratory tract of adults, but these are rare occurrences. Some situations may be the result of trauma or found in patients with mental illness. Foreign bodies may be inorganic or organic. Inorganic foreign bodies, such as plastic or metal objects, may cause no symptoms and be incidentally discovered on routine examination. Organic foreign bodies, such as food, may cause a local inflammatory reaction and nasal discharge, which may become purulent and foul smelling if the object stays in the nasal cavity for an extended time. Foreign bodies can cause pain, difficulty breathing, and nasal bleeding. Foreign bodies should be removed from the nose through the route of entry. Sneezing or blowing the nose with the opposite nostril closed may be effective in removing the foreign object. Avoid irrigating the nose or pushing the object backward, since these could cause aspiration and airway obstruction. If sneezing or blowing the nose does not remove the object, consult an HCP.

Problems of Pharynx Acute Pharyngitis Acute pharyngitis is an acute inflammation of the pharyngeal walls. It may include the tonsils, palate, and uvula. It can be caused by a viral, bacterial, or fungal infection. Viral pharyngitis accounts for about 90% of cases. Bacterial pharyngitis (“strep throat”) usually results from group A β-hemolytic streptococci and accounts for 5% to 10% of cases. Fungal pharyngitis, such as candidiasis, can develop with the prolonged use of antibiotics or inhaled corticosteroids. It can also occur in immunosuppressed patients, especially those with human

immunodeficiency virus (HIV) infection. Other causes of pharyngitis include dry air, smoking, GERD, allergy and postnasal drip, ET intubation, chemical fumes, and cancer.

Clinical Manifestations Symptoms of acute pharyngitis range in severity from a “scratchy” throat to pain so severe that swallowing is difficult. Because both viral and streptococcal infections appear as a red and edematous pharynx (with or without patchy exudates), it may be hard to distinguish between them. Four classic manifestations present in bacterial pharyngitis include: (1) fever greater than 100.4° F (38° C); (2) anterior cervical lymph node enlargement; (3) tonsillar or pharyngeal exudate; and (4) absence of cough.19 However, appearance is not always diagnostic. When 2 or 3 of these criteria are present, a rapid antigen detection test and/or a throat culture can help establish the cause and direct treatment. White, irregular patches on the oropharynx suggest fungal infection with Candida albicans.

Interprofessional and Nursing Care The goals of nursing management are infection control, symptom relief, and prevention of secondary complications. For viral pharyngitis, antibiotics are not recommended. For bacterial pharyngitis caused by group A β-hemolytic streptococci, penicillin is the drug of choice. This antibiotic must be taken several times a day for a full 10 days to prevent complications, such as rheumatic fever. For patients allergic to penicillin, erythromycin and clindamycin are appropriate substitutes.20 Other antibiotics, such as azithromycin (Zithromax) or a 1st generation cephalosporin, are options. Most people with streptococcal infections are contagious until they have been on antibiotics for 24 to 48 hours. Repeat throat cultures after antibiotic therapy are not required. Candida infections are treated with nystatin, an antifungal antibiotic. Teach patients to swish the preparation in their mouths for as long as

possible before swallowing it. Treatment should continue until symptoms are gone. Patients taking inhaled corticosteroids are at risk for infection with Candida organisms. Thoroughly rinsing the mouth with water after using corticosteroids can prevent this infection. Teach patients to use ibuprofen or acetaminophen for pain relief. Encourage the patient to increase fluid intake. For symptom relief, have patients to gargle with warm salt water (½ tsp of salt in 8 oz of water); drink warm or cold liquids; and suck on popsicles, hard candies, or throat lozenges. Cool, bland liquids and gelatin will not irritate the pharynx. Citrus juices are often irritating. Encourage the patient to use a cool mist vaporizer or humidifier.

Peritonsillar Abscess Peritonsillar abscess is a complication of tonsillitis. It is most often caused by group A β-hemolytic streptococci. The abscess causes pain, swelling, and blockage of the throat (when severe), threatening airway patency. The patient may have a high fever, chills, leukocytosis, difficulty swallowing, and a muffled voice. Treatment consists of IV antibiotic therapy and needle aspiration or incision and drainage of the abscess. In some cases an emergency tonsillectomy is done or an elective tonsillectomy is scheduled after the infection has subsided.

Problems of Larynx and Trachea Laryngeal Polyps Laryngeal polyps develop on the vocal cords from vocal abuse (e.g., excessive talking, singing) or irritation (e.g., intubation, cigarette smoking). The most common sign is hoarseness. Polyps are treated conservatively with voice rest and adequate hydration. Large polyps may cause dysphagia, dyspnea, and stridor and may need surgically removed. Polyps are usually benign but may be removed because they can become cancerous.

Acute Laryngitis Acute laryngitis is swelling and inflammation of the voice box (larynx). A virus (e.g., flu, common cold) is the most common cause. Other causes include inflammatory or infectious conditions of the upper respiratory tract (e.g., tonsillitis, acute bronchitis), overuse of one’s voice (e.g., yelling loudly at a concert or a sporting event), exposure to smoke-filled environments, or chemical inhalation. The classic hallmark signs of acute laryngitis include a tingling or burning sensation at the back of the throat, a persistent need to clear the throat, and hoarseness, which may be accompanied by complete loss of voice. The patient may have a low-grade fever, persistent cough, or feeling of fullness in the throat. Symptoms will appear suddenly, increase in severity over 2 to 3 days, then gradually subside over the next 7 to 10 days as the condition improves. It usually resolves within 21 days. Diagnosis of acute laryngitis is made based on the history, clinical presentation, and changes in voice. Treatment for acute laryngitis is supportive. The patient is strongly encouraged to limit use of the larynx. This includes no talking or singing, which realistically is almost impossible to do. Patients will want to whisper when communicating but whispering places increased strain on the vocal cords that may worsen the pain. Acetaminophen, cough suppressants, throat lozenges, and use of a humidifier are helpful for throat discomfort. Have the patient increase fluid intake. They should avoid caffeine and alcohol, which may worsen a sore throat. Encourage smoking cessation. If a bacterial cause is known, such as acute bronchitis or tonsillitis, antibiotics should help resolve the condition. If symptoms last longer than 3 weeks, patients should return to their HCP for further investigation and treatment.

Airway Obstruction Acute airway obstruction is a medical emergency. Airway obstruction

can be caused by aspiration of food or a foreign body, allergic reactions, edema and inflammation caused by infections or burns, peritonsillar or retropharyngeal abscesses, cancer, laryngeal or tracheal stenosis, and trauma. Airway obstruction may be partial or complete. The presentation of an airway obstruction often depends on the cause of the obstruction and/or location of the blockage. For example, objects lodged within the larynx may cause voice hoarseness or complete airway obstruction. Tracheal obstruction may produce wheezing. Objects lodged within the lower respiratory system (e.g., bronchus) may produce a cough or decreased air entry on the affected side. Manifestations include choking, stridor, use of accessory muscles, suprasternal and intercostal retractions, flaring nostrils, wheezing, restlessness, tachycardia, cyanosis, and change in level of consciousness.21 Prompt assessment and treatment are essential because partial obstruction may quickly progress to complete obstruction. Complete airway obstruction can result in permanent brain damage or death if not corrected within 3 to 5 minutes. Your immediate priority is to ensure the patient has a patent airway. Interventions to reestablish a patent airway include the obstructed airway (Heimlich) maneuver (see Appendix A), cricothyroidotomy, ET intubation, or tracheostomy. Unexplained partial airway obstruction or recurrent symptoms indicate the need for more tests, including a chest x-ray, laryngoscopy, and rigid bronchoscopy.

Tracheostomy A tracheostomy is a surgically created stoma (opening) in the anterior part of the trachea (Fig. 26.3, A). A tracheostomy may be done to (1) establish a patent airway, (2) bypass an upper airway obstruction, (3) facilitate removal of secretions, (4) permit long-term mechanical ventilation, and (5) assist with weaning from mechanical ventilation.22 The tracheostomy tube is shorter in length and slightly wider in diameter than an ET tube. This makes it easier to keep the tube clean

and facilitates better oral and bronchial hygiene. A tracheostomy (compared to an ET tube) may increase patient comfort because no tube is present in the mouth. There is also less risk for long-term damage to vocal cords.

FIG. 26.3 Tracheostomy tube. A, Placement of a tracheostomy tube. B, Parts of a tracheostomy tube.

A variety of tracheostomy tubes are available to meet specific patient needs (Table 26.6). All tracheostomy tubes have a faceplate, or flange, which rests against the neck, and an obturator, which is used to help insert the tube. Many tracheostomy tubes have an outer cannula (which keeps the airway patent), and an inner cannula (which can be disposable or nondisposable and removed for cleaning) (Fig. 26.3). Cuffed and uncuffed tracheostomy tubes are available. A tracheostomy tube with an inflated cuff (balloon) is used the most, especially if the patient needs mechanical ventilation. The cuff, inflated via the balloon inflation port on the tracheostomy tube, ensures the patient receives the volume of air delivered by the ventilator, and helps decrease the risk for aspiration. Cuffless tubes are primarily used for patients with longer term tracheostomies, when mechanical ventilation is not required and the risk for aspiration has decreased. They make talking and eating easier. The outer and/or inner cannula may be fenestrated or non-fenestrated. A fenestrated tube has an opening (a hole) on the dorsal surface of the tube. This tube promotes spontaneous breathing. For example, with the use of a cuffed, fenestrated tracheostomy tube, when the cuff is deflated and the inner cannula removed, air can pass from the lungs up through the opening in the tracheostomy tube through the vocal cords and larynx, into the upper airway, and out the mouth and nose. This allows the patient to breathe spontaneously and speak with the tracheostomy tube in place. When the cuff is reinflated and the inner cannula reinserted, air cannot pass from the lungs through the vocal cords. Most patients who need mechanical ventilation first have an ET tube, because we can quickly insert one an emergency. Care of the patient with an ET tube is discussed in Chapter 65. When swelling, trauma, or upper airway obstruction prevents ET intubation, an emergent surgical cricothyroidotomy (also known as a cricothyrotomy) is needed. This procedure, which can be completed in minutes, involves making an incision through the skin and

cricothyroid membrane on the anterior surface of the neck. Most surgical tracheostomies are done in the operating room using general anesthesia. The HCP makes a horizontal incision on the anterior part of the trachea. After inserting the tracheostomy tube, the HCP sutures the incision and applies a sterile dressing. A newer surgical technique is the percutaneous tracheostomy. Using local anesthesia, sedation, and under video-assisted guidance, the ET tube is withdrawn up to the level of the glottis. A needle is placed between the second and third tracheal rings, into the middle of the trachea. A dilator is then placed over the top of the needle. The HCP makes the opening progressively larger (with increasingly larger dilators) until the hole is big enough for insertion of the tracheostomy tube. Percutaneous tracheostomy approaches have less risk for bleeding and fewer postoperative complications.23 Both surgical and percutaneous tracheostomies may be done at the patient’s bedside in the emergency department or ICU.

Nursing Management: Tracheostomy Acute Care Before the tracheostomy procedure (and time permitting), explain the purpose of the procedure to both the patient and caregiver. If the patient is having the tracheostomy in the operating room, follow all hospital policies and procedures for preparing the patient for surgery (see care of the preoperative patient in Chapter 17).

TABLE 26.6 Nursing Management of

Tracheostomies

If the procedure is being done at the patient’s bedside, ensure all appropriate personnel, including respiratory therapist, are present.

Emergency resuscitation equipment, including a bag-valve-mask (BVM), should be readily available and functional. Record vital signs, including heart rate, respiratory rate and rhythm, BP, and SpO2. Ensure an existing IV line is patent and that bedside suction is working. Help assemble and set up all necessary equipment. Position the patient supine. Give analgesia and sedation as ordered by the HCP, ensuring correct identification of times and dosages. Monitor patient response to analgesia and/or sedatives. Observe patient’s tolerance to the procedure. Immediately after the procedure, the tracheostomy cuff (balloon) is inflated. We use several different methods to confirm tracheostomy tube placement: (1) auscultation of the patient’s chest for air entry, (2) end-tidal CO2 capnography, and (3) passage of a suction catheter through the tracheostomy tube. After placement is confirmed, the ET tube (if present) is removed. The tracheostomy tube is sutured and secured in place with cotton tracheostomy ties, tracheostomy tapes, or Velcro straps.

TABLE 26.7 Complications of Tracheostomy Closely monitor patients with a tracheostomy for the following potential complications: • Air leak • Airway obstruction • Altered body image • Aspiration • Bleeding • Fistula formation • Impaired cough • Infection: wound or respiratory tract • Subcutaneous emphysema

• Tracheal necrosis • Tracheal stenosis • Tube displacement Monitor and record the patient’s heart rate, respiratory rate, BP, and SpO2. SpO2 readings should remain stable. Note and record the mechanical ventilator settings, including mode, FIO2, and positive end-expiratory pressure (PEEP). (Care of the patient receiving mechanical ventilation is discussed in Chapter 65.) Observe the amount of blood at the tracheostomy insertion site. Notify the HCP if bleeding persists. A chest x-ray should be obtained after the procedure. Many different complications can occur because of tracheostomy (Table 26.7). You must be aware of them, especially airway obstruction, bleeding, and infection. There is considerable variation in the care of a patient with a new tracheostomy. In some places, it is the nurse who is primarily responsible; in others, it is a shared responsibility between nursing and respiratory therapy. You need to be familiar with your agency’s policies and procedures. The following discussion highlights general guidelines when caring for a patient with a tracheostomy during the first few days after the procedure. At a minimum, you must assess the tracheostomy site every shift. Confirm the patency of the tracheostomy tube. Observe the site for any redness, inflammation, edema, ulceration, or signs of infection. Sterile dressing changes should be done every 12 hours. Clean around the stoma with normal saline and apply a sterile pre-cut dressing around the tracheostomy tube site. You can complete dressing changes more often based on your assessment. Because an inflated tracheostomy cuff exerts pressure on the tracheal mucosa, it is important to inflate the cuff with the least volume of air needed to obtain an airway seal. We can measure cuff inflation pressure with a hand-held cuff manometer. Monitor the pressure at least every 8 hours. Cuff inflation pressure should not exceed 20 to 25 cm H2O. Higher pressures may compress tracheal

capillaries, limit blood flow, and predispose the patient to tracheal necrosis. The minimal occlusion volume (MOV) is one way we often use to inflate the tracheostomy cuff (Table 26.6). Routine cuff deflation is not recommended.24 Suction the airway via the tracheostomy tube as needed (Fig. 26.4 and Table 26.8). Try to avoid suctioning through the newly created tracheostomy in the first few hours after the procedure, as this may aggravate discomfort and promote bleeding. Suctioning may be done using sterile glove and catheter technique, or an existing in-line suction catheter. Each time the patient is suctioned, note and record the amount, color, clarity, and patient tolerance to the procedure. At first, patients should receive humidified air to compensate for the loss of the upper airway to warm and moisturize secretions. Humidification is essential to keep secretions thin and decrease formation of mucous plugs.

FIG. 26.4 Suctioning tracheostomy with closed system suction catheter. From Potter PA, Perry AG: Basic nursing: Essentials for practice, ed 7,

St Louis, 2011, Mosby.

If the inner cannula is disposable, replace as per manufacturer and agency guidelines. Clean a nondisposable inner cannula at least every shift. Cleaning removes mucus from the inside of the tube to prevent airway obstruction (Table 26.9). Change the tracheostomy tapes after the first 24 hours and then as needed (Fig. 26.5 and Table 26.9). A 2-person technique, 1 person to stabilize the tracheostomy and the other to change the tapes, is best practice to ensure that the tracheostomy does not become accidentally dislodged during the procedure. In some places, the HCP and/or respiratory therapist may complete this task. At the end of the procedure, place 2 fingers underneath the tapes to ensure they are not too tight around the neck. When turning and repositioning the patient, take care not to dislodge the tracheostomy tube. Because tube replacement may be difficult in the immediate postoperative period, several precautions are required, including (1) keep a replacement tube of equal or smaller size at the bedside, readily available for emergency reinsertion; (2) do not change tracheostomy tapes for at least 24 hours after the surgical procedure; and (3) if needed, the HCP performs the first tube change usually no sooner than 7 days after the tracheostomy. If the tube is accidentally dislodged, immediately call for help. While waiting for the HCP, a respiratory therapist, or other designated individual to arrive, several options may be used (depending on your nursing scope of practice and specific agency policies and procedures). It is essential that you know and understand your role and scope of practice for care of the patient with a tracheostomy. Immediately call for help. Quickly assess the patient’s level of consciousness, ability to breathe, and the presence or absence of any respiratory distress. If respiratory distress is present, you can quickly use a hemostat to spread the opening where the tube was displaced. Insert the obturator in the replacement (spare) tracheostomy tube, lubricate with saline, and insert the tube into the stoma. Once the tube is inserted, remove the obturator at once so that air can flow through

the tube. Another option is to insert a suction catheter to allow passage of air and serve as a guide for insertion. Thread the tracheostomy tube over the catheter and remove the suction catheter. Trying to reinsert will be easier if the stoma tract is mature or older than 1 week.

TABLE 26.8 Suctioning a Tracheostomy Assess the need for suctioning hourly. Indications include visible coughing, coarse crackles or wheezes over large airways, moist cough, increase in peak inspiratory pressure on mechanical ventilator, and restlessness or agitation. Neurologic patients may not show any signs and/or symptoms of the need to be suctioned, so suctioning once per shift (at minimum) is recommended. Do not suction routinely. 1. If suctioning is indicated, explain procedure to patient. 2. Collect necessary sterile equipment: suction catheter (no larger than half the lumen of the tracheostomy tube), sterile water, cup, and personal protective equipment (PPE). If a closed tracheal suction system is used, the catheter is enclosed in a plastic sleeve and reused (Fig. 26.4). No other equipment is needed. 3. Check suction source and regulator. Adjust suction pressure to no greater than 125 mm Hg pressure with tubing occluded. 4. Assess heart rate and rhythm, respiratory rate and SpO2 to provide baseline for detecting changes in patient condition during suctioning. 5. Wash hands and put on PPE. 6. Use sterile technique to open package, fill cup with sterile water, put on sterile gloves, and connect catheter to suction tubing. Designate one hand as contaminated for (1) connecting and disconnecting the tubing at the suction catheter, (2) using the manual bag-valve-mask (BVM), and (3) operating the suction

control. Suction sterile water through the catheter to test the system. 7. Provide preoxygenation for a minimum of 30 seconds by (1) adjusting ventilator to deliver 100% O2 or (2) using a reservoirequipped BVM connected to 100% O2. The method chosen depends on whether the patient is attached to a mechanical ventilator or has a tracheostomy tube in place but is spontaneously breathing and receiving supplemental O2. The patient who has a long-term chronic tracheostomy and is not acutely ill may be able to tolerate suctioning without using a BVM. 8. Gently insert catheter without suction to the point at which the patient coughs. Do not insert the catheter until you meet resistance (this is the carina, and repeated trauma with suction catheter can promote bleeding). Apply suction as you slowly begin to withdraw the catheter. 9. Apply continuous suction for no more than 10 to 15 seconds. 10. Observe the patient during the suctioning procedure. Immediately stop suctioning and remove the suction catheter from the patient’s trachea if the patient becomes bradycardic or hypotensive, a dysrhythmia occurs, or SpO2 decreases to less than 90%. A vagal response may have occurred. 11. After each suction pass, wait at least 30 seconds before suctioning again. Always hyperoxygenate for at least 30 seconds (via mechanical ventilator or BVM with 5 or 6 breaths) in between each suctioning pass. 12. Repeat procedure until airway is clear. Limit insertion of suction catheter to as few times as possible. If airway is not clear after 3 suction passes, allow the patient to rest before additional suctioning. 13. Return O2 concentration to prior setting. 14. Rinse catheter. If using the in-line suction catheter (via mechanical ventilation), ensure that normal saline used to flush out the suction catheter does not enter the patient’s airway. For disposable suction catheters, dispose of catheter by wrapping it

around fingers of gloved hand and pulling glove over catheter. Discard equipment in proper waste container. 15. Suction the oropharynx or use mouth suction. 16. Reassess heart rate and rhythm and SpO2. Auscultate to assess changes in lung sounds. 17. Record time, amount, and character of secretions and patient response to suctioning. If the tube cannot be replaced because of tract immaturity (less than 1 week old) or other circumstances, immediately place the patient in semi-Fowler’s position to decrease dyspnea. Cover the stoma with a sterile dressing and provide ventilation with the BVM over the nose and mouth. If a patient has had a total laryngectomy, there will be complete separation between the upper airway and trachea. Ventilate this patient through the tracheostomy stoma. Severe dyspnea may progress to respiratory arrest.

TABLE 26.9 Tracheostomy Care The following are general guidelines for basic tracheostomy care. Become familiar with the specific policies and/or procedures in your agency: 1. Explain procedure to patient. 2. Use tracheostomy care kit or collect necessary sterile equipment (e.g., suction catheter, 1 pair sterile gloves, 1 pair nonsterile gloves, water basin, tracheostomy ties, tube brush or pipe cleaners, 4 × 4–inch gauze pads, sterile water or normal saline, tracheostomy dressing [optional]). NOTE: Clean rather than sterile technique is used at home. 3. Place patient in semi-Fowler’s position. 4. Assemble needed materials on bedside table next to patient. 5. Wash hands. Put on PPE. 6. Auscultate chest sounds. If wheezes or coarse crackles are present, suction the patient if unable to cough up secretions

(Table 26.8). Remove soiled dressing and clean gloves. 7. Open sterile equipment, pour sterile H2O or normal saline into 2 compartments of sterile container or 2 basins, and put on sterile gloves. NOTE: Hydrogen peroxide (3%) is only used if an infection is present. If it is used, rinse the inner cannula and skin with sterile H2O or normal saline afterward to prevent trauma to tissue. 8. If present, unlock and remove inner cannula. Many tracheostomy tubes do not have inner cannulas. Care for these tubes includes all steps except for inner cannula care. 9. Replace a disposable inner cannula with a new cannula. With a nondisposable cannula: • Immerse inner cannula in sterile solution and clean inside and outside of cannula using tube brush or pipe cleaners. • Rinse cannula in sterile solution. Remove from solution and shake to dry. • Insert inner cannula into outer cannula with the curved part downward, and lock in place. 10. Remove dried secretions from stoma using 4 × 4–inch gauze pad soaked in sterile water or saline. Gently pat area around the stoma dry. Be sure to clean under the tracheostomy flange (faceplate), using cotton swabs to reach this area. 11. Place dressing around tube (Fig. 26.5). Use a pre-cut tracheostomy dressing or unlined gauze. Do not cut the gauze because threads may be inhaled or wrap around the tracheostomy tube. Change the dressing as needed. Wet dressings promote infection and stoma irritation. 12. Change tracheostomy tapes, using a 2-person change technique. Tie tracheostomy tapes securely with room for 2 fingers between tapes and skin (Fig. 26.5). To prevent accidental tube removal, secure the tracheostomy tube by gently applying pressure to the flange of the tube during the tape changes. Do not change tracheostomy tapes for 24 hours after the tracheostomy procedure.

13. Some patients prefer tracheostomy tapes made of Velcro, which are easier to adjust. 14. Repeat care 3 times/day and as needed.

Check Your Practice You are caring for a patient who had a surgically created tracheostomy 6 hours ago. While suctioning the patient, he coughs, dislodging the tracheostomy tube. • What should you do?

FIG. 26.5 Changing tracheostomy tapes. A, A slit is cut about 1 in (2.5 cm) from the end. The slit end is put into the opening of the cannula. B, A loop is made with the other end of the tape. C, The tapes are tied together with a double knot on the side of the neck. D, A Velcro tracheostomy tube holder. D, Courtesy Dale Medical Products.

Chronic Care Some patients will never be able to be weaned from mechanical ventilation and will need a tracheostomy for life. Care of the patient with a long-term tracheostomy includes all the same care as patients with a new tracheostomy. This includes observing the tracheostomy site, cleaning the inner cannula, suctioning, and changing tracheostomy tapes. The tracheostomy tube should be changed around 1 month after the first tube change and every 1 to 3 months thereafter. When a tracheostomy has been in place for several months, the healed tract should be well formed. Changing the tracheostomy tube is important as it permits assessment of the stoma and cleaning of the tube. The patient may be taught to observe for signs and symptoms of infection and how to change the tube at home using a clean technique. Engaging patients to take part in their care may help decrease the incidence of complications, including infection, and promote an overall feeling of well-being.

Swallowing Dysfunction An inflated tracheostomy tube cuff may result in swallowing problems by interfering with the normal function of muscles used to swallow. Therefore, for long-term tracheostomy patients, it is important to evaluate the patient’s swallowing ability and risk for aspiration. A speech therapist is often the one who assesses the patient’s ability to swallow. Using different consistencies of thickened fluids, the patient is evaluated for aspiration and/or microaspiration under videofluoroscopy or with a fiberoptic endoscopy. If the patient can swallow without aspiration when the cuff is deflated, the cuff may be left deflated or a cuffless tube substituted. At this time, patients may be allowed varying levels of thickened fluids and soft foods.

FIG. 26.6 Speaking tracheostomy tubes. A, Fenestrated tracheostomy tube with cuff deflated, inner cannula removed, and tracheostomy tube capped to allow air to pass over the vocal cords. B,

Speaking tracheostomy tube. One tube is used for cuff inflation. The second tube is connected to a source of compressed air or O2. When the port on the second tube is occluded, air flows up over the vocal cords, allowing speech with an inflated cuff.

Speech With a Tracheostomy Tube Several techniques promote speech in the patient with a tracheostomy. When the patient needs mechanical ventilation, provide the patient with a paper and pencil, a white board, or cellular phone for texting. A communication board with pictures of common needs is convenient for patients who may speak other languages. A visual alphabet for spelling words is useful for patients who are weak or have difficulty writing. The spontaneously breathing patient may be able to talk with a tracheostomy. Several options are available depending upon the type of tracheostomy. For example, if the patient is at low risk for aspiration, (1) remove the inner cannula (if non-fenestrated), (2) deflate the cuff, and (3) place the cap on the tube (Fig. 26.6). When the tracheostomy cuff is deflated, exhaled air can flow upward over the vocal cords. When a fenestrated cannula is first used, frequently assess the patient for signs and symptoms of respiratory distress. If the patient is unable to tolerate the procedure, remove the cap, insert a non-fenestrated cannula, and reinflated the cuff. Monitor for improvement in patient condition. The Passy-Muir valve is a simple device that attaches to the hub of the tracheostomy tube (Fig. 26.7). With the cuff deflated, the valve redirects airflow through the vocal cords. On inspiration, the valve on the device opens, allowing the patient to inhale. When the patient exhales, the valve closes and air flows upward around the tracheostomy and through the vocal cords. The patient exhales through the nose and mouth instead of through the tracheostomy, allowing speech. The patient may initially be able to tolerate only short periods of use until they become accustomed to exhaling through the mouth. Remove the valve immediately if there are any signs and symptoms of respiratory distress. Advocating for the use of

speaking devices may help improve self-care and increase self-esteem for the patient with a long-term tracheostomy.

FIG. 26.7 Passy-Muir speaking tracheostomy valve. The valve is placed over the hub of the tracheostomy tube after the cuff is deflated. Multiple options are available and can be used for ventilated and nonventilated patients. The 1-way valve allows air to enter the lungs during inspiration and redirects air upward over the vocal cords into the mouth during expiration. Courtesy Passy-Muir, Irvine, CA.

Decannulation Removal of the tracheostomy from the trachea is known as decannulation. Removal is possible when the primary condition for which the patient initially received a tracheostomy has been resolved. In addition, the patient needs to (1) be hemodynamically stable; (2)

have a stable, intact respiratory drive; (3) be able to adequately exchange air, and (4) independently expectorate secretions. Immediately prior to decannulation, explain to the patient what will occur. Monitor and record vital signs. Suction the patient prior to decannulation through the tracheostomy. Clear the mouth of any oral secretions. Loosen and/or cut the tracheostomy tapes, and remove any visible sutures holding the tracheostomy in place. Most importantly, ensure that the tracheostomy cuff is deflated. Pull the tracheostomy tube outward in one smooth motion. Stop if you meet any resistance and notify the appropriate personnel immediately. After the tracheostomy tube is removed, care involves applying a sterile occlusive dressing and monitoring the site for bleeding. The dressing must be changed if it gets soiled or wet. If necessary, close the stoma with tape strips. Monitor the patient’s respiratory status and O2 saturation for any evidence of airway compromise or difficulty breathing. Apply an alternative method of O2 delivery (e.g., nasal prongs) if needed. Teach the patient to splint the stoma with the fingers when coughing, swallowing, or speaking. Epithelial tissue begins to form in 24 to 48 hours, and the opening closes within 4 or 5 days. Surgical intervention to close the tracheostomy is usually not needed.

Nursing Management Suctioning and Tracheostomy Care Suctioning and tracheostomy care are complex nursing activities. Every nurse who performs suctioning and tracheostomy care is responsible for knowing the scope of practice and policies and procedures of the agency in which they work for all health care personnel. Collaborate with respiratory therapy staff, who will play a key role in the patient’s care. For unstable patients:

• Assess for the need for suctioning. • Suction the ET or tracheostomy tube. • Assess for adverse effects during suctioning, such as dysrhythmias. • Evaluate the patient’s respiratory status after suctioning. • Maintain appropriate cuff inflation pressure at 20 to 25 cm H2O or use minimal leak technique to maintain cuff pressure. • Assess tracheostomy site at least once per shift for any signs of inflammation or infection. • Replace the tracheostomy tube or ventilate the patient with a bagvalve-mask device after accidental tracheostomy dislodgment if needed. • Assess swallowing ability and risk for aspiration. • Develop plan to avoid aspiration in a patient with a tracheostomy. • Teach patient and caregiver about home tracheostomy care. • Delegate care of the stable patient to the licensed practical/vocational nurse (LPN/VN): • Determine the need for suctioning • Suction the tracheostomy • Evaluate patient status after suctioning • Provide tracheostomy care using sterile technique • Notify the RN of any changes in the patient’s respiratory status • Oversee the UAP in providing oral care to patient with a tracheostomy. • Collaborate with the respiratory therapist: • Ensure proper equipment is available for suctioning and tracheotomy care • Measure tracheal cuff pressures • Replace tracheostomy tube after accidental dislodgement • Assist with bronchoscopy

• Assist with decannulation

Head and Neck Cancer Head and neck cancer is classified according to the area where it occurs. These cancers may involve the nasal cavity and paranasal sinuses, nasopharynx, oropharynx, larynx, oral cavity, and/or salivary gland. (Cancer of the oral cavity is discussed in Chapter 41.) Most head and neck cancers arise from squamous cells that line the mucosal surfaces of the head and neck. More than 52,000 new cases of head and neck cancer are diagnosed each year in the United States.25 Tobacco use causes 85% of head and neck cancers. Excess alcohol consumption is another major risk factor. Head and neck cancer most often occurs in people over age 50 and twice as often in men compared to women. Head and neck cancers in those younger than 50 years are often associated with human papillomavirus (HPV) infection. Other risk factors include exposure to the sun, asbestos, industrial carcinogens, marijuana use, radiation therapy to the head and neck, and poor oral hygiene.26 Unfortunately, most patients have locally advanced disease at the time of diagnosis. Disability from both the disease and subsequent treatment is significant because of the potential loss of voice, adverse effects from chemotherapy and/or radiation, disfigurement, and social concerns.

Clinical Manifestations The early manifestations of head and neck cancer vary with the location of the tumor. For example, patients with pharyngeal cancer may have what feels like a lump in the throat or a sore throat that does not get better with treatment. Some have white or red patches in the mouth or a change in the quality of the voice. Hoarseness that lasts more than 2 weeks may be a symptom of early laryngeal cancer. Other manifestations may include ear pain or ringing in the ears, swelling or lumps in the neck, constant coughing, and coughing up

blood. Swelling of the jaw can cause dentures to fit poorly or become uncomfortable. Unintentional weight loss and difficulty with chewing, swallowing, moving the tongue or jaw, and breathing are typically late symptoms. A partially or fully obstructed airway is often a late manifestation of head and neck cancer.

Diagnostic Studies Early detection is key to patient survival. Physical assessment involves a focused assessment of the ears, nose, throat, mouth, and neck. Thoroughly examine the mouth, including the area under the tongue and dentures, with a flashlight. There may be thickening of the normally soft and pliable oral mucosa. Inspect the floor of the mouth and tongue. Leukoplakia (white patch) or erythroplakia (fiery red patch) may be present. Both leukoplakia and carcinoma in situ (localized to a defined area) may precede invasive carcinoma by many years. Palpate the lymph nodes in the neck. If lesions are suspected, the HCP will examine upper airways may be examined using indirect pharyngoscopy and laryngoscopy (which involves using a laryngeal mirror). The larynx and vocal cords are visually inspected for lesions and tissue mobility. Typically, multiple biopsy specimens are obtained to help determine the extent of the disease. A CT scan or MRI may be done to detect local and regional spread. Positron emission tomography (PET) scanning is also used in diagnosis. The interprofessional care of head and neck cancer is outlined in Table 26.10.

TABLE 26.10 Interprofessional CareHead and

Neck Cancer

Diagnostic Assessment • History and physical examination • Indirect pharyngoscopy and laryngoscopy

• Endoscopy • Biopsy • Chest x-ray • Barium swallow

Management • Surgery • Vocal cord stripping • Laser surgery • Cordectomy • Partial or total laryngectomy • Pharyngectomy • Lymph node removal with neck dissection • Tracheostomy • Reconstructive procedures • Radiation therapy • Chemotherapy • Targeted therapy • Respiratory therapy • Physical therapy • Occupational therapy • Speech therapy

Staging of Head and Neck Cancer Head and neck cancer is staged based on the size of the tumor (T), number and location of involved lymph nodes (N), and extent of metastasis (M). This is referred to as TNM staging.27 Staging is slightly different for each type of cancer. Generally, stage 0 is in situ, or confined to where it began, through stage 4, with more advanced disease. Oral cancer staging considers a patient’s HPV status. TNM staging is discussed in Chapter 15.

Interprofessional Care The choice of treatment for head and neck cancer is based on many factors. These include the location of tumor, TNM stage, patient’s age and overall general health, urgency of treatment, cosmetic and functional considerations (e.g., ability to talk, swallow, chew), and patient choice. Treatment options include surgery, radiation therapy, chemotherapy, targeted therapy, or any combination of these modalities.28

Surgical Therapy Surgery is often the first-line treatment option for head and neck cancers. Some patients may be treated with surgery alone. For other patients, combining surgery with radiation therapy and/or chemotherapy may be appropriate. Depending on the location and stage of cancer, surgical options include: • Vocal cord stripping: Removal of outer layers of tissue on the vocal cords. This approach may be used for a biopsy or to treat some stage 0 cancers confined to the vocal cords. Vocal cord stripping rarely affects speech. • Laser surgery: An endoscope with a laser is inserted down the throat, and the tumor can be vaporized or removed. • Cordectomy: Removal of part or all the vocal cords. There may be changes in tone of voice. Removing part of a vocal cord may lead to a hoarse voice. If both vocal cords are removed, speech will no longer be possible. • Partial or total laryngectomy: Removal of part or all the larynx. A total laryngectomy will change airflow in and out of the lungs and normal voice production will not be possible (Fig. 26.8). • Pharyngectomy: Removal of part or all the throat. • Tracheostomy: A tracheostomy is done to create an alternate pathway for breathing by creating a stoma in the trachea. Lymph node removal: Head and neck cancer sometimes spreads

to the lymph nodes. The amount of tissue and number of lymph nodes that are removed depend on how far the cancer has spread. • Neck dissection surgery: There are 3 main types: • Radical neck dissection: Removal of all the tissue on the side of the neck from the mandible to the clavicle. This includes the muscle, nerve, salivary gland, and major blood vessels. • Modified radical neck dissection: This is the most common type of neck dissection for cancer. All lymph nodes are removed. Less neck tissue is taken out than in radical dissection. This surgery may spare the nerves in the neck and, sometimes, the blood vessels or muscle. • Selective neck dissection: If cancer has not spread far, fewer lymph nodes are removed. The muscle, nerve, and blood vessels in the neck may be saved. After extensive surgery to remove head and neck cancer, reconstructive operations can help restore both the structure and function of the affected areas.

Radiation Therapy Radiation therapy can be delivered by either external-beam therapy or internal implants (brachytherapy). Brachytherapy is a concentrated and localized method of delivering radiation that involves placing a radioactive source near or into the tumor. The goal is to deliver high doses of radiation to the target area while limiting exposure of surrounding tissues. Thin, hollow, plastic needles are inserted into the tumor area, and radioactive seeds are placed in the needles. The seeds emit continuous radiation. Radiation therapy and brachytherapy are discussed in Chapter 15.

FIG. 26.8 Airflow in and out of the lungs after total laryngectomy. There is no anatomic connection between the nose, mouth, and throat. Inhaled and exhaled air enters the lungs through a surgically created stoma (hole) in the neck.

Radiation therapy is often preferred for patients with early head and neck cancer because it offers the patient good results with voice preservation. Some patients refuse surgical intervention for advanced lesions because of the extent of the procedure and potential risks involved. In this situation, radiation therapy is used as the sole treatment or in combination with chemotherapy. Other patients may opt for surgery and a combination of either radiation and/or chemotherapy treatments.

Chemotherapy and Targeted Therapy Chemotherapy is used in combination with radiation therapy for patients with stage 3 or 4 head and neck cancers. Chemotherapy agents currently recommended include cisplatin, 5-fluorouracil, carboplatin, docetaxel (Taxotere), paclitaxel, methotrexate, and bleomycin.29 Cetuximab (Erbitux), a targeted therapy, is used with chemotherapy to treat patients with late-stage head and neck cancer. The drug targets epidermal growth factor receptor (EGFR), a specific protein within cancer cells, and stops the cells from growing. Targeted therapy is discussed in Chapter 15 and Table 15.13.

Nutritional Therapy Many patients with head and neck cancer are malnourished even before treatment begins. Treatment modalities increase the risk for malnutrition. For example, after radical neck surgery, the patient may be unable to consume nutrients orally because of swelling, the location of sutures, or difficulty with swallowing. Side effects from chemotherapy and radiation therapy can impair the patient’s ability to maintain adequate nutrition. Painful oral mucositis often leads to breaks in treatment if the patient is relying solely on oral intake for nutrition. A thorough nutritional assessment and prophylactic placement of a gastrostomy tube in high-risk patients are vital to maintaining adequate nutrition. Enteral nutrition may be started before initiating treatment to obtain and maintain optimal nutritional status needed for tissue repair. (Enteral nutrition is described in Chapter 39.) Elevate the head of the bed while the patient is eating. Observe for feeding intolerance and adjust the amount, time, and/or formula if nausea, vomiting, diarrhea, or distention occurs. Teach the patient and caregiver about the enteral feedings. Patients who are not candidates for or who refuse enteral feedings need to be monitored closely for weight loss. Antiemetics or analgesics given before meals can reduce nausea and mouth pain. Bland foods are easier for patients to tolerate. Patients can increase caloric intake by adding dry milk to foods during preparation, eating foods high in calories, and using oral supplements. It is helpful to add mild sauces and gravy to food. This adds calories and moistens food so that it is more easily swallowed. Expect swallowing problems when the patient resumes eating after surgery. The type and degree of difficulty varies depending on the surgical procedure. Videofluoroscopic swallowing studies may be used to evaluate the safety of swallowing postoperatively. When the patient can successfully swallow with low or no risk for aspiration, small amounts of thickened liquids or pureed foods may be given with the patient in high-Fowler’s position. Avoid thin, watery fluids because they are hard to swallow and increase the risk for aspiration. Closely monitor

and observe for any signs or symptoms of respiratory distress and/or choking when eating resumes. Oral suctioning may be done to prevent aspiration.

Physical Therapy After surgery for head and neck cancer, the physical therapist will help teach the patient how to use the upper extremities to assist with support and movement of the head. In the immediate postoperative period, the patient should begin an exercise program to maintain strength and movement in the shoulders and neck. Without exercise, the patient could be left with a “frozen” shoulder and limited range of neck motion. The patient should continue the exercise program after discharge to prevent future functional disabilities.

Speech Therapy Preoperatively, a speech therapist should meet with the patient and caregiver to discuss any effect that surgery will have on the voice and potential adaptations or voice restoration options. The International Association of Laryngectomees, an association of laryngectomy patients, focuses on helping patients reestablish speech. Local groups, such as “Lost Chord” or “New Voice,” often have volunteers to visit patients before surgery.

FIG. 26.9 A, The sound waves created by the electrolarynx allow the person to speak. B, The Blom-Singer voice prosthesis and valve.

Three major approaches are used to restore oral communication: (1) electrolarynx, (2) tracheoesophageal puncture (TEP) voice restoration, and (3) esophageal speech. An electrolarynx is a hand-held, batterypowered device that creates speech with the use of sound waves (Fig. 26.9, A). This option allows for speech immediately after surgery. It needs little maintenance and is easy to learn. The primary disadvantage of the electrolarynx is the mechanical sound quality, which many patients find unacceptable. In transesophageal puncture (TEP), a fistula is created in the tracheoesophageal wall that diverts pulmonary air across the pharyngoesophageal mucosa for phonation when the tracheostoma is occluded. A 1-way prosthetic valve is placed in the tract. The valve prevents aspiration of food or saliva from the esophagus into the tracheostomy. To speak, the patient manually blocks the stoma with the finger. Air moves from the lungs, through the prosthesis, into the esophagus, and out the mouth. Speech is made by the air vibrating against the esophagus and is formed into words by moving the tongue and lips. A common voice prosthesis is the Blom-Singer prosthesis (Fig. 26.9, B). TEP offers the best speech quality with the highest degree of patient satisfaction.

Esophageal speech depends upon air that is introduced into the esophagus and then expelled past the pharyngoesophageal segment, the vibratory source for sound production. The primary disadvantages of developing esophageal speech are the length of time needed to learn the technique and the reduction in voice quality.

Nursing Management: Head and Neck Cancer Nursing Assessment Table 26.11 presents subjective and objective data to obtain from a person with head and neck cancer.

Nursing Diagnoses Nursing diagnoses for the patient with head and neck cancer include: • Impaired airway clearance • Risk for aspiration TA B L E 2 6 . 11  N u r s i n g A s s e s s m e n t H e a d a n d N e c k C a n c e r

Subjective Data Important Health Information Past health history: Positive family history; prolonged tobacco use (cigarettes, pipes, cigars, chewing tobacco, smokeless tobacco); prolonged, heavy alcohol use; poor intake of fruits and vegetables Medications: Prolonged use of over-the-counter medication for sore throat, decongestants Functional Health Patterns Health perception–health management: Does not take part in preventive health measures, long history of alcohol and tobacco use

Nutritional-metabolic: Mouth ulcer that does not heal, change in fit of dentures, change in appetite, sudden or unexplained weight loss, swallowing difficulty (e.g., sensation of lump in throat, pain with swallowing, aspiration when swallowing) Activity-exercise: Fatigue with minimal exertion Cognitive-perceptual: Sore throat, pain on swallowing, referred ear pain Objective Data Respiratory Hoarseness, change in voice quality, chronic laryngitis, nasal voice, palpable neck mass and lymph nodes (tender, hard, fixed), tracheal deviation; dyspnea, stridor (late sign)

Gastrointestinal White (leukoplakia) or red (erythroplakia) patches inside mouth, ulceration of mucosa, asymmetric tongue, exudate in mouth or pharynx, mass or thickening of mucosa

Possible Diagnostic Findings Mass on direct or indirect laryngoscopy; tumor on soft tissue x-ray, CT scan, or MRI; positive biopsy

• Difficulty coping • Impaired communication More information on nursing diagnoses and the care of the patient with head and neck cancer is presented in eNursing Care Plan 26.2 on the website for this chapter.

Planning The overall goals are that the patient will have (1) a patent airway, (2) an acceptable body image, (3) no complications related to therapy, (4) adequate nutritional intake, (5) minimal to no pain, and (6) the ability to communicate.

Nursing Implementation Health Promotion

Most head and neck cancers can be prevented. The development of head and neck cancer is closely related to personal habits, mainly tobacco use and excess alcohol use. Poor oral hygiene and HPV infection are also risk factors for head and neck cancer. Include information about risk factors in health teaching. Encourage good oral hygiene. Teach patients about safe sex practices to prevent HPV infection (e.g., use condoms, encourage monogamous relationships, choose a partner who has had no or few previous partners). If cancer has been diagnosed, tobacco and alcohol cessation are still important. The chance of a cure, by any treatment modality, for a patient with head and neck cancer who continues to smoke and use alcohol is decreased. Also, the risk for a second primary cancer is significantly increased. Give patients information about smoking cessation programs and techniques for success. If needed, refer to an alcohol treatment program. Smoking cessation and treatment of alcohol use are discussed in Chapter 10.

Acute Care Teach the patient and caregiver about the type of treatment to be performed, care needed, and reason for treatment and care. Help prepare them to deal with the psychological impact of the diagnosis of cancer, change in physical appearance, possible need for enteral feedings, and use of other communication methods because of loss of voice. Care plans should include assessment of the patient’s support system. The patient may not have someone to help after discharge or may have a job that cannot be continued, leaving the patient unemployed.

Surgical Therapy Preoperatively assess the patient’s physical and psychosocial needs. Physical preparation is the same as for any major surgery, with an emphasis on oral hygiene. Assess knowledge and understanding of the planned surgical procedure and clarify misinformation or misunderstanding as needed. When possible, include the caregiver in

preoperative teaching. Tailor teaching to the planned surgical procedure. For example, include information about expected changes in speech after a laryngectomy. Alphabet boards, writing materials, pictorial guides, laptops, and hand signals are useful methods for communicating. Programmable speech-generating devices allow use of recorded messages that are matched with a graphic representing each message. Integration of newer technology into patient care enhances the patient’s ability to communicate basic needs after surgery.

Informatics in Practice Communication Devices for Patient With Laryngectomy • Assisting with communication will improve a patient’s quality of life after a laryngectomy. • Use a tablet or smartphone and download a text-to-speech application. These applications allow the patient to type in text, and then a computer voice says the text aloud. • You can teach the patient how to use a keyboard-based communication program. The patient types on a traditional keyboard and generates speech that is transmitted through handheld speakers. Immediately after surgery, nursing care priorities include airway management, wound care, nutrition, communication, and psychosocial issues related to body image changes. Maintaining a patent airway is essential. Inflammation in the surgical area may compress the trachea. Keep the patient in a semi-Fowler’s position to decrease edema and limit tension on suture lines. Give analgesic drugs as needed for pain control. Because patients may not be able to speak, have them nonverbally rate their pain (e.g., visual pain scale) to help assess the effectiveness of the medication.

(Pain management is discussed in Chapter 8.) Monitor vital signs frequently. Be alert for hemorrhage, as many of the structures in the head and neck area are very vascular. Pay careful attention to heart rate, blood pressure, SpO2, and the patient’s hemoglobin value. The patient with a laryngectomy needs frequent suctioning via the tracheostomy tube. Secretions typically change in amount and consistency over time. The patient may initially have a large amount of blood-tinged secretions that gradually diminish and thicken. Maintain adequate fluid intake (IV, enteral) and humidification of inspired gases to keep secretions liquid and mucous membranes moist. Encourage deep breathing and coughing. Pressure dressings, packing, or drainage tubes may be present, depending on the type of surgical procedure. Do not change any dressing unless you have a specific order from the HCP. If skin flaps are used, dressings are typically not present. This allows better visualization of the flap and avoids excess pressure on tissue. Skin flaps must initially be checked hourly for color and any change in size or edema. Doppler ultrasound may be used to determine the presence of a pulse, depending upon the location of the skin flap. Hemovac, Jackson-Pratt, and Penrose drains are some of the drainage devices that may be used. Drainage may initially be bloody, then serosanguineous, and gradually decrease in volume over 24 to 48 hours. Monitor patency of drainage tubes every hour in the first few hours after surgery, then every 4 hours to ensure proper functioning. If tubing becomes obstructed, fluid will accumulate under the skin flap and predispose the patient to formation of hematomas or seromas, impair wound healing, and increase the risk for infection. After drainage tubes are removed, closely monitor the area to detect any swelling. Closely monitor incision sites for signs of infection. The patient may have a nasogastric tube inserted during surgery to remove gastric contents via intermittent suction for the first 24 to 48 hours until peristalsis returns. Because the nasogastric tube lies close to internal incision lines, do not manipulate or move the tube. When bowel sounds return, start enteral feedings slowly and advance to

meet nutritional needs.

Radiation Therapy Dry mouth (xerostomia), a frequent and annoying problem, typically occurs within a few weeks of treatment. The patient’s saliva decreases in volume and becomes thick. This change may be temporary or permanent. Pilocarpine hydrochloride (Salagen) is often effective in increasing saliva production.

Check Your Practice Your 64-yr-old male patient with oral cancer has been receiving radiation therapy for 3 weeks. He has developed xerostomia and oral mucositis. He asks if you have any suggestions to help relieve his symptoms. • How would you respond? Once patients can have foods or fluids by mouth, they can get symptom relief by increasing fluid intake, chewing sugarless gum or sugarless candy, using nonalcoholic mouth rinses (baking soda, glycerin solutions), and using artificial saliva. Teach patients to always carry a water bottle with them. Fluoride gels or treatments can help prevent dental deterioration caused by xerostomia. Oral mucositis can cause irritation, ulceration, and pain. Teach the patient on oral care basics, including the use of a soft toothbrush and regular flossing. Empty fluoride gel trays, along with bite blocks, athletic mouth guards, or gauze pads, can be worn during radiation treatments. This prevents radiation scatter to the tongue and cheek from metal work in the mouth. Warm bland rinses, like those with salt and baking soda, 4 to 6 times daily may be helpful. Sucking on ice chips can also help with the pain. Patients should avoid commercial mouthwashes and hot, spicy, or acidic foods because they are irritating.

Skin over the irradiated area often becomes reddened and sensitive to touch. Teach patients to use only prescribed lotions and skin products while undergoing radiation therapy and to not use any lotions within 2 hours before treatment. Skin care for patients having radiation therapy is discussed in Chapter 15. Fatigue is a common side effect of radiation therapy as well as chemotherapy. Encourage patients to walk 15 to 30 minutes each day since regular exercise can give them more energy. Teach patients to do activities that are most important to them and to rest during periods of low energy. Identify support systems and encourage patients to ask for help.

Stoma Care Should the patient have a stoma after surgery, teach the patient proper care of the stoma. The patient should wash the area around the stoma daily with a moist cloth. A nasal wash spray (e.g., Alkalol) can be used every 1 to 2 hours to keep the stoma moist and prevent crusting. Dried secretions can be removed with tweezers. If a laryngectomy tube is in place, the patient must remove the entire tube at least daily and clean it in the same manner as a tracheostomy tube. The inner cannula may have to be removed and cleaned more often. A scarf or loose shirt can hide the stoma. The patient should cover the stoma when coughing (because mucus may be expectorated) and during any activity (e.g., shaving, applying makeup) that may lead to inhalation of foreign materials. Because water can easily enter the stoma, the patient should wear a plastic collar when taking a shower. Swimming is contraindicated. Initially, humidification is given with mechanical ventilation or, after extubation, with a tracheostomy mask. After discharge, the patient can use a bedside humidifier.

Psychosocial Needs Psychosocial care of the patient with head and neck cancer is of utmost importance. Issues concerning depression, change in body image, and sexuality are common. Although changes are discussed

before surgery, the patient may not be psychologically prepared for the extent of these changes. If the patient has a significant other, this person’s reaction to the patient’s altered appearance is important. Acceptance by another person can promote an improved self-image. Depression may occur for many reasons: inability to speak because of surgical procedure and/or presence of ET or tracheostomy tube, altered physical appearance due to the surgery and edema, loss of independence and reliance upon others, and feelings of helplessness and hopelessness. Depression also may be related to concern about the prognosis. Allow the patient and caregiver to express their feelings and emotions. Convey acceptance to help patients regain positive feelings about their body image and self-concept. Encourage participation in support groups. Information about available groups can be obtained through the local branch of the American Cancer Society. A psychiatric referral may be needed for the patient who has prolonged or severe depression. Surgery and surgical devices such as tracheostomy and gastrostomy tubes may dramatically affect body image. Xerostomia and fatigue can physically affect sexuality. It may be hard for the patient to talk about sexual problems because of changes in communication. Help the patient and partner by allowing them to talk about their sexuality and how surgery and treatment may affect their relationship. Helping the patient see that sexuality involves much more than appearance may relieve some anxiety.

Ambulatory Care The patient may be discharged with a tracheostomy and a nasogastric or gastrostomy feeding tube. Some patients initially need a home health care referral and assessment to evaluate the patient’s or caregiver’s ability to perform self-care activities. Both patient and caregiver need to learn how to manage tubes and whom to call if there are problems. Provide pictorial instructions for tracheostomy care, suctioning, stoma and skin care, and enteral feeding as appropriate. Encouraging the patient to take part in self-care is an important part of

rehabilitation. Teach the patient the importance of wearing a Medic Alert bracelet or other identification that alerts emergency personnel of the possible changes in breathing status because of surgery. Because the patient no longer breathes through the nose, the ability to smell smoke and taste food is often lost. Teach the patient to install smoke and carbon monoxide detectors in the home. Encourage preparation of food that is colorful, attractive, and nutritious because taste may be decreased due to the loss of smell and radiation therapy. Refer to a dietitian as needed. The patient can resume exercise, recreation, and sexual activity when able. Most patients can return to work 1 to 2 months after surgery. However, many never return to full-time employment. The changes that follow a total laryngectomy can be upsetting. Loss of speech, loss of the ability to taste and smell, inability to produce audible sounds (including laughing and weeping), and the presence of a permanent tracheal stoma that produces undesirable mucus are often overwhelming to patients.

Evaluation Expected outcomes for the patient with head and neck cancer who is treated surgically are that the patient will: • Have effective coughing and secretion clearance • Swallow oral foods without aspiration • Uses effective coping strategies • Use techniques to effectively communicate

Case Study Laryngeal Cancer

© iStockphoto/Thinkstock.

Patient Profile M.R., a 69-yr-old retired baker, was admitted to the hospital for influenza. He told his HCP that he has “a cough that just won’t go away,” difficulty swallowing, and “a sore throat that really hasn’t gotten better” over the past year. His wife passed away 6 years ago. He has 3 adult children; 1 daughter lives in the same city. He has a history of hypertension, smoking, alcohol use, gastroesophageal

reflux disease (GERD), and type 2 diabetes.

Subjective Data • States that his symptoms worsened in the past 3 months • Has used various cough and cold remedies over the past 6 months to relieve symptoms without relief • Has lost weight because of decrease in appetite and difficulty swallowing • Has smoked 3 packs of cigarettes a day for the past 50 yrs • Consumes 4 to 6 cans of beer a day

Objective Data Physical Examination • Vital signs: Temperature 102.4° F (39.1° C), heart rate 99 beats/min (pulse strong, regular), respiratory rate 24 breaths/min (short, shallow, slightly labored), BP 176/84 (cuff), SpO2 87% on room air • Inspection: Awake and alert, appears gray, malnourished, dehydrated. Small, irregular white patches on the sides of oral cavity • Palpation: Enlarged cervical nodes bilaterally (nontender) • Auscultation: Adequate and clear air entry to upper lung fields; slightly decreased air entry to bases with occasional fine crackles on expiration

Diagnostic Studies • Chest x-ray: lung fields clear • Laryngoscopy: mass in subglottic area (requires further evaluation) • CT scan: subglottic lesion with lymph node involvement

• Diagnosis: laryngeal cancer

Interprofessional Care • Surgery: suggests a total laryngectomy • Oncology: suggests radiation and chemotherapy postoperatively • Gastroenterology: percutaneous gastrostomy tube preoperatively for enteral feeding • Dietary: explain nutritional options with/without ET tube/tracheostomy • Physical therapy: visit pre-surgery to explain postoperative exercise routine • Social worker: determine social supports available postoperatively

Discussion Questions 1. What assessment information suggests that M.R. is at risk for laryngeal cancer? 2. Priority Decision: What are your priority teaching strategies for M.R. before his total laryngectomy? Postoperative teaching priorities? 3. How would you explain the gastrostomy tube to M.R.? 4. Is there anything in his history that may affect wound healing after surgery?

Progression of Case M.R. is transferred to the clinical unit after 24 hours in ICU. He is awake, alert, but slightly confused. Vital signs are stable. BP 168/94. Large surgical dressing on neck with 3 Jackson-Pratt drains. Tracheostomy tube in place. Receiving O2 via tracheal mask. Enteral feeding at 30 mL/hr via gastrostomy tube. Foley catheter patent, draining a moderate amount of amber urine. M.R. is picking at his

surgical drains, and when you try to reassure him, he just starts waving his hands at you. 5. Collaboration: What information would you want to know from the ICU nurse who has just transported M.R. to the clinical unit? 6. Priority Decision: Based on the assessment data presented, what are your priority nursing diagnoses? Are there any collaborative problems? 7. Evidence-Based Practice: How could you best meet M.R.’s communication needs during the first few postoperative days? 8. Four hours after transfer to the clinical unit, M.R. is tearful and is staring at the wall. What should you do? 9. Patient-Centered Care: What teaching is required to help him assume self-care after his surgery? What precautions should he take because of his stoma? Answers available at http://evolve.elsevier.com/Lewis/medsurg.

Bridge to Nclex Examination The number of the question corresponds to the same-numbered outcome at the beginning of the chapter.

1. A patient is seen in the clinic for a nosebleed, which is controlled by placement of anterior nasal packing. During discharge teaching, the nurse teaches the patient to a. use aspirin for pain relief. b. remove the packing later that day. c. avoid vigorous nose blowing and strenuous activity. d. insert more packing into the nose if rebleeding occurs. 2. A patient with allergic rhinitis reports severe nasal

congestion; sneezing; and watery, itchy eyes and nose at various times of the year. When teaching the patient about how to control these symptoms, the nurse teaches the patient to a. avoid all intranasal sprays and oral antihistamines. b. limit the usage of nasal decongestant spray to 10 days. c. use oral decongestants at bedtime to prevent symptoms during the night. d. keep a diary of when the allergic reaction occurs and what precipitates it. 3. A patient is seen at the clinic with fever, muscle aches, sore throat with yellowish exudate, and headache. The nurse anticipates that the interprofessional management will include (select all that apply) a. antiviral agents to treat influenza. b. treatment with antibiotics starting ASAP. c. a throat culture or rapid strep antigen test. d. supportive care, including cool, bland liquids. e. comprehensive history to determine possible cause. 4. The best method for determining the risk for aspiration in a patient with a tracheostomy is to a. consult a speech therapist for swallowing assessment. b. have the patient drink plain water and assess for coughing. c. ask the patient to rate the perceived degree of swallowing difficulty. d. assess for sputum changes 48 hours after the patient drinks small amount of blue dye.

5. Which nursing action would be of highest priority when suctioning a patient with a tracheostomy? a. Auscultating lung sounds after suctioning is complete b. Giving antianxiety medications 30 minutes before suctioning c. Instilling 5 mL of normal saline into the tracheostomy tube before suctioning d. Assessing the patient’s oxygen saturation before, during, and after suctioning 6. When planning health care teaching to prevent or detect early head and neck cancer, which people would be the priority to target (select all that apply)? a. 65-year-old man who has used chewing tobacco most of his life b. 45-year-old rancher who uses snuff to stay awake while driving his herds of cattle c. 21-year-old college student who drinks beer on weekends with his fraternity brothers d. 78-year-old woman who has been drinking liquor since her husband died 15 years ago e. 22-year-old woman who has been diagnosed with human papilloma virus of the cervix 7. While in the recovery room, a patient with a total laryngectomy is suctioned and has bloody mucus with some clots. Which nursing interventions would apply? (select all that apply) a. Notify the health care provider at once. b. Place the patient in semi-Fowler’s position.

c. Use a bag-valve-mask (BVM) and begin rescue breathing for the patient d. Instill 10 mL of normal saline into the tracheostomy tube to loosen secretions. e. Continue patient assessment, including O2 saturation, respiratory rate, and breath sounds. 8. Appropriate discharge teaching for the patient with a permanent tracheostomy after a total laryngectomy for cancer would include (select all that apply) a. encouraging regular exercise such as swimming. b. washing around the stoma daily with a moist washcloth. c. encouraging participation in postlaryngectomy support group. d. providing pictures and “hands-on” instruction for tracheostomy care. e. teaching how to hold breath and trying to gag to promote swallowing reflex. 1. c, 2. d, 3. c, d, e, 4. a, 5. d, 6. a, b, d, e, 7. b, e, 8. b, c, d For rationales to these answers and even more NCLEX review questions, visit http://evolve.elsevier.com/Lewis/medsurg.

Evolve Website/Resources List http://evolve.elsevier.com/Lewis/medsurg

Review Questions (Online Only) Key Points Answer Keys for Questions • Rationales for Bridge to NCLEX Examination Questions

• Answer Guidelines for Case Study on p. 499 Student Case Study • Patient With Head and Neck Cancer/Laryngectomy With Tracheostomy Nursing Care Plans • eNursing Care Plan 26.1: Patient With a Tracheostomy • eNursing Care Plan 26.2: Patient Having Total Laryngectomy and/or Radical Neck Surgery Conceptual Care Map Creator Supporting Media • Animation • Tracheotomy Audio Glossary Content Updates

References 1. American Academy of Otolaryngology: Deviated septum. Retrieved from https://www.enthealth.org/nose-landing-page/. 2. Paton K.T, Thibodeau G.A. Anatomy and physiology. ed 9. St Louis: Mosby; 2016. 3. Haraldson SJ: Nasal fracture. Retrieved from https://emedicine.medscape.com/article/84829-overview. 4. Good V.S, Kirkwood P.L. Advanced critical care nursing. ed 2. St Louis: Elsevier; 2018. 5. Rothrock J.C. Alexander’s care of the patient in surgery. ed 16. St Louis: Elsevier; 2019.

6. Shiffman M.A, DiGiuseppe A. Advanced aesthetic rhinoplasty: Art, science, and new clinical technologies. New York: Springer; 2013 (Classic). 7. DeWit S.C, Stromberg H.K, Dallred C. Medicalsurgical nursing: Concepts and practice. ed 3. St Louis: Elsevier; 2017. 8. Nguyen QA: Epistaxis treatment and management. Retrieved from https://emedicine.medscape.com/article/863220-treatment. 9. Sheikh J: Allergic rhinitis. Retrieved from https://emedicine.medscape.com/article/134825overview#a5. Scadding G.K, Kariyawasam H.H, Scadding G, et al. BSACI guideline for the diagnosis and management of allergic and non-allergic rhinitis. Clin Exp Allergy. 2017;47:856.

11. American Academy of Asthma, Allergy and Immunology: Hay fever and allergy medications. Retrieved from www.aaaai.org/conditions-andtreatments/library/allergy-library/hay-fever-medications. 12. Centers for Disease Control and Prevention: Seasonal influenza-associated hospitalizations in the United States. Retrieved from www.cdc.gov/flu/about/qa/hospital.htm. 13. Centers for Disease Control and Prevention: Estimating seasonal influenza-associated deaths in the United States. Retrieved from www.cdc.gov/flu/about/disease/us_flu-related_deaths.htm. 14. University of California Irvine Health: How long is the flu contagious? Retrieved from www.ucirvinehealth.org/blog/2017/02/flu-contagious. 15. US Food and Drug Administration: Influenza (flu) antiviral drugs and related information. Retrieved

from www.fda.gov/drugs/drugsafety/informationbydrugclass/ucm100228.h Hanson C, Lepule K. Management of acute and chronic sinusitis. S Afr Pharm J. 2017;84:45. Arina A.M, Chan M.M. Current concepts in adult acute rhinosinusitis. Am Fam Physician. 2016;94:97.

18. Newson L: Nasal polyps. Retrieved from https://patient.info/health/nasal-polyps-leaflet. 19. Hermann J: Say ahh: Acute pharyngitis diagnosis and management. Retrieved from http://contemporaryclinic.pharmacytimes.com/journals/issue/2017/de Ahh-Acute-Pharyngitis-Diagnosis-and-Management. 20. Carrillo-Marquez MA: Bacterial pharyngitis treatment and management. Retrieved from https://emedicine.medscape.com/article/225243-treatment. Lynch J, Crawley S.M. Management of airway obstruction. BJA Education. 2018;18:46.

22. Urden L.D, Stacy K.M, Lough M.E. Critical care nursing: Diagnosis and management. ed 8. St. Louis: Elsevier; 2018. Mehta C, Mehta Y. Percutaneous tracheostomy. Ann Card Anaesth. 2017;20:S19.

24. Salisbury NHS Foundation Trust: Tracheostomy cuffs —Management of. Retrieved from www.icid.salisbury.nhs.uk/CLINICALMANAGEMENT/ENT/Pages 25. American Cancer Society: Key statistics for oral and oropharyngeal cancers. Retrieved from www.cancer.org/cancer/oral-cavity-and-oropharyngealcancer/about/key-statistics.html. 26. American Society of Clinical Oncology Cancer.Net: Head and neck cancer: Risk factors and prevention. Retrieved from www.cancer.net/cancer-types/head-and-

neck-cancer/risk-factors-and-prevention. 27. Cancer Treatment Centers of America: TNM system for head and neck cancer. Retrieved from www.cancercenter.com/head-and-neck-cancer/stages/. 28. Australian Government Cancer Australia: Head and neck cancer treatment options. Retrieved from https://head-neck-cancer.canceraustralia.gov.au/treatment. 29. Cancer Treatment Centers of America: Head and neck cancer drug information. Retrieved from www.cancercenter.com/head-and-neck-cancer/diagnosticsand-treatments/tab/drug-information/. ∗Evidence-based information for clinical practice.

27

Lower Respiratory Problems Eugene Mondor

LEARNING OUTCOMES 1. Compare and contrast the clinical manifestations and nursing and interprofessional management of patients with acute bronchitis and pertussis. 2. Distinguish among the types of pneumonia and their etiology. 3. Describe the pathophysiology, clinical manifestations, diagnostic studies, and interprofessional and nursing management of patients with pneumonia. 4. Describe the pathogenesis, classification, clinical manifestations, complications, diagnostic abnormalities, and interprofessional and nursing management of patients with tuberculosis. 5. Describe the causes, clinical manifestations, and nursing and interprofessional management of patients with pulmonary fungal infections. 6. Explain the pathophysiology, clinical manifestations, and nursing and interprofessional management of a patient with a lung abscess. 7. Identify the causative factors, clinical manifestations, and nursing and interprofessional management of patients with environmental lung diseases. 8. Describe the etiology, risk factors, pathophysiology, clinical manifestations, and interprofessional and nursing management of

lung cancer. 9. Compare and contrast the pathophysiology, clinical manifestations, and nursing and interprofessional management of fractured ribs, flail chest, and pneumothorax. 10. Describe the purpose, function, and nursing responsibilities related to chest tubes and chest drainage systems. 11. Explain the types of chest surgery and appropriate preoperative and postoperative care. 12. Describe the etiology, clinical manifestations, and nursing and interprofessional management of patients with restrictive lung disorders. 13. Describe the pathophysiology, clinical manifestations, and nursing and interprofessional management of pulmonary embolism, pulmonary hypertension, and cor pulmonale. 14. Discuss the use of lung transplantation as a treatment for pulmonary disorders, emphasizing nursing and interprofessional management of the postoperative lung transplant patient.

KEY TERMS acute bronchitis, p. 502 community-acquired pneumonia (CAP), p. 504 cor pulmonale, p. 535 empyema, p. 531 flail chest, p. 524 hemothorax, p. 525 hospital-acquired pneumonia (HAP), p. 504 lung abscess, p. 515 pertussis, p. 503

pleural effusion, p. 531 pleurisy (pleuritis), p. 531 pneumoconiosis, p. 516 pneumonia, p. 503 pneumothorax, p. 524 pulmonary edema, p. 532 pulmonary embolism (PE), p. 532 pulmonary hypertension, p. 534 tension pneumothorax, p. 525 thoracentesis, p. 530 thoracotomy, p. 529 tuberculosis (TB), p. 509 To know even one life has breathed easier because you have lived, that is to have succeeded. Ralph Waldo Emerson http://evolve.elsevier.com/Lewis/medsurg/

Conceptual Focus Cellular Regulation Clotting Functional Ability Gas Exchange Infection A variety of problems affect the lower respiratory system. This chapter discusses lower respiratory tract diseases that influence the concept of gas exchange. It focuses on infectious, environmental,

oncologic, traumatic, restrictive, and vascular problems that impair gas exchange. Gas exchange is related with multiple concepts, as a problem has profound consequences because of the need of adequate oxygenation for life.

Lower Respiratory Tract Infections Lower respiratory tract infection is both a common and serious occurrence. It is the reason for thousands of clinic and emergency department (ED) visits and hospital admissions each year. In the United States, pneumonia and influenza cause more than 57,000 deaths annually.1

Acute Bronchitis Acute bronchitis is a self-limiting inflammation of the bronchi in the lower respiratory tract. It is the reason for 10% of all clinic visits and 100 million ED visits per year.2 Most acute bronchial infections are caused by viruses. Air pollution, dust, inhalation of chemicals, smoking, chronic sinusitis, and asthma are other triggers. Cough, which is the most common symptom, may last for up to 3 weeks. It is the main reason for seeking medical care. Clear sputum is often present, although some patients have purulent sputum. The presence of colored (e.g., green) sputum is not a reliable indicator of bacterial infection. Other symptoms may include headache, fever, malaise, hoarseness, myalgias, dyspnea, and chest pain. Diagnosis is based on the assessment. Assessment may reveal normal breath sounds or crackles or wheezes, usually on expiration and with exertion. Consolidation (which occurs when fluid accumulates in the lungs), suggestive of pneumonia, is absent with bronchitis. Chest x-rays are normal and not needed unless pneumonia or some other pulmonary disorder is suspected. The goal of treatment is to relieve symptoms and prevent pneumonia. Treatment is supportive. It includes cough suppressants (e.g., dextromethorphan), encouraging oral fluid intake, and using a humidifier. Throat lozenges, hot tea, and honey may help relieve cough. β2-Agonist (bronchodilator) inhalers are useful for patients with wheezes or underlying pulmonary conditions. Antibiotics are not prescribed for viral infections because they have side effects and promote antibiotic resistance. Antibiotics may be given to patients with underlying chronic conditions who have a prolonged infection associated with systemic symptoms. Encourage patients not to smoke, to avoid secondhand smoke, and to wash their hands often. If the acute bronchitis is due to an influenza virus, treatment with antiviral drugs may be started. If patients with acute bronchitis develop a fever, have difficulty breathing, or have symptoms last longer than 4 weeks, they should see their HCP.

Pertussis Pertussis is a highly contagious infection of the respiratory tract caused by the gram-negative bacillus Bordetella pertussis. The bacteria attach to the cilia of the respiratory tract and release toxins that damage the cilia, causing inflammation and swelling. The incidence of pertussis has been steadily increasing in the United States since the 1980s. The largest increase is seen in adults. We think that immunity from childhood tetanus, diphtheria, and pertussis vaccine (Tdap) vaccination may decrease over time, allowing a milder (but still contagious) infection. The Centers for Disease Control and Prevention (CDC) currently recommends that all adolescents (11 years and older) and adults who have not received a dose of Tdap receive a one-time vaccination as soon as possible.3 Manifestations of pertussis occur in stages. The first stage, lasting 1 to 2 weeks, manifests as a mild upper respiratory tract infection (URI) with a low-grade or no fever, runny nose, watery eyes, generalized malaise, and mild, nonproductive cough. The second stage, from the second to tenth week of infection, is characterized by paroxysms of cough. The last stage lasts 2 to 3 weeks. It is characterized by a less severe cough and weakness.

Promoting Population Health Preventing Respiratory Diseases • Wash hands often to prevent and avoid spreading infections. • Avoid cigarette smoking and exposure to environmental smoke. • Get a pneumococcal vaccine and yearly flu vaccine as directed by the HCP. • Avoid exposure to allergens, indoor pollutants, and ambient air pollutants.

• Wear proper personal protective equipment when working in an occupation with prolonged exposure to dust, fumes, or gases. The hallmark characteristic of pertussis is uncontrollable, violent coughing. Inspiration after each cough produces the typical “whooping” sound as the patient tries to breathe in air against an obstructed glottis. The “whoop” is often not present in teens and adults (especially those who have been vaccinated). Like acute bronchitis, the coughing is more frequent at night. Vomiting may occur with coughing. Unlike acute bronchitis, the cough with pertussis may last from 6 to 10 weeks. In the community, diagnosis is primarily by history and examination. In the clinical setting, the CDC recommends nasopharyngeal cultures, polymerase chain reaction (PCR) of nasopharyngeal secretions, or serology testing.4 The treatment is macrolide (erythromycin, azithromycin [Zithromax]) antibiotics to minimize symptoms and prevent spread of the disease. For the patient who cannot take macrolides, trimethoprim/sulfamethoxazole is used. The patient is infectious from the beginning of the first stage through the third week after onset of symptoms or until 5 days after antibiotic therapy has been started. Routine and droplet precautions are required for hospitalized patients. Patients should not use cough suppressants and antihistamines as they are ineffective and may induce coughing episodes. Corticosteroids and bronchodilators are also not helpful. The CDC recommends postexposure antibiotics to those who have had close contact with the patient.

Pneumonia Pneumonia is an acute infection of the lung parenchyma. Despite remarkable progress in the development of antibiotics to treat pneumonia, pneumonia is still associated with significant morbidity and mortality. The CDC reports that pneumonia and influenza are the 8th leading cause of death in the United States.5

Etiology Normally, various defense mechanisms protect the airway distal to the larynx from infection. Mechanisms that create a mechanical barrier to microorganisms entering the tracheobronchial tree include air filtration, epiglottis closure over the trachea, cough reflex, mucociliary escalator mechanism, and reflex bronchoconstriction (see Chapter 25). Immune defense mechanisms include secretion of immunoglobulins A and G and alveolar macrophages. Pneumonia is more likely to occur when defense mechanisms become incompetent or are overwhelmed by the virulence or quantity of infectious agents. A weakened cough or epiglottal reflex may allow aspiration of oropharyngeal contents into the lungs. Tracheal intubation bypasses normal filtration processes and interferes with the cough reflex and mucociliary escalator mechanism. Air pollution, cigarette smoking, viral URIs, and normal changes that occur with aging can impair the mucociliary mechanism. Chronic diseases can suppress the immune system’s ability to inhibit bacterial growth. The risk factors for pneumonia are listed in Table 27.1. Pathogens that cause pneumonia reach the lung in 3 ways: 1. Aspiration of normal flora from the nasopharynx or oropharynx. Many organisms that cause pneumonia are normal inhabitants of the pharynx in healthy adults. 2. Inhalation of microbes present in the air. Examples include Mycoplasma pneumoniae and fungal pneumonias.

3. Hematogenous spread from a primary infection elsewhere in the body. Examples are streptococci and Staphylococcus aureus from infective endocarditis.

TABLE 27.1 Risk Factors for Pneumonia • Abdominal or chest surgery • Age >65 years • Air pollution • Altered consciousness: alcoholism, head injury, seizures, anesthesia, drug overdose, stroke • Bed rest and prolonged immobility • Chronic diseases: chronic lung and liver disease, diabetes, heart disease, cancer, chronic kidney disease • Debilitating illness • Exposure to bats, birds, rabbits, and farm animal droppings (excrement) • Immunosuppressive disease and/or therapy (corticosteroids, cancer chemotherapy, HIV infection, immunosuppressive therapy after organ transplant) • Inhalation or aspiration of noxious substances • Intestinal and gastric feedings via nasogastric or nasointestinal tubes • IV drug use • Malnutrition • Recent antibiotic therapy • Resident of a long-term care facility • Smoking • Tracheal intubation (endotracheal intubation, tracheostomy) • URI

Classifications of Pneumonia There is no universally accepted classification system for pneumonia. Some suggest classifying pneumonia according to the causative pathogens (e.g., bacterial, viral, fungal, etc.), characteristics of the disease, or radiographic appearance on chest x-ray. The most widely recognized and effective way to classify pneumonia is as either community-acquired or hospital-acquired pneumonia. This classification helps the HCP identify the most likely cause (Table 27.2) and the choice of antimicrobial therapy.

Community-Acquired Pneumonia Community-acquired pneumonia (CAP) is an acute infection of the lung occurring in patients who have not been hospitalized or lived in a long-term care facility within 14 days of the onset of symptoms. The decision to treat the patient at home or admit to hospital is based on several factors. These include the patient’s age, vital signs, mental status, presence of co-morbid conditions, and current physiologic condition. We can use tools such as the expanded CURB-65 scale (Table 27.3) to supplement clinical judgment.

Hospital-Acquired Pneumonia Hospital-acquired pneumonia (HAP), also known as nosocomial pneumonia, is pneumonia in a nonintubated patient that begins 48 hours or longer after admission to hospital and was not present at the time of admission. Ventilator-associated pneumonia (VAP), a type of HAP, refers to pneumonia that occurs more than 48 hours after endotracheal intubation.6 VAP is discussed in Chapter 65. Both HAP and VAP are associated with longer hospital stays, increased associated costs, sicker patients, and increased risk for morbidity and mortality. Once the diagnosis of CAP, HAP, or VAP is made, treatment is started based on known risk factors, early versus late onset, presentation, underlying medical conditions, hemodynamic stability, and the likely causative pathogen. Empiric antibiotic therapy, the

initiation of treatment before a definitive diagnosis or causative agent is confirmed, should be started as soon as pneumonia is suspected. Empiric antibiotic therapy is based on the knowledge of drugs known to be effective for the likely cause. Antibiotic therapy can be adjusted once the results of sputum cultures identify the exact pathogen.

TABLE 27.2 Organisms Causing Pneumonia

Community-Acquired Pneumonia • Chlamydophila pneumoniae • Chlamydophila psittaci • Coxiella burnettii • Gram-negative bacilli • Fungi • Influenzae • Influenza A and B • Klebsiella pneumoniae • Legionella pneumophila∗ • MRSA∗ • Moraxella catarrhalis • Mycobacterium tuberculosis • Mycoplasma pneumoniae • Oral anaerobes (e.g., alcoholism, IV drug use) • Pseudomonas aeruginosa • Respiratory viruses • S. pneumoniae∗

Hospital-Acquired Pneumonia

• Acinetobacter species† • Enterobacter species • Escherichia coli† • H. influenzae • Klebsiella pneumoniae† • Proteus species • Pseudomonas aeruginosa† • S. aureus • S. pneumoniae



Most common cause of community-acquired pneumonia (CAP). † Most common causes of hospital-acquired pneumonia (HAP).

TABLE 27.3 Assessing Pneumonia Severity Using

Expanded CURB-65 The Expanded CURB-65 scale may be used as a supplement to clinical judgment to determine the severity of pneumonia and if patients need to be hospitalized.

Identifying the Level of Risk Patients receive 1 point for each of the following indicators: • C: Confusion (compared to baseline) • U: BUN >20 mg/dL • R: Respiratory rate ≥30 breaths/min • B: Systolic blood pressure 230 µ/L • Albumin: 5 cm and more than one tumor in a different lobe of the lung

IV

Distant metastasis

B

OR 5–7 cm with visceral and parietal pleura, diaphragm, phrenic nerve involvement

Tumor

Staging Staging of NSCLC is done using the TNM staging system (see Table 15.5). Under the TNM system, cancer is grouped into 4 stages with A or B subtypes. A simplified version of staging of NSCLC is shown in Table 27.17. Patients with stages I, II, and IIIA disease may be surgical candidates. However, stage IIIB or IV disease is usually inoperable and has a poor prognosis. Staging of SCLC by TNM has not been useful because this cancer is aggressive and is always considered systemic. The stages of SCLC are limited and extensive. Limited means that the tumor is only on 1 side of the chest and regional lymph nodes. Extensive SCLC means that the cancer extends beyond the limited stage. Most patients with SCLC have extensive disease at time of diagnosis.

Screening for Lung Cancer The American College of Chest Physicians recommends screening for

high-risk patients.28 Adults ages 55 to 77 with a history of smoking (30 pack-year smoking history or currently smoke) or who quit smoking but less than 15 years ago should have annual screening for lung cancer. Screening is done using low-dose CT. Several other groups have endorsed these guidelines, including the American Cancer Society.29

Interprofessional Care Surgical Therapy Surgical resection is the treatment of choice in NSCLC stages I to IIIA without mediastinal involvement. Resection gives the best chance for a cure. Factors that affect survival include the size of the primary tumor and preexisting co-morbidities. For other NSCLC stages, patients may have surgery in conjunction with radiation therapy, chemotherapy, and targeted therapy. Many NSCLCs are not resectable at the time of diagnosis. Surgical procedures include segmental or wedge resection procedures, lobectomy (removal of 1 or more lobes of the lung), or pneumonectomy (removal of 1 entire lung). VATS may be used to treat lung cancers near the outside of the lung. Surgery is generally not done for SCLC because of its rapid growth and dissemination at the time of diagnosis. When the tumor is considered operable, the patient’s cardiopulmonary status must be evaluated to determine the ability to have surgery. Pulmonary function studies, ABGs, and anesthesia and critical care consults are often done before surgery to assess the patient’s cardiopulmonary status.

Radiation Therapy Radiation therapy may be used as treatment for both NSCLC and SCLC. Radiation therapy may be given as curative therapy, palliative therapy (to relieve symptoms), or adjuvant therapy in combination with surgery, chemotherapy, or targeted therapy. Radiation therapy may be used as primary therapy in the person

who is unable to tolerate surgical resection because of co-morbidities. Radiation therapy relieves symptoms of dyspnea and hemoptysis from bronchial obstructive tumors and treats superior vena cava syndrome. It can treat pain from metastatic bone lesions or brain metastasis. Radiation before surgery can reduce the tumor mass before surgical resection. Complications of radiation therapy include esophagitis, skin irritation, nausea and vomiting, anorexia, and radiation pneumonitis (see Chapter 15). Stereotactic body radiotherapy (SBRT), also called stereotactic radiosurgery (SRS), is a newer lung cancer treatment. It is a type of radiation therapy that uses high doses of radiation delivered to tumors outside the CNS. SBRT uses special positioning procedures and radiology techniques to deliver a higher dose of radiation to the tumor and expose only a small part of healthy lung. It does not destroy the tumor, but damages tumor DNA. Therapy is given over 1 to 3 days. SBRT provides an option for patients with early-stage lung cancers who are not surgical candidates for other medical reasons.

Chemotherapy Chemotherapy is the main treatment for SCLC. In NSCLC, chemotherapy may be used in the treatment of nonresectable tumors or as adjuvant therapy to surgery. We use a variety of chemotherapy drugs and multidrug protocols. Chemotherapy for lung cancer typically consists of combinations of 2 of the following drugs: etoposide (VP-16), carboplatin, cisplatin, paclitaxel (Taxol), vinorelbine (Navelbine), docetaxel (Taxotere), gemcitabine (Gemzar), and pemetrexed (Alimta).

Targeted Therapy Targeted therapy uses drugs that block the growth of molecules involved in specific aspects of tumor growth (see Chapter 15). Because this type of therapy inhibits growth rather than directly killing cancer cells, targeted therapy may be less toxic than chemotherapy. One type of targeted therapy for patients with NSCLC inhibits tyrosine kinase, an enzyme associated with speeding up molecular reactions. Tyrosine

kinase inhibitors, which block signals for growth in the cancer cells, include cetuximab (Erbitux), erlotinib (Tarceva), afatinib (Gilotrif), gefitinib (Iressa), osimertinib (Tagrisso), and necitumumab (Portrazza). Another type of kinase inhibitor is used to treat patients with NSCLC who have an abnormal anaplastic lymphoma kinase (ALK) gene. Drugs in this class include crizotinib (Xalkori), brigatinib (Alunbrig), and ceritinib (Zykadia). These drugs directly inhibit the kinase protein made by the ALK gene that is responsible for cancer development and growth. Another type of targeted therapy used to treat lung cancer inhibits the growth of new blood vessels (angiogenesis) by targeting vascular endothelial growth factor. Bevacizumab (Avastin) is an angiogenesis inhibitor.

Immunotherapy Nivolumab (Opdivo), atezolizumab (Tecentriq), and pembrolizumab (Keytruda) are drugs that target PD-1, a protein on T cells that normally helps keep these cells from attacking other cells in the body. By blocking PD-1, these drugs boost the immune response against cancer cells. This can shrink some tumors or slow their growth. Nivolumab and pembrolizumab can be used in people with metastatic NSCLC whose cancer has progressed after other treatments and with tumors that express PD-1.

Other Therapies Prophylactic Cranial Irradiation Patients with SCLC have early metastases, especially to the CNS. Most chemotherapy does not penetrate the blood-brain barrier. As a result, after successful systemic treatment, the patient is at risk for brain metastases. Prophylactic radiation can decrease the incidence of brain metastases and may improve survival rates in patients with limited SCLC.30

Bronchoscopic Laser Therapy Bronchoscopic laser therapy makes it possible to remove obstructing bronchial lesions. The laser’s thermal energy is transmitted to the target tissue. It is a safe and effective treatment of endobronchial obstructions from tumors. Symptoms of airway obstruction are relieved due to thermal necrosis and shrinkage of the tumor. The procedure may be repeated as needed.

Photodynamic Therapy Photodynamic therapy (PDT) is a form of treatment for early-stage lung cancers that uses a combination of a drug and a specific type of light. Cancer cells are killed when the drug, known as a photosynthesizer, is exposed to a specific wavelength of light. Porfimer (Photofrin) is the most used photosynthesizer. After an IV injection, it selectively concentrates in tumor cells in the esophagus and outer layers of the airways. After a set time (usually 48 hours), the tumor is exposed to laser light via bronchoscopy, activating the drug and causing cell death. Necrotic tissue is removed with bronchoscopy a few days later. This process can be repeated as needed. PDT can affect nutrient delivery to cancer cells and stimulate the immune system to attack the cancer cells.

Airway Stenting Stents are used alone or in combination with other techniques for relief of dyspnea, cough, or respiratory insufficiency. The stent is inserted during a bronchoscopy. The advantage of an airway stent is that it supports the airway wall against collapse or external compression and can delay extension of tumor into the airway lumen. At this time, we do not know which patients will benefit most from airway stents.

Radiofrequency Ablation Radiofrequency ablation therapy is used to treat small NSCLC lung tumors that are near the outer edge of the lungs. This therapy is an

alternative to surgery in patients who cannot or elect not to have surgery. A thin, needle-like probe is inserted through the skin into the tumor. CT scans are used to guide placement. An electric current is then passed through the probe, which heats and destroys tumor cells. Local anesthesia is used for this outpatient procedure.

Nursing Management: Lung Cancer Nursing Assessment It is important to determine the patient and caregiver’s understanding of the current medical condition, diagnostic tests (those completed as well as those planned), diagnosis or potential diagnosis, treatment options, and prognosis. Assess the patient’s level of anxiety and support provided by the patient’s significant others. Subjective and objective data that should be obtained from a patient with lung cancer are described in Table 27.18.

Nursing Diagnoses Nursing diagnoses for the patient with lung cancer may include: • Impaired airway clearance • Impaired breathing • Impaired gas exchange • Anxiety

Planning The overall goals are that the patient with lung cancer will have (1) adequate airway clearance, (2) effective breathing patterns, (3) adequate oxygenation of tissues, (4) minimal to no discomfort, and (5) a realistic outlook about treatment and prognosis.

Nursing Implementation Health Promotion The best way to halt the epidemic of lung cancer is to prevent people from smoking, help smokers stop smoking, and decrease exposure to environmental pollutants. Because most smokers start in the teenage

years, prevention of teen smoking has the most significant role in reducing the incidence of lung cancer. A wealth of material is available to the smoker who is interested in smoking cessation. (See Chapter 10.) Modeling healthy behavior by not smoking, promoting smoking cessation programs, and actively supporting education and policy changes related to smoking are important nursing activities. Many changes have occurred because of the recognition that secondhand smoke is a health hazard. Laws prohibit smoking in most public places and limit public smoking to designated areas. Most hospital environments are now completely smoke free, prohibiting smoking by employees and patients. A new trend is for hospitals to refuse employment to anyone testing positive for nicotine.

TABLE 27.18 Nursing AssessmentLung Cancer

Subjective Data Important Health Information Past health history: Exposure to secondhand smoke, airborne carcinogens (e.g., asbestos, radon, hydrocarbons), or other pollutants. Urban living environment. Chronic lung disease (e.g., TB, COPD, bronchiectasis). History of cancer. Medications: Cough medicines, bronchodilators, expectorants, or other respiratory medications

Functional Health Patterns Health perception–health management: Smoking history, including what was smoked, amount per day, and number of years. Family history of lung cancer. Frequent respiratory tract infections Nutritional-metabolic: Anorexia, nausea, vomiting, weight loss,

dysphagia (late). Activity-exercise: Fatigue. Persistent cough (productive or nonproductive). Dyspnea at rest or with exertion, hemoptysis (late symptom) Cognitive-perceptual: Chest pain or tightness, shoulder and arm pain, headache, bone pain (late symptom)

Objective Data General Fever, nose and/or throat infection, neck and axillary lymphadenopathy, paraneoplastic syndrome (e.g., syndrome of inappropriate ADH secretion)

Integumentary Edema of neck and face (superior vena cava syndrome), digital clubbing. Jaundice (liver metastasis).

Respiratory Wheezing, hoarseness, stridor, dyspnea on exertion (unilateral diaphragm paralysis), pleural effusions (late signs)

Cardiovascular Pericardial effusion, cardiac tamponade, dysrhythmias (late signs)

Neurologic Confusion, disorientation, unsteady gait (brain metastasis)

Musculoskeletal Pathologic fractures, muscle wasting (late)

Possible Diagnostic Findings Observance of lesion on chest x-ray, CT scan, or PET scan. MRI findings of vertebral, spinal cord, or mediastinal invasion. Positive sputum or bronchial washings for cytologic studies. Positive fiberoptic bronchoscopy and biopsy findings ADH, Antidiuretic hormone; PET, positron emission tomography.

Acute Care Care of the patient with lung cancer initially involves support and reassurance during diagnostic evaluation. It is important to recognize the multiple stressors that occur when someone receives a lung cancer diagnosis. The stress response is a normal and adaptive response but can become detrimental when stress is overwhelming and intense. Patients have the stress of their symptoms, including dyspnea and cough. Diagnostic and therapeutic interventions provide more stress by placing patients in unfamiliar environments with unusual and perhaps painful procedures. Emotional stressors include waiting for test results and awareness of the high mortality rate associated with lung cancer and the causal effect of cigarette smoking. Worries about role performance and ability to care for their family while undergoing cancer treatment provide further stress. Carefully assess the patient since each will have unique stressors. The insight gained will help the patient and caregiver cope with the stress of both illness and treatment. Care of the patient undergoing chest surgery is discussed later in this chapter on pp. 529–530. Care of the patient undergoing radiation therapy and chemotherapy is discussed in Chapter 15. Individualized

care depends on the plan for treatment. Assessment and intervention in symptom management are pivotal, as is teaching the patient to recognize signs and symptoms that may indicate progression or recurrence of disease. Teach signs and symptoms to report (e.g., hemoptysis, dysphagia, chest pain, hoarseness). Provide patient comfort, teach methods to reduce pain, monitor for side effects of prescribed drugs, foster appropriate coping strategies for both the patient and caregiver, assess smoking cessation readiness, and help the patient access resources to deal with the illness.

Check Your Practice You are completing discharge teaching with a 72-yr-old woman who had a lobectomy for NSCLC. She tells you, “I’m not going to give up smoking my cigarettes because I am just going to die anyhow. I might as well enjoy smoking while I still can.” • How would you respond?

Ambulatory Care Counseling patients on smoking cessation and prevention is essential in decreasing morbidity and mortality risks associated with lung cancer. Encourage the patient and family to provide a smoke-free environment. This may include smoking cessation for multiple family members. If the treatment plan includes home O2, the teaching plan must include the safe use of O2. For many patients with lung cancer, little can be done to significantly prolong their lives. Radiation therapy and chemotherapy can provide palliative relief from distressing symptoms. Constant pain may become a major problem. Measures used to relieve pain are discussed in Chapter 8. Care of the patient with cancer is discussed in Chapter 15. The palliative care team should be involved as the patient and family move toward the end of life (see Chapter 9). The team can

provide information about disability, financial planning, and community resources for end-of-life care, such as hospice and home care.

Evaluation The expected outcomes are that the patient with lung cancer will: • Have adequate breathing patterns • Maintain adequate oxygenation • Have minimal to no pain • Convey feelings openly and honestly, with a realistic attitude about prognosis

Other Types of Lung Tumors SCLC and NSCLC account for 95% of lung tumors. The other 5% include: • Hamartomas, the most common benign tumor, is a slowgrowing congenital tumor composed of fibrous tissue, fat, and blood vessels. • Mucous gland adenoma is a benign tumor arising in the bronchi that consists of columnar cystic spaces. • Mesotheliomas are either malignant or benign and start in the visceral pleura. Malignant mesotheliomas are associated with exposure to asbestos. Benign mesotheliomas are localized lesions. Secondary metastases from other cancers can occur. Cancer cells from another part of the body reach the lungs through the pulmonary capillaries or lymphatic network. The main cancers that spread to the lungs often start in the breast, GI, or genitourinary tract.

Chest Trauma and Thoracic Injuries Traumatic injuries to the chest contribute to many deaths. Chest injuries range from simple rib fractures to cardiorespiratory arrest. We describe the primary mechanisms of injury responsible for chest trauma as either blunt trauma or penetrating trauma. Blunt trauma occurs when the chest strikes or is struck by an object. The impact can cause shearing and compression of chest structures. The external injury may appear minor, but internally organs may have been severely damaged. Rib and sternal fractures can lacerate lung tissue. In a high-velocity impact, shearing forces can result in laceration or tearing of the aorta. Compression of the chest may result in contusion, crush injury, and organ rupture. Penetrating trauma is an injury in which a foreign object impales or passes through the body tissues, creating an open wound. Examples include knife wounds, gunshot wounds, and injuries with other sharp objects. Emergency care of the patient with a chest injury is outlined in Table 27.19. The most common chest emergencies and their management are described in Table 27.20.

Fractured Ribs Rib fractures are the most common type of chest injury from blunt trauma. Ribs 5 through 9 are most often fractured because they are the least protected by chest muscles. A fractured rib that is splintered or displaced can damage the pleura, lungs, heart, and other internal organs. Manifestations of fractured ribs include pain at the site of injury, especially during inspiration and with coughing. The patient splints the affected area and takes shallow breaths to try to decrease the pain. Atelectasis and pneumonia may develop because of decreased chest wall movement and retained secretions. The goal of treatment is to decrease pain so that the patient can breathe adequately and clear secretions. Strapping the chest with tape or using a thoracic binder is not recommended. These limit chest expansion and predispose the person to atelectasis. NSAIDs, opioids, and thoracic nerve blocks can be used to reduce pain and assist with deep breathing and coughing. Patient teaching should emphasize deep breathing, coughing, incentive spirometry, and appropriate use of pain medications.

TABLE 27.19 Emergency ManagementChest

Trauma

TABLE 27.20 Emergency ManagementChest

Injuries

Flail Chest Flail chest results from the fracture of 3 or more consecutive ribs, in 2 or more separate places, causing an unstable segment (Fig. 27.5). It also can be caused by fracture of the sternum and several consecutive ribs. The resulting instability of the chest wall causes paradoxical movement during breathing. The affected (flail) area moves in the opposite direction with respect to the intact part of the chest. During inspiration, the affected part is sucked in, and during expiration, it bulges out. This paradoxical chest movement prevents adequate ventilation and increases the work of breathing. The underlying injured lung may be contused, aggravating hypoxemia. A flail chest is usually apparent on physical examination. The patient has rapid, shallow respirations and tachycardia. Movement of the thorax is asymmetric and uncoordinated. The patient may ventilate poorly and try to splint the chest to assist with breathing. Observation of abnormal chest cavity movement, palpation for crepitus near the rib fractures, and chest x-ray all assist in the diagnosis. Initial therapy consists of ensuring adequate ventilation and supplemental O2 therapy. The goal is to promote lung expansion and ensure adequate oxygenation. Analgesia can help promote adequate respiration. Although many patients can be managed without mechanical ventilation, intubation and ventilation may be needed. In cases of extreme chest trauma, surgical fixation of the flail segment may be done. The lung parenchyma and fractured ribs heal with time. Some patients continue to have intercostal pain several weeks after the flail chest has resolved.

FIG. 27.5 Flail chest causes paradoxical respiration. On inspiration, the flail section moves inward with mediastinal shift to the uninjured side. On expiration, the flail section bulges outward with mediastinal shift to the injured side.

Pneumothorax A pneumothorax is caused by air entering the pleural cavity. Normally, negative (subatmospheric) pressure exists between the visceral pleura (surrounding the lung) and parietal pleura (lining the chest cavity), known as the pleural space. The pleural space has a few milliliters of lubricating fluid to reduce friction when the tissues move. When air enters this space, the change to positive pressure causes a partial or complete lung collapse (Fig. 27.6). As the volume of air in the pleural space increases, lung volume decreases. Pneumothorax can be classified as open (air entering through an opening in the chest wall) or closed (no external wound). Penetrating trauma allows air to enter the pleural space through an opening in the chest wall (Fig. 27.6). A penetrating chest wound may be referred to as a sucking chest wound, since air enters the pleural space through the chest wall during inspiration. A pneumothorax should be suspected after any trauma to the chest wall. If a pneumothorax is small, mild tachycardia and dyspnea may be the only manifestations. If the pneumothorax occupies a large area, respiratory distress may be present, including short, shallow, rapid respirations; dyspnea; air hunger; and O2 desaturation. On auscultation, breath sounds are absent over the affected area. Time permitting, a chest x-ray will show air or fluid in the pleural space and reduction in lung volume.

Types of Pneumothorax Spontaneous Pneumothorax A spontaneous pneumothorax typically occurs due to the rupture of small blebs (air-filled sacs) on the surface of the lung. These blebs can occur in healthy, young people or from lung disease, such as COPD, asthma, cystic fibrosis, and pneumonia. Smoking increases the risk for bleb formation. Other risk factors include being tall and thin, male gender, family history, and previous spontaneous pneumothorax.

Iatrogenic Pneumothorax Iatrogenic pneumothorax can occur due to laceration or puncture of the lung during medical procedures. For example, transthoracic needle aspiration, subclavian catheter insertion, pleural biopsy, and transbronchial lung biopsy all have the potential to injure the lung. Barotrauma from excessive ventilatory pressure during manual or mechanical ventilation can rupture alveoli, creating a pneumothorax. Esophageal procedures may result in a pneumothorax. For example, tearing of the esophageal wall during insertion of a gastric tube can allow air from the esophagus to enter the mediastinum and pleural space.

FIG. 27.6 Open pneumothorax resulting from collapse of lung due to disruption of chest wall and outside air entering.

Tension Pneumothorax Tension pneumothorax occurs when air enters the pleural space but

cannot escape. The continued accumulation of air in the pleural space causes increasingly elevated intrapleural pressures. This results in compression of the lung on the affected side and pressure on the heart and great vessels, pushing them away from the affected side (Fig. 27.7). The mediastinum shifts toward the unaffected side, compressing the “good” lung, which further compromises oxygenation. As the pressure increases, venous return decreases and cardiac output falls. Tension pneumothorax may result from either an open or a closed pneumothorax. In an open chest wound, a flap may act as a one-way valve. Thus air can enter on inspiration but cannot escape. Tension pneumothorax can occur with mechanical ventilation and resuscitative efforts. It can also occur if chest tubes are clamped or become blocked in a patient with a pneumothorax. Unclamping the tube or relieving the obstruction may correct this situation. Tension pneumothorax is a medical emergency. It affects both the respiratory and cardiovascular systems. Manifestations include severe dyspnea, marked tachycardia, tracheal deviation, decreased or absent breath sounds on the affected side, neck vein distention, cyanosis, and profuse diaphoresis. If the tension in the pleural space is not relieved, the patient is likely to die from inadequate cardiac output or severe hypoxemia.

Hemothorax Hemothorax is an accumulation of blood in the pleural space from injury to the chest wall, diaphragm, lung, blood vessels, or mediastinum. When it occurs with pneumothorax, it is called a hemopneumothorax. The patient with a traumatic hemothorax needs immediate insertion of a chest tube for evacuation of the blood. Recovered blood can be reinfused for a short time after the injury. (Autotransfusion is discussed in Chapter 30.)

Chylothorax Chylothorax is the presence of lymphatic fluid in the pleural space. The thoracic duct is disrupted either traumatically or from cancer,

allowing lymphatic fluid to fill the pleural space. This milky white fluid is high in lipids. Normal lymphatic flow through the thoracic duct is 1500 to 2500 mL/day. This amount can be increased up to 10fold after ingestion of fats. Some cases heal with conservative treatment (chest drainage, bowel rest, dietary modifications). Octreotide may reduce the flow of lymphatic fluid. Surgery (thoracic duct ligation) and pleurodesis (the artificial production of adhesions between the parietal and visceral pleura) are options for refractory cases.

FIG. 27.7 Tension pneumothorax. As pleural pressure on the affected side increases, mediastinal displacement ensues, causing respiratory and cardiovascular compromise. Tracheal deviation is an external (but late) manifestation of the mediastinal shift.

Interprofessional Care Treatment of a pneumothorax depends on its severity, underlying cause, and hemodynamic stability of the patient. If the patient is stable and has minimal air and/or fluid accumulated in the intrapleural space, no treatment may be needed since the condition may resolve spontaneously. Emergency treatment consists of covering the wound with an occlusive dressing that is secured on 3 sides (vent dressing). During inspiration, as negative pressure is created in the chest, the dressing pulls against the wound, preventing air from entering the pleural space. During expiration, as the pressure rises in the pleural space, the dressing is pushed out and air escapes through the wound and from under the dressing. If the object that caused the open chest wound is still in place, do not remove it. Stabilize the impaled object with a bulky dressing. Wait until an HCP is present or arrange transport to the nearest medical facility. The most definitive and common treatment of pneumothorax and hemothorax is to insert a chest tube and connect it to water-seal drainage. Repeated spontaneous pneumothorax may need surgical treatment with a partial pleurectomy, stapling, or pleurodesis to promote adherence of the pleurae to one another. Tension pneumothorax is a medical emergency, requiring urgent needle decompression followed by chest tube insertion to water-seal drainage.

Chest Tubes and Pleural Drainage If enough fluid or air accumulates in the pleural space, the normally negative subatmospheric pressure becomes positive and the lungs collapse. Inserting a chest tube can drain the pleural space, reestablish negative pressure, and allow for proper lung expansion. Chest tubes are about 20 in (51 cm) long and vary in size from 12F to 40F. The size inserted depends on the patient’s condition. Large (36F to 40F) tubes are used to drain blood, medium (24F to 36F) tubes are used to drain fluid, and small (12F to 24F) tubes are used to drain air. Pigtail tubes are very small (10F to 14F) tubes with a curly end designed to keep them in place. Pigtail tubes are a safe and effective alternative to larger-bore chest tubes for treatment of pneumothorax.

Chest Tube Insertion Insertion of a chest tube can take place in the ED, the operating room, or at the patient’s bedside. Time permitting, a chest x-ray is used to confirm the affected side. The patient is positioned with the arm raised above the head on the affected side to expose the midaxillary area, the standard site for insertion. Elevate the patient’s head 30 to 60 degrees, when possible, to lower the diaphragm and reduce the risk for injury. The area is cleansed with an antiseptic solution. The HCP infiltrates the chest with a local anesthetic and makes a small incision over a rib. The chest tube is advanced up and over the top of the rib to avoid the intercostal nerves and blood vessels that are behind the rib inferiorly (Fig. 27.8). Once inserted, the HCP secures (sutures) the tube in place and closes the incision with sutures. The tube is connected to a pleural drainage system (Fig. 27.9). The wound is covered with an occlusive dressing. Most HCPs prefer to seal the wound around the chest tube with petroleum (airtight) gauze. Proper tube placement is confirmed by chest x-ray.

FIG. 27.8 Placement of chest tubes.

The insertion of a chest tube and its presence in the pleural space are painful. Monitor the patient’s comfort frequently and use appropriate pain-relieving interventions.

Flutter or Heimlich Valve A flutter valve (also called the Heimlich valve) is used to remove air from the pleural space (Fig. 27.10). This device consists of a one-way rubber valve within a rigid plastic tube. It is attached to the external end of the chest tube. It has 2 nozzles. The inlet nozzle allows the air to pass in the valve through the chest drainage tube attached to it. The outlet nozzle allows the air to pass to the environment or a collecting device during expiration. During inspiration, when pressure in the chest decreases, the valve closes. During expiration, when intrathoracic pressure increases, the valve closes. The flutter valve can be used for small to moderate-sized pneumothorax. It also allows for patient mobility. The smaller drainage bag can be hidden under the clothes while the patient ambulates. Drainage bags attached to the flutter valve must have a vent to the atmosphere to prevent a tension pneumothorax. This is done by simply cutting a small slit in the top of any drainage bag that does not have a built-in vent. Patients may go home with a flutter valve in place.

Pleural Drainage A chest tube is usually attached to a drainage device or chamber to collect fluid, air, and/or blood from the chest cavity. Several different disposable chest drainage units are currently available. All drainage units have 3 basic compartments (Fig. 27.9).

FIG. 27.9 Chest drainage unit. Both units have 3 chambers: (1) collection chamber; (2) water-seal chamber; and (3) suction control chamber. Suction control chamber requires a connection to a wall suction source that is dialed up higher than the prescribed suction for the suction to work. A, Water suction. This unit uses water in the suction control chamber to control the wall suction pressure. B, Dry suction. This unit controls wall suction by using a regulator control dial. From Atrium Medical Corporation, Hudson, NH.

The first compartment, or collection chamber, receives fluid and air from the pleural space. The drained fluid stays in this chamber while expelled air vents to the second compartment. The second compartment, the water-seal chamber, contains 2 cm of water, which acts as a oneway valve. Incoming air enters from the collection chamber and bubbles up through the water. The water prevents backflow of air into the patient. Brisk bubbling of air often occurs in this chamber when a pneumothorax is first evacuated. Intermittent bubbling during exhalation, coughing, or sneezing (when the patient’s intrathoracic pressure is increased) may be seen as long as there is air in the pleural space. Eventually, as the air leak resolves and the lung becomes more fully expanded, bubbling ceases. Normal fluctuation of the water within the water-seal chamber is called tidaling. This up and down movement of water in concert with respiration reflects intrapleural pressure changes during inspiration and expiration. If tidaling stops suddenly, assess the chest tube as this may signify an occluded chest tube. As the lung reexpands, tidaling gradually slows then eventually stops.

FIG. 27.10 A, Heimlich chest drain valve is a specially designed flutter valve that is used in place of a chest drainage unit for small uncomplicated pneumothorax with little or no drainage and no need for suction. The valve allows for escape of air but prevents the reentry of air into the pleural space. B, Placement of valve between chest tube and vented drainage bag, which can be worn under a person’s clothes. A, Courtesy and © Becton, Dickinson and Company.

The third compartment, the suction control chamber, applies suction to the chest drainage unit. There are 2 main types of suction control: water and dry. The water suction control chamber uses a column of water to control the amount of suction from the wall regulator. The chamber is typically filled with 20 cm of water. The amount of suction applied to the chest drainage unit is regulated by the amount of water in this chamber and not by the amount of suction applied to

the system. An increase in wall suction does not result in an increase in negative pressure to the system because any excess suction merely draws in air through the vent on top of the third chamber. The suction pressure is usually ordered to be −20 cm H2O. Higher pressures (−40 cm H2O) are sometimes needed to evacuate the pleural space. Lower pressure (−10 cm H2O) may be used for frail and older patients at risk for tissue damage with higher pressures. When the negative pressure generated by the suction source exceeds the set –20 cm H2O, air from the atmosphere enters the chamber through a vent on top of the chest drainage unit and the air bubbles up through the water, causing a suction-breaker effect. As a result, excess pressure is relieved. To start suction, adjust (increase) the vacuum source until gentle bubbling is present in the third chamber. Excessive bubbling does not increase the amount of suction but does increase the rate of evaporation of the water and the amount of noise made by the device. Dry suction chest drainage systems do not contain water. They often have a visual alert that shows if the suction is working. It uses either a restrictive device or a regulator to dial the desired negative pressure; this is internal in the chest drainage system. To increase the suction pressures, turn the dial on the drainage system. Increasing the vacuum source does not increase the pressure. When decreasing suction, depress the manual vent to reduce excess vacuum to the lower prescribed level. A variety of disposable plastic chest drainage systems are available. Manufacturers include directions for set-up and use with each unit.

Informatics in Practice Chest Drainage System • You find yourself in a situation in which you need to set up a chest drainage system. You have not done this since simulation in nursing school.

• On the Internet, find a procedure manual or watch a video or podcast on this procedure.

Nursing Management: Chest Drainage General guidelines for nursing care of the patient with chest tubes and water-seal drainage systems are shown in Table 27.21. Clamping of chest tubes during transport or when the tube is accidentally disconnected is no longer advocated. The danger of rapid accumulation of air in the pleural space, causing tension pneumothorax, is far greater than that of a small amount of atmospheric air that enters the pleural space. If a chest tube becomes disconnected, the immediate priority is to reestablish the water-seal system. In some agencies, when disconnection occurs, the chest tube is immersed in sterile water to act as a water seal until a new system can be set up and chest drainage reestablished. It is important to know the unit protocol, the clinical situation (whether an air leak exists), and HCP preference before any chest tube clamping occurs. Chest tubes may be momentarily clamped to change the drainage apparatus or to check for air leaks. Appearance of a new air leak warrants assessment of the drainage system to identify whether the air leak is coming from the patient or the system. Again, you must be familiar with the policies and procedures of your agency about specific clinical situations when you may clamp a chest tube. Closely monitor the patient for complications associated with chest tube placement and drainage. If volumes from 1 to 1.5 L of fluid and/or blood are removed rapidly, reexpansion pulmonary edema or severe, symptomatic hypotension can occur. Subcutaneous emphysema can occur from air leaking into the tissue surrounding the chest tube insertion site. A “crackling” sensation will be felt when palpating the skin. A small amount of subcutaneous air is harmless and will be reabsorbed. However, severe subcutaneous emphysema can cause drastic swelling of the head and neck with potential airway compromise. Meticulous sterile technique during dressing changes can reduce the incidence of infected chest tube insertion sites. Nursing care and patient teaching can minimize the risk for atelectasis and shoulder

stiffness. Encourage coughing, deep breathing, incentive spirometer use, and range-of-motion exercises. Inspect the integrity of the chest tube system. Monitor the color and amount of drainage hourly in the first few hours after chest tube insertion. Drainage greater than 200 mL in the first hour, development of subcutaneous emphysema, or any signs and symptoms of respiratory distress should be reported to the HCP at once.

Check Your Practice You are caring for a 26-yr-old male patient who has chest injuries from a motorcycle accident. He has 2 chest tubes in place that are each attached to a chest drainage system. While turning him, you accidentally disconnect one of the chest tubes from the drainage system. • What is your most immediate priority?

TABLE 27.21 Chest Tubes and Water-Seal

Drainage

Set-Up and Insertion 1. Make sure patient is aware of the procedure and informed consent is obtained. 2. Gather equipment. • Thoracotomy or chest tube insertion tray • Chest drainage unit (CDU) • Chest tube • Bottle of sterile water • 1% lidocaine • Suction tubing and collection container

• Occlusive dressing 3. Prepare CDU. • Wet suction: Add sterile water to 2-cm mark in waterseal chamber and to 20-cm mark (or as ordered) in suction control chamber. • Dry suction: Add sterile water to the fill line of the air leak meter. Attach suction tubing and increase suction until the bellows-like float moves across the display window. 4. Position and support the patient to minimize movement during procedure.

Drainage System 1. Keep all tubing loosely coiled below chest level. Tubing should drop straight from bed or chair to drainage unit. Do not let it be compressed. 2. Keep all connections between chest tubes, drainage tubing, and the drainage collector tight, and tape all connections. 3. Observe for air fluctuations (tidaling) and bubbling in the waterseal chamber. • If tidaling (rising with inspiration and falling with expiration in the spontaneously breathing patient) is not seen, the drainage system is blocked, the lungs are reexpanded, or the system is attached to suction. • If bubbling increases, there may be an air leak in the drainage system or a leak from the patient (bronchopleural leak). 4. If the chest tube is connected to suction, disconnect from wall suction to check for tidaling. 5. Suspect a system leak when bubbling is continuous. • Retape tubing connections. • Ensure that dressing is air occlusive. • If leak persists, briefly clamp the chest tube at the patient’s chest. If the leak stops, the air is coming from

the patient∗ • If the air leak persists, briefly and methodically move the clamps down the tubing away from the patient until the air leak stops. The leak will then be present between the last 2 clamp points. If the air leak persists all the way to the drainage unit, replace the unit.∗ 6. High fluid levels in the water seal indicate residual negative pressure. • The chest system may have to be vented by using the high-negativity release valve available on the drainage system to release residual pressure from the system. • Do not lower water-seal column when wall suction is not operating or when patient is on gravity drainage.

Patient’s Clinical Status 1. Monitor the patient’s clinical status. Assess vital signs, lung sounds, and pain. 2. Assess for reaccumulation of air and fluid in the chest (↓ or absent breath sounds), significant bleeding (>100 mL/hr), infection at chest tube insertion site (drainage, erythema, fever, ↑ WBCs), or poor wound healing. Notify HCP for management plan. 3. Evaluate for subcutaneous emphysema at chest tube site. 4. Encourage the patient to breathe deeply periodically to promote lung expansion and encourage range-of-motion exercises to the shoulder on the affected side. Encourage use of incentive spirometry every hour while awake to prevent atelectasis or pneumonia.

Chest Drainage 1. Never elevate the drainage system to the level of the patient’s chest because this will cause fluid to drain back into the lungs.

Change the unit if the collection chamber is full. Do not try to empty it. 2. Mark the time of measurement and the fluid level on the drainage unit according to the unit standards. Report any change in the quantity or characteristics of drainage (e.g., clear yellow to bloody) to the HCP and record the change. Notify HCP if >100 mL/hr drainage. 3. Check the position of the chest drainage container. If the drainage system is overturned and the water seal is disrupted, return it to an upright position and encourage the patient to take a few deep breaths, followed by forced exhalations and cough maneuvers. 4. If the drainage system breaks, place the distal end of the chest tubing connection in a sterile water container at a 2-cm level as an emergency water seal. 5. Position tubing so that drainage flows freely.

Monitoring Wet Versus Dry Suction Chest Drainage Systems Suction Control Chamber in Wet Suction System 1. Keep the suction control chamber at the right water level by adding sterile water as needed to replace water lost to evaporation. 2. Keep the cover over the suction control chamber in place to prevent more rapid evaporation of water and to decrease the noise of the bubbling. 3. After filling the suction control chamber to the ordered suction amount (generally 20 cm H2O suction), connect the suction tubing to the wall suction. 4. Dial the wall suction regulator until there is continuous gentle bubbling in the suction control chamber (generally 80 to 120 mm Hg). Vigorous bubbling is not necessary and will increase the rate of evaporation.

5. If there is no bubbling in the suction control chamber, (1) there is no suction, (2) suction is not high enough, or (3) the pleural air leak is so large that suction is not high enough to evacuate it.

Suction Control Chamber in Dry Suction System (see manufacturer’s directions) 1. After connecting patient to system, turn the dial on the chest drainage system to amount ordered (generally −20 cm H2O pressure), connect suction tubing to wall suction source, and increase the suction until the float appears in the window of the CDU. 2. If ordered to decrease suction, turn the dial down, depress the high-negativity vent, and assess for a rise in the water level of the water-seal chamber.

Chest Tube Dressings 1. Change dressing according to unit protocol and HCP preference. 2. Remove old dressing carefully. Assess the site for inflammation or infection and culture site as needed. 3. Cleanse the site according to protocol, maintaining strict sterile asepsis. 4. Redress with occlusive dressing. Some HCPs prefer the use of petroleum gauze dressing around the tube to prevent air leak. Date the dressing and document dressing change.



As per agency policy and procedures.

Chest Tube Removal

Chest tubes are removed when the lungs are reexpanded and fluid drainage has ceased or is minimal. In some centers, suction is discontinued, and the chest drain is allowed to drain by gravity for 24 hours before the tube is removed. Give the patient pain medication about 30 to 60 minutes before tube removal. Gather dressing supplies, including petroleum jelly and dry gauze dressing. Explain the procedure to the patient. In most settings, the tube is removed by the HCP or an advanced practice nurse. The suture is cut, and with the patient holding his or her breath or bearing down (Valsalva maneuver), the tube is removed. The site is immediately covered with the airtight dressing to prevent air from entering the pleural space. The pleura will seal off, and the wound usually heals in a few days. A chest x-ray is done 30 to 60 minutes after chest tube removal to evaluate for pneumothorax or fluid accumulation. Observe the wound for drainage and reinforce the dressing if needed. Monitor and record vital signs. Assess the patient for respiratory distress, which may signify a recurrence of the original problem.

Chest Surgery Chest surgery is done for various reasons, including lung, heart, vascular, and esophageal disorders. The most common types of chest surgery are described in Table 27.22.

Surgical Procedures Thoracotomy A thoracotomy is a surgical incision into the chest to gain access to the heart, lungs, esophagus, thoracic aorta, or anterior spine. Two common approaches to a thoracotomy are the median sternotomy and lateral thoracotomy. The median sternotomy involves splitting the sternum. It is primarily used for surgery involving the heart. The lateral thoracotomy incision can be done using a posterolateral or anterolateral incision. The posterolateral incision is used for most surgeries involving the lung. The incision is made from front to back at the level of the 4th, 5th, or 6th intercostal space. Strong mechanical retractors are used to separate the ribs and gain access to the lung. The anterolateral incision is made in the 4th or 5th intercostal space from the sternal border to the midaxillary line. This procedure is often done for surgery or trauma victims, mediastinal operations, and wedge resections of the upper and middle lobes of the lung.

TABLE 27.22 Chest Surgeries

Video-Assisted Thoracic Surgery Video-assisted thoracoscopic surgery (VATS) is a widely used, minimally invasive surgical approach. It provides a real-time 2-dimensional video image of the inside of the chest cavity. It is used for diagnosis and treatment of diseases of the pleura, pulmonary masses and nodules, mediastinal masses, and interstitial lung disease. Through

incisions just large enough to insert the instruments, the HCP can inspect the chest cavity, biopsy suspicious areas, obtain samples of fluids for analysis, and remove tissue. VATS is increasingly being used for patients with chest trauma. The HCP can examine, diagnose, and manage injuries in both blunt and penetrating trauma, including injuries to the diaphragm. A chest tube is placed in the pleural space through 1 or more of the incisions at the end of the procedure, secured with sutures, and connected to a drainage unit in the usual manner. The advantages of VATS include less discomfort, faster return to normal activity level, reduced length of hospital stay, lower postoperative morbidity risk, and fewer complications.31 Patients who have marginal respiratory reserve or are too debilitated to tolerate an open thoracotomy approach may benefit from the VATS procedure.

Preoperative Care Assess the patient’s cardiopulmonary status to determine their ability to tolerate the surgery and provide a baseline reference for postoperative care. Diagnostic studies may include chest x-ray, electrocardiogram (ECG), ABGs, pulmonary function studies, blood urea nitrogen (BUN), serum creatinine, blood glucose, serum electrolytes, prothrombin time/international normalized ratio (PT/INR), activated partial thromboplastin time (aPTT), and CBC. An anesthesia consult is usually completed. The patient should be in the best possible health and, if applicable, stop smoking before elective surgery. Anxiety associated with anticipated surgery makes smoking cessation more difficult. Provide encouragement, support, and teaching about various methods to help stop smoking before surgery (see Chapter 10). Teach the patient what to expect after surgery. Include the use of O2, the chance of intubation, administration of blood and IV fluids, and the purpose and function of chest tubes. Reassure the patient that adequate medication will be used to reduce pain. Explain how to use patient-controlled analgesia (PCA), if planned. Preoperative teaching

should always include exercises for effective deep breathing and use of incentive spirometry. If the patient practices these techniques before surgery, they will be easier to perform after surgery. Show the patient how to splint the incision with a pillow to promote deep breathing. Teach and have the patient provide a return demonstration of range-of-motion exercises on the surgical side (similar to those for the mastectomy patient [see Fig. 51.8]). The thought of losing part of a vital organ is often frightening. Reassure the patient that the lungs have a large degree of functional reserve. Even after the removal of 1 lung, enough lung tissue is left to maintain adequate oxygenation. Be available to answer the patient and caregiver’s questions. Answer questions openly and honestly. Encourage the expression of concerns, feelings, and questions.

Postoperative Care The thoracotomy incision is the most painful surgical incision for patients and one of the most difficult for nurses to manage. Pain after a thoracotomy is typically intense because respiratory muscles are cut during surgery. For most chest surgeries, chest tubes are placed in the pleural space to allow for lung reexpansion. In a pneumonectomy, chest tubes may or may not be placed in the space from which the lung was removed. Adequate pain management is a priority to prevent respiratory compromise. The use of PCA, epidural infusions, and intercostal nerve blocks allows patients to breathe deeply, cough, and move the arm and shoulder on the operative side. Nursing care priorities in the postoperative period include assessment of respiratory function, including observation of respiratory rate and effort, breath sounds, sputum volume and color, and chest tube function and drainage. Daily chest x-rays are often ordered. Assessment of pain, monitoring of temperature, and observation of the surgical site are similar to care provided for other postoperative patients (see Chapter 19). Care after thoracotomy is presented in eNursing Care Plan 27.2 (available on the website for this chapter).

Thoracentesis Thoracentesis is aspiration of intrapleural fluid for diagnostic and therapeutic purposes. For a thoracentesis, the patient may sit on the edge of a bed and lean forward over a bedside table. A chest x-ray or ultrasound images are used to determine the optimal puncture site. The skin is cleansed with an antiseptic solution and injected with a local anesthetic. The thoracentesis needle is inserted into the intercostal space (see Fig. 25.12). Fluid is aspirated with a syringe, or tubing is connected to the needle to allow fluid to drain into a sterile container. After the fluid is removed, the needle is withdrawn, and a bandage is applied over the insertion site. Usually no more than 1000 to 1200 mL of pleural fluid is removed at one time. Rapid removal of a large volume can result in hypotension, hypoxemia, or reexpansion pulmonary edema. A chest x-ray may be done after the procedure to assess for complications, such as pneumothorax. During and after the procedure, monitor vital signs and pulse oximetry. Observe the patient for respiratory distress.

Restrictive Respiratory Disorders Disorders that impair the ability of the chest wall and diaphragm to move with respiration are called restrictive respiratory disorders. There are 2 categories: extrapulmonary conditions, in which the lung tissue is normal, and intrapulmonary conditions, in which the cause is the lung or pleura. Examples of extrapulmonary and intrapulmonary conditions that alter respiratory functioning are listed in Table 27.23. These disorders are further described in their respective chapters. Pulmonary function tests are the best means of distinguishing between restrictive and obstructive respiratory disorders. The hallmark characteristic of a restrictive lung disorder is a reduced total lung capacity (TLC). The hallmark characteristic of an obstructive disorder is reduced forced expiratory volume (FEV1). Mixed obstructive and restrictive disorders sometimes occur together. For example, a patient may have both asthma (an obstructive problem) and pulmonary fibrosis (a restrictive problem).

TABLE 27.23 Common Causes of Restrictive Lung

Disease

Intrapulmonary Causes Pleural Disorders • Pleural effusion • Pleurisy (pleuritis) • Pneumothorax

Parenchymal Disorders • Acute respiratory distress syndrome (ARDS)

• Atelectasis • Interstitial lung diseases • Pneumonia

Extrapulmonary Causes Central Nervous System • Head injury, central nervous system lesion (e.g., tumor, stroke) • Opioid and barbiturate overdose

Neuromuscular System • Amyotrophic lateral sclerosis • Guillain-Barré syndrome • Muscular dystrophy • Myasthenia gravis

Chest Wall • Kyphoscoliosis • Obesity-hypoventilation syndrome (Pickwickian syndrome)

Atelectasis Atelectasis is a lung condition characterized by collapsed, airless alveoli. There may be decreased or absent breath sounds and dullness to percussion over the affected area. The most common cause of atelectasis is obstruction of the small airways with secretions. This is common in bedridden patients and in postoperative abdominal and chest surgery patients. Normally the pores of Kohn (see Fig. 25.1) provide collateral passage of air from one alveolus to another. Deep inspiration opens the pores effectively. For this reason, deep-breathing exercises, coughing, incentive spirometry, and early mobility are important to prevent atelectasis and treat the patient at risk. (The prevention and treatment of atelectasis are discussed in Chapter 19.)

Pleurisy Pleurisy (pleuritis) is an inflammation of the pleura. It can be caused by infectious diseases, cancer, autoimmune disorders, chest trauma, GI disease, and certain medications. The inflammation usually subsides with adequate treatment of the primary disease. The pain of pleurisy is typically abrupt, sharp in onset, and worse with inspiration. The patient’s breathing is shallow and rapid to avoid unnecessary movement of the pleura and chest wall. A pleural friction rub may occur. This is the sound heard over areas where inflamed visceral pleura and parietal pleura rub over one another during inspiration. This sound, like a squeaking door, is usually loudest at peak inspiration. It may be heard during exhalation as well. Treatment of pleurisy is aimed at treating the underlying disease and providing pain relief. Teach the patient to splint the rib cage when coughing. If the pain is severe, intercostal nerve blocks may be considered.

Pleural Effusion Types The pleural space normally holds 5 to 15 mL of fluid that acts as a lubricant between the chest wall (parietal pleura) and lungs (visceral pleura). Pleural effusion is an abnormal collection of fluid in this space. It is not a disease but a sign of disease. A balance among hydrostatic pressure, oncotic pressure, and capillary membrane permeability governs movement of fluid in and out of the pleural space. Fluid accumulation can be due to increased pulmonary capillary pressure, decreased oncotic pressure, increased pleural membrane permeability, or obstruction of lymphatic flow. We classify pleural effusions as transudative or exudative depending on the protein content. A transudate occurs primarily in noninflammatory conditions. It is an accumulation of protein-poor, cell-poor fluid. The fluid is clear, pale yellow. These effusions are caused by (1) increased hydrostatic pressure found in HF or (2) decreased oncotic pressure (from hypoalbuminemia) found in chronic liver or renal disease. An exudative effusion results from increased capillary permeability due to an inflammatory reaction. They most often occur with an infection or cancer (called a malignant effusion). An empyema is the collection of purulent fluid in the pleural space. It is often caused by pneumonia, TB, lung abscess, and infected surgical wounds of the chest. Treatment options include antibiotic therapy (to eradicate the causative organism), percutaneous drainage, chest tube insertion, VATS, intrapleural fibrinolytic therapy (instilled through the chest tube) to dissolve fibrous adhesions, decortication, and open window thoracostomy.

Clinical Manifestations Common manifestations of pleural effusion are dyspnea, cough, and occasional sharp, non-radiating chest pain that is worse on inhalation. Physical examination of the chest may show decreased movement of

the chest on the affected side, dullness to percussion, and decreased breath sounds over the affected area. A chest x-ray and CT reveal the volume and location of the effusion. Indications of an empyema include the manifestations of pleural effusion as well as fever, night sweats, cough, and weight loss.

Interprofessional Care The management of pleural effusions is to treat the underlying cause. For example, adequate treatment of HF with diuretics and sodium restriction may result in a decreased incidence of pleural effusion. The treatment of malignant effusions is more difficult. These effusions often reoccur and reaccumulate quickly after thoracentesis. Chemical pleurodesis is done to obliterate the pleural space and prevent reaccumulation of effusion fluid. This procedure first requires chest tube drainage of the effusion. Once the fluid is drained, a chemical slurry is instilled into the pleural space. Talc is the most effective agent for pleurodesis. Other agents that can be used include doxycycline and bleomycin. The chest tube is clamped for 8 hours while the patient is turned in different positions to allow the chemical to contact the entire pleural space. After 8 hours the chest tube is unclamped and attached to a drainage unit. Chest tubes are left in place until fluid drainage is less than 150 mL/day and no air leaks are noted. Fever and chest pain are the most common side effects associated with pleurodesis.

Interstitial Lung Diseases Interstitial lung disease (ILD), also called diffuse parenchymal lung disease, refers to more than 200 lung disorders in which the tissue between the air sacs of the lungs (the interstitium) is affected by inflammation or scarring (fibrosis).32 Most ILDs are extremely rare. Many times, the cause is unknown. Two common ILDs of unknown cause are idiopathic pulmonary fibrosis and sarcoidosis. Other ILDs are caused by inhalation of occupational and environmental toxins, certain medications, radiation therapy, connective tissue disorders, cancer, and infection. Treatment is aimed at reducing exposure to the causative agent and/or treating the underlying disease process. Although scarring is irreversible, treatment with corticosteroids and immunosuppressant drugs can minimize progression. A lung transplant may be an option for some patients.

Idiopathic Pulmonary Fibrosis Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive disorder characterized by chronic inflammation and formation of scar tissue in the connective tissue. Risk factors include a history of cigarette smoking and exposure to wood and metal dust. IPF affects more men than women. It typically first appears between the ages of 50 and 70 years. There is no known cure for IPF. Manifestations include exertional dyspnea; dry, nonproductive cough; clubbing of the fingers; and inspiratory crackles. Fatigue, weakness, anorexia, and weight loss may occur as the disease progresses. Chest x-ray findings are generally nonspecific. Pulmonary function tests may be abnormal, with evidence of restriction (reduced vital capacity) and impaired gas exchange. Open lung biopsy using VATS often helps to confirm the pathology and is considered the gold standard for diagnosis. The course of IPF is variable and the prognosis is poor. The 5-year survival rate is 30% to 50% after diagnosis. Many people diagnosed with IPF are first treated with a corticosteroid (prednisone), sometimes in combination with other drugs that suppress the immune system (e.g., methotrexate, cyclosporine). Kinase inhibitor drugs, which block multiple pathways that involved with scarring, include nintedanib (Ofev) and pirfenidone (Esbriet). O2 therapy and pulmonary rehabilitation should be prescribed for all patients. Lung transplantation may be an option for those who meet the criteria. (Lung transplantation is discussed later in this chapter on p. 537.)

Sarcoidosis Sarcoidosis is a chronic, multisystem granulomatous disease of unknown cause that primarily affects the lungs. The disease may also involve the skin, eyes, liver, kidney, heart, and lymph nodes. Those at higher risk include blacks and those with a family history of sarcoidosis. Signs and symptoms vary depending on what organs are affected. Pulmonary symptoms include dyspnea, cough, and chest pain. Many patients do not have symptoms. Staging and treatment decisions are based on pulmonary function and disease progression. Some patients have a spontaneous remission. Treatment is aimed at suppressing the inflammatory response. Patients are followed every 3 to 6 months with pulmonary function tests, chest x-ray, and CT scan to monitor disease progression.

TABLE 27.24 Causes of Pulmonary Edema

• Acute respiratory distress syndrome (ARDS) • Altered capillary permeability of lungs: aspiration, inhaled toxins, inflammation (e.g., pneumonia), severe hypoxia, near-drowning • Anaphylactic (allergic) reaction • Hypoalbuminemia: nephrotic syndrome, liver disease, nutritional disorders • Left ventricular (heart) failure • Lymph system cancer (e.g., non-Hodgkin’s lymphoma) • Overhydration with IV fluids • O2 toxicity • Unknown causes: neurogenic condition, opioid overdose, reexpansion pulmonary edema, high altitude

FIG. 27.11 Large embolus from the femoral vein lying in the main left and right pulmonary arteries. From the teaching collection of the Department of Pathology, University of Texas Southwestern Medical School, Dallas, TX. In Kumar V, Abbas AK, Aster JC, Fausto N, eds: Robbins and Cotran pathologic basis of disease, ed 8, Philadelphia, 2010, Saunders.

Vascular Lung Disorders Pulmonary Edema Pulmonary edema is an abnormal accumulation of fluid in the alveoli and interstitial spaces of the lungs. It is a complication of various heart and lung diseases (Table 27.24). In severe cases, pulmonary edema can be a life-threatening medical emergency. The most common cause of pulmonary edema is left-sided HF. (HF is discussed in Chapter 34.)

Pulmonary Embolism Etiology and Pathophysiology Pulmonary embolism (PE) is the blockage of 1 or more pulmonary arteries by a thrombus, fat or air embolus, or tumor tissue. The word embolus derives from a Greek word meaning “plug” or “stopper.” Emboli are mobile clots that generally do not stop moving until they lodge at a narrowed part of the circulatory system. A PE consists of material that gains access to the venous system and then to the pulmonary circulation. The embolus travels with blood flow through ever-smaller blood vessels until it lodges and obstructs perfusion of the alveoli (Fig. 27.11). The lower lobes of the lung are most often affected. Most PEs arise from deep vein thrombosis (DVT) in the deep veins of the legs. Venous thromboembolism (VTE) is the preferred term to describe the spectrum of pathologic conditions from DVT to PE (see Table 37.7). Other sites of origin of PE include femoral or iliac veins, right side of the heart (atrial fibrillation), and pelvic veins (especially after surgery or childbirth). Upper extremity DVT sometimes occurs in the presence of central venous catheters or arterial lines. These cases may resolve with the removal of the catheter. A saddle embolus refers to a large thrombus lodged at an arterial bifurcation. Less common causes include fat emboli (from fractured long bones), air emboli (from improperly administered IV therapy), bacterial vegetation on heart valves, amniotic fluid, and cancer. Risk factors for PE include immobility or reduced mobility, surgery within the last 3 months (especially pelvic and lower extremity surgery), history of VTE, cancer, obesity, oral contraceptives, hormone therapy, cigarette smoking, prolonged air travel, HF, pregnancy, and clotting disorders.

Clinical Manifestations The signs and symptoms of PE are varied and nonspecific, making diagnosis difficult. Manifestations depend on the type, size, and

extent of emboli. Small emboli may go undetected or cause vague, transient symptoms. Symptoms may begin slowly or appear suddenly. Dyspnea is the most common presenting symptom, occurring in 85% of patients with PE. Mild to moderate hypoxemia may occur. Other manifestations include tachypnea, cough, chest pain, hemoptysis, crackles, wheezing, fever, accentuation of pulmonic heart sound, tachycardia, and syncope. Massive PE may cause a sudden change in mental status, hypotension, and feelings of impending doom.

Complications About 10% of patients with massive PE die within the first hour. Treatment with anticoagulants significantly reduces mortality. Complications include pulmonary infarction and pulmonary hypertension. Pulmonary infarction (death of lung tissue) is most likely when there is: (1) occlusion of a large or medium-sized pulmonary vessel (more than 2 mm in diameter), (2) insufficient collateral blood flow from the bronchial circulation, or (3) preexisting lung disease. Infarction results in alveolar necrosis and hemorrhage. Sometimes the necrotic tissue becomes infected and an abscess may develop. Concomitant pleural effusion is frequent. Pulmonary hypertension results from hypoxemia or from involvement of more than 50% of the area of the normal pulmonary bed. As a single event, a PE rarely causes pulmonary hypertension. Recurrent PEs gradually reduce capillary bed blood flow and eventually cause pulmonary hypertension. Dilation and hypertrophy of the right ventricle can develop due to pulmonary hypertension. Depending on the degree of pulmonary hypertension and how quickly it develops, outcomes can vary, with some patients dying within months of the diagnosis and others living for decades.

Diagnostic Studies D-dimer is a laboratory test that measures the amount of cross-linked fibrin fragments. These fragments are the result of clot degradation

and are rarely found in healthy people. The disadvantage of D-dimer testing is that it is neither specific (many other conditions cause elevation) nor sensitive, because up to 50% of patients with a small PE have normal results. Patients with suspected PE and an elevated Ddimer level but normal venous ultrasound may need a spiral CT or lung scan. A spiral (helical) CT scan (also known as CT angiography or CTA) is the most common test to diagnose PE. An IV injection of contrast media is needed to view the pulmonary blood vessels. The scanner continuously rotates around the patient while obtaining views (slices) of the pulmonary vasculature. This allows visualization of all anatomic regions of the lungs. Computer software reconstructs the data to give a 3-dimensional picture and assist in seeing PEs. If a patient cannot have contrast media, a ventilation-perfusion (V/Q) scan is done. The V/Q scan has 2 parts. It is most accurate when both are done: 1. Perfusion scanning involves IV injection of a radioisotope. A scanning device images the pulmonary circulation. 2. Ventilation scanning involves inhalation of a radioactive gas, such as xenon. Scanning reflects the distribution of gas through the lung. The ventilation portion requires the patient’s cooperation. It may not be possible to perform in the critically ill patient, especially if the patient is intubated. ABG analysis is important but not diagnostic. The PaO2 may be low because of inadequate oxygenation from occluded pulmonary vasculature preventing matching of perfusion to ventilation. The pH is often normal unless respiratory alkalosis develops because of prolonged hyperventilation or to compensate for lactic acidosis caused by shock. Abnormal findings may be seen on a chest x-ray (atelectasis, pleural effusion) and ECG (ST segment and T wave changes), but they are not diagnostic for PE. Serum troponin levels and b-type natriuretic peptide (BNP) levels are often increased but not diagnostic.

Interprofessional Care To reduce mortality risk, treatment is started as soon as PE is suspected (Table 27.25). The goals are to (1) provide adequate tissue perfusion and respiratory function, (2) prevent further growth or extension of thrombi in the lower extremities, (3) prevent embolization from the upper or lower extremities to the pulmonary vascular system, and (4) prevent further recurrence of PE.

TABLE 27.25 Interprofessional CareAcute

Pulmonary Embolism

Diagnostic Assessment • History and physical examination • Chest x-ray • Continuous ECG monitoring • Arterial blood gases • Spiral (helical) CT scan • Ventilation-perfusion (V/Q) lung scan • D-dimer level • Troponin level, b-natriuretic peptide level

Management • Supplemental O2, intubation if needed • Monitor hemoglobin, assess patient for bleeding • Monitor activated partial thromboplastin time and international normalized ratio levels • Balance activity and rest • Inferior vena cava filter

• Pulmonary embolectomy in life-threatening situation

Drug Therapy • Fibrinolytic agent • Unfractionated heparin IV • Low-molecular-weight heparin (e.g., enoxaparin [Lovenox]) • Warfarin (Coumadin) for long-term therapy • Analgesia Immediate assessment should focus on the patient’s cardiopulmonary status, which can vary according to the size and location of the PE. O2 should be given by mask or cannula when hypoxemia is present. The concentration of FIO2 is titrated based on ABG analysis. In some situations, endotracheal intubation and mechanical ventilation are needed to maintain adequate oxygenation and ventilation. Respiratory measures, including turning, coughing, deep breathing, and incentive spirometry, are important to help prevent or treat atelectasis. If manifestations of shock are present, IV fluids and vasopressor agents are given as needed to support circulation (see Chapter 66). If HF is present, diuretics are used (see Chapter 34). Pain from pleural irritation or reduced coronary blood flow is treated with opioids.

Drug Therapy Immediate anticoagulation is required for patients with PE. Subcutaneous administration of low-molecular-weight heparin (LMWH) (e.g., enoxaparin [Lovenox]) or fragmin [Dalteparin] or fondaparinux) is the recommended treatment for patients with acute PE. LMWH is safer and more effective than unfractionated heparin.33 Advantages of LMWH over unfractionated heparin include greater bioavailability, subcutaneous administration, once daily dosing, and longer duration of therapeutic effect. Monitoring the aPTT is not

necessary or useful with LMWH. Unfractionated IV heparin can be as effective but is hard to titrate to therapeutic levels. Warfarin (Coumadin), an oral anticoagulant, should also be started at the time of diagnosis.34 Warfarin should be given for at least 3 months and then reevaluated. Alternatives to warfarin include apixaban (Eliquis), dabigatran (Pradaxa), and edoxaban (Savaysa). Anticoagulant therapy may be contraindicated if the patient has complicating factors, such as liver problems causing changes in the clotting, overt bleeding, a history of hemorrhagic stroke, heparininduced thrombocytopenia (HIT), or other blood dyscrasias. Some HCPs use direct thrombin inhibitors (see Table 37.10) in the treatment of PE. Similarly, fibrinolytic agents, such as tissue plasminogen activator (tPA) or alteplase (Activase), may help dissolve the PE and the source of the thrombus in the pelvis or deep leg veins, thereby decreasing the risk for recurrent emboli. Fibrinolytic therapy is discussed in Chapter 33.

Surgical Therapy Hemodynamically unstable patients with massive PE in whom thrombolytic therapy is contraindicated may be candidates for pulmonary embolectomy. Embolectomy, the removal of emboli, can be achieved through a diagnostic imaging (vascular catheter) or surgical approach. It can help decrease right ventricular afterload, Surgical outcomes have improved in recent years, in part due to rapid diagnosis and enhanced surgical procedures. Percutaneous catheter embolectomy or endovascular ultrasound delivered thrombolysis are newer, moderately invasive procedures for PE. In patients who are at high risk and patients for whom anticoagulation is contraindicated, an inferior vena cava (IVC) filter may be the treatment of choice. This device, inserted percutaneously through the femoral vein, is placed at the level of the renal veins in the inferior vena cava. Once inserted, the filter expands and prevents migration of large clots into the pulmonary system. Complications associated with this device are rare but include misplacement, migration, and perforation.

Nursing Management: Pulmonary Embolism Prevention of PE begins with prevention of DVT. Nursing measures aimed at prevention of PE are similar to those for prophylaxis of VTE (see Chapter 37). These include the use of intermittent pneumatic compression devices, early ambulation, and anticoagulant medications. The prognosis of a patient with PE is good if therapy is started immediately. Keep the patient on bed rest in a semi-Fowler’s position to facilitate breathing. Assess the patient’s cardiopulmonary status with careful monitoring of vital signs, cardiac rhythm, pulse oximetry, ABGs, and lung sounds. Apply O2 therapy as ordered. Maintain a patent IV line for medications and fluid therapy. Monitor laboratory results to ensure therapeutic ranges of INR (for warfarin) and aPTT (for IV heparin). Monitor platelet counts for thrombocytopenia and the development of HIT. Observe the patient for complications of anticoagulant and fibrinolytic therapy (e.g., bleeding, hematomas, bruising). Provide appropriate interventions related to immobility and fall precautions once the patient is permitted out of bed. The patient may be anxious because of pain, inability to breathe, and fear of death. Carefully explain the situation and the medications. Provide emotional support and reassurance to help relieve the patient’s anxiety. Patient teaching about long-term anticoagulant therapy is essential. Anticoagulant therapy continues for at least 3 months. Patients with large or recurrent emboli may be treated indefinitely with anticoagulants. INR levels are drawn at intervals and warfarin dosage is adjusted. Some patients are monitored by nurses in an anticoagulation clinic. Long-term management of PE is similar to that for the patient with VTE (see discussion of VTE in Chapter 37). Discharge planning is aimed at preventing worsening of the condition and avoiding

complications and recurrence. Reinforce the need for the patient to return to the HCP for regular follow-up examinations.

Pulmonary Hypertension Pulmonary hypertension is characterized by elevated pulmonary artery pressure from an increase in resistance to blood flow through the pulmonary circulation. Normally the pulmonary circulation is characterized by low resistance and low pressure. In pulmonary hypertension the pulmonary pressures are high, with the mean pulmonary artery pressure greater than 25 mm Hg at rest (normal is 12 to 16 mm Hg) or greater than 30 mm Hg with exercise. The World Health Organization (WHO) has identified 5 classes of pulmonary hypertension.35 Each group is based on cause of the disorder. Group 1: Attributed to medication, specific diseases, genetic (inherited) link, or idiopathic Group 2: Related to left-sided HF Group 3: Related to the lungs and hypoxemia Group 4: Related to the cardiovascular system and thromboembolic occlusion Group 5: Multifactorial (and often unclear) origins with hematologic or metabolic involvement Pulmonary hypertension can occur as a primary disease (idiopathic pulmonary arterial hypertension) or as a secondary complication of a respiratory, heart, autoimmune, liver, or connective tissue disorder (secondary pulmonary arterial hypertension).

FIG. 27.12 Pathogenesis of pulmonary hypertension and cor pulmonale.

Idiopathic Pulmonary Arterial Hypertension Idiopathic pulmonary arterial hypertension (IPAH) is pulmonary hypertension that occurs without an apparent cause. It was previously known as primary pulmonary hypertension (PPH). If untreated, IPAH can rapidly progress, causing right-sided HF and death within a few years. Although new drug therapy has greatly improved survival, the disease is not curable.

Etiology and Pathophysiology The cause of IPAH is unknown. It is related to connective tissue diseases, cirrhosis, and HIV. The exact relationship between these disorders and IPAH is unclear. Similarly, the pathophysiology of IPAH is poorly understood. We think that some type of insult (e.g., hormonal, mechanical) to the pulmonary endothelium may occur, causing a cascade of events leading to vascular scarring, endothelial dysfunction, and smooth muscle proliferation (Fig. 27.12). IPAH affects females more than males.

Clinical Manifestations and Diagnostic Studies The classic symptoms are dyspnea on exertion and fatigue. Exertional chest pain, dizziness, and syncope may occur. These are related to the inability of cardiac output to increase in response to increased O2 demand. Abnormal heart sounds may be heard, including an S3. Eventually, as the disease progresses, dyspnea occurs at rest. Pulmonary hypertension increases the workload of the right ventricle and causes right ventricular hypertrophy (a condition called cor pulmonale) and eventually HF. Right-sided cardiac catheterization is the definitive test to diagnose any type of pulmonary hypertension. It gives an accurate measurement of pulmonary artery pressures, cardiac output, and

pulmonary vascular resistance. Confirmation of IPAH requires a thorough workup to exclude conditions that may cause secondary pulmonary hypertension. Diagnostic evaluation often includes ECG, chest x-ray, pulmonary function tests, echocardiogram, and CT scan. The mean time between onset of symptoms and the diagnosis is about 2 years. By the time patients become symptomatic, the disease is already in the advanced stages and the pulmonary artery pressure is 2-3 times normal values.

Interprofessional and Nursing Care Early recognition is essential to interrupt the vicious cycle responsible for progression of the disease. Encourage patients to report unexplained shortness of breath, syncope, chest discomfort, and edema of the feet and ankles to their HCP. Although IPAH has no cure, treatment can relieve symptoms, improve quality of life, and prolong life. Drug therapy consists of agents that promote vasodilation of the pulmonary blood vessels, reduce right ventricular overload, and reverse remodeling (Table 27.26). Diuretics are used to manage peripheral edema. Anticoagulants are beneficial in pulmonary complications related to thrombus formation. Because hypoxia is a potent pulmonary vasoconstrictor, low-flow O2 gives symptomatic relief. The goal is to keep O2 saturation 90% or greater. Surgical interventions include pulmonary thromboendarterectomy (PTE), in which clots are removed from the pulmonary arteries. It is a technically demanding procedure and is done only at certain centers. Atrial septostomy (AS) is a palliative procedure that involves the creation of an intraatrial right-to-left shunt to decompress the right ventricle. It is used for a select group of patients awaiting lung transplantation. Lung transplantation is an option for patients who do not respond to drug therapy and progress to severe right-sided HF. Recurrence of the disease has not been reported in persons who had a transplant.

Secondary Pulmonary Arterial Hypertension Secondary pulmonary arterial hypertension (SPAH) occurs when another disease causes a chronic increase in pulmonary artery pressures. The specific primary disease pathology can cause anatomic or vascular changes that cause the pulmonary hypertension. SPAH can develop due to parenchymal lung disease, left ventricular dysfunction, intracardiac shunts, chronic PE, or systemic connective tissue disease. The symptoms can reflect the underlying disease, but some are directly attributable to SPAH, including dyspnea, fatigue, lethargy, and chest pain. The initial physical findings can include right ventricular hypertrophy and signs of right-sided HF (increased pulmonic heart sound, S4 heart sound, peripheral edema, hepatomegaly). Diagnosis of SPAH is like that of IPAH. Treatment of SPAH consists of treating the underlying primary disorder. When irreversible pulmonary vascular damage has occurred, therapies used for IPAH are started. A PTE may offer a cure for patients with chronic pulmonary hypertension caused by PE.

Cor Pulmonale Cor pulmonale is enlargement of the right ventricle caused by a primary disorder of the respiratory system. Almost any disorder that affects the respiratory system can cause cor pulmonale. The most common cause is COPD. Pulmonary hypertension is usually a preexisting condition in the person with cor pulmonale. Overt HF may be present. Fig. 27.12 outlines the cause and pathogenesis of pulmonary hypertension and cor pulmonale.

TABLE 27.26 Drug TherapyPulmonary

Hypertension

Clinical Manifestations and Diagnostic Studies

Manifestations are subtle and often masked by symptoms of the pulmonary condition. Common symptoms include exertional dyspnea, tachypnea, cough, and fatigue. Physical signs include evidence of right ventricular hypertrophy on ECG and an increase in intensity of S2. Chronic hypoxemia leads to polycythemia and increased total blood volume and viscosity of the blood. Polycythemia is often present in cor pulmonale from COPD. If HF accompanies cor pulmonale, manifestations, including peripheral edema, weight gain, distended neck veins, full, bounding pulse, and enlarged liver, may occur. We use various laboratory tests and imaging studies to confirm the diagnosis of cor pulmonale (Table 27.27).

Interprofessional and Nursing Care Early identification is essential before changes to the heart occur that may be irreversible. Management is directed at determining the cause and treating the underlying problem (Table 27.27). Long-term O2 therapy, the mainstay of treatment to correct the hypoxemia, reduces vasoconstriction and pulmonary hypertension. All other interventions are tailored for each patient. If fluid, electrolyte, and/or acid-base imbalances are present, they must be corrected. Diuretics may help decrease plasma volume and reduce the workload on the heart but must be used with extreme caution. In some cases, decreases in fluid volume from diuresis can worsen heart function. Bronchodilator therapy is needed if the underlying respiratory problem is due to an obstructive disorder.

TABLE 27.27 Interprofessional CareCor

Pulmonale

Diagnostic Assessment • History and physical examination

• Arterial blood gases, SpO2 • Serum and urine electrolytes • b-Type natriuretic peptide (BNP) • ECG • Chest x-ray • Echocardiography • CT scan, MRI • Cardiac catheterization

Management • O2 therapy • Low-sodium diet

Drug Therapy • Bronchodilators • Diuretics • Vasodilators (if indicated) • Calcium channel blockers (if indicated) • Inotropic agents Other treatments may include vasodilator therapy, calcium channel blockers, anticoagulants, digitalis, and phlebotomy. All have varying degrees of success. Chronic management of cor pulmonale from COPD is like that described for COPD (see Chapter 28).

Lung Transplantation Lung transplantation has become an important alternative option for patients with end-stage lung disease. Unfortunately, the limiting factor for this therapy is the lack of donors. A variety of pulmonary disorders are potentially treatable with lung transplantation (Table 27.28). Better patient selection criteria, improvements in surgical techniques, enhanced methods of immunosuppression, and excellent postoperative care have resulted in improved survival rates.

Preoperative Care Patients being considered for lung transplantation need to undergo extensive evaluation. Absolute contraindications for lung transplant include cancer within past 2 years (some types of skin cancer are excluded), chronic active hepatitis B or C, HIV, untreatable advanced dysfunction of another major organ system (e.g., liver or renal failure), current smoker, poor nutritional status, poor rehabilitation potential, and significant psychosocial problems. The patient and family must be able to cope with a complex postoperative regimen (e.g., strict adherence to immunosuppressive therapy, continuous monitoring for early signs of infection, prompt reporting of manifestations of infection). Many transplant centers require preoperative outpatient pulmonary rehabilitation to maximize physical conditioning. In the United States, the United Network for Organ Sharing (UNOS) is a private, non-profit organization that works with the federal government to manage organ transplantation. UNOS designates recipients of donor lungs based on a lung allocation score (LAS). The LAS helps to prioritize waiting list recipients based on the urgency of need and expected posttransplant survival expectations. Patients who are accepted as transplant candidates must always carry a pager in case a donor organ becomes available. They must be prepared to be at their transplant center at a moment’s notice. Patients may be encouraged to limit their travel within a certain geographic

region to facilitate rapid transportation to a transplant center.

TABLE 27.28 Common Indications for Lung

Transplantation

• α1-Antitrypsin deficiency • Chronic obstructive pulmonary disease (COPD) • Cystic fibrosis • Idiopathic pulmonary arterial hypertension • Idiopathic pulmonary fibrosis

Surgical Procedure Four types of transplant procedures are available: single-lung transplantation, bilateral lung transplantation, heart-lung transplantation, and transplantation of lobes from a living-related donor. Single-lung transplantation involves a thoracotomy incision on the side of the chest. The opposite lung is ventilated while the diseased lung is excised and the donor lung implanted. Three anastomoses are done: bronchus, pulmonary artery, and pulmonary veins. In bilateral lung transplantation, the incision is made across the sternum and the donor lungs are implanted separately. A median sternotomy incision is used for a heart-lung transplant procedure. Lobar transplantation from living donors is reserved for those who urgently need transplantation and are unlikely to survive until a donor becomes available. Most of these recipients are patients with cystic fibrosis, and donors are their parents or relatives. Once anastomosis is complete, the lung is gently reinflated, perfusion is reestablished, chest tubes are inserted, and the surgical incision is closed.

Postoperative Care Early postoperative care often includes ventilatory support, hemodynamic management, IV fluid therapy, immunosuppression, nutritional support, detection of early rejection, and prevention or treatment of complications, including infection. Once hemodynamic stability has been achieved, the patient is often transferred from the ICU to a high-acuity observation or surgical unit. Maintaining accurate fluid balance is vital after surgery. Lung transplant recipients are at high risk for multiple complications. Infections are the leading cause of death at all time points after lung transplant. Bacterial bronchitis and pneumonia are the most common infections. CMV, fungi, viruses, and mycobacteria are also causative agents. Noninfectious issues may include VTE, diaphragmatic dysfunction, and cancer. Immunosuppressive therapy usually includes a 3-drug regimen of tacrolimus, mycophenolate mofetil (CellCept), and prednisone. The mechanisms of action of these drugs are discussed in Table 13.17 and Fig. 13.13.) Drug levels are monitored on a regular basis. Lung transplant recipients usually receive higher levels of immunosuppressive therapy than other organ recipients. Acute rejection is fairly common in lung transplantation. It typically occurs in the first 5 to 10 days after surgery. Signs of rejection include low-grade fever, fatigue, dyspnea, dry cough, and O2 desaturation. Accurate diagnosis of rejection is by transtracheal biopsy. Treatment consists of high doses of IV corticosteroids for 3 days, followed by high doses of oral prednisone. In patients with persistent or recurrent acute rejection, antilymphocyte therapy may be useful. Bronchiolitis obliterans (BOS) is a manifestation of chronic rejection in lung transplant patients. BOS is characterized by airflow obstruction that progresses over time. The onset is often subacute, with gradual development of exertional dyspnea, nonproductive cough, wheezing, and/or low-grade fever. Airway obstruction is not responsive to bronchodilators and corticosteroid therapy. Although not proven effective, additional immunosuppressive agents may be used to treat chronic rejection. Because acute rejection is a major risk factor for BOS,

preventing acute rejection is key to decreasing the incidence of chronic rejection. Before discharge, the patient needs to be able to perform self-care activities, including medication management and activities of daily living, and to know when to call the transplant team. Patients are taught pulmonary clearance measures, including aerosolized bronchodilators, chest physiotherapy, and deep-breathing and coughing techniques, to help minimize complications. Home spirometry is useful in monitoring trends in lung function. Teach patients to keep medication logs, laboratory results, and spirometry records. Patients are placed in an outpatient rehabilitation program to improve physical endurance. After discharge, the transplant team follows patients for transplantrelated issues. Patients return to their HCP for health maintenance and routine illnesses. As transplant procedures become more frequent, transplant patients will return to hospitals for other routine procedures. Coordination of care among the transplant team, inpatient team, and primary care team is essential for ongoing successful management of these patients. (Organ transplantation, histocompatibility, rejection, and immunosuppressive therapy are discussed in Chapter 13.)

Case Study Pneumonia and Lung Cancer

(© iStockphoto/Thinkstock.)

Patient Profile J.H. is a 52-yr-old white man who comes to the ED with shortness of breath. He has not seen an HCP for many years.

Subjective Data

• Has a 38 pack-year history of cigarette smoking • Has had 25-lb weight loss despite a normal appetite in the past few months • Admits to a “smoker’s cough” for the past 2 to 3 years; recently coughing up blood • Is married and the father of 3 adult children

Objective Data Physical Examination • Thin, pale man who looks older than stated age • Height 6 ft (182.9 cm); weight 135 lb (61.2 kg) • Intermittently confused and anxious • Lung auscultation reveals coarse crackles on left side that clear with cough; right side has decreased breath sounds • Chest wall has limited excursion on right side • Vital signs: temperature 102.6° F (39.2° C), heart rate 120, respiratory rate 36, BP 98/54; short, shallow respirations

Diagnostic Studies • Arterial blood gases: pH 7.51, PaO2 62 mm Hg, PaCO2 30 mm Hg, HCO3− 22 mEq/L, O2 saturation 88% (room air) • Chest x-ray: consolidation of the right lung, especially in the base with mass around right bronchus; pleural effusion on the right side • Bronchoscopy with biopsy of mass: small cell lung cancer

Interprofessional Care • Diagnosis: pneumonia with small cell lung cancer

• Follow-up with patient and family to consider treatment options

Discussion Questions 1. How would you classify J.H.’s pneumonia? Why is this important? 2. What is your analysis of J.H.’s arterial blood gas results? 3. Priority Decision: Based on the assessment data presented, what are the priority nursing diagnoses? Are there any collaborative problems? 4. Priority Decision: What are the priority nursing interventions for J.H.? 5. Collaboration: Identify activities that can be delegated to unlicensed assistive personnel (UAP). 6. Patient-Centered Care: You are planning a meeting with J.H. and his family to discuss their needs. The HCP tells you that J.H. is terminally ill. Who will you include in this meeting? 7. Evidence-Based Practice: J.H.’s children tell you that they are worried they will get lung cancer, since their father has it and they grew up around his secondhand smoke. They want to know what kind of screening is available for them. How will you respond? • What is the goal if radiation therapy is used for J.H.? • Patient-Centered Care: What issues should be addressed in your teaching of J.H. and his wife as you prepare him for discharge and care at home? Answers available at http://evolve.elsevier.com/Lewis/medsurg.

Lung Abscess Etiology and Pathophysiology A lung abscess is necrosis of lung tissue. It typically results from bacteria aspirated from the oral cavity in patients with periodontal disease. They can also result from IV drug use, cancer, pulmonary emboli, TB, and various parasitic and fungal diseases. The abscess usually develops slowly, beginning with an enlarging area of infection that becomes necrotic and eventually forms a cavity filled with purulent material. Abscesses usually contain more than 1 type of microbe, most often reflecting the anaerobic flora of the mouth. The area of the lung most often affected due to aspiration is the posterior segment of the upper lobes. The abscess may erode into the bronchial system, causing the production of foul-smelling or sourtasting sputum. It may grow toward the pleura and cause pleuritic pain. Multiple small abscesses, sometimes referred to as necrotizing pneumonia, can occur within the lung.

TABLE 27.14 Fungal Infections of the Lung

Clinical Manifestations and Complications Manifestations usually occur slowly over a period of weeks to months,

especially if anaerobic organisms are the cause. Symptoms of abscess caused by aerobic bacteria develop more acutely and resemble bacterial pneumonia. The most common is cough-producing purulent sputum (often dark brown) that is foul smelling and foul tasting. Hemoptysis is common, especially when an abscess ruptures into a bronchus. Other manifestations include fever, chills, prostration, night sweats, pleuritic pain, dyspnea, anorexia, and weight loss. Lung assessment reveals dullness to percussion and decreased breath sounds on auscultation over the involved segment of lung. Bronchial breath sounds may be transmitted to the periphery if the communicating bronchus becomes patent and the segment begins to drain. Crackles may be present in the later stages as the abscess drains. The infection can spread through the bloodstream and cause several possible complications. Pulmonary abscess, bronchopleural fistula, bronchiectasis, and empyema from perforation of the abscess into the pleural cavity can occur.22

Diagnostic Studies A chest x-ray is often the only test needed to diagnose a lung abscess. The presence of a single cavitary lesion with an air-fluid level and local infiltrate confirms the diagnosis. CT scanning may be helpful if the cavitation is not clear on chest x-ray. If there is drainage via the bronchus, sputum will contain the microorganisms that are present in the abscess. However, expectorated sputum samples are contaminated with oral flora, making it hard to determine the responsible organism(s). Bronchoscopy may be used to (1) avoid oropharyngeal contamination, (2) collect a specimen if drainage is delayed, or (3) investigate for an underlying cancer. Pleural fluid and blood cultures may be useful to identify the offending organisms. Although nonspecific, an elevated neutrophil count from a complete blood count (CBC) may indicate an infectious process. Necrotic pulmonary lesions also can be caused by lung infarction, pulmonary embolism,

and sarcoidosis.

Interprofessional and Nursing Care Monitor the patient’s vital signs, level of consciousness, and respiratory status for any signs of hypoxemia. Note any signs and symptoms of respiratory distress. Apply O2 as needed. IV antibiotic therapy should be started as soon as possible. Clindamycin is first-line therapy for its effectiveness against Staphylococcus and anaerobic organisms. Parenteral antibiotics are switched to oral antibiotics once the patient shows clinical and chest x-ray signs of improvement. Because of the need for prolonged antibiotic therapy, the patient must be aware of the importance of continuing the medication for the prescribed period. To avoid the risk for a secondary or worsening infection, all antibiotics should be taken as directed for the entire prescribed period. Sometimes the patient is asked to return periodically during the course of antibiotic therapy for repeat cultures and sensitivity tests to ensure that the infecting organism is not becoming resistant to the antibiotic. When antibiotic therapy is complete, the patient is reevaluated. Teach the patient how to cough effectively (see Table 28.21). Chest physiotherapy and postural drainage are not recommended because they may promote movement of microorganisms into other bronchi, extending infection. Rest, optimal nutrition, and adequate fluid intake are supportive measures to promote recovery. If dentition is poor and dental hygiene is not adequate, encourage the patient to obtain dental care. Collaborate with the social worker to evaluate available options for dental care if the patient has limited resources. If the patient does not adequately respond to antibiotic treatment, percutaneous drainage of the abscess may be done. A small catheter, guided by CT or ultrasound, may be placed to drain the abscess. Surgery is sometimes done when reinfection of a large cavitary lesion occurs, when an empyema develops, or to establish a diagnosis when there is evidence of an underlying problem, such as cancer. The usual procedure in such cases is a lobectomy. A pneumonectomy may be

needed for multiple abscesses.

Bridge to Nclex Examination The number of the question corresponds to the same-numbered outcome at the beginning of the chapter.

1. When caring for a patient with acute bronchitis, the nurse will prioritize interventions by a. auscultating lung sounds. b. encouraging fluid restriction. c. administering antibiotic therapy. d. teaching the patient to avoid cough suppressants. 2. Which patients have the greatest risk for aspiration pneumonia? (select all that apply) a. Patient with seizures b. Patient with head injury c. Patient who had thoracic surgery d. Patient who had a myocardial infarction e. Patient who is receiving nasogastric tube feeding 3. An appropriate nursing intervention to assist a patient with pneumonia manage thick secretions and fatigue would be to a. perform postural drainage every hour. b. provide analgesics as ordered to promote patient comfort. c. administer O2 as prescribed to maintain optimal O2 levels. d. teach the patient how to cough effectively and expectorate secretions.

4. A patient with TB has been admitted to the hospital and is placed on airborne precautions and in an isolation room. What should the nurse teach the patient? (select all that apply) a. Expect routine TB testing to evaluate the infection. b. No visitors will be allowed while in airborne isolation. c. Adherence to precautions includes coughing into a paper tissue. d. Take all medications for full length of time to prevent multidrug-resistant TB. e. Wear a standard isolation mask if leaving the airborne infection isolation room. 5. A patient has been receiving high-dose corticosteroids and broad-spectrum antibiotics for treatment of an infection after a traumatic injury. The nurse plans care for the patient knowing that the patient is most susceptible to a. candidiasis. b. cryptococcosis. c. histoplasmosis. d. coccidioidomycosis. 6. When caring for a patient with a lung abscess, what is the nurse’s priority intervention? a. Postural drainage b. Antibiotic administration c. Obtaining a sputum specimen d. Patient teaching about home care 7. You are caring for patients exposed to a chlorine leak from

a local factory. The nurse would closely monitor these patients for a. pulmonary edema. b. anaphylactic shock. c. respiratory alkalosis. d. acute tubular necrosis. 8. The nurse receives an order for a patient with lung cancer to receive influenza vaccine and pneumococcal vaccines. The nurse will a. call the health care provider to question the order. b. give both vaccines at the same time in different arms. c. give the pneumococcal vaccine and obtain a nasal influenza vaccine. d. give the flu shot and tell the patient to come back in 1 week to have the pneumococcal vaccine. 9. The nurse identifies a flail chest in a trauma patient when a. multiple rib fractures are determined by x-ray. b. a tracheal deviation to the unaffected side is present. c. paradoxical chest movement occurs during respiration. d. there is decreased movement of the involved chest wall. 10. The nurse notes tidaling of the water level in the waterseal chamber in a patient with closed chest tube drainage. The nurse should a. continue to monitor the patient. b. check all connections for a leak in the system. c. lower the drainage collector further from the chest. d. clamp the tubing at a distal point away from the patient.

11. After a pneumonectomy, an appropriate nursing intervention is a. monitoring chest tube drainage and functioning. b. positioning the patient on the unaffected side or back. c. doing range-of-motion exercises on the affected upper limb. d. auscultating frequently for lung sounds on the affected side. 12. A priority nursing intervention for a patient who has just undergone a chemical pleurodesis for recurrent pleural effusion is a. giving ordered analgesia. b. monitoring chest tube drainage. c. sending pleural fluid for laboratory analysis. d. monitoring the patient’s level of consciousness. 13. When planning care for a patient at risk for pulmonary embolism, the nurse prioritizes a. maintaining the patient on bed rest. b. using intermittent pneumatic compression devices. c. encouraging the patient to cough and deep breathe. d. teaching the patient how to use the incentive spirometer. 14. Which statement(s) describe(s) the management of a patient following lung transplantation (select all that apply)? a. High doses of O2 are administered around the clock. b. Using a home spirometer will help to monitor lung function. c. Immunosuppressant therapy usually involves a 3-drug

regimen. d. Most patients have an acute rejection episode within the first 2 days. e. A lung biopsy is done using a transtracheal method if rejection is suspected. 1. a, 2. a, b, e, 3. d, 4. c, d, e, 5. a, 6. b, 7. a, 8. b, 9. c, 10. a, 11. c, 12. a, 13. b, 14. b, c, e For rationales to these answers and even more NCLEX review questions, visit http://evolve.elsevier.com/Lewis/medsurg.

Evolve Website/Resources List http://evolve.elsevier.com/Lewis/medsurg

Review Questions (Online Only) Key Points Answer Keys for Questions • Rationales for Bridge to NCLEX Examination Questions • Answer Guidelines for Case Study on p. 538 Student Case Studies • Patient With Lung Cancer • Patient With Pulmonary Embolism and Respiratory Failure Nursing Care Plans • eNursing Care Plan 27.1: Patient With Pneumonia • eNursing Care Plan 27.2: Patient After Thoracotomy Conceptual Care Map Creator Audio Glossary

Content Updates

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15. Lange C, Chesov D, Hevckendorf J, et al. Drugresistant tuberculosis: an update on disease burden, diagnosis and treatment. Respirology. 2018;23:656. 16. Sloan D.J, Lewis J.M. Management of multidrug resistant TB: Novel treatments and their expansion to low resource settings. T Roy Soc Trop Med Hyg. 2016;3:163. 17. Sharma R, Gaillard F. Ghon lesion Retrieved from. www.radiopaedia.org/articles/ghon-lesion. 18. Centers for Disease Control and Prevention, . Tuberculin skin testing Retrieved from. www.cdc.gov/tb/publications/factsheets/testing/skintesting.htm Lewinsohn D.M, Leonard M.K, LoBue P.A, et al. Official American

Thoracic Society/Infectious Diseases Society of America/CDC clinical practice guidelines: Diagnosis of tuberculosis in adults and children. Clin Infect Dis. 2017;64:111. World Health Organization Guidelines for treatment of drugsusceptible tuberculosis and patient care (2017 update). Retrieved from www.who.int/tb/publications/2017/dstb_guidance_2017/en/. Reyes-Montes M.D.R, Perez-Huitron M.A, Ocana-Monroy J.L, et al. The habitat of Coccidioides spp. and the role of animals as reservoirs and disseminators in nature. BMC Infect Dis. 2016;16:550.

22. Sethi S. Lung abscess Retrieved from. www.merckmanuals.com/enca/professional/pulmonary-disorders/lung-abscess/lungabscess. 23. American Cancer Society, . Key statistics for lung cancer Retrieved from. www.cancer.org/cancer/nonsmall-cell-lung-cancer/about/key-statistics.html. 24. American Lung Association, . Lung cancer fact sheet Retrieved from. www.lung.org/lung-health-anddiseases/lung-disease-lookup/lung-cancer/resourcelibrary/lung-cancer-fact-sheet.html. 25. National Cancer Institute, . Harms of cigarette smoking and health benefits of quitting Retrieved from. www.cancer.gov/about-cancer/causesprevention/risk/tobacco/cessation-fact-sheet. 26. Chandra A.M. Cigarette smoking is the main cause of lung cancer Retrieved from. www.healthxchange.sg/cancer/lungcancer/cigarette-smoking-main-cause-lung-cancer. 27. Lung Cancer.org. Types and staging of lung cancer Retrieved from. www.lungcancer.org/find_information/publications/163lung_cancer_101/268-types_and_staging.

Mazzone P.J, Silvestri G.A, Patel S, et al. Screening for lung cancer: chest guideline and expert panel report. Chest. 2018;153:954. American Cancer Society, . Lung cancer screening guidelines Retrieved from. www.cancer.org/health-careprofessionals/american-cancer-society-prevention-early-detectionguidelines/lung-cancer-screening-guidelines.html. Groen H.J.M, Dingemans A.M.C, Belderbos J, et al. Prophylactic cranial irradiation versus observation in radically treated stage III non-small cell lung cancer. J Clin Oncol. 2017;35:s8502.

31. Simoglou C, Gymnopoulos D. Video-assisted thoracoscopic surgery. Scientific Chronicles. 2017;22:150. 32. Lee J. Overview of interstitial lung disease Retrieved from. www.merckmanuals.com/enca/professional/pulmonary-disorders/interstitial-lungdiseases/overview-of-interstitial-lung-disease. 33. Ryan J. Pulmonary embolism: New treatments for an old problem. Emerg Medicine. 2016;8:87. 34. Ouellette D.R. Pulmonary embolism treatment and management Retrieved from. https://emedicine.medscape.com/article/300901treatment#d9. 35. Pulmonary Hypertension Association, . Types of pulmonary hypertension Retrieved from. https://phassociation.org/patients/aboutph/types-ofph/. ∗Evidence-based information for clinical practice.

28

Obstructive Pulmonary Diseases Eugene Mondor

LEARNING OUTCOMES 1. Describe the etiology, pathophysiology, and clinical manifestations of asthma. 2. Explain the difference between an acute asthma exacerbation and status asthmaticus. 3. Describe the interprofessional and nursing management of the patient with asthma. 4. Identify the classifications of drugs used in the treatment of asthma and chronic obstructive pulmonary disease (COPD). 5. Describe the etiology, pathophysiology, clinical manifestations, and interprofessional care of the patient with COPD. 6. Relate the indications for O2 therapy, methods of delivery, and complications of O2 administration. 7. Explain the nursing management of the patient with COPD. 8. Describe the pathophysiology, clinical manifestations, and interprofessional and nursing management of the patient with cystic fibrosis. 9. Describe the pathophysiology, clinical manifestations, and interprofessional and nursing management of the patient with bronchiectasis.

KEY TERMS α1-antitrypsin deficiency (AATD), p. 561 asthma, p. 542 bronchiectasis, p. 580 chest physiotherapy (CPT), p. 571 chronic bronchitis, p. 560 chronic obstructive pulmonary disease (COPD), p. 560 cor pulmonale, p. 563 cystic fibrosis (CF), p. 576 emphysema, p. 560 O2 toxicity, p. 567 postural drainage, p. 571 pursed-lip breathing (PLB), p. 570 status asthmaticus, p. 545 Kindness is a breath of fresh air to someone who feels they are suffocating. Franklin D. Roosevelt http://evolve.elsevier.com/Lewis/medsurg/

Cenceptual Focus Fatigue Functional Ability Gas Exchange Infection Self-Management

Imagine needing to consciously think about every breath that you take each minute, each hour, and every day of your life. You are tired and weak and have not been sleeping well. Your appetite is poor. The stress of living with these symptoms makes you feel anxious and depressed. You have been absent from work and are having some financial problems. Many people with obstructive lung disease have this experience. The obstructive pulmonary diseases are the most common chronic lung diseases. They are characterized by increased resistance to airflow because of airway obstruction or airway narrowing. There are 4 major types of obstructive lung disease: asthma, chronic obstructive pulmonary disease (COPD), cystic fibrosis (CF), and bronchiectasis. Asthma causes inflammation with variable degrees of airflow obstruction. Between acute exacerbations, or attacks, the patient with asthma is often asymptomatic with normal lung function. On the other hand, in COPD there is progressive limitation in airflow that is not fully reversible. The limitation in expiratory airflow in COPD is generally more constant day-to-day and worsens over time. Emphysema and chronic bronchitis are 2 related respiratory conditions often responsible for COPD.1 The pathophysiology of asthma and the response to therapy differs from COPD. However, patients with asthma who have less responsive airflow obstruction are hard to tell from COPD patients. In fact, some patients share features of both asthma and COPD. This is known as asthma-COPD overlap syndrome.2 It is characterized by significantly worse respiratory signs and symptoms, an increased number of hospitalizations, and a much poorer quality of life than asthma or COPD alone.3 CF is an inherited genetic disorder. It produces airway obstruction because of changes in exocrine glandular secretions, resulting in increased mucus production. There are about 30,000 people in the United States living with CF, with 52.7% being adults.4 Bronchiectasis is characterized by dilated bronchioles, making it hard to clear secretions. It most often results from poorly treated or untreated pulmonary infections, immune system problems, or genetic

factors.

Promoting Health Equity Obstructive Pulmonary Diseases

Asthma • Asthma prevalence rates are 38% higher among blacks than whites. • Hispanics, especially those from Puerto Rico, have higher rates of asthma and age-adjusted death rates than all other racial and ethnic subgroups. • Black females have the highest mortality rates from asthma.

COPD • Whites have the highest incidence of COPD despite higher rates of smoking among other ethnic groups. • Hispanics have lower death rates from COPD than other ethnic groups.

Cystic Fibrosis • Whites have the highest incidence of CF. • CF is uncommon among blacks, Hispanics, and Asian Americans.

Asthma Asthma is a heterogenous disease characterized by bronchial hyperreactivity with reversible expiratory airflow limitation. Signs and symptoms can be variable. They often include episodes of wheezing, breathlessness, chest tightness, and cough, particularly at night or in the early morning. These episodes are associated with widespread, variable airflow obstruction that is usually reversible, either spontaneously or with treatment. The clinical course of asthma is unpredictable, ranging from periods of adequate control to attacks with poor control of symptoms. Asthma affects around 20.4 million adult Americans.5 It is a major public health concern, with more than 1.7 million emergency department (ED) visits each year.5 After a long period of an increasing incidence of asthma, the mortality and use of health care services for asthma have decreased over the past 10 years. Unfortunately, more than 3600 people still die each year from asthma.5

Gender Differences Asthma

Men • Before puberty, more boys are affected than girls.

Women • In adulthood, women are much more likely to be affected than men. • Women who present to the ED are more likely to need

hospitalization than men. • Mortality is higher in women than in men.

Risk Factors for Asthma and Triggers of Asthma Attacks Risk factors for asthma and triggers of asthma attacks can be related to the patient (e.g., genetic factors) or the environment (e.g., pollen) (Table 28.1). Important factors and triggers are discussed in this section.

Nose and Sinus Problems Most patients with asthma have a history of allergic rhinitis. Treatment of allergic rhinitis usually improves the symptoms of asthma. Acute and chronic sinusitis, especially bacterial rhinosinusitis, may worsen asthma. Patients with asthma often have chronic sinus problems that cause inflammation of the mucous membranes and can trigger an asthma attack. Sinusitis must be treated and large nasal polyps removed for an asthma patient to have good control. (Sinusitis is discussed in Chapter 27.)

TABLE 28.1 Triggers of Asthma Attacks

Air Pollutants • Aerosol sprays • Cigarette smoke • Exhaust fumes • Oxidants • Perfumes • Sulfur dioxides

Allergen Inhalation • Animal dander (e.g., cats, mice, guinea pigs) • Cockroaches • House dust mite • Molds • Pollens

Drugs • Aspirin • β-Adrenergic blockers • Nonsteroidal antiinflammatory drugs

Food Additives • Beer, wine, dried fruit, shrimp, processed potatoes • Monosodium glutamate • Sulfites (bisulfites and metabisulfites) • Tartrazine

Occupational Exposure • Agriculture, farming • Industrial chemicals and plastics • Laundry detergents • Metal salts • Paints, solvents • Wood and vegetable dusts

Viral or Bacterial Infection • Sinusitis, allergic rhinitis • Viral URI

Other Factors • Exercise and cold, dry air • Gastroesophageal reflux disease (GERD) • Hormones, menses • Stress

Respiratory Tract Infections Respiratory tract infections are often a major trigger of an acute asthma attack. Acute infection can decrease the diameter of the airways and induce airway hyperresponsiveness. Viral-induced changes in epithelial cells, the accumulation of inflammatory cells, edema of airway walls, and exposure of airway nerve endings contribute to altered respiratory function. These changes may exacerbate asthma.

Allergens Allergens cause varying degrees of allergic reactions in susceptible persons. Indoor and outdoor allergens, such as cockroaches, furry animals, fungi, pollen, and molds, can trigger asthma attacks. However, their role in the actual development of asthma is not as clear.6

Cigarette Smoke The Centers for Disease Control and Prevention (CDC) estimates that 21% of asthma patients smoke.7 In a person with asthma, smoking is associated with a faster decline of lung function, increased disease

severity, more frequent visits to the HCP, and a decreased response to treatment. The smoke exhaled by a smoker, known as secondhand smoke, is also a risk factor.

Air Pollutants Various air pollutants, such as wood smoke or vehicle exhaust, can trigger asthma attacks. In heavily industrialized or densely populated areas, climate conditions often lead to concentrated pollution in the atmosphere, especially with thermal inversions and stagnant air masses. News sources report ozone alert days. Patients with breathing problems should minimize outdoor activity during these times.

Occupational Factors Occupational asthma is the most common job-related respiratory disorder. These irritants cause a change in the responsiveness of the airways. However, the development of symptoms may not occur until the patient has had months to years of exposure. These agents are diverse and include wood dusts, laundry detergents, metal salts, chemicals, paints, solvents, and plastics. Often, people with occupational asthma give a history of arriving at work feeling well but gradually develop symptoms, which may become progressively worse, by the end of the day.

Exercise Asthma that is induced or worse during physical exertion is called exercise-induced asthma (EIA) or exercise-induced bronchospasm (EIB). Typically, symptoms of EIA are pronounced during activities in which there is exposure to cold, dry air. For example, swimming in an indoor heated pool is less likely to cause symptoms than downhill skiing. Airway obstruction may occur due to changes in the airway mucosa caused by hyperventilation during exercise, with either cooling or rewarming of air and capillary leakage in the airway wall. EIB occurs after vigorous exercise, not during it (e.g., jogging, aerobics, walking briskly, climbing stairs).

Drugs and Food Additives Some people with asthma have what we call the asthma triad: nasal polyps, asthma, and sensitivity to aspirin and nonsteroidal antiinflammatory drugs (NSAIDs). Some persons with asthma who use salicylic acid (e.g., aspirin) or NSAIDs develop wheezing within 2 hours. In addition, there is usually profound rhinorrhea, congestion, tearing, and even angioedema. Avoiding salicylic acid and NSAIDs is required. Teach the patient to read labels. Salicylic acid is in many OTC drugs and some foods, beverages, and flavorings. Under the care of an allergist, daily administration of the drug can desensitize some patients. β-Adrenergic blockers in oral form (e.g., metoprolol [Toprol-XL]) or topical eye drops (e.g., timolol [Timoptic]) may trigger an asthma attack because they can cause bronchospasm. Angiotensin-converting enzyme (ACE) inhibitors (e.g., lisinopril) may cause a dry, hacking cough in susceptible persons, making asthma symptoms worse. Asthma attacks can occur after the use of sulfite-containing preservatives found in topical ophthalmic solutions, IV corticosteroids, and some inhaled bronchodilator solutions. Food and drug additives that may trigger asthma in the susceptible person are tartrazine (yellow dye no. 5) and sulfiting agents. They are widely used as preservatives and sanitizing agents. Sulfiting agents are in fruits, beer, and wine. They are used in salad bars to protect vegetables from oxidation. Food allergies triggering asthma reactions in adults are rare. Avoidance diets are not recommended until testing has proven an allergy is present.

Gastroesophageal Reflux Disease Gastroesophageal reflux disease (GERD) is more common in people with asthma than in the general population. GERD can worsen asthma symptoms because reflux may trigger bronchoconstriction and cause aspiration. Asthma drugs may worsen GERD symptoms. β2Agonists used to treat asthma (especially when given orally) relax the lower esophageal sphincter. This allows stomach contents to reflux into the esophagus and be aspirated into the lungs. Effective treatment

for GERD can improve nocturnal asthma control, improve quality of life, and prevent asthma symptoms in some patients. (GERD is discussed in Chapter 41.)

Genetics Asthma has an inherited component, but the genetics are complex. Numerous genes may be involved in the development of asthma. They are likely responsible for varying responses among patients to different types of asthma drugs. Atopy, the genetic predisposition to develop an allergic (immunoglobulin E [IgE]–mediated) response to common allergens, is a major risk factor for asthma.

Immune Response The hygiene hypothesis suggests that a newborn baby’s immune system must be conditioned so that it will function properly during infancy and the rest of life. People who have a lower incidence of asthma were exposed to certain infections early in life, used fewer antibiotics, were around other children (e.g., siblings, day care), or lived in rural settings or with pets. People for whom these factors are not present in childhood have a higher incidence of asthma.

Psychological Factors Asthma is not a psychosomatic disease. However, many people with asthma report that symptoms worsen with stress. An asthma attack caused by any triggering event can produce panic, stress, and anxiety. These emotions, and other psychological factors, can cause bronchoconstriction through stimulation of the cholinergic reflex pathways. Extreme behavioral expressions (e.g., crying, laughing, anger, fear) can lead to hyperventilation and hypocapnia, which can cause airway narrowing.

Pathophysiology The main pathophysiologic process in asthma is persistent but variable inflammation of the airways. Airflow is limited because

inflammation results in bronchoconstriction, airway hyperresponsiveness (hyperreactivity), and edema of the airways. Exposure to allergens or irritants initiates the inflammatory cascade (Fig. 28.1). A variety of inflammatory cells are involved, including mast cells, macrophages, eosinophils, neutrophils, T and B lymphocytes, and epithelial cells of the airways. As the inflammatory process begins, mast cells (found beneath the basement membrane of the bronchial wall) degranulate and release multiple inflammatory mediators (Fig. 28.2). IgE antibodies are linked to mast cells, and the allergen cross-links the IgE. As a result, inflammatory mediators, such as leukotrienes, histamine, cytokines, prostaglandins, and nitric oxide, are released. Inflammatory mediators have effects on the (1) blood vessels, causing vasodilation and increasing capillary permeability (runny nose); (2) nerve cells, causing itching; (3) smooth muscle cells, causing bronchial spasms and airway narrowing; and (4) goblet cells, causing mucus production (Fig. 28.3). This whole process is sometimes referred to as the early-phase response in asthma. Clinically, it occurs within 30 to 60 minutes after exposure to an allergen or irritant. Symptoms can recur 4 to 6 hours after the early response because of the influx of many inflammatory cells, which are set in motion by the initial response. At this later time, the patient may develop symptoms again or worsening of symptoms. This is called the late-phase response. It occurs in about 50% of people with asthma. In the late-phase response, more inflammatory cells are recruited and activated, with continuing inflammation of the airways. Thus bronchoconstriction with symptoms lasts for 24 hours or more. Corticosteroids are effective in treating inflammation in this phase. Chronic inflammation may cause structural changes in the bronchial wall, known as remodeling. A progressive loss of lung function occurs that therapy cannot fully reverse. The changes in structure may include fibrosis of the subepithelium, hypertrophy of the smooth muscle of the airways, mucus hypersecretion, continued inflammation, and angiogenesis (proliferation of new blood vessels).8 We think remodeling explains why some persons have persistent

asthma and limited response to therapy.

FIG. 28.1 Pathophysiology of asthma. Adapted from McCance KL, Huether SE, Brashers, VL, Rote, NS, editors: Pathophysiology: The biologic basis for disease in adults and children, ed 7, St Louis, 2015, Elsevier.

FIG. 28.2 Allergic asthma is triggered when an allergen cross-links IgE receptors on mast cells, which are then activated to release histamine and other inflammatory mediators (early-phase response). A late-phase response may occur due to further inflammation.

FIG. 28.3 Factors causing expiratory obstruction in asthma. A, Cross section of a bronchiole occluded by muscle spasm, swollen mucosa, and mucus in the lumen. B, Longitudinal section of a bronchiole. Redrawn from Price SA, Wilson LM: Pathophysiology: Clinical concepts of disease processes, ed 6, St Louis, 2003, Mosby.

Clinical Manifestations The characteristic manifestations are wheezing, cough, dyspnea, and chest tightness after exposure to a risk factor or trigger. Normally the

bronchioles constrict during expiration. However, in asthma, the airways become narrower than usual because of bronchospasm, edema, and mucus. As a result, it takes longer for the air to move out of the bronchioles (airflow obstruction). This causes the characteristic wheezing, air trapping, and hyperinflation of the lungs. As a result, expiration may be prolonged. The most common finding during an acute asthmatic event is wheezing on auscultation. For wheezing to occur, the patient must be able to move enough air to make the sound. Wheezing usually occurs first on exhalation. As asthma progresses, the patient may wheeze during inspiration and expiration. However, wheezing is an unreliable sign to gauge the severity of an attack. Many patients with minor attacks wheeze loudly. Others with severe attacks do not wheeze. The patient with a severe asthma attack may wheeze only during forced expiration or have no audible wheezing because of the marked reduction in airflow. Decreased or absent breath sounds may signal a significant decrease in air movement resulting from exhaustion and an inability to generate enough muscle force to breathe. Severely decreased breath sounds, often referred to as the “silent chest,” are an ominous sign. It means severe airway obstruction and impending respiratory failure.

Safety Alert Silent Chest • If the patient has been wheezing, then there is an absence of a wheeze (e.g., silent chest) and the patient is obviously struggling, this is a life-threatening situation. The patient may need mechanical ventilation. Hyperventilation occurs during an asthma attack as lung receptors respond to increased lung volume from trapped air and airflow

limitation. Decreased perfusion and ventilation of the alveoli and increased alveolar gas pressure lead to ventilation-perfusion abnormalities in the lungs. The patient is hypoxemic early on with decreased PaCO2 and increased pH (respiratory alkalosis) because they are is hyperventilating. As the airflow limitation worsens with air trapping, the patient works much harder to breathe. The PaCO2 normalizes as the patient tires, and then it increases to produce respiratory acidosis. This is an ominous sign of respiratory failure. In some patients with asthma, cough is the only symptom. This is termed cough variant asthma. Bronchospasm is not present or may not be severe enough to cause airflow obstruction or wheezing, but it can increase bronchial tone and cause irritation with stimulation of the cough receptors. The cough may be nonproductive or with secretions. Sputum may be thick, tenacious, and gelatinous, which makes removal difficult. The examination of the patient with asthma may be normal, especially between attacks. A runny nose, swollen nasal passages, and nasal polyps may be seen. The patient may have eczema and hives, which have been linked to asthma.

Check Your Practice Your patient with a history of asthma was admitted to the ED in acute respiratory distress. He has been receiving therapy and seems to be responding. You notice he is no longer wheezing. • Should you consider this finding a sign that he is doing better?

Asthma Classifications There are several sets of guidelines for classifying asthma. Each set of guidelines has a slightly different perspective about asthma and how to classify the severity when attacks occur. Asthma severity is used to guide treatment decisions. Current guidelines focus on (1) assessing

the severity of the disease at diagnosis and initial treatment and then (2) monitoring periodically to control the disease. All groups endorse the use of short-acting bronchodilators for an acute asthma attack and the importance of an “asthma action plan” to help prevent future attacks from occurring. They promote patient education and adherence to prescribed therapy. Many HCPs use the 2007 the National Heart, Lung, and Blood Institute classification of asthma severity (Table 28.2). It describes asthma as intermittent, mild persistent, moderate persistent, or severe persistent.

Complications Asthma is characterized by an unpredictable and variable course. Asthma attacks range from minor interferences in breathing to lifethreatening episodes. Depending on a person’s response, asthma can rapidly progress from normal breathing to an acute, severe attack or a life-threatening medical emergency within a few minutes. While asthma attacks may have an abrupt onset, most of the time, symptoms occur more gradually. Attacks may last for a few minutes to several hours. Between attacks, the patient may be asymptomatic with normal or near-normal spirometry, depending on the severity of disease. In some people, compromised pulmonary function (indicated by abnormal spirometry results) may lead to a state of continuous symptoms and chronic debilitation. Pneumonia, tension pneumothorax, status asthmaticus, and acute respiratory failure can occur.

Status Asthmaticus A life-threatening medical emergency, status asthmaticus is the most extreme form of an acute asthma attack. It is characterized by hypoxia, hypercapnia, and acute respiratory failure.9 The patient is unresponsive to treatment with bronchodilators and corticosteroids. The patient may have chest tightness, a severely marked increase in shortness of breath, or suddenly be unable to speak. Hypotension, bradycardia, and respiratory and/or cardiac arrest may occur if we do

not recognize that the patient’s condition is getting worse. The patient must be immediately intubated, and mechanical ventilation started. Hemodynamic monitoring of the patient is critical. Analgesia and sedation are essential. Continuous analgesic infusions (e.g., ketamine, morphine) and sedation with drugs such as propofol (Diprivan) help decrease work of breathing (WOB) and facilitate patient synchrony with the ventilator. In some circumstances, neuromuscular blocking agents may be used. Inhaled anesthetics, such as isoflurane or halothane, are an option for those not responding to conventional treatment. IV magnesium sulfate, which has a bronchodilator effect, may be given to patients with a very low FEV1 (forced expiratory volume in 1 second) or peak flow (less than 40% of predicted or personal best) or those who do not respond to initial treatment.

Diagnostic Studies The tests we use to diagnose asthma are shown in Table 28.3. In general, the HCP should consider a diagnosis of asthma if various indicators (e.g., manifestations, health history, peak flow variability, spirometry) are positive. Underdiagnosis of asthma is common. A detailed history is important to determine if a person has had similar attacks, which are often precipitated by a known trigger. Because wheezing and cough occur with a variety of disorders (e.g., COPD, GERD, vocal cord problems, heart failure), it is important to determine if asthma or some other disease process is the cause of these problems. A comparison of asthma and COPD is shown in Table 28.4.

TABLE 28.2 Classification of Asthma Severity

ercent predicted values for FEV1 or ratio of FEV1/FVC. Normal FEV1/FVC: 8–19 yr, 85%; 20– 39 yr, 80%; 40–59 yr, 75%; 60–80 yr, 70%. †

Consider short-term corticosteroid therapy.

Guidelines for Using Table • Assign patients to the most severe step in which any feature occurs. Clinical features may overlap across steps. Determine level of severity by assessment of both impairment and risk. Assess impairment by patient’s recall of previous 2–4 wk spirometry results. • A person’s classification should change over time with treatment. After treatment, the focus switches to the level of control, not the classification of severity. • Patients at any level of severity of chronic asthma can have mild, moderate, or severe asthma attacks. Some patients with intermittent asthma have severe and life-threatening attacks separated by long periods of normal lung function and no symptoms. Source: Adapted from National Asthma Education and Prevention Program, National Heart, Lung, and Blood Institute: Expert Panel Report 3: Guidelines for the diagnosis and management of asthma, NIH pub

no 08-4051, Bethesda, MD, 2007, National Institutes of Health.

Table 28.3  Interprofessional CareAsthma

Diagnostic Assessment • History and physical examination • Spirometry, including response to bronchodilator therapy • Peak expiratory flow rate (PEFR) • Chest x-ray • Measurement of oximetry • Allergy skin testing (if indicated) • Blood level of eosinophils and IgE (if indicated)

Management • Identify and avoid or eliminate triggers • Patient and caregiver teaching • Drug therapy (Tables 28.6 and 28.7 and Figs. 28.4 and 28.5) • Asthma action plan (Fig. 28.9) • Desensitization (immunotherapy) if indicated • Assess for control (e.g., Asthma Control Test [ACT])∗

Acute Attacks • SaO2 monitoring • ABGs • Inhaled β2-adrenergic agonists • Inhaled anticholinergics

• O2 by nasal cannula or mask • IV or oral corticosteroids • IV fluids • IV magnesium • Intubation and assisted ventilation



See www.asthmacontroltest.com.

The peak expiratory flow rate (PEFR) measured by the peak flow meter (at home or in a health care setting) is a test of lung function (see Table 25.17). PEFR measurements can help predict an asthma attack or monitor the severity of disease. Test results depend on the patient’s age, gender, and height. Since types of peak flow meters vary, PEFR should be compared with the patient’s own previous best measurements using their own meter. Spirometry is usually normal between asthma attacks if the patient has no other underlying pulmonary disease. However, the patient with asthma may show an obstructive pattern including a decrease in forced vital capacity (FVC), FEV1, PEFR, and FEV1 to FVC ratio (FEV1/FVC) (see Table 25.16). When spirometry is scheduled, the patient must stop taking any bronchodilator drugs for 6 to 12 hours before the test. Spirometry can be done before and after the administration of a bronchodilator to determine the degree of the response. This helps determine reversibility of airway obstruction, which is critical information for diagnosing asthma. A positive (favorable) response to the bronchodilator is an increase of more than 200 mL and an increase of more than 12% between preadministration and postadministration values.10 We can use a hand-held, point-of-care device to measure fractional exhaled nitric oxide (FENO). FENO levels are increased in people with asthma associated with eosinophilic-induced airway inflammation. FENO may be used to gauge loss of asthma control and

attacks, assess a patient’s adherence to therapy, or determine if more inhaled or oral antiinflammatory medication is needed.11

TABLE 28.4 Comparison of Asthma and COPD∗



Patients may have features of both asthma and COPD.

Increased serum eosinophil counts and IgE levels are highly suggestive of atopy. Allergy skin testing may be used to determine sensitivity to specific allergens. However, a positive skin test does not necessarily mean that the allergen is causing the asthma attack. On the

other hand, a negative allergy test does not mean that the asthma event is not allergy related. (Allergy testing is discussed in Chapter 13.) A chest x-ray in an asymptomatic patient with asthma is usually normal. A routine chest x-ray is usually not done unless other manifestations, such as fever, chills, or upper airway stridor, are present. It can show if something else is causing symptoms similar to those of asthma (e.g., pneumonia, foreign body in the airway.) A sputum specimen for culture and sensitivity may be done to rule out bacterial infection, especially if the patient has purulent sputum, a history of upper respiratory tract infection (URI), a fever, or an increased white blood cell (WBC) count. However, most asthma attacks are viral, and sputum cultures are rarely done on an outpatient basis.

Interprofessional Care The goal of care is to achieve and maintain control of the disease. Once the patient is diagnosed, guidelines provide direction about medications (based on steps) the patient needs (Fig. 28.4). The HCP will step up the medication therapy as asthma symptoms worsen and step down the medication as the patient achieves control (Table 28.5). The level of control is determined by the patient’s medication use, symptoms, and PEFR or FEV1. During an acute attack, signs and symptoms, medication use, and PEFR or FEV1 measurements can be used to help identify the severity of an asthma attack and guide us in providing the most appropriate treatment. The goal is to achieve rapid control of the symptoms and return the patient to their daily functioning at the best possible level. Management of acute asthma attacks is shown in Fig. 28.5. Patients with mild or moderate asthma attacks are often seen in the community at an outpatient clinic. These attacks occur no more than twice per week, with minimal interference in day-to-day activity. The patient is alert, oriented, and speaks in sentences. The patient may describe chest tightness, varying degrees of difficulty breathing, and a

slight increase in the use of asthma drugs. O2 saturation is usually greater than 90% on room air and PEFR greater than 50% of predicted or personal best. Inhaled bronchodilators and oral corticosteroids are the mainstays of treatment for mild to moderate asthma attacks. Monitor the patient’s vital signs. Most improve within 60 minutes of starting therapy. Teach the patient the importance of a follow-up appointment with the HCP. Oral corticosteroids will be part of the discharge plan for a moderate attack and, based on the patient’s history and HCP preference, sometimes for a mild attack. If the patient’s condition is slow to respond, does not respond, or the HCP suspects that some other condition may be occurring or contributing to the acute attack, the patient should be transferred to an acute care facility. In a severe attack the patient is still alert and oriented, but may be tachycardic, tachypneic, and focused on breathing. Respiratory rates greater than 30 breaths/min may be present. Accessory muscle use may be seen. The patient may be agitated from hypoxemia. If not immediately audible, auscultation of the lungs may reveal inspiratory or expiratory wheezing. The patient often sits forward to maximize diaphragmatic movement. Time permitting, percussion of the lungs indicates hyperresonance. PEFR is 50% or less of predicted or of personal best. Symptoms may re-occur, sometimes daily, and there is interference with activities of daily living (ADLs). A severe acute attack is usually frightening enough for patients to go to the ED. In many cases, a severe attack will warrant hospital admission. Management of the patient with a severe attack focuses on correcting hypoxemia and continually observing and/or improving ventilation. Supplemental O2 is given by nasal cannula or mask to achieve a PaO2 of at least 60 mm Hg or O2 saturation greater than 93%. O2 monitoring should be continuous with pulse oximetry.

FIG. 28.4 Stepwise approach to asthma treatment. Modified from GINA evidence-based strategy document, 2018. Retrieved from https://ginasthma.org.

TABLE 28.5 Components of Asthma Control

Source: Adapted from National Asthma Education and Prevention

Program, National Heart, Lung, and Blood Institute: Expert Panel Report 3: Guidelines for the diagnosis and management of asthma, NIH pub no 08-4051, Bethesda, MD, 2007, National Institutes of Health. Bedside PEFR may be used to monitor airflow obstruction. Serial PEFR results, oximetry, and measurement of arterial blood gases (ABGs) give information about the severity of the attack and the response to therapy. Obtaining a PEFR during a severe asthma attack is usually not possible. However, if it can be obtained and is less than 200 L/min, it indicates severe obstruction in all but very small adults. Careful monitoring of the patient’s heart rate, respiratory rate and rhythm, and BP are essential. Bronchodilators and oral corticosteroids will be part of the treatment plan. The “silent chest” is an ominous clinical finding. It often signals impending respiratory failure. Immediate notification of the HCP is required.

Drug Therapy Drug therapy for asthma can be complex and overwhelming for many practitioners, including you. It is important to understand the intended purpose, desired effect, side effects, and when to use different drugs. Asthma drugs are divided into 2 general types: (1) quick relief, or rescue medications, to treat attacks, and (2) long-term control medications (Table 28.6).

FIG. 28.5 Management of patient with acute asthma attack. Modified from GINA evidence-based strategy document, 2018. Retrieved from https://ginasthma.org.

The patient’s medical history, medication plan, and severity of

attack helps the HCP determine which types of drugs are best suited to control asthma symptoms. Current guidelines all suggest a stepwise approach to drug therapy. Common drugs used in asthma therapy are discussed in Table 28.7. The mainstay of asthma treatment is inhalation of short-acting β2adrenergic agonist (SABA) bronchodilators. All patients need a quickrelief or “rescue” medication. Short-acting SABAs, such as albuterol (ProAir HFA, Proventil HFA, Ventolin HFA), are the most effective rescue drugs for asthma. In patients with a moderate to severe attack, inhaled ipratropium (Atrovent) is used in conjunction with a SABA. Combivent is a combination of both ipratropium and albuterol. Oral and, in some situations, IV corticosteroids may be given to patients who do not initially respond to SABA alone. Patients with asthma who have frequent attacks also must be on a long-term (“controller”) medication. Inhaled corticosteroids (ICSs) (e.g., fluticasone [Flovent Diskus or HFA]) are the most effective longterm controllers to treat inflammation. Some ICSs are used in combination with long-acting bronchodilators (LABAs) to gain better asthma control.

Bronchodilators The 3 classes of bronchodilator drugs used in asthma therapy are β2adrenergic agonists (also referred to as β2-agonists), methylxanthines and derivatives, and anticholinergics.

β2-Adrenergic Agonist Drugs These drugs may be SABAs or LABAs. Because inhaled SABAs are the most effective drugs for relieving acute bronchospasm (as seen in an acute attack), they are known as rescue medications. These drugs have an onset of action within minutes and are effective for 4 to 8 hours. They act by stimulating β-adrenergic receptors in the bronchioles, thus producing bronchodilation. They also increase mucociliary clearance.

TABLE 28.6 Drug TherapyQuick Relief vs. Long-

Term Control of Asthma

Quick-Relief (“Rescue”) Medications Bronchodilators Short-acting inhaled β2-adrenergic agonists (e.g., albuterol [Proventil HFA]) Anticholinergics (inhaled) (e.g., ipratropium [Atrovent HFA])∗

Antiinflammatory Drugs Corticosteroids (systemic) (e.g., prednisone)†

Long-Term (“Controller”) Medications Antiinflammatory Drugs Corticosteroids • Inhaled (e.g., fluticasone [Flovent Diskus or HFA]) • Oral (e.g., prednisone) LTMAs (e.g., montelukast [Singulair]) Anti–IgE (omalizumab [Xolair])

Bronchodilators Long-acting inhaled β2-adrenergic agonists (e.g., salmeterol [Serevent]) Long-acting oral β2-adrenergic agonists (e.g., albuterol [VoSpire ER]) Methylxanthines (e.g., theophylline [Theo-24])



Used as alternative if patient has intolerable side effects to albuterol or in ED for severe attacks. † Considered quick-relief drugs when used in a short burst (3–10 days) at the start of therapy or during a period of gradual deterioration. Corticosteroids are not used for immediate relief of an ongoing attack. β2-Adrenergic agonists are useful in preventing bronchospasm triggered by exercise and other stimuli because they prevent the release of inflammatory mediators from mast cells. They do not inhibit the late-phase response of asthma or have antiinflammatory effects. If used often, inhaled β2-adrenergic agonists may cause tremors, anxiety, tachycardia, palpitations, and nausea. Too frequent use of β2-adrenergic agonists indicates poor asthma control, may mask asthma severity, and may lead to reduced drug effectiveness. The use of SABAs should be limited to less than 2 times weekly. SABA inhalers should last for months. SABAs are not to be used for long-term control. They should not be used alone for recurrent, repeated asthma attacks. Use of long-term bronchodilators with inhaled corticosteroids or other drugs can achieve this goal better if prescribed and used properly. LABAs, including salmeterol (Serevent Diskus) and formoterol (Foradil), are effective for 12 hours. LABAs are added to a daily dose of ICSs for long-term control of moderate to severe persistent asthma and prevention of symptoms, particularly at night. When LABAs are added to a patient’s daily regimen of corticosteroids, they decrease the need for SABAs and allow patients to achieve better asthma control with a lower dosage of ICSs. LABAs should never be used alone as asthma therapy. They should only be used if the patient is on an ICS. Tell patients that these drugs should not be used to treat acute symptoms or to obtain quick relief from bronchospasm. Teach the patient that these drugs are used only once every 12 hours. Combination therapy using an ICS and a LABA is available in

several inhalers (e.g., fluticasone/salmeterol [Advair] and budesonide/formoterol [Symbicort]). The combinations are more convenient, improve adherence, and ensure that patients receive the LABA together with an ICS.

Drug Alert β2-Adrenergic Agonists • Use with caution in patients with cardiac disorders. • Both SABAs and LABAs may cause increased BP and heart rate, central nervous system stimulation, and dysrhythmias.

Drug Alert Long-Acting β2-Adrenergic Agonists (LABAs) • Should not be the first or only drug used to treat asthma. • Should be added to the treatment plan only if other controller medicines do not control asthma. • Do not use to treat wheezing that is getting worse. • Always use a SABA to treat sudden wheezing.

Methylxanthines Sustained-release methylxanthine (theophylline) preparations are not a first-line controller medication. They are used only as an alternative therapy. Methylxanthine is a bronchodilator with mild antiinflammatory effects. The exact mechanism of action is unknown. The main problems with theophylline are the high incidence of interaction with other drugs and the side effects. These include

nausea, headache, insomnia, gastrointestinal (GI) distress, tachycardia, dysrhythmias, and seizures. Because theophylline has a narrow margin of safety, monitor serum blood levels regularly to determine if drug levels are within therapeutic range.

Drug Alert Theophylline • Teach patient to report signs of toxicity: nausea, vomiting, seizures, insomnia. • Avoid caffeine to prevent intensifying adverse effects.

Anticholinergic Drugs Anticholinergic drugs affect the muscles around the bronchi (large airways). When the lungs are irritated, these bands of muscle can tighten, causing bronchoconstriction via the parasympathetic nervous system. Anticholinergics work by preventing these muscles from tightening. Consequently, these drugs promote bronchodilation. Anticholinergic drugs are less effective than equivalent doses of SABAs in asthma. However, they are more effective in COPD patients. Therefore short-acting anticholinergic drugs are not used in the routine management of asthma, except for in severe acute asthma attacks.

Antiinflammatory Drugs Corticosteroids Chronic inflammation is a key component of asthma. Corticosteroids are antiinflammatory drugs that reduce bronchial hyperresponsiveness, block the late-phase response, and inhibit migration of inflammatory cells. Corticosteroids are more effective in improving asthma control than any other long-term drug.

To gain prompt control in acute attacks, oral corticosteroids are used. ICSs must be used for 1 to 2 weeks before maximum therapeutic effects can be seen. Some ICSs (e.g., fluticasone, budesonide [Pulmicort Flexhaler]) begin to have a therapeutic effect in 24 hours. Long-term, maintenance doses of oral corticosteroids may be needed to control asthma in patients with severe chronic asthma. ICSs must be used on a fixed schedule.

TABLE 28.7 Drug TherapyAsthma and Chronic

Obstructive Pulmonary Disease (COPD)

When ICSs are used, asthma can usually be controlled without significant systemic side effects since little systemic drug absorption

occurs from these drugs. However, ICSs at the highest dosage levels have been associated with side effects (e.g., easy bruising, decreased bone mineral density). Oropharyngeal candidiasis, hoarseness, and dry cough are local side effects caused by inhalation of corticosteroids. These problems can be reduced or prevented by using a spacer with the metered-dose inhaler (MDI) and by gargling with water or mouthwash after each use. Using a spacer or holding device can help get more medication into the lungs. Women, especially postmenopausal women, who have asthma and use corticosteroids should take adequate amounts of calcium and vitamin D and take part in regular weight-bearing exercise. (Osteoporosis is discussed in Chapter 63.)

Leukotriene Modifiers Leukotrienes are inflammatory mediators produced from arachidonic acid metabolism. They are potent bronchoconstrictors. Some leukotrienes cause airway edema and inflammation, contributing to the symptoms of asthma. Leukotriene modifying agents (LTMAs) block the release of some substances from mast cells and eosinophils, thereby producing both bronchodilator and antiinflammatory effects. LTMAs include leukotriene receptor blockers (zafirlukast [Accolate], montelukast [Singulair]) and leukotriene synthesis inhibitors (zileuton [Zyflo CR]). These drugs interfere with the synthesis or block the action of leukotrienes. LTMAs do not reverse bronchospasm in acute asthma attacks. They are used only for prophylactic and maintenance therapy. One advantage of these drugs is that they are taken orally.

Anti-IgE Omalizumab (Xolair) is a monoclonal antibody to IgE that decreases circulating free IgE levels. Omalizumab prevents IgE from attaching to mast cells, thus preventing the release of chemical mediators. This drug is indicated for patients with moderate to severe asthma, or those not controlled with ICSs alone. Omalizumab is given subcutaneously every 2 to 4 weeks. The drug has a risk for

anaphylaxis, so patients must receive the medication in an HCP’s office where this potential emergency can be treated.

Anti-Interleukin 5 Mepolizumab (Nucala) and reslizumab (Cinqair) are monoclonal antibodies to interleukin-5 (IL-5). IL-5 is a major cytokine involved in the inflammatory response in asthma by promoting eosinophil activity. By inhibiting IL-5, these drugs inhibit the production and survival of eosinophils. They are used for patients who have a history of severe asthma attacks despite using current asthma medication.

Nonprescription Combination Drugs Several nonprescription combination drugs are available OTC. They are usually combinations of a bronchodilator (ephedrine) and an expectorant (guaifenesin). Often patients seek OTC drugs because they are less expensive than prescription medication. Many people consider these drugs safe because they can be obtained without a prescription. In general, they should be avoided due to their potential side effects. Inhalers containing epinephrine may be available. These agents are advertised as drugs to relieve bronchospasm. Those containing ephedrine and epinephrine are potentially dangerous because they stimulate the central nervous and cardiovascular systems, causing nervousness, heart palpitations and dysrhythmias, tremors, insomnia, and increased BP. Many respiratory products containing ephedrine are behind the counter at pharmacies or need a prescription. This limited access is to prevent the diversion of ephedrine to the production of methamphetamine. Many OTC products have been reformulated with phenylephrine, instead of ephedrine, which works well topically but has modest effects in the oral form. It is important to teach patients about the dangers associated with nonprescription combination drugs. These drugs are high risk and possibly unsafe to a patient with underlying heart problems because tachycardia and hypertension often occur. For the patient who insists on taking these drugs, caution them to read and follow the directions

on the label.

Inhalation Devices for Drug Delivery Many asthma drugs are given by inhalation because the onset of action is faster and systemic side effects are reduced. Inhalation devices include MDIs, dry powder inhalers (DPIs), and nebulizers.

Inhalers MDIs are small, hand-held, pressurized devices that deliver a measured dose of drug with each activation. The dosing is usually 1 or 2 puffs. Depending on the specific MDI, a spacer or holding chamber (e.g., AeroChamber, InspirEase [Fig. 28.6]) is used to reduce the amount of drug delivered to the oropharynx and improve the amount of drug delivered to the lungs. Spacers also help people who have hand-breath coordination problems.

FIG. 28.6 Example of an AeroChamber spacer used with a metereddose inhaler. From Potter PA, Perry AG, Stockert P, et al: Fundamentals of nursing, ed 9, St Louis, 2017, Mosby.

TABLE 28.8 Problems Using a Metered-Dose

Inhaler (MDI) • Not coordinating activation with inspiration • Activating MDI in the mouth while breathing through nose • Inspiring too rapidly • Not holding the breath for 10 sec (or as close to 10 sec as possible)

• Holding MDI upside down or sideways • Inhaling more than 1 puff with each inspiration • Not shaking MDI before use (if indicated) • Not waiting enough time between each puff • Not opening mouth wide enough (if using open mouth technique), causing medication to bounce off teeth, tongue, or palate • Not having adequate strength to activate MDI • Not being able to understand and follow directions International law mandates all MDIs have an ozone-friendly propellant that is a hydrofluoroalkane (HFA). This propellant is nontoxic, evaporates almost instantly once it forces medicine out of the MDI canister, and is not harmful to the patient. The number of times an MDI must be primed and the frequency of priming vary widely, so read the package insert with the patient. The patient who needs to use several MDIs is often unclear about the order in which to take the medications. Historically it was recommended that SABAs be used first to open the airway and improve the delivery of subsequent medication. However, this recommendation is not evidence based. It is also a potential source of confusion to patients because SABAs are usually used on an asneeded basis. One of the major problems with metered-dose drugs is the potential for overuse (more than 2 canisters per month) rather than seeking needed medical care (Table 28.8). As the patient has more asthmatic symptoms, they may use the β2-adrenergic agonist MDI much more often. β2-Adrenergic agonists help by relieving bronchospasm. They do not treat the inflammatory response. Therefore teach the patient the correct therapeutic use of these drugs. Another problem is technique. Any MDI is effective only if taken properly. Review MDI technique during each visit as a standard part of care. The patient needs to know the correct way to determine whether the MDI is empty and how to effectively clean and care for

the device (Fig. 28.7).

FIG. 28.7 How to use your metered-dose inhaler correctly.

DPIs are simpler to use than MDIs. The DPI contains dry, powdered

medication and is breath activated (Fig. 28.8). No propellant is used. Instead, an aerosol is created when the patient inhales through a reservoir containing a dose of powder. DPIs have several advantages over MDIs: (1) less manual dexterity is needed, (2) there is no need to coordinate device puffs with inhalation, and (3) no spacer is needed. Disadvantages are that some common drugs are not yet available in DPIs, and the medication may clump if exposed to humidity. Since the medicine is delivered only by the patient’s inspiratory effort, patients with a low FEV1 (less than 1 L) may not be able to inspire the medication. Table 28.9 describes how to effectively use a DPI. Differences between MDIs and DPIs are described in Table 28.10. Aerosolized medication delivery systems, when used with comparable drug doses, provide equivalent efficacy. Therefore patients should use the device best suited to their needs.

Nebulizers Nebulizers are small machines used to convert drug solutions into mists. The mist can be inhaled through a face mask or mouthpiece held between the teeth. Nebulizers are usually used for those who have severe asthma or difficulty with the MDI inhalation. They do not provide better delivery of medication than a spacer with an inhaler. Nebulizers are usually powered by a compressed air or O2 generator. At home, the patient may have an air-powered compressor. In the hospital, wall O2 or compressed air powers the nebulizer. Aerosolized medication orders must include the medication, dose, diluent, and whether it is to be nebulized with O2 or compressed air. The advantage of nebulization therapy is that it is easy to use. Medications that are routinely nebulized include albuterol and ipratropium.

FIG. 28.8 Example of a dry powder inhaler (DPI). From Potter PA, Perry AG, Stockert P, et al: Fundamentals of nursing, ed 9, St Louis, 2017, Mosby.

TABLE 28.9 Patient TeachingHow to Use a Dry

Powder Inhaler (DPI) Include the following instructions when teaching a patient to use a DPI: 1. Remove mouthpiece cap or open the device according to manufacturer’s instructions. Check for dust or dirt. If there is an external counter, note the number of doses left. 2. Load the medicine into the inhaler or engage the lever to allow the medicine to become available. Some DPIs re held upright while loading. Others are held sideways or in a horizontal

position. 3. Do not shake your medicine. 4. Tilt your head back slightly and breathe out, getting as much air out of your lungs as you can. Do not breathe into your inhaler because this could affect the dose. 5. Close your lips tightly around the mouthpiece of the inhaler. 6. Breathe in deeply and quickly. This will ensure that the medicine moves down deeply into your lungs. You may not taste or sense the medicine going into your lungs. 7. Hold your breath for 10 seconds or as long as you can to disperse the medicine into your lungs. 8. If there is an external counter, note the number of doses left. It should be 1 less than the number in step 1 above. 9. Do not keep your DPI in a humid place, such as a shower room, because the medicine may clump. The patient is placed in an upright position that allows for most efficient breathing to ensure adequate penetration and deposition of the aerosolized medication. The patient must breathe slowly and deeply through the mouth and hold each inspiration for 2 to 3 seconds. Deep diaphragmatic breathing helps ensure delivery of the medication. Tell the patient to breathe normally in between large, inhaled breaths. After treatment, have the patient cough effectively. To reduce the potential for bacterial growth, review cleaning procedures for home respiratory equipment with the patient. An effective home-cleaning method is to wash the nebulizer daily in soap and water, rinse it with water, and soak it for 20 to 30 minutes in a 1:1 white vinegar–water solution, followed by a water rinse and air drying.

Patient Teaching Related to Drug Therapy One of the major factors determining success in asthma management is the correct administration of drugs. The drug regimen can be confusing and complex. When teaching patients about their medications, include the name, purpose, dosage, method of

administration, and when to use. It is essential that the patient understand the difference between rescue and controller medications, the importance of monitoring their response to therapy, and, most importantly, when to recognize that symptoms are not improving and help is required. Review side effects, appropriate action if side effects occur, and how to properly prime, use, and clean devices. Some patients may benefit from keeping a diary to record medication use, wheezing, or coughing, PEFR, side effects of drugs, and activity level. This information will help the HCP adjust the medication if needed.

TABLE 28.10 Comparison of Metered-Dose and

Dry Powder Inhalers

Metered-Dose Inhaler (MDI) Shake before use

May be needed for some (e.g., albuterol), but not for others (Read package insert)

Inspiration

Slow

May be used with inhaled corticosteroids or for more effective delivery (Read package insert) Counting device Many have an external device, but some do not

Dry Powder Inhaler (DPI) No Rapid

Spacer

Not used

Inhalations/dose Often 2/dose

Most preloaded forms include counter Often 1/dose

Cleaning

Use water for plastic case

Avoid moisture

Several factors can affect the correct use of inhalation devices. These include advanced age, changes in physical dexterity (e.g., arthritis in hands, coordination), psychologic state (e.g., cognition), affordability, convenience, and administration time and preference. Poor adherence with medication therapy is a major challenge in the long-term management of chronic asthma. Lack of adherence often occurs when the patient is symptom free and does not use the longterm therapy (e.g., ICS) regularly because no immediate benefit is felt.

The patient does not realize that ICSs are needed to treat the ongoing inflammatory process. Explain the importance and purpose of taking the long-term therapy regularly, emphasizing that maximum improvement may take 1 week or longer. Tell the patient that without regular use, swelling in the airways may progress and asthma will likely worsen over time. Collaborate with social services to help lower income patients obtain medications. Make sure that patients understand exactly how to use their inhaler device (Fig. 28.7). Give them printed instructions. At every clinic visit or hospitalization, reassess the patient’s inhaler technique. If package inserts are available, you can review them before teaching the patient.

Nursing Management: Asthma Nursing Assessment If a patient is not in acute distress, obtain a detailed health history, including information about triggers and what has helped alleviate asthma attacks in the past. Subjective and objective data that should be obtained from a patient with asthma are outlined in Table 28.11.

TABLE 28.11 Nursing AssessmentAsthma

Subjective Data Important Health Information Past health history: Allergic rhinitis, sinusitis, or skin allergies. Previous asthma attack and hospitalization or intubation. Symptoms worsened by triggers in the environment. GERD. Occupational exposure to chemical irritants (e.g., paints, dust) Medications: Adherence to medication, inhaler technique. Use of antibiotics. Pattern and amount of short-acting β2-adrenergic agonist used per week. Medications that may trigger an attack in susceptible persons, such as aspirin, NSAIDs, β-adrenergic blockers

Functional Health Patterns Health perception–health management: Family history of allergies or asthma. Recent URI or sinus infection Activity-exercise: Fatigue, decreased or absent exercise tolerance. Dyspnea, cough (especially at night), productive cough with yellow or green sputum or sticky sputum. Chest tightness, feelings of suffocation, air hunger, talking in short sentences or

words or phrases, sitting upright to breathe Sleep-rest: Awakened from sleep because of cough or breathing difficulties, insomnia Coping–stress tolerance: Emotional distress, stress in work environment or home

Objective Data General Restlessness or exhaustion, confusion, upright or forwardleaning body position

Integumentary Diaphoresis, cyanosis (circumoral, nail bed), eczema

Respiratory Nasal discharge, nasal polyps, mucosal swelling. Crackles, decreased or absent breath sounds, and wheezes (inspiratory, expiratory, or both) on auscultation. Hyperresonance on percussion. Sputum (thick, white, tenacious), ↑ work of breathing with use of accessory muscles. Intercostal and supraclavicular retractions. Tachypnea with hyperventilation. Prolonged expiration

Cardiovascular Tachycardia, pulsus paradoxus, jugular venous distention, hypertension or hypotension, premature ventricular contractions

Possible Diagnostic Findings Abnormal ABGs during attacks, ↓ O2 saturation, serum and sputum eosinophilia, ↑ serum IgE, positive skin tests for allergens, chest x-ray showing hyperinflation with attacks, abnormal pulmonary function tests showing ↓ flow rates; FVC, FEV1, PEFR, and FEV1/FVC ratio that improve between attacks and with bronchodilators

Nursing Diagnoses Nursing diagnoses for the patient with asthma may include: • Impaired breathing • Activity intolerance • Anxiety • Lack of knowledge Additional information on nursing diagnoses and interventions is presented in eNursing Care Plan 28.1 on the website for this chapter.

Planning The overall goals are that the patient with asthma will achieve asthma control, as evidenced by (1) minimal symptoms during the day and night, (2) acceptable activity levels (including exercise), (3) maintaining greater than 80% of personal best PEFR, (4) few or no adverse effects of therapy, (5) no acute attacks of asthma, and (6) adequate knowledge to carry out the plan of care.

Nursing Implementation Health Promotion Your role in preventing asthma attacks or decreasing their severity

focuses primarily on teaching both the patient and caregiver. Teach the patient to identify and avoid known personal triggers for asthma (e.g., cigarette smoke, pet dander) and irritants (e.g., cold air, aspirin, foods, cats, indoor air pollution) (Table 28.1). Washing bedclothes in hot water or cooler water with detergent and bleach has some effect on allergen levels. Avoiding furred animals is suggested, but pet allergens are impossible to avoid. Pet allergens can be found in many public areas for months even after removal of the animal. Many people are allergic to cockroach remains and the dried droppings, so measures to avoid or control cockroaches are partly effective in removing allergens. When cold air cannot be avoided, dressing properly with scarves or using a mask helps reduce the risk for an asthma attack. Aspirin and NSAIDs should be avoided if they are known to trigger an attack. Many OTC drugs contain aspirin. Teach the patient to read the labels carefully. Nonselective β-blockers (e.g., propranolol [Inderal]) are contraindicated because they inhibit bronchodilation. Selective βblockers (e.g., atenolol [Tenormin]) should be used with caution. Desensitization (immunotherapy) may be partially effective in decreasing the patient’s sensitivity to known allergens (see Chapter 13). Prompt diagnosis and treatment of URIs and sinusitis may prevent an asthma attack. If occupational irritants are involved, the patient may need to consider changing jobs. Those who are obese often find that weight loss improves asthma control. Encourage the patient to maintain a fluid intake of 2 to 3 L/day, adequate nutrition, and plenty of rest. If exercise is planned or if the patient has asthma only with exercise, the HCP can suggest a medication regimen for pretreatment or long-term control of symptoms to prevent bronchospasm.

Acute Care A major goal in asthma care is to maximize the patient’s ability to safely manage acute asthma using an asthma action plan developed in conjunction with the HCP (Fig. 28.9). Action plans are important for all people with asthma, especially those who have frequent, acute

attacks. They are based on the patient’s asthma symptoms and PEFR. The action plan dictates what symptoms or PEFR necessitates a change in asthma management to gain control. The patient can take 2 to 4 puffs of a SABA every 20 minutes, up to 3 times, as a rescue plan. Depending on the response (e.g., alleviation of symptoms, improved PEFR), continued SABA use and/or oral corticosteroids may be a part of the home management plan. If symptoms persist or if the patient’s PEFR is less than 50% of the personal best, the HCP or emergency medical services must be contacted at once. When the patient is in the health care agency with an acute attack, it is important to monitor the patient’s respiratory and cardiovascular systems. This includes (1) monitoring heart rate and rhythm, respiratory rate and WOB, and BP; (2) monitoring pulse oximetry, PEFR, and ABGs; and (3) auscultating lung sounds.

FIG. 28.9 Asthma action plan. Source: National Heart, Lung, and Blood Institute, Bethesda, MD.

Give drugs as ordered. Louder wheezing may actually occur in airways that are responding to therapy as airflow increases. As improvement continues and airflow increases, breath sounds increase and wheezing decreases. The disappearance of most bronchospasm,

resolution of edema and cellular infiltration of airway mucosa, and the elimination of viscous mucous plugs may take several days to improve. As a result, therapy must be continued even after clinical improvement. Always evaluate the patient’s response to therapy. An important nursing goal during an acute attack is to decrease the patient’s anxiety and sense of panic. Position the patient comfortably (usually sitting, in semi- to high-Fowler’s position) to maximize chest expansion. A calm, quiet, reassuring attitude may help the patient relax. A technique called “talking down” can help the patient remain calm. In talking down, you gain eye contact with the patient. In a firm, calm voice, coach the patient to use pursed-lip breathing. Pursed-lip breathing keeps the airways open by maintaining positive pressure (Table 28.12). Stay with the patient until the respiratory rate has slowed.

TABLE 28.12 Patient TeachingPursed-Lip

Breathing (PLB) Teach the patient how to do PLB using the following guidelines: 1. Use PLB before, during, and after any activity causing you to be short of breath. 2. Inhale slowly and deeply through the nose. 3. Exhale slowly through pursed lips, as if whistling. 4. Relax your facial muscles without puffing your cheeks—like whistling—while you are exhaling. 5. Make breathing out (exhalation) 3 times as long as breathing in (inhalation). 6. The following activities can help you get the “feel” of PLB: • Blow through a straw in a glass of water with the intent of forming small bubbles. • Blow a lit candle enough to bend the flame without blowing it out. • Steadily blow a table-tennis ball across a table.

• Blow a tissue held in the hand until it gently flaps. 7. Practice 8-10 repetitions of PLB 3 or 4 times a day. When the acute attack subsides, provide rest and a quiet, calm environment. When the patient is less exhausted, can breathe easier, and beginning to recover, try to obtain a health history and do a physical assessment. If caregivers are present, they may be able to provide information about the patient’s health history. This information is important in planning and implementing an individualized nursing care plan.

Ambulatory Care Control of symptoms can be achieved by teaching the patient about drug therapy and monitoring. Review the written asthma action plan. As part of the plan, the patient must measure PEFR at least daily. PEFR monitoring, when done correctly, is a reliable, objective measurement of asthma control (Table 28.13). Some patients may not perceive changes in their breathing and may have a significant decrease in lung function without any symptoms other than a change in PEFR.

TABLE 28.13 Patient TeachingHow to Use Your

Peak Flow Meter Include the following instructions when teaching the patient to use a peak flow meter:

Why Use a Peak Flow Meter? • Peak flow meters are used to check your asthma the way that BP cuffs are used to check BP. A peak flow meter is a device that measures how well air moves out of your lungs. • During an asthma episode, the airways of the lungs usually begin to narrow slowly. The peak flow meter may tell you if there is

narrowing in the airways hours, sometimes even days, before you have any asthma symptoms. • By taking your medicines early (before symptoms), you may be able to stop the episode quickly and avoid a severe asthma episode. • The peak flow meter is used to help you and your HCP: • Learn what makes your asthma worse. • Decide if your treatment plan is working well. • Decide when to add or stop medicine. • Decide when to seek emergency care.

How to Use Your Peak Flow Meter Complete the following 5 steps with your peak flow meter: 1. Move the indicator to the bottom of the numbered scale. 2. Stand up. 3. Take a deep breath, filling your lungs completely. 4. Place the mouthpiece in your mouth and close your lips around it. Do not put your tongue inside the hole. 5. Blow out as hard and fast as you can in a single blow. • Write down the number you get. But if you cough or make a mistake, do not write down the number. Perform the action again. • Repeat steps 1 through 5 two more times. Write down the best of the 3 blows in your asthma diary.

Find Your Personal Best Peak Flow Number • Your personal best peak flow number is the highest peak flow number you can achieve over a 2-week period when your asthma is under good control. Good control is when you feel good and do not have any asthma symptoms. • Each patient’s asthma is different. Your best peak expiratory flow

rate (PEFR) may be higher or lower than the peak flow of someone of your height, weight, and gender. This means that it is important for you to find your own personal best peak flow number, which is the basis for your treatment plan. • To find your personal best peak flow number, take peak flow readings: • At least twice a day for 2-3 weeks, between 12 noon and 2 PM when your peak flow is the highest • 15 to 20 minutes after taking inhaled short-acting β2agonist (SABA) for quick relief • As instructed by your HCP

The Peak Flow Zone System Once you know your personal best peak flow number, your HCP will put the peak flow numbers into zones that are set up like a traffic light. This will help you know what to do when your peak flow number changes. For example: ▪Green Zone (more than __L/min [80% of your personal best number]) signals good control. No asthma symptoms are present. Take your medicines as usual. ▪Yellow Zone (between __ and __L/min [50% to 40 in (102 cm)

Respiratory Increased work of breathing; wheezing; rapid, shallow breathing

Cardiovascular Hypertension, tachycardia, dysrhythmias

Musculoskeletal Decreased joint mobility and flexibility; knee, hip, and low back pain

Reproductive

Gynecomastia and hypogonadism in men

Possible Diagnostic Findings Elevated serum glucose, cholesterol, triglycerides; chest x-ray showing enlarged heart; ECG showing dysrhythmia; abnormal liver function test results When assessing a person who is overweight or obese, be sensitive and nonjudgmental in asking specific and leading questions about weight, diet, and exercise (Table 40.4). In doing so, you can often obtain information that the patient may have withheld out of embarrassment or shyness. Patients need to understand the reason for questions asked about weight or dietary habits. You must be ready to respond to their concerns.

Check Your Practice You are working in the hypertension clinic, and the provider has asked you to do an assessment on a 54-yr-old man for referral to a weight loss program. He is 5 ft, 9 in and weighs 242 lb. His BP has been hard to control with drugs and diet. While you are trying to do an assessment (using the questions in Table 40.4), he interrupts you and asks you if he can leave. He angrily tells you, “I do not want to give up my favorite foods, quit drinking, or exercise. Do you understand that?” • How would you respond to him? Assess a patient’s willingness to change and potential for change. If people are not ready for change, offer them the opportunity to return for further discussion when they are ready to discuss their weight again and make lifestyle changes.

When obtaining the history, explore genetic and endocrine factors, such as hypothyroidism, hypothalamic tumors, Cushing syndrome, hypogonadism in men, and polycystic ovary syndrome in women. Laboratory tests of liver function and thyroid function, a fasting glucose level, and a lipid panel (triglyceride level, LDL and HDL cholesterol levels) aid in evaluating the cause and effects of obesity. When no organic cause (e.g., hypothyroidism) is associated with obesity, the disorder should be considered a chronic, complex disease. Assess for any co-morbid diseases associated with obesity (e.g., hypertension, sleep apnea). These obesity-related complications require special treatment.

TABLE 40.4 Assessing Patients With Obesity When assessing patients with obesity and before selecting a weight loss strategy, ask the following questions: • What is your history with weight gain and weight loss? • Are other family members overweight? • How has your body weight affected your health? • What do you think contributes to your weight? • What does food mean to you? How do you use food (e.g., to relieve stress, provide comfort)? • Describe your motivation for losing weight. • What have you already tried to lose weight? Was it successful? If not, why not? • Would you like to manage your weight differently? If so, how? • What sort of barriers do you think impede your weight loss efforts? • Are there any major stresses that will make it hard to focus on weight control? • How much time can you devote to exercise on a daily or weekly basis?

• Describe the support you have from family and/or friends for losing weight. As part of the initial nursing physical examination, assess each body system with particular attention to the organ system in which the patient has expressed a problem or concern. Measurements used with the obese person may include height (without shoes), weight (obtain in a private location and in a gown, if possible), waist circumference, and BMI. Have the right equipment to take these measurements. Provide special chairs, examination tables, and scales that can accommodate an obese person.

Classifications of Body Weight and Obesity An important part of your patient assessment is to determine and classify a patient’s body weight. Common assessment methods include BMI, waist circumference, waist-to-hip ratio (WHR), and body shape. The most widely used and endorsed measures are BMI and waist circumference. These measures are cost-effective, reliable, and easily used in all practice settings.

Body Mass Index The most common measure of obesity is the body mass index (BMI). BMI is calculated by dividing a person’s weight (in kilograms) by the square of the height in meters (Fig. 40.6). Table 40.5 shows the classification of overweight and obesity by BMI. Persons with a BMI less than 18.5 kg/m2 are considered underweight. A BMI between 18.5 and 24.9 kg/m2 reflects a normal body weight. A BMI of 25 to 29.9 kg/m2 is classified as being overweight. Those with values at 30 kg/m2 or above are considered obese. The term extreme obesity (morbid or severe obesity) is used for those with a BMI greater than 40 kg/m2.

FIG. 40.6 Body mass index (BMI) chart. Healthy weight: BMI 18 to 24.9 kg/m2; overweight: BMI 25 to 29.9 kg/m2; obesity: BMI 30 kg/m2. BMI = weight (kg)/height (m2).

TABLE 40.5 Classification of Overweight and

Obesity

Source: National Heart, Lung, and Blood Institute: Classification of overweight and obesity by BMI, waist circumference, and associated disease risks. Retrieved from www.nhlbi.nih.gov/health/public/heart/obesity/lose_wt/bmi_dis.htm. Though BMI provides an overall assessment of fat mass, we must consider BMI in relation to the patient’s age, gender, and body build. For example, a body builder may have a BMI associated with obesity, but because of a high muscle mass, the BMI would not be an accurate assessment. In contrast, in those who have lost body mass (e.g., older adults), the BMI would underestimate the degree of obesity. For this reason, other measures must be combined with the BMI for an accurate evaluation of a person’s weight.

Waist Circumference Waist circumference is another way to assess and classify a person’s weight. The average waist size has increased by more than 1 inch (from 37.6 inches to 38.8 inches) in the past decade. Health risks increase if the waist circumference is greater than 40 inches in men and greater than 35 inches in women.9 People who have visceral fat with android obesity have an increased risk for CVD and metabolic syndrome (discussed later in this chapter).

Waist-to-Hip Ratio The waist-to-hip ratio (WHR) is another method used to assess obesity. This ratio describes the distribution of both subcutaneous and visceral adipose tissue. Calculate the WHR by dividing the waist measurement by the hip measurement. A WHR less than 0.8 is best. A WHR greater than 0.8 indicates more truncal fat, which puts a person at a greater risk for health complications.

Body Shape Body shape is another way of identifying those who are at a higher risk for health problems (Table 40.6). People with fat primarily in the abdominal area, an apple-shaped body, have android obesity. Those with fat distribution in the upper legs, a pear-shaped body, have gynoid obesity. Genetics has an important role in determining a person’s body shape and weight.

Nursing Diagnoses Nursing diagnoses for the patient with obesity may include: • Obesity • Activity intolerance • Impaired physical mobility • Disturbed body image

Planning The overall goals are that the obese patient will (1) modify eating patterns, (2) take part in a regular physical activity program, (3) achieve and maintain weight loss to a specified level, and (4) minimize or prevent health problems related to obesity.

Nursing Implementation Obesity is one of the most challenging health problems. For most

patients, successful weight management will be a hard, lifelong project. Obesity treatment begins with patients understanding their weight history and deciding on a plan that is best for them. It is rare to find an obese person who has not tried to lose weight. Some people have met with limited and temporary success, and others have met only with failure.

TABLE 40.6 Relationship Between Body Shape

and Health Risks

You are in a key position to help obese patients by (1) helping them explore and deal with their negative experiences and (2) teaching other health professionals about stigma and biases experienced by obese patients. Although health care for obese people has greater demands, HCPs often do not address these needs. HCPs are often reluctant to counsel patients about obesity for a variety of reasons,

including (1) time constraints during appointments make it hard, (2) weight management may be viewed as professionally unrewarding, (3) reimbursement for weight management services is hard to obtain, and (4) many HCPs do not feel knowledgeable about giving weight loss advice. Despite knowing benefits of weight loss, most people find the process tough. Achieving an “ideal” BMI is not necessary and may not be a realistic goal. Modest weight loss of even 3% to 5% of starting weight can have clinical benefits, and greater weight losses produce greater benefits.10 In general, the average weight loss program (except for bariatric surgery) results in a 10% reduction of body weight. This average should not be considered a failure since it is associated with significant health benefits.10 Exploring a person’s motivation for weight loss is essential for overall success. Using principles from motivational interviewing (see Chapter 4), you can help patients understand their desire to lose weight and gain confidence in achieving weight loss. Focusing on the reasons for wanting to lose weight may help patients develop strategies for a weight loss program. Any supervised plan of care must be directed at 2 different processes: (1) successful weight loss, which requires a short-term energy deficit, and (2) successful weight control, which requires long-term behavior changes. Together with other members of the interprofessional care team, you have a key role in planning for and managing the care of an obese patient. A holistic approach for weight loss must be used that includes nutritional therapy, exercise, behavior modification, and, for some, drugs or surgical intervention (Table 40.7). Combining more than one aspect supports more effective weight loss and weight control efforts. While teaching patients, stress healthy eating habits and adequate physical activity as lifestyle patterns to develop and maintain.

Promoting Population Health Maintaining a Healthy Weight

• Weigh yourself regularly. • Consume 5 or more servings of fruits and vegetables daily. • Choose whole grain foods, such as brown rice and whole wheat bread. • Avoid highly processed foods made with refined white sugar, flour, and saturated fat. • Avoid foods that are high in “energy density” or have a lot of calories in a small amount of food. • Take part in physical activity: • 150 minutes of moderate-intensity aerobic activity (i.e., brisk walking) every week • Muscle-strengthening activities on 2 or more days a week

Nutritional Therapy There are no “magic” diets for weight loss. No one diet is superior for weight loss. All diets can work if they reduce caloric intake compared to expenditure and are one to which the patient will adhere.11 The ability to adhere to a diet and degree of weight loss strongly depends on the patient’s motivation. Restricting dietary intake so that it is below energy requirements is a cornerstone for any weight loss or maintenance program. Table 40.8 presents an example of a 1200calorie diet. It is best to recommend a dietary approach in which calorie restriction includes all food groups. In general, recommend a diet that includes adequate amounts of fruits and vegetables, gives enough bulk to prevent constipation, and meets daily vitamin A and vitamin C requirements. Lean meat, fish, and eggs provide sufficient protein and the B-complex vitamins. Patients will find it easier to incorporate such a change into their lifestyle and not become as bored with their food options.

TABLE 40.7 Interprofessional Care

Obesity

Diagnostic Assessment • History and physical examination • Family history • BMI, waist circumference, waist-to-hip ratio • Assessment of health risks and co-morbidities

Management • Management of co-morbidities • Lifestyle interventions • Taking part in weight loss program • Support groups • Behavior modification • Nutritional therapy • Exercise • Behavior modification • Support groups • Drug therapy (Table 40.9) • Surgical therapy (Table 40.10) A very-low-calorie diet plan that limits calories to a total of 800 or less per day may be prescribed if rapid weight loss is needed.11 These diets are not sustainable on a long-term basis. They should be provided only by trained professionals in a medical care setting. Persons on very-low-calorie diets need frequent professional monitoring because the severe energy restriction places them at risk for multiple health complications. Many people try to lose weight by following one of the many fad diets that offer the enticement of quick weight loss with little effort. Often, these quick weight-reduction diets (found in the popular media) advocate eliminating one category of foods (e.g., carbohydrates). Therefore these should be discouraged. Low-

carbohydrate diets do produce a rapid weight loss but reduce the ability to get adequate amounts of fiber, vitamins, and minerals. Restrictive diets are hard to maintain on a long-term basis. The more restrictive the diet, the greater the demand for intense discipline in the face of an intense desire to eat foods not allowed on the diet. The degree of success of any diet depends in part on the amount of weight to be lost. A moderately obese person will obviously reach a weight goal more easily than a person with extreme obesity. Because men have a higher percent of lean body mass, they are often able to lose weight more quickly than women. Women have a higher percent of body fat, which is metabolically less active than muscle tissue. Postmenopausal women are particularly prone to weight gain, especially increased abdominal fat.

TABLE 40.8 Nutritional Therapy

1200-Calorie–

Restricted Weight-Reduction Diet

General Principles 1. Eat regularly. Do not skip meals. 2. Measure foods to determine the correct portion size. 3. Avoid concentrated sweets, such as sugar, candy, honey, pies, cakes, cookies, and regular sodas. 4. Reduce fat intake by baking, broiling, or steaming foods. 5. Maintain a regular exercise program for successful weight loss.

Sample Meal Plan

Setting a realistic and healthy goal, such as losing 1 to 2 lb per week, should be mutually agreed on at the beginning of a weight loss program. Trying to lose too much too fast usually results in a sense of frustration and failure for the patient. You can help patients understand that losing large amounts of weight in a short period causes skin and underlying tissue to lose elasticity and tone. Slower weight loss offers better cosmetic results. Inevitably, the patient reaches plateau periods during which no weight is lost. These plateaus may last from several days to several weeks. Remind the patient that plateaus are normal occurrences during weight reduction. A weekly check of body weight is a good method of monitoring progress. Daily weighing is not recommended because of fluctuations that result from retained water (including urine) and feces. Teach the patient to record the weight at the same time of the day, wearing the same type of clothing.

Evidence-Based Practice Obesity Interventions and Faith-Based Organizations

J.W. is a 39-yr-old black woman who is 5 ft, 6 in tall and weighs 196 lb. You work in the clinic that she visits for health care. Your clinic is referring patients who would benefit from losing weight to community and hospital-based weight loss programs. She tells you she has been trying to lose weight by “watching what she eats” and that she is “not sure what else she can do.” In further talks with her, you learn she is an active member of her neighborhood church.

Making Clinical Decisions Best Available Evidence. Obesity is highest among racial and ethnic minority groups in the United States. Many faith-based organizations (FBOs) provide programs that have helped obese persons improve weight-related behaviors (e.g., increase in physical activity and fruit and vegetable intake) and lose weight. Successes in these programs have been more notable for females. Overall, programs that offer comprehensive and intensive behavioral interventions for weight loss are an option for weight management. Clinician Expertise. You know it is important for J.W. to engage in a weight loss program that will help her to adopt and maintain healthy behaviors. You also know that FBOs can play a major role in providing health promotion programs in the black community. Patient Preferences and Values. J.W. says she is interested in learning about a weight loss program at her church.

Implications for Nursing Practice 1. Why is it important to discuss with J.W. her motivation for starting a weight loss program at her church? 2. How will you help J.W. to set realistic short- and long-term goals related to weight loss? How may these goals differ? 3. At each clinic visit, how will you support J.W.’s efforts to lose weight?

References for Evidence Lv N, Azar K.M, Rosas L.G, et al. Behavioral lifestyle interventions for moderate and severe obesity: a systematic review. Prev Med. 2017;100:180. Tucker C.M, Wippold G.M, Williams J.L, et al. A CBPR study to test the impact of a church-based health empowerment program on health behaviors and health outcomes of black adult churchgoers. J Racial Ethn Health Disparities. 2017;4:70. There is no clear consensus on the number of meals a person on a diet should eat. Some advocate several small meals per day because the body’s metabolic rate is temporarily increased right after eating. However, patients eating several small meals a day might consume more calories unless they carefully adhere to portion sizes and total daily calorie allotment. When a person first starts a weight loss program, food portion sizes must be carefully determined to stay within the dietary guidelines. Portion sizes over the past 40 years have increased considerably (Table 40.2). Food portions can be weighed using a scale, or everyday objects can be used as a visual cue to determine portion sizes. The size of a woman’s fist or a baseball is equivalent to a serving of vegetables or fruit. The recommended portion size of meat is 3 oz. This is about the size of a person’s palm or a deck of cards. A serving of cheese is about the size of a thumb or 6 dice. The standard size for chopped vegetables is ½ cup, according to MyPlate guidelines (see Table 39.9). A portion size quiz is available at www.nhlbi.nih.gov/health/educational/wecan/eat-right/portiondistortion.htm. Another aspect of the American diet to consider is which foods contribute the most calories—animal sources, fruits, grains, or vegetables. Two thirds or more of a person’s diet should be plantsource foods, and the other one third or less should be from animal protein. Being aware of personal consumption habits and striving for the two-thirds to one-third ratio is a simple goal that one can achieve

without weighing and measuring foods at every meal. Once this ratio is part of meal planning, the patient can gradually reduce portions as they gradually increase activity levels to achieve healthy weight loss. A list of healthy or low-calorie foods serves as a good reference and allows the patient to dine out on occasion. Furthermore, the patient who carefully follows the prescribed diet may not need to take vitamin supplements. Encourage the appropriate fluid intake in the form of water. Alcoholic and sugary beverages should be limited or avoided, since they increase caloric intake and are low in nutritional value.

Exercise Exercise is an essential part of a weight loss program. Patients should exercise daily, preferably 30 minutes to an hour, with a goal of more than 10,000 steps per day.11 There is no evidence that increased activity promotes an increase in appetite or leads to dietary excess. In fact, exercise has the opposite effect. The addition of exercise results in more weight loss than dieting alone and has a favorable effect on body fat distribution. The type of exercise (e.g., high intensity versus low intensity) does not seem to affect overall weight loss. More intensive activity may result in weight loss with a reduced time commitment, making it preferable to some people. Exercise is especially important in supporting weight loss. Higher levels of physical activity, 200 to 300 minutes per week, are recommended to maintain weight loss or minimize weight regain in the long term.11 Explore ways to incorporate exercise in daily routines. It may be as simple as parking farther from their place of employment or taking the stairs versus an elevator. Encourage a person to use a pedometer to track progress toward meeting the 10,000 steps a day goal. However, success may be walking one third of the recommended steps with incremental increases over time. Patients can swim and cycle, which both have long-term benefits. Joining a health club can be another way of getting exercise. Stress to patients that engaging in weekend exercise only or in spurts of strenuous activity is not helpful

and can be dangerous.

Behavior Modification The assumptions behind behavior modification are: (1) obesity is a learned disorder caused by overeating and (2) often the critical difference between an obese person and a person of normal weight is the cues that regulate eating behavior. Therefore most behaviormodification programs deemphasize the diet and focus on how and when to eat. Ideally, behavior intervention should begin with counseling sessions with a trained interventionist. Persons who are in a behavioral therapy program are more successful in maintaining their losses over an extended time than those who do not take part in such training.12 Various behavioral techniques for patients engaged in a weight loss program include (1) self-monitoring, (2) stimulus control, and (3) rewards. Self-monitoring may involve keeping a record of the type and time food was consumed, what the person was doing, and how the person was feeling when eating. By looking at the cues and events before eating, the person can identify areas in which to make behavior changes to break the chain of events and prevent overeating. These eating behaviors must be changed, or any weight loss will only be temporary. Stimulus control is aimed at eliminating cues in the environment that trigger eating. For example, if the patient overeats while watching television, limiting eating to a certain area (e.g., kitchen table) can be an effective way to weaken the link between eating and television watching. The more often the person does not eat in front of the television, the less likely television watching will trigger overeating. Rewards may be incentives for weight loss. Short- and long-term goals are useful benchmarks for earning rewards. It is important that the reward for a specified weight loss not be associated with food, such as dinner out or a favorite treat. Reward items do not need to have a monetary component. For example, time for a hot bath or an hour of pleasure reading would be an enjoyable reward for many people. Praise your patient’s successes, even small ones, at every

opportunity. Changing existing behaviors is hard.

Support Groups People who are on a weight management plan are often encouraged to join a group in which others are also trying to change their eating habits. Many self-help groups offer support and information on dieting tips. For example, Take Off Pounds Sensibly (TOPS) (www.tops.org) is the oldest nonprofit organization of this type. Behavior modification is an integral part of the program, along with nutrition education. Weight Watchers International (www.weightwatchers.com), Jenny Craig (www.jennycraig.com), and Nutrisystem (www.nutrisystem.com) are probably the most successful commercial weight-loss programs.13 Weight Watchers offers a food plan that is nutritionally balanced and practical to follow. Group leaders, all of whom have successfully lost weight with Weight Watchers, teach members various behavior-modification techniques. There are many commercial weight-reduction centers. Most programs are staffed by nurses and dietitians. These weight-reduction centers are cost prohibitive for those with limited financial resources. Most programs offer special prepackaged foods and supplements that a person must buy as part of the weight-reduction plan. The person only consumes these prescribed foods and drinks until an agreed-on amount of weight is lost. The person is encouraged to buy the same type of foods for the maintenance phase of the program, lasting from 6 months to 1 year. Behavior-modification training is part of these programs. People must learn how to adjust their diet once they are no longer using the commercial products. This can be challenging for many. The person may regain weight lost once the restricted food program is completed.13 In recent years, many employers have begun weight loss programs at the workplace. The reason for such programs is that better health repays the cost of the programs through improved work performance, decreased absenteeism, less hospitalization, and lower insurance costs. Both employees and employers report benefiting from such programs.

Drug Therapy Drugs should never be used alone. Rather, drugs should be part of a comprehensive weight loss program that includes reduced-calorie diet, exercise, and behavior modification. They should be reserved for adults with a BMI of 30 kg/m2 or greater (obese) or adults with a BMI of 27 kg/m2 or greater (overweight) who have at least 1 weight-related condition, such as hypertension, type 2 diabetes, or dyslipidemia.10,14 There are currently 5 obesity drugs for long-term management approved by the FDA (Table 40.9).

Appetite-Suppressing Drugs Sympathomimetic amines suppress appetite by increasing the availability of norepinephrine in the brain, thus stimulating the CNS. Sympathomimetics fall into 2 groups: amphetamines and nonamphetamines. Amphetamines have a much higher abuse potential than nonamphetamines. The FDA does not recommend or approve amphetamines for either short- or long-term weight loss. We usually do not use nonamphetamines for weight loss because of the potential for abuse. If used, they should be used only short term (for 3 months or less). These drugs include phentermine (Adipex, Lomaira, Suprenza), diethylpropion (Tenuate), and phendimetrazine (Bontril). Adverse effects include palpitations, tachycardia, overstimulation, restlessness, dizziness, insomnia, weakness, and fatigue.

Nursing Interventions Related to Drug Therapy Drugs will not cure obesity. People must understand that without substantial changes in food intake and increased physical activity, they will gain weight when drug therapy is stopped. As with any drug treatment, there are side effects (Table 40.9). Careful evaluation for other medical conditions can help determine which drugs, if any, would be advisable for a given patient. Many insurance companies do not cover the cost of weight loss drugs. Your role related to drug therapy is to teach the patient about

proper administration, side effects, and how the drugs fit into the overall weight loss plan. Changing drug dosages without consultation with the HCP can have detrimental effects. Stress that diet and exercise plans are the cornerstones of permanent weight loss. Finally, discourage patients from buying over-the-counter diet aids unless recommended by an HCP.

Bariatric Surgical Therapy Bariatric surgery, surgery on the stomach and/or intestines to help a person with extreme obesity lose weight, has become a viable option for treating obesity. Surgery is currently the only treatment that has a successful and lasting impact for sustained weight loss for those with extreme obesity.15 Criteria guidelines for bariatric surgery include having a BMI of 40 kg/m2 or more or a BMI of 35 kg/m2 or more with other significant comorbidities (e.g., hypertension, type 2 diabetes, heart failure, sleep apnea).

TABLE 40.9 Drug TherapyObesity

Most people who undergo bariatric surgery successfully improve their overall quality of life. In addition to losing weight, outcomes include improved glucose control with improvement or reversal of diabetes, normalization of BP, decreased total cholesterol and triglycerides, decreased GERD, and decreased sleep apnea.16 Insurance coverage for bariatric surgery varies. Those who cover surgery often require extensive documentation. This often includes taking part in a supervised weight loss program for around 6 months and a psychologic evaluation. Although overall mortality is very low, several complications can arise from surgery. Therefore, having surgery is carefully considered. Candidates for surgery must be screened for psychologic, physical, and behavioral conditions that have been associated with poor surgical outcomes. These include untreated depression, binge eating disorders, and drug and alcohol abuse that may interfere with a commitment to lifelong behavioral changes. Other contraindications to surgery include illnesses that are known to reduce life expectancy and are not likely to improve with weight reduction. These include advanced cancer; end-stage kidney, liver, and cardiopulmonary disease; severe coagulopathy; or inability to follow nutritional recommendations.

Bariatric surgeries fall into 1 of 3 broad categories: restrictive, malabsorptive, or a combination of malabsorptive and restrictive (Table 40.10 and Fig. 40.7). In restrictive procedures, the stomach is reduced in size (less food eaten). In malabsorptive procedures, the small intestine is shortened or bypassed (less food absorbed). Most procedures are done laparoscopically. These patients have fewer wound infections, shorter hospital stays, and a faster recovery period.

Restrictive Surgeries Restrictive bariatric surgery reduces either the size of the stomach, which causes the patient to feel full more quickly, or the amount allowed to enter the stomach. In these surgeries, digestion is not altered, so the risk for anemia or cobalamin deficiency is low. The most common restrictive surgeries include adjustable gastric banding and sleeve gastrectomy.

Adjustable Gastric Banding Laparoscopic adjustable gastric banding (AGB) involves limiting the stomach size with an inflatable band placed around the fundus of the stomach (Fig. 40.7, A). This restrictive procedure can be done using a Lap-Band or Realize Band system. The band is connected to a subcutaneous port that can be inflated or deflated (by fluid injection in the HCP’s office) to change the stoma size to meet the patient’s needs as weight is lost. The restrictive effect of the band creates a sense of fullness as the upper part of the stomach now accommodates less than the average stomach. The band then causes a delay in stomach emptying, providing patients with further satiety. The procedure can be either modified or reversed at a later date, if needed. AGB is the preferred option for patients who are surgical risks because it is a less invasive approach. Because it is restrictive only, patients must follow a strict diet to lose weight and not regain weight.

Sleeve Gastrectomy (Gastric Sleeve)

In the sleeve gastrectomy (gastric sleeve), about 75% of the stomach is removed, leaving a sleeve-shaped stomach (Fig. 40.7, B). Although the stomach is drastically reduced in size, its function is preserved. Removing most of the stomach results in the elimination of hormones made in the stomach that stimulate hunger, such as ghrelin. Research is ongoing on a new procedure called endoscopic sleeve gastroplasty. It involves using an endoscope rather than making a surgical incision. When the endoscope reaches the stomach, the surgeon places sutures in the stomach, making it smaller and changing its shape.

Gastric Plication Gastric plication is a minimally invasive weight-loss surgery that reduces the size of the stomach. It is done by folding the stomach wall inward, and then sutures are placed to secure the folded stomach wall. This reduces the stomach volume by as much as 70%. An advantage is reversibility, since there is no gastric resection.

TABLE 40.10 Surgical Therapy for Obesity

Intragastric Balloons Intragastric balloon weight-loss systems use a gastric balloon to occupy space in the stomach. The balloon does not change or alter the

stomach’s natural anatomy. It is designed to help patients feel more full, curb the appetite, and reduce food intake. Patients should follow a diet and exercise plan to help with weight loss efforts. The balloons are less invasive than having gastric bypass surgery. Most are placed endoscopically, while the patient is under mild sedation. The HCP places the balloon into the stomach through the mouth. Once in place, the balloon is filled with saline so that it expands. The balloon can be filled with different amounts of saline (from 400 to 700 mL).

FIG. 40.7 Bariatric surgical procedures. A, Adjustable gastric banding (AGB) uses a band to create a gastric pouch. B, Sleeve gastrectomy involves creating a sleeve-shaped stomach by removing about 75% of the stomach. C, Biliopancreatic diversion (BPD) with duodenal switch procedure creates an anastomosis between the stomach and intestine. D, Roux-en-Y gastric bypass procedure involves constructing a gastric pouch whose outlet is a Y-shaped limb of small intestine.

With newer balloons, the patient swallows the balloon in a capsule that is attached to a microcatheter. The balloon is inflated with nitrogen gas through the microcatheter. After inflation, the catheter is detached and removed, leaving the balloon in the stomach.17 When it is time to remove a balloon, it is first deflated and then removed using another endoscopic procedure.

Balloons should not be used in patients who have had gastrointestinal or bariatric surgery or who have inflammatory bowel disease, large hiatal hernia, delayed gastric emptying, or active Helicobacter pylori infection. Patients may have vomiting, nausea, abdominal pain, and feelings of indigestion. Other potential risks are gastric ulcers and balloon deflation.

Combination of Restrictive and Malabsorptive Surgery Roux-en-Y Gastric Bypass The Roux-en-Y gastric bypass (RYGB) procedure is a combination of restrictive and malabsorptive surgery. This surgical procedure is the most common bariatric procedure done in the United States. It is considered the gold standard among bariatric procedures. Overall, it has low complication rates, has excellent patient tolerance, and sustains long-term weight loss. The RYGB involves creating a small gastric pouch and attaching it directly to the small intestine using a Y-shaped limb of the small bowel (Fig. 40.7, D). After the procedure, food bypasses 90% of the stomach, the duodenum, and a small segment of jejunum. A complication of the RYGB is dumping syndrome, in which gastric contents empty too rapidly into the small intestine, overwhelming its ability to digest nutrients. Symptoms can include vomiting, nausea, weakness, sweating, faintness, and, on occasion, diarrhea. Patients are discouraged from eating sugary foods after surgery to avoid dumping syndrome. Because sections of the small intestine are bypassed, poor absorption of iron can cause iron-deficiency anemia. Patients need to take a multivitamin with iron and calcium supplements. Chronic anemia caused by cobalamin deficiency may occur. This problem can usually be managed with parenteral or intranasal cobalamin.

Implantable Gastric Stimulation An implantable gastric stimulation device (e.g., Maestro Rechargeable

System) consists of a pacemaker-like electrical pulse generator, wire leads, and electrodes that are implanted in the abdomen (Fig. 40.8). The Maestro System works by sending intermittent electrical pulses to the vagus nerve, which is involved in regulating stomach emptying and signaling to the brain that the stomach feels empty or full. External controllers allow the patient to charge the device and allow HCPs to adjust the device’s settings to provide optimal therapy. Adverse events include nausea, heartburn, problems swallowing, belching, and chest pain.

FIG. 40.8 The Maestro Rechargeable System is an electrical stimulator that is surgically implanted into the abdomen. It works by sending intermittent electrical pulses to the vagus nerve, which is involved in regulating stomach emptying and signaling to the brain that the stomach feels empty or full.

Nursing Management: Perioperative Care of The Obese Patient Nursing Implementation This section discusses general nursing considerations for the care of the obese patient who is having surgery. Special nursing considerations are described for the patient who is having bariatric surgery (Table 40.11). See Chapters 17 through 19 for more on care of the surgical patient.

Preoperative Care Special considerations are needed for the obese patient, especially the patient with extreme obesity, who is having surgery. Before surgery, interview the patient to identify past and current health information and any assistive devices currently in use (e.g., continuous positive airway pressure [CPAP] for sleep apnea). Co-morbidities related to obesity increase the risk for complications in the perioperative period. You may need to coordinate care with the patient’s specialists. Have a plan in place before the patients arrive so that they receive optimal care and do not feel like they are a burden to the nursing staff. You must have available appropriate-size hospital gowns, beds that accommodate an increased body size, and necessary patient transfer equipment. A larger BP cuff size is needed to avoid measurement errors. Ensure that an oversized BP cuff is available and placed in the patient’s room. Consider how the patient will be weighed and transported throughout the hospital. A wheelchair with removable arms that is large enough to safely accommodate the patient and pass easily through doorways should be available. You may need to use alternative assessment techniques to perform assessment of heart, lung, and bowel sounds. For example, because of the large chest wall, breath and heart sounds are often distant. You can use an electronic stethoscope to amplify lung, heart, and bowel sounds.

Teach the patient proper coughing and deep breathing techniques and methods of turning and positioning to prevent pulmonary complications after surgery. If possible, show how to use a spirometer before surgery. Spirometer use helps prevent and treat postoperative lung congestion. Practicing these strategies preoperatively can help the patient perform them correctly postoperatively. If the patient uses CPAP at home for sleep apnea, make arrangements for the use of a machine while the patient is hospitalized.

TABLE 40.11 Nursing ManagementCare of the

Patient Undergoing Bariatric Surgery

Preoperative • Assess for use of assistive devices. Note any physical limitations or mobility issues. • Perform baseline assessment, including vital signs, pulse oximetry, height, weight, BMI, skin condition, nutrition status, and heart, lung, and bowel sounds. • Assess baseline laboratory values and diagnostic test results (e.g., pulmonary function tests). • Teach patient and caregiver about procedure and postoperative care. Review proper coughing and deep breathing techniques, incentive spirometer use, and methods of turning and positioning to prevent pulmonary complications. • Explain the need for frequent assessment and interventions to prevent VTE. • Have available proper-sized hospital gowns, beds, BP cuffs, and transfer equipment.

Immediate Postoperative

• Perform assessment and compare to baseline: vital signs, pulse oximetry, and heart and lung sounds. • Assess abdominal wound for the amount and type of drainage, condition of the incision, and signs of infection. • Observe for anastomosis leak (tachycardia, fever, tachypnea, chest and abdominal pain). • Help patient turn, cough and deep breath, and use incentive spirometer at least every 2 hrs. • Protect the incision against any straining that accompanies turning and coughing. • Give pain medications as needed. • Position the patient upright at a minimum of a 45-degree angle. • Maintain IV and/or oral fluid intake and monitor urine output. • Institute measures to prevent VTE. • Nutrition • Start with room temperature water and low-sugar clear liquids. • Teach the patient to avoid drinking with a straw. • Begin with 15 mL every 10–15 minutes, gradually increase to 90 mL every 30 min. • Move to a low-fat, full-liquid diet after 48 hrs if tolerating clear liquids. • Observe for dehydration (thirst, decreased urine output, headache, dizziness). Excess adipose tissue may make obtaining venous access difficult. A longer IV catheter is helpful (longer than 1 in) to go through the overlying tissue to the vein. It is important that the cannula is far enough into the vein so it is not dislodged or infiltrated.

Special Considerations for Bariatric Surgery Ensure that the patient scheduled for bariatric surgery understands the surgical procedure. Your teaching depends on the type of

procedure and surgical approach (Table 40.10). Stress that we will frequently assess vital signs and general assessment to monitor for complications. Tell the patient that they will be assisted with ambulation soon after surgery and encouraged to cough and deep breathe to prevent pulmonary complications.

Postoperative Care The initial postoperative care focuses on careful assessment and immediate intervention for cardiopulmonary complications, thrombus formation, anastomosis leaks, and electrolyte imbalances. The transfer from surgery may require many staff members. During the transfer, keep the patient’s airway stabilized and give attention to managing the patient’ pain. Maintain the patient’s head at a 45-degree angle to reduce abdominal pressure and increase lung expansion.18 The body stores anesthetics in adipose tissue, thus placing patients with excess adipose tissue at risk for resedation. As adipose cells release anesthetics back into the bloodstream, the patient may become sedated after surgery. If this happens, be prepared to perform a headtilt or jaw-thrust maneuver and keep the patient’s oral and nasal airways open. Diligence in turning and ambulation postoperatively will prevent complications from surgery. The patient will typically begin walking the evening after surgery and then at least 3 or 4 times each day. Assist the patient as needed. The patient may be reluctant to move or may not have the stamina to walk even a short distance. In either situation, you will need help moving an obese patient. Obesity can cause a patient’s breathing to become shallow and rapid. The extra adipose tissue in the chest and abdomen compresses the diaphragmatic, thoracic, and abdominal structures. This compression restricts the chest’s ability to expand, preventing the lungs from working as efficiently as they would otherwise. The patient retains more CO2 with less O2 delivered to the lungs. This results in hypoxemia, pulmonary hypertension, and polycythemia. After surgery, the risk for venous thromboembolism (VTE) is increased. Intermittent pneumatic compression devices or

compression stockings with low-dose heparin decrease the risk for VTE. Active and passive range-of-motion exercises are a frequent part of daily care.18 Wound infection, dehiscence, and delayed healing are potential problems for all obese patients. Assess the patient’s skin for any complications related to wound healing. Keep skinfolds clean and dry to prevent dermatitis and bacterial or fungal infections.

Special Considerations for Bariatric Surgery Patients have considerable abdominal pain after bariatric surgery (Table 40.11). Give pain medications as needed during the immediate postoperative period (first 24 hours). Be aware that pain could be from an anastomosis leak rather than typical surgical pain. Abdominal wounds require frequent observation for the amount and type of drainage, condition of the incision, and signs of infection. Monitor vital signs to help identify problems, such as infection or anastomosis leak. Give room temperature water and low-sugar clear liquids as soon as the patient is fully awake and there is no evidence of any anastomosis leaks. Begin with 15-mL increments every 10 to 15 minutes. Gradually increase intake to a goal of 90 mL every 30 minutes by postoperative day 1. Teach the patient to avoid gulping fluids or drinking with a straw to reduce the incidence of air swallowing. The patient who tolerates clear liquids may begin a lowfat, full-liquid diet on postoperative day 3.

Ambulatory and Home Care Special Considerations for Bariatric Surgery The patient who has undergone major surgical treatment for obesity has not been successful in the past in following or maintaining a prescribed diet. Now the patient must reduce oral intake because of the anatomic changes from the surgical procedure. The patient must clearly understand the proper diet. A dietitian is usually part of the bariatric team and helps the patient with the transition to the new

diet. Patients usually are discharged on a full-liquid diet. Within 10 to 14 days after surgery, depending on tolerance, the patient may begin a pureed or soft foods diet with vitamin supplementation. Most patients transition to the usual diet 4 to 6 weeks after surgery.19 The usual diet is high in protein and low in carbohydrates, fat, and roughage. It should consist of 6 small feedings daily. Many need a protein supplement once or twice a day for the first few months after surgery to meet their protein needs.19 Patient should not consume fluids with meals. Fluids and foods high in carbohydrate tend to promote diarrhea and symptoms of dumping syndrome. Caloriedense foods should be avoided to permit more nutritionally sound food to be consumed. Teach the patient to eat slowly and stop eating when feeling full. Weight loss is considerable during the first 6 to 12 months. Although behavior modification is not necessarily an intended outcome with these surgical procedures, it becomes an unexpected secondary gain. For example, a person who has had bariatric surgery cannot overeat or binge eat without consequences (e.g., vomiting, abdominal pain). The patient may fail to lose weight if the stomach pouch is too large. An outlet that is much too small may result in the patient losing too much weight. Some patients have been known to overeat when they return home and gain rather than lose weight. Stress the importance of long-term follow-up care, in part because of potential complications. Teach patients to inform the HCP of any changes in their physical or emotional condition. Nutritional deficiencies are expected after malabsorptive bariatric surgery, including anemia, vitamin deficiencies, and diarrhea. Patients should take multivitamins with folate, calcium, vitamin D, iron, and vitamin B12 for life.20 Peptic ulcer formation, dumping syndrome, and small bowel obstruction may be seen late in the recovery and rehabilitation stage.

Informatics in Practice Use of Smart Phone for Weight Loss • Phone apps (e.g., My Fitness Pal) are available to help track calories, weight, exercise, and eating patterns. • Tracking systems give immediate access to nutritional information for better dietary decision making. • Some apps can scan the barcode of foods in the grocery store and give nutritional information. • Calorie tracker apps can be used to monitor daily calorie intake and keep a record of weight loss progress. • With text messaging, a phone “buddy” can provide support when a person’s will power is lacking. • Share progress with friends and family. Some weight loss apps sync with social media accounts so that a person can share milestones on Twitter and Facebook. Several potential psychologic problems may arise after surgery. Assess social functioning, self-esteem, sexual life, and activities of daily living in follow-up care. Some patients feel guilty that they had to achieve weight loss by surgical intervention rather than by the “sheer willpower” of reduced dietary intake and exercise. Be ready to provide support and assist the patient in moving away from such negative feelings.

FIG. 40.9 A, Preoperative view of a 37-yr-old woman with massive weight loss who had gastric bypass surgery. B, Postoperative view 2½ years after abdominoplasty. She underwent breast surgery, thigh lift, back lift with excision of excess skin of the lower back and upper buttocks, and upper arm surgery. From Shermak MA: Contouring the epigastrium, Aesthet Surg J 25:506, 2005.

By 6 to 8 months after surgery, most patients have lost considerable weight and are able to see how much their appearance has changed. Help the patient adjust to a new body image. Massive weight loss may leave the patient with large quantities of flabby skin that can result in problems related to altered body image (Fig. 40.9). Discuss this possible outcome with the patient before surgery and again during the rehabilitation phase. Cosmetic surgery may alleviate this situation. Do not hesitate to encourage counseling for unresolved psychologic issues. Often one result of bariatric surgery is the return of fertility in women. Pregnancy complications can result from anemia and nutritional deficiencies. Furthermore, depending on the type of

surgery, intestinal obstructions and hernias may occur with pregnancy. Women must carefully consider the risk for pregnancy after bariatric surgery. In general, encourage women to postpone pregnancy for 12 to 18 months after bariatric surgery.

Check Your Practice You are working in the bariatric surgery outpatient clinic. When you walk into the clinic room where a 36-yr-old woman is waiting for her follow-up visit, you find her distraught and crying. You ask her what is wrong. She responds, “I am a total failure. I have been fat all my life, and I had to have this horrible surgery to help me. Why couldn’t I do it on my own?” • What is an effective way for you to handle this situation?

Evaluation The expected outcomes are that the obese patient will • Have long-term weight loss • Have improvement in obesity-related co-morbidities • Integrate healthy practices into daily routines • Monitor for adverse side effects of surgical therapy • Have an improved self-image

Gerontologic Considerations: Obesity in Older Adults The prevalence of obesity is increasing in older people. The number of obese older persons has markedly risen because of increases in both the total number of older persons and the percent of the older adults who are obese. Obesity is more common in older women than in older men. A decrease in energy expenditure is an important contributor to

a gradual increase in body fat with age. Obesity in older adults can worsen age-related declines in physical function and lead to frailty and disability. Obesity is associated with decreased survival. Those who are obese live 6 to 7 years less than people of normal weight. Obesity worsens many changes associated with aging. Excess body weight places more demands on arthritic joints. The mechanical strain on weight-bearing joints can lead to premature immobility. Excess intraabdominal weight can cause problems with urinary incontinence. Excess weight may contribute to hypoventilation and sleep apnea. Obesity affects the quality of life for older adults. Weight loss can improve physical functioning and obesity-related health complications. The same therapeutic approaches for obesity discussed earlier also apply to the older adult.

Cosmetic Surgical Therapy Lipectomy Lipectomy (adipectomy) is done to remove unsightly flabby folds of adipose tissue (Fig. 40.9). There is no evidence that regeneration of adipose tissue occurs at the surgical sites. However, Stress to the patient that surgical removal does not prevent obesity from recurring, especially if lifetime eating habits stay the same. Although body image and self-esteem may improve with such procedures, these operations are not without complications. Do not underestimate the dangerous effects of anesthesia and the potential for poor wound healing in the obese patient.

Liposuction Another cosmetic surgical procedure is liposuction, or suction-assisted lipectomy. It is used for cosmetic purposes and not for weight reduction. This surgical intervention helps improve facial appearance or body contours. A good candidate is a person who has achieved

weight reduction and has excess fat under the chin, along the jaw line, in the nasolabial folds, over the abdomen, or around the waist and upper thighs. A long, hollow, stainless steel cannula is inserted through a small incision over the fatty tissue to be suctioned. This surgical procedure is not usually recommended for an older person because the skin is less elastic and will not accommodate the new underlying shape.

Metabolic Syndrome Metabolic syndrome is a group of metabolic risk factors that increase a person’s chance of developing CVD, stroke, and diabetes. About 1 in 3 adults have metabolic syndrome. The syndrome is more prevalent in those 60 years of age and older.21 Metabolic syndrome is a cluster of health problems, including obesity, hypertension, abnormal lipid levels, and high blood glucose. Metabolic syndrome is diagnosed if a person has 3 or more of the conditions listed in Table 40.12.

Etiology and Pathophysiology The main underlying risk factor for metabolic syndrome is insulin resistance related to excess visceral fat (Fig. 40.10). Insulin resistance is the decreased ability of the body’s cells to respond to the action of insulin. The pancreas compensates by secreting more insulin, resulting in hyperinsulinemia.

TABLE 40.12 Criteria for Metabolic Syndrome Any 3 of the 5 measures are needed to diagnose metabolic syndrome:

Source: National Heart, Lung, and Blood Institute: How is metabolic syndrome diagnosed? Retrieved from www.nhlbi.nih.gov/health/healthtopics/topics/ms/diagnosis. Other characteristics include hypertension, increased risk for clotting, and abnormalities in cholesterol levels. The net effect of these conditions is an increased prevalence of coronary artery disease.

Clinical Manifestations and Diagnostic Studies The signs of metabolic syndrome are impaired fasting blood glucose, hypertension, abnormal cholesterol levels, and obesity. Medical problems develop over time if the condition is not addressed. Patients with this syndrome are at a higher risk for heart disease, stroke, diabetes, renal disease, and polycystic ovary syndrome. Patients who have metabolic syndrome and smoke are at an even higher risk.

Nursing and Interprofessional Management: Metabolic Syndrome There is no specific management of metabolic syndrome. Interventions focus on reducing the major risk factors of CVD and

type 2 diabetes: reducing LDL cholesterol, stopping smoking, lowering BP, losing weight, and reducing glucose levels. There are no specific medications for metabolic syndrome. Patients receive cholesterol-lowering and antihypertensive drugs as needed. Metformin (Glucophage) can lower glucose levels and enhance the cells’ sensitivity to insulin. Obese patients may be candidates for bariatric surgery.

FIG. 40.10 Relationship among insulin resistance, obesity, diabetes, and CVD.

For long-term risk reduction, the person needs to maintain a healthy weight, increase physical activity, and follow healthy diet habits. You can help patients by giving information on healthy diets, exercise, and positive lifestyle changes. The diet, which should be low in saturated fats, should promote weight loss. Weight reduction and maintaining a lower weight are a priority in those with abdominal obesity and metabolic syndrome. Because sedentary lifestyles contribute to metabolic syndrome, increasing regular physical activity will lower a patient’s risk factors. In addition to helping with weight reduction, regular exercise decreases triglyceride levels and increases HDL cholesterol levels in those with metabolic syndrome.

Case Study Obesity

© Thinkstock.

Patient Profile S.R. is a 48-yr-old white woman who comes to the clinic reporting hip pain.

Subjective Data • States that it is “getting hard to get around”

• Reports gradual weight gain of 40 lbs over past 20 yrs • Lives in a rural community with no sidewalks • Spends her free time watching television • Reports a history of type 2 diabetes, shortness of breath, hypertension, and osteoarthritis • Had knee replacement surgery at age 46 for osteoarthritis • Tried orlistat (Xenical) but hated the side effects

Objective Data Physical Examination • 5 ft, 6 in tall; weighs 230 lb; BMI 37 kg/m2, waist circumference of 40 in • Has obese, nontender, soft round, abdomen • BP 160/100 mm Hg • Moderate pain with range of motion of both hips

Laboratory Results • Fasting blood glucose 250 mg/dL (13.9 mmol/L) • Total cholesterol 205 mg/dL (5.3 mmol/L) • Triglyceride 298 mg/dL (3.36 mmol/L) • HDL cholesterol 31 mg/dL (0.8 mmol/L) • LDL cholesterol 114 mg/dL

Interprofessional Care • Referral to a community weight loss program • Consultation with bariatric surgeon • Diagnosed with bilateral osteoarthritis of the hips

Discussion Questions 1. What are S.R.’s risk factors for obesity? 2. Of the possible complications of obesity, which ones does S.R. have? Why did she develop them? 3. Patient-Centered Care: How would you help S.R. in designing a successful weight loss and weight management program? 4. Collaboration: How could a comprehensive community weight loss program be beneficial to S.R.? 5. What are S.R.’s risk factors for metabolic syndrome? 6. Is S.R. a candidate for bariatric surgery? Why or why not? 7. Evidence-Based Practice: S.R. tells you that she is not sure surgery will work for her. She asks you, “What is the best surgery for me?” Answers available at http://evolve.elsevier.com/Lewis/medsurg.

Bridge to Nclex Examination The number of the question corresponds to the same-numbered outcome at the beginning of the chapter.

1. Which statement best describes the etiology of obesity? a. Obesity primarily results from a genetic predisposition. b. Psychosocial factors can override the effects of genetics in causing obesity. c. Obesity is the result of complex interactions between genetic and environmental factors. d. Genetic factors are more important than environmental factors in the etiology of obesity. 2. Health risks associated with obesity include (select all that apply)

a. colorectal cancer. b. rheumatoid arthritis. c. polycystic ovary syndrome. d. nonalcoholic steatohepatitis. e. systemic lupus erythematosus. 3. The obesity classification that is most often associated with cardiovascular health problems is a. primary obesity. b. secondary obesity. c. gynoid fat distribution. d. android fat distribution. 4. The best nutritional therapy plan for a person who is obese a. is high in animal protein. b. is fat-free and low in carbohydrates. c. restricts intake to under 800 calories per day. d. lowers calories with foods from all the basic groups. 5. This bariatric surgical procedure involves creating a gastric pouch that is reversible, and no malabsorption occurs. Which surgical procedure is this? a. Vertical gastric banding b. Biliopancreatic diversion c. Roux-en-Y gastric bypass d. Adjustable gastric banding 6. A patient with extreme obesity has undergone Roux-en-Y gastric bypass surgery. In planning postoperative care, the nurse anticipates that the patient

a. may have severe diarrhea early in the postoperative period. b. will not be allowed to ambulate for 1 to 2 days postoperatively. c. will require nasogastric suction until the drainage is pale yellow. d. may have limited amounts of oral liquids during the early postoperative period. 7. Which criteria must be met for a diagnosis of metabolic syndrome? (select all that apply) a. Hypertension b. High triglycerides c. Elevated plasma glucose d. Increased waist circumference e. Decreased low-density lipoproteins 1. c, 2. a, c, d, 3. d, 4. d, 5. d, 6. d, 7. a, b, c, d For rationales to these answers and even more NCLEX review questions, visit http://evolve.elsever.com/Lewis/medsurg.

Evolve Website/Resources List http://evolve.elsevier.com/Lewis/medsurg

Review Questions (Online Only) Key Points Answer Keys for Questions • Rationales for Bridge to NCLEX Examination Questions • Answer Guidelines for Case Study on p. 886 Student Case Study

• Patient With Obesity and Osteoarthritis Conceptual Care Map Creator Audio Glossary Content Updates

References 1. Centers for Disease Control and Prevention: Overweight and obesity. Retrieved from www.cdc.gov/obesity/data/adult.html. Albuquerque D, Nóbrega C, Manco L, et al: The contribution of genetics and environment to obesity, BMJ 123:73, 2017. Dimitriadis GK, Randeva MS, Miras AD: Potential hormone mechanisms of bariatric surgery, Curr Obes Rep 6:253, 2017. Shibata R, Ouchi N, Ohashi K, et al: The role of adipokines in cardiovascular disease, J Cardiol 70:329, 2017.

5. Robert Wood Johnson Foundation. The state of obesity. Retrieved from https://stateofobesity.org/resources/. Björnson E, Adiels M, Taskinen MR, et al : Kinetics of plasma triglycerides in abdominal obesity, Curr Opin Lipidol 28:11, 2017.

7. The link between obesity and cancer (editorial), Lancet 390:1716, 2017. Rotenberg KJ, Bharathi C, Davies H, et al: Obesity and the social withdrawal syndrome, Eating Behaviors 26:167, 2017.

9. Centers for Disease Control and Prevention: Assessing your weight. Retrieved from www.cdc.gov/healthyweight/assessing/index.html. Acosta A, Streett S, Kroh MD, et al: White paper AGA: POWER— Practice guide on obesity and weight management, education and resources, Clin Gastroenterol Hepat 515:631, 2017.

11. Bray GA, Frühbeck G, Ryan DH, et al: Management of obesity, Lancet 387:1947, 2016. Lv N, Azar KM, Rosas LG, et al: Behavioral lifestyle interventions for moderate and severe obesity: A systematic review, Prev Med 100:180, 2017.

13. Alfaris N, Minnick A, Hong P, et al: A review of commercial and proprietary weight loss programs. In: Mechanik J, Kushner R, eds: Lifestyle medicine: A manual for clinical practice, New York, 2016, Springer. 14. Igel LI, Kumar RB, Saunders KH, et al: Practical use of pharmacotherapy for obesity, Gastroenterol 152:1765, 2017. Gadde KM, Martin CK, Berthoud HR, et al: Obesity: Pathophysiology and management, J Am Coll Cardiol 71:69, 2018. Adams TD, Davidson LE, Litwin SE, et al: Weight and metabolic outcomes 12 years after gastric bypass, NEJM 377:1143, 2017.

17. Genco A, Maselli R, Casella G, et al: Intragastric balloon treatment for obesity, New York, 2016, Springer. Thorell A, MacCormick AD, Awad S, et al: Guidelines for perioperative care in bariatric surgery: Enhanced Recovery After Surgery (ERAS) Society recommendations, World J Surg 40:2065, 2016. Dagan SS, Goldenshluger A, Globus I, et al: Nutritional recommendations for adult bariatric surgery patients, Adv Nutr 8:382, 2017. Cooley M: Preventing long-term poor outcomes in the bariatric patient postoperatively, DCCN 36:30, 2017. Moore JX, Chaudhary N, Akinyemiju T: Metabolic syndrome prevalence by race/ethnicity and sex in the United States, PCD 14:24, 2017. ∗Evidence-based information for clinical practice.

41

Upper Gastrointestinal Problems Kara Ann Ventura

LEARNING OUTCOMES 1. Describe the etiology, complications, and interprofessional and nursing management of nausea and vomiting. 2. Relate the etiology, clinical manifestations, and interprofessional and nursing management of common oral inflammations and infections. 3. Describe the etiology, clinical manifestations, complications, and interprofessional and nursing management of oral cancer. 4. Explain the types, pathophysiology, clinical manifestations, complications, and interprofessional and nursing management of gastroesophageal reflux disease and hiatal hernia. 5. Relate the pathophysiology, clinical manifestations, complications, and interprofessional management of esophageal cancer, diverticula, achalasia, and esophageal strictures. 6. Distinguish between acute and chronic gastritis, including the etiology, pathophysiology, and interprofessional and nursing management. 7. Compare and contrast gastric and duodenal ulcers, including the etiology, pathophysiology, clinical manifestations, complications, and interprofessional and nursing management. 8. Describe the clinical manifestations and interprofessional and nursing management of stomach cancer.

9. Explain the common etiologies, clinical manifestations, and interprofessional and nursing management of upper gastrointestinal bleeding. 10. Identify common types of foodborne illnesses and nursing responsibilities related to food poisoning.

KEY TERMS achalasia, p. 904 Barrett’s esophagus, p. 897 dysphagia, p. 894 esophageal cancer, p. 901 esophagitis, p. 897 gastritis, p. 915 gastroesophageal reflux disease (GERD), p. 896 hiatal hernia, p. 900 Mallory-Weiss tear, p. 891 nausea, p. 889 peptic ulcer disease (PUD), p. 904 stomach (gastric) cancer, p. 911 stress-related mucosal disease (SRMD), p. 917 vomiting, p. 889 Anywhere I see suffering that is where I want to be, doing what I can. Princess Diana http://evolve.elsevier.com/Lewis/medsurg

Conceptual Focus Fluids and Electrolytes Nutrition Pain Sleep Stress Tissue Integrity Several upper gastrointestinal (GI) problems and the care of the patient undergoing upper GI surgery are discussed in this chapter. These include nausea and vomiting, oral and gastric cancers, gastroesophageal reflux, ulcerative disease, inflammatory and infectious bowel disorders, GI bleeding, and structural problems. Conceptually, patients with impaired GI function may have malnutrition from impaired nutritional intake. Many are at risk for altered fluid, electrolyte, and acid-base balance. Problems with eating, drinking, or talking may cause pain and impair the ability to communicate. Pain can disrupt sleep and cause fatigue. Difficulty swallowing increases the risk for aspiration.

Nausea and Vomiting Nausea and vomiting are the most common manifestations of GI disease. Although nausea and vomiting can occur independently, they are closely related and usually treated as one problem. Nausea is a feeling of discomfort in the epigastrium with a conscious desire to vomit. Vomiting is the forceful ejection of partially digested food and secretions (emesis) from the upper GI tract.

Etiology and Pathophysiology Nausea and vomiting occur in a wide variety of GI disorders and in many conditions unrelated to GI disease. These include pregnancy; infection; central nervous system (CNS) problems (e.g., meningitis, tumor); cardiovascular disease (CVD) (e.g., myocardial infarction, heart failure); metabolic disorders (e.g. psychologic factors (e.g., stress, fear); and when the GI tract becomes overly irritated, excited, or distended. Patients may have nausea and vomiting after surgery with general anesthesia or as a drug side effect (e.g., chemotherapy, opioids). Women are more likely to have nausea and vomiting associated with anesthesia and motion sickness.1 A vomiting center in the medulla coordinates the multiple components involved in vomiting. This center receives input from various stimuli. Neural impulses reach the vomiting center via afferent pathways through branches of the autonomic nervous system. Receptors for these afferent fibers are found in the GI tract, kidneys, heart, and uterus. When stimulated, these receptors relay information to the vomiting (emetic) center, which then initiates the vomiting reflex (Fig. 41.1). Vomiting is a complex act. It requires the coordinated activity of several structures: closure of the glottis, deep inspiration with contraction of the diaphragm in the inspiratory position, closure of the pylorus, relaxation of the stomach and lower esophageal sphincter (LES), and contraction of the abdominal muscles with increasing

intraabdominal pressure. These simultaneous activities force the stomach contents up through the esophagus, into the pharynx, and out the mouth. The chemoreceptor trigger zone (CTZ), found in the brainstem, responds to chemical stimuli from drugs, toxins, and labyrinthine stimulation (e.g., motion sickness). Once stimulated, the CTZ transmits impulses directly to the vomiting center. This action activates the autonomic nervous system, resulting in both parasympathetic and sympathetic stimulation. Sympathetic activation causes tachycardia, tachypnea, and diaphoresis. Parasympathetic stimulation causes relaxation of the LES, an increase in gastric motility, and a pronounced increase in salivation.

Clinical Manifestations Nausea is subjective. Anorexia (lack of appetite) usually accompanies nausea. When nausea and vomiting occur over a long period, dehydration can develop rapidly. Water and essential electrolytes (e.g., potassium, sodium, chloride, hydrogen) are lost. As vomiting persists, the patient may have severe electrolyte imbalances, extracellular fluid volume loss, decreased plasma volume, and eventually circulatory failure.

FIG. 41.1 Stimuli involved in the act of vomiting. CTZ, Chemoreceptor trigger zone. Modified from McKenry L, Tessier E, Hogan M: Mosby’s pharmacology in nursing, ed 22, St Louis, 2006, Mosby.

Metabolic alkalosis can result from loss of gastric hydrochloric (HCl) acid. Metabolic acidosis can occur with vomiting of small intestine contents. However, metabolic acidosis is less common than metabolic alkalosis. Weight loss resulting from fluid loss can occur in a short time with severe vomiting.

Interprofessional Care

In managing nausea and vomiting, the goals of care are to determine and treat the underlying cause, recognize and correct any complications, and provide symptomatic relief.

Drug Therapy The use of drugs to treat nausea and vomiting depends on the cause of the problem (Table 41.1). Many antiemetic drugs act in the CNS via the CTZ to block the neurochemicals that trigger nausea and vomiting. When the cause has not been determined, use drugs with caution. Using antiemetics before knowing the cause can mask the underlying disease process and delay diagnosis and treatment.

Drug Alert Promethazine Injection • Do not give into an artery or under the skin because of the risk for severe tissue injury. • When given IV, it can leak out of the vein and cause severe damage to surrounding tissue. • Deep muscle injection is the preferred route of injection administration. 5-HT3 (Serotonin) receptor antagonists are effective in reducing chemotherapy-induced vomiting (CINV), postoperative nausea and vomiting (PONV), and nausea and vomiting related to migraine headache and anxiety. Dexamethasone is given with other antiemetics to manage acute and delayed CINV. Neurokinin-1 receptor antagonists (NK1RAs) (e.g., aprepitant [Emend], rolapitant [Varubi]), can treat CINV and PONV.2

Drug Alert Metoclopramide (Reglan) • Chronic use or high doses carry the risk for tardive dyskinesia. • Tardive dyskinesia is a neurologic condition characterized by involuntary and repetitive movements of the body (e.g., extremity movements, lip smacking). • Tardive dyskinesia may persist after stopping the drug. An oral cannabinoid (e.g., dronabinol) may be part of the regimen to manage CINV. Because of the potential for abuse as well as drowsiness and sedation, this is an option only when other therapies are not effective.

Nursing Management: Nausea and Vomiting Nursing Assessment Each patient with a history of prolonged and persistent nausea or vomiting needs a thorough nursing assessment. You should have a basic understanding of the common conditions associated with nausea and vomiting and be able to identify the patient who is at high risk. Assess the patient for precipitating factors and describe the contents of the emesis. Table 41.2 presents subjective and objective data to obtain from a patient with nausea and vomiting. When food is the precipitating cause of nausea and vomiting, help the patient identify the specific food. Determine when it was eaten, prior history with the food, and whether anyone else who ate the food is sick. Emesis containing partially digested food several hours after a meal indicates gastric outlet obstruction or delayed gastric emptying. The presence of fecal odor and bile after prolonged vomiting suggests intestinal obstruction below the level of the pylorus. Bile in the emesis suggests obstruction below the ampulla of Vater.

TABLE 41.1 Drug TherapyNausea and Vomiting

The color of the emesis helps determine the presence and source of any bleeding. Bright red blood occurs with active bleeding. This could be due to a Mallory-Weiss tear (disruption of the mucosal lining near the esophagogastric junction), esophageal varices, gastric or duodenal ulcer, or cancer. Vomitus with a “coffee-grounds” appearance is related to gastric bleeding. The blood changes to dark brown because of its interaction with HCl acid. It is important to discern among vomiting, regurgitation, and projectile vomiting. Regurgitation is an effortless process in which partially digested food slowly comes up from the stomach. Retching or vomiting rarely occurs before it. Projectile vomiting is a forceful expulsion of stomach contents without nausea. It often occurs with brain and spinal cord tumors. The timing of nausea and vomiting can help determine its cause.

Early morning vomiting is common in pregnancy. Emotional stressors may elicit vomiting during or right after eating. Those with cyclic vomiting syndrome have recurring episodes of nausea, vomiting, and fatigue that last from a few hours up to 10 days.

Nursing Diagnoses Nursing diagnoses for the patient with nausea and vomiting may include: • Nausea • Fluid imbalance • Electrolyte imbalance • Impaired nutritional intake More information on nursing diagnoses and interventions are in eNursing Care Plan 41.1 (available on the website for this chapter).

Planning The overall goals are that the patient with nausea and vomiting will (1) have minimal or no nausea and vomiting, (2) have normal electrolyte levels and hydration status, and (3) return to a normal pattern of fluid balance and nutrient intake.

Nursing Implementation Acute Care Most people with nausea and vomiting are at home. When nausea and vomiting persist, the patient may need hospitalized to diagnose the underlying problem. Until we confirm a diagnosis, the patient is NPO and given IV fluids. The patient with persistent vomiting, a possible bowel obstruction, or paralytic ileus may need a nasogastric (NG) tube connected to suction to decompress the stomach. Secure the NG tube to prevent its movement in the nose and back of the throat,

because this can stimulate nausea and vomiting.

TABLE 41.2 Nursing AssessmentNausea and

Vomiting

Subjective Data Important Health Information Past health history: GI disorders, chronic indigestion, food allergies, pregnancy, infection, CNS problems, recent travel, eating disorders, metabolic disorders, cancer, CVD, renal disease Medications: Antiemetics, digitalis, opioids, ferrous sulfate, aspirin, aminophylline, alcohol, antibiotics, chemotherapy. General anesthesia Surgery or other treatments: Recent surgery

Functional Health Patterns Nutritional-metabolic: Amount, frequency, character, and color of vomitus. Dry heaves. Anorexia, weight loss Activity-exercise: Weakness, fatigue Cognitive-perceptual: Abdominal tenderness or pain Coping–stress tolerance: Stress, fear

Objective Data General Lethargy, sunken eyeballs

Integumentary

Pallor, dry mucous membranes, poor skin turgor

Gastrointestinal Amount, frequency, character (e.g., projectile), content (undigested food, blood, bile, feces), and color of vomitus (red, coffee-grounds, green-yellow)

Urinary Decreased output, concentrated urine

Possible Diagnostic Findings Altered serum electrolytes (especially hypokalemia), metabolic alkalosis, abnormal upper GI findings on endoscopy or abdominal x-rays With prolonged vomiting, there is a chance of dehydration and acid-base and electrolyte imbalances. Record intake and output, monitor vital signs, and assess for signs of dehydration. Provide physical and emotional support. Maintain a quiet, odor-free environment. Observe for changes in the patient’s physical comfort and mentation. The risk for pulmonary aspiration is a concern when vomiting occurs in older or unconscious patients or in patients with conditions that impair the gag reflex. To prevent aspiration, put the patient who cannot manage self-care in a semi-Fowler’s or side-lying position.

Nutritional Therapy The patient with severe vomiting needs IV fluid therapy with electrolyte and glucose replacement until able to tolerate oral intake. Start oral nutrition beginning with clear liquids once symptoms have

subsided. A patient may be reluctant to resume fluid intake because of fear of symptoms recurring. Water is the initial fluid of choice for oral rehydration. Have the patient sip small amounts of fluid (5 to 15 mL) every 15 to 20 minutes. Other options include carbonated beverages with the carbonation removed at room temperature and warm tea. Extremely hot or cold liquids are often hard to tolerate. Broth and sports drinks (e.g., Gatorade) are high in sodium, so give them with caution. Dry toast, crackers, and plain gelatin may be helpful. As the patient’s condition improves, provide a diet high in carbohydrates and low in fat. Bland foods, such as a baked potato, rice, cooked chicken, and cereal, are ideal. Many patients do not tolerate coffee, spicy foods, highly acidic foods, and those with strong odors. Tell the patient to eat food slowly and in small amounts to prevent overdistending the stomach. Liquids taken between meals rather than with meals reduce overdistention. Consult a dietitian about nutritious foods that the patient can tolerate.

Check Your Practice You are caring for a newly admitted 76-yr-old man who reports vomiting for the past 3 days. He says, “I cannot keep anything down, not even water.” • What assessment do you need to perform? • What findings would show he is dehydrated? • What are your priority nursing interventions?

Ambulatory Care Teach the patient and caregiver (1) how to manage the unpleasant sensation of nausea, (2) methods to prevent nausea and vomiting, and (3) ways to maintain fluid and nutritional intake. Tell them to keep the immediate environment quiet, free of noxious odors, and well ventilated. Avoiding sudden changes of position and unnecessary

activity are helpful. Encourage the use of relaxation techniques, frequent rest periods, effective pain management strategies, and diversional tactics. Cleansing the face and hands with a cool washcloth and providing mouth care between episodes increase the person’s comfort level. When symptoms occur, stop all foods and drugs until the acute phase is over. If you suspect a medication is the cause, notify the (HCP at once. The HCP can change the dose or prescribe a new drug. Tell the patient that stopping the drug without consulting the HCP may have adverse effects on the person’s health. The patient should take an antiemetic drug only if prescribed by the HCP. Taking over-the-counter (OTC) drugs to relieve symptoms may make the problem worse. Some patients find that acupressure or acupuncture at specific points is effective in reducing PONV.3 Others use herbs, such as ginger and peppermint oil. Relaxation breathing exercises, changes in body position, or exercise may help some patients.

Complementary & Alternative Therapies Ginger

Scientific Evidence • May be effective for nausea and vomiting in pregnancy when used at recommended doses for short periods • May help CINV if used with antiemetic drugs

Nursing Implications • Few adverse effects reported with short-term use • May interact with anticoagulants and increase risk for bleeding • Use with caution in people with gallbladder disease

Source: www.nccih.nih.gov/health/ginger.

TABLE 41.3 Infections and Inflammation of the

Mouth

Evaluation The expected outcomes are that the patient with nausea and vomiting will

• Be comfortable, with minimal or no nausea and vomiting • Have electrolyte levels within normal range • Be able to maintain adequate intake of fluids and nutrients

Gerontologic Considerations: Nausea and Vomiting The older adult with nausea and vomiting needs careful assessment and monitoring, especially during periods of fluid loss and rehydration therapy. They are more likely to have cardiac or renal problems that places them at greater risk for life-threatening fluid and electrolyte imbalances. Excess fluid and electrolytes replacement may have adverse consequences for a person with heart failure or renal disease. The older adult with a decreased level of consciousness has a high risk for aspirating. Close monitoring of the patient’s physical status and level of consciousness during episodes of vomiting is important. Older adults are particularly susceptible to the CNS side effects of antiemetic drugs. These drugs may cause confusion and increase fall risk. Doses should be reduced and efficacy closely evaluated. Use safety precautions for these patients (e.g., removing rugs that may cause slipping).

Oral Inflammation and Infections Inflammations and infections of the oral cavity are shown in Table 41.3. They may be due to specific mouth diseases or related to systemic disorders, such as leukemia or vitamin deficiency. The patient who is immunosuppressed (e.g., receiving chemotherapy for cancer) or using corticosteroid inhalant treatment for asthma is at risk for oral infections (e.g., candidiasis). Oral infections may predispose the patient to infections in other body organs. For example, the oral cavity is a potential reservoir for respiratory pathogens. Oral pathogens are associated with diabetes and heart disease.4 Managing these problems focuses on identifying the cause, eliminating infection, providing comfort measures, and maintaining nutritional intake. They can severely impair oral ingestion. Regular and good oral and dental hygiene reduces oral infections and inflammation.

Oral Cancer There are 2 types of oral cancer: oral cavity cancer, which starts in the mouth, and oropharyngeal cancer, which develops in the part of the throat just behind the mouth (the oropharynx). Head and neck squamous cell carcinoma (HNSCC) is a broad term used for cancers of the oral cavity, pharynx, and larynx. Most oral cancer lesions occur on the lower lip. Other common sites are the lateral border and undersurface of the tongue, labial commissure, and buccal mucosa. Annually 51,540 Americans are diagnosed with oral cancer. An estimated 10,030 people die from the disease.5 Oral cancer is more common after age 35. The average age at diagnosis is 65 years. It is 2 times more common in men than in women. The 5-year survival rate is 84% for localized cancer and 65% for all stages of oral cavity and pharynx cancer combined.5 Lip cancer has the most favorable prognosis of any of the oral tumors. The visibility of lip lesions usually leads to an earlier diagnosis.

Promoting Health Equity Oral, Pharyngeal, and Esophageal Problems

Nausea and Vomiting • Asian Americans, Middle Easterners, and blacks are more likely to have nausea and vomiting than whites

Cancers of Oral Cavity and Pharynx • Incidence and mortality rates are higher in black men than in whites • Death rates from oral cancer are decreasing in whites and

increasing in nonwhites

Esophageal Cancer • Highest incidence is in non-Hispanic white men • Lowest incidence occurs in Asian Americans, Pacific Islanders, and Hispanics.

Stomach Cancer • Asian Americans and Pacific Islanders, Hispanics, and blacks have higher rates of stomach cancer than non-Hispanic whites • Asian Americans have higher survival rates than other ethnic groups

Etiology and Pathophysiology Although the exact cause of oral cancer is unknown, there are predisposing factors (Table 41.4). Of those with oral cancer, 75% to 90% report either using tobacco or a history of frequent alcohol use. More than 30% of patients with cancer of the lip have outdoor occupations, showing that prolonged exposure to sunlight is a risk factor. Irritation from the pipe stem resting on the lip is a factor in pipe smokers. Human papillomavirus (HPV) contributes to 25% of oral cancer cases. HPV-associated oropharyngeal cancer is associated with multiple sexual partners, especially multiple oral sex partners.6

Clinical Manifestations The common manifestations are shown in Table 41.4. Patients may report nonspecific symptoms such as chronic sore throat, sore mouth, and voice changes. Leukoplakia, called “smoker’s patch,” is a white patch on the mouth mucosa or tongue. It is a precancerous lesion, although less than 15% actually transform into cancer cells. The patch

becomes keratinized (hard and leathery). This is described as hyperkeratosis. Leukoplakia is the result of chronic irritation, especially from smoking. Erythroplasia (erythroplakia), a red velvety patch on the mouth or tongue, is another precancerous lesion. More than 50% of cases of erythroplasia progress to squamous cell cancer. About 30% of patients with oral cancer have an asymptomatic neck mass. Cancer of the lip usually appears as an indurated, painless ulcer on the lip. The first sign of cancer of the tongue is an ulcer or area of thickening. Soreness or pain of the tongue may occur, especially when eating hot or highly seasoned foods. Lesions are most likely to develop in the proximal half of the tongue. Some patients have limited tongue movement. Later symptoms include increased salivation, slurred speech, dysphagia (difficulty swallowing), toothache, and earache.

Diagnostic Studies Diagnostic tests are done to identify oral dysplasia, which is a precursor to oral cancer (Table 41.5). Oral exfoliative cytologic study involves scraping the suspicious lesion and spreading the scraping on a slide for microscopic examination. The toluidine blue test is a screening test for oral cancer. When toluidine blue is applied topically to stain an area, cancer cells preferentially take up the dye. A negative cytologic smear or negative toluidine blue test does not necessarily rule out cancer. Once cancer is diagnosed, CT scan, MRI, and positron emission tomography (PET) are used for staging cancer.

TABLE 41.4 Types and Characteristics of Oral

Cancer

Interprofessional Management: Oral Cancer Management usually consists of surgery, radiation, chemotherapy, or a combination of these. The curative treatments are usually surgery and radiation.

Surgical Therapy Surgery is the most effective treatment, especially for early-stage disease.7 The procedure done depends on the location and extent of the tumor. Some patients with small tumors in the mouth and throat are candidates for minimally invasive robotic-assisted surgery. However, many of the operations are radical procedures involving extensive resections. Some examples are partial mandibulectomy (removal of the mandible), hemiglossectomy (removal of half of the tongue), glossectomy (removal of the tongue), resections of the buccal mucosa and floor of the mouth, and radical neck dissection. Radical neck dissection includes wide excision of the primary lesion with removal of the regional lymph nodes, the deep cervical lymph nodes, and their lymphatic channels. The following structures are removed or transected depending on the extent of the primary lesion: sternocleidomastoid muscle and other closely associated muscles, internal jugular vein, mandible, submaxillary gland, part of the thyroid and parathyroid glands, and spinal accessory nerve. The patient usually has a tracheostomy. Drainage tubes inserted into the

surgical area are connected to suction to remove fluid and blood. Head and neck surgery is described in more detail in Chapter 26.

Nonsurgical Therapy Radiation therapy may be used alone to treat small cancers or when lesions cannot be removed. Patients usually do not have radiation before surgery because it is hard to remove radiated tissue. The tissue becomes fibrotic and heals slower. Most patients begin radiation about 6 weeks after surgery. Chemotherapy can shrink lesions before surgery, decrease metastasis, sensitize cancer cells to radiation, or treat distant metastases. Common chemotherapy drugs include fluorouracil, cisplatin, carboplatin, paclitaxel, docetaxel, and hydroxyurea. A common combination is cisplatin and fluorouracil.8 This combination is more effective than either drug alone. (Chemotherapy is discussed in Chapter 15.) Palliative treatment is the best management when the prognosis is poor, the cancer is inoperable, or the patient decides against surgery. Palliation aims to treat the symptoms and make the patient more comfortable. If it becomes hard for the patient to swallow, placing a gastrostomy tube will allow for adequate nutritional intake. Give analgesic drugs freely. Frequent suctioning of the oral cavity is needed when swallowing becomes difficult. Other palliative and end-of-life nursing measures are discussed in Chapter 9.

Nutritional Therapy Many patients are malnourished before surgery. They may need placement of a percutaneous endoscopic gastrostomy (PEG) and enteral nutrition (EN) before radiation treatment or surgery. After radical neck surgery, the patient may be unable to ingest nutrients orally because of mucositis, swelling, location of sutures, or difficulty swallowing. PN is given for the first 24 to 48 hours. After that time, EN is given via NG, gastrostomy, or jejunostomy tube. (See Chapter 39 for information on EN.) Cervical esophagostomy and pharyngostomy are options for some patients.

TABLE 41.5 Interprofessional CareOral Cancer

Diagnostic Assessment • History and physical examination • Biopsy • Oral exfoliative cytology • Toluidine blue test • CT, MRI, PET scans

Management • Surgical therapy • Surgical excision of the tumor • Radical neck dissection • Radiation therapy • Chemotherapy • Nutrition therapy Assess for feeding tolerance and adjust the amount, time, and formula if nausea, vomiting, diarrhea, or distention occurs. Give small amounts of water when the patient can swallow. Observe for choking. Suctioning may be needed to prevent aspiration.

Nursing Management: Oral Cancer Nursing Assessment Subjective and objective data to obtain from a patient with oral cancer are outlined in Table 41.6.

Nursing Diagnoses Nursing diagnoses for the patient with oral cancer may include the following: • Impaired nutritional intake • Acute pain • Anxiety

Planning The overall goals are that the patient with cancer of the oral cavity will (1) have a patent airway, (2) be able to communicate, (3) have adequate nutritional intake to promote wound healing, and (4) have relief of pain and discomfort.

TABLE 41.6 Nursing AssessmentOral Cancer

Subjective Data Important Health Information Past health history: Recurrent oral herpetic lesions, HPV infection or vaccination, syphilis, exposure to sunlight Medications: Immunosuppressants Surgery or other treatments: Removal of prior tumors or lesions

Functional Health Patterns Health perception–health management: Alcohol and tobacco use, pipe smoking. Poor oral hygiene Nutritional-metabolic: Reduced oral intake, weight loss, difficulty chewing food, increased salivation, intolerance to certain foods or temperatures of food Cognitive-perceptual: Mouth or tongue soreness or pain, toothache, earache, neck stiffness, dysphagia, difficulty speaking

Objective Data Integumentary Indurated, painless ulcer on lip. Painless neck mass

Gastrointestinal Areas of thickening or roughness, ulcers, leukoplakia, or erythroplakia on the tongue or oral mucosa. Limited tongue movement. Increased salivation, drooling. Slurred speech. Foul breath odor

Possible Diagnostic Findings Positive exfoliative smear cytology (microscopic examination of cells removed by scraping), positive biopsy

Nursing Implementation You play a key role in the early detection and treatment of oral cancer. Identify patients at risk (Table 41.4) and provide information about predisposing factors. Review information about smoking cessation

with the patient who smokes. Warn adolescents and teenagers about the danger of using snuff or chewing tobacco and electronic cigarettes. Smoking cessation is discussed in Chapter 10 and Tables 10.3 to 10.6. Because early detection of oral cancer is important, teach the patient to report unexplained pain or soreness of the mouth, unusual bleeding, dysphagia, sore throat, voice changes, or swelling or lump in the neck. Refer any person with an ulcerative lesion that does not heal within 2 to 3 weeks to the HCP.

Promoting Population Health Health Impact of Good Oral Hygiene • Improves quality of life • Lowers risk for teeth loss • Reduces pain and disability • Aids in early detection of oral and craniofacial cancers • Decreases cost of care needed from dental professionals • Decreases risk for periodontal disease, gingivitis, and dental caries Preoperative care for the patient who will have a radical neck dissection must consider the patient’s physical and psychosocial needs. Physical preparation is the same as that for any major surgery, with special emphasis on oral hygiene. Explanations and emotional support should include information on postoperative communication and feeding. Explain the surgical procedure and ensure that the patient understands the information. See Chapter 26 and eNursing Care Plan 26.2 for more information about the nursing management of a patient undergoing a radical neck dissection.

Evaluation

The expected outcomes are that the patient with oral cancer will • Have no respiratory complications • Be able to communicate • Maintain an adequate nutritional intake to promote wound healing • Have minimal pain and discomfort with eating, drinking, and talking

Esophageal Disorders Gastroesophageal Reflux Disease Gastroesophageal reflux disease (GERD) is a chronic symptom of mucosal damage caused by reflux of stomach acid into the lower esophagus. GERD is not a disease but a syndrome. GERD is the most common upper GI problem. About 15 million Americans have GERD symptoms (heartburn or regurgitation) each day.9

Etiology and Pathophysiology GERD has no one single cause (Fig. 41.2). GERD results when the reflux of acidic gastric contents into the esophagus overwhelms the esophageal defenses. Gastric HCl acid and pepsin secretions in refluxate cause esophageal irritation and inflammation (esophagitis). If it contains intestinal proteolytic enzymes (e.g., trypsin) and bile, this further irritates the esophageal mucosa. The degree of inflammation depends on the amount and composition of the gastric reflux and on the esophagus’s mucosal defense mechanisms.

FIG. 41.2 Factors involved in the pathogenesis of GERD.

TABLE 41.7 Factors Affecting Lower Esophageal

Sphincter Pressure

Decrease Pressure • Alcohol • Chocolate (theobromine) • Drugs • Anticholinergics • β-Adrenergic blockers • Calcium channel blockers • Diazepam (Valium) • Morphine sulfate • Nitrates • Progesterone • Theophylline • Fatty foods • Nicotine • Peppermint, spearmint • Tea, coffee (caffeine)

Increase Pressure • Bethanechol (Urecholine) • Metoclopramide (Reglan) One of the primary factors causing GERD is an incompetent LES. Normally, the LES acts as an antireflux barrier. An incompetent LES lets gastric contents move from the stomach to the esophagus when the patient is supine or has an increase in intraabdominal pressure. Decreased LES pressure can be due to certain foods and drugs (Table 41.7). Obesity is a risk factor. In an obese person the intraabdominal pressure is increased, which can worsen GERD. Cigarette and cigar smoking can contribute to GERD. Hiatal hernia, discussed in the next section, often causes GERD.

Clinical Manifestations The symptoms of GERD vary from person to person. Persistent mild symptoms (i.e., more than twice a week) or moderate to severe symptoms once a week is considered GERD. Heartburn (pyrosis) is the most common symptom. Heartburn is a burning, tight sensation felt intermittently beneath the lower sternum and spreading upward to the throat or jaw. It may occur after ingesting food or drugs that decrease the LES pressure or directly irritate the esophageal mucosa. An HCP should evaluate heartburn that occurs more than twice a week, is severe, is associated with dysphagia, or occurs at night and wakes a person from sleep. Older adults who report the recent onset of heartburn should receive medical evaluation.

FIG. 41.3 Esophagitis with esophageal ulcerations.

GERD-related chest pain can mimic angina. It is described as burning; squeezing; or radiating to the back, neck, jaw, or arms. Chest pain is more common in older adults with GERD. Unlike angina, GERD-related chest pain is relieved with antacids. Patients may have dyspepsia or regurgitation. Dyspepsia is pain or discomfort centered in the upper abdomen (mainly in or around the midline as opposed to the right or left hypochondrium). Regurgitation is often described as hot, bitter, or sour liquid coming into the throat or mouth. A person with GERD may report respiratory symptoms, including wheezing, coughing, and dyspnea. Nighttime discomfort and coughing can awaken the person, resulting in disturbed sleep patterns. Otolaryngologic symptoms include hoarseness, sore throat, a

globus sensation (sense of a lump in the throat), hypersalivation, and choking.

Complications Complications of GERD are due to the direct local effects of gastric acid on the esophageal mucosa. Esophagitis (inflammation of the esophagus) is a common complication of GERD. Esophagitis with esophageal ulcerations is shown in Fig. 41.3. Repeated esophagitis may lead to scar tissue formation, stricture, and dysphagia. Another complication of chronic GERD is Barrett’s esophagus (BE) (esophageal metaplasia). Metaplasia is the reversible change from one type of cell to another type because of an abnormal stimulus. In BE, the flat epithelial cells in the distal esophagus change into columnar epithelial cells. These cell changes are primarily due to GERD. However, some people with no history of GERD develop BE. About 5% to 20% of people with chronic GERD have BE.10 Other risk factors include being over age 60, being male, being white, and having central obesity. BE is a precancerous lesion that increases the patient’s risk for esophageal cancer. Because of this risk, those with BE undergo surveillance endoscopy or radiofrequency ablation as recommended. Respiratory complications of GERD include cough, bronchospasm, laryngospasm, and cricopharyngeal spasm. These complications are due to gastric secretions irritating the upper air∗way. Asthma, chronic bronchitis, and pneumonia may develop from aspiration into the respiratory system. Dental erosion, especially in the posterior teeth, may result from acid reflux into the mouth.

TABLE 41.8 Interprofessional CareGERD and

Hiatal Hernia

Diagnostic Assessment

• History and physical examination • Upper GI endoscopy with biopsy and cytologic analysis • Esophagram (barium swallow) • Motility (manometry) studies • pH monitoring (laboratory or 24 hr ambulatory) • Radionuclide studies

Management Conservative • Elevate head of bed on 4- to 6-in blocks • Avoid reflux-inducing foods (fatty foods, chocolate, peppermint) • Avoid alcohol • Reduce or avoid acidic pH beverages (colas, red wine, orange juice)

Drug Therapy (Table 41.10) • PPIs • H2 receptor blockers • Antacids • Prokinetic drug therapy

Surgical Therapy • Nissen fundoplication • Toupet fundoplication

Endoscopic Therapy

• Intraluminal valvuloplasty • Radiofrequency ablation

Diagnostic Studies GERD is often diagnosed based on symptoms and the patient’s response to behavioral and drug therapies. Diagnostic tests are done when usual therapy is ineffective or when complications are suspected. Diagnostic studies done to determine the cause of the GERD are shown in Table 41.8. Endoscopy is useful in assessing the LES competence and the degree of inflammation (if present), potential scarring, and strictures. Biopsy and cytologic specimens can distinguish stomach or esophageal cancer from BE. In addition, the degree of dysplasia (low grade versus high grade) is determined. Manometric studies measure pressure in the esophagus and LES and esophageal motility function. Ambulatory esophageal pH monitoring is an option for those with refractory symptoms and no evidence of mucosal inflammation. Radionuclide tests can detect reflux of gastric contents and the rate of esophageal clearance.

Nursing and Interprofessional Management: GERD Most patients with GERD can successfully manage the condition through lifestyle modifications, drug therapy, and nutrition therapy. These approaches require patient teaching and adherence to therapies. When these therapies are ineffective, surgery is an option (Table 41.8).

Lifestyle Modifications Teach the patient with GERD to avoid factors that trigger symptoms. The head of the bed is elevated 30 degrees. This can be done using pillows or with 4- to 6-in blocks under the bed. The patient should not be supine for 2 to 3 hours after a meal. A patient and caregiver teaching guide is shown in Table 41.9. Encourage patients who smoke to stop. If needed, refer the patient to community resources for help in stopping smoking. See Chapter 10 for more information related to smoking cessation. If stress causes symptoms, discuss measures to cope with stress. (See Chapter 6 for stress management techniques.)

TABLE 41.9 Patient & Caregiver TeachingGERD Include the following instructions when teaching the patient and caregiver about managing GERD: 1. Explain the reason for a low-fat diet. 2. Have the patient to eat small, frequent meals to prevent gastric distention. 3. Explain the reason for avoiding alcohol, smoking (causes an almost immediate, marked decrease in lower esophageal sphincter pressure), and beverages that contain caffeine.

4. Tell the patient to not lie down for 2–3 hr after eating, wear tight clothing around the waist, or bend over (especially after eating). 5. Have the patient avoid eating within 3 hr of bedtime. 6. Have the patient to sleep with head of bed elevated on 4- to 6-in blocks (gravity fosters esophageal emptying). 7. Provide information about drugs, including reason for their use and common side effects. 8. Discuss strategies for weight reduction if appropriate. 9. Encourage patient and caregiver to share concerns about lifestyle changes and living with a chronic problem.

Drug Therapy Drug therapy for GERD focuses on decreasing the volume and acidity of reflux, improving LES function, increasing esophageal clearance, and protecting the esophageal mucosa (Table 41.10). Proton pump inhibitors (PPIs) and histamine (H2) receptor blockers are the most common and effective treatments for symptomatic GERD.11 The goal of HCl acid suppression treatment is to reduce the acidity of the gastric refluxate. Patients who are symptomatic with GERD but do not have esophagitis (nonerosive GERD) achieve symptom relief with PPIs and H2 receptor blockers. Both PPIs and H2 receptor blockers are available in prescription or OTC preparations. Teach the patient about side effects. Tell the patient to take medications as prescribed and not to stop without checking with the HCP. Have patients contact the HCP if symptoms persist. PPIs are more effective in healing esophagitis than H2 receptor blockers. PPIs also decrease the incidence of esophageal strictures, a complication of chronic GERD. Therapy should start with once-daily dosing, taken before the first meal of the day. Long-term use of PPIs may be associated with decreased bone density, kidney disease, vitamin B12 and magnesium deficiency, and increased risk for dementia.12

Drug Alert Proton Pump Inhibitors (PPIs) • Long-term use or high doses may increase the risk for fractures of hip, wrist, and spine. • Patients should take the lowest dose for the shortest duration needed to treat their condition. • Use may increase the risk for C. difficile infection in hospitalized patients.12 H2 receptor blockers reduce symptoms and promote esophageal healing in 50% of patients. The onset of action of H2 receptor blockers is 1 hour. Depending on the specific drug, therapeutic effects last up to 12 hours. We can give famotidine, ranitidine, and cimetidine orally or IV. Nizatidine is only available orally. Some preparations combine an H2 receptor blocker with an antacid. For example, Pepcid Complete includes famotidine, calcium carbonate, and magnesium hydroxide. Adjunctive treatments include antacids and prokinetic drugs. Antacids produce quick, short-lived relief of heartburn. Common antacids consist of magnesium hydroxide or aluminum hydroxide as single preparations or in various combinations (Table 41.10). The neutralizing effects of antacids taken on an empty stomach last only 20 to 30 minutes. They are most effective taken 1 to 3 hours after meals and at bedtime. When taken after meals, their effects may last 3 to 4 hours. Antacids with or without alginic acid (e.g., Gaviscon) may be useful in patients with mild, intermittent heartburn. In patients with moderate to severe or frequent symptoms or patients with esophagitis, antacids are not effective in relieving symptoms or healing lesions. After an acute phase of bleeding, antacids may be given hourly, either orally or through the NG tube. If an NG tube is in place, periodically aspirate the stomach contents and test the pH level.

If pH is less than 5, intermittent suction may be used, or the frequency or dosage of the antacid or antisecretory agent increased. The type and dosage of antacid given depend on side effects and potential drug interactions. Antacids high in sodium are used cautiously in older adults and patients with CVD, liver, and renal disease. Patients with renal failure should not take magnesium preparations because of the risk for magnesium toxicity. An antacid combination of aluminum and magnesium decreases the side effects of both. Antacids can interact unfavorably with many drugs. They enhance the effects of some drugs, like benzodiazepines and pseudoephedrine. In many instances, antacids decrease the absorption rates of other drugs, such as thyroid hormones, phenytoin, and tetracycline. Before antacid therapy begins, inform the HCP of any drugs that a patient is taking. Prokinetics increase LES pressure and improve gastric emptying, which may result in a small improvement in regurgitation and vomiting. Common agents include cisapride, metoclopramide (Reglan), bethanechol, and baclofen. However, many have significant side effects, so their use is limited only to those with known delayed gastric emptying.13

Nutritional Therapy No specific diet is used to treat GERD. Some patients may need to avoid foods that decrease LES pressure, such as chocolate, peppermint, fatty foods, coffee, and tea (Table 41.7), which predispose them to reflux. Certain foods (e.g., tomato-based products, orange juice, cola, red wine) may irritate the esophagus. Tell the patient to avoid late evening meals, nighttime snacking, and milk, especially at bedtime, since it increases gastric acid secretion. Small, frequent meals and drinking fluids between meals help prevent overdistention of the stomach. Increased saliva production by chewing gum and oral lozenges may help with mild symptoms. Recommend weight reduction if the patient is overweight.

Surgical Therapy Surgical therapy (antireflux surgery) is reserved for patients with complications, such as esophagitis, medication intolerance, stricture, BE, and persistent severe symptoms. The goal of surgical therapy is to reduce reflux by enhancing the integrity of the LES. Most surgical procedures are done laparoscopically. The fundus of the stomach is wrapped around the lower part of the esophagus to reinforce and repair the defective barrier. Nissen and Toupet fundoplications are common laparoscopic antireflux surgeries.

TABLE 41.10 Drug TherapyGERD and Peptic

Ulcer Disease (PUD)

Laparoscopic fundoplication is often an outpatient procedure. However, patients at risk for complications, including those with prior upper abdominal surgeries or co-morbidities (e.g., cardiac disease, obesity), may be hospitalized after the procedure. A small number of patients have complications, including gastric or esophageal injury, splenic injury, pneumothorax, perforation, bleeding, infection, and pneumonia. After surgery, reflux symptoms should decrease. However,

recurrence is possible. In the first month after surgery, the patient may report mild dysphagia caused by edema, but it should resolve. Teach the patient to report persistent symptoms, such as heartburn and regurgitation. A LINX Reflux Management System is an option for patients who have symptoms despite maximum medical management. A LINX system is a ring of small, flexible magnets enclosed in titanium beads and connected by titanium wires. Once implanted laparoscopically into the LES, the ring strengthens the weak LES. Under resting (nonswallowing) conditions, the magnetic attraction between the beads helps keep a weak LES closed to prevent reflux. When the person swallows, the force of pressure associated with the movement of fluids or foods overwhelms the magnetic forces and the fluid or food passes to the stomach. Adverse events with the system include difficulty swallowing, nausea, and pain when swallowing food. Tell patients who have a LINX system not to have an MRI as it could cause serious harm.

FIG. 41.4 Nissen fundoplication. A, Fundus of stomach is wrapped around distal esophagus. B, The fundus is then sutured to itself. Modified from Doughty DB, Jackson DB: Mosby’s clinical nursing series: Gastrointestinal disorders, St Louis, 1993, Mosby.

Endoscopic Therapy Alternatives to surgical therapy include endoscopic mucosal resection (EMR) and radiofrequency ablation. The heat energy delivered through radiofrequencies creates lesions, which we think thicken the LES. For patients with high-grade dysplasia, EMR can be used as a diagnostic test to obtain biopsy samples. Biopsy results determine whether cancer is present.

Hiatal Hernia Hiatal hernia is herniation of part of the stomach into the esophagus through an opening, or hiatus, in the diaphragm. We also call it a diaphragmatic hernia or esophageal hernia. Hiatal hernias are the most common abnormality found on x-ray examination of the upper GI tract. They are common in older adults and occur more often in women. There are 2 types of hiatal hernias (Fig. 41.4): 1. Sliding: The junction of the stomach and esophagus is above the diaphragm, and a part of the stomach slides through the hiatal opening in the diaphragm. This occurs when the patient is supine. The hernia usually goes back into the abdominal cavity when the patient is standing upright. This is the most common type. 2. Paraesophageal or rolling: The fundus and greater curvature of the stomach roll up through the diaphragm, forming a pocket alongside the esophagus. The esophagogastric junction stays in the normal position. Acute paraesophageal hernia is a medical emergency.

Etiology and Pathophysiology Many factors contribute to the development of a hiatal hernia. Structural changes (weakening of the muscles in the diaphragm around the esophagogastric opening) occur with aging. Factors that increase intraabdominal pressure may predispose patients to developing a hiatal hernia. These include obesity, pregnancy, ascites, tumors, intense physical exertion, and heavy lifting on a continual basis.

Clinical Manifestations and Complications

Some people with hiatal hernia are asymptomatic. When present, manifestations of hiatal hernia are similar to those described for GERD on pp. 896-897. Complications that may occur with hiatal hernia include GERD, esophagitis, hemorrhage from erosion, stenosis (narrowing of the esophagus), ulcerations of the herniated part of the stomach, strangulation of the hernia, and regurgitation with tracheal aspiration.

FIG. 41.5 A, Sliding hiatal hernia. B, Rolling or paraesophageal hernia.

Diagnostic Studies An esophagram (barium swallow) may show the protrusion of gastric mucosa through the esophageal hiatus. Endoscopic visualization of the lower esophagus gives information on the degree of mucosal inflammation or other abnormalities. Other tests done are the same as those for GERD (Table 41.8).

Nursing and Interprofessional Management: Hiatal Hernia Conservative therapy of hiatal hernia is similar to that described for GERD (pp. 897-898). Teach the patient to reduce intraabdominal pressure by eliminating constricting garments and avoiding lifting and straining. Surgical approaches to hiatal hernias can include reduction of the herniated stomach into the abdomen, herniotomy (excision of the hernia sac), herniorrhaphy (closure of the hiatal defect), fundoplication, and gastropexy (attachment of the stomach below the diaphragm to prevent reherniation). The goals are to reduce the hernia, provide an acceptable LES pressure, and prevent movement of the gastroesophageal junction. Surgery to repair hiatal hernia is often done laparoscopically by either Nissen or Toupet techniques (Fig. 41.5). The approach used (thoracic or abdominal) depends on the patient.

Gerontologic Considerations: GERD and Hiatal Hernia The incidence of hiatal hernia and GERD increases with age. Hiatal hernia is associated with weakening of the diaphragm, obesity, kyphosis, or other factors (e.g., wearing girdles) that increase intraabdominal pressure. Older patients may take drugs known to decrease LES pressure (e.g., nitrates, calcium channel blockers, antidepressants). Other agents, such as nonsteroidal antiinflammatory drugs (NSAIDs) and potassium, can irritate the esophageal mucosa, causing medication-induced esophagitis. Some older adults with hiatal hernia and GERD are asymptomatic or have less severe symptoms. The first sign may be a serious problem, such as esophageal bleeding from esophagitis or respiratory complications (e.g., aspiration pneumonia) due to aspiration of gastric

contents. The clinical course and management of GERD and hiatal hernia in the older adult are similar to those for the younger adult. Changes in lifestyle, including smoking cessation and elevating the head of the bed on blocks may be challenging for the older adult. Laparoscopic procedures reduce the risk associated with surgical repair. An older patient with heart and lung problems may not be a good candidate for surgical intervention.

Esophageal Cancer Esophageal cancer is not common. However, the rates are increasing. In the United States, around 17,280 new cases are diagnosed and 15,850 deaths occur from esophageal cancer each year.5 The overall 5year survival rate is 19%. Most esophageal cancers are adenocarcinomas. The others are squamous cell tumors. Adenocarcinomas arise from the glands lining the esophagus and resemble cancers of the stomach and small intestine. The incidence of esophageal cancer increases with age. Those between 65 and 75 are at greatest risk. The incidence is higher in men than in women.

Etiology and Pathophysiology The cause of esophageal cancer is unknown. Key risk factors include BE, smoking, excess alcohol use, and obesity. For example, current smoking or a history of smoking is associated with a twofold higher risk for esophageal cancer. Those with injury to the esophageal mucosa (e.g., from occupational exposure to asbestos and cement dust) are at greater risk. Achalasia, a condition marked by delayed emptying of the lower esophagus, is associated with squamous cell cancer. Most esophageal tumors occur in the middle and lower portions of the esophagus. The tumor usually appears as an ulcerated lesion. It may penetrate the muscular layer and extend outside the wall of the esophagus. Many patients have advanced disease at the time of diagnosis. The cancer spreads via the lymph system, with the liver and lung being common sites of metastasis.

Clinical Manifestations and Complications By the time the patient has symptoms, the tumor is often advanced. Progressive dysphagia is the most common symptom. It may be

described as a substernal feeling that food is not passing. Initially the dysphagia occurs only with meat, then with soft foods, and eventually with liquids. Pain develops late. It occurs in the substernal, epigastric, or back areas and usually increases with swallowing. The pain may radiate to the neck, jaw, ears, and shoulders. If the tumor is in the upper third of the esophagus, symptoms, such as sore throat, choking, and hoarseness, may occur. Most patients lose weight. When esophageal stenosis (narrowing) is severe, regurgitation of blood-flecked esophageal contents is common. Hemorrhage occurs if the cancer erodes through the esophagus and into the aorta. Esophageal perforation with fistula formation into the lung or trachea sometimes develops. The tumor may enlarge enough to cause esophageal obstruction, particularly in the later stages.

TABLE 41.11 Interprofessional CareEsophageal

Cancer

Diagnostic Assessment • History and physical examination • Endoscopy of esophagus with biopsy • Endoscopic ultrasonography • Esophagram (barium swallow) • Bronchoscopy • CT, MRI, PET scans

Management • Surgical therapy • Esophagectomy • Esophagoenterostomy

• Esophagogastrostomy • Endoscopic therapy • Dilation • Endoscopic mucosal resection • Laser therapy • Photodynamic therapy • Radiofrequency ablation • Stent or prosthesis placement • Radiation therapy • Chemotherapy

Diagnostic Studies Endoscopic biopsy is required to diagnose esophageal cancer. Endoscopic ultrasonography (EUS) is important in staging esophageal cancer. Esophagram (barium swallow) may show narrowing of the esophagus at the tumor site (Table 41.11).

Interprofessional Management The treatment of esophageal cancer depends on the tumor’s location and whether invasion or metastasis is present. Esophageal cancer usually has a poor prognosis because it is often diagnosed at an advanced stage. The best results occur with a multimodal approach, including surgery, endoscopic ablation, chemotherapy, and radiation therapy. Depending on the location and cancer spread, only chemotherapy and radiation may be used. Palliative therapy consists of restoring swallowing function and maintaining nutrition and hydration.

Surgical Therapy The types of surgical procedures done are (1) removal of part or all of the esophagus (esophagectomy) with use of a Dacron graft to replace the resected part, (2) resection of a portion of the esophagus and anastomosis of the remaining portion to the stomach

(esophagogastrostomy), and (3) resection of a portion of the esophagus and anastomosis of a segment of colon to the remaining portion (esophagoenterostomy). The surgical approaches may be open (thoracic, abdominal incision) or laparoscopic. Minimally invasive esophagectomy (e.g., laparoscopic vagal nerve– sparing surgery) is being done more often. It has the advantage of using smaller incisions, decreasing intensive care unit (ICU) and hospital stays, and producing fewer pulmonary complications.

Endoscopic Therapy Endoscopic therapy includes photodynamic therapy, EMR, and radiofrequency ablation. In photodynamic therapy, the patient receives an IV injection of porfimer sodium (Photofrin), a photosensitizer. Although most tissues absorb porfimer, cancer tissue absorbs it to a greater degree. The HCP directs light towards the cancerous area using a fiber passed through an endoscope. The light reacts with porfimer, starting a reaction that destroys the cancer cells. Patients must avoid direct sunlight for up to 6 weeks after the procedure. EMR is an option for some small, very early stage cancers. It involves the removal of cancer tissue using an endoscope. Radiofrequency ablation uses electric currents to kill cancer cells by heating them. Dilation, stent placement, or both can relieve obstruction. Dilation increases the lumen of the esophagus. It often relieves dysphagia and allows for improved nutrition. There are various types of dilators. Placement of stents or expandable stents may help when dilation is no longer effective. Stents allow food and liquid to pass through the stenotic area of the esophagus. Self-expandable metal stents are available with features to prevent stent migration and tumor ingrowth. Stents placed before surgery may help improve the patient’s nutritional status. Endoscopic laser therapy may be used in combination with dilation. Laser therapy can be repeated if obstruction recurs as the tumor grows. Sometimes these procedures are combined with radiation

therapy.

Radiation Therapy Depending on the type and stage of esophageal cancer, the patient may receive chemotherapy with or without radiation therapy. Concurrent therapy is given for palliation of symptoms, especially dysphagia, and to increase survival. Some patients receive radiation therapy before surgery.

Chemotherapy Many different chemotherapy drugs can be used to treat esophageal cancer. The preferred regimens are carboplatin and paclitaxel, cisplatin with capecitabine (Xeloda), cisplatin and fluorouracil, and oxaliplatin with either fluorouracil or capecitabine. DCF (docetaxel, cisplatin, fluorouracil) is an option for metastatic disease. Other treatments include ECF (epirubicin [Ellence], cisplatin, fluorouracil) and irinotecan (Camptosar).14 Chemotherapy is discussed in Chapter 15.

Targeted Therapy Some esophageal cancers have too much HER-2 protein on their cell surfaces, which helps cancer cells to grow. Trastuzumab (Herceptin) is a drug that targets the HER-2 protein and kills the cancer cells. This drug can cause heart damage, so it is not given with other chemotherapy drugs that also cause heart damage, such as epirubicin.14 Ramucirumab (Cyramza), an angiogenesis inhibitor, binds to the receptor for vascular endothelial growth factor (VEGF), a compound that stimulates blood vessel growth. Thus it prevents VEGF from binding to the receptor and signaling the body to make more blood vessels. This can help slow or stop the growth and spread of cancer. Ramucirumab treats advanced cancers that start at the gastroesophageal junction. Targeted therapies are discussed in Chapter 15.

Nutritional Therapy After esophageal surgery IV fluids are given. A jejunostomy, gastrostomy, or esophagostomy feeding tube may be placed to feed the patient depending on the type of surgery (e.g., esophagogastrectomy). A swallowing study is often done before allowing the patient to have oral fluids. When starting fluids, give water (30 to 60 mL) hourly and gradually progress to small, frequent, bland meals. Place the patient in an upright position for 2 hours after to prevent regurgitation. With EN, observe the patient for signs of intolerance to the feeding or leakage of the feeding into the mediastinum. Symptoms that indicate leakage are pain, increased temperature, and dyspnea. (EN is discussed in Chapter 39.)

Nursing Management: Esophageal Cancer Nursing Assessment Ask the patient about a history of GERD, hiatal hernia, achalasia, BE, and tobacco and alcohol use. Assess the patient for progressive dysphagia and odynophagia (burning, squeezing pain while swallowing). Ask about the type of substances (e.g., meats, soft foods, liquids) that cause dysphagia. Assess the patient for pain (substernal, epigastric, or back areas), choking, heartburn, hoarseness, cough, anorexia, weight loss, and regurgitation.

Nursing Diagnoses Nursing diagnoses for the patient with esophageal cancer include: • Chronic pain • Impaired nutritional intake • Impaired nutritional status • Risk for aspiration • Anxiety

Planning The overall goals are that the patient with esophageal cancer will (1) have relief of symptoms, including pain and dysphagia; (2) achieve optimal nutritional intake; and (3) have a quality of life appropriate to stage of disease and prognosis.

Nursing Implementation Health Promotion Counsel the patient with GERD, BE, or hiatal hernia about the

importance of regular follow-up evaluation. Health counseling should focus on smoking cessation and reducing risk factors for GERD (Table 41.7). Maintaining good oral hygiene and dietary habits (e.g., intake of fresh fruits and vegetables) is important. Encourage patients to seek medical attention for any esophageal problems, especially dysphagia.

Acute Care Preoperative Care The patient and caregiver usually react with shock, disbelief, and depression when given the diagnosis of esophageal cancer. Provide emotional and physical support, provide information, clarify test results, and maintain a positive attitude with respect to the patient’s immediate recovery and long-term survival. In addition to general preoperative teaching and preparation, pay attention to the patient’s nutritional needs. Many are poorly nourished because of the inability to ingest adequate amounts of food and fluids. A high-calorie, high-protein diet is recommended. Some patients need a liquid form of this diet. Others may need IV fluid replacement or parenteral nutrition (PN). Teach the patient and caregiver how to keep an intake and output record and assess for signs of fluid and electrolyte imbalance. Some treatment protocols include preoperative radiation and chemotherapy. Meticulous oral care is essential. Cleanse the mouth thoroughly, including the tongue, gingivae, and teeth or dentures. It may be necessary to use swabs or a gauze pad and to scrub the mouth, including the tongue. Milk of Magnesia with mineral oil helps remove crust formation. Teaching should include information about chest tubes (with a planned open thoracic approach), IV lines, NG tubes, pain management, gastrostomy or jejunostomy feeding, turning, coughing, and deep breathing. (General preoperative care is discussed in Chapter 17.)

Postoperative Care

During the immediate postoperative period, the patient usually receives care in the ICU for 1 to 2 days. In addition to usual postoperative complications, dysrhythmias may result from the proximity of the pericardium to the surgical site. Other complications include anastomotic leaks, fistula formation, interstitial pulmonary edema, and acute respiratory distress related to the disruption of the mediastinal lymph nodes. The patient usually has an NG tube in place for 5 to 7 days. The drainage may be bloody for 8 to 12 hours. The drainage gradually changes to greenish yellow. Assessing the drainage, maintaining the tube, and providing oral and nasal care are key nursing responsibilities. Do not irrigate the NG tube, reposition it, or reinsert it without consulting the HCP. If the chest cavity is entered, postoperative drainage is achieved with chest tube insertion. Assess the amount and type of drainage. Notify the HCP of excess drainage (e.g., over 400 to 600 mL in 8 hours). Chest surgery and drainage tubes are discussed in Chapter 27. Because of the location of the surgery and the patient’ general condition, implement measures to prevent respiratory complications. Have the patient turn, cough and deep breathe, and use an incentive spirometer every 2 hours. Follow VTE prophylaxis measures and provide effective pain management. Position the patient in a semiFowler’s or Fowler’s position to prevent reflux and aspiration of gastric secretions. When the patient can drink fluids or eat, maintain the upright position for at least 2 hours after eating to assist with gastric emptying.

Ambulatory Care Many patients need long-term follow-up care after surgery for esophageal cancer. The patient may need chemotherapy and radiation treatment after surgery. Encourage and assist the patient in maintaining adequate nutrition. A permanent feeding gastrostomy may be needed. The patient usually is afraid and anxious about the cancer diagnosis. Know what the HCP has told the patient about the prognosis and provide appropriate counseling.

Referral to a palliative care or home health nurse may be needed. (See Chapter 15 for the care of the cancer patient and Chapter 9 for a discussion of palliative and end-of-life care.)

Evaluation The expected outcomes are that the patient with esophageal cancer will • Maintain a patent airway • Have relief of pain • Be able to swallow comfortably and consume adequate nutritional intake • Have a quality of life appropriate to stage of disease and prognosis

Other Esophageal Disorders Eosinophilic Esophagitis Eosinophilic esophagitis (EoE) is characterized by swelling of the esophagus from an infiltration of eosinophils. People with EoE often have a personal or family history of other allergic diseases. The most common food triggers are milk, egg, wheat, rye, and beef. Environmental allergens, such as pollens, molds, cat, dog, and dust mite allergens, may be involved in the development of EoE. Patients may have severe heartburn, difficulty swallowing, food impaction in the esophagus, nausea, vomiting, and weight loss. The diagnosis is based on symptoms and biopsy findings of eosinophils infiltrating esophageal tissue obtained from endoscopy. Allergy skin testing helps to determine the person’s allergens. A trial of avoiding the foods to which the person has positive allergy tests is the first treatment. Other common treatments include the use of PPIs (Table 41.10) and corticosteroids. Corticosteroids are used to treat EoE when avoiding allergic triggers does not relieve symptoms. Corticosteroids may be used orally (prednisone) or as a topical therapy with inhaled corticosteroids (e.g., fluticasone [Flovent]). The patient takes a puff of fluticasone, and rather than inhaling it, swallows the medication. This directly delivers the drug to the esophagus. The most common side effect is a yeast infection of the throat (esophageal candidiasis).

FIG. 41.6 Sites for esophageal diverticula. These hollow outpouchings may occur just above the upper esophageal sphincter (Zenker’s), near the midpoint of the esophagus (traction), and just above the lower esophageal sphincter (epiphrenic). Modified from Price SA, Wilson LM: Pathophysiology: Clinical concepts of disease processes, ed 6, St Louis, 2003, Mosby.

Esophageal Diverticula Esophageal diverticula are saclike outpouchings of 1 or more layers of the esophagus. They occur in 3 main areas: (1) above the upper esophageal sphincter (Zenker’s diverticulum), which is the most common location; (2) near the esophageal midpoint (traction diverticulum); and (3) above the LES (epiphrenic diverticulum) (Fig. 41.6). Zenker’s diverticula occur commonly in people older than 60 years. Typical symptoms include dysphagia, regurgitation, chronic cough, aspiration, and weight loss. Food becomes trapped in the outpouches. This causes tasting sour food and smelling a foul odor. Complications

include malnutrition, aspiration, and perforation. Endoscopy or barium studies can easily establish a diagnosis. There is no specific treatment. Some patients find that they can empty the pocket of food that collects by applying pressure at a certain point on the neck. The diet may have to be limited to foods that pass more readily (e.g., blenderized foods). Surgical treatment may be needed if nutrition is disrupted. Endoscopic stapling diverticulotomy or diverticulostomy is associated with decreased complications compared with the open approaches. The most serious surgical complication is esophageal perforation.

Esophageal Structures The most common cause of esophageal strictures (or narrowing) is chronic GERD. The ingestion of strong acids or alkalis, external beam radiation, and surgical anastomosis can also create strictures. Trauma, such as throat lacerations and gunshot wounds, can lead to strictures because of scar formation. Strictures can cause dysphagia and regurgitation, leading to weight loss. Strictures can be dilated using mechanical bougies (dilating instruments) or balloons. Dilation may be done with or without endoscopy, or with fluoroscopy. Surgical excision with anastomosis is sometimes needed. The patient may have a temporary or permanent gastrostomy.

FIG. 41.7 Esophageal achalasia. A, Early stage, showing tapering of lower esophagus. B, Advanced stage, showing dilated, tortuous esophagus.

Achalasia In achalasia, peristalsis of the lower two thirds (smooth muscle) of the esophagus is absent. Achalasia is a rare, chronic disorder. The exact cause is unknown. With achalasia, the pressure in the LES increases along with incomplete relaxation. Esophageal obstruction at or near the diaphragm occurs. Food and fluid accumulate in the lower esophagus. The result is dilation of the esophagus above the tapered affected segment of the lower esophagus (Fig. 41.7). There is a selective loss of inhibitory neurons, resulting in unopposed contraction of the LES. The onset of achalasia is usually slow. Dysphagia is the most common symptom and occurs with both liquids and solids. Patients

may report a globus sensation and/or substernal chest pain (similar to angina pain) during or right after a meal. About a third have nighttime regurgitation. Halitosis (foul-smelling breath) and the inability to eructate (belch) can occur. Patients may report symptoms of GERD and regurgitation of sour-tasting food and liquids, especially when they are lying down. Weight loss is common. Diagnosis is made with esophagram (barium swallow), manometric evaluation (high-resolution manometry), and/or endoscopic evaluation. Treatment focuses on symptom management. The goals of treatment are to relieve dysphagia and regurgitation, improve esophageal emptying by disrupting the LES, and prevent the development of megaesophagus (enlargement of the lower esophagus). Endoscopic pneumatic dilation involves dilating the LES muscle using balloons of progressively larger diameter (3.0, 3.5, and 4.0 cm) (Fig. 41.8). It is an outpatient procedure. If this is ineffective, the next option is a Heller myotomy, done laparoscopically. In this procedure, the HCP cuts through the muscles of the LES, allowing food to pass. Because GERD with esophagitis and stricture is a common complication, the patient often has anti-reflux surgery at the same time. The patient typically returns to usual activities 1 to 2 weeks afterward. Medical therapy is less effective than invasive procedures. The injection of botulinum toxin endoscopically into the LES gives shortterm relief of symptoms and improves esophageal emptying. It works by promoting relaxation of the smooth muscle. This treatment is used for older patients for whom surgery and pneumatic dilation may not be appropriate due to other chronic illnesses. Nitrates (e.g., isosorbide dinitrate) and calcium channel blockers (e.g., nifedipine [Procardia]) relax the LES and may improve dysphagia. They are taken sublingually 10 to 30 minutes before meals. Side effects (e.g., headache), drug tolerance, and short duration of action limit their use. Symptomatic treatment consists of eating a semisoft diet, eating slowly, drinking fluid with meals, and sleeping with the head elevated.

FIG. 41.8 Pneumatic dilation can treat achalasia by maintaining an adequate lumen and decreasing lower esophageal sphincter (LES) tone. Modified from Price SA, Wilson LM: Pathophysiology: Clinical concepts of disease processes, ed 6, St Louis, 2003, Mosby.

Esophageal Varices Esophageal varices are dilated, tortuous veins occurring in the lower part of the esophagus because of portal hypertension. Esophageal varices are a common complication of liver cirrhosis. They are discussed in Chapter 43.

Disorders of the Stomach and Upper Small Intestine Peptic Ulcer Disease Peptic ulcer disease (PUD) is a condition characterized by erosion of the GI mucosa from the digestive action of HCl acid and pepsin. Any part of the GI tract that is in contact with gastric secretions is susceptible to ulcer development. This includes the lower esophagus, stomach, duodenum, and margin of a gastrojejunal anastomosis after surgical procedures. PUD affects about 4.5 million people in the United States each year.15

Types Peptic ulcers are classified as acute or chronic, depending on the degree and duration of mucosal involvement, and gastric or duodenal, according to the location. The acute ulcer (Fig. 41.9) is associated with superficial erosion and minimal inflammation. It is of short duration and resolves quickly when the cause is identified and removed. A chronic ulcer (Fig. 41.10) is one of long duration, eroding through the muscular wall with the formation of fibrous tissue. It is present continuously for many months or intermittently throughout the person’s lifetime. Chronic ulcers are more common than acute erosions. Although gastric and duodenal ulcers are both considered PUD, they are different in their incidence and presentation (Table 41.12).

FIG. 41.9 Peptic ulcers, including an erosion, an acute ulcer, and a chronic ulcer. Both the acute ulcer and the chronic ulcer may penetrate the entire wall of the stomach. Modified from Price SA, Wilson LM: Pathophysiology: Clinical concepts of disease processes, ed 6, St Louis, 2003, Mosby.

FIG. 41.10 Peptic ulcer of the duodenum. From Kumar V, Abbas AK, Aster JC, Fausto N: Robbins and Cotran pathologic basis of disease, ed 8, Philadelphia, 2010, Saunders.

Etiology and Pathophysiology Peptic ulcers develop only in an acid environment. However, an excess of HCl acid is not necessary for ulcer development. Pepsinogen, the precursor of pepsin, changes to pepsin in the presence of HCl acid and a pH of 2 to 3. When food or antacids neutralize the stomach acid level or drugs block acid secretion, the pH increases to 3.5 or more. At a pH of 3.5 or more, pepsin has little or no proteolytic activity. The pathophysiology of ulcer development is outlined in Fig. 41.11. The back diffusion of HCl acid into the gastric mucosa results in cellular destruction and inflammation. Histamine is released from the damaged mucosa. This results in vasodilation, increased capillary permeability, and further secretion of acid and pepsin. Fig. 41.12 shows the interrelationship between the mucosal blood flow and disruption of the gastric mucosal barrier. Several factors damage the

mucosal barrier.

Helicobacter Pylori The major risk factor for PUD is infection with Helicobacter pylori. 80% of gastric and 90% of duodenal ulcers are related to H. pylori. In the United States, H. pylori affects 20% of persons younger than 30 years and 50% of those older than 60 years. Infection likely occurs during childhood with transmission from family members to the child, possibly through a fecal-oral or oral-oral route. The rate is highest in black and Hispanic people.15 Although most people with H. pylori never develop ulcers, it appears that those infected with CagA-positive strains are more likely to have PUD.16 In the stomach, the bacteria can survive a long time by colonizing the gastric epithelial cells within the mucosal layer. The bacteria make urease, which metabolizes urea-producing ammonium chloride and other damaging chemicals. Urease activates the immune response with both antibody production and the release of inflammatory cytokines. This leads to increased gastric secretion and causes tissue damage, leading to PUD.

TABLE 41.12 Comparison of Gastric and

Duodenal Ulcers

Medication-Induced Injury NSAID use is responsible for most non–H. pylori peptic ulcers. NSAIDs inhibit prostaglandin synthesis, increase gastric acid secretion, and reduce the integrity of the mucosal barrier. NSAID use in the presence of H. pylori further increases the risk for PUD. Patients taking corticosteroids or anticoagulants with NSAIDs have a higher risk for PUD.15 Corticosteroids affect mucosal cell renewal and decrease its protective effects.

Lifestyle Factors High alcohol intake is associated with acute mucosal lesions. Alcohol and smoking stimulate acid secretion. Coffee (caffeinated and decaffeinated) is a strong stimulant of gastric acid secretion. Smoking and psychologic distress, including stress and depression, can delay the healing of ulcers once they have developed.

Gastric Ulcers Gastric ulcers can occur in any part of the stomach. They most often occur in the antrum. Gastric ulcers are less common than duodenal

ulcers. Gastric ulcers are more prevalent in women and those over 50 years of age. Because of the peak incidence of gastric ulcers in older adults, the mortality rate from gastric ulcers is greater than that from duodenal ulcers. Gastric ulcers are more likely than duodenal ulcers to cause an obstruction. H. pylori, NSAIDs, and bile reflux are the main risk factors.

FIG. 41.11 Disruption of gastric mucosa and pathophysiologic consequences of back diffusion of acids.

FIG. 41.12 Relationship between mucosal blood flow and disruption of the gastric mucosal barrier.

Duodenal Ulcers Duodenal ulcers account for about 80% of all peptic ulcers. Duodenal ulcers occur at any age, but the incidence is especially high between 35 and 45 years of age. Although many factors are associated with the development of duodenal ulcers, H. pylori is the most common. The development of duodenal ulcers is often associated with a high HCl acid secretion. Those at high risk include people with chronic

obstructive pulmonary disease (COPD), cirrhosis, pancreatitis, hyperparathyroidism, chronic kidney disease, and Zollinger-Ellison syndrome (ZES). ZES is a rare condition characterized by severe peptic ulceration and HCl acid hypersecretion. Duodenal ulcers tend to occur continuously for a few weeks or months and then disappear for a time, only to recur some months later.

Stress-Related Mucosal Disease (SRMD) SRMD is described later in this chapter in the section on acute upper GI bleeding on p. 917.

Clinical Manifestations In gastric ulcers, the discomfort is generally high in the epigastrium and occurs about 1 to 2 hours after meals. The pain is described as “burning” or “gaseous.” If the ulcer has eroded through the gastric mucosa, food tends to worsen the pain. For some patients, the earliest symptoms are due to a serious complication, such as perforation. In duodenal ulcers, symptoms occur when gastric acid comes in contact with the ulcers. With meal ingestion, food is present to help buffer the acid. Symptoms occur generally 2 to 5 hours after a meal. The pain is described as “burning” or “cramplike.” It is most often in the midepigastric region beneath the xiphoid process. Duodenal ulcers can also cause back pain. Some patients have bloating, nausea, vomiting, and early feelings of fullness. Not all patients with ulcers will have pain or discomfort. Silent peptic ulcers are more likely to occur in older adults and those taking NSAIDs. The presence or absence of symptoms is not related to the size of the ulcer or the degree of healing.

Diagnostic Studies Endoscopy is the most accurate procedure to determine the presence and location of an ulcer.15 It allows for direct viewing of the gastric and duodenal mucosa (Fig. 41.13). During endoscopy, tissue

specimens are taken to determine if H. pylori is present and rule out stomach cancer. Endoscopy can also assess the degree of ulcer healing after treatment. Several noninvasive and invasive tests are available to confirm H. pylori infection. The gold standard for diagnosing H. pylori infection is a biopsy of the antral mucosa with testing for urease (rapid urease testing). Urea is a by-product of the metabolism of H. pylori bacteria. Noninvasive tests include serology, stool, and breath testing. The urea breath and stool antigen tests can identify active infection. Stool tests are not as accurate as the urea breath test. Antibody tests for H. pylori can remain positive for years. They are not good for evaluating treatment results. A barium contrast study may be used to diagnose gastric outlet obstruction or for ulcer detection in those who cannot undergo endoscopy. High fasting serum gastrin levels may show the presence of a possible gastrinoma (ZES). A secretin stimulation test can discern a gastrinoma from other causes of hypergastrinemia. Laboratory tests, including a CBC, liver enzyme studies, serum amylase, and stool examination, may be done. A CBC may show anemia from ulcer bleeding. Liver enzyme studies help detect any liver problems (e.g., cirrhosis) that may complicate ulcer treatment. Stools are tested for blood. A serum amylase evaluates pancreatic function if we suspect posterior duodenal ulcer penetration of the pancreas.

FIG. 41.13 Esophagogastroduodenoscopy (EGD) directly visualizes the mucosal lining of the stomach with a flexible endoscope. Ulcers or tumors can be directly seen and biopsies obtained.

Interprofessional Management

Conservative Care Treatment begins after diagnostic studies confirm the presence of PUD (Table 41.13). The regimen consists of adequate rest, drug therapy, smoking cessation, dietary modifications (if needed), and long-term follow-up care. The aim of treatment is to decrease gastric acidity and enhance mucosal defense mechanisms. Patients are generally treated in ambulatory care clinics. Pain disappears after 3 to 6 days, but ulcer healing is much slower. Complete healing may take 3 to 9 weeks, depending on ulcer size, treatment plan, and patient adherence. Endoscopic examination is the most accurate method to monitor ulcer healing. The usual follow-up endoscopic evaluation is done 3 to 6 months after diagnosis and treatment. Aspirin and nonselective NSAIDs are stopped for 4 to 6 weeks. When aspirin must be continued, co-administration with a PPI, H2 receptor blocker, or misoprostol may be prescribed. Patients receiving low-dose aspirin (LDA) for CVD and stroke risk who have a history of ulcer disease or complications may need to receive long-term treatment with a PPI. Enteric-coated aspirin decreases localized irritation but does not reduce the overall risk for GI bleeding. Smoking has an irritating effect on the mucosa and delays mucosal healing. The patient should either stop or severely reduce smoking. (See Chapter 10 for ways to promote smoking cessation.) Adequate rest, both physical and emotional, is important for ulcer healing and may require some changes in the patient’s daily routine. Avoiding or restricting alcohol use will enhance healing.

Drug Therapy Medications are a key part of therapy (Table 41.10). Drug therapy focuses on reducing gastric acid secretion and, if needed, eliminating H. pylori infection. Patients with H. pylori infection need treatment with antibiotics and a PPI. After the ulcer has healed, many patients can stop PPI therapy. Some may need to continue low-dose maintenance therapy.

TABLE 41.13 Interprofessional CarePeptic Ulcer

Disease

Diagnostic Assessment • History and physical examination • Upper GI endoscopy with biopsy • Endoscopic ultrasound • H. pylori testing of breath, urine, blood, tissue • Complete blood cell count • Liver enzymes • Serum amylase • Stool testing for blood

Management Conservative Therapy • Adequate rest • Smoking and alcohol cessation • Stress management (see Chapter 6)

Drug Therapy (Tables 41.10 and 41.14) • Antibiotics for H. pylori • PPIs • Adjunctive therapy • H2-receptor blockers • Cytoprotective drugs • Antacids

Acute Exacerbation Without Complications • NPO • NG suction • Adequate rest • IV fluid replacement

Drug Therapy (Tables 41.10 and 41.14) • Antibiotics for H. pylori • PPIs • Adjunctive therapy • H2 receptor blockers • Cytoprotective drugs • Antacids • Sedatives

Acute Exacerbation With Complications (Hemorrhage, Perforation, Obstruction) • NPO • NG suction • IV PPI • Bed rest • IV fluid replacement (lactated Ringer’s solution) • Blood transfusions • Stomach lavage (possible)

Surgical Therapy

• Gastric outlet obstruction: Pyloroplasty and vagotomy • Perforation: Simple closure with omentum graft • Ulcer removal or reduction • Billroth I and II • Vagotomy and pyloroplasty Because ulcers often recur, interrupting or stopping therapy can have harmful results. Strict adherence to the prescribed drug regimen is important. Encourage the patient to adhere to therapy and continue with follow-up care as prescribed. Teach the patient and caregiver about each drug prescribed, why it is ordered, and the expected benefits. Review what to do if pain and discomfort recur or there is blood in vomitus or stools.

TABLE 41.14 Drug TherapyH. pylori Infection

Antibiotic Therapy Eradicating H. pylori is the most important part of treating PUD in patients positive for H. pylori. Antibiotic therapy is prescribed concurrently with a PPI for 14 days (Table 41.14). If the patient has a penicillin allergy, metronidazole is used instead of amoxicillin in the triple-drug regimen. Bismuth can be given alone or as part of a combination capsule (Pylera) containing bismuth, tetracycline, and metronidazole. Because of the existence of antibiotic-resistant organisms, a growing number of patients do not have H. pylori

eradicated with a single round of therapy. Proton Pump Inhibitors PPIs are more effective than H2 receptor blockers in reducing gastric acid secretion and promoting ulcer healing. PPIs are used in combination with antibiotics to treat ulcers caused by H. pylori. Cytoprotective Drug Therapy Sucralfate is used for short-term ulcer treatment. It provides mucosal protection for the esophagus, stomach, and duodenum. Sucralfate does not have acid-neutralizing capabilities. Since it is most effective at a low pH, give it at least 60 minutes before or after an antacid. Adverse side effects are minimal. It binds with cimetidine, digoxin, warfarin, phenytoin, and tetracycline, reducing their bioavailability. Adjunct Drugs H2 receptor blockers and antacids may be used as adjunct therapy to promote ulcer healing. Antacids increase gastric pH by neutralizing HCl acid. As a result, they reduce the acid content of chyme reaching the duodenum. Some antacids (e.g., aluminum hydroxide) can bind to bile salts, thus decreasing the damaging effects of bile on the gastric mucosa. Misoprostol is a synthetic prostaglandin analog prescribed to prevent gastric ulcers caused by NSAIDs and LDA. It has protective and some antisecretory effects on gastric mucosa. People who need chronic NSAID therapy, such as those with osteoarthritis, may benefit from its use. However, it can cause diarrhea and abdominal pain. It is teratogenic and must be used with caution in women of childbearing potential. Tricyclic antidepressants (e.g., imipramine, doxepin) may be prescribed for some patients. They may contribute to overall pain relief through their effects on afferent pain fiber transmission. In addition, they have varying degrees of anticholinergic properties, which result in reduced acid secretion. Anticholinergic drugs are sometimes used for PUD treatment.

Anticholinergics are associated with several side effects, such as dry mouth, warm skin, flushing, thirst, tachycardia, dilated pupils, blurred vision, and urine retention.

Nutritional Therapy There is no specific diet used to treat PUD. Patients should eat and drink foods and fluids that do not cause any distressing symptoms. Foods that may cause gastric irritation include pepper, carbonated beverages, broth (meat extract), and hot, spicy foods. Caffeinecontaining beverages and foods can increase symptoms in some patients. Teach the patient to avoid alcohol use because it can delay healing.

FIG. 41.14 Duodenal ulcer of the posterior wall penetrating the head of the pancreas, resulting in walled-off perforation.

Surgical Therapy With the use of drug therapy and endoscopic therapy to treat PUD, surgery is used less often. Surgery is done on patients with complications that are unresponsive to medical management or concerns about stomach cancer. Gastric surgeries are described later in this chapter on p. 914.

Complications

The 3 major complications of chronic PUD are hemorrhage, perforation, and gastric outlet obstruction.16 All these complications are considered emergency situations and may need surgical intervention.

Hemorrhage Hemorrhage is the most common complication of PUD. Duodenal ulcers cause more upper GI bleeding episodes than gastric ulcers.

Perforation Perforation is considered the most lethal complication of PUD. Perforation risk is highest with large penetrating duodenal ulcers (Fig. 41.14). However, the mortality rate associated with perforation of gastric ulcers is higher. The patient with gastric ulcers is older and often has concurrent medical problems, which accounts for the higher mortality rate. With perforation, the ulcer penetrates the serosal surface with spillage of either gastric or duodenal contents into the peritoneal cavity. The contents entering the peritoneal cavity may contain air, saliva, food particles, HCl acid, pepsin, bacteria, bile, and pancreatic fluid and enzymes. The manifestations of perforation are sudden and dramatic in onset. During the initial phase (0 to 2 hours after perforation), the patient has sudden, severe upper abdominal pain that quickly spreads throughout the abdomen. The pain radiates to the back and shoulders. Food or antacids do not relieve the pain. The abdomen appears rigid and boardlike as the abdominal muscles try to protect from further injury. The patient’s respirations become shallow and rapid. The heart rate is elevated, and the pulse is weak. Bowel sounds are usually absent. Nausea and vomiting may occur. If the condition is untreated, bacterial peritonitis may occur within 6 to 12 hours. The intensity of peritonitis is proportional to the amount and duration of the spillage through the perforation. It is hard to determine from symptoms alone whether a gastric or duodenal ulcer has perforated, because the manifestations of peritonitis are the same

(see Chapter 42). The immediate focus of managing a patient with a perforation is to stop the spillage of gastric or duodenal contents into the peritoneal cavity and restore blood volume. An NG tube can provide continuous aspiration and gastric decompression to stop spillage through the perforation. For duodenal aspiration, the tube is placed as near to the perforation site as possible to facilitate decompression. Circulating blood volume is replaced with lactated Ringer’s and albumin solutions. These solutions substitute for the fluids lost from the vascular and interstitial space as peritonitis develops. Blood replacement in the form of packed RBCs may be needed. A central venous pressure line and an indwelling urinary catheter may be inserted and monitored hourly. The patient with a history of heart disease needs ECG monitoring or placement of a pulmonary artery catheter for accurate assessment of left ventricular function. Broadspectrum antibiotic therapy is started immediately to treat bacterial peritonitis. Small perforations may spontaneously seal themselves and symptoms cease. Spontaneous sealing occurs because of fibrin production in response to the perforation. This can lead to fibrinous fusion of the duodenum or gastric curvature to adjacent tissue (mainly the liver) and strictures that can obstruct the flow of intestinal contents and the passage of stool. Larger perforations need immediate surgical closure. Whether the patient has an open or laparoscopic repair depends on the location of the ulcer and HCP preference. The procedure involving the least risk to the patient is simple oversewing of the perforation and reinforcement of the area with a graft of omentum. Excess gastric contents are suctioned from the peritoneal cavity during the surgical procedure.

Gastric Outlet Obstruction Both acute and chronic PUD can cause gastric outlet obstruction. Obstruction in the distal stomach and duodenum is the result of edema, inflammation, pylorospasm, or fibrous scar tissue formation.

With obstruction the patient reports discomfort or pain that is worse toward the end of the day as the stomach fills and dilates. Belching or self-induced vomiting may provide some relief. Vomiting is common and often projectile. The vomitus may contain food particles that were ingested hours or days before. Constipation occurs because of dehydration and decreased diet intake from anorexia. Over time dilation of the stomach and visible swelling in the upper abdomen may occur. The aim of therapy for obstruction is to decompress the stomach, correct any existing fluid and electrolyte imbalances, and improve the patient’s general state of health. An NG tube is used as described previously. With continuous decompression for several days, the ulcer can begin healing and the inflammation and edema will subside. Pain relief results from the decompression.

TABLE 41.15 Nursing AssessmentPeptic Ulcer

Disease

Subjective Data Important Health Information Past health history: Chronic kidney disease, pancreatic disease, COPD, serious illness or trauma, hyperparathyroidism, cirrhosis of the liver, ZES Medications: Aspirin, corticosteroids, NSAIDs Surgery or other treatments: Complicated or prolonged surgery

Functional Health Patterns Health perception–health management: Chronic alcohol use, smoking, caffeine use. Family history of PUD Nutritional-metabolic: Weight loss, anorexia, nausea and vomiting, hematemesis, dyspepsia, heartburn, belching

Elimination: Black, tarry stools Cognitive-perceptual: • Duodenal ulcers: Burning, midepigastric or back pain occurring 2–5 hr after meals and relieved by food; nighttime pain common • Gastric ulcers: High epigastric pain occurring 1–2 hr after meals. Food may precipitate or worsen pain. Coping–stress tolerance: Acute or chronic stress

Objective Data General Anxiety, irritability

Gastrointestinal Epigastric tenderness

Possible Diagnostic Findings Anemia. Guaiac-positive stools. Positive blood, urine, breath, or stool tests for H. pylori. Abnormal upper GI endoscopic and barium studies IV fluids and electrolytes are replaced according to the degree of dehydration, vomiting, and electrolyte imbalance shown by laboratory studies. A PPI or H2 receptor blocker is used if the obstruction is due to an active ulcer. Balloon dilation can open a pyloric obstruction. Surgery may be needed to remove scar tissue.

Nursing Management: Peptic Ulcer Disease Nursing Assessment Subjective and objective data to obtain from a patient with PUD are outlined in Table 41.15.

Nursing Diagnoses Nursing diagnoses related to PUD may include: • Acute pain • Lack of knowledge • Nausea Additional information on nursing diagnoses and interventions for the patient with PUD are in eNursing Care Plan 41.2 available on the website for this chapter.

Planning The overall goals are that the patient with PUD will (1) adhere to the prescribed therapeutic regimen, (2) see a reduction in or absence of discomfort, (3) have no signs of GI complications, (4) have complete healing of the peptic ulcer, and (5) make appropriate lifestyle changes to prevent recurrence.

Nursing Implementation Health Promotion You play an important role in identifying patients at risk for PUD. Early detection and effective treatment of ulcers are important aspects of reducing morbidity risks associated with PUD. Patients who are

taking ulcerogenic drugs (e.g., NSAIDs, LDA) are at risk for PUD. Encourage patients to take these drugs with food. Teach patients to report symptoms related to gastric irritation, including epigastric pain, to their HCP.

Acute Care During an acute exacerbation, the patient often reports increased pain, nausea, and vomiting. Some may have bleeding. Initially, many patients try to cope with the symptoms at home before seeking medical care. During the acute phase, the patient may be NPO for a few days, have an NG tube connected to intermittent suction, and receive IV fluid replacement. Explain to the patient and caregiver the reasons for these therapies so they understand that the advantages far outweigh any temporary discomfort. Regular mouth care relieves the dry mouth. Cleaning and lubricating the nares facilitate breathing and decrease soreness. Analysis of gastric contents may include pH testing and analysis for blood, bile, or other substances. When the stomach is empty of gastric secretions, pain decreases and ulcer healing begins. The volume of fluid lost, the patient’s signs and symptoms, and laboratory test results (hemoglobin, hematocrit, electrolytes) determine the type and amount of IV fluids given. Take vital signs initially and then at least hourly to detect and treat shock. Give IV fluids as ordered and record intake and output. Physical and emotional rest is helpful to ulcer healing. The patient’s environment should be quiet and restful. Give pain medications as ordered. A mild sedative or tranquilizer has beneficial effects when the patient is anxious and apprehensive. Use good judgment before sedating a person who is becoming increasingly restless because the drug could mask the signs of shock from upper GI bleeding.

Hemorrhage Changes in vital signs and an increase in the amount and redness of aspirate often signal massive upper GI bleeding. With bleeding, the patient’s pain often decreases because the blood helps neutralize the

acidic gastric contents. It is important to maintain the patency of the NG tube so that blood clots do not obstruct the tube. If the tube becomes blocked, the patient can develop abdominal distention. Use interventions similar to those described for upper GI bleeding on pp. 918–920.

Perforation If the patient with an ulcer develops manifestations of a perforation, notify the HCP immediately. Take vital signs promptly and record them every 15 to 30 minutes. Temporarily stop all oral or NG drugs and feedings. If perforation exists, anything taken orally can add to the spillage into the peritoneal cavity and increase discomfort. Give IV fluid as ordered to replace the depleted plasma volume. Giving pain medications provides comfort. Those with confirmed perforation will start on antibiotic therapy. If the perforation does not seal spontaneously, surgical closure is needed. Since surgery is done as soon as possible, there may not be time to prepare the patient and family.

Gastric Outlet Obstruction Gastric outlet obstruction can happen at any time. It is most likely to occur in the patient whose ulcer is close to the pylorus. The onset of symptoms is usually gradual. Constant NG aspiration of stomach contents can help relieve symptoms. This allows edema and inflammation to subside and permits normal flow of gastric contents through the pylorus. Regularly irrigate the NG tube with a normal saline solution per agency policy to assist proper functioning. It may be helpful to reposition the patient from side to side so that the tube tip is not constantly lying against the mucosal surface. Maintain accurate intake and output records, especially of the gastric aspirate. To check for ongoing obstruction, clamp the NG tube intermittently and measure the gastric residual volume. The frequency and amount of time the tube is clamped are related to the amount of aspirate obtained and the patient’s comfort level. A common method is to

clamp the tube overnight (usually 8 to 12 hours) and measure the gastric residual volume in the morning. When the aspirate falls below 200 mL, it is within a normal range and the patient can begin oral intake of clear liquids. Oral fluids begin at 30 mL/hr and then gradually increase in amount. As the amount of gastric residual decreases, solid foods are added, and the tube removed. If the patient has resumed oral feedings and you note symptoms of obstruction, promptly inform the HCP. Generally, all that is needed to treat the problem is to resume gastric aspiration so that the edema and inflammation resulting from the acute episode resolve. IV fluids with electrolyte replacement keep the patient hydrated during this period. If conservative treatment is not successful, surgery is done after the acute phase has passed.

Ambulatory Care Patients with PUD have specific needs to prevent recurrence and complications. Teaching should cover aspects of the disease process, drugs, lifestyle changes (alcohol use, smoking), and regular follow-up care. Table 41.16 provides a patient and caregiver teaching guide for PUD. Knowing the causes of PUD may motivate the patient to become involved in care and improve adherence to therapy. Work with the dietitian to elicit a dietary history and plan ways to incorporate any needed dietary modifications into the patient’s home and work setting. Teach the patient about prescribed drugs, including their actions, side effects, and dangers if omitted for any reason. Make sure the patient knows not to take OTC drugs (e.g., NSAIDs, LDA) unless approved by the HCP. Some H2 receptor blockers and PPIs are available without a prescription. Tell the patient to check with the HCP before switching from a prescription to an OTC preparation to avoid side effects and incorrect dosing. Obtain information about the patient’s psychosocial status. Knowledge of lifestyle, occupation, and coping behaviors can be helpful in planning care. The patient may be reluctant to talk about personal subjects, the stress at home or on the

job, the usual methods of coping, or dependence on drugs or alcohol.

TABLE 41.16 Patient & Caregiver TeachingPeptic

Ulcer Disease (PUD) Include the following instructions when teaching the patient and caregiver about management of PUD: 1. Avoiding foods that cause epigastric distress, such as acidic foods. 2. Avoid cigarettes. Smoking promoting ulcer development and delays ulcer healing. 3. Reduce or eliminate alcohol use. 4. Avoid OTC drugs unless approved by the HCP. Many preparations contain ingredients, such as aspirin, that should not be taken unless approved by the HCP. Check with the HCP about the use of NSAIDs. 5. Do not interchange brands of PPIs, antacids, or H2 receptor blockers that you can buy OTC without checking with the HCP. This can lead to harmful side effects. 6. Take all medications as prescribed. This includes both antisecretory and antibiotic drugs. Not taking medications as prescribed can cause a relapse. 7. It is important to report any of the following: • Increased nausea or vomiting • Increased epigastric pain • Bloody emesis or tarry stools 8. Stress can be related to signs and symptoms of PUD. Learn and use stress management strategies (see Chapter 6). 9. Share concerns about lifestyle changes and living with a chronic illness. The patient may not be honest about habitual use of alcohol or cigarettes. Provide information about the negative effects of alcohol

and cigarettes on PUD and ulcer healing. Changes such as smoking cessation and alcohol abstinence are hard for many people. The patient may do better in reducing, rather than totally eliminating, use of these substances. However, the goal is total cessation. PUD is a chronic, recurring disorder. Teach patients with chronic PUD about potential complications, and what to do until they see the HCP. Emphasize the need for long-term follow-up care. Encourage the patient to seek immediate intervention if symptoms return. Some patients do not adhere to the plan of care and have repeated exacerbations. Patients quickly learn that they often have no discomfort when they omit prescribed drugs, smoke, or drink alcohol. Consequently, they make no or few changes in their lifestyle. After an acute exacerbation, the patient is likely to be more amenable to following the plan of care and open to suggestions for changes in lifestyle.

Evaluation Expected outcomes are that the patient with PUD will • Have pain controlled without the use of analgesics • States an understanding of the treatment plan • Commit to self-care and management of the disease • Have no complications (hemorrhage, perforation)

Gerontologic Considerations: Peptic Ulcer Disease The morbidity and mortality rates associated with PUD in older adults are higher than for younger adults because of concurrent health problems and a decreased ability to withstand hypovolemia. Monitor older adults who use NSAIDs for osteoarthritis for PUD. In older patients, pain may not be the first symptom associated with an ulcer. For some patients the first sign is frank gastric bleeding or a decrease in hematocrit.

The treatment and management of PUD in older adults are similar to those in younger adults. The emphasis is on preventing gastritis and PUD. This includes teaching the patient to take NSAIDs and other gastric-irritating drugs with food, milk, or antacids. Teach the patient to avoid irritating substances, adhere to the PPI therapy as prescribed, and report abdominal pain or discomfort to the HCP.

Stomach Cancer Stomach (gastric) cancer is an adenocarcinoma of the stomach wall (Fig. 41.15). It accounts for more than 26,240 new cancer cases and 10,800 deaths annually.5 The rate of stomach (particularly distal) cancer has been steadily declining in the United States. However, cancer in the proximal gastric and gastroesophageal junction is increasing. Asian Americans, Pacific Islanders, Hispanics, and blacks have higher rates of stomach cancer than non-Hispanic whites. In the United States the incidence is higher in men than in women by a 2:1 ratio. Stomach cancer mostly affects older people. The average age of people at the time of diagnosis is 68.5 At the time of diagnosis, only 10% to 20% of patients have disease confined to the stomach. The 5-year survival rate in this group is 71%. However, more than 50% have advanced metastatic disease. The overall 5-year survival rate of all people with stomach cancer is about 31%.5

Etiology and Pathophysiology While many factors are implicated in the development of stomach cancer, no single causative agent has been identified. Stomach cancer probably begins with a nonspecific mucosal injury because of infection (H. pylori), autoimmune-related inflammation, repeated exposure to irritants such as bile or NSAIDs, and tobacco use. Stomach cancer has been associated with diets high in smoked foods, salted fish and meat, and pickled vegetables. Whole grains and fresh fruits and vegetables are associated with reduced rates of stomach cancer. Infection with H. pylori, especially at an early age, is a risk factor for stomach cancer. It is possible that H. pylori and resulting cell changes can induce a sequence of transitions from dysplasia to cancer. People with lymphoma of the stomach (mucosa-associated lymphoid tissue [MALT]) are at higher risk of stomach cancer.

Other predisposing factors include atrophic gastritis, pernicious anemia, adenomatous polyps, hyperplastic polyps, and achlorhydria (absent or low production of gastric HCl). Smoking and obesity both increase the risk for stomach cancer. Although first-degree relatives of patients with stomach cancer are at increased risk, only about 10% of stomach cancers have an inherited component.17 Stomach cancer spreads by direct extension and typically infiltrates rapidly to the surrounding tissue and liver. Seeding of tumor cells into the peritoneal cavity occurs late in the course of the disease.

Clinical Manifestations Stomach cancers often spread to adjacent organs before any distressing symptoms occur. Manifestations include unexplained weight loss, indigestion, abdominal discomfort or pain, and signs and symptoms of anemia. The patient may report early satiety, or a sense of being full sooner than usual. Anemia is common. It is caused by chronic blood loss as the lesion erodes through the mucosa or from pernicious anemia (caused by loss of intrinsic factor). The person appears pale and weak. They may report fatigue, weakness, dizziness, and, in extreme cases, shortness of breath. The stool may be positive for occult blood. Supraclavicular lymph nodes that are hard and enlarged suggest metastasis via the thoracic duct. The presence of ascites is a poor prognostic sign.

FIG. 41.15 Stomach cancer. Gross photograph showing an ill-defined, excavated central ulcer (arrow) surrounded by irregular, heaped-up borders. From Kumar V, Abbas AK, Aster JC, Fausto N: Robbins and Cotran pathologic basis of disease, ed 8, Philadelphia, 2010, Saunders.

TABLE 41.17 Interprofessional CareStomach

Cancer

Diagnostic Assessment • History and physical examination • Endoscopy and biopsy • CT, MRI, PET scans • Upper GI barium study • Exfoliative cytologic study

• Endoscopic ultrasonography • CBC • Liver enzymes • Urinalysis • Stool examination • Serum amylase • Tumor markers • α-Fetoprotein • Carbohydrate antigen (CA)-19-9, CA-125, CA 72-4 • Carcinoembryonic antigen (CEA)

Management • Surgical therapy • Subtotal gastrectomy (Billroth I or II procedure) • Total gastrectomy with esophagojejunostomy • Chemotherapy • Radiation therapy • Targeted therapy

Diagnostic Studies The diagnostic studies for stomach cancer are outlined in Table 41.17. Upper GI endoscopy is the best diagnostic tool. The stomach can be distended with air during the procedure, stretching the mucosal folds. Tissue biopsy and histologic examination are important in diagnosing stomach cancer. Endoscopic ultrasound, CT, MRI, and PET scanning can be used to stage the disease. Laparoscopy is done to determine peritoneal spread. Blood studies detect anemia and determine its severity. Increased liver enzymes and serum amylase levels may mean liver and pancreatic involvement. Stool examination provides evidence of occult or gross bleeding. The presence of tumor markers can help

diagnose cancer.

Interprofessional Management The treatment of choice for stomach cancer is surgical removal of the tumor. Preoperative management focuses on correcting nutritional deficits and treating anemia. Transfusions of packed RBCs correct the anemia. If gastric outlet obstruction occurs, gastric decompression may be needed before surgery.

Surgical Therapy The surgical aim is to remove as much of the stomach as required to remove the tumor and a margin of normal tissue. The location and extent of the lesion, the patient’s physical condition, and the HCP’s preference determine the specific surgery used (e.g., open versus laparoscopic). Lesions in the antrum or pyloric region are generally treated by either a Billroth I or II procedure (Fig. 41.16). When the lesion is in the fundus, a total gastrectomy with esophagojejunostomy is done (Fig. 41.17). When metastasis has occurred to adjacent organs, such as the spleen, ovaries, or bowel, the surgical procedure is extended as needed. If the tumor extends into the transverse colon, partial colon resection is done.

FIG. 41.16 A, Billroth I procedure (subtotal gastric resection with gastroduodenostomy anastomosis). B, Billroth II procedure (subtotal gastric resection with gastrojejunostomy anastomosis).

Chemotherapy and Radiation Therapy A number of chemotherapy drugs can be used to treat stomach cancer. These include fluorouracil, capecitabine (Xeloda), carboplatin, cisplatin, docetaxel (Taxotere), epirubicin (Ellence), irinotecan (Camptosar), oxaliplatin (Eloxatin), and paclitaxel. Combination therapies are preferred as the drugs affect different phases of the cell cycle. Examples of combination therapy include ECF (epirubicin, cisplatin, fluorouracil) and docetaxel, irinotecan, oxaliplatin, or cisplatin with fluorouracil or capecitabine.18 Intraperitoneal administration of chemotherapy agents may also be used to treat metastatic disease. Chemotherapy is discussed in Chapter 15. Radiation therapy may be used together with chemotherapy to reduce the recurrence or as a palliative measure to decrease tumor mass and provide temporary relief of obstruction.

Targeted Therapy Trastuzumab (Herceptin) and ramucirumab (Cyramza) are targeted therapies used to treat stomach cancer. About 20% of patients with stomach cancer have too much HER-2 on the surface of the cancer cells. Trastuzumab targets the HER-2 protein and kills the cancer cells. Ramucirumab binds to the receptor for VEGF and prevents VEGF from binding to the receptor, thus preventing the growth and spread of cancer. These drugs are used to treat esophageal cancer and were discussed on p. 902.

FIG. 41.17 Total gastrectomy for stomach cancer. A, Normal anatomic structure of the stomach. B, Removal of the stomach (total gastrectomy). C, Anastomosis of the esophagus with the jejunum (esophagojejunostomy).

Nursing Management: Stomach Cancer Nursing Assessment The assessment of a person with stomach cancer is similar to that for PUD (Table 41.15). Important data to obtain from the patient and caregiver include a nutritional assessment, a psychosocial history, the patient’s perceptions of the health problem and need for care, and a physical examination. The nutritional assessment obtains information about appetite and changes in eating patterns over the previous 6 months. Determine the patient’s normal weight and any recent weight changes. Unexplained weight loss and anorexia are common. Evaluate the patient’s nutritional status. Cachexia may be present if oral intake has been reduced for an extended period. A malnourished patient does not respond well to chemotherapy or radiation therapy and is a poor surgical risk. The patient may report a history of vague abdominal symptoms, including dyspepsia and intestinal gas discomfort or pain. If the patient reports pain, explore where and when it occurs and how it is relieved. Determine the patient’s personal perception of the health problem and method of coping with hospitalization, diagnostic tests, and procedures. A possible diagnosis of cancer and a treatment plan that may include surgery, chemotherapy, or radiation treatment is stressful. If surgery is planned, assess the patient’s expectations about surgery (cure or palliation) and how the patient has responded to previous surgical procedures.

Nursing Diagnoses Nursing diagnoses for the patient with stomach cancer include: • Impaired nutritional intake

• Impaired nutritional status • Acute pain • Anxiety

Planning The overall goals are that the patient with stomach cancer will (1) have minimal discomfort, (2) achieve optimal nutritional status, and (3) maintain a degree of spiritual and psychologic well-being appropriate to the disease stage.

Nursing Implementation Health Promotion Your role in the early detection of stomach cancer focuses on identifying the patient at risk because of specific disorders such as H. pylori infection, pernicious anemia, and achlorhydria. Be aware of symptoms associated with stomach cancer and the significant findings on physical examination. Symptoms often occur late and mimic other conditions, such as PUD. Poor appetite, weight loss, fatigue, and persistent stomach distress are symptoms of stomach cancer. Encourage patients with a positive family history of stomach cancer to undergo diagnostic evaluation if anemia, PUD, or vague epigastric distress are present. It is important that you recognize the possibility of stomach cancer in a patient who is treated for PUD and does not get relief with prescribed therapy.

Acute Care When diagnostic tests confirm cancer, the patient and family generally react with shock, disbelief, and depression. Provide emotional and physical support, provide information, clarify test results, and maintain a positive attitude with respect to the patient’s immediate recovery and long-term survival. Because of changes in appetite and early satiety, the patient may be malnourished. Surgery may be delayed until the patient is more

physically able to withstand it. A positive nutritional state enhances wound healing and the ability to deal with infection and other possible postoperative complications. The patient may better tolerate several small meals a day than 3 regular meals. It may be challenging to persuade the patient to eat when he or she has no appetite and is depressed. Getting the patient’s caregiver to help with meals and encourage intake may be beneficial. Diet may be supplemented by commercial liquid supplements and vitamins. If the patient is unable to ingest oral feedings, the HCP may prescribe EN or PN (see Chapter 39). If needed, packed RBCs and fluid volume restoration may be given during the preoperative period. The preoperative teaching plan and the postoperative care of the patient having stomach cancer surgery is described in the next section on gastric surgery. Radiation therapy or chemotherapy is used as an adjuvant to surgery or for palliation. Your role is to provide detailed instructions, reassure the patient, and ensure completion of the designated number of treatments. Start by assessing the patient’s knowledge of these therapies. Teach the patient about skin care, need for nutrition and fluid intake, and the use of antiemetic drugs. Specific care of the patient receiving chemotherapy and radiation therapy is discussed in Chapter 15.

Ambulatory Care When chemotherapy or radiation treatment is continuing after discharge, a referral to home health care may be beneficial. The home health nurse can help with recovery, determine the degree of patient adherence, and provide support to the patient and caregiver. Provide the patient with a list of community agencies (e.g., American Cancer Society) that are available before the patient goes home. Encourage the patient to adhere to the prescribed therapies, keep appointments for chemotherapy administration or radiation treatments, and keep the HCP informed of changes in physical condition. Recurrence of cancer is common, and patients need regular follow-up examinations and imaging assessments. Long-term management of the cancer patient is

discussed in Chapter 15.

Evaluation Expected outcomes are that the patient with stomach cancer will • Have no or minimal discomfort, pain, or nausea • Achieve optimal nutritional status • Maintain a degree of psychologic well-being appropriate to the disease stage

Gastric Surgery Gastric surgeries are done to treat stomach cancer, as well as polyps, perforation, chronic gastritis, and PUD. Surgeries include partial gastrectomy, gastrectomy, vagotomy, and pyloroplasty. Partial gastrectomy with removal of the distal two thirds of the stomach and anastomosis of the gastric stump to the duodenum is a gastroduodenostomy or Billroth I operation (Fig. 41.16, A). If the gastric stump is anastomosed to the jejunum, the surgery is a gastrojejunostomy or Billroth II operation (Fig. 41.16, B). A total gastrectomy involves resection of the lower esophagus, removal of the entire stomach, and anastomosis of the esophagus to the jejunum. Vagotomy is the severing of the vagus nerve, either totally (truncal) or selectively (highly selective vagotomy). These procedures decrease gastric acid secretion. Pyloroplasty consists of surgical enlargement of the pyloric sphincter to facilitate the easy passage of contents from the stomach. It is often done after vagotomy or to enlarge an opening that is constricted from scar tissue.

Postoperative Complications As with all surgeries, acute postoperative bleeding at the surgical site can occur. Monitoring of patients is similar to that described later under acute upper GI bleeding. The most common long-term postoperative complications from gastric surgery are (1) dumping syndrome, (2) postprandial hypoglycemia, and (3) bile reflux gastritis.

Dumping Syndrome Dumping syndrome is the direct result of surgical removal of a large part of the stomach and pyloric sphincter. Normally, gastric chyme enters the small intestine in small amounts. After surgery, the stomach no longer has control over the amount of gastric chyme entering the small intestine. Therefore a large bolus of hypertonic fluid enters the intestine and causes fluid to be drawn into the bowel lumen. This

creates a decrease in plasma volume, distention of the bowel lumen, and rapid intestinal transit. Symptoms begin within 15 to 30 minutes after eating. The patient usually describes feelings of generalized weakness, sweating, palpitations, and dizziness. These symptoms are due to the sudden decrease in plasma volume. The patient may have abdominal cramps, borborygmi (audible abdominal sounds made by hyperactive intestinal peristalsis), and the urge to defecate. These manifestations usually last less than 1 hour after eating. A short rest period after each meal reduces the chance of dumping syndrome.

Postprandial Hypoglycemia Postprandial hypoglycemia is a variant of dumping syndrome. It is the result of uncontrolled gastric emptying of a bolus of fluid high in carbohydrate into the small intestine. The bolus of concentrated carbohydrate results in hyperglycemia and the release of excess amounts of insulin into the circulation. This results in reflex hypoglycemia. Symptoms are similar to those of any hypoglycemic reaction and include sweating, weakness, mental confusion, palpitations, tachycardia, and anxiety. Symptoms generally occur 2 hours after eating.

Bile Reflux Gastritis Gastric surgery that involves either reconstruction or removal of the pylorus can result in reflux of bile into the stomach. Prolonged contact with bile causes damage to the gastric mucosa, chronic gastritis, and PUD. The main symptom is continuous epigastric distress that increases after meals. Vomiting relieves the distress, but only temporarily. Although only a small number of patients have bile reflux gastritis, caution the patient to notify the HCP of any continuous epigastric distress after meals. Cholestyramine (Questran), given before or with meals, has been used successfully to treat this problem. Cholestyramine binds with the bile salts that are the source of gastric irritation.

Nursing Management: Gastric Surgery Preoperative Care Surgery can involve either laparoscopic or open surgical techniques. The HCP will provide the necessary information about the procedure and expected outcomes, so the patient can make an informed decision. Help the patient and caregiver by answering their questions. Teach them what to expect after surgery, including comfort measures, pain relief, coughing and breathing exercises, use of an NG tube, and IV fluid administration (see Chapter 17 for more on preoperative care).

Postoperative Care Postoperative care focuses on maintaining fluid and electrolyte balance, preventing respiratory complications, maintaining comfort, and preventing infection. Complications include atelectasis, pneumonia, anastomotic leak, deep vein thrombosis, pulmonary embolus, and bleeding. Morbidly obese patients have a higher risk for many postoperative complications. After surgery, an NG tube is used for decompression. This decreases pressure on suture lines and allows edema and inflammation resulting from surgical trauma to resolve. Observe the gastric aspirate for color, amount, and odor. Small volumes of bloody drainage from the NG can be expected for the first 2 to 3 hours because bleeding at the anastomotic site is common. Report bright red bleeding that does not decrease after this period or bleeding that becomes excessive (more than 75 mL/hr) immediately to the HCP. The NG aspirate should gradually darken within the first 24 hours after surgery. Normally the color changes to yellow-green within 36 to 48 hours. After total gastrectomy, the NG tube does not drain a large quantity of secretions because removing the stomach has eliminated the reservoir capacity. Observe the NG tube closely because blood easily clots and clogs the tube. Notify the HCP immediately if the tube stops draining or

appears obstructed with blood. If the tube becomes clogged, the HCP may order periodic gentle irrigations with normal saline solution. It is essential that the NG suction is working and that the tube stays patent so that accumulated gastric secretions do not put a strain on the anastomosis. This can lead to distention of any remaining part of the stomach and result in (1) rupture of the sutures, (2) leakage of gastric contents into the peritoneal cavity, (3) hemorrhage, and (4) abscess formation. If the tube must be replaced or repositioned, call the HCP to perform this task because of the danger of perforating the gastric mucosa or disrupting the suture line. While the NG tube is connected to suction, maintain IV therapy. Before the NG tube is removed, the patient begins clear liquids to determine the tolerance level. In a partial gastrectomy, the stomach may be aspirated within 1 or 2 hours to assess the amount remaining and its color and consistency. When fluids are well tolerated, the NG tube is removed. Solids are added gradually with the goal of resuming a normal diet. Closely observe the patient for an anastomotic leak and notify the HCP at once if one is suspected. A leak occurs when there is a breakdown of the suture line in an anastomosis that allows gastric or intestinal contents to enter the abdomen or mediastinum. It requires immediate treatment to prevent sepsis and death. Signs and symptoms include tachycardia, dyspnea, fever, abdominal pain, anxiety, and restlessness. Since most procedures are done laparoscopically, the risk for respiratory complications is reduced. In an open surgical approach, the incision is relatively high in the epigastrium and respiratory complications may occur. Respiratory assessment includes respiratory rate and rhythm, pulse rate and rhythm, and signs of pneumothorax (e.g., dyspnea, chest pain, cyanosis). Have the patient cough and deep breathe to expand the lungs. Pain may interfere with deep breathing and coughing. Encourage the patient to splint the area with a pillow. Splinting also protects the abdominal suture line from rupturing during deep breathing and coughing. Encourage early ambulation and frequent position changes.

Give pain medications as needed. Be aware that pain could be from an anastomosis leak rather than typical surgical pain. Abdominal wounds need frequent observation for the amount and type of drainage, condition of the incision, and signs of infection. Monitor vital signs to help identify problems such as infection, hemorrhage, or anastomosis leak. Implement measures to control nausea and vomiting. Measure and record the intake and output and obtain daily weights.

Nutritional Therapy Understanding the patient’s surgery and the resulting anatomy is important. Long-term, many patients have malnutrition, metabolic bone disease, anemia, and weight loss. Nutrition interventions help minimize the occurrence of expected complications and maximize nutrient intake (Table 41.18). Start nutrition teaching as soon as the immediate postoperative period has passed. The dietitian usually provides dietary instructions. You must reinforce them. Following dietary measures will decrease symptoms and is essential to longterm adherence. Postoperative wound healing may be impaired because of poor nutritional intake. Give potassium and vitamin supplements as ordered. For those who were malnourished preoperatively, a small bowel feeding tube may be placed intraoperatively. EN may be started on postoperative day 1 and adjusted depending on how oral intake is tolerated. Some may be discharged with nighttime tube feedings. PN is an option if the patient is not able to tolerate oral nutrition. Pernicious anemia is a long-term complication of total gastrectomy and may occur after partial gastrectomy. It is due to the loss of intrinsic factor, which is made by the parietal cells. Intrinsic factor is essential for the absorption of cobalamin in the terminal ileum. Because it is essential for the growth and maturation of RBCs, the lack of cobalamin results in pernicious anemia and neurologic complications. The patient will require cobalamin replacement therapy (see Chapter 30). Patients should take multivitamins with

folate, calcium, vitamin D, and iron for life.

TABLE 41.18 Nutritional

TherapyPostgastrectomy Dumping Syndrome The amount of time these restrictions should be followed varies. The HCP decides the proper amount of time to remain on this prescribed diet according to the patient’s clinical condition and progress.

Purposes • Slow the rapid passage of food into the intestine • Control symptoms of dumping syndrome (dizziness, sense of fullness, diarrhea, tachycardia), which sometimes occurs after a partial or total gastrectomy

Diet Principles • Divide meals into 6 small feedings to avoid overloading the stomach and intestine at mealtimes. • Do not take fluids with meals but at least 30–45 min before or after meals. This helps prevent distention or a feeling of fullness. • Avoid concentrated sweets (e.g., honey, sugar, jelly, jam, candies, sweet pastries, and sweetened fruit) because they sometimes cause dizziness, diarrhea, and a sense of fullness. • Protein consumption is unlimited to promote rebuilding of body tissues. Meat and eggs are specific foods to increase in the diet. • Milk contains lactose, which may be hard to digest. Introduce milk and milk products slowly several weeks after surgery. • Avoid carbonated beverages and foods that are gas forming to help prevent gastric distention. • Low-roughage and raw foods are allowed as tolerated a few weeks after surgery.

• Increase complex carbohydrates (e.g., bread, vegetables, rice, potatoes) and fats to meet energy needs. Because partial gastrectomy decreases the stomach’s reservoir, patients must reduce their meal size accordingly. For the first few weeks after surgery, the patient should consume soft, bland foods with low fiber and high complex carbohydrates and protein content. Teach the patient to eat in small portions and not to drink fluids with meals. Simple sugars, lactose, and fried foods should be avoided. Teach the patient to avoid extreme temperatures in food and to chew food thoroughly. To avoid hypoglycemic episodes, teach the patient to limit the amount of sugar consumed with each meal and eat small, frequent meals with moderate amounts of protein and fat. The immediate ingestion of sugared fluids or candy relieves hypoglycemic symptoms.

Ambulatory Care Patients who have had a total gastrectomy and are debilitated may need skilled care after discharge. For those going home, assist the patient and caregiver with symptom management. Make plans for pain relief, including comfort measures and the judicious use of analgesics. Teach wound care (if needed) to the primary caregiver. Dressings, special equipment, or special services may be needed. Collaborate with the dietitian to provide teaching about the diet that will optimize nutrition.

Gastritis Gastritis, an inflammation of the gastric mucosa, is one of the most common problems affecting the stomach. Gastritis may be acute or chronic and diffuse or localized.

Etiology and Pathophysiology Gastritis occurs as the result of a breakdown in the normal gastric mucosal barrier. This mucosal barrier normally protects the stomach tissue from the corrosive action of HCl acid and pepsin. When the barrier is broken, HCl acid and pepsin can diffuse back into the mucosa. This back diffusion results in tissue edema, disruption of capillary walls with loss of plasma into the gastric lumen, and possible hemorrhage.

TABLE 41.19 Causes of Gastritis

Drugs • Aspirin • Bisphosphonates • Corticosteroids • Digitalis • Iron supplements • Nonsteroidal antiinflammatory drugs (NSAIDs)

Diet • Alcohol • Large amounts of spicy, irritating foods

Microorganisms • H. pylori • Cytomegalovirus • Mycobacterium species • Salmonella organisms • Staphylococcus organisms • Treponema pallidum (syphilis)

Environmental Factors • Radiation • Smoking

Diseases/Disorders • Burns • Crohn’s disease • Large hiatal hernia • Physiologic stress • Reflux of bile and pancreatic secretions • Renal failure • Sepsis • Shock

Other Factors • Endoscopy procedures • Nasogastric tube • Psychologic stress

Risk Factors Risk factors and causes of gastritis are listed in Table 41.19. Some risk factors are discussed in this section.

Drug-Related Gastritis Drugs contribute to the development of acute and chronic gastritis. NSAIDs and corticosteroids inhibit the synthesis of prostaglandins that are protective to the gastric mucosa. This makes the mucosa more susceptible to injury. Factors that increase the risk for NSAID-induced gastritis include being female; being over age 60; having a history of ulcer disease; taking anticoagulants, LDA, or corticosteroids; and having a chronic disorder, such as CVD. Some drugs such as digoxin and alendronate (Fosamax) have direct irritating effects on the gastric mucosa.

Diet Dietary indiscretions can cause acute gastritis. After an alcoholic drinking binge, acute damage to the gastric mucosa can range from localized injury of superficial epithelial cells to destruction of the mucosa with mucosal congestion, edema, and hemorrhage. Prolonged damage induced by repeated alcohol use results in chronic gastritis. Eating large quantities of spicy, irritating foods can cause acute gastritis.

Helicobacter Pylori A key cause of chronic gastritis is H. pylori infection. H. pylori infection causes acute gastritis in most infected persons. Chronic gastritis may develop in some. Prolonged inflammation leads to functional changes in the stomach and may cause stomach cancer. H. pylori was discussed earlier in this chapter on p. 905.

Other Risk Factors Although not as common as H. pylori, other bacterial, viral, and fungal infections are associated with chronic gastritis. Gastritis can occur

from reflux of bile salts from the duodenum into the stomach because of anatomic changes after surgical procedures (e.g., gastroduodenostomy, gastrojejunostomy). Prolonged vomiting may cause reflux of bile salts. Intense emotional responses and CNS lesions may cause inflammation of the mucosal lining from hypersecretion of HCl acid.

Autoimmune Gastritis Autoimmune metaplastic atrophic gastritis (also called autoimmune atrophic gastritis) is an inherited condition in which there is an immune response directed against parietal cells. It most often affects women of northern European descent. Patients often have other autoimmune disorders. The loss of parietal cells leads to low chloride levels, inadequate production of intrinsic factor, cobalamin (vitamin B12) malabsorption, and pernicious anemia. It is associated with an increased risk of stomach cancer.

Clinical Manifestations The symptoms of acute gastritis include anorexia, nausea and vomiting, epigastric tenderness, and a feeling of fullness. Hemorrhage is often associated with alcohol use and at times, is the only symptom. Acute gastritis is self-limiting, lasting from a few hours to a few days. Complete healing of the mucosa is expected. The manifestations of chronic gastritis are like those of acute gastritis. Some patients are asymptomatic. However, when parietal cells are lost because of atrophy, the source of intrinsic factor is also lost. Intrinsic factor is essential for cobalamin absorption. The lack of cobalamin results in pernicious anemia. Cobalamin deficiency anemia is discussed in Chapter 30.

Diagnostic Studies Acute gastritis is usually diagnosed based on the patient’s symptoms and a history of drug or alcohol use. Occasionally, an endoscopic

examination with biopsy is required to make the diagnosis. Breath, urine, serum, stool, and gastric tissue biopsy tests are done to assess for H. pylori infection. A CBC may show anemia from blood loss or lack of intrinsic factor. Stools are tested for occult blood. Serum tests for antibodies to parietal cells and intrinsic factor may be done. A tissue biopsy can rule out gastric cancer.

Nursing and Interprofessional Management: Gastritis Acute Gastritis Eliminating the cause and preventing or avoiding it in the future are generally all that is needed to treat acute gastritis. The plan of care is supportive and similar to that described for nausea and vomiting. If vomiting is present, rest, NPO status, and IV fluids may be prescribed. Antiemetics are given (Table 41.1). Monitor for dehydration. It can occur rapidly in acute gastritis with vomiting. In severe cases of acute gastritis, an NG tube may be used to (1) monitor for bleeding, (2) lavage the precipitating agent from the stomach, or (3) keep the stomach empty and free of noxious stimuli. Clear liquids are resumed when symptoms have subsided. Reintroduce solids gradually. If the patient is at risk for hemorrhage, frequently check vital signs and test the vomitus for blood. All the management strategies discussed in the section on upper GI bleeding apply to the patient with severe gastritis (see pp. 917–920). Drug therapy focuses on reducing irritation of the gastric mucosa and providing symptomatic relief. H2 receptor blockers (e.g., ranitidine, cimetidine) or PPIs (e.g., omeprazole) reduce gastric HCl acid secretion (Table 41.10). Teach the patient about the therapeutic effects of PPIs and H2 receptor blockers.

Chronic Gastritis The treatment of chronic gastritis focuses on evaluating and eliminating the specific cause (e.g., cessation of alcohol use, abstinence from drugs, H. pylori eradication). Antibiotic combinations are used to eradicate H. pylori (Table 41.14). The patient with pernicious anemia needs lifelong cobalamin therapy (see Chapter 30).

TABLE 41.20 Types of Upper GI Bleeding

The patient undergoing treatment for chronic gastritis may have to adapt to lifestyle changes and strictly adhere to a drug regimen. Some patients find a nonirritating diet consisting of 6 small feedings a day helpful. Smoking is contraindicated in all forms of gastritis. An interprofessional team approach in which the HCP, nurse, dietitian, and pharmacist provide consistent information and support will increase the patient’s success in making these changes.

Upper Gastrointestinal Bleeding In the United States, 250,000 hospital admissions occur each year for upper GI bleeding.19 About 60% of these are adults over age 65. Though the mortality rate is still around 2.5%, this rate has decreased over the past few decades due to advances in the prevention and treatment of upper GI bleeding.

Etiology and Pathophysiology Although the most serious loss of blood from the upper GI tract is characterized by a sudden onset, insidious occult bleeding can be a major problem. The severity of bleeding depends on whether the origin is venous, capillary, or arterial. Types of upper GI bleeding are described in Table 41.20. Bleeding from an arterial source is profuse, and the blood is bright red because it has not been in contact with gastric HCl acid secretion. In contrast, coffee-grounds vomitus means that the blood has been in the stomach for some time. Melena (black, tarry stools) occurs with slow bleeding from an upper GI source. The longer the passage of blood through the intestines, the darker the stool color because of the breakdown of hemoglobin and release of iron. Discovering the cause of the bleeding is not always easy. A variety of areas in the GI tract may be involved. Table 41.21 lists the common causes of upper GI bleeding.

Stomach and Duodenal Origin Peptic ulcers, due to H. pylori infection and the use of NSAIDS, are the most common causes of upper GI bleeding. About 25% of people on chronic NSAIDs (e.g., ibuprofen) develop ulcer disease; of these, 2% to 4% will bleed. Even LDA is associated with a risk for GI bleeding. Many OTC preparations contain aspirin. Obtain a careful medication history whenever upper GI bleeding is suspected. Stress-related mucosal disease (SRMD), also called physiologic stress ulcers, describes mucosal damage in the GI tract ranging from

small single lesions to multiple gastric ulcers and major bleeding. SRMD most often occurs in critically ill patients who have had severe burns, trauma, or major surgery. Patients with coagulopathy, liver disease, or organ failure and those receiving renal replacement therapy are at highest risk for SRMD.20

TABLE 41.21 Causes of Upper GI Bleeding

Stomach and Duodenum • Drug-induced • Corticosteroids • NSAIDs • Salicylates • Erosive gastritis • Polyps • PUD • Stress-related mucosal disease • Stomach cancer

Esophagus • Esophageal varices • Esophagitis • Mallory-Weiss tear

Systemic Diseases • Blood dyscrasias (e.g., leukemia, aplastic anemia) • Renal failure

Esophageal Origin Bleeding from the esophagus is likely due to chronic esophagitis, Mallory-Weiss tear, or esophageal varices. Chronic esophagitis can be caused by GERD, smoking, alcohol use, and the ingestion of drugs irritating to the mucosa. Esophageal varices most often occur from cirrhosis of the liver. Esophageal varices are discussed in Chapter 43.

Diagnostic Studies Endoscopy is the primary tool for diagnosing the source (e.g., esophageal varices, PUD, gastritis) of upper GI bleeding. Angiography is used when endoscopy cannot be done or when bleeding persists after endoscopic therapy. Angiography requires preparation and setup time and may not be appropriate for a highrisk, unstable patient. In this procedure, a catheter is inserted into the femoral artery and advanced to the left gastric or superior mesenteric artery until the site of bleeding is found. Laboratory studies include CBC, blood urea nitrogen (BUN), serum electrolytes, prothrombin time, partial thromboplastin time, liver enzymes, arterial blood gases (ABGs), and a type and crossmatch for possible blood transfusions. All vomitus and stools are tested for gross and occult blood. Monitor the patient’s laboratory studies to estimate the effectiveness of therapy. The hemoglobin and hematocrit values are not of immediate help in estimating the degree of blood loss, but they provide a baseline for guiding further treatment. The initial hematocrit may be normal and may not reflect the loss until 4 to 6 hours after fluid replacement, since initially the loss of plasma and RBCs is equal. Assess the patient’s BUN level. During a significant hemorrhage, GI tract bacteria break down proteins, resulting in increased BUN levels. An increased BUN level may also show renal hypoperfusion or renal disease.

Interprofessional Management

A massive upper GI hemorrhage is a loss of more than 1500 mL of blood or 25% of intravascular blood volume. Although 80% to 85% of patients with massive hemorrhage spontaneously stop bleeding, the cause must be identified and treatment started at once.

Emergency Assessment and Management A complete history of events leading to the bleeding episode is deferred until emergency care has been started. To facilitate early intervention, focus your physical examination on identifying signs and symptoms of shock, such as tachycardia, weak pulse, hypotension, cool extremities, prolonged capillary refill, and apprehension. (Shock is discussed in Chapter 66.) Urine output is one of the best measures of vital organ perfusion. An indwelling urinary catheter is inserted so that hourly output can be accurately assessed. Hemodynamic monitoring provides an accurate and quick assessment of blood flow and pressure in the cardiovascular system (see Chapter 65). A central venous pressure line may be used for fluid volume status assessment. If the patient has a history of valvular heart disease, coronary artery disease, or heart failure, a pulmonary artery catheter may be needed. Give supplemental O2 to increase blood O2 saturation. The patient is at risk for perforation and peritonitis. Do a thorough abdominal examination. Note the presence of a tense, rigid, boardlike abdomen and the presence or absence of bowel sounds. The type and amount of fluids infused are based on physical and laboratory findings. Generally, an isotonic crystalloid solution (e.g., lactated Ringer’s solution) is started. Whole blood, packed RBCs, and fresh frozen plasma may be used for volume replacement in massive hemorrhage. When upper GI bleeding is less profuse, infusion of isotonic saline solution followed by packed RBCs restores the hematocrit more quickly and does not create complications related to fluid volume overload. (The use of blood transfusions and volume expanders is discussed in Chapter 30.)

Endoscopic Therapy

The first-line management of upper GI bleeding is endoscopy. Endoscopy within the first 24 hours of bleeding is important for diagnosis, determining the need for surgical intervention, and providing treatment. The goal of endoscopic hemostasis is to coagulate or thrombose the bleeding vessel. Several techniques are used, including (1) mechanical therapy with clips or bands, (2) thermal ablation, and (3) injection (e.g., epinephrine, alcohol). Clips and bands directly compress the bleeding vessel. Thermal ablation cauterizes tissue through applying heat to the bleeding site. Common devices include neodymium:yttrium-aluminum-garnet (YAG) laser, monopolar or bipolar electrocoagulation, heater probes, and argon plasma coagulation (APC).21 For variceal bleeding, other strategies include variceal ligation, injection sclerotherapy, and balloon tamponade (see Chapter 43).

Surgical Therapy Surgical intervention is needed when bleeding continues regardless of the therapy provided and when the site of the bleeding has been identified. Surgery may be done if the patient continues to bleed after rapid transfusion of up to 2000 mL of whole blood or is still in shock after 24 hours. The site of the hemorrhage determines the choice of surgery. Mortality rates increase considerably in older patients.

Drug Therapy During the acute phase of upper GI bleeding, drugs are used to decrease bleeding, decrease HCl acid secretion, and neutralize the HCl acid that is present. Empiric PPI therapy with high-dose IV bolus and subsequent infusion to decrease acid secretion is often started before endoscopy (Table 41.10). Efforts are made to reduce acid secretion because the acidic environment can alter platelet function and interfere with clot stabilization. This may decrease the amount of bleeding and need for endoscopic therapy. After an acute phase of bleeding, antacids may be given hourly, either orally or through the NG tube. If an NG tube is in place, the

stomach contents should be aspirated and tested periodically for pH level. If pH is less than 5, intermittent suction may be used or the frequency or dosage of the antacid or antisecretory agent increased.

Nursing Management: Upper Gastrointestinal Bleeding Nursing Assessment A thorough nursing assessment is an essential first step as you begin care of the patient admitted with upper GI bleeding. The patient may not be able to give specific information about the cause of the bleeding until immediate physical needs are met. Perform an immediate nursing assessment while you are getting the patient ready for initial treatment. The assessment includes the patient’s level of consciousness, vital signs, skin color, and capillary refill. Check the abdomen for distention, guarding, and peristalsis. Immediate determination of vital signs indicates whether the patient is in shock from blood loss and provides a baseline BP and pulse for monitoring the progress of treatment. Signs and symptoms of shock include low BP; rapid, weak pulse; increased thirst; cold, clammy skin; and restlessness. Monitor vital signs every 15 to 30 minutes. Inform the HCP of any significant changes. Once the immediate interventions have begun, the patient or caregiver should answer the following questions: Is there a history of bleeding episodes? Has the patient received blood transfusions? Were there any transfusion reactions? Are there any other illnesses (e.g., liver disease, cirrhosis) or medications that may contribute to bleeding or interfere with treatment? Does the patient have a religious preference that prohibits the use of blood or blood products? Subjective and objective data to obtain from the patient or caregiver are outlined in Table 41.22.

Nursing Diagnoses Nursing diagnoses for the patient with upper GI bleeding include: • Impaired cardiac output

• Fluid imbalance • Ineffective tissue perfusion • Anxiety

Planning The overall goals are that the patient with upper GI bleeding will (1) have no further GI bleeding, (2) have the cause of the bleeding identified and treated, (3) return to a normal hemodynamic state, and (4) have minimal or no symptoms of pain or anxiety.

Nursing Implementation Health Promotion Although not all cases of upper GI bleeding can be prevented, you have an important role in identifying patients at high risk. Always consider the patient with a history of chronic gastritis, cirrhosis, or PUD at high risk. The patient who has had an upper GI bleeding episode is more likely to have another bleed. Patients on daily LDA to reduce CVD risk are at risk for upper GI bleeding, especially those over 60 years old with a history of PUD. Teach the patient who takes regular doses of drugs that cause GI toxicity (peptic ulcer formation, bleeding), such as corticosteroids and NSAIDs, about the risk for GI bleeding. They may need to receive long-term treatment with a PPI, H2 receptor blocker, or misoprostol. Taking these drugs with meals or snacks lessens their direct irritation.

TABLE 41.22 Nursing AssessmentUpper GI

Bleeding

Subjective Data Important Health Information

Past health history: Precipitating events before bleeding episode, prior bleeding episodes and treatment, PUD, esophageal varices, esophagitis, acute and chronic gastritis, stress-related mucosal disease Medications: Aspirin, NSAIDs, corticosteroids, anticoagulants

Functional Health Patterns Health perception–health management: Family history of bleeding, smoking, alcohol use Nutritional-metabolic: Nausea, vomiting, weight loss, thirst Elimination: Diarrhea. Black, tarry stools. Decreased urine output. Sweating Activity-exercise: Weakness, dizziness, fainting Cognitive-perceptual: Epigastric pain, abdominal cramps Coping–stress tolerance: Acute or chronic stress

Objective Data General Fever

Integumentary Clammy, cool, pale skin. Pale mucous membranes, nail beds, and conjunctivae. Spider angiomas, jaundice, peripheral edema

Respiratory Rapid, shallow respirations

Cardiovascular Tachycardia, weak pulse, orthostatic hypotension, slow capillary refill

Gastrointestinal Red or coffee-grounds vomitus. Tense, rigid abdomen, ascites. Hypoactive or hyperactive bowel sounds. Black, tarry stools

Urinary Decreased urine output, concentrated urine

Neurologic Agitation, restlessness. Decreasing level of consciousness

Possible Diagnostic Findings ↓ Hematocrit and hemoglobin, hematuria. Guaiac-positive stools, emesis, or gastric aspirate. ↓ Levels of clotting factors, ↑ liver enzymes, abnormal endoscopy results Teach the at-risk patient to avoid known gastric irritants, such as alcohol and smoking, and to take only prescribed medications. OTC drugs can be harmful because they may contain ingredients (e.g., aspirin) that increase the risk for bleeding. Review how to test vomitus or stools for occult blood. Teach them to report positive results promptly to the HCP. Stress the importance of treating an upper respiratory tract infection promptly. Severe coughing or sneezing can increase pressure on the already fragile varices and may

result in massive hemorrhage (see Chapter 43). Patients with blood dyscrasias (e.g., aplastic anemia) or liver dysfunction or those who are taking chemotherapy drugs are at risk due to a decrease in clotting factors and platelets. Teach patients about their disease process, drugs, and increased risk for GI bleeding.

TABLE 41.23 Emergency ManagementAcute GI

Bleeding

Acute Care Emergency management of acute GI bleeding is outlined in Table 41.23. Place IV lines, preferably 2, with a 16- or 18-gauge needle for fluid and blood replacement. Give fluid or blood replacement as ordered. An accurate intake and output record is essential so that the patient’s hydration status can be assessed. Measure the urine output hourly. If a central venous pressure line or pulmonary artery catheter in place, record these readings every 1 to 2 hours. Use ECG monitoring to evaluate cardiac function. Close monitoring of vital signs, especially in the patient with CVD, is important because dysrhythmias may occur.

Check Your Practice You are admitting a 71-yr-old man to the unit from the emergency department. He has a diagnosis of upper GI bleeding. He reports heartburn and pain (6 on a scale of 10) in the upper epigastric region and has just had a 250 mL coffee-grounds emesis. • What assessment data do you need to obtain? • What are the priority nursing interventions for this man? Observe the older adult or the patient with CVD closely for signs of fluid overload. However, volume overload and pulmonary edema are concerns in all patients who are receiving large amounts of IV fluids within a short time. Auscultate breath sounds and closely observe the respiratory effort. Keep the head of the bed elevated to provide comfort and prevent aspiration. When an NG tube is present, pay special attention to keeping it in proper position and checking the aspirate for blood. Although gastric lavage (room temperature, cool, or iced) is used in some agencies, its effectiveness as a treatment for upper GI bleeding is questionable. When lavage is used, around 50 to 100 mL of fluid is instilled at a time into the stomach. The lavage fluid may be aspirated from the stomach or drained by gravity. When aspiration is the method used, it is important not to aspirate if you feel resistance. The tip of the NG tube may be up against the gastric mucosal lining. When resistance is a factor, use the gravity method.

TABLE 41.24 Bacterial Food Poisoning

Approach the patient in a calm manner to help decrease the level of anxiety. Use caution when giving sedatives for restlessness because it is one of the warning signs of shock and may be masked by the drugs. Assess the stools for blood (black-tarry, bright red). Black, tarry stools are not usually associated with a brisk hemorrhage but are indicative of prolonged bleeding. Determine if menses or bleeding are possible sources of blood in the stools. When vomitus contains blood, but the stool contains no gross or occult blood, the hemorrhage is thought to be of short duration. When beginning oral nourishment, observe the patient for symptoms of nausea and vomiting and a recurrence of bleeding. Feedings initially consist of clear fluids. They are given hourly until tolerance is determined. Gradually introduce foods if the patient has no signs of discomfort. When hemorrhage is the result of chronic alcohol use, closely observe the patient for delirium tremens as alcohol withdrawal takes place. Symptoms indicating the onset of delirium tremens are

agitation, uncontrolled shaking, sweating, and hallucinations. (Alcohol withdrawal is discussed in Chapter 10.)

Ambulatory Care Teach the patient and caregiver how to avoid future bleeding episodes. Ulcer disease, drug or alcohol use, liver and respiratory diseases can all cause upper GI bleeding. Help the patient and caregiver to be aware of the consequences of not adhering to drug therapy. Emphasize not to take any drugs (especially aspirin, NSAIDs) other than those prescribed by the HCP. Support the patient in smoking and alcohol cessation because they are sources of irritation and interfere with tissue repair. Long-term follow-up care may be needed because of possible recurrence. Teach the patient and caregiver what to do if an acute hemorrhage occurs in the future.

Evaluation The expected outcomes are that the patient with upper GI bleeding will • Have no upper GI bleeding • Maintain normal fluid volume • Return to a normal hemodynamic state • Understand potential risk factors and make lifestyle modifications

Foodborne Illness Foodborne illness (food poisoning) is a nonspecific term that describes acute GI symptoms such as nausea, vomiting, diarrhea, and cramping abdominal pain caused by the intake of contaminated food or liquids.22 There are more than 250 foodborne illnesses. Each year 1 in 6 Americans, or 48 million, gets a foodborne illness. Of these, 128,000 are hospitalized and around 3000 die.22 Bacteria account for most foodborne illnesses. The most common source is raw foods that become contaminated during growing, harvesting, processing, storing, shipping, or final preparation. Bacteria multiply quickly when the temperature of food is between 40 and 140 degrees. So, bacteria can multiply if hot food is not kept hot enough or cold food not cold enough. The most common bacterial food poisonings are described in Table 41.24. Focus interventions on preventing infection. Teaching includes correct food preparation and cleanliness, adequate cooking, and refrigeration (Table 41.25). For the hospitalized patient, emphasize correcting fluid and electrolyte imbalances from diarrhea and vomiting. With botulism, additional assessment and care related to neurologic symptoms are indicated (see Chapter 60).

TABLE 41.25 Patient & Caregiver

TeachingPreventing Food Poisoning Include these instructions when teaching the patient and caregiver how to prevent food poisoning. 1. Cook all ground beef and hamburger thoroughly. • Use a digital instant-read meat thermometer to ensure thorough cooking (ground beef can turn brown before disease-causing bacteria are killed). • Cook ground beef until a thermometer inserted into

several parts of the patty, including the thickest part, reads at least 160° F. • People who cook ground beef without using a thermometer can decrease their risk for illness by not eating ground beef patties that are still pink in the middle. 2. If you are served an undercooked hamburger or other ground beef product in a restaurant, send it back for further cooking. Ask for a new bun and a clean plate. 3. Avoid spreading harmful bacteria. Keep raw meat separate from ready-to-eat foods. Wash hands, counters, and utensils with hot soapy water after they touch raw meat. Never place cooked hamburgers or ground beef on the unwashed plate that held raw patties. Wash meat thermometers in between tests of patties that need more cooking. 4. Drink only pasteurized milk, juice, or cider. Commercial juice with an extended shelf-life that is sold at room temperature (e.g., juice in cardboard boxes, vacuum-sealed juice in glass containers) has been pasteurized. Juice concentrates are heated enough to kill pathogens. 5. Wash fruits and vegetables thoroughly, especially those you will not be cooking. 6. Do not eat raw food products that are supposed to be cooked. Follow package directions for cooking at proper temperatures. 7. People who are immunocompromised should avoid eating alfalfa sprouts until the safety of the sprouts can be ensured.

Escherichia coli O157:H7 Poisoning Most strains of Escherichia coli are harmless and live in the intestines of healthy humans and animals. E, coli O157:H7 makes a powerful toxin and can cause severe illness with hemorrhagic colitis and kidney failure. In the very young and older adults, E. coli O157:H7 can be life threatening. E. coli O157:H7 is found primarily in undercooked meats, particularly poultry and hamburger. E. coli outbreaks have occurred

with contaminated leafy vegetables, fruits, and nuts. Infection can occur after drinking raw milk, unpasteurized or contaminated fruit juices and after swimming in or drinking sewage-contaminated water. Person-to-person contact in families, nursing homes, and child care centers is an important mode of transmission. Illness starts 1 to 10 days after swallowing the organism and lasts 5 to 10 days. Manifestations include diarrhea (often bloody), vomiting, and abdominal cramping pain. The diarrhea is variable, ranging from mild to bloody. It may start out as watery but may progress to bloody. Systemic complications, including hemolytic uremia and thrombocytopenic purpura, and even death can occur. Infection with E. coli O157:H7 is diagnosed by detecting the bacteria in the stool. All people who suddenly have diarrhea with blood should have a stool culture for E. coli O157:H7. Treatment involves hydration to maintain blood volume. There is no evidence that antibiotic therapy improves the course of disease. We think that treatment with some antibiotics may precipitate kidney complications. Patients should avoid antidiarrheal agents, such as loperamide (Imodium). Other therapies may include dialysis and plasmapheresis. A small number of patients, especially young children and older adults, develop hemolytic uremic syndrome (HUS). With HUS, the RBCs are destroyed and the kidneys fail. It is a life-threatening condition usually treated in an ICU. Blood transfusions and kidney dialysis are often needed. The mortality rate is around 5%. About one third of people with HUS have abnormal kidney function for years afterward. A few need long-term dialysis. Other long-term complications of HUS include hypertension, seizures, blindness, and paralysis.

Case Study Peptic Ulcer Disease

© iStockphoto/Thinkstock.

Patient Profile F.H., a 40-yr-old male immigrant from Vietnam, has a 1-yr history of epigastric distress. Increasingly, it is not relieved by over-the-counter omeprazole (Prilosec). He is scheduled for an upper endoscopy this morning.

Subjective Data • Reports increasing substernal pain, especially 2 to 3 hr after

eating • Currently avoids alcohol and is taking an over-the-counter PPI • Smoking history of 1 pack of cigarettes per day for 20 yr • Has had increasing fatigue with exercise • Reports occasional black bowel movement • Takes Chinese medicine for frequent back pain

Objective Data Physical Examination • Height 5 ft, 5 in tall and weight 140 lb

Diagnostic Studies • Endoscopy reveals a duodenal ulcer • Hgb 10.2 g/dL; Hct 30% • Histology of biopsied tissue reveals H. pylori infection

Interprofessional Care • omeprazole 20 mg twice daily × 10 days • clarithromycin 500 mg twice daily × 10 days • amoxicillin 1 gram twice daily × 10 days

Discussion Questions 1. Explain the pathophysiology of peptic ulcer disease. 2. What are the risk factors for duodenal ulcers? Which of these did F.H. have? 3. What is the pathophysiology of H. pylori? 4. Priority Decision: Based on the assessment data provided, what

are the priority nursing diagnoses? Are there any collaborative problems? 5. Patient-Centered Care: How will you consider F.H.’s cultural preferences in planning care? 6. Priority Decision: What are the priority nursing interventions for F.H.? 7. What lifestyle interventions would you recommend for F.H.? 8. Evidence-Based Decision: F.H. asks you if the treatment will work and this will be the end of his problems. How will you respond? 9. Collaboration: What referrals may be indicated? Answers available at http://evolve.elsevier.com/Lewis/medsurg.

Bridge to NCLEX Examination The number of the question corresponds to the same-numbered outcome at the beginning of the chapter.

1. M.J. calls the clinic and tells the nurse that her 85-yr-old mother has been nauseated all day and has vomited twice. Before the nurse hangs up and calls the HCP, she should tell M.J. to a. administer antiemetic drugs and assess her mother’s skin turgor. b. give her mother sips of water and elevate the head of her bed to prevent aspiration. c. offer her mother large quantities of Gatorade to decrease the risk for sodium depletion. d. give her mother a high-protein liquid supplement to drink to maintain her nutritional needs. 2. The nurse explains to the patient with Vincent’s infection that treatment will include a. tetanus vaccinations. b. viscous lidocaine rinses. c. amphotericin B suspension. d. topical application of antibiotics. 3. The nurse teaching young adults about behaviors that put them at risk for oral cancer includes a. discouraging use of chewing gum. b. avoiding use of perfumed lip gloss. c. avoiding use of smokeless tobacco.

d. discouraging drinking of carbonated beverages. 4. Which instructions would the nurse include in a teaching plan for a patient with mild gastroesophageal reflux disease (GERD)? a. “The best time to take an as-needed antacid is 1 to 3 hours after meals.” b. “A glass of warm milk at bedtime will decrease your discomfort at night.” c. “Do not chew gum; the excess saliva will cause you to secrete more acid.” d. “Limit your intake of foods high in protein because they take longer to digest.” 5. A patient who has undergone an esophagectomy for esophageal cancer develops increasing pain, fever, and dyspnea when a full-liquid diet is started postoperatively. The nurse recognizes that these symptoms are most indicative of a. an intolerance to the feedings. b. extension of the tumor into the aorta. c. leakage of fluids into the mediastinum. d. esophageal perforation with fistula formation into the lung. 6. The pernicious anemia that may accompany gastritis is due to a. chronic autoimmune destruction of cobalamin stores in the body. b. progressive gastric atrophy from chronic breakage in the mucosal barrier and blood loss.

c. a lack of intrinsic factor normally produced by acidsecreting cells of the gastric mucosa. d. hyperchlorhydria from an increase in acid-secreting parietal cells and degradation of RBCs. 7. The nurse is teaching the patient and family that peptic ulcers are a. caused by a stressful lifestyle and other acid-producing factors, such as H. pylori. b. inherited within families and reinforced by bacterial spread of Staphylococcus aureus in childhood. c. promoted by factors that cause oversecretion of acid, such as excess dietary fats, smoking, and alcohol use. d. promoted by a combination of factors that cause erosion of the gastric mucosa, including certain drugs and H. pylori. 8. An optimal teaching plan for an outpatient with stomach cancer receiving radiation therapy should include information about a. cancer support groups, alopecia, and stomatitis. b. nutrition supplements, ostomy care, and support groups. c. prosthetic devices, wound and skin care, and grief counseling. d. wound and skin care, nutrition, drugs, and community resources. 9. The teaching plan for the patient being discharged after an acute episode of upper GI bleeding includes information about the importance of (select all that apply)

a. limiting alcohol intake to 1 serving per day. b. only taking aspirin with milk or bread products. c. avoiding taking aspirin and drugs containing aspirin. d. only taking drugs prescribed by the health care provider. e. taking all drugs 1 hour before mealtime to prevent further bleeding. 10. Several patients come to the urgent care center with nausea, vomiting, and diarrhea that began 2 hours ago while attending a large family reunion potluck dinner. You ask the patients specifically about foods they ingested containing a. beef. b. meat and milk. c. poultry and eggs. d. home-preserved vegetables. 1. b, 2. d, 3. c, 4. a, 5. c, 6. c, 7. d, 8. d, 9. c, d, 10. b For rationales to these answers and even more NCLEX review questions, visit http://evolve.elsevier.com/Lewis/medsurg.

Evolve Website/Resources List http://evolve.elsevier.com/Lewis/medsurg

Review Questions (Online Only) Key Points Answer Keys for Questions • Rationales for Bridge to NCLEX Examination Questions • Answer Guidelines for Case Study on p. 921

Student Case Studies • Patient With Oral Cancer • Patient With Peptic Ulcer Disease Nursing Care Plans • eNursing Care Plan 41.1: Patient With Nausea and Vomiting • eNursing Care Plan 41.2: Patient With Peptic Ulcer Disease Conceptual Care Map Creator Audio Glossary Content Updates

References Matthews C. A review of nausea and vomiting in the anaesthetic and post anaesthetic environment. J Perioper Pract. 2017;27:224. Bošnjak S.M, Gralla R.J, Schwartzberg L. Prevention of chemotherapyinduced nausea. Support Care Cancer. 2017;25:1661. Nguyen L.A, Lee L. Complementary and alternative medicine for nausea and vomiting. In: Koch KL, Hasler WL, eds: Nausea and vomiting. New York: Springer; 2017. Dietrich T, Webb I, Stenhouse L, et al. Evidence summary: The relationship between oral and cardiovascular disease. British Dental Jour. 2017;222:381.

5. National Cancer Institute: SEER stat fact sheets. Retrieved from http://seer.cancer.gov/statfacts/html. de Martel C, Plummer M, Vignat J, et al. Worldwide burden of cancer attributable to HPV by site, country and HPV type. Int J Cancer. 2017;141:664.

7. The Oral Cancer Foundation. Surgery for oral cancer. Retrieved from https://oralcancerfoundation.org/treatment/surgery/. 8. American Cancer Society. Treating oral cancer. Retrieved from www.cancer.org/cancer/oral-cavity-andoropharyngeal-cancer/treating.html. 9. American Gastroenterological Association. GERD. Retrieved from www.gastro.org/patient-care/conditionsdiseases/gerd. Mansour N.M, El-Serag H.B, Anandasabapathy S. Barrett’s esophagus: Best practices for treatment and post-treatment surveillance. Ann Cardiothoracic Surg. 2017;6:75. Sandhu D.S, Fass R. Current trends in the management of gastroesophageal reflux disease. Gut Liver. 2018;12(7). Nehra A.K, Alexander J.A, Loftus C.G, et al. Proton pump inhibitors: Review of emerging concerns. Mayo Clinic Proc. 2018;93:240. Gyawali C.P, Fass R. Management of gastroesophageal reflux disease. Gastroenterology. 2018;154:302.

14. American Cancer Society. Treating esophageal cancer. Retrieved from www.cancer.org/cancer/esophaguscancer/treating.html. 15. Prasad MA, Friedman LS, Anania FA: Peptic ulcer disease. In: Srinivasan S, Friedman L, eds:Sitaraman and Friedman’s essentials of gastroenterology, ed 2, Oxford, United Kingdom, 2018, John Wiley & Sons Ltd. 16. Lanas A, Chan F.K. Peptic ulcer disease. Lancet. 2017;390:613. 17. Gigek CO, Chen ES, Smith MA: Epigenetic alterations in stomach cancer. In: Patel V, Preedy VR, eds: Handbook of nutrition, diet, and epigenetics, New York, 2017, Springer

18. American Cancer Society. Treating stomach cancer. Retrieved from www.cancer.org/cancer/stomachcancer/treating.html. Abougergi M.S. Epidemiology of upper gastrointestinal hemorrhage in the USA: Is the bleeding slowing down? Digestive Diseases and Science. 2018;63:1091. Barletta J.F, Mangram A.J, Sucher J.F, et al. Stress ulcer prophylaxis in neurocritical care. Neurocrit Care. 2017;19(1).

21. Rey J.W, Hoffman A, Teubner D, et al. Therapeutic endoscopy in the gastrointestinal tract. New York: Springer; 2018. 22. National Digestive Diseases Information Clearinghouse. Bacteria and foodborne illness. Retrieved from www.niddk.nih.gov/healthinformation/health-topics/digestive-diseases/foodborneillnesses/Pages/facts.aspx. ∗Evidence-based information for clinical practice.

42

Lower Gastrointestinal Problems Mariann M. Harding

LEARNING OUTCOMES 1. Explain the common etiologies and interprofessional and nursing management of diarrhea, fecal incontinence, and constipation. 2. Describe common causes of acute abdominal pain and nursing management of the patient after a laparotomy. 3. Describe the interprofessional and nursing management of acute appendicitis, peritonitis, and gastroenteritis. 4. Compare and contrast the inflammatory bowel diseases of ulcerative colitis and Crohn’s disease, including pathophysiology, clinical manifestations, complications, and interprofessional and nursing management. 5. Distinguish among small and large bowel obstructions, including causes, clinical manifestations, and interprofessional and nursing management. 6. Describe the clinical manifestations and interprofessional and nursing management of colorectal cancer. 7. Select nursing interventions to manage the care of the patient after bowel resection and ostomy surgery. 8. Distinguish between diverticulosis and diverticulitis, including clinical manifestations and interprofessional and nursing management. 9. Compare and contrast the types of hernias, including etiology

and surgical and nursing management. 10. Describe the types of malabsorption syndromes and interprofessional care of celiac disease, lactase deficiency, and short bowel syndrome. 11. Describe the types, clinical manifestations, and interprofessional and nursing management of anorectal conditions.

KEY TERMS anal fistula, p. 965 appendicitis, p. 937 celiac disease, p. 960 constipation, p. 929 Crohn’s disease, p. 939 diarrhea, p. 924 diverticulitis, p. 957 fecal incontinence, p. 928 fistula, p. 958 gastroenteritis, p. 939 hemorrhoids, p. 963 hernia, p. 959 inflammatory bowel disease (IBD), p. 939 intestinal obstruction, p. 945 irritable bowel syndrome (IBS), p. 936 lactase deficiency, p. 962 ostomy, p. 952 paralytic ileus, p. 945

peritonitis, p. 938 short bowel syndrome (SBS), p. 962 steatorrhea, p. 960 ulcerative colitis (UC), p. 939 In this life we cannot do great things. We can only do small things with great love. Mother Teresa http://evolve.elsevier.com/Lewis/medsurg

Conceptual Focus Acid-Base Balance Elimination Fluids and Electrolytes Inflammation Nutrition Pain Stress The wide variety of gastrointestinal (GI) problems discussed in this chapter include diarrhea, constipation, and fecal incontinence; inflammatory and infectious bowel problems; bowel trauma; bowel obstructions; colorectal cancer; abdominal and bowel surgery (including ostomy formation); and malabsorption problems. Conceptually, patients often have problems with impaired elimination and nutrition. Many have inflammation and pain and are at risk for altered fluid and electrolyte balance. Promoting optimal bowel habits and nutrition are common goals.

Diarrhea Diarrhea is the passage of at least 3 loose or liquid stools per day.1 It may be acute, lasting 14 days or less, or persistent, lasting longer than 14 days. Chronic diarrhea lasts 30 days or longer.

Etiology and Pathophysiology The primary cause of acute diarrhea is ingesting infectious organisms (Table 42.1). Viruses cause most cases of infectious diarrhea in the United States. While some viral infections can be deadly, most are mild and last less than 24 hours. So, most patients rarely seek treatment.

TABLE 42.1 Causes and Manifestations of Acute

Infectious Diarrhea

Bacterial infection with Escherichia coli O157:H7, a type of enterohemorrhagic E. coli, is a common cause of bloody diarrhea in the United States. It is transmitted by undercooked beef or chicken contaminated with the bacteria or in fruits and vegetables exposed to

contaminated manure. Other pathologic E. coli strains are endemic in developing countries and often cause traveler’s diarrhea. Giardia lamblia is the most common intestinal parasite that causes diarrhea in the United States. Infectious organisms attack the intestines in different ways. Some organisms (e.g., Rotavirus A, Norovirus, G. lamblia) change the secretion and/or absorption of enterocytes in the small intestine and do not cause inflammation. Other organisms (e.g., Clostridium difficile) impair absorption by destroying cells, causing inflammation in the colon, and producing toxins that cause damage. Secretory diarrhea is a common result of bacterial or viral infections. It occurs when ingested pathogens survive in the GI tract long enough to absorb into the enterocytes. The resulting chain reaction changes cell permeability and causes the oversecretion of water and sodium and chloride ions into the bowel. Organisms enter the body in contaminated food (e.g., Salmonella in undercooked eggs and chicken) or contaminated drinking water (G. lamblia in contaminated lakes or pools). Travelers often get diarrhea, especially if they travel to countries with poorer sanitation than their own. Infection can spread from person to person via the fecal-oral route. For example, adult day care workers can transmit infection from one resident to another if they do not wash their hands after changing soiled diapers or linens. A person’s age, gastric acidity, intestinal microflora, and immune status influence susceptibility to pathogenic organisms. Older adults are most likely to have life-threatening diarrhea. Since stomach acid kills ingested pathogens, taking drugs to decrease stomach acid (e.g., proton pump inhibitors [PPIs]) increases the chance that pathogens will survive.2 The healthy human colon contains short-chain fatty acids and bacteria, such as E. coli. These organisms aid in fermentation and provide a microbial barrier against pathogenic bacteria. Antibiotics kill the normal flora, making the person more susceptible to pathogenic organisms. For example, patients receiving broadspectrum antibiotics (e.g., carbapenems, cephalosporins,

piperacillin/tazobactam) are susceptible to pathogenic strains of C. difficile.2 C. difficile infection (CDI) causes the most serious antibioticassociated diarrhea and is a common cause of hospital-acquired GI illness in the United States. People who are immunocompromised because of disease (e.g., human immunodeficiency virus [HIV]) or immunosuppressive drugs are susceptible to GI tract infection. Immunocompromised patients receiving jejunal enteral nutrition (EN) are especially prone to CDI and other foodborne infections. Jejunostomy and nasointestinal feedings, which bypass the stomach’s acid environment, do not contain the poorly digestible fiber that normal colonic bacteria need for survival. Diarrhea is not always due to infection. Drugs and specific food intolerances can cause diarrhea. Large amounts of undigested carbohydrate in the bowel, lactose intolerance, and certain laxatives (e.g., lactulose, sodium phosphate, magnesium citrate) produce osmotic diarrhea. Osmotic diarrhea results from rapid GI transit that prevents fluid and electrolyte absorption. Bile salts and undigested fats lead to excess fluid secretion into the GI tract. Diarrhea from celiac disease and short bowel syndrome result from malabsorption in the small intestine.

Clinical Manifestations Infections that attack the upper GI tract (e.g., Norovirus, G. lamblia) usually produce large-volume, watery stools, cramping, and periumbilical pain (Table 42.1). Patients have either a low-grade or no fever and often have nausea and vomiting before the diarrhea begins. Infections of the colon and distal small bowel (e.g., Shigella, Salmonella, C. difficile) cause fever and frequent bloody diarrhea with a small volume. Leukocytes, blood, and mucus may be present in the stool, depending on the causative agent. Severe diarrhea may cause lifethreatening dehydration, electrolyte problems (e.g., hypokalemia), and acid-base imbalances (metabolic acidosis). CDI can progress to

severe colitis and intestinal perforation.

Diagnostic Studies Stool cultures are usually done only in patients who are very ill; have a fever, bloody diarrhea, or diarrhea lasting longer than 3 days; or were exposed during an outbreak.1 Those with travelers’ diarrhea lasting 14 days or longer should be evaluated for parasitic infections. Stools are examined for blood, mucus, white blood cells (WBCs), and parasites. Cultures reliably identify infectious organisms. Multiplepathogen stool tests can detect common viral, parasitic, and bacterial organisms from a single stool sample.

TABLE 42.2 Drug TherapyAntidiarrheal Drugs

Drug bismuth subsalicylate (Pepto-Bismol)

Mechanism of Action Decreases secretions and has weak antibacterial activity. Used to prevent traveler’s diarrhea

calcium polycarbophil (FiberCon)

Bulk-forming agent that absorbs excess fluid from diarrhea to form a gel. Used when intestinal mucosa cannot absorb fluid

diphenoxylate with atropine (Lomotil)

Opioid and anticholinergic. Decreases peristalsis and intestinal motility

loperamide (Imodium, Pepto Diarrhea Control)

Inhibits peristalsis, delays transit, increases absorption of fluid from stools

octreotide acetate (Sandostatin)

Suppresses serotonin secretion, stimulates fluid absorption from GI tract, decreases intestinal motility

paregoric (camphorated tincture of opium)

Opioid. Decreases peristalsis and intestinal motility

Blood cultures should be done in those with signs of sepsis or systemic infection (e.g., high fever) or who are immunocompromised.1 The WBC count may be high. People with long-standing diarrhea can develop anemia from iron and folate deficiencies. Increased

hematocrit, blood urea nitrogen (BUN), and creatinine levels are signs of fluid deficit. In patients with chronic diarrhea, measuring stool electrolytes, pH, and osmolality helps determine whether the diarrhea is from decreased fluid absorption or increased fluid secretion. Measuring stool fat and undigested muscle fibers may show fat and protein malabsorption conditions. Some patients with secretory diarrhea have high serum levels of GI hormones, such as vasoactive intestinal polypeptide and gastrin.

Interprofessional Care Treatment of diarrhea depends on the cause. Acute infectious diarrhea is usually self-limiting. The major concerns are preventing transmission, replacing fluid and electrolytes, and protecting the skin. Most patients tolerate oral fluids. Solutions containing glucose and electrolytes (e.g., Pedialyte) may be enough to replace losses from mild diarrhea. If losses are severe, it will be necessary to give parenteral fluids, electrolytes, vitamins, and nutrition. Teach the patient to avoid foods and drugs that cause diarrhea. Antidiarrheal agents have limited short-term use. They coat and protect mucous membranes, absorb irritating substances, inhibit intestinal transit, decrease intestinal secretions, or decrease central nervous system stimulation of the GI tract (Table 42.2). Antidiarrheal agents are contraindicated in treating some infectious diarrheas because they potentially prolong exposure to the organism.1 They are used cautiously in inflammatory bowel disease (IBD) because of the danger of causing toxic megacolon (colonic dilation greater than 5 cm). Antibiotics rarely have a role in treating acute diarrhea. They are given only for certain infections or when the infected person is severely ill or immunosuppressed. The 2 antibiotics recommended for empiric therapy in adults are a fluoroquinolone, such as ciprofloxacin, and azithromycin.1

Clostridium difficile infection

CDI is a particularly hazardous health care–associated infection (HAI). The risk for contracting CDI is highest in patients receiving antimicrobial, chemotherapy, gastric acid–suppressing, or immunosuppressive agents. C. difficile spores can survive for up to 70 days on objects, including commodes, telephones, bedside tables, and floors. Health care workers who do not adhere to strict infection control precautions can transmit C. difficile from patient to patient. Meticulous hand washing with soap and water is extremely important in limiting the spread of C. difficile. Lactobacillus probiotics may be used to prevent CDI or as an adjunct therapy to help prevent the risk for recurrent CDI.3 CDI is treated with either oral vancomycin (125 mg 4 times a day) or fidaxomicin (200 mg twice daily) for 10 days. All nonessential antibiotics, stool softeners, laxatives, and antidiarrheal agents should be stopped. Metronidazole is an option when patients are unable to be treated with vancomycin or fidaxomicin. Patients with severe, complicated CDI with shock, hypotension, ileus, or megacolon should receive vancomycin 500 mg 4 times daily orally with IV metronidazole. Patients with ileus can receive vancomycin via enema. Recurrent CDI occurs in about 20% of patients. The risk increases with the use of additional antibiotics and CDI recurrences. Fecal microbiota transplantation (FMT) is emerging as the most effective treatment for recurrent CDI.3 FMT reestablishes healthy intestinal flora by infusing fecal bacteria obtained from healthy donor stool into the patient’s colon. To perform an FMT, feces obtained from the donor is pureed into a liquid, slurry consistency using saline, water, or pasteurized cow’s milk. The donor stool is then placed in the GI tract via an enema, nasoenteral tube, or during colonoscopy. The major concern with FMT is the potential for transmitting infectious agents in the donor stool. Using feces from donors who have intimate physical contact with the recipient and careful screening minimize this risk. Most patients have diarrhea immediately after the procedure.

Nursing Management: Acute Infectious Diarrhea Nursing Assessment Begin the nursing assessment with a thorough history and physical examination (Table 42.3). Ask the patient to describe their stool pattern and associated symptoms. Focus on the duration, frequency, character, and consistency of stool and the relationship to other symptoms, such as pain and vomiting. Ask about medical conditions that may cause diarrhea and whether the person is taking drugs, such as antibiotics and laxatives, which are known to cause diarrhea, decrease stomach acidity, or cause immunosuppression. Determine whether the patient has traveled to a foreign country or been at a day care facility recently and if other family members are ill. Ask about food preparation practices, food intolerances (e.g., milk), and changes in diet and appetite. Assess for fever and signs of dehydration (dry skin, low-grade fever, orthostatic changes in pulse and BP, decreased and concentrated urine). Assess the abdomen for distention, pain, and guarding. Inspect the perineal skin for signs of redness and breakdown from the diarrhea.

TABLE 42.3 Nursing AssessmentDiarrhea

Subjective Data Important Health Information Past health history: Recent travel, hospitalization, infections, stress. Diverticulitis or malabsorption, metabolic disorders, IBD, IBS Medications: Laxatives or enemas, magnesium-containing antacids, sorbitol-containing suspensions or elixirs, antibiotics,

methyldopa, digitalis, colchicine; OTC antidiarrheal drugs Surgery or other treatments: Stomach or bowel surgery, radiation

Functional Health Patterns Health perception–health management: Chronic laxative use, malaise Nutritional-metabolic: Ingestion of fatty and spicy foods, food intolerances. Anorexia, nausea, vomiting, weight loss. Thirst Elimination: Increased stool frequency, volume, and looseness. Change in color and character of stools. Steatorrhea, abdominal bloating. Decreased urine output Cognitive-perceptual: Abdominal tenderness, abdominal pain and cramping, tenesmus

Objective Data General Lethargy, sunken eyeballs, fever, malnutrition

Integumentary Pallor, dry mucous membranes, poor skin turgor, perianal irritation

Gastrointestinal Frequent soft to liquid stools that may alternate with constipation, altered stool color. Abdominal distention, hyperactive bowel sounds. Pus, blood, mucus, or fat in stools. Fecal impaction

Urinary Decreased output, concentrated urine

Possible Diagnostic Findings Abnormal serum electrolyte levels. Anemia, leukocytosis, eosinophilia, hypoalbuminemia. Positive stool cultures. Ova, parasites, leukocytes, blood, or fat in stool. Abnormal sigmoidoscopy or colonoscopy findings. Abnormal lower GI series

Nursing Diagnoses Nursing diagnoses for the patient with acute infectious diarrhea include: • Diarrhea • Fluid imbalance • Electrolyte imbalance For more information on nursing diagnoses and interventions for diarrhea, see eNursing Care Plan 42.1 on the website for this chapter.

Planning The overall goals are that the patient with diarrhea will have (1) cessation of diarrhea and resumption of normal bowel patterns; (2) normal fluid, electrolyte, and acid-base balance; (3) normal nutritional status; and (4) no perianal/perineal skin breakdown.

Nursing Implementation Consider all cases of acute diarrhea as infectious until the cause is

known. Strict infection control precautions are needed to prevent the illness from spreading to others. Wash your hands with soap and water before and after contact with each patient and when handling body fluids of any kind. Flush vomitus and stool in the toilet. Teach the patient principles of hygiene, infection control, and the potential dangers of an illness that is infectious to themselves and others. Discuss proper food handling, cooking, and storage with the patient and caregiver (see Tables 41.24 and 41.25). Viruses and C. difficile spores are extremely hard to kill. Alcoholbased hand cleaners and ammonia-based disinfectants are ineffective. Vigorous cleaning with soap and water does not kill everything. Immediately put patients with CDI in isolation. Ensure that visitors and all providers wear gloves and gowns. Give infected patients their own disposable stethoscopes and thermometers. Consider all objects in the room contaminated. Ensure surfaces and equipment are disinfected with a 10% bleach solution or a disinfectant labeled as C. difficile sporicidal.

Fecal Incontinence Etiology and Pathophysiology Fecal incontinence is the involuntary passage of stool. It occurs when the normal structures that maintain continence are damaged or disrupted. Defecation is a voluntary action when the neuromuscular system is intact (see Chapter 38). Problems with motor function (contraction of sphincters and rectal floor muscles) and/or sensory function (ability to perceive the presence of stool or have the urge to defecate) can result in fecal incontinence. Contributing factors include altered bowel habits, weakness or disruption of the internal or external anal sphincter, damage to the pudendal nerve or other nerves that innervate the anorectum, and damage to the anal tissue (Table 42.4). For women, obstetric trauma is the most common cause of sphincter disruption. Childbirth, aging, and menopause contribute to the development of fecal incontinence. Anorectal surgery can damage the sphincters and pudendal nerves. Radiation for prostate cancer decreases rectal compliance. Neurologic conditions, including stroke and multiple sclerosis, interfere with defecation. People with normal functioning defecation can have incontinence if immobility prevents prompt access to a toilet or stool is accidentally discharged with diarrhea. Chronic constipation can lead to fecal impaction, a collection of hardened feces in the rectum or sigmoid colon that a person cannot expel. Incontinence occurs as liquid stool seeps around the hardened feces. Fecal impaction is a common problem in older adults with limited mobility. Constipated persons tend to strain during defecation. Straining contributes to incontinence because it weakens the pelvic floor muscles.

Diagnostic Studies and Interprofessional Care The diagnosis and effective management of fecal incontinence require a thorough health history and physical examination. Ask the patient

about the number of incontinent episodes per week, stool consistency and volume, and the degree that incontinence interferes with work and social activities. A rectal examination can reveal reduced anal canal muscle tone and contraction strength of the external sphincter, as well as detect internal prolapse, rectocele, hemorrhoids, masses, and fecal impaction. Other tests, such as anorectal manometry, anorectal ultrasonography, and anal electromyography, are done when symptoms persist after treating underlying problems or certain problems need further evaluation.4

TABLE 42.4 Common Causes of Fecal

Incontinence

Anal Sphincter Weakness • Anorectal infection • Injury • Anorectal surgery for hemorrhoids, fistula, and fissures • Childbirth injury • Perineal trauma or pelvic fracture • Internal sphincter thinning

Functional • Physical or mobility impairments affecting toileting ability (e.g., frail older person who cannot get to the bathroom in time)

Inflammatory • Inflammatory bowel disease • Radiation

Neurologic Disease • Brain tumor • Congenital abnormalities (e.g., spina bifida, myelomeningocele) • Dementia • Diabetes • Multiple sclerosis • Neuropathy • Spinal cord lesions • Stroke

Pelvic Floor Dysfunction • Fistula • Rectal prolapse

Other • Chronic constipation • Denervation of pelvic muscles from chronic straining • Diarrhea • Fecal impaction Treatment of incontinence depends on the cause. Maintaining normal stool consistency and a bowel management program are important. This includes regular defecation, a high-fiber diet, and increased intake of caffeine-free fluids. Dietary fiber supplements or bulk-forming laxatives, like psyllium (e.g., Metamucil), increase stool bulk, firm consistency, and promote the sensation of rectal filling. Patients may need to reduce the intake of foods that cause diarrhea and rectal irritation. Common triggers include caffeine, products

containing artificial sweeteners, dairy products, high gas–producing vegetables (e.g., broccoli, cabbage, cauliflower), and vegetables containing insoluble fiber (e.g., lettuce, tomatoes, corn). Fecal incontinence from fecal impaction usually resolves after manual removal of the hard feces and cleansing enemas. Antidiarrheal agents (e.g., loperamide) are useful in slowing intestinal transit. Physical therapy and biofeedback training can improve awareness of rectal sensation, coordinate internal and external anal sphincters, and increase the strength of external sphincter contraction. Biofeedback training requires intact sensory and motor nerves and motivation to learn. It is a safe, painless, and effective treatment.4 Mild electrical stimulation of the sacral nerves targets communication problems between the brain and nerves that control the pelvic floor muscles and sphincters. Electrical stimulation can improve quality of life. Some patients may achieve complete continence.4 For patients who do not respond to conservative measures, treatment with dextranomer/hyaluronic acid gel (Solesta) may be used. In this treatment, the gel is injected into the deep submucosa of the patient’s anal canal. It works by building up tissue in the anal area, narrowing the anal canal and allowing muscles to more adequately close. No anesthesia is given. Postinjection pain and bleeding may occur. Surgery (e.g., sphincter repair procedures) is an option when other conservative treatments fail, the patient has a full-thickness prolapse, or the anal sphincter needs repair. A colostomy is sometimes needed.

Nursing Management: Fecal Incontinence Nursing Assessment Fecal incontinence is embarrassing, uncomfortable, and irritating to the skin. Its unpredictable nature makes it hard to maintain school and work activities and hampers social or intimate contact. Be sensitive to the patient’s feelings when discussing incontinence. Ask about bowel patterns before the incontinence developed; current bowel habits; stool consistency, volume, and frequency; and symptoms, including pain during defecation and a feeling of incomplete evacuation (tenesmus). The Bristol Stool Scale is helpful to assess stool consistency. Assess whether the patient has a sensation of urgency to evacuate the bowel or sensation of passing flatus and leaking stool. Ask about daily activities (mealtimes and work), diet, and family and social activities and the degree that incontinence interferes with these activities. Check the perineal area for irritation or breakdown. Patients who have fecal incontinence are at risk for incontinence-associated dermatitis (IAD).4 IAD results from chemical irritants in the feces causing skin damage. Symptoms include redness, skin loss, and rash. The location of IAD is usually the perianal or perineal area, buttocks, or upper thighs. Fungal infection is common and seen as a dark red center surrounded by satellite lesions. Your assessment is important in distinguishing IAD from pressure injury development.

Nursing Implementation Regardless of the cause of fecal incontinence, bowel training is effective for many patients. Bowel elimination occurs at regular intervals in most people. Knowing the patient’s usual bowel pattern can help you plan a bowel program that will achieve optimal stool consistency and establish predictable bowel elimination patterns. For

the hospitalized patient, placement on a bedpan, help to a bedside commode, or walks to the bathroom at a regular time daily help to establish regular defecation. The best time to schedule elimination is within 30 minutes after breakfast. If these techniques are not effective in reestablishing bowel regularity, administer bisacodyl, a glycerin suppository, or a small phosphate enema 15 to 30 minutes before the usual evacuation time. These preparations stimulate the anorectal reflex. Since stimulation will not occur unless the suppository or enema touches the rectal wall, first check for stool in the rectum and digitally remove it before inserting the laxative. Once a regular pattern is established, stop these drugs. Digital stimulation is another method for stimulating the anorectal reflex. It is often included in bowel programs for people with neurogenic bowels (e.g., from spinal cord injury). Irrigating the rectum and colon (usually with tap water) at regular intervals is another way to achieve continence in patients with neurogenic bowel. Maintaining perineal skin integrity is a priority, especially in the bedridden patient. Feces can contaminate wounds, damage skin, cause bladder infections, and spread infections such as C. difficile. Fecal containment is essential. One way to contain stool is a stool management system (e.g., Flexi-Seal, DigniCare, Actiflo). These systems funnel liquid stool from the rectum into a containment system. Common features include a retention cuff that sits above the anal sphincter and soft tubing that extends from this cuff to a secure hub that allows a person to change the containment canister when it is full. A system can remain in place for weeks. Their use may decrease the risk for CDI, skin damage from exposure to stool, IAD, and pressure injuries. Do not use a rectal tube or urinary catheter as a stool catheter. They can reduce the responsiveness of the rectal sphincter and irritate or ulcerate the rectal mucosa. Perform frequent skin assessments when using absorbent products. Incontinence pads are an option when the patient is in bed. Briefs should be used only during ambulation or when sitting in a chair. Make sure they are changed promptly after each episode of incontinence.

Use absorbent products in combination with a defined skin care program. This includes prompt cleansing, moisturizing, and skin protection. Cleanse the skin gently, using a skin cleanser rather than soap and water. Options include a cotton cloth moistened with a hydrating skin cleansing foam, incontinence clean-up cloths, or baby wipes. Avoid products that contain alcohol as they can cause drying of the skin and discomfort if skin is irritated. Pat the skin dry or use a blow dryer on a cool setting. Do not rub the skin dry. Apply a moisture barrier and, if needed, a skin barrier cream for more protection. For patients unable to care for themselves at home, you should teach caregivers how to maintain skin integrity. Fecal incontinence is an overwhelming burden for most patients. Be sensitive to their fears. Teach them ways to reduce incontinence episodes and better cope with them when they do occur. Help patients identify food triggers that may worsen symptoms. Encourage them to avoid those foods and exercise after meals. Tell them to try to use bathrooms when they are available. Patients may be more confident when they use discreet, disposable briefs or pads. Have them wear dark-colored clothing that they can quickly remove for toileting. Ready access to a spare set of clothing and cleansing cloths is important.

Constipation Constipation is characterized by difficult or infrequent bowel movements, often accompanied by excessive exertion during defecation or a feeling of incomplete evacuation.5 Constipation is a symptom, not a disease. It can be acute, usually lasting less than 1 week, or chronic, lasting over 3 months.

Etiology and Pathophysiology Risk factors associated with chronic constipation include a low-fiber diet, decreased physical activity, or ignoring the defecation urge. Ignoring the urge to defecate for a prolonged period can cause the muscles and mucosa of the rectum to become insensitive to the presence of feces. In addition, the prolonged retention of feces results in drying of stool due to water absorption. The harder and drier the feces, the harder it is to expel. Emotions, including anxiety, depression, and stress, affect the GI tract and can contribute to constipation. Constipation occurs with diseases that slow GI transit and hamper neurologic function, such as diabetes, Parkinson’s disease, and multiple sclerosis (Table 42.5). Many drugs, especially opioids, cause constipation (Table 42.6).5 Some people think they are constipated if they do not have a daily bowel movement. This can result in chronic laxative use and cathartic colon syndrome, a condition in which the colon becomes dilated and atonic (lacking muscle tone). Ultimately, the person cannot defecate without a laxative.

Clinical Manifestations The clinical presentation varies from a mild discomfort to a more severe event mimicking an “acute abdomen.” Stools are absent or hard, dry, and difficult to pass. Abdominal distention, bloating,

increased flatulence, and increased rectal pressure may be present.

TABLE 42.5 Diseases Associated With

Constipation

Colonic Disorders • Cancer • Diverticular disease • Inflammatory bowel disease • Intestinal stenosis • Intussusception • Luminal or extraluminal obstructing lesions • Rectocele • Prolapse

Systemic Disorders Collagen Vascular Disease • Amyloidosis • Systemic lupus erythematosus • Systemic sclerosis (scleroderma)

Metabolic/Endocrine • Chronic renal failure • Diabetes • Hypercalcemia/hyperparathyroidism • Hypokalemia • Hypothyroidism

• Pheochromocytoma • Pregnancy

Neurologic Disorders • Autonomic neuropathy (from diabetes) • Hirschsprung’s megacolon • Multiple sclerosis • Neurofibromatosis • Parkinson’s disease • Spinal cord lesions or injury • Stroke

TABLE 42.6 Drugs Associated With Constipation

Hemorrhoids are a common complication of chronic constipation. They result from venous engorgement caused by repeated Valsalva maneuvers (straining) and venous compression from hard, impacted stool. The Valsalva maneuver may have serious outcomes for patients with heart failure, cerebral edema, hypertension, and coronary artery

disease. During straining, the patient inspires deeply and holds the breath while contracting abdominal muscles and bearing down. This increases both intraabdominal and intrathoracic pressures and reduces venous return to the heart. The heart rate temporarily decreases along with a decrease in cardiac output. This results in a transient drop in arterial pressure. When the patient relaxes, thoracic pressure falls, resulting in a sudden flow of blood into the heart, increased heart rate, and an immediate rise in arterial pressure. These changes may be fatal for the patient who cannot compensate for the sudden increased blood flow returning to the heart. Rectal mucosal ulcers and fissures may occur from stool stasis or straining. Diverticulosis is another potential complication of chronic constipation. It is more common in older patients. In the presence of obstipation (absolute constipation with no passage of gas or stool) or fecal impaction secondary to constipation, colonic perforation may occur. Perforation, which is life threatening, causes abdominal pain, nausea, vomiting, fever, and a high WBC count.

Diagnostic Studies and Interprofessional Care In most patients, the diagnosis of constipation is based on findings from a thorough history and physical examination. The physical should include an abdominal examination, inspection of the perianal and rectal region, and a digital rectal examination. Concerning signs include a sudden, persistent change in bowel habits (>6 weeks) in those over 50 years, rectal bleeding or bloody stools, iron deficiency anemia, weight loss, significant abdominal pain, family or personal history of colorectal cancer (CRC) or inflammatory bowel disease and palpable mass.5 If any of these are present, tests are needed to rule out serious disease, such as CRC. These may include abdominal x-rays, barium enema, and colonoscopy or sigmoidoscopy. Increasing dietary fiber, fluid intake, and exercise can prevent many cases of constipation.6 Laxatives (Table 42.7) and enemas are an option in treating constipation. All promote bowel movements, but each class works differently. Which one a patient receives depends on the

severity and duration of the constipation and the patient’s health. Daily bulk-forming laxatives (psyllium) can prevent constipation because they work like dietary fiber and do not cause dependence. In patients with chronic constipation who do not respond to diet and lifestyle modifications, osmotic laxatives are the next recommended treatment. Stimulant laxatives are given to patients who do not respond to osmotic laxatives. Enemas are fast acting and can give immediate treatment of constipation but must be used cautiously. Agents containing sodium phosphate and magnesium can cause electrolyte imbalances in older adults and patients with heart and kidney problems. Other therapies target specific patient needs. Peripherally acting opioid receptor antagonists (e.g., methylnaltrexone, naldemedine, naloxegol) decrease constipation caused by opioid use. They do not block the analgesic effects of opioids. Biofeedback therapy may help patients who have constipation because of anismus (uncoordinated contraction of the anal sphincter during straining). A patient with severe constipation related to bowel motility or mechanical disorders may need more intense treatment. Diagnostic studies include anorectal manometry, GI tract transit studies, balloon expulsion test, and defecography. A patient with unrelenting constipation may need a colostomy, ileostomy, or continent fecal diversion. These procedures are discussed later in this chapter.6

Nutritional Therapy Diet is a key factor in preventing and treating constipation. Many patients have improved symptoms when they increase their dietary fiber intake. Dietary fiber is found in fruits, vegetables, and grains (Table 42.8). Wheat bran and prunes are especially effective for preventing and treating constipation. Whole wheat and bran are high in insoluble fiber. Dietary fiber adds to the stool bulk directly by attracting water. Adequate fluid intake (2 L/day) is essential. Large, bulky stools move through the colon much more quickly than small stools. However, the recommended fluid intake may be contraindicated in a patient with

heart disease or renal failure. Tell the patient that increasing fiber intake may initially increase gas production because of fermentation in the colon, but this effect decreases over several days.

TABLE 42.7 Drug TherapyConstipation

Evidence-Based Practice Probiotics and Constipation L.R. is an 82-yr-old woman with decreased mobility due to a recent

hip fracture. During a check-up visit at the orthopedic clinic, L.R. states she is having discomfort due to constipation. She tells you she is following her discharge instructions, “drinking lots of water,” and trying to increase fiber in her diet.

Making Clinical Decisions Best Available Evidence. Quality of life decreases with increased severity in constipation symptoms. Many patients with constipation have modifiable risk factors related to their lifestyle. These include low-fiber diet, poor hydration, and/or sedentary lifestyle. In adults with constipation, there is an association between the use of probiotics, especially products containing Bifidobacterium longum and Bifidobacterium lactis, and significant improvements in gut transit time, stool frequency, and stool consistency. Clinician Expertise. You know that diet, fluid intake, and activity can play a key role in treating and preventing constipation. You recently read about the potential benefit of probiotics in relieving constipation. Patient Preferences and Values. L.R. asks if you know of anything else she can do as she does not want to take any more drugs.

Implications for Nursing Practice 1. What information would you share with L.R. about probiotics and constipation? 2. What data would you want from L.R. about her diet, activity, medications, and fluid intake? 3. Why is it important for you to know about alternative therapies? What is your role in supporting patients who want alternatives to drug therapy?

References for Evidence Martinez-Martinez M.I, Calabuig-Tulsa R, Cauli O. The effects of probiotics as a treatment for constipation in elderly people: A systematic review. Arch Gerontol Geriatr. 2017;71:142. Serra J, Mascort-Roca J, Marzo-Castillejo M, et al. Clinical practice guidelines for the management of constipation in adults: Part 2: Diagnosis and treatment. Gastroenterol Hepatol. 2017;40:303.

TABLE 42.8 Nutritional TherapyHigh-Fiber

Foods

Acute Abdominal Pain and Laparotomy Etiology and Pathophysiology Acute abdominal pain is pain of recent onset. It may signal a lifethreatening problem, so it requires immediate attention. Causes include damage to organs in the abdomen and pelvis, which leads to inflammation, infection, obstruction, bleeding, and perforation (Fig. 42.1). Perforation of the GI tract results in irritation of the peritoneum (serous membrane lining the abdominal cavity) and peritonitis. Hypovolemic shock occurs from bleeding or obstruction and peritonitis causing large amounts of fluid to move from the vascular space into the abdomen.

TABLE 42.10 Patient & Caregiver

TeachingConstipation Include the following instructions when teaching the patient and caregiver about management of constipation. 1. Eat Dietary Fiber Eat 20 to 30 g of fiber per day. Gradually increase the amount of fiber eaten over 1 to 2 wk. Fiber softens hard stool and adds bulk to stool, promoting evacuation. Eat prunes or drink prune juice daily. Prunes stimulate defecation. • Foods high in fiber: raw vegetables and fruits, beans, breakfast cereals (All Bran, oatmeal) • Fiber supplements: Metamucil, Citrucel, FiberCon 2. Drink Fluids

Fluid softens hard stools. Drink 2 L per day. Drink water or fruit juices. Avoid caffeinated coffee, tea, and cola. Caffeine stimulates fluid loss through urination. 3. Exercise Regularly Walk, swim, or bike at least 3 times per wk. Contract and relax abdominal muscles when standing or by doing sit-ups to strengthen muscles and prevent straining. Exercise stimulates bowel motility and moves stool through the colon. 4. Establish a Regular Time to Defecate First thing in the morning or after the first meal of the day is the best time because people often have the urge to defecate at this time. 5. Do Not Delay Defecation Respond to the urge to have a bowel movement as soon as possible. Delaying defecation results in hard stools and a decreased “urge” to defecate. Water is absorbed from stool by the intestine over time. The colon becomes less sensitive to the presence of stool in the rectum. 6. Record Your Bowel Elimination Pattern Develop a habit of recording on your calendar when you have a bowel movement. Regular monitoring of bowel movement will help you identify a problem early. 7. Avoid Laxatives and Enemas Do not overuse laxatives and enemas, because they cause dependence. People who overuse them become unable to have a bowel movement without them.

FIG. 42.1 Cause of acute abdominal pain and pathophysiologic sequelae.

Clinical Manifestations Pain is the most common symptom of an acute abdominal problem. The patient may have nausea, vomiting, diarrhea, constipation, flatulence, fatigue, fever, rebound tenderness, and bloating.

Diagnostic Studies and Interprofessional Care Diagnosis begins with a complete history and physical examination. Description of the pain (frequency, timing, duration, location), accompanying symptoms, and sequence of symptoms (e.g., pain before or after vomiting) provide vital clues about the origin of the problem. Note the patient’s position. The fetal posture is common

with peritoneal irritation (e.g., appendicitis), a supine posture with outstretched legs with visceral pain, and restlessness with a seated posture with bowel obstructions or obstructions from kidney stones and gallstones.

TABLE 42.11 Emergency ManagementAcute

Abdominal Pain

Physical examination includes examination of the abdomen, rectum, and pelvis. A complete blood count (CBC), urinalysis, abdominal xray, and ECG are done, along with an ultrasound or CT scan. Women of childbearing age may need a pregnancy test to rule out an ectopic pregnancy. Emergency management of the patient with acute abdominal pain is

shown in Table 42.11. The goal of management is to identify and treat the cause and monitor and treat complications, especially shock. Carefully use pain medications (e.g., morphine) to provide pain relief without interfering with diagnostic accuracy when patients have nontraumatic acute abdominal pain. An immediate surgical consult may be needed. The HCP may perform a diagnostic laparoscopy to inspect the surface of abdominal organs, obtain biopsy specimens, perform laparoscopic ultrasounds, and remove organs. A laparotomy is done when laparoscopic techniques are inadequate. If the cause of the acute abdomen can be surgically removed (e.g., inflamed appendix) or surgically repaired (e.g., ruptured abdominal aneurysm), surgery is considered definitive therapy.

Nursing Management: Acute Abdominal Pain Nursing Assessment For the patient with acute abdominal pain, take vital signs immediately and again at frequent intervals. Increased pulse and decreasing BP indicate impending shock. A fever suggests an inflammatory or infectious process. Intake and output measurement gives essential information about the adequacy of vascular volume. Altered mental status occurs with poor cerebral perfusion. Skin color, skin temperature, and peripheral pulse strength give information about perfusion. Inspect the abdomen for distention, masses, abnormal pulsation, symmetry, hernias, rashes, scars, and pigmentation changes. Auscultate bowel sounds. Decreased or absent bowel sounds in a quadrant may occur with a bowel obstruction, peritonitis, or paralytic ileus. Perform gentle palpation to help determine the location and level of the patient’s pain. Assess for involuntary guarding and rigidity, which occur with peritoneal irritation. Ask the patient about the onset, location, intensity, duration, frequency, and character of pain. Note whether the pain has spread or moved to new sites (quadrants) and what makes the pain worse or better. Ask if the pain is associated with other symptoms, such as nausea, vomiting, changes in bowel and bladder habits, or vaginal discharge in women. Assessment of vomiting includes the amount, color, consistency, and odor of the emesis. Ask about usual and changes in bowel patterns and habits.

Nursing Diagnoses Nursing diagnoses for the patient with acute abdominal pain include: • Acute pain

• Fluid imbalance • Risk for infection

Planning The overall goals are that the patient with acute abdominal pain will have (1) relief of abdominal pain, (2) resolution of inflammation, (3) freedom from complications (especially hypovolemic shock), and (4) normal nutritional status.

Nursing Implementation General care for the patient with acute abdominal pain involves managing fluid and electrolyte imbalances, pain, and anxiety. Assess the quality and intensity of pain at regular intervals. Provide medication and other comfort measures. Maintain a calm environment and give information to help decrease anxiety. A nasogastric (NG) tube with low suction may decrease vomiting and relieve discomfort from gastric distention. Conduct ongoing assessments of vital signs, intake and output, and level of consciousness, which are key indicators of hypovolemic shock.

Acute Care Preoperative Care Preoperative care includes the emergency care of the patient described in Table 42.11 and general care of the preoperative patient (see Chapter 17).

Postoperative Care Postoperative care depends on the type of surgical procedure. See eNursing Care Plan 19.1, a general plan for the postoperative patient, on the website for Chapter 19. After surgery, some patients will have an NG tube with low suction to empty the stomach and prevent gastric dilation. If the upper GI

tract was entered, drainage from the NG tube may be dark brown to dark red for the first 12 hours. Later it should be light yellowish brown, or it may have a greenish tinge because of bile. If a dark red color continues or you see bright red blood, notify the HCP because of the risk for hemorrhage. “Coffee-grounds” granules in the drainage mean the blood has been changed by acidic gastric secretions. Nausea and vomiting are common after a laparotomy and result from the surgery, decreased peristalsis, or pain medications. Antiemetics, such as ondansetron (Zofran), promethazine (Phenergan), and aprepitant (Emend), may be ordered. Monitor fluid and electrolyte status along with BP, heart rate, and respirations. See Chapter 41 for further discussion of managing nausea and vomiting. Swallowed air and reduced peristalsis from decreased mobility, manipulation of the abdominal organs during surgery, and anesthesia can result in abdominal distention and gas pains. Early ambulation helps restore peristalsis, expel flatus, and reduce gas pain. Gradually, as intestinal activity increases, distention and gas pain disappear.

Ambulatory Care Preparation for discharge begins soon after surgery. Teach the patient and caregiver about any modifications in activity, care of the incision, diet, and drug therapy. Initially the patient starts on clear liquids after surgery and then, if tolerated, progresses to a regular diet. Early ambulation speeds recovery, but normal activities are resumed gradually, with planned rest periods. Patients generally have restrictions not to lift anything heavier than a few pounds. The patient and caregiver should be aware of any possible complications. Teach them to notify the HCP at once if fever is greater than 101°F (38.6°C), vomiting, pain, weight loss, incisional drainage, or changes in bowel function occur.

Evaluation The expected outcomes are that the patient with acute abdominal pain will:

• Have resolution of the cause of the acute abdominal pain • Experience relief of abdominal pain and discomfort • Be free from complications, especially hypovolemic shock and sepsis • Have normal fluid, electrolyte, and nutritional status

Abdominal Trauma Etiology and Pathophysiology Injuries to the abdominal area usually are a result of blunt trauma or penetrating injuries. Common injuries of the abdomen include lacerated liver, ruptured spleen, mesenteric artery tears, diaphragm rupture, urinary bladder rupture, great vessel tears, renal or pancreas injury, and stomach or intestine rupture. Blunt trauma often occurs with motor vehicle accidents, direct blows, and falls. It may not be obvious because it does not leave an open wound. Both compression injuries (e.g., direct blow to the abdomen) and shearing injuries (e.g., rapid deceleration in a motor vehicle crash allowing some tissue to move forward while other tissues stay stationary) occur with blunt trauma. Penetrating injuries occur when a gunshot or stabbing produces an obvious, open wound into the abdomen. When solid organs (liver, spleen) are injured, bleeding can be profuse, resulting in hypovolemic shock. When contents from hollow organs (e.g., bladder, stomach, intestines) spill into the peritoneal cavity, the patient is at risk for peritonitis. In addition, abdominal compartment syndrome can develop. Abdominal compartment syndrome, or abdominal hypertension, is excessively high pressure in the abdomen. Anything that increases the volume in the abdominal cavity (e.g., edematous organs, bleeding) increases abdominal pressure. This high pressure restricts ventilation, potentially leading to respiratory failure. The high pressure decreases cardiac output, venous return, and arterial perfusion of organs. Decreased perfusion to the kidneys can lead to renal failure.

Clinical Manifestations Careful assessment provides important clues to the type and severity of injury. Intraabdominal injuries are often associated with rib fractures, fractured pelvis, spinal injury, and thoracic injury. If the

patient was in an automobile accident, a contusion or abrasion across the lower abdomen may indicate internal organ trauma due to seat belt use. Seat belts can produce blunt trauma to abdominal organs by pressing the intestine and pancreas into the spinal column. Classic manifestations of abdominal trauma are (1) guarding and splinting of the abdominal wall (indicating peritonitis); (2) a hard, distended abdomen (occurs with intraabdominal bleeding); (3) decreased or absent bowel sounds; (4) abrasions or bruising over the abdomen; (5) abdominal pain; (6) hematemesis or hematuria; and (7) signs of hypovolemic shock (Table 42.12). Ecchymosis around the umbilicus (Cullen’s sign) or flanks (Grey Turner’s sign) may mean retroperitoneal hemorrhage. Loss of bowel sounds occurs with peritonitis. If the diaphragm ruptures, you can hear bowel sounds (if present) in the chest. Auscultation of bruits is indicative of arterial damage.

Diagnostic Studies Laboratory tests include a baseline CBC and urinalysis. Even when bleeding, the patient will have normal hemoglobin and hematocrit because fluids are lost at the same rate as the red blood cells. Deficiencies are evident after fluid resuscitation begins. Blood in the urine may be a sign of kidney or bladder damage. Other laboratory work includes arterial blood gases, prothrombin time, electrolytes, BUN and creatinine, and type and crossmatch (in anticipation of possible blood transfusions). An abdominal CT scan and focused abdominal ultrasound are the most common diagnostic methods, but the patient must be stable before going for CT.

TABLE 42.12 Emergency ManagementAbdominal

Trauma

Diagnostic peritoneal lavage can detect blood, bile, intestinal contents, and urine in the peritoneal cavity. It is generally used only for unstable patients to identify blood in the peritoneum.

Interprofessional and Nursing Care Emergency management of abdominal trauma is outlined in Table 42.12. Volume expanders or blood given if the patient is hypotensive. An NG tube with low suction will decompress the stomach and prevent aspiration. Frequent ongoing assessment is needed to monitor fluid status, detect deterioration in condition, and determine the need for surgery. The decision about whether to do surgery depends on clinical findings, diagnostic test results, and the patient’s response to conservative management. Do not remove an impaled object until skilled care is available. Removal may cause further injury and bleeding.

Chronic Abdominal Pain Chronic abdominal pain may originate from abdominal structures or be referred from a site with the same or a similar nerve supply. The pain is often described as dull, aching, or diffuse. Common causes of chronic abdominal pain include irritable bowel syndrome (IBS), peptic ulcer disease, chronic pancreatitis, hepatitis, pelvic inflammatory disease, adhesions, and vascular insufficiency. Diagnosing the cause of chronic abdominal pain begins with a thorough history and description of specific pain characteristics, including severity, location, frequency, duration, and onset. The assessment includes factors that increase or decrease the pain, such as eating, defecation, and activities. Endoscopy, CT scan, MRI, laparoscopy, and barium studies may be done. Treatment for chronic abdominal pain depends on the underlying cause.

Irritable Bowel Syndrome Irritable bowel syndrome (IBS) is a disorder characterized by chronic abdominal pain or discomfort and alteration of bowel patterns. Patients may have diarrhea or constipation, alternating periods of both. IBS has no known organic cause. Psychologic stressors (e.g., depression, anxiety, panic disorders, posttraumatic stress disorder) are associated with the development and exacerbation of IBS. Patients often have a history of GI infections and adverse reactions to food. Dietary intolerances that may contribute to symptoms include gluten and fermentable oligo-, di-, and monosaccharides and polyols (FODMAPs).7 Examples of oligosaccharides are wheat and rye products, some fruits and vegetables, onions, garlic, legumes, and nuts. The disaccharide lactose is found in milk and milk products. Fructose is a monosaccharide found in honey, apples, pears, and highfructose corn syrup. Polyols are found in apples, pears, stone fruits, cauliflower, mushrooms, and artificial sweeteners, like sorbitol.8 IBS is diagnosed solely on symptoms. The Rome IV criteria for diagnosing IBS require the presence of abdominal pain and/or discomfort at least 1 day per week for 3 months that is associated with 2 or more of the following: related to defecation, change in stool frequency, or change in the stool form.7 Depending on the stool patterns, IBS is categorized as IBS with constipation (IBS-C), IBS with diarrhea (IBS-D), IBS mixed, and IBS unsubtyped. Other common symptoms include abdominal distention, nausea, flatulence, bloating, urgency, mucus in the stool, and sensation of incomplete evacuation. Non-GI symptoms may include fatigue, headache, and sleep problems.

Gender Differences

Irritable Bowel Syndrome (IBS)

Men • More likely to have IBS with diarrhea • Less likely to admit to symptoms or seek help for them

Women • Overall affects women 2 to 2.5 times more often than men • More likely to have IBS with constipation • Report more severe abdominal pain, gas, and bloating • Have a lower quality of life with higher levels of fatigue and depression The key to accurate diagnosis is a thorough history and physical examination. Ask patients to describe symptoms, health history (including psychosocial factors, such as stress and anxiety), family history, and drug and diet history. Determine if and how IBS symptoms interfere with school, work, or recreational activities. Diagnostic tests are used to rule out other disorders, such as colorectal cancer, IBD, endometriosis, and malabsorption disorders (lactose intolerance, celiac disease). No single therapy is effective for all patients with IBS. Treatment may include dealing with psychologic factors, dietary changes, and drugs to regulate stool output and reduce discomfort. Patients may benefit from keeping a diary of symptoms, diet, and episodes of stress to help identify any factors that trigger the IBS symptoms. Cognitive behavior therapy and stress management techniques may help a patient cope. Participating in regular exercise reduces bloating and constipation and reduces stress-related symptoms. Review with the patient foods that are high in FODMAPs and teach them to follow a low-FODMAP diet.8 If dairy products tend to cause symptoms, yogurt may be the best option because of the lactobacillus

bacteria it contains. Probiotics can improve symptoms. Tell the patient with flatulence to avoid common gas-producing foods, such as broccoli and cabbage. For those with constipation, encourage an intake of enough dietary fiber to produce soft, painless bowel movements. Drug therapy focuses on the dominant bowel symptom and pain. The opioid agonist eluxadoline (Viberzi) decreases colonic contractions to reduce diarrhea and pain. It is contraindicated in those without a gallbladder. An option for women with IBS-D is alosetron (Lotronex). Because of serious side effects (e.g., severe constipation, ischemic colitis), it is available only in a restricted access program. Other treatments for IBS-D include loperamide, antidepressants, and antispasmodic medications (hyoscyamine, dicyclomine). Antispasmodics decrease GI motility and smooth muscle spasms, reducing pain and diarrhea.8

Drug Alert Alosetron (Lotronex) • Taking this drug can cause severe constipation and ischemic colitis (reduced blood flow to intestines). • Teach the patient to stop the drug and contact the HCP if constipation, rectal bleeding, bloody diarrhea, or abdominal pain occurs. Women with IBS-C may benefit from lubiprostone (Amitiza). Men or women with IBS-C can take linaclotide (Linzess). It is contraindicated in patients with a history of mechanical obstruction or prior bowel surgery.

FIG. 42.2 In appendicitis the blood supply of the appendix is impaired by inflammation and bacterial infection, which may result in gangrene.

Inflammatory Disorders Appendicitis Appendicitis is inflammation of the appendix, a narrow blind tube that extends from the inferior part of the cecum (Fig. 42.2). It is the most common reason for emergency abdominal surgery.

Etiology and Pathophysiology About 7% of people will develop appendicitis sometime during their lifetime.9 It is most common in those 10 to 30 years of age. A common cause of appendicitis is obstruction of the lumen by a fecalith (accumulated feces). Obstruction results in distention; venous engorgement; and the accumulation of mucus and bacteria, which can lead to gangrene, perforation, and peritonitis.

Clinical Manifestations Diagnosis can be difficult because many patients do not have classic symptoms. Appendicitis typically begins with dull periumbilical pain, followed by anorexia, nausea, and vomiting. The pain is persistent and continuous, eventually shifting to the right lower quadrant and localizing at McBurney’s point (halfway between the umbilicus and right iliac crest). A low-grade fever may develop. Further assessment reveals localized tenderness, rigidity, rebound tenderness, and muscle guarding. Coughing, sneezing, and deep inhalation worsen pain. The patient usually prefers to lie still, often with the right leg flexed. The older adult may report less severe pain, slight fever, and discomfort in the right iliac fossa.

Diagnostic Studies and Interprofessional Care Patient examination includes a complete history, physical examination, and a differential WBC count. Most patients have a mildly to moderately high WBC count. A urinalysis is done to rule out

genitourinary conditions that mimic appendicitis. CT scan is the preferred diagnostic procedure. However, ultrasound and MRI are options. If there is a delay in diagnosis and treatment, the appendix can rupture and the resulting peritonitis can be fatal. The standard treatment of appendicitis is an immediate appendectomy (surgical removal of appendix).9 If the inflammation is localized, surgery should be done as soon as the diagnosis is made. Antibiotics and fluid resuscitation are started before surgery. If the appendix has ruptured and there is evidence of peritonitis or an abscess, giving parenteral fluids and antibiotic therapy for 6 to 8 hours before the appendectomy helps prevent dehydration and sepsis.

Nursing Management: Appendicitis Managing the patient who has manifestations of appendicitis focuses on preventing fluid volume deficit, relieving pain, and preventing complications. To ensure the stomach is empty in case surgery is needed, keep the patient NPO until the HCP evaluates the patient. Monitor vital signs and perform ongoing assessment to detect any deterioration in condition. Give IV fluids, analgesics, and antiemetics as ordered. Provide comfort measures. Postoperative care for the patient who had an appendectomy is similar to the patient after a laparotomy (see p. 935). Patients are usually discharged within 24 hours after an uncomplicated laparoscopic appendectomy. Ambulation begins a few hours after surgery, and the diet is advanced as tolerated. Those who had a perforation usually have a longer length of stay and need IV antibiotic therapy. Most patients resume normal activities 2 to 3 weeks after surgery.

Check Your Practice A 28-yr-old female patient comes to the emergency department with acute abdominal pain. • What manifestations would make you suspect appendicitis is the cause of the patient’s abdominal pain?

Peritonitis Etiology and Pathophysiology Peritonitis results from a localized or generalized inflammatory process of the peritoneum. Causes of peritonitis are listed in Table 42.13. Primary peritonitis occurs when blood-borne organisms enter the peritoneal cavity. For example, the ascites that occurs with cirrhosis of the liver provides an excellent liquid environment for bacteria to flourish. Organisms can enter the peritoneum during peritoneal dialysis. Secondary peritonitis is much more common. It occurs when abdominal organs perforate or rupture and release their contents (bile, enzymes, and bacteria) into the peritoneal cavity. Common causes include a ruptured appendix, perforated gastric or duodenal ulcer, severely inflamed gallbladder, and trauma from gunshot or knife wounds. Intestinal contents and bacteria irritate the normally sterile peritoneum and produce an initial chemical peritonitis. Bacterial peritonitis develops a few hours later. The resulting inflammatory response leads to massive fluid shifts (peritoneal edema) and adhesions as the body tries to wall off the infection.

Clinical Manifestations Abdominal pain is the most common symptom of peritonitis. A universal sign is tenderness over the involved area. Rebound tenderness, muscular rigidity, and spasm are other signs of peritoneal irritation. Patients may lie still and take only shallow breaths because movement worsens the pain. Abdominal distention, fever, tachycardia, tachypnea, nausea, vomiting, and altered bowel habits may be present. These manifestations vary, depending on the severity and acuteness of the underlying condition. Complications include hypovolemic shock, sepsis, intraabdominal abscess formation, paralytic ileus, and acute respiratory distress syndrome. Peritonitis

can be fatal if treatment is delayed.

TABLE 42.13 Causes of Peritonitis

Primary • Blood-borne organisms • Cirrhosis with ascites • Genital tract organisms

Secondary • Appendicitis with rupture • Blunt or penetrating trauma to abdominal organs • Diverticulitis with rupture • Ischemic bowel disorders • Pancreatitis • Perforated intestine • Perforated peptic ulcer • Peritoneal dialysis • Postoperative (breakage of anastomosis)

TABLE 42.14 Interprofessional CarePeritonitis

Diagnostic Assessment • History and physical examination • CBC, including WBC differential • Serum electrolytes

• Abdominal x-ray • Abdominal paracentesis and culture of fluid • CT scan or ultrasound • Peritoneoscopy

Management Preoperative or Nonoperative • NPO status • IV fluid replacement • NG to low-intermittent suction • O2 PRN • Parenteral nutrition as needed

Drug Therapy • Antibiotic therapy • Analgesics (e.g., morphine) • Antiemetics as needed

Postoperative • NPO status • NG to low-intermittent suction • Semi-Fowler’s position • IV fluids with electrolyte replacement • PN as needed • Blood transfusions as needed

Drug Therapy

• Antibiotic therapy • Sedatives and opioids • Antiemetics as needed

Diagnostic Studies and Interprofessional Care A CBC is done to determine elevations in WBC count and hemoconcentration from fluid shifts (Table 42.14). Peritoneal aspiration may be done with the fluid analyzed for blood, bile, pus, bacteria, fungus, and amylase content. An abdominal x-ray may show dilated loops of bowel consistent with paralytic ileus, free air if perforation has occurred, or air and fluid levels if an obstruction is present. Ultrasound and CT scans may be useful in identifying ascites and abscesses. Peritoneoscopy may be helpful in the patient without ascites. It allows for direct examination of the peritoneum and the ability to obtain biopsy specimens for diagnosis. Patients with milder cases of peritonitis or those who are poor surgical risks receive conservative care. Treatment consists of antibiotics, NG suction, analgesics, and IV fluid administration. Surgery is indicated to locate the cause of the inflammation, drain purulent fluid, and repair any damage (e.g., perforated organs).

Nursing Management: Peritonitis Nursing Assessment Assessment of the patient’s pain, including the location, is important and may help to determine the cause of peritonitis. Assess for the presence and quality of bowel sounds, increasing abdominal distention, abdominal guarding, nausea, fever, and manifestations of hypovolemic shock.

Nursing Diagnoses Nursing diagnoses for the patient with peritonitis include: • Acute pain • Fluid imbalance • Impaired gas exchange • Risk for infection

Planning The overall goals are that the patient with peritonitis will have (1) resolution of inflammation, (2) relief of abdominal pain, (3) freedom from complications (especially sepsis and hypovolemic shock), and (4) normal nutritional status.

Nursing Implementation The patient with peritonitis is extremely ill and needs skilled supportive care. Establish IV access so that you can give replacement fluids lost to the peritoneal cavity and have access for antibiotic therapy. Monitor the patient for pain and response to analgesics. You may position the patient with knees flexed to increase comfort. Sedatives may relieve anxiety and promote rest. Accurate monitoring of intake and output and electrolyte status is

essential to determine replacement therapy. Frequently monitor vital signs. Give antiemetics to decrease nausea and vomiting and prevent further fluid and electrolyte losses. Place the patient on NPO status. The patient may need an NG tube to decrease gastric distention and further leakage of bowel contents into the peritoneum. Give low-flow oxygen therapy as needed. If the patient had an open surgical procedure, drains are inserted to remove purulent drainage and excess fluid. Postoperative care is similar to that for the patient who had a laparotomy (see p. 935).

Gastroenteritis Gastroenteritis is an inflammation of the mucosa of the stomach and small intestine. Features of acute gastroenteritis are sudden diarrhea accompanied by nausea, vomiting, fever, and abdominal cramping. Viruses are the most common cause of gastroenteritis (Table 42.1). Norovirus is a leading cause of foodborne outbreaks of acute gastroenteritis. Laboratory testing to identify norovirus is useful when a number of people simultaneously have gastroenteritis and there is a clear avenue for virus transmission, such as a shared location or food. Most cases of gastroenteritis are self-limiting. Encourage oral fluids containing glucose and electrolytes (e.g., Pedialyte) to prevent and treat dehydration. Older adults and chronically ill patients may be unable to consume enough fluids to make up for fluid loss. If dehydration occurs, IV fluid replacement may be needed. Nursing management of the patient with gastroenteritis is the same as for the patient with acute diarrhea (see p. 927).

Inflammatory Bowel Disease Inflammatory bowel disease (IBD) is a chronic inflammation of the GI tract characterized by periods of remission interspersed with periods of exacerbation. We classify IBD as either Crohn’s disease or ulcerative colitis (UC) based on clinical manifestations (Table 42.15). As the name suggests, ulcerative colitis is usually limited to the colon. Crohn’s disease can involve any segment of the GI tract from the mouth to the anus. About 1.3 million Americans have IBD. It often begins during the teenage years and early adulthood. IBD has a second peak in the 6th decade. The incidence and frequency of IBD varies depending on geographic location and racial or ethnic background. The highest rates are in the Northern Hemisphere and industrialized nations.10 The risk for having IBD is greater in urban compared with rural areas and those of white and Ashkenazic Jewish origin than in other racial and ethnic groups.10 The strongest risk factor is family history. Many people with IBD have a family member with the disorder.

Etiology and Pathophysiology We do not know the exact cause of IBD. IBD is an autoimmune disease involving an immune reaction to a person’s own intestinal tract. We think that it results from an overactive, inappropriate, or sustained immune response to environmental and bacterial triggers, probably in a genetically susceptible person. The resulting inflammation causes widespread tissue destruction. Environmental factors, such as diet, smoking, and stress, increase susceptibility by changing the environment of the GI microbial flora. We think that dietary factors unique to industrialized countries contribute to the development of IBD. High intake of refined sugar, total fats, polyunsaturated fatty acid (PUFA), and omega-6 fatty acids is associated with an increased risk for IBD. Eating fewer raw fruits, vegetables, omega-3−rich foods, and dietary fiber decrease risk.11 Use

of nonsteroidal antiinflammatory drugs (NSAIDs), antibiotics, and oral contraceptives are associated with increased risk.12

Genetic Link IBD occurs more often in family members of people with IBD, especially monozygotic twins. To date, we have found over 200 genes associated with IBD. Certain genetic mutations are associated with Crohn’s disease, others with UC, and many with both. The number of gene variations suggests that IBD is a group of diseases that produce similar types of mucosal destruction. The path from genetic mutation to abnormal immune responses varies depending on which gene or genes are affected. Several of the genes are involved in protective functions of the intestines. Others have a role in the immune system, especially in the maturation and function of T cells. Genetic variation may explain differences in patient responses to drug therapies for IBD.

TABLE 42.15 Comparison of Ulcerative Colitis

and Crohn’s Disease

Many of the major genes related to Crohn’s disease, including NOD2, ATG16L1, IL23R, and IRGM, are involved in immune system function. The proteins made from these genes help the immune system sense and respond appropriately to bacteria in the lining of the GI tract. NOD2 gene changes are associated with a form of Crohn’s disease that affects the ileum in persons of northern European descent. Changes in the NOD2 gene trigger an abnormal immune response that allows bacteria to grow unchecked and invade intestinal cells. This causes chronic inflammation and digestive problems.13 IBD is more likely to occur in those with other genetic syndromes, including cystic fibrosis. An increased prevalence occurs in the presence of other inflammatory disorders with genetic susceptibility, such as psoriasis and multiple sclerosis.

Pattern of Inflammation in Ulcerative Colitis vs. Crohn’s

Disease The pattern of inflammation differs between Crohn’s disease and UC (Fig. 42.3). Crohn’s disease can occur anywhere in the GI tract from the mouth to the anus. It most often involves the distal ileum and proximal colon. Segments of normal bowel can occur between diseased portions, so-called “skip” lesions. The inflammation in Crohn’s disease involves all layers of the bowel wall. Typically, ulcerations are deep, longitudinal, and penetrate between islands of inflamed edematous mucosa, causing the classic cobblestone appearance. Strictures at the areas of inflammation can cause bowel obstruction. Since the inflammation goes through the entire wall, microscopic leaks can allow bowel contents to enter the peritoneal cavity and form abscesses or produce peritonitis. In active Crohn’s disease, fistulas are common.

FIG. 42.3 Comparison of distribution patterns of Crohn’s disease and ulcerative colitis.

UC usually starts in the rectum and moves in a continual fashion toward the cecum. Although mild inflammation may occur in the terminal ileum, UC is a disease of the colon and rectum. The inflammation and ulcerations occur in the mucosal layer, the innermost layer of the bowel wall. Fistulas and abscesses are rare since inflammation does not extend through all bowel wall layers. Because water and electrolytes are not absorbed through inflamed mucosa, diarrhea with large fluid and electrolyte losses is common. Breakdown of cells results in protein loss through the stool. Areas of inflamed mucosa form pseudopolyps, tongue-like projections into the

bowel lumen.

FIG. 42.4 Extraintestinal manifestations of IBD.

Clinical Manifestations Both forms of IBD are chronic disorders with mild to severe acute exacerbations that occur at unpredictable intervals over many years. Although the manifestations of Crohn’s disease and UC are similar (diarrhea, weight loss, abdominal pain, fever, fatigue), there are differences (Table 42.15). In Crohn’s disease, diarrhea and cramping abdominal pain are common symptoms. If the small intestine is involved, weight loss occurs from inflammation of the small intestine causing malabsorption. Rectal bleeding sometimes occurs with Crohn’s disease, although not as often as with UC. In UC, the primary problems are bloody diarrhea and abdominal pain. Pain may vary from the mild lower abdominal cramping associated with diarrhea to severe, constant pain associated with acute perforations. With mild disease, diarrhea may consist of no more than 4 semiformed stools daily that contain small amounts of blood. The patient may have no other manifestations. In moderate disease, the patient has increased stool output (up to 10 stools/day), increased bleeding, and systemic symptoms (fever, malaise, mild anemia, anorexia). In severe disease, diarrhea is bloody, contains mucus, and occurs 10 to 20 times a day. In addition, fever, rapid weight loss greater than 10% of total body weight, anemia, tachycardia, and dehydration are present.

Complications Patients with IBD have both local (confined to the GI tract) and systemic (extraintestinal) complications (Fig. 42.4). GI tract complications include hemorrhage, strictures, perforation (with possible peritonitis), abscesses, fistulas, CDI, and colonic dilation (toxic megacolon). Toxic megacolon is more common with UC. Patients with toxic megacolon are at risk for perforation and may need an emergency colectomy. Perineal abscess and fistulas occur in up to a third of patients with Crohn’s disease. CDI increases in frequency and severity in patients with IBD.

IBD is related to an increased risk for colorectal cancer. Those with Crohn’s disease are at increased risk for small intestinal cancer. Cancer screening at regular intervals is important in persons with IBD. People with IBD may have systemic complications, such as multiple sclerosis and ankylosing spondylitis. Some are related to the inflammatory activity in the bowel. They occur with active inflammation and improve when the IBD improves. Other complications include malabsorption, liver disease (primary sclerosing cholangitis), and osteoporosis. Routine liver function tests are important because primary sclerosing cholangitis can lead to liver failure. Both men and women with IBD are at risk for osteoporosis. They need a bone density scan at baseline and every 2 years.

Diagnostic Studies The diagnosis of IBD includes ruling out diseases with similar symptoms and figuring out whether the patient has Crohn’s disease or UC. The symptoms of early Crohn’s disease are like those of IBS. Diagnostic studies provide information about disease severity and complications. A CBC typically shows iron-deficiency anemia from blood loss. A high WBC count may be a sign of toxic megacolon or perforation. Decreased serum sodium, potassium, chloride, bicarbonate, and magnesium levels occur due to fluid and electrolyte losses from diarrhea and vomiting. Hypoalbuminemia is present with severe disease because of poor nutrition or protein loss. Increased erythrocyte sedimentation rate, C-reactive protein, and WBCs reflect inflammation. The stool is examined for blood, pus, and mucus. Stool cultures can determine if infection is present. Imaging studies, such as double-contrast barium enema, small bowel series (small bowel follow through), transabdominal ultrasound, CT, and MRI, are useful for diagnosing IBD. Colonoscopy allows for examination of the entire large intestine lumen and sometimes the most distal ileum. The HCP can determine the extent of inflammation, ulcerations, pseudopolyps, and strictures and obtain biopsy specimens for a definitive diagnosis. Since a colonoscope can

enter only the distal ileum, capsule endoscopy (see Chapter 38) may be needed to diagnose Crohn’s disease in the small intestine.

Interprofessional Care The goals of treatment of IBD are to (1) rest the bowel, (2) control the inflammation, (3) combat infection, (4) correct malnutrition, (5) provide symptomatic relief, and (6) improve quality of life. There is no cure for IBD. Treatment relies on drugs to treat the inflammation and maintain remission (Table 42.16). Several drugs are available to treat IBD. Since the recurrence rate is high after surgical treatment of Crohn’s disease, drugs are the preferred treatment. Hospitalization is needed if the patient does not respond to drug therapy, the disease is severe, or complications are suspected.

Drug Therapy The goal of drug treatment in IBD is to induce and maintain remission. Five major classes of drugs are used: aminosalicylates, antimicrobials, corticosteroids, immunomodulators, and biologic therapies (Table 42.17). Drug choice depends on the location and severity of inflammation. Patients are treated with either a “step-up” or a “step-down” approach. With the step-up approach, the patient with mild symptoms begins with an aminosalicylate or antimicrobial and adds a more toxic medication (e.g., biologic therapies) when initial therapies do not work. The step-down approach uses immunosuppressant and biologic therapy first.14

TABLE 42.16  Interprofessional

CareInflammatory Bowel Disease

Diagnostic Assessment • History and physical examination

• CBC, erythrocyte sedimentation rate • Serum chemistries • Testing of stool for occult blood and infection • Capsule endoscopy • Radiologic studies with barium contrast • Sigmoidoscopy and/or colonoscopy with biopsy

Management • High-calorie, high-vitamin, high-protein, low-residue, lactosefree (if lactase deficiency) diet • Elemental diet or PN • Drug therapy (Table 42.17) • Aminosalicylates • Antimicrobials • Biologic therapies • Corticosteroids • Immunosuppressants • Physical and emotional rest • Referral for counseling or support group • Surgical therapy (Table 42.18) Drugs containing 5-aminosalicylic acid (5-ASA) remain the mainstay to achieve and maintain remission and prevent flare-ups of IBD. They include sulfasalazine (Azulfidine) and the new generation of sulfa-free drugs (olsalazine, mesalamine). Aminosalicylates can treat both UC and Crohn’s disease. They are much more effective for UC.14 The exact mechanism of action of 5-ASA is unclear. We think topical application to the intestinal mucosa suppresses proinflammatory cytokines and other inflammatory mediators. People can take aminosalicylates orally or rectally. Oral forms are available with different coatings that affect where the medication is released along

the GI tract. This allows more effective treatment of specific symptoms. Rectal forms include suppositories and enemas. Rectal use offers the advantage of delivering the 5-ASA directly to the affected tissue. This is useful in treating inflammation in the rectum and/or large intestine. The combination of oral and rectal therapy is better than oral or rectal therapy alone. Corticosteroids can help achieve remission in IBD. They are given for the shortest possible time because of the side effects associated with long-term use. Patients with disease in the left colon, sigmoid, and rectum benefit from suppositories, enemas, and foams because they deliver the corticosteroid directly to the inflamed tissue with minimal systemic effects. Oral prednisone is given to patients with mild to moderate disease who did not respond to either 5-ASA or topical corticosteroids. Those with severe inflammation may need a short course of IV corticosteroids. Corticosteroids must be tapered to very low levels when surgery is planned to prevent postoperative complications (e.g., infection, delayed wound healing, fistula formation).

TABLE 42.17 Drug TherapyInflammatory Bowel

Disease

Immunosuppressants (6-mercaptopurine, azathioprine) are given for several reasons. They can maintain remission after corticosteroid therapy. Patients who do not respond to aminosalicylates, corticosteroids, or antibiotics; have side effects from corticosteroids; or have fistulas may benefit. These drugs require regular CBC monitoring because they can suppress the bone marrow and lead to inflammation of the pancreas or liver. They have a delayed onset of action and are not useful for acute flare-ups. Methotrexate is most useful in patients with Crohn’s disease who cannot stop corticosteroid use without a flare-up or in whom other drugs have been ineffective. Many patients have flu-like symptoms with use. Some develop bone marrow depression and liver dysfunction. Correct dosing is critical to minimize the risk for toxicity. Careful monitoring of the CBC and liver enzymes is essential. Advise women of childbearing age to avoid pregnancy because use causes birth defects and fetal death. Biologics reduce IBD-related inflammation by blocking specific proteins that play a role in inflammation. There are 2 main classes: anti–tumor necrosis factor (TNF) agents and integrin receptor antagonists. The anti-TNF agent infliximab (Remicade) is given IV to induce and maintain remission in patients with Crohn’s disease and in patients with draining fistulas who do not respond to conventional drug therapy. The other anti-TNF agents are given subcutaneously.15 The anti-TNF agents have similar side effects. The most common ones are upper respiratory and urinary tract infections, headaches, nausea, joint pain, and abdominal pain. More serious effects include reactivation of hepatitis and tuberculosis (TB); opportunistic infections; and cancers, especially lymphoma. Patients need to know the risks before starting therapy. They are tested for TB and hepatitis before treatment begins and cannot receive live virus immunizations. Teaching includes how to prevent infection and recognize early signs and symptoms (e.g., fever, cough, malaise, dyspnea). Integrin receptor antagonists include natalizumab (Tysabri) and vedolizumab (Entyvio). They inhibit leukocyte adhesion by blocking

α4-integrin, an adhesion molecule. Use is limited to those who have not had an adequate response with other therapies (corticosteroids, immunosuppressants, anti-TNF agents). Both are given by IV infusion. Their use is associated with increased risk for infection, hepatotoxicity, and hypersensitivity reactions. Because of the risk for progressive multifocal leukoencephalopathy, natalizumab is available only through a restricted program.

TABLE 42.18 Indications for Surgical Therapy for

IBD • Drainage of abdominal abscess • Failure to respond to conservative therapy • Fistulas • Inability to decrease corticosteroids • Intestinal obstruction • Massive hemorrhage • Perforation • Severe anorectal disease • Suspicion of cancer The biologic agents do not work for everyone. They are costly and may produce allergic reactions. They are immunogenic, meaning that patients receiving them often make antibodies against them. Immunogenicity leads to acute infusion reactions and delayed hypersensitivity-type reactions. The drugs are most effective when given at regular intervals. Infusion reactions are more likely if a drug is stopped and then restarted.

Surgical Therapy

Ulcerative Colitis Indications for surgery for UC are outlined in Table 42.18. Surgical procedures used include (1) total proctocolectomy with ileal pouch/anal anastomosis (IPAA) and (2) total proctocolectomy with permanent ileostomy. Since UC affects only the colon, a total proctocolectomy is curative. The most common surgical procedure for UC is a total proctocolectomy with IPAA. For more detail, see the discussion on bowel resection and ostomy surgery later in this chapter on p. 952.

Crohn’s Disease Surgery for Crohn’s disease is usually done for complications such as strictures, obstructions, bleeding, and fistula (Table 42.18). Most patients with Crohn’s disease eventually need surgery. The most common surgery involves resecting the diseased segments with reanastomosis of the remaining intestine. Unfortunately, the disease often recurs at the anastomosis site. Repeated removal of sections of the small intestine can lead to short bowel syndrome. Short bowel syndrome (SBS) occurs when either surgery or disease leaves too little small intestine surface area to maintain normal nutrition and hydration. Lifetime fluid boluses and parenteral nutrition (PN) may be needed. For more detail, see the discussion on short bowel syndrome later in this chapter on p. 962. The other common surgery for Crohn’s disease is a strictureplasty. This opens narrowed areas obstructing the bowel. Since the intestine stays intact, it reduces the risk for developing short-bowel syndrome and its associated complications. Recurrences at the site are uncommon.

Nutritional Therapy An individualized diet is an important part of treating IBD. Patients with IBD need a balanced, healthy diet with enough calories, protein, and nutrients. Consult a dietitian about dietary recommendations. The goals of diet management are to (1) provide adequate nutrition without worsening symptoms, (2) correct and prevent malnutrition,

(3) replace fluid and electrolyte losses, and (4) prevent weight loss. Nutritional deficiencies are due to decreased oral intake, blood loss, and, depending on the location of the inflammation, impaired absorption. Patients may reduce food intake to reduce diarrhea. Inflammatory mediators reduce appetite. Blood loss and malabsorption lead to iron-deficiency anemia (see Chapter 30). The patient may need oral iron supplements. Parenteral or IV iron is an option for those who cannot tolerate oral iron or if anemia is severe. Zinc deficiency can result from ostomies or diarrhea. Zinc supplements may be needed.16 Disease of the terminal ileum reduces absorption of cobalamin and bile acids. Reduced cobalamin contributes to anemia. Those who develop anemia should receive cobalamin injections. Bile salts are important for fat absorption and contribute to osmotic diarrhea. Cholestyramine, an ion-exchange resin that binds unabsorbed bile salts, helps control diarrhea. Drug therapy can contribute to nutritional problems. Patients taking sulfasalazine should take 1 mg folate (folic acid) daily.16 Those receiving corticosteroids are prone to osteoporosis and need calcium supplements. Potassium supplements may be needed with corticosteroids. During an acute exacerbation, patients with IBD may not be able to tolerate a regular diet. Liquid enteral feedings are preferred over PN because atrophy of the gut and bacterial overgrowth occur when the GI tract is not used. EN is high in calories and nutrients, lactose free, and easily absorbed. They help achieve remission and improve nutritional status. EN is discussed in Chapter 39. There are no universal food triggers for IBD, but some may find that certain foods cause diarrhea. A food diary helps to identify problem foods to avoid. Patients are typically taught to then avoid or limit foods that cause GI distress or worsen symptoms.

Nursing Management: Inflammatory Bowel Disease Nursing Assessment Table 42.19 outlines the subjective and objective data you should obtain from a patient with IBD.

Nursing Diagnoses Nursing diagnoses for the patient with IBD include: • Diarrhea • Impaired nutritional status • Difficulty coping • Chronic pain For more information on nursing diagnoses and interventions for IBD, see eNursing Care Plan 42.2 on the website for this chapter.

TABLE 42.19 Nursing AssessmentInflammatory

Bowel Disease

Subjective Data Important Health Information Past health history: Infection, autoimmune disorders Medications: Antidiarrheal drugs

Functional Health Patterns

Health perception–health management: Family history of ulcerative colitis or Crohn’s disease. Fatigue, malaise Nutritional-metabolic: Nausea, vomiting; anorexia. Weight loss Elimination: Diarrhea. Blood, mucus, or pus in stools Cognitive-perceptual: Lower abdominal pain (worse before defecation), cramping, tenesmus

Objective Data General Intermittent fever, emaciated appearance, fatigue

Integumentary Pale skin with poor turgor, dry mucous membranes. Skin lesions, anorectal irritation, skin tags, cutaneous fistulas

Gastrointestinal Abdominal distention, hyperactive bowel sounds, abdominal cramps

Cardiovascular Tachycardia, hypotension

Possible Diagnostic Findings Anemia, leukocytosis. Electrolyte imbalance, hypoalbuminemia, vitamin, and trace metal deficiencies. Guaiac-positive stool. Abnormal sigmoidoscopy, colonoscopy, and/or barium enema

findings

Planning The overall goals are that the patient with IBD will (1) have fewer and less severe acute exacerbations, (2) maintain normal fluid and electrolyte balance, (3) be free from pain or discomfort, (4) adhere to medical regimens, (5) maintain nutritional balance, and (6) have an improved quality of life.

Nursing Implementation Acute Care During the acute phase, focus your attention on hemodynamic stability, pain control, fluid and electrolyte balance, and nutritional support. Maintain accurate intake and output records. Monitor the number and appearance of stools. Assess for the presence of blood in stools and emesis. Give IV fluids, electrolytes, analgesics, and antiinflammatory drugs as prescribed. Monitor serum electrolytes, CBC, and vital signs, being alert for changes related to diarrhea and dehydration. If the patient has orthostatic hypotension, teach the patient to change position slowly and use safety precautions. Help the patient stay clean, dry, and free of odor until the diarrhea is under control. Place a deodorizer in the room. Meticulous perianal skin care using plain water (no harsh soap) with a moisturizing skin barrier cream prevents skin breakdown. Dibucaine, witch hazel, sitz baths, and other soothing compresses or ointments may reduce perianal irritation and pain. Calculate the adequacy of the daily calorie intake. Obtain a daily weight. Assess the abdomen, including bowel sounds, as needed. Consult with a dietitian about diet modifications and the need for nutritional supplements. Postoperative care after surgical procedures for IBD is similar to that described later in this chapter in the intestinal and ostomy surgery section (see p. 952) and in the general nursing care plan for

the postoperative patient (see eNursing Care Plan 19.1 on the website for Chapter 19).

Ambulatory Care IBD is a chronic illness. Assist the patient in accepting the chronicity of IBD and learning ways to cope with its recurrent, unpredictable nature. Teaching includes (1) the importance of rest and diet management, (2) perianal care, (3) drug action and side effects, (4) symptoms of recurrence of disease, (5) when to seek medical care, and (6) ways to reduce stress. Excellent teaching resources, written in easily comprehensible language are available from the Crohn’s and Colitis Foundation of America (www.crohnscolitisfoundation.org). It is important to establish rapport and encourage the patient to talk about self-care. Ask patients what you can do to promote their selfcare. An explanation of all procedures and treatments helps to build trust, decrease apprehension, and increase self-control. Once you have established a therapeutic relationship, talk with smokers who have Crohn’s disease about quitting since smoking is associated with more severe disease. The patient and caregiver may need your help setting realistic short- and long-term goals. Patients may have severe fatigue, which limits their energy for physical activity. Rest is important. Patients may lose sleep because of frequent episodes of diarrhea and abdominal pain. Nutritional deficiencies and anemia worsen fatigue and leave the patient feeling weak. Teach them to schedule activities around rest periods. Many patients have intermittent exacerbations and remissions of symptoms. Given the chronicity and uncertainty related to the frequency and severity of flares, the patient may have frustration, depression, and anxiety. Psychotherapy and behavioral therapies may help patients deal with their feelings about the disease and help to manage their symptoms. Because of the relationship between emotions and the GI tract, teach the patient ways to manage stress (see Chapter 6). Suggest the patient seek support through a local or online support group from the Crohn’s and Colitis Foundation of America.

Evaluation The expected outcomes are that the patient with IBD will • Have a decrease in the number of diarrhea stools • Maintain body weight within a normal range • Be free from pain and discomfort • Use effective coping strategies

Gerontologic Considerations: Inflammatory Bowel Disease A second peak in occurrence of IBD is in the 6th decade. The cause, natural history, and clinical course of IBD are similar to those seen in younger patients. However, in the older patient, proctitis and leftsided UC are more common. Diagnosis is sometimes difficult in older adults since IBD can be confused with CDI, diverticulitis, or colitis. The interprofessional care of IBD is also similar; however, challenges exist. Drug therapy and surgery have an increased risk for adverse events, hospitalization, and mortality. Older adults are more prone to adverse events from corticosteroids. Immunosuppressant and biologic therapies have a higher risk for infection and cancer. Anemia and malnutrition are more common.17 They are more vulnerable to volume depletion from diarrhea. Those with physical limitations may have trouble handling fecal urgency and multiple trips to the bathroom without help.

Intestinal Obstruction Intestinal obstruction occurs when intestinal contents cannot pass through the GI tract. The obstruction may occur in the small (SBO) or large (LBO) intestine. It can be partial or complete, simple or strangulated. Partial obstructions do not completely occlude the intestinal lumen, allowing for some fluid and gas to pass through. They usually resolve with conservative treatment. A complete obstruction totally occludes the lumen and usually requires surgery. A simple obstruction has an intact blood supply; a strangulated one does not.

Types of Intestinal Obstruction The causes of intestinal obstruction are either mechanical or nonmechanical.

Mechanical In mechanical obstruction, there is a physical obstruction of the intestinal lumen. Most intestinal obstructions occur in the small intestine. Surgical adhesions are the most common cause of SBO.18 They can occur within days of surgery or years later (Fig. 42.5). Other causes of SBO are hernia, cancer, strictures from Crohn’s disease, and intussusception after bariatric surgery. The most common cause of LBO is colorectal cancer (malignant obstruction) followed by diverticular disease. Other causes include adhesions, ischemia, volvulus, and Crohn’s disease.19

Nonmechanical A nonmechanical obstruction occurs with reduced or absent peristalsis due to altered neuromuscular transmission of the parasympathetic innervation to the bowel. It may result from a neuromuscular or vascular disorder. Paralytic ileus (lack of intestinal peristalsis and

bowel sounds) is the most common form of nonmechanical obstruction. It occurs to some degree after any abdominal surgery. It can be hard to know if a postoperative obstruction is due to paralytic ileus or adhesions. One clue is that bowel sounds usually return before postoperative adhesions develop. Other causes of paralytic ileus include peritonitis, inflammatory responses (e.g., acute pancreatitis, acute appendicitis), electrolyte abnormalities (especially hypokalemia), and thoracic or lumbar spinal fractures. Pseudo-obstruction is a mechanical obstruction without any cause found on radiologic imaging. It is a GI motility disorder. There are several conditions associated with pseudo-obstruction. These include major surgery, electrolyte imbalance, neurologic conditions, medications, sepsis, cancer, trauma, and burns.20 Vascular obstructions are rare. They are the result of an interference with the blood supply to a part of the intestines. The most common causes are emboli and atherosclerosis of the mesenteric arteries. Emboli may originate from thrombi in patients who have chronic atrial fibrillation, diseased heart valves, and prosthetic valves. Venous thrombosis may occur in conditions of low blood flow, such as heart failure and shock.

Etiology and Pathophysiology About 6 to 8 L of fluid enter the small intestine daily. Most of the fluid is absorbed before it reaches the colon. Around 75% of intestinal gas is swallowed air. When an obstruction occurs, fluid, gas, and intestinal contents accumulate proximal to the obstruction. Distention reduces fluid absorption and initially stimulates intestinal secretions. Distal to the obstruction, the bowel empties, and then collapses. As distention increases in the proximal bowel, intraluminal bowel pressure rises. The increased pressure leads to an increase in capillary permeability and extravasation of fluids and electrolytes into the peritoneal cavity. Eventually the intestinal muscle becomes fatigued, and peristalsis stops. Retention of fluids in the intestine and peritoneal cavity leads to a severe reduction in circulating blood volume. This leads to

hypotension and hypovolemic shock.

FIG. 42.5 Bowel obstructions. A, Adhesions. B, Strangulated inguinal hernia. C, Ileocecal intussusception. D, Intussusception from polyps. E, Mesenteric occlusion. F, Neoplasm. G, Volvulus of the sigmoid colon.

If blood flow is inadequate, bowel tissue becomes ischemic, then necrotic, and the bowel may perforate. In the most dangerous situation the bowel becomes so distended that the blood flow stops, causing edema, cyanosis, and gangrene of a bowel segment. This is called intestinal strangulation or intestinal infarction. If not quickly corrected, the bowel will become necrotic and rupture, leading to infection, septic shock, and death. The location of the obstruction determines the extent of fluid, electrolyte, and acid-base imbalances. If the obstruction is high (e.g., upper duodenum), metabolic alkalosis may result from the loss of gastric hydrochloric (HCl) acid through vomiting or NG intubation

and suction. When the obstruction is in the small intestine, dehydration occurs rapidly. Dehydration and electrolyte imbalances do not occur early in large bowel obstruction. If the obstruction is below the proximal colon, solid fecal material accumulates until symptoms of discomfort appear.

Clinical Manifestations The 4 hallmark clinical manifestations of an obstruction are abdominal pain, nausea and vomiting, distention, and constipation. The order and degree these appear vary by the cause, location, and type of obstruction (Table 42.20). Colicky abdominal pain is usually the first symptom. In SBO, the pain is often of sudden onset. It occurs at 4- to 5-minute intervals for proximal obstructions and less often for distal obstructions. The nature of the vomiting gives a clue to the level of obstruction. In a proximal obstruction, patients rapidly develop nausea and vomiting. It may be projectile and contain bile. Vomiting usually gives temporary relief from abdominal pain in higher obstructions. Vomiting from a more distal small bowel obstruction is more gradual in onset and more fecal and foul smelling. Bowel sounds may be high-pitched above the area of obstruction. Bowel sounds are usually absent with paralytic ileus.

TABLE 42.20 Manifestations of Small and Large

Intestinal Obstructions

Signs of LBO include abdominal distention, either obstipation or a marked change in bowel function, and lack of flatus. The patient has persistent, cramping abdominal pain. Bowel sounds are usually present and become progressively hypoactive. Vomiting is rare. Strangulation causes severe, constant pain that is rapid in onset.19 With both types, abdominal tenderness and rigidity occur. The patient appears acutely ill, with signs of dehydration and sepsis. These include tachycardia, dry mucous membranes, and hypotension. The patient’s temperature may rise above 100°F (37.8°C).

Diagnostic Studies Perform a thorough history and physical examination. Imaging can identify an obstruction and guide decisions about surgery. Abdominal x-rays, CT scan, or contrast enema may be done. Sigmoidoscopy or colonoscopy provides direct visualization of an LBO. Blood tests include a CBC and blood chemistries. A high WBC count may mean strangulation or perforation. Increased hematocrit values may reflect hemoconcentration. Decreased hemoglobin and hematocrit values may mean bleeding from cancer or strangulation with necrosis. Serum electrolytes, BUN, and creatinine are monitored to assess the degree of dehydration. Metabolic alkalosis can develop from vomiting.

Interprofessional Care Treatment of a bowel obstruction depends on the cause. If a strangulated obstruction or perforation is present, the patient will need emergency surgery to relieve the obstruction and survive. In some, especially those due to surgical adhesions, an obstruction may resolve without surgery. Surgery may involve simply resecting the obstructed segment of bowel and anastomosing the remaining healthy bowel back together. Partial or total colectomy, colostomy, or ileostomy may be done when extensive obstruction or necrosis is present. Sometimes, an obstruction can be removed nonsurgically. Colonoscopy offers a means to remove

polyps, dilate strictures, and remove and destroy tumors with a laser. The initial treatment includes placing the patient on NPO status, providing IV fluid therapy with either normal saline or lactated Ringer’s solution, and giving IV antiemetics. If needed, insert an NG tube for decompression and give ordered electrolyte replacement. Obtain blood cultures and start IV antibiotic therapy. Some patients need PN to allow bowel rest and improve nutritional status before surgery. The treatment goal for a patient with a malignant obstruction is to regain patency and resolve the obstruction. Stents can be placed via endoscopic or fluoroscopic procedures. They are used for palliative purposes or as “a bridge to surgery,” allowing a patient to avoid emergency surgery.19 This gives the interprofessional team time to correct fluid volume problems and treat other problems, thus improving surgical outcomes. Corticosteroids with antiemetic properties that decrease edema and inflammation may be used with stent placement.

Nursing Management: Intestinal Obstruction Nursing Assessment Intestinal obstruction is a potentially life-threatening condition. Major concerns are preventing fluid and electrolyte deficiencies and early recognition of deterioration in the patient’s condition (e.g., hypovolemic shock, sepsis, bowel strangulation). Nursing assessment begins with a detailed patient history and physical examination. Determine the location, duration, intensity, and frequency of abdominal pain. Record the onset, frequency, color, odor, and amount of vomitus. Assess bowel function, including the passage of flatus. Auscultate for bowel sounds and document their character and location. Inspect the abdomen for scars, visible masses, and distention. Assess whether abdominal tenderness or rigidity is present. Measure the abdominal girth. Check for signs of peritoneal irritation (e.g., muscle guarding, rebound pain). If the HCP decides to wait to see if the obstruction resolves on its own, assess the patient regularly. Notify the HCP of changes in vital signs, changes in bowel sounds, decreased urine output, increased abdominal distention, and pain. Maintain a strict intake and output record, including emesis and tube drainage. A urinary catheter allows for hourly monitoring of urine output. Report if the urine output is less than 0.5 mL/kg of body weight per hour. This indicates inadequate vascular volume and the potential for acute kidney injury. Rising serum creatinine and BUN levels are other indicators of acute kidney injury.

Nursing Diagnoses Nursing diagnoses for the patient with intestinal obstructions include: • Acute pain

• Fluid imbalance

Planning The overall goals are that the patient with an intestinal obstruction will have (1) relief of the obstruction and return to normal bowel function, (2) minimal to no discomfort, and (3) normal fluid and electrolyte and acid-base status.

Nursing Implementation Monitor the patient closely for signs of dehydration and electrolyte imbalances. Give IV fluids as ordered. Assess for signs and symptoms of fluid imbalance. Some patients, especially older adults, may not tolerate rapid fluid replacement. Monitor serum electrolyte levels closely. A patient with a high intestinal obstruction is more likely to have metabolic alkalosis. A patient with a low obstruction is at greater risk for metabolic acidosis. The patient is often restless and constantly changes position to relieve the pain. Provide comfort measures and promote a restful environment. Nursing care of the patient after surgery for an intestinal obstruction is similar to care of the patient after a laparotomy (see p. 935). With an NG tube in place, oral care is extremely important. Vomiting leaves an unpleasant taste in the patient’s mouth, and fecal odor may be present. The patient breathes through the mouth, drying the mouth and lips. Provide frequent oral care and water-soluble lubricant for the lips. Check the nose for signs of irritation from the NG tube. Clean and dry this area daily, apply water-soluble lubricant, and retape the tube. Check the NG tube every 4 hours for patency.

Polyps of Large Intestine Colonic polyps arise from the mucosal surface of the colon and project into the lumen. They may be sessile (flat, broad based, and attached directly to the intestinal wall) or pedunculated (attached to the intestinal wall by a thin stalk). Polyps tend to be sessile when small and become pedunculated as they enlarge (Fig. 42.6). They may be found anywhere in the large intestine. As patients age, polyps are increasingly present in the proximal colon. Rectal bleeding and occult blood in the stool are the most common signs, but most patients with polyps are asymptomatic.

Types of Polyps The most common types of polyps are hyperplastic and adenomatous. Hyperplastic polyps are noncancerous. They rarely grow larger than 5 mm and never cause clinical symptoms. Other benign polyps include inflammatory polyps, lipomas, and juvenile polyps.

FIG. 42.6 Endoscopic image of pedunculated polyp in descending colon. Courtesy David Bjorkman, MD, University of Utah School of Medicine, Department of Gastroenterology. In McCance KL, Huether SE: Pathophysiology: The biologic basis for disease in adults and children, ed 6, St Louis, 2010, Mosby.

Adenomatous polyps are neoplastic and closely linked to colorectal adenocarcinoma. There are 3 types: tubular, tubulovillous, and villous. Villous or large adenomatous polyps are more likely to have cancers develop in them. Removing adenomatous polyps decreases the occurrence of colorectal cancer.

Genetic Link Familial adenomatous polyposis (FAP) is the most common polyposis syndrome (see the Genetics in Clinical Practice box), causing 1% of all CRCs. FAP is a genetic disorder characterized by hundreds or

sometimes thousands of polyps in the colon that appear during adolescence and early adulthood. They eventually become cancerous, usually by age 40. Since CRC is inevitable,

Genetics in Clinical Practice Familial Adenomatous Polyposis (FAP)

Genetic Basis • Autosomal dominant FAP • Classic form of disease • Mutations in adenomatous polyposis coli (APC) gene • Normally this is a tumor suppressor gene involved in DNA repair • Normally this gene makes a protein that keeps polyps from developing in the colon • 50% of the offspring of a patient with FAP carry the FAP gene • Autosomal recessive FAP • Autosomal recessive disorder • Mutations in the mutY homolog (MUTYH) gene • Normally this gene is involved in DNA repair • Characterized by fewer polyps, typically 10 lb) for 6 to 8 weeks.

FIG. 42.15 A, Umbilical hernia. B, Femoral hernias (note swelling below the inguinal ligaments). C, Right inguinal hernia. A and B, From Zitelli BJ, McIntire SC, Nowalk AJ: Zitelli and Davis’ atlas of pediatric physical diagnosis, ed 6, Philadelphia, 2012, Saunders. C, From Swartz MH: Textbook of physical diagnosis: History and examination, ed 6, Philadelphia, 2010, Saunders.

Malabsorption Syndrome Malabsorption results from impaired absorption of fats, carbohydrates, proteins, minerals, and vitamins. The stomach, small intestine, liver, and pancreas regulate normal digestion and absorption. Digestive enzymes ordinarily break down nutrients so that absorption can take place. Malabsorption may occur if this process is interrupted at any point. Several problems can cause malabsorption (Table 42.31). Lactose intolerance is the most common malabsorption disorder, followed by IBD, celiac disease, tropical sprue, and cystic fibrosis. The most common signs of malabsorption are weight loss, diarrhea, and steatorrhea (bulky, foul-smelling, yellow-gray, greasy stools with putty-like consistency) (Table 42.32). Steatorrhea does not occur with lactose intolerance. Tests to determine the cause of malabsorption include qualitative examination of stool for fat (e.g., Sudan III stain), a 72-hour stool collection for quantitative measurement of fecal fat, serologic testing for celiac disease, and fecal elastase testing to determine if there is pancreatic insufficiency. Near-infrared reflectance analysis (NIRA) for fecal fat is available at some centers in the United States. Other diagnostic studies include a CT scan and endoscopy to obtain a small bowel biopsy specimen. A small bowel barium enema can identify abnormal mucosal patterns. Capsule endoscopy is useful in assessing the small intestine for changes in mucosal integrity and inflammation. Tests for carbohydrate malabsorption include the Dxylose test and the lactose tolerance test. Laboratory studies include a CBC, measurement of prothrombin time (to see if vitamin K absorption is adequate), serum vitamin A and carotene levels, serum electrolytes, cholesterol, and calcium. Treatment depends on the cause.

TABLE 42.31 Causes of Malabsorption

Bacterial Proliferation • Parasitic infection • Tropical sprue

Biochemical or Enzyme Deficiencies • Biliary tract obstruction • Chronic pancreatitis • Cystic fibrosis • Lactase deficiency • Pancreatic insufficiency • Zollinger-Ellison syndrome

Disturbed Lymphatic and Vascular Circulation • Heart failure • Ischemia • Lymphangiectasia • Lymphoma

Small Intestinal Mucosal Disruption • Celiac disease • Crohn’s disease • Whipple’s disease

Surface Area Loss • Billroth II gastrectomy

• Distal ileal resection, disease, or bypass • Short bowel syndrome

Celiac Disease Celiac disease is an autoimmune disease that causes damage to the small intestinal mucosa. It is triggered by ingesting gluten, a protein in wheat, barley, and rye.27 It can occur at any age and has a wide variety of symptoms. Celiac sprue and gluten-sensitive enteropathy are other names for celiac disease. Celiac disease is not the same disease as tropical sprue, a chronic disorder occurring primarily in tropical areas. Tropical sprue causes progressive disruption of jejunal and ileal tissue, resulting in nutrition problems. It is treated with folic acid and tetracycline.

TABLE 42.32 Manifestations of Malabsorption

Celiac disease affects about 1 in 100 people worldwide.28 Firstdegree relatives of someone with celiac disease have a 4% to 15% chance of developing the disorder. It is associated with other autoimmune diseases, particularly rheumatoid arthritis, type 1 diabetes, and thyroid disease. It is slightly more common in women. Symptoms often begin in childhood.

Etiology and Pathophysiology Three factors necessary for developing celiac disease are genetic predisposition, gluten ingestion, and an immune-mediated response.

Genetic Link

About 90% to 95% of patients with celiac disease have human leukocyte antigen (HLA) allele HLA-DQ2. The other 5% to 10% have HLA-DQ8. However, not everyone with these genetic markers develops celiac disease, and some people with celiac disease do not have these HLA alleles. As with other autoimmune diseases, the tissue destruction that occurs with celiac disease is the result of chronic inflammation. Gluten contains specific peptides called prolamines. Partial digestion of gluten releases the prolamine peptides, which are absorbed into the intestinal submucosa. In genetically susceptible persons, the peptides bind to HLA-DQ2 and/or HLA-DQ8 and activate an inflammatory response. Inflammation damages the microvilli and brush border of the small intestine, decreasing the amount of surface area available for nutrient absorption. Damage is most severe in the duodenum, probably because it has more exposure to gluten. The inflammation lasts as long as gluten ingestion continues.

Clinical Manifestations Classic manifestations of celiac disease include foul-smelling diarrhea, abdominal pain, flatulence, abdominal distention, and malnutrition.27 Some people have no obvious GI symptoms and may instead have atypical signs and symptoms. These include joint pain, osteoporosis, dental enamel hypoplasia, fatigue, peripheral neuropathy, and reproductive problems. An intensely pruritic, vesicular skin lesion, called dermatitis herpetiformis, is sometimes present and occurs as a rash on the buttocks, scalp, face, elbows, and knees. Protein, fat, and carbohydrate absorption is affected. Weight loss, muscle wasting, and other signs of malnutrition may be present. Abnormal serum folate, iron, and cobalamin levels can occur. Irondeficiency anemia is common. Patients may have lactose intolerance and need to refrain from lactose-containing products until the disease is under control. Inadequate calcium intake and vitamin D absorption can lead to decreased bone density and osteoporosis.

Diagnostic Studies Early diagnosis and treatment can prevent complications. Screening is recommended for close relatives of patients known to have the disease, young patients with decreased bone density, those with anemia if other causes are ruled out, and certain autoimmune diseases. Celiac disease is confirmed by a combination of findings from the history and physical examination, serology testing, and histologic analysis of small intestine biopsies.27 Have the patient complete diagnostic testing before starting a gluten-free diet, since the diet will change the results. Serologic testing for immunoglobulin A (IgA) antitissue transglutaminase and IgA endomysial antibody offer good sensitivity and specificity. Histologic evidence is the gold standard for confirming the diagnosis. Biopsies show flattened mucosa and noticeable losses of villi. Genotyping involves testing for HLA-DQ2 and/or HLA-DQ8 antigens.

Interprofessional and Nursing Care A gluten-free diet (Table 42.33) is the only effective treatment for celiac disease. Most patients need to stay on a gluten-free diet for the rest of their lives. Periodic nutrition evaluations and laboratory monitoring are done to monitor for anemia and malnutrition. The patient should undergo bone density screening every 2 to 3 years.28 Refer all patients for a dietary consultation. You can work with a dietitian to teach the patient how to eat a nutritionally adequate diet while staying within a budget. Teach the patient to avoid wheat, barley, oats, and rye products. Although pure oats do not contain gluten, wheat, rye, and barley can contaminate oat products during the milling process. Teach the patient to read medication and food labels. Some medications and many food additives, preservatives, and stabilizers contain gluten. The patient needs to know where to buy gluten-free products. Good sources are health food stores, many grocery stores, and through Internet sites. Maintaining a gluten-free diet can be hard, particularly when

traveling or eating in restaurants. Many with celiac disease describe feeling embarrassed or like a burden when having to discuss glutenfree menu options with restaurant staff or when dining in other’s homes. Mobile phone users will find apps listing gluten-free menu options at popular restaurants helpful. Many restaurants now indicate which food choices are gluten free. The Celiac Sprue Association website (www.csaceliacs.info) and the Celiac Disease Foundation (www.celiac.org) provide suggestions for maintaining a gluten-free diet and living with celiac disease.

TABLE 42.33 Nutritional TherapyCeliac Disease

Foods to Eat • Butter • Cheese, cottage cheese • Coffee, tea, and cocoa • Corn tortillas • Eggs • Flax, corn, and rice • Fresh fruits • Gluten-free flour breads, crackers, pasta, and cereals • Meat, fish, poultry (not marinated or breaded) • Peanut butter • Potatoes • Soy products • Tapioca • Unflavored milk • Yogurt

Foods to Avoid

• Baked goods, including muffins, cookies, cakes, pies • Barley • Bread, including wheat bread, white bread, “potato” bread • Flour • Gluten stabilizers • Oats • Pasta, pizza, bagels • Rye • Wheat

Lactase Deficiency Lactase deficiency is a condition in which the lactase enzyme is deficient or absent. Lactase is the enzyme that breaks down lactose into 2 simple sugars: glucose and galactose. Primary lactase insufficiency is often a result of genetic factors. Certain ethnic or racial groups, especially those with Asian or African ancestry, develop low lactase levels in childhood. Less common causes include low lactase levels resulting from premature birth and congenital lactase deficiency, a rare genetic disorder. Lactose malabsorption can occur when conditions leading to bacterial overgrowth promote lactose fermentation in the small bowel or when intestinal mucosal damage interferes with absorption. The latter occurs with IBD and celiac disease. Symptoms of lactose intolerance include bloating, flatulence, cramping abdominal pain, and diarrhea. Diarrhea results from the excess, undigested lactose in the small intestine attracting water molecules, which prevents them from being properly absorbed. Symptoms generally occur within 30 minutes to several hours after drinking a glass of milk or ingesting a milk product. Lactose intolerance is diagnosed with a lactose tolerance test, a lactose hydrogen breath test, or genetic testing. Treatment consists of eliminating lactose from the diet by avoiding milk and milk products, and/or replacing lactase with commercially available preparations. A lactose-free diet generally results in prompt resolution of symptoms. Many lactose-intolerant persons are aware of their condition. They likely have been avoiding lactose-containing products and using lactose-free milk products. Lactase enzyme (Lactaid) is available as an over-the-counter (OTC) product. It breaks down the lactose present in ingested milk. A number of milk products treated with lactase enzyme are readily available. The diet may gradually advance to a low-lactose diet as tolerated. Many lactose-intolerant persons may not have symptoms if they have lactose in small amounts. Cheese has less lactose than milk and ice

cream. Live culture yogurt has less lactose because the bacteria help digest the lactose. Teach the patient to read labels to detect any hidden sources of milk products. Some people tolerate lactose better if taken with meals. Teach the patient that adhering to the diet is important. Since avoiding milk and milk products can lead to calcium deficiency, supplements may be needed to prevent osteoporosis.

Short Bowel Syndrome Short bowel syndrome (SBS) is a condition in which the small intestine does not have enough surface area to absorb enough nutrients. This leaves the person unable to meet energy, fluid, electrolyte, and nutritional needs to stay healthy on a normal diet. Causes of SBS include diseases that damage the intestinal mucosa, surgical removal of too much small intestine (e.g., with Crohn’s disease, cancer), and congenital defects. SBS is likely to develop in patients with a loss of around 75% of the small intestine. The length and area of the remaining small intestine and the presence of the colon affect the patient’s outcome. If the terminal ileum and ileocecal valve are intact, the remaining intestine undergoes adaptive changes that are most pronounced in the ileum. The villi and crypts increase in size, and the absorptive capacity of the remaining intestine increases. When the colon is present, fluid and electrolyte absorption increase. Those with an end jejunostomy often have little to no adaptation.

Clinical Manifestations SBS results in reduced nutrient, fluid, and electrolyte absorption. This leads to dehydration, weight loss, diarrhea, malnutrition, vitamin deficiencies, and electrolyte imbalances. Other manifestations include abdominal pain, flatulence, and steatorrhea. The patient may develop lactase deficiency and bacterial overgrowth. Those who do not receive appropriate nutrition may have manifestations associated with specific deficiencies. For example, patients may have peripheral neuropathy from vitamin B12, vitamin E, copper, or thiamine deficiencies or fatigue due to anemia from decreased folate or iron.29

Interprofessional Care The treatment goals are that the patient will have fluid and electrolyte

balance, normal nutritional status, and control of diarrhea. The main treatment is nutritional support involving PN, EN, medications, and a tailored diet. In the immediate period after massive bowel resection, patients receive PN to replace fluid, electrolyte, and nutrient losses and to rest the bowel. Those with severe resections will need PN indefinitely. EN and a normal diet are gradually resumed to stimulate the remaining intestine to function better. Some can eventually stop PN. Refer the patient to a dietitian. The ideal diet is high in protein and complex carbohydrates and low in fat and concentrated sweets. Oral supplements of calcium, zinc, and multivitamins may be needed. Soluble fiber is encouraged if the colon is present. The patient should eat at least 6 small meals per day to increase the time of contact between food and the intestine. Oral intake may be supplemented with elemental nutrient formulas and tube feeding during the night. Patients with severe malabsorption may need PN (see Chapter 39). Patients often take multiple medications to help control fecal output. PPIs, H2 blockers, α-adrenergic receptor agonists (e.g., clonidine), or octreotide reduce excess fluid secretion. Opioid antidiarrheal drugs decrease intestinal motility (Table 42.2). For patients who have limited ileal resections, cholestyramine reduces diarrhea resulting from unabsorbed bile acids by increasing their excretion in feces. Bile acids stimulate intestinal fluid secretion and reduce colonic fluid absorption. Antibiotic therapy is used if bacterial overgrowth is contributing to diarrhea. Three drugs have FDA approval for the treatment of SBS: somatropin, glutamine, and teduglutide (Gattex). Somatropin enhances intestinal adaption and increases the flow of water, electrolytes, and nutrients into the bowel. Glutamine improves intestinal absorption. Teduglutide increases the surface area of the intestine and improves intestinal absorption of fluids and nutrients. Intestinal transplantation is done at a few specialized transplant centers in the United States. It is considered the only long-term treatment option for patients with intestinal failure who have significant complications from PN or nutrition failure. The leading

cause of intestinal failure is SBS. Transplantation may include the intestine alone, liver and intestine, or multivisceral combinations (stomach, duodenum, jejunum, ileum, colon, and/or pancreas).

Gastrointestinal Stromal Tumors Gastrointestinal stromal tumors (GISTs) are a rare form of cancer that originates in cells found in the wall of the GI tract. These cells, known as interstitial cells of Cajal, help control the movement of food and liquid through the stomach and intestines. About 60% of GISTs are in the stomach; 25% are in the small intestine; and the rest are in the esophagus, colon, or peritoneum.30 Most GISTs occur in people between the ages of 50 and 70. While the exact cause of GISTs is unknown, genetic mutations likely play a role. A few GISTs occur in people with familial mutations in either the KIT or platelet-derived growth factor receptor a (PDGFRa) or in those with neurofibromatosis type 1.30 The manifestations of GISTs depend on the part of the GI tract affected. Early manifestations are often subtle, including early satiety, fatigue, bloating, nausea or vomiting, and a change in bowel habits. Because these manifestations are like those of many other GI problems, early detection of the cancer is difficult. Later manifestations may include GI bleeding and obstruction caused by growth of the tumor. GISTs are often found during imaging for other problems. Diagnosis is based on histologic examination of biopsied tissue. Endoscopic ultrasound, CT, or MRI are used to determine the extent of disease. Surgery offers the only permanent cure. Often, though, GISTs have metastasized by the time of diagnosis or commonly recur. GISTs are unresponsive to conventional chemotherapy. The discovery of genetic mutations led to the development of tyrosine kinase inhibitor drugs (e.g., imatinib mesylate [Gleevec], sunitinib, regorafenib [Stivarga]) that are effective against certain GISTs.31

Anorectal Problems Hemorrhoids Hemorrhoids are dilated hemorrhoidal veins. They may be internal (occurring above the internal sphincter) or external (occurring outside the external sphincter) (Figs. 42.16 and 42.17). In affected persons, hemorrhoids appear periodically, depending on the amount of anorectal pressure.

Etiology and Pathophysiology Hemorrhoids develop because of increased anal pressure and weakening of the connective tissue that supports the hemorrhoidal veins. Weakened supporting tissue allows for downward displacement of the hemorrhoidal veins, causing them to dilate. Blood flow through the veins of the hemorrhoidal plexus is impaired. An intravascular clot in the venule results in a thrombosed external hemorrhoid. Many factors increase the risk for hemorrhoids, including pregnancy, constipation, straining to defecate, diarrhea, heavy lifting, prolonged standing and sitting, obesity, and ascites.31

Clinical Manifestations Hemorrhoids are the most common reason for bleeding with defecation. Internal hemorrhoids most often cause painless bright red bleeding with stools, on the toilet paper, or dripping into the toilet water. If internal hemorrhoids become constricted, the patient will report pain. Internal hemorrhoids can prolapse into the anal canal or externally. Symptoms of prolapse include pressure with defecation and a protruding mass.

FIG. 42.16 Anatomic structures of the rectum and anus with external and internal hemorrhoids.

FIG. 42.17 Thrombosed external hemorrhoids. From Townsend CM, Beauchamp RD, Evers BM, et al: Sabiston textbook of surgery: The biological basis of modern surgical practice, ed 19, Philadelphia, 2012, Saunders.

External hemorrhoids are reddish blue and seldom bleed. There may be itching, burning, and edema. They usually do not cause pain unless thrombosis (blood clots) is present. Thrombosed hemorrhoids are a bluish-purple tinge and palpable at the anal orifice. They usually cause pain and inflammation. The clot can erode through the overlying stretched skin, causing bleeding with defecation. Constipation or diarrhea can worsen these symptoms.

Diagnostic Studies and Interprofessional Care It is easy to diagnose external hemorrhoids visual inspection and digital examination. Digital examination, anoscopy, and sigmoidoscopy are used to diagnose internal hemorrhoids. Therapy is based on the cause and the patient’s symptoms. A high-

fiber diet and increased fluid intake prevent constipation and reduce straining, which allows engorgement of the veins to subside. The resulting stool bulk may decrease stool leakage and itching. Ointments, such as dibucaine; creams, suppositories, and impregnated pads that contain antiinflammatory agents (e.g., hydrocortisone); or astringents and anesthetics (e.g., witch hazel, benzocaine), may shrink the mucous membranes and relieve discomfort. Topical corticosteroids use should be limited to 1 week or less to prevent side effects, such as contact dermatitis and mucosal atrophy. Stool softeners can keep the stools soft. Sitz baths help relieve pain. External hemorrhoids are usually managed by conservative therapy unless they become thrombosed. For internal hemorrhoids, nonsurgical approaches (rubber band ligation, infrared coagulation, sclerotherapy, laser treatment) are options.31 Rubber band ligation is the most widely used technique. The HCP inserts an anoscope to identify the hemorrhoid and then ligates it with a rubber band. The rubber band around the hemorrhoid constricts circulation. The tissue becomes necrotic, separates, and sloughs off. There is some local discomfort with this procedure, but no anesthetic is needed. A hemorrhoidectomy is the surgical excision of hemorrhoids. Surgery is needed when there is marked prolapse, excessive pain or bleeding, or large or multiple thrombosed hemorrhoids. After removing the hemorrhoids, the tissue is either sutured and the wound heals by primary intention or the area is left open and healing takes place by secondary intention.

Nursing Management: Hemorrhoids Conservative nursing management includes teaching ways to prevent constipation and to avoid prolonged standing or sitting and proper use of OTC drugs for hemorrhoidal symptoms. Teach the patient to seek medical care for severe symptoms of hemorrhoids (e.g., excessive pain and bleeding, prolapsed hemorrhoids). Sitz baths (15 to 20 minutes, 2 or 3 times each day) may help to reduce discomfort and swelling associated with hemorrhoids. Nursing care after a hemorrhoidectomy focuses on pain control and promoting wound healing. Be aware that although the procedure is minor, the pain is severe and feared by many. There are several analgesic regimens, using a combination of medications. Most patients receive multimodal analgesia. This may involve an opioid and NSAID in conjunction with topical preparations that provide anesthesia or reduce internal sphincter spasms, such as topical lidocaine, 2% diltiazem, and glyceryl trinitrate. The patient usually dreads the first bowel movement and often resists the urge to defecate. Give pain medication before the bowel movement to reduce discomfort. Stool softeners (e.g., docusate) and bulking agents are given to help form a soft, bulky stool that is easier to pass. If the patient does not have a bowel movement within 2 or 3 days, an oil-retention enema is given. Sitz baths are started 1 or 2 days after surgery and continued for 1 to 2 weeks. A warm sitz bath provides comfort and keeps the anal area clean. A sponge ring in the sitz bath helps relieve pressure on the area. Initially, do not leave the patient alone because of the possibility of weakness or fainting. Teach the patient that pressure relief cushions are acceptable to ease discomfort when sitting. Tell the patient not to use a pressure relief ring or “doughnut” because they can reduce blood flow to the area. The patient may have packing in the rectum to absorb drainage, with a T-binder to hold the dressing in place. Packing is usually removed on the first or second postoperative day. Assess for rectal

bleeding, especially in patients taking clopidogrel or oral anticoagulants. The patient may be embarrassed when the dressing is changed. Provide as much privacy as possible. Teach the patient care of the anal area, symptoms of complications (especially bleeding), and ways to avoid constipation and straining. Hemorrhoids may recur. Sometimes, anal strictures develop, requiring dilation. Regular checkups are important to prevent any further problems.

Anal Fissure An anal fissure is a skin ulcer or a crack in the lining of the anal wall. Many times, the inciting event is trauma from passing hard stools. Other fissures are related to trauma (anal intercourse, foreign body insertion, such as endoscope), local infection (syphilis, gonorrhea, Chlamydia, herpes simplex virus, HIV), or inflammation. An anal fissure is acute when it is of recent onset (less than 6 weeks), and chronic if it has been present for a longer period. Chronic fissures have a characteristic appearance that includes perianal skin tag and fibrotic edges.32 Anal tissue ulcerates because of ischemia caused by a combination of high pressure in the internal anal sphincter and poor blood supply to the area. The ischemic tissue may ulcerate spontaneously or when traumatized by factors such as hard stools, which would not normally cause tissue breakdown. Ischemia must be corrected for a fissure to heal. The hallmark of an anal fissure is severe anal pain. It tends to be worse with defecation and with direct pressure on the site (e.g., sitting). Acute fissures tend to bleed slightly. Patients may report red blood on the toilet paper. Constipation results because of fear of pain associated with bowel movements. Anal fissures are easy to diagnose with a physical examination. Conservative care with fiber supplements, increased fluid intake, sitz baths, and topical analgesics is successful in most cases, especially if the fissure is acute. Topical preparations, including nitrates and calcium channel blockers, decrease rectal anal pressure and allow the fissure to heal without sphincter damage. Local injections of botulinum toxin can decrease rectal anal pressure. They are most effective when combined with nitrates. Pain is managed by softening stools with a bulk-producing agent (psyllium) or stool softener and warm sitz baths (15 to 20 minutes, 3 times per day).32 If conservative treatment fails, a lateral internal sphincterotomy is the recommended surgical procedure. It carries the risk for

postoperative incontinence. Postoperative nursing care is the same as the care for the patient who had a hemorrhoidectomy.

Anorectal Abscess An anorectal abscess is a collection of perianal pus (Fig. 42.18). The abscess results from obstruction of the anal glands, leading to infection and abscess formation. Abscess formation occurs with anal fissures, trauma, or IBD. The most common causative organisms are E. coli, staphylococci, and streptococci. Manifestations include local severe pain and swelling, foul-smelling drainage, tenderness, and fever. Sepsis can occur as a complication. Anorectal abscesses are diagnosed by rectal examination. Anorectal abscesses require surgical drainage. Larger abscesses need packing afterward with impregnated gauze or placement of drains (e.g., Penrose) to promote drainage. The area then heals by granulation. Patients who have diabetes or cellulitis or are immunocompromised (e.g., chemotherapy) may need antibiotic therapy. Nursing care includes warm, moist heat applications and changing packing daily. The patient is usually more comfortable lying on the abdomen or side. A low-fiber diet is given. The patient may leave the hospital with the wound still open. Teach the patient about wound care and the importance of sitz baths, thorough cleaning after urinating or bowel movements, and follow-up visits with the HCP.

FIG. 42.18 Common sites of anorectal abscesses and fistula formation.

Anal Fistula An anal fistula is an abnormal tunnel leading from the anus or rectum. It may extend to the outside of the skin, vagina, or buttocks and often precedes an abscess. Anal fistulas are a complication of Crohn’s disease and may resolve when drug treatment achieves remission of the disease. About 50% of anal fistulas are due to anorectal abscess. Feces may enter the fistula and cause an infection. There may be persistent, bloody or purulent discharge, or stool leakage from the fistula. The patient may need to wear a pad to avoid staining clothes. Surgical treatment of an anal fistula depends on the location and nature of the fistula. In a fistulotomy, the HCP opens the fistula and healthy tissue is allowed to granulate in the wound. Care is the same as after a hemorrhoidectomy. Options for complex fistulas include ligation of the intersphincteric fistula tract (LIFT) or the use of rectal flaps, setons, plugs, or fibrin glue injections to seal the fistula.

Anal Cancer Anal cancer is uncommon in the general population, but the incidence is increasing. In the United States around 8200 people are diagnosed with anal cancer each year.33 It mainly occurs in older adults, with the average age being in the early 60s. Human papillomavirus (HPV) is associated with about 80% of the cases of anal cancer. Those at high risk for anal cancer include smokers, HIV-positive homosexual men, people who are immunocompromised (e.g., posttransplant immunosuppression), and women with cervical, vaginal, or vulvar cancer.33 Rectal bleeding is the most common presenting sign. Other symptoms include rectal pain, fullness, and changes in bowel habits. Some patients have no symptoms, which leads to delayed diagnosis and treatment. It is especially important to screen high-risk persons using digital rectal examination (DRE) and anal Pap tests. In an anal Pap test, the anal lining is swabbed and the cells examined to identify any cell changes (e.g., dysplasia, neoplasia). High-resolution anoscopy allows for visualization of the mucosa and biopsy. An endoanal (endorectal) ultrasound may be done. Treatment of anal cancer depends on the size and depth of the lesions. Cancer therapy involves surgery or a combination of low-dose radiation and chemotherapy. Chemotherapy regimens include combinations of mitomycin, cisplatin, and fluorouracil.33 Options for precancerous lesions are surgical removal or treatment with topical imiquimod (Aldara) and fluorouracil. If the tumor involves the rectum and is large enough to require removing the anal sphincters, the anus will be sutured shut and a permanent ostomy created.

Pilonidal Sinus A pilonidal sinus is a small tract under the skin between the buttocks in the sacrococcygeal area. It is thought to be of congenital origin. It may have several openings and is lined with epithelium and hair, hence the name pilonidal (“a nest of hair”). The skin is moist, and movement of the buttocks causes the short, wiry hair to penetrate the skin. If the irritated skin becomes infected, it forms a pilonidal cyst or abscess. There are no symptoms with a pilonidal sinus unless there is an infection. Then the patient may have pain and swelling at the base of the spine. An abscess requires incision and drainage. The wound may be closed or left open to heal by secondary intention. The wound is packed, and sitz baths ordered. Nursing care includes warm, moist heat applications when an abscess is present. The patient is usually more comfortable lying on the abdomen or side. Teach the patient to avoid contaminating the dressing when urinating or defecating and to avoid straining whenever possible.

Case Study Colorectal Cancer

©iStockphoto/Thinkstock

Patient Profile L.C., a 58-yr-old Native American man, is from a Pueblo tribe in northern New Mexico. L.C.’s wife and family drove 50 miles to take him to the Indian Health Service hospital because of his deteriorating health (see the case study in Chapter 38 on p. 835).

Subjective Data See the case study in Chapter 38 on p. 838.

Objective Data

Physical Examination See the case study in Chapter 38 on p. 840.

Laboratory Tests • CT scan and colonoscopy show 2 medium-sized tumors in the transverse colon

Interprofessional Care Surgical Procedure • Had a transverse hemicolectomy with lymph node biopsies • Pathology results: Adenocarcinoma, has invaded the muscle wall of colon, 2 of 5 lymph nodes are positive for cancer

Postoperative • Feels like his life has ended and does not want to leave hospital • States that there is “no one” to take care of him at his home and he is far away from the hospital

Follow-Up Treatment Scheduled for outpatient chemotherapy

Discussion Questions 1. What signs and symptoms of colorectal cancer did L.C. have (see the case study in Chapter 38)? 2. What stage of CRC does L.C. probably have? What treatment is recommended for this stage of CRC? 3. How could you provide emotional support to L.C. and his family? 4. Patient-Centered Care: What is a culturally sensitive way for

you to support L.C. and his family in making decisions about his continued health care? 5. Priority Decision: Based on the assessment data, what are the priority nursing diagnoses? Are there any collaborative problems? 6. Priority Decision: What are the priority nursing interventions for L.C. at this stage of his illness? 7. Collaboration: What referrals may be indicated at this time? 8. Evidence-Based Practice: L.C. is worried that other members of his family may have colon cancer. What can you tell him about the recommendations for colorectal cancer screening? 9. Quality Improvement: What outcomes would indicate nursing interventions were successful? Answers available at http://evolve.elsevier.com/Lewis/medsurg.

Nursing Management: Constipation Nursing Assessment Determine the patient’s usual defecation patterns and habits. Ask the patient about the onset and duration of symptoms; the shape and consistency of the stool; and any difficulty with evacuation. Is the patient straining during defecation? Is there a feeling of incomplete evacuation or the need to use fingering to expel the feces? Ask about diet, exercise, laxative use, and history that could contribute to problems with defecation. Table 42.9 outlines the subjective and objective data you should obtain from a patient with constipation.

Nursing Implementation Tailor the nursing management of constipation to your assessment of the patient’s symptoms. Teach the patient about the role of diet, adequate fluid intake, and regular exercise in preventing and treating constipation (Table 42.10). Emphasize the importance of a high-fiber diet. Teach the patient to establish a regular time to defecate and not to suppress the urge to defecate. Discourage the use of laxatives and enemas. Defecation is easiest when the person is sitting on a commode with the knees higher than the hips. The sitting position allows gravity to aid defecation, and flexing the hips straightens the angle between the anal canal and rectum so that stool flows out more easily. Place a footstool in front of the toilet to promote flexion of the hips. It is challenging to defecate while sitting on a bedpan. For a patient in bed, raise the head of the bed as high as the patient can tolerate.

TABLE 42.9 Nursing AssessmentConstipation

Subjective Data

Important Health Information Past health history: Colorectal disease, neurologic dysfunction, bowel obstruction, environmental changes, cancer, IBD, diabetes Medications: Aluminum and calcium antacids, antidepressants, hypolipidemics, antipsychotics, diuretics, opioids, iron, PPIs, antidiarrheals

Functional Health Patterns Health perception–health management: Chronic laxative or enema use. Rigid beliefs about bowel function. Malaise Nutritional-metabolic: Changes in diet or mealtime. Fiber and fluid intake. Anorexia, nausea Elimination: Change in usual bowel patterns. Hard, difficult-topass stool, decrease in stool frequency and amount. Flatus, abdominal distention. Straining, tenesmus, rectal pressure. Fecal incontinence (if impacted) Activity-exercise: Daily activity routine. Immobility, sedentary lifestyle Cognitive-perceptual: Dizziness, headache, anorectal pain. Abdominal pain on defecation Coping–stress tolerance: Acute or chronic stress

Objective Data General Lethargy

Integumentary

Anorectal fissures, hemorrhoids, abscesses

Gastrointestinal Abdominal distention. Hypoactive or absent bowel sounds. Palpable abdominal mass. Fecal impaction. Small, hard, dry stool. Stool with blood

Possible Diagnostic Findings Guaiac-positive stools. Abdominal x-ray showing stool in lower colon The sights, odors, and sounds of defecation embarrass most people. Provide as much privacy as possible and use an odor eliminator. Encourage patients to maintain abdominal muscle tone. Prompt patients to contract abdominal muscles several times a day. Sit-ups and straight-leg raises can help improve abdominal muscle tone. For the patient whose perceived constipation is related to rigid beliefs about bowel function, start a discussion about these concerns. Give appropriate information on normal bowel function and discuss the adverse consequences of overuse of laxatives and enemas.

Bridge to Nclex Examination The number of the question corresponds to the same-numbered outcome at the beginning of the chapter.

1. The most appropriate therapy for a patient with acute diarrhea caused by a viral infection is to a. increase fluid intake. b. administer an antibiotic. c. administer an antimotility drug. d. quarantine the patient to prevent spread of the virus. 2. A 35-yr-old female patient is admitted to the emergency department with acute abdominal pain. Which medical diagnoses should you consider as possible causes of her pain? (select all that apply) a. Gastroenteritis b. Ectopic pregnancy c. Gastrointestinal bleeding d. Irritable bowel syndrome e. Inflammatory bowel disease 3. Assessment findings suggestive of peritonitis include (select all that apply) a. rebound tenderness. b. a soft, distended abdomen. c. dull, intermittent abdominal pain. d. shallow respirations with bradypnea. e. observing that the patient is lying still.

3. In planning care for the patient with Crohn’s disease, the nurse recognizes that a major difference between ulcerative colitis and Crohn’s disease is that Crohn’s disease a. often results in toxic megacolon. b. causes fewer nutritional deficiencies than ulcerative colitis. c. often recurs after surgery, while ulcerative colitis is curable with a colectomy. d. is manifested by rectal bleeding and anemia more often than is ulcerative colitis. 4. The nurse performs a detailed assessment of the abdomen of a patient with a possible bowel obstruction, knowing that manifestations of an obstruction in the large intestine are (select all that apply) a. persistent abdominal pain. b. marked abdominal distention. c. diarrhea that is loose or liquid. d. colicky, severe, intermittent pain. e. profuse vomiting that relieves abdominal pain. 5. A patient with stage I colorectal cancer is scheduled for surgery. Patient teaching for this patient would include an explanation that a. chemotherapy will begin after the patient recovers from the surgery. b. both chemotherapy and radiation can be used as palliative treatments. c. follow-up colonoscopies will be needed to ensure that

the cancer does not recur. d. a wound, ostomy, and continence nurse will visit the patient to identify the site for the ostomy. 6. The nurse determines a patient undergoing ileostomy surgery understands the procedure when the patient states a. “I should only have to change the pouch every 4 to 7 days.” b. “The drainage in the pouch will look like my normal stools.” c. “I may not need to wear a drainage pouch if I irrigate it daily.” d. “Limiting my fluid intake should decrease the amount of output.” 7. In contrast to diverticulitis, the patient with diverticulosis a. has rectal bleeding. b. often has no symptoms. c. usually develops peritonitis. d. has localized cramping pain. 8. A nursing intervention that is most appropriate to decrease postoperative edema and pain after an inguinal herniorrhaphy is to a. apply a truss to the hernia site. b. allow the patient to stand to void. c. support the incision during coughing. d. apply a scrotal support with an ice bag. 9. The nurse determines that the goals of dietary teaching have been met when the patient with celiac disease selects

from the menu a. scrambled eggs and sausage. b. buckwheat pancakes with syrup. c. oatmeal, skim milk, and orange juice. d. yogurt, strawberries, and rye toast with butter. 10. What should a patient be taught after a hemorrhoidectomy? a. Take mineral oil before bedtime. b. Eat a low-fiber diet to rest the colon. c. Use oil-retention enemas to empty the colon. d. Take prescribed pain medications before a bowel movement. 1. a, 2. a, b, c, d, e, 3. a, e, 4. c, 5. a, b, 6. c, 7. a, 8. b, 9. d, 10. a, 11. d For rationales to these answers and even more NCLEX review questions, visit http://evolve.elsevier.com/Lewis/medsurg.

Evolve Website/Resources List http://evolve.elsevier.com/Lewis/medsurg

Review Questions (Online Only) Key Points Answer Keys for Questions • Rationales for Bridge to NCLEX Examination Questions • Answer Guidelines for Case Study on p. 966 Student Case Study • Patient With Ulcerative Colitis Nursing Care Plans

• eNursing Care Plan 42.1: Patient With Acute Infectious Diarrhea • eNursing Care Plan 42.2: Patient With Inflammatory Bowel Disease • eNursing Care Plan 42.3: Patient With a Colostomy/Ileostomy Conceptual Care Map Creator Audio Glossary Content Updates

References Shane AL, Mody RK, Crump JA, et al: 2017 IDSA clinical practice guidelines for the diagnosis and management of infectious diarrhea, Clin Infect Dis 65:e45, 2017. Watson T, Hickok J, Fraker S, et al: Evaluating the risk factors for hospital-onset Clostridium difficile infections in a large healthcare system, Clin Infect Dis 66:1957-1959, 2018. McDonald LC, Gerding DN, Johnson S, et al: Clinical practice guidelines for Clostridium difficile infection in adults and children: 2017 Update by the IDSA and SHEA, Clin Infect Dis 66:e1, 2018.

4. Chabkraborty S, Bharucha AE: Fecal incontinence. In: Barden E, Shaker R, eds: Gastrointestinal motility disorders, New York, 2018, Springer. Serra J, Mascort-Roca J, Marzo-Castillejo M, et al: Clinical practice guidelines for the management of constipation in adults: Definition, etiology and clinical manifestations, Gastroenterol Hepatol 40:132, 2017.

6. Camilleri M, Ford AC, Mawe GM, et al: Chronic constipation, Nat Rev Dis Primers 3:1, 2017.

7. Weaver KR, Melkus GD, Henderson WA: Irritable bowel syndrome, AJN 117:48, 2017. Ireton-Jones C: The low FODMAP diet: Fundamental therapy in the management of IBS, Curr Opin Clin Nutr Metab Care 20:414, 2017.

9. Braslow B: Management of appendicitis. In: Khwaja KA, Diaz JJ (eds.), Minimally invasive acute care surgery, New York, 2018, Springer. 10. Centers for Disease Control and Prevention: Epidemiology of the IBD. Retrieved from www.cdc.gov/ibd/ibd-epidemiology.htm. Shivashankar R, Lewis JD: The role of diet in inflammatory bowel disease, Curr Gastroenter Reports 19:22, 2017. Shouval D, Rufo P: The role of environmental factors in the pathogenesis of IBD, JAMA Pediatric 171:999, 2017. Venema U, Werna TC, Voskuil MD, et al: The genetic background of inflammatory bowel disease: from correlation to causality, J Pathol 241:146, 2017.

14. Crohn’s and Colitis Foundation: IBD medications. Retrieved from www.ibdetermined.org/ibdinformation/ibd-treatment/ibd-medication.aspx. Bots S, Gecse K, Barclay M, et al: Combination immunosuppression in IBD, Inflamm Bowel Dis 24:539, 2018.

16. Flier LC, Welstead LA: Nutrition matters. In: Cohen R, ed: Inflammatory bowel disease, New York, 2017, Humana Press. John ES, Katz K, Saxena M, et al: Management of inflammatory bowel disease in the elderly, Curr Treat Options Gastroenterol 14:285, 2016. Reddy SR, Cappell MS: A systematic review of the clinical presentation, diagnosis, and treatment of small bowel obstruction, Curr Gastroenterol Rep 9:28, 2017.

19. Alavi K, Friel CM: Large bowel obstruction. In: Steele SR, Hull TL, Read TE, Saclarides TJ, Senagore AJ,

Whitlow CB, eds: The ASCRS textbook of colon and rectal surgery, New York, 2016, Springer. 20. Toevs CC, Mazellan K, Kohr R: Ogilvie’s syndrome, Am Surg 83:217, 2017. 21. American Cancer Society: Key statistics for colorectal cancer. Retrieved from www.cancer.org/cancer/colonrectal-cancer/about/key-statistics.html. Ansa BE, Coughlin SS, Alema-Mensah E, et al: Evaluation of colorectal cancer incidence trends in the United States (2000–2014), J Clin Med 7:22, 2018.

23. American Cancer Society: Colorectal cancer screening guidelines. Retrieved from www.cancer.org/cancer/colon-rectal-cancer/detectiondiagnosis-staging/acs-recommendations.html. 24. National Cancer Institute: Colon cancer treatment. Retrieved from www.cancer.gov/types/colorectal/hp/colon-treatmentpdq#link/_125. Ellison DL: Acute diverticulitis management, Crit Care Nurs Clin North Am 30:67, 2018. Ortiz LA, Zhang B, McCarthy MW, et al: Treatment of enterocutaneous fistulas, then and now, Nutr Clin Pract 32:508, 2017. Leonard MM, Sapone A, Catassi C, et al: Celiac disease and nonceliac gluten sensitivity, JAMA 318:647, 2017.

28. Celiac Disease Foundation: Celiac disease. Retrieved from https://celiac.org/celiac-disease/understandingceliac-disease-2/what-is-celiac-disease/. 29. Boutte HJ, Rubin DC: Short bowel syndrome. In: Barden E, Shaker R, eds: Gastrointestinal motility disorders, New York, 2018, Springer. Nishida T, Blay JY, Hirota S, et al: The standard diagnosis, treatment, and follow-up of gastrointestinal stromal tumors based on

guidelines, Gastric Cancer 19:3, 2016. American Society of Colon and Rectal Surgeons: Clinical practice guidelines for the management of hemorrhoids. Retrieved from www.fascrs.org/physicians/clinical-practice-guidelines.

32. American Society of Colon and Rectal Surgeons: Anal fissure, Dis Colon Rectum 61:293, 2018. 33. Eng C, Shridhar R, Chan E, et al: Anal cancer. The American Cancer Society’s Oncology in Practice: Clinical Management 9:149, 2018. ∗Evidence-based information for clinical practice.

43

Liver, Biliary Tract, and Pancreas Problems Mary C. Olson

LEARNING OUTCOMES 1. Distinguish among the types of viral hepatitis, including etiology, pathophysiology, clinical manifestations, and complications. 2. Describe the interprofessional and nursing management of the patient with viral hepatitis. 3. Describe the pathophysiology, clinical manifestations, complications, and interprofessional care of the patient with nonalcoholic fatty liver disease. 4. Explain the etiology, pathophysiology, clinical manifestations, complications, and interprofessional and nursing management of the patient with cirrhosis. 5. Describe the clinical manifestations and management of liver cancer. 6. Distinguish between acute and chronic pancreatitis related to pathophysiology, clinical manifestations, complications, interprofessional care, and nursing management. 7. Explain the clinical manifestations and interprofessional and nursing management of the patient with pancreatic cancer. 8. Describe the pathophysiology, clinical manifestations, and interprofessional care of gallbladder disorders.

9. Describe the nursing management of the patient undergoing surgical treatment of cholecystitis and cholelithiasis.

KEY TERMS acute liver failure, p. 989 acute pancreatitis, p. 992 ascites, p. 982 asterixis, p. 984 cholecystitis, p. 998 cholelithiasis, p. 998 chronic pancreatitis, p. 996 cirrhosis, p. 980 esophageal varices, p. 982 gastric varices, p. 982 hepatic encephalopathy, p. 983 hepatitis, p. 968 hepatorenal syndrome, p. 984 jaundice, p. 971 nonalcoholic fatty liver disease (NAFLD), p. 979 nonalcoholic steatohepatitis (NASH), p. 979 paracentesis, p. 985 portal hypertension, p. 982 spider angiomas, p. 980 Never define yourself by your relationship status, income, or looks. It is your kindness, generosity, and compassion that counts.

Brigette Nicole http://evolve.elsevier.com/Lewis/medsurg

Conceptual Focus Infection Inflammation Nutrition Pain Nursing management of patients with a wide range of liver, pancreatic, and gallbladder problems is the focus of this chapter. These organs are closely positioned together anatomically and highly associated in their digestive functions. Liver and pancreatic problems can lead to altered nutrient absorption and use, causing malnutrition and impaired elimination. Inflammation may be present, with the patient having pain, nausea, and vomiting. Nursing care focuses on helping the patient and caregiver manage symptoms and develop ways to cope with the diagnosis and, sometimes, prognosis. Health promotion focuses on reducing risk through immunizations and avoiding substance use.

Disorders of The Liver Hepatitis Hepatitis is inflammation of the liver. Hepatitis is most often caused by viruses. It also can be caused by substances (e.g., alcohol, medications, chemicals), autoimmune diseases, and metabolic problems.

Viral Hepatitis There are several types of viral hepatitis. We designate each type by a letter (A, B, C, D, E). The different types have similar manifestations, but their modes of transmission and disease course vary (Table 43.1). Some can lead to chronic liver disease. Other less common viruses can also cause liver disease. These include cytomegalovirus (CMV), Epstein-Barr virus (EBV), herpesvirus, coxsackievirus, and rubella virus.

TABLE 43.1 Characteristics of Hepatitis Viruses

Hepatitis A Virus Hepatitis A is a self-limiting infection that can cause a mild flu-like illness and jaundice. In more severe cases, it can cause acute liver failure. Hepatitis A virus (HAV) is a ribonucleic acid (RNA) virus. It is transmitted primarily through the fecal-oral route. It often occurs in small outbreaks caused by fecal contamination of food or drinking water. Poor hygiene, improper handling of food, crowded situations, and poor sanitary conditions are contributing factors. Transmission occurs between family members, institutionalized persons, and children in day care centers. Foodborne outbreaks are usually due to food contaminated by an infected food handler. People at increased risk for infection include drug users (both injection and noninjection drugs), men who have sex with men (MSM), and persons traveling to developing countries. The greatest risk for transmission occurs before clinical symptoms appear. The virus is found in feces 1 to 2 weeks before the onset of symptoms and at least 1 week after the onset of illness (Fig. 43.1). This

means it can be carried and transmitted by persons who have undetectable, subclinical infections. It is present only briefly in blood, usually less than 3 weeks. Fecal excretion can occur in infants for months. Anti-HAV (antibody to HAV) immunoglobulin M (IgM) appears during the acute phase. Detection of hepatitis A IgM indicates acute hepatitis. Hepatitis A IgG without anti-HAV IgM indicates past infection. IgG antibody provides lifelong immunity (Fig. 43.2). HAV vaccination and thorough hand washing are the best measures to prevent outbreaks. In the United States, the incidence of infection has declined since we started vaccinating at-risk persons and children (beginning 12 to 24 months).1

FIG. 43.1 Jaundiced patient. From Butcher GP: Gastroenterology: An illustrated colour text, London, 2004, Churchill Livingstone.

Hepatitis B Virus Hepatitis B virus (HBV) is a blood-borne pathogen that can cause either acute or chronic hepatitis. The incidence of HBV infection has

decreased in areas where the use of the HBV vaccine is widespread.2 Asians and Pacific Islanders have an incidence of HBV of up to 8%. Perinatal transmission is the most common mode of transmission in this population and often results in chronic HBV infection.2

FIG. 43.2 Course of infection with hepatitis A virus (HAV). ALT, Alanine aminotransferase. From McCance KL, Huether SE: Pathophysiology: The biologic basis for disease in adults and children, ed 6, St Louis, 2010, Mosby.

HBV is a deoxyribonucleic acid (DNA) virus. It can be transmitted in several ways: (1) perinatally from mothers infected with HBV to their infants; (2) percutaneously (e.g., IV drug use, accidental needlestick punctures); or (3) via small cuts on mucosal surfaces and exposure to infectious blood, blood products, or other body fluids

(e.g., semen, vaginal secretions, saliva). Sexual transmission is a common mode of HBV transmission. MSM (especially those practicing unprotected anal intercourse) are at an increased risk for HBV infection. Most believe that casual encounters, like hugging, kissing, and sharing utensils, do not transmit the disease. Other at-risk persons include those who live with chronically HBVinfected persons, patients on hemodialysis, health care personnel, public safety workers, IV drug users, recipients of blood products, and Native Alaskans, Pacific Islanders, and Native Americans. HBV has been detected in almost every body fluid. Infected semen, cervicovaginal secretions, and saliva contain much lower concentrations of HBV than blood, but the virus can be transmitted via these secretions. If gastrointestinal (GI) bleeding occurs, feces can be contaminated with the virus from the blood. There is no evidence of fecal-oral transmission. Organ and tissue transplantation is another potential source of infection. However, in some patients with acute hepatitis B, there is no readily identifiable risk factor. HBV is a complex structure with 3 distinct antigens: surface antigen (HBsAg), core antigen (HBcAg), and e antigen (HBeAg). Each antigen, along with its corresponding antibody, may appear or disappear in serum depending on the phase of infection and immune response. In most people who acquire HBV infection as an adult, the infection completely resolves without any long-term complications. In those who develop chronic HBV infections, the liver may range from a normal-appearing liver to severe liver inflammation and scarring (fibrosis). Around 25% of those who become chronically HBV-infected in childhood die from complications of chronic liver disease, including liver cancer.3 Screening for HBV usually includes identifying those at high risk for infection and testing the blood for the presence of hepatitis B surface antigen (HBsAg), hepatitis B antibody (anti-HBs), and hepatitis B core antibody (anti-HBc). The presence of anti-HBs in the blood indicates immunity from the HBV vaccine or from past HBV infection (Fig. 43.3). HBsAg in the serum for 6 months or longer after

infection indicates chronic HBV infection.

FIG. 43.3 Course of infection with hepatitis B virus (HBV). ALT, Alanine aminotransferase; anti-HBc, antibody to hepatitis B core antigen; anti-HBe, antibody to HBeAg; anti-HBs, antibody to HBsAg; HBeAg, hepatitis B e antigen; HBsAg, hepatitis B surface antigen. From McCance KL, Huether SE: Pathophysiology: The biologic basis for disease in adults and children, ed 6, St Louis, 2010, Mosby.

Hepatitis C Virus Hepatitis C virus (HCV) causes a type of hepatitis that can result in both acute illness and chronic infection. Acute hepatitis C, which can be mild in presentation, can be hard to detect unless a diagnosis is made with laboratory testing. The most common causes of acute hepatitis C outbreaks are among injection drug users and MSM with HIV infection. HCV is an RNA virus that is blood-borne and primarily transmitted percutaneously. The most common mode of HCV transmission is the

sharing of contaminated needles and equipment among injection drug users. High-risk sexual behavior (e.g., unprotected sex, multiple partners), especially among MSM, is associated with increased risk for transmission. After a needle-stick exposure or sharps exposure to HCV-positive blood, the transmission rate is 0.1%. The risk for perinatal HCV transmission is 4% to 7% per pregnancy. Persons who were given blood or blood products before 1992 (when blood product testing for HCV began) are at higher risk for chronic HCV infection and should be routinely tested.4 Some patients with HCV infection cannot identify a source of infection. Most patients usually develop chronic infection. However, because signs and symptoms of HCV infection are generally mild, most people are unaware of their infection. HCV is the most common cause of chronic liver disease and liver failure. About 20% to 30% develop cirrhosis and eventually liver failure and/or liver cancer.4 Along with chronic HBV, HCV accounts for most cases of liver cancer. HCV hepatitis is the most common reason for liver transplantation in the United States. Because of the 15- to 20-year delay between infection and the manifestations of liver damage, long-term effects of HCV infection pose important health care challenges. Persons at risk for HCV infection are also at risk for HBV and HIV infections. About 30% to 40% of HIV-infected patients also have HCV. This high rate of co-infection is primarily related to IV drug use. Coinfection with HIV and HCV places the patient at greater risk for progression to cirrhosis. People in the United States born between 1945 and 1965 and those at increased risk should be screened for HCV infection. This includes people who engage in high-risk sexual practices, injection drug users, those who may have had blood or blood products prior to 1992, and/or those who have abnormal liver function tests. A positive antibody test for HCV (anti-HCV) is usually enough for a diagnosis.2 However, a positive viral load is needed to confirm active infection because anti-HCV can also indicate a past infection.

Evidence-Based Practice Screening and Testing of Hepatitis C You are caring for S.B., a 32-yr-old man who often visits the community clinic with health concerns. He arrives today saying he feels “tired.” He tells you a friend was recently diagnosed with HCV and he wants “a shot” to keep from “getting it.” You see on S.B.’s medical record that he injects drugs and has not been tested for HCV.

Making Clinical Decisions Best Available Evidence. Currently, most HCV-infected persons are undiagnosed and therefore untreated. It is recommended that patients with known risk factors for HCV be tested. Rapid diagnostic tests (RDTs), including oral HCV antibody (Ab) RDTs, have excellent sensitivity and specificity compared to laboratory-based methods for HCV Ab detection. Clinician Expertise. You know a major risk factor for HCV is injection drug use. You understand early diagnosis of HCV is important for best patient outcomes and prevention of transmission to others. Patient Preferences and Values. S.B. tells you he is “busy today,” but he can come back tomorrow for HCV testing.

Implications for Nursing Practice 1. What information would you provide to S.B. on HCV testing, symptoms, and transmission? 2. Since S.B. is now willing to be tested for HCV, how would you determine barriers to the informed consent process? 3. Should S.B. test positive for HCV, what other information will you provide him?

References for Evidence Center for Disease Control and Prevention. Viral Hepatitis: Hepatitis C FAQs for Health Professionals Retrieved from. www.cdc.gov/hepatitis/hcv/hcvfaq.htm. Tang W, Chen W, Amini A, et al. Diagnostic accuracy of tests to detect hepatitis C antibody: A meta-analysis and review of the literature. BMC Infect Dis. 2017;17:695.

Hepatitis D Virus Hepatitis D virus (HDV), also called delta virus, is uncommon in the United States. HDV is a defective single-stranded RNA virus that cannot survive on its own. It requires HBV surface Ag to serve as its outer shell. So, only those who are infected with HBV can be infected with HDV. It can be acquired at the same time as HBV or a person with HBV can be infected with HDV later. HDV is transmitted like HBV. It can cause a range of illness, from an asymptomatic chronic carrier state to acute liver failure. There is no vaccine for HDV. However, vaccination against HBV reduces the risk for HDV coinfection.3

Hepatitis E Virus Like hepatitis A, the hepatitis E virus (HEV) is an RNA virus transmitted by the fecal-oral route. The usual mode of transmission is drinking contaminated water. HEV infection occurs primarily in developing countries, with epidemics reported in India, Asia, Mexico, and Africa. Only a few cases of HEV have been reported in the United States. These have been primarily in persons who recently traveled to an HEV-endemic area. It is generally acute and self-resolving, but chronicity in immunosuppressed persons, such as liver transplant recipients, has been reported. Pregnant women may be affected severely, with reported mortality rates of up to 10%. An IgM antibody assay is available to test for acute hepatitis E.3

Pathophysiology Liver In viral hepatitis, hepatocytes become targets of the virus in one of 2 ways: through direct action of the virus (as in HCV infection) or through a cell-mediated immune response to the virus (as in HBV and HCV infection).3 During acute viral hepatitis, large numbers of infected hepatocytes are destroyed. The destruction of hepatocytes leads to a wide range of liver-related dysfunction. Bile production, coagulation, blood glucose, and protein metabolism can be affected. Detoxification and processing of drugs, hormones, and metabolites (e.g., ammonia from protein catabolism) may be disrupted. After resolution of an acute infection, liver cells can regenerate. If no complications occur, the liver can resume its normal appearance and function. In certain cases, the acute hepatitis can become so severe and irreversible that people develop liver failure or die. Chronic viral hepatitis can be insidious and silent, causing persistent and continual destruction of infected hepatocytes. Over time scar tissue can develop, which leads to fibrosis and compromised liver function. Fibrosis can lead to cirrhosis and liver failure. Cirrhosis is a generally irreversible condition that can increase one’s risk for liver dysfunction, portal hypertension, and primary liver cancer. Cirrhosis is discussed later in this chapter.

Systemic Effects In the early phases of hepatitis infection, antigen-antibody complexes between the virus and its corresponding antibody may form circulating immune complexes. The circulating immune complexes activate the complement system (see Chapter 11). The manifestations of this activation are rash, angioedema, arthritis, fever, and malaise. Cryoglobulinemia (abnormal proteins found in the blood), glomerulonephritis, vasculitis, and involvement of other organs can occur from immune complex activation.

Clinical Manifestations and Complications The manifestations of the different viral hepatitis infections can be classified into acute hepatitis and chronic hepatitis (Table 43.2).

Acute Hepatitis Many patients with acute hepatitis have no symptoms and may not even know they have been infected. However, others may have intermittent or ongoing anorexia, lethargy, nausea, vomiting, skin rashes, diarrhea or constipation, malaise, fatigue, myalgias, arthralgias, other flu-like symptoms, and right upper quadrant tenderness (caused by liver inflammation). Although the acute phase of viral hepatitis varies depending on the type of hepatitis, it usually lasts from 1 to 6 months. During this time, the patient may have a decreased sense of smell and find food repugnant. Smokers may have distaste for cigarettes. Physical examination often reveals hepatomegaly, lymphadenopathy, abdominal tenderness, and sometimes splenomegaly. The acute phase is the period of maximal infectivity. A patient in the acute phase of hepatitis may be icteric (jaundiced) or anicteric. Jaundice, a yellowish discoloration of body tissues, results from a change in normal bilirubin metabolism or disruption of the flow of bile into the hepatic or biliary duct systems. The types of jaundice are described in Table 43.3. The urine may appear darker due to excess bilirubin being excreted by the kidneys. If conjugated bilirubin cannot pass into the intestines from the liver because of obstruction or inflammation of the bile ducts, the stools will be clay colored. Pruritus (intense generalized itching) sometimes accompanies jaundice. It occurs from the accumulation of bile salts beneath the skin. Itching can be intolerable to the patient. As jaundice fades, the convalescent phase begins. The convalescent phase can last for weeks to months, with an average of 2 to 4 months. During this period, patients typically have malaise and easy fatigability. Hepatomegaly remains for several weeks. Splenomegaly (if present) subsides during this period.

TABLE 43.2 Manifestations of Hepatitis

Acute Hepatitis • Anorexia • Clay-colored stools • Dark urine • Decreased sense of taste and smell • Diarrhea or constipation • Fatigue, lethargy, malaise • Flu-like symptoms (e.g., headache) • Hepatomegaly • Jaundice • Low-grade fever • Lymphadenopathy • Myalgias and/or arthralgias • Nausea, vomiting • Pruritus • Right upper quadrant tenderness • Splenomegaly • Weight loss

Chronic Hepatitis • ALT, AST elevations (may be normal in some people) • Ascites and lower extremity edema • Asterixis (“liver flap”) • Bleeding abnormalities (thrombocytopenia, easy bruising, prolonged clotting time) • Fatigue, malaise

• Hepatic encephalopathy: confusion, difficulty concentrating, easy agitation • Hepatomegaly • Increased bilirubin • Jaundice • Myalgias and/or arthralgias • Palmar erythema • Spider angiomas Most patients with acute viral hepatitis recover completely. Almost all cases of acute hepatitis A resolve. However, some patients may have a relapse in the first 2 to 3 months after the infection. The disappearance of jaundice does not mean the patient has totally recovered. Some HBV infections and most HCV infections result in chronic hepatitis. The overall mortality rate for acute hepatitis is less than 1%. The mortality rate is higher in older adults and those with underlying debilitating illnesses (including chronic liver disease). Complications that can result from acute hepatitis are acute liver failure, chronic hepatitis, cirrhosis of the liver, portal hypertension, and liver cancer. Acute Liver Failure Sometimes, acute liver failure (fulminant hepatic failure) may occur, which is a serious condition with a poor prognosis. Manifestations include encephalopathy, GI bleeding, disseminated intravascular coagulation (DIC), fever with leukocytosis, renal manifestations (oliguria, azotemia), ascites, edema, hypotension, respiratory failure, hypoglycemia, bacterial infections, thrombocytopenia, and coagulopathies. Liver transplantation is usually the cure for these patients. Acute liver failure is discussed in this chapter on p. 989.

Chronic Hepatitis Manifestations of chronic hepatitis are shown in Table 43.2. Chronic

HBV is more likely to develop in infants born to infected mothers and in those who acquire the infection before age 5 than in those who acquire the virus after age 5.3 Problems with the patient’s cellular immune response may be important in the development of the chronic HBsAg carrier state and the progression of acute HBV to chronic HBV. More than 50% of immunocompromised adults who are acutely infected with HBV progress to chronic infection.3 HCV infection is more likely than HBV to become chronic. As previously mentioned, many patients with chronic HCV infection develop chronic liver disease, cirrhosis, portal hypertension, and liver cancer. Risk factors for progression to cirrhosis include male gender, alcohol use, concomitant fatty liver disease, and excess iron deposition in the liver. In some patients, co-infection with HIV may cause complications or require treatment modification. Manifestations of chronic hepatitis include anemia and coagulation problems (easy bruising, bleeding). Since the liver produces clotting factors, clotting and bleeding times can be impaired or prolonged.

TABLE 43.3 Classification of Jaundice

Skin manifestations may include spider angiomas, palmar erythema, and gynecomastia. Some patients have spleen, liver, or cervical lymph node enlargement. In patients with severe liver damage, hepatic encephalopathy is a potentially life-threatening spectrum of neurologic, psychiatric, and motor disturbances. Hepatic encephalopathy results from the liver’s inability to remove toxins (especially ammonia) from the blood. Hepatic encephalopathy is discussed later in this chapter on p. 983.) Ascites, a common manifestation of hepatitis (especially chronic hepatitis), is the accumulation of excess fluid in the peritoneal cavity. Fluid accumulates due to reduced protein levels in the blood, which reduces the plasma oncotic pressure. Ascites is discussed later in this chapter on p. 982.

Diagnostic Studies The only definitive way to distinguish among the types of viral hepatitis is by testing the patient’s blood for the specific antigen or antibody. In some types of viral hepatitis, the blood can be tested for the viral load (viral level). Tests for the different types of viral hepatitis are outlined in Table 43.4. Many liver function tests show

significant abnormalities, as shown in Table 43.5. Several tests are available to determine the presence of HCV. The screening test for HCV infection is HCV antibody testing. Antibodies can be detected within 4 weeks of infection. If the antibody test is positive, HCV RNA testing is done to assess for chronic infection. A positive result confirms chronic infection. A few patients may have a false-positive HCV antibody result with a negative HCV RNA test. If recent HCV infection is suspected, HCV RNA testing is usually done because it may take several weeks or longer for HCV antibodies to develop. HCV RNA testing may be used for immunocompromised patients (e.g., patient with HIV). Because of altered or delayed antibody response to HCV, these patients may not have detectable antibody levels even if they are infected with HCV. Viral genotype testing is done in patients undergoing drug therapy for HBV or HCV infection. HBV has at least 8 different genotypes (A to H). In some centers, HBV genotyping is done before starting treatment. HBV genotype may be useful in predicting disease course and treatment outcomes. HBV core Ab (HBVcAb) IgG indicates that the patient has a history of HBV infection. HBV may reactivate in these patients if they become immunosuppressed. HCV has 6 genotypes and more than 50 subtypes. In the United States, 75% of HCV infections are caused by HCV genotype 1. For patients who test positive for HCV, genotyping is done before drug therapy is started. The genotype determines the choice and duration of therapy. It is one of the strongest predictors of a patient’s response to drug therapy. A liver biopsy is done in acute hepatitis only if diagnosis is in doubt. In chronic hepatitis, a liver biopsy allows for histologic examination of liver cells and determination of the degree of inflammation, fibrosis, or cirrhosis that may be present. A patient who has a bleeding disorder may not be a candidate for a percutaneous liver biopsy because of the risk for bleeding. In these patients, a transjugular biopsy may be an alternative. This type of biopsy consists of obtaining liver tissue through a rigid cannula introduced into a

hepatic vein, typically using jugular venous access. Techniques for noninvasive assessment of liver fibrosis are increasingly replacing the need for liver biopsy. One option is the use of ultrasound elastography (e.g., FibroScan), which uses an ultrasound transducer to determine the degree of liver fibrosis.5 FibroSure (FibroTest) is an example of one of several biomarkers that uses the results of serum tests to assess the extent of hepatic fibrosis.

TABLE 43.4 Diagnostic StudiesViral Hepatitis

A, Hepatitis A virus (HAV); B, hepatitis B virus (HBV); C, hepatitis C virus (HCV); D, hepatitis D virus (HDV); E, hepatitis E virus (HEV).

TABLE 43.5 Diagnostic Findings in Acute

Hepatitis

Interprofessional Care There is no specific treatment for acute viral hepatitis. Most patients are managed at home. Emphasis is on providing adequate nutrition and measures to rest the body and help the liver to regenerate and repair (Table 43.6). Rest reduces the metabolic demands on the liver and promotes liver cell regeneration. The degree of rest depends on the severity of symptoms, but usually alternating periods of activity and rest are adequate. Counseling should include the importance of avoiding alcohol and notifying contacts for testing and prophylaxis, if indicated. In patients with chronic viral hepatitis, care may involve hepatologists, infectious disease specialists, pharmacists, dietitians, and mental health or substance use specialists. The role and extent of involvement of team members is based on the patient’s specific needs.

Drug Therapy Acute Hepatitis There are no drug therapies for treating acute HAV infection. Treatment of acute HBV may be indicated only in patients with severe

hepatitis and liver failure. In acute hepatitis C, some patients may choose to be monitored for spontaneous clearance of the infection. For patients who choose treatment, one of the direct-acting antivirals (DAAs) may be used.6 DAAs are discussed later in the section on chronic hepatitis. Supportive drug therapy may include antihistamines for generalized itching and antiemetics for nausea. These drugs include promethazine (Phenergan) and ondansetron (Zofran).

TABLE 43.6 Interprofessional CareViral

Hepatitis

Diagnostic Assessment • History and physical examination • Liver function tests (ALT, AST, alkaline phosphatase, bilirubin, γglutamyl transpeptidase [GGT]) • PT time and INR • Hepatitis testing • Hepatitis A: Anti-HAV IgM, anti-HAV IgG, or HAV total antibody • Hepatitis B: HBsAg, anti-HBs, HBeAg, anti-HBe, antiHBc IgM and IgG, HBV DNA quantitation, HBV genotyping • Hepatitis C: Anti-HCV, HCV RNA quantitation, HCV genotyping • Hepatitis D: Anti-HDV, HDV Ag • FibroScan • FibroSure (FibroTest)

Management Acute and Chronic

• Well-balanced diet • Vitamin supplements • Rest (degree of strictness varies) • Avoiding alcohol and drugs detoxified by liver

Chronic HBV and HCV • Drug therapy (Table 43.7) HAV, Hepatitis A virus; HB, hepatitis B; HBeAg, hepatitis B e antigen; HBsAg, hepatitis B surface antigen; HBV, hepatitis B virus; HCV, hepatitis C virus; HDV Ag, hepatitis D antigen; HDV, hepatitis D virus.

Complementary & Alternative Therapies Milk Thistle (Silymarin)

Scientific Evidence People have used milk thistle for liver disorders, including hepatitis, cirrhosis, and gallbladder problems. • Clinical trials of milk thistle for liver diseases have mixed results. • Silymarin was no better than placebo for chronic hepatitis C in people who had not responded to standard antiviral treatment. • The 2008 Hepatitis C Antiviral Long-Term Treatment Against Cirrhosis (HALT-C) study found that patients with hepatitis C who used silymarin had fewer and milder symptoms of liver disease and better quality of life but no change in virus activity or liver inflammation.

Nursing Implications

• Well tolerated in recommended doses. Some people report GI side effects • May lower blood glucose • May interfere with the liver’s cytochrome P450 enzyme system Source: National Center for Complementary and Alternative Therapy: Milk thistle. Retrieved from www.nccih.nih.gov/health/milkthistle/ataglance.htm. Chronic Hepatitis B Drug therapy for chronic HBV focuses on decreasing the hepatitis B viral load and liver enzymes, and in turn, slowing the rate of disease progression. Long-term goals are preventing the development of cirrhosis, portal hypertension, liver failure, and liver cancer. Current drug therapies for chronic HBV do not eradicate the virus but suppress viral replication and prevent complications of infection. First-line therapies now include primarily nucleoside and nucleotide analogs (Table 43.7) and sometimes interferon therapy.7

TABLE 43.7 Drug TherapyViral Hepatitis B and C



Use of all oral or noninterferon therapies for chronic hepatitis C is preferred.



Used only in combination therapy.



CYP3A inhibitor used to enhance the pharmacokinetics of the other agents.

Nucleoside and nucleotide analogs Nucleoside and nucleotide analogs inhibit viral DNA replication. HBV reproduces by making copies of its viral DNA nucleosides and nucleotides. The nucleoside and nucleotide analog drugs mimic normal building blocks for DNA but are actually faulty viral DNA building blocks. Once they become incorporated into the viral DNA, they halt DNA synthesis. Nucleoside and nucleotide analogs do not prevent all viral reproduction, but they can substantially lower the amount of virus in the body. These medications include lamivudine (Epivir), adefovir (Hepsera), entecavir (Baraclude), telbivudine (Tyzeka), and tenofovir (Viread). These oral medications are used to treat chronic HBV when there is evidence of significant active viral replication and liver

inflammation.7 These drugs also reduce viral load, decrease liver damage, and decrease serum liver enzyme levels. Most patients with HBV need long-term treatment. When these drugs are stopped, many patients’ (except those who have seroconverted) HBV DNA and liver enzyme levels return to pretreatment levels. Severe exacerbations of hepatitis B can develop after ending treatment. If these drugs are stopped for any reason, closely monitor liver function for several months. Interferon Interferon is a naturally occurring immune protein made by the body during an infection to recognize and respond to pathogens. It has antiviral, antiproliferative, and immune-modulating effects. (Interferon is discussed in Chapter 13). Pegylated interferon (PEGIntron, Pegasys) is given by subcutaneous injection. The many side effects with interferon therapy, including flu-like symptoms (e.g., fever, malaise, fatigue), make adhering to therapy hard for some patients. Currently, the availability of better tolerated and more effective oral treatments limits interferon use. However, it is still among the first-line options recommended by hepatology societies. Patients receiving interferon should have blood counts and liver function tests every 4 to 6 weeks. Depression is a side effect of interferon. Patients must be screened for depression and other mood disorders before starting interferon treatment and monitored frequently while on therapy. Chronic Hepatitis C Treatment of chronic hepatitis C is patient specific and based on the genotype of the HCV, severity of liver disease, and presence of other health problems (e.g., HIV). The goal of drug therapy is eradicating the virus and preventing HCV-related complications. Treatment for HCV primarily includes the use of DAAs (Table 43.7), which block proteins needed for HCV replication.

With DAAs, patients typically complete a 12-week regimen with oral drugs. Almost all (>95%) of those who complete treatment with the DAAs are now able to cure their chronic HCV infection.6

Drug Alert Ribavirin (Rebetol, Ribasphere) • May cause severe birth defects. During treatment, women taking the drug and women whose male partners are taking the drug must avoid pregnancy. • Monitor hemoglobin and hematocrit as it may cause anemia. • Used only for specific populations. Many patients with HIV also have HCV. Patients who have stable HIV and intact immune systems (CD4+ counts greater than 200/µL) receive HCV treatment with the goal of eradicating HCV and reducing the risk for progression to cirrhosis. HCV treatment may reduce CD4+ counts and increase the patient’s risk for anemia and leukopenia. Patients with advanced fibrosis or cirrhosis can undergo drug therapy if liver decompensation (e.g., ascites, variceal rupture, jaundice, wasting, encephalopathy) is not present.

Nutritional Therapy No special diet is needed in the treatment of viral hepatitis. Emphasis is placed on a well-balanced diet that the patient can tolerate. During acute viral hepatitis, adequate calories are important because the patient usually loses weight. If fat content is poorly tolerated because of decreased bile production, it should be reduced. Vitamin supplements, particularly B-complex and vitamin K, are often given. If anorexia, nausea, and vomiting are severe, IV solutions of glucose

or supplemental enteral nutrition (EN) therapy may be used. Fluid and electrolyte balance must be maintained.

Nursing Management: Viral Hepatitis Nursing Assessment Subjective and objective data that should be obtained from a person with hepatitis are outlined in Table 43.8.

Nursing Diagnoses Nursing diagnoses for the patient with viral hepatitis may include: • Impaired nutritional intake • Activity intolerance • Risk for bleeding Additional information on nursing diagnoses and interventions for the patient with hepatitis is presented in eNursing Care Plan 43.1 available on the website for this chapter.

Planning The overall goals are that the patient with viral hepatitis will (1) have relief of discomfort, (2) be able to resume normal activities, and (3) return to normal liver function without complications.

Nursing Implementation Health Promotion Viral hepatitis is a public health problem. Your role is important in the prevention and control of this disease. It is helpful to understand the epidemiology of the different types of viral hepatitis when considering appropriate control measures. Preventive and control measures for hepatitis A, B, and C are outlined in Table 43.9. A suggested guideline for general practice to prevent you from

contracting viral hepatitis from diagnosed and undiagnosed patients and carriers is for you to wear disposable gloves, goggles, and gowns (sometimes) when fecal or blood contamination is likely in handling (1) soiled bedpans, urinals, and catheters and (2) when the patient’s bed linens are soiled by body excreta or secretions.

Hepatitis A Viral hepatitis outbreaks are usually due to HAV. Preventive measures include personal and environmental hygiene and health education to promote good sanitation. Hand washing is the most important precaution. Teach about careful hand washing after bowel movements and before eating. Vaccination is the best protection against HAV. All children at 1 year of age should receive the vaccine. Adults at risk should also receive the vaccine. These include people who travel to areas with increased rates of hepatitis A, MSM, injecting and noninjecting drug users, persons with clotting factor disorders (e.g., hemophilia), and persons with chronic liver disease.

TABLE 43.8 Nursing AssessmentHepatitis ∗

Subjective Data Important Health Information Past health history: Hemophilia, cancer, exposure to infected persons, ingestion of contaminated food or water. Exposure to benzene, carbon tetrachloride, or other hepatotoxic agents. Crowded, unsanitary living conditions. Exposure to contaminated needles. Recent travel, organ transplant recipient, exposure to new drug regimens, hemodialysis, transfusion of blood or blood products before 1992. HIV status (if known) Medications: Use and misuse of acetaminophen, new prescription, over-the-counter, or herbal medications or supplements

Functional Health Patterns Health perception–health management: IV drug and chronic alcohol use. Malaise, distaste for cigarettes (in smokers), high-risk sexual behaviors Nutritional-metabolic: Weight loss, anorexia, nausea, vomiting. Feeling of fullness in right upper quadrant Elimination: Dark urine, light-colored stools, constipation or diarrhea, skin rashes, hives Activity-exercise: Fatigue, arthralgias, myalgias Cognitive-perceptual: Right upper quadrant pain and liver tenderness, headache, itching Role-relationship: Exposure as health care worker, resident in long-term care institution, incarceration, homelessness

Objective Data General Low-grade fever, lethargy, lymphadenopathy

Integumentary Rash or other skin changes, jaundice, icteric sclera, injection sites

Gastrointestinal Hepatomegaly, splenomegaly

Possible Diagnostic Findings Elevated liver enzyme levels. ↑ Serum total bilirubin, hypoalbuminemia, anemia, bilirubin in urine and increased

urobilinogen, prolonged PT time, positive tests for hepatitis, including anti-HAV IgM, HBsAg, anti-HBs, HBeAg, anti-HBe, anti-HBc IgM and IgG, HBV DNA quantitation, anti-HCV, HCV RNA quantitation, anti-HDV, HDV Ag. Abnormal liver scan, abnormal results on liver biopsy HAV, Hepatitis A virus; HBcAg, hepatitis B core antigen; HBeAg, hepatitis B e antigen; HBsAg, hepatitis B surface antigen; HBV, hepatitis B virus; HCV, hepatitis C virus; HDV Ag, hepatitis D antigen; HDV, hepatitis D virus.



Tailor history questions to the type of hepatitis.

HAV vaccine is inactivated HAV protein. There are 2 forms of HAV vaccine in the United States: Havrix and Vaqta. Primary immunization consists of 1 dose given IM in the deltoid muscle. A booster is recommended 6 to 12 months after the first dose to ensure adequate antibody titers and long-term protection. Primary immunization provides immunity within 30 days after 1 dose in more than 95% of those vaccinated. Twinrix, a combined HAV and HBV vaccine, is available for people over 18 years of age. Immunization consists of 3 doses, given on a 0-, 1-, and 6-month schedule, the same schedule as that used for the single HBV vaccine. Twinrix may be given to high-risk persons, including patients with chronic liver disease, users of illicit IV drugs, patients on hemodialysis, MSM, and people with clotting factor disorders who receive therapeutic blood products. The side effects of the vaccine are mild and usually limited to soreness and redness at the injection site.

TABLE 43.9 Preventive Measures for Viral

Hepatitis

Hepatitis A General Measures • Hand washing • Proper personal hygiene • Environmental sanitation • Control and screening (signs, symptoms) of food handlers • Serologic screening for those carrying virus • Active immunization: HAV vaccine

Use of Immune Globulin • Early administration (1–2 wk after exposure) to those exposed • Prophylaxis for travelers to areas where hepatitis A is common if not vaccinated with HAV vaccine

Special Considerations for Health Care Personnel • Wash hands after contact with a patient or removal of gloves • Use infection control precautions

Hepatitis B and C Percutaneous Transmission • Screening of donated blood • HBV: HBsAg • HCV: Anti-HCV • Use of disposable needles and syringes

Sexual Transmission • Acute exposure: HBIG administration to sexual partner of HBsAg-positive person • HBV vaccine series given to uninfected sexual partners • Condoms used for sexual intercourse

General Measures • Hand washing • Avoid sharing toothbrushes and razors • HBIG administration for one-time exposure (needle stick, contact of mucous membranes with infectious material) • Active immunization: HBV vaccine

Special Considerations for Health Care Personnel • Use infection control precautions • Reduce contact with blood or blood-containing secretions • Handle the blood of patients as potentially infective • Dispose of needles properly • Use needleless IV access devices when available HAV, Hepatitis A virus; HBIG, hepatitis B immune globulin; HBsAg, hepatitis B surface antigen; HBV, hepatitis B virus; HCV, hepatitis C virus. Isolation is not needed for HAV infection. For a patient with HAV infection, use infection control precautions. Place the patient who is incontinent of stool or has poor personal hygiene in a private room. Both hepatitis A vaccine and immune globulin (IG) are used to

prevent HAV infection after exposure to an infected person (postexposure prophylaxis). The vaccine is used for preexposure prophylaxis. IG can be given either before or after exposure. IG gives temporary (1 to 2 months) passive immunity and is effective for preventing hepatitis A if given within 2 weeks after exposure. IG is recommended for persons who do not have anti-HAV antibodies and were exposed by close (household, day care center) contact with persons who have HAV or foodborne exposure. Because patients with HAV are most infectious just before the onset of symptoms (the preicteric phase), those exposed through household contact or foodborne outbreaks should receive IG. Although IG may not prevent infection in all persons, it may lessen the illness to a subclinical infection. When hepatitis A occurs in a food handler, IG should be given to all other food handlers at the establishment. Patrons may need to receive IG. Persons exposed to HAV who have received a dose of HAV vaccine more than 1 month previously or who have a history of laboratoryconfirmed HAV infection do not need IG.

Hepatitis B The best way to reduce HBV infection is to identify those at risk, screen them for HBV, and vaccinate those who are not infected. Teach those at high risk for contracting HBV to reduce risks by following good hygienic practices, including hand washing and using gloves when expecting contact with blood. Patients should not share razors, toothbrushes, and other personal items. Teach patients to use a condom for sexual intercourse. In addition, the partner should be vaccinated. The HBV vaccine is the best means of prevention. The HBV vaccines (Recombivax HB, Engerix-B) contain HBsAg, which promotes the synthesis of specific antibodies directed against HBV. The vaccine is given in a series of 3 IM injections in the deltoid muscle. The second dose is given within 1 month of the first dose and the third dose within 6 months of the first. The vaccine is more than 95% effective. Minor reactions include transient fever and soreness at the injection

site. The vaccine can be given in pregnancy. The first dose of hepatitis B vaccine should be given at birth, with the vaccine series completed by age 6 to 18 months. Older children and adolescents who did not receive the hepatitis B vaccine should be vaccinated.3 It is important to vaccinate adults who are in the at-risk groups and are not immune. Household members of the patient with HBV should be tested and vaccinated if they are HBsAg and antibody negative. Hepatitis vaccination is recommended for patients with chronic kidney disease before they start dialysis. Dialysis patients should routinely have their antibody titer levels checked to determine the need for revaccination. For postexposure prophylaxis, the HBV vaccine series and hepatitis B immune globulin (HBIG) are given. HBIG has antibodies to HBV and confers temporary passive immunity. HBIG is prepared from plasma of donors with a high titer of anti-HBs. HBIG is recommended for postexposure prophylaxis in cases of needle stick, mucous membrane contact, or sexual exposure and for infants born to mothers who are positive for HBsAg. Ideally HBIG should be given within 24 hours of exposure. Giving antiviral therapy (e.g., tenofovir) to pregnant women in the third trimester with viral levels over 200,000 IU/mL can prevent the small risk for neonatal infection that may occur even with postnatal immunization and vaccination. The Centers for Disease Control and Prevention (CDC) recommends following standard precautions for the patient with HBV (see Table 14.9). This includes using disposable needles and syringes and disposing of them in puncture-resistant units without recapping, bending, or breaking.

Hepatitis C No vaccine is currently available for hepatitis C. Therefore it is important to identify those at high risk for contracting HCV and teach them how to reduce their risks. Primary measures to prevent HCV transmission include (1) screening of blood, organ, and tissue donors; (2) using infection control precautions; and (3) modifying high-risk behavior.

In the United States, there are many people who have undiagnosed hepatitis C. Therefore the CDC recommends universal screening for all persons born between 1945 and 1965.4 The CDC does not recommend IG or antiviral agents (e.g., interferon) for postexposure prophylaxis for HCV infection (e.g., needle-stick exposure from an infected patient). After an acute exposure (e.g., needle stick), the person should have anti-HCV testing done. For the person exposed to HCV, baseline anti-HCV and ALT levels should be measured, with follow-up testing at 4 to 6 months. Testing for HCV RNA may be done after 4 to 10 weeks.4

Acute Care In patients with hepatitis, assess for the presence and degree of jaundice. In light-skinned persons, jaundice is usually seen first in the sclera of the eyes and later in the skin. In dark-skinned persons, jaundice is seen in the hard palate of the mouth and inner canthus of the eyes. The urine may have a dark brown or brownish red color from bilirubin excretion from the kidneys. Comfort measures to relieve itching, headache, and arthralgias are helpful.

Check Your Practice You are caring for a 32-yr-old man who has acute hepatitis A. He has severe nausea and vomiting. He is admitted to the hospital for IV hydration and monitoring. The patient says, “I’m so weak and I feel like I’m going to vomit all the time. Isn’t there something you can do to help me?” • How would you handle this situation? • What information and teaching will you give him? Ensuring that the patient receives adequate nutrition is not always easy. The anorexia and distaste for food may cause nutritional

problems. Assess the patient’s tolerance of specific foods and eating pattern. Small, frequent meals may be preferable to 3 large ones and may help prevent nausea. Often a patient with hepatitis finds that anorexia is not as severe in the morning, so it is easier to eat a good breakfast than a large dinner. Include measures to stimulate the appetite, such as mouth care, antiemetics, and attractively served meals in pleasant surroundings, in the care plan. Drinking carbonated beverages and avoiding very hot or cold foods may help ease anorexia. Adequate fluid intake (2500 to 3000 mL/day) is important. Rest is a critical factor in promoting hepatocyte regeneration. Assess the patient’s response to the rest and activity plan. Modify it as needed based on liver function tests and symptoms. Psychologic and emotional rest is as essential as physical rest. Limited activity may produce anxiety and restlessness in some patients. Diversion activities, such as reading and hobbies, may help a patient cope with the plan of care and ensure adequate rest.

Ambulatory Care Most patients with viral hepatitis are cared for at home. Assess the patient’s knowledge of nutrition and provide any needed dietary teaching. Caution the patient about overexertion and the need to follow the HCP’s advice about when to return to work. For patients who have fatigue, tell them to plan activities after periods of rest when energy levels are highest. Teach the patient and caregiver how to prevent transmission to other family members and symptoms to report to the HCP. Assess the patient for any signs of complications. These include bleeding tendencies with increasing prothrombin (PT) time values, manifestations of encephalopathy, sudden increase in weight and abdominal girth (may indicate fluid retention and/or ascites), bloody or tarry stools, vomiting of blood, or elevated liver enzymes. Teach the patient to have regular follow-ups for at least 1 year after the diagnosis of hepatitis. Because relapses occur with hepatitis B and C, teach the patient the symptoms of recurrence and the need for follow-up evaluations. All patients with chronic HBV or HCV should

avoid alcohol as it can accelerate disease progression. Note that patients who are positive for HBsAg (chronic carrier status) or HCV antibody cannot be blood donors.

Evaluation Expected outcomes are that the patient with hepatitis will • Maintain food and fluid intake adequate to meet nutritional needs • Avoid alcohol and other hepatotoxic agents • Show gradual increase in activity tolerance • Perform daily activities with scheduled rest periods

Drug- and Chemical-Induced Liver Diseases Alcohol use is the most frequent cause of both acute and chronic liver disease. It can cause injury and necrosis of liver tissue. Alcohol use can cause a spectrum of manifestations, ranging from mild elevation in liver enzymes to acute alcoholic hepatitis. It may also cause advanced fibrosis and cirrhosis, which usually occurs after decades of excess alcohol use. Patients may have serious liver disease caused by another chronic disease (e.g., chronic HCV infection) in combination with alcoholic liver disease, which can compound the problem. Acute alcoholic hepatitis is a syndrome of hepatomegaly, jaundice, elevated liver enzymes (AST, ALT, alkaline phosphate), and lowgrade fever with possible ascites and prolonged PT time. These manifestations may improve if alcohol intake ceases. Even at the end-stage of cirrhosis, abstinence can result in significant reversal in some patients. If liver function does not recover after abstaining from alcohol for 6 months or longer, liver transplantation may be considered. Chemical hepatotoxicity is liver injury caused by exposure to certain compounds (e.g., carbon tetrachloride, gold compounds). Some agents can cause hepatotoxicity, while others may induce cholestasis, necrosis, or liver cancer. Fortunately, because of the decreased use of these agents, the incidence of chemically induced liver toxicity has decreased since the 1980s. Drug-induced liver injury (DILI) can present similarly to other forms of liver disease. The main cause of DILI is antimicrobial agents, especially amoxicillin-clavulanate. Many drugs (prescription, OTC, diet and herbal supplements) can cause an increase in liver enzymes and, in severe cases, jaundice and acute liver failure. The pattern of injury depends on the drug causing the reaction. The most common cause of acute liver failure is acetaminophen. In patients with chemical hepatotoxicity or DILI, all drugs identified as the cause of

liver injury should be stopped.3

Drug Alert Acetaminophen (Tylenol) • Safe when taken at recommended levels. • Its prevalence in a variety of pain relievers, fever reducers, and cough medicines may mean that patients do not realize they are taking several drugs that all contain acetaminophen and overdose may occur. • Acute liver failure can occur because of overdosing, either intentionally or unintentionally. • The FDA has asked drug manufacturers to limit the strength of acetaminophen in prescription drug products to 325 mg per tablet, capsule, or other dosage unit, making these products safer. • Combining the drug with alcoholic beverages increases the risk for liver damage.

Autoimmune, Genetic, and Metabolic Liver Diseases Autoimmune Hepatitis Autoimmune hepatitis is a chronic inflammatory disorder of the liver in which the patient’s own immune system attacks the liver. The cause of this condition is unknown. Autoimmune hepatitis is characterized by the presence of autoantibodies and high levels of serum immunoglobulins. It often occurs with other autoimmune diseases. Most patients with autoimmune hepatitis are women. Laboratory tests useful in the diagnosis include antinuclear antibody (ANA), anti– smooth muscle antibody (ASMA), and antimitochondrial antibody (AMA) testing. A liver biopsy is often done to confirm the diagnosis and guide the treatment decision.8 Although autoimmune hepatitis can cause acute liver failure, the spectrum of disease is variable. Most patients develop chronic hepatitis. Untreated autoimmune hepatitis can progress to cirrhosis. Prednisone with or without azathioprine (Imuran) is the recommended treatment for active autoimmune hepatitis. Cyclosporine (Gengraf), tacrolimus (Prograf, FK506), budesonide (Entocort), methotrexate, mercaptopurine, and mycophenolate mofetil (CellCept) are options in those who do not respond to prednisone and azathioprine.8 Mycophenolate is most often used for patients intolerant to azathioprine.

Wilson’s Disease Wilson’s disease is an autosomal recessive disorder involving cellular copper transport. A defect in biliary excretion leads to accumulation of copper in the liver, causing progressive liver injury and cirrhosis. About 30 people per million have Wilson’s disease. It usually appears between ages 5 and 35.9 Once cirrhosis occurs, copper leaks into the plasma, leading to

multiple complications, including neurologic, hematologic, and renal disease. The hallmark of Wilson’s disease is corneal Kayser-Fleischer rings. These are brownish red rings seen in the cornea near the limbus on eye examination. Low serum ceruloplasmin levels and markedly elevated copper concentrations from liver biopsy samples are present. Diagnosis is based on clinical findings, including the corneal rings and neurologic symptoms. First-degree relatives of patients with Wilson’s disease should be screened for the disease. The recommended first treatment of symptomatic patients or those with active disease is chelating agents, such as D-penicillamine (Cuprimine) or trientine (Syprine). They promote the excretion of urinary copper. Zinc acetate (Galzin), another therapy, interferes with copper absorption. Once we have reduced the amount of copper in the body, treatment focuses on preventing copper from building up again. Liver transplantation may be an option with severe liver damage.

Hemochromatosis Hemochromatosis is a condition in which excess iron accumulates in the body. It is primarily caused by a genetic defect (hereditary hemochromatosis). It also can be caused by liver disease and chronic blood transfusions used to treat thalassemia and sickle cell disease. Hemochromatosis is discussed in Chapter 30.

Primary Biliary Cholangitis Primary biliary cholangitis (PBC), formerly known as primary biliary cirrhosis, is a chronic disease of the small bile ducts of the liver.3 In PBC, there is a T cell–mediated attack of the small bile duct cells, resulting in loss of bile ducts and cholestasis (blockage of bile flow). Over time, this leads to liver fibrosis and cirrhosis. Most patients diagnosed with PBC are middle-aged women. The disease is associated with other autoimmune disorders, such as rheumatoid arthritis, Sjögren’s syndrome, and scleroderma. High serum alkaline phosphatase levels, AMAs, ANAs, and serum lipid levels occur in patients with PBC.

The goals of treatment are suppressing ongoing liver damage, preventing complications, and symptom management. Drugs for PBC include ursodeoxycholic acid (ursodiol [Actigall]), a bile acid, and obeticholic acid (Ocaliva). It decreases bile in the liver. Management focuses on preventing or minimizing malabsorption, skin disorders, such as itching and xanthomas (cholesterol deposits in the skin), hyperlipidemia, vitamin deficiencies, anemia, and fatigue. Cholestyramine is used to treat itching. Patients are monitored for progression to cirrhosis. Liver transplantation is an option for endstage liver disease in patients with PBC.

Primary Sclerosing Cholangitis Primary sclerosing cholangitis (PSC) is a disease of unknown cause characterized by chronic inflammation, fibrosis, and strictures (narrowing) of the medium and large bile ducts both inside and outside the liver.3 Most patients with PSC also have ulcerative colitis or, less often, Crohn’s disease. Complications of PSC can include cholangitis, cholestasis with jaundice, bile duct cancer, and cirrhosis. Drug therapy has no proven benefit, although many HCPs use ursodiol. Treatment is directed at reducing the incidence of biliary complications and screening for bile duct and colorectal cancer, which is related to the high incidence of ulcerative colitis. Patients with advanced liver disease may need liver transplantation.

Nonalcoholic Fatty Liver Disease and Nonalcoholic Steatohepatitis Nonalcoholic fatty liver disease (NAFLD) refers to a wide spectrum of liver diseases ranging from a fatty liver (steatosis) to nonalcoholic steatohepatitis (NASH) to cirrhosis. The term nonalcoholic is used because NAFLD and NASH occur in people who do not consume excess amounts of alcohol. The fundamental characteristic of NAFLD is the accumulation of fatty infiltration in the hepatocytes. In NASH, the fat accumulation is

associated with varying degrees of inflammation and fibrosis of the liver. If NASH is untreated, it can become a serious liver disease leading to cirrhosis, liver cancer, and liver failure. Currently, NAFLD is increasing because of the growing number of people who are obese. NAFLD occurs in 90% to 95% of severely obese children and adults. NASH occurs in 8% to 20% of obese persons with NAFLD.3 NAFLD should be considered in patients with risk factors, including obesity, diabetes, hyperlipidemia, and hypertension (also known as metabolic syndrome). Elevated liver function tests (ALT, AST) are often the first sign of NAFLD. Ultrasound and CT scans can be used to diagnose NAFLD. Definitive diagnosis is by a liver biopsy. There is no currently approved medication for NAFLD.10 The goal of therapy is weight loss of at least 10% of body weight, if overweight or obese and exercise. Reducing risk factors, including hyperlipidemia, hypertension, and diabetes, is important.

Promoting Health Equity Liver, Pancreas, and Gallbladder Disorders

Hepatitis • Hepatitis C has a higher incidence among blacks than whites. • Hepatitis B has a higher incidence among Asian Americans and Pacific Islanders. • Deaths caused by hepatitis C are more common in blacks.

Liver and Pancreatic Cancer • Primary liver cancer has a highest incidence in Hispanics, followed by blacks and whites. • Pancreatic cancer occurs more often among blacks than whites.

Gallbladder Disease • Whites and Native Americans have a higher incidence of gallbladder disease than blacks or Asian Americans

Cirrhosis Cirrhosis is the end stage of liver disease. Cirrhosis is characterized by extensive degeneration and destruction of the liver cells. This results in the replacement of liver tissue by fibrosis (scar tissue) and regenerative nodules that occur from the liver’s attempt to repair itself (Fig. 43.4). The development of cirrhosis usually happens after decades of chronic liver disease.

Etiology and Pathophysiology Any chronic liver disease, including disease from excess alcohol use and NAFLD, can cause cirrhosis. The most common causes of cirrhosis in the United States are chronic hepatitis C infection and alcohol-induced liver disease. In patients with alcohol-induced liver disease, controversy exists as to the degree to which malnutrition adds to the damage caused by the alcohol itself. Some cases of nutrition-related cirrhosis have resulted from extreme dieting, malabsorption, and obesity. Environmental factors and genetic predisposition may lead to the development of cirrhosis, regardless of dietary or alcohol intake. Around 20% of patients with chronic hepatitis C and 25% of those with chronic hepatitis B develop cirrhosis.3 Chronic inflammation and cell necrosis from viral hepatitis can result in progressive fibrosis and cirrhosis. Chronic hepatitis combined with alcohol use has a synergistic effect in accelerating liver damage. Biliary causes of cirrhosis include primary biliary cholangitis (PBC) and primary sclerosing cholangitis (PSC). Both are described earlier in this chapter.

FIG. 43.4 Cirrhosis that developed from alcohol use. The characteristic diffuse nodularity of the surface is due to the combination of regeneration and scarring of the liver. From Kumar V, Abbas AK, Aster JC, et al: Robbins and Cotran pathologic basis of disease, ed 8, Philadelphia, 2010, Saunders.

Cardiac cirrhosis includes a spectrum of hepatic problems that result from long-standing, severe, right-sided heart failure. It causes hepatic venous congestion, parenchymal damage, necrosis of liver cells, and fibrosis over time. Treatment is aimed at managing the patient’s underlying heart failure. In cirrhosis, the liver cells try to regenerate, but the regenerative process is disorganized. This results in abnormal blood vessel and bile duct architecture. The overgrowth of new and fibrous connective tissue distorts the liver’s normal lobular structure, resulting in lobules of irregular size and shape with impeded blood flow. Eventually, irregular and disorganized liver regeneration, poor cellular nutrition, and hypoxia (from inadequate blood flow and scar tissue) result in decreased liver function.

Clinical Manifestations Early Manifestations Patients may be unaware of their liver condition because there are few symptoms in early-stage disease. If a person does have symptoms, these may include fatigue or an enlarged liver. Blood tests may show normal liver function (compensated cirrhosis). The diagnosis of cirrhosis is often made later when a patient presents with symptoms of more advanced liver disease.

Late Manifestations Late manifestations result from liver failure and portal hypertension (Fig. 43.5). Jaundice, peripheral edema, and ascites develop gradually. Other late manifestations include skin lesions, hematologic problems, endocrine problems, and peripheral neuropathies (Fig. 43.6). In the advanced stages, the liver becomes small and nodular. Liver function is dramatically impaired.

Jaundice Jaundice results from decreased ability to conjugate and excrete bilirubin into the small intestines (Table 43.3). There is an overgrowth of connective tissue in the liver, which compresses the bile ducts and leads to an obstruction. This results in an increase in the bilirubin in the vascular system, and jaundice occurs. The jaundice may be minimal or severe, depending on the degree of liver damage.

Skin Lesions Various skin manifestations often occur with cirrhosis. Spider angiomas (telangiectasia or spider nevi) are small, dilated blood vessels with a bright red center point and spiderlike branches. They occur on the nose, cheeks, upper trunk, neck, and shoulders. Palmar erythema (a red area that blanches with pressure) occurs on the palms of the hands. Both lesions are due to an increase in circulating estrogen due to the damaged liver’s inability to metabolize steroid hormones.

FIG. 43.5 Continuum of liver dysfunction in cirrhosis and resulting manifestations. Adapted from Huether SE, McCance KL: Understanding pathophysiology, ed 5, St Louis, 2012, Mosby.

Hematologic Problems Hematologic problems include thrombocytopenia, leukopenia, anemia, and coagulation disorders. We think thrombocytopenia, leukopenia, and anemia are caused by the splenomegaly that results from backup of blood from the portal vein into the spleen (portal hypertension). Overactivity of the enlarged spleen results in increased removal of blood cells from circulation. Anemia can result from

inadequate red blood cell (RBC) production and survival, poor diet, poor absorption of folic acid, and bleeding from varices. The coagulation problems result from the liver’s inability to make prothrombin and other factors essential for blood clotting. Manifestations of coagulation problems (bleeding tendencies) include epistaxis, purpura, petechiae, easy bruising, gingival bleeding, and heavy menstrual bleeding.

Endocrine Problems The liver plays a vital role in the metabolism of hormones, such as estrogen and testosterone. In men with cirrhosis, gynecomastia (benign growth of the glandular tissue of the male breast), loss of axillary and pubic hair, testicular atrophy, and impotence with loss of libido may occur because of increased estrogen levels. Younger women with cirrhosis may develop amenorrhea, and older women may have vaginal bleeding. If the liver does not metabolize aldosterone properly, it can lead to hyperaldosteronism with sodium and water retention and potassium loss.

Peripheral Neuropathy Peripheral neuropathy is a common finding in alcoholic cirrhosis. It is probably due to a dietary deficiency of thiamine, folic acid, and cobalamin. The neuropathy usually results in sensory and motor symptoms, but sensory symptoms may predominate.

Complications Major complications of cirrhosis are portal hypertension, esophageal and gastric varices, peripheral edema, abdominal ascites, hepatic encephalopathy (mental status changes, including coma), and hepatorenal syndrome. Patients who are cirrhotic but who have no obvious complications have compensated cirrhosis. Those who have 1 or more complications of their liver disease have decompensated cirrhosis.

FIG. 43.6 Systemic manifestations of liver cirrhosis.

Portal Hypertension and Esophageal and Gastric Varices In patients with cirrhosis, the liver undergoes structural changes. These changes lead to obstruction of blood flow in and out of the liver. This results in increased pressure within the liver’s circulatory system (portal hypertension). Portal hypertension is characterized by increased venous pressure in the portal circulation, splenomegaly, large collateral veins, ascites, and gastric and esophageal varices. As a way of reducing pressure, the body develops alternate

circulatory pathways, referred to as collateral circulation. The collateral channels often form in the lower esophagus, anterior abdominal wall, parietal peritoneum, and rectum. Varicosities (distended veins) develop in areas where the collateral and systemic circulations communicate, resulting in esophageal and gastric varices, caput medusae (ring of varices around the umbilicus), and hemorrhoids. Esophageal varices are a complex of tortuous, enlarged veins at the lower end of the esophagus. Gastric varices are found in the upper part of the stomach. These varices are fragile and do not tolerate high pressure, so they can bleed easily. Large varices are more likely to bleed. Esophageal varices can cause variceal hemorrhages with a 5year mortality of 20%.11 The patient may present with melena or hematemesis. Ruptured esophageal varices are the most lifethreatening complication of cirrhosis and considered a medical emergency.

Peripheral Edema and Ascites Peripheral edema occurs in the lower extremities and presacral area. Peripheral edema can occur before, concurrently with, or after ascites development. Edema results from decreased colloidal oncotic pressure from impaired liver synthesis of albumin and increased portacaval pressure from portal hypertension. Ascites is the accumulation of serous fluid in the peritoneal or abdominal cavity. It is a common manifestation of cirrhosis. Several mechanisms lead to ascites. One mechanism of ascites occurs with portal hypertension, which causes proteins to shift from the blood vessels into the lymph space (Fig. 43.7). When the lymphatic system is unable to carry off the excess proteins and water, they leak into the peritoneal cavity. The osmotic pressure of the proteins pulls more fluid into the peritoneal cavity (Table 43.10). A second mechanism of ascites formation is hypoalbuminemia resulting from the liver’s decreased ability to synthesize albumin. The hypoalbuminemia results in decreased colloidal oncotic pressure. A third mechanism of ascites is hyperaldosteronism, which occurs when the damaged hepatocytes metabolize aldosterone. The increased

aldosterone level causes increased sodium reabsorption by the renal tubules. Sodium retention, combined with an increase in antidiuretic hormone in blood, leads to further water retention and edema. Edema decreases intravascular volume with decreased renal blood flow and glomerular filtration. Ascites is manifested by abdominal distention with weight gain (Fig. 43.8). If the ascites is severe, the increase in abdominal pressure from the fluid accumulation may cause eversion of the umbilicus. Abdominal striae with distended abdominal wall veins may be present. Patients may have signs of dehydration (e.g., dry tongue and skin, sunken eyeballs, muscle weakness) and a decrease in urine output. Hypokalemia is common. It is due to an excessive loss of potassium caused by hyperaldosteronism. Low potassium levels can also result from diuretic therapy used to treat the ascites.

FIG. 43.7 Mechanisms for development of ascites. Adapted from Huether SE, McCance KL: Understanding pathophysiology, ed 5, St Louis, 2012, Mosby.

TABLE 43.10 Factors Involved in Ascites

Because of decreased immune function associated with cirrhosis, patients with ascites are at risk for spontaneous bacterial peritonitis (SBP). SBP is a bacterial infection of the ascitic fluid. In SBP, bacteria normally found in the intestines move into the peritoneal space. The bacteria most often responsible for the infection are a gram-negative enteric pathogen, such as Escherichia coli. SBP is a common complication of hospitalized patients with cirrhosis and ascites. Worsening vasodilation contributes to the development of SBP.11

FIG. 43.8 Gross ascites.

From Butcher GP: Gastroenterology: An illustrated colour text, London, 2004, Churchill Livingstone.

Hepatic Encephalopathy Hepatic encephalopathy is a neuropsychiatric manifestation of liver disease. The pathogenesis is multifactorial. It includes the neurotoxic effects of ammonia, abnormal neurotransmission, astrocyte swelling, and inflammatory cytokines. A major source of ammonia is the bacterial and enzymatic deamination of amino acids in the intestines. The ammonia that results from deamination normally goes to the liver via the portal circulation and is converted to urea. The kidneys then excrete urea. When blood is shunted past the liver via the collateral vessels or the liver is so damaged that it is unable to convert ammonia to urea, the levels of ammonia in the systemic circulation increase. The ammonia crosses the blood-brain barrier and produces neurologic toxic manifestations. Factors that increase ammonia in the circulation may precipitate hepatic encephalopathy (Table 43.11). Hepatic encephalopathy can occur after placement of a transjugular intrahepatic portosystemic shunt (TIPS). TIPS reduces portal hypertension by diverting blood flow around the liver. (TIPS is discussed on p. 986.) Manifestations include changes in neurologic and mental responsiveness; impaired consciousness; and inappropriate behavior, ranging from sleep problems to trouble concentrating to deep coma. Changes may occur (1) suddenly from an increase in ammonia in response to bleeding varices or infection or (2) gradually as blood ammonia levels slowly increase. We often use a grading system to classify the stages of hepatic encephalopathy (Table 43.12).

TABLE 43.11 Factors Precipitating Hepatic

Encephalopathy

A characteristic manifestation is asterixis (flapping tremors). This may take several forms, with the most common involving the arms and hands. When asked to hold the arms and hands stretched out, the patient is unable to hold this position and performs a series of rapid flexion and extension movements of the hands. Impairments in writing involve difficulty in moving the pen or pencil from left to right and apraxia (inability to construct simple figures). Other signs include hyperventilation, hypothermia, tongue fasciculations, and grimacing and grasping reflexes. Fetor hepaticus (musty, sweet odor of the patient’s breath) occurs in some patients. This odor is from the accumulation of digestive by-products that the liver is unable to degrade.

Hepatorenal Syndrome Hepatorenal syndrome is a type of renal failure with azotemia, oliguria, and intractable ascites. In this syndrome, the kidneys have no structural abnormality. The cause is complex. The final common pathway is likely to be portal hypertension along with liver decompensation, resulting in splanchnic and systemic vasodilation and decreased arterial blood volume. As a result, renal vasoconstriction occurs, and renal failure follows. Liver transplantation can reverse renal failure. In the patient with cirrhosis, hepatorenal syndrome can follow diuretic therapy, GI hemorrhage, or paracentesis.

Diagnostic Studies Patients with cirrhosis have abnormalities in most of their liver function tests. Enzyme levels, including alkaline phosphatase, AST, ALT, and γ-glutamyl transpeptidase (GGT), are initially high due to their release from inflamed liver cells. However, in end-stage liver disease, AST and ALT levels may be normal due to the death and loss of hepatocytes. Patients will also have low serum total protein and albumin, increased serum bilirubin (Table 43.3) and globulin levels, and prolonged PT time. Low cholesterol levels reflect the changes in fat metabolism. Although a liver ultrasound may be able to detect cirrhosis, it is not a reliable diagnostic test for cirrhosis. Ultrasound elastography (Fibroscan) is a noninvasive test used to quantify the degree of liver fibrosis. A liver biopsy, which may be done to identify liver cell changes, is the gold standard for a definitive diagnosis of cirrhosis.

Interprofessional Care The goal of treatment is to slow the progression of cirrhosis and to prevent and treat any complications. Interprofessional care measures are listed in Table 43.13. Management of specific problems associated with cirrhosis is described next.

Ascites Management of ascites focuses on sodium restriction, diuretics, and fluid removal.12 Patients may need to limit sodium intake to 2 g/day. Very low sodium intake can result in reduced nutritional intake and malnutrition. The patient is usually not on restricted fluids unless severe ascites develops. When caring for patients with ascites, accurately monitor fluid and electrolyte balance. An albumin infusion may help maintain intravascular volume and adequate urine output by increasing plasma colloid oncotic pressure.

TABLE 43.12 Grading Scale for Hepatic

Encephalopathy

TABLE 43.13 Interprofessional CareCirrhosis of

the Liver

Diagnostic Assessment • History and physical examination • Liver function tests (ALT, AST, alkaline phosphatase, bilirubin, γglutamyl transpeptidase [GGT]) • Serum albumin • Serum electrolytes • PT time • Complete blood count • Liver biopsy (percutaneous needle) • Liver ultrasound (e.g., FibroScan) • Upper endoscopy (esophagogastroduodenoscopy) • CT scan, MRI

Management

Conservative Therapy • Rest • B-complex vitamins • Avoiding alcohol • Minimizing or avoiding aspirin, acetaminophen, and NSAIDs

Ascites • Low-sodium diet • Diuretics • Paracentesis (if needed)

Esophageal and Gastric Varices • Endoscopic band ligation or sclerotherapy • Balloon tamponade • Transjugular intrahepatic portosystemic shunt (TIPS)

Drug Therapy • Nonselective β-blocker (e.g., propranolol [Inderal]) • octreotide (Sandostatin) • vasopressin

Hepatic Encephalopathy Drug Therapy • Antibiotics (rifaximin [Xifaxan]) • lactulose

Diuretic therapy is an important part of management. Often a combination of drugs that work at multiple sites of the nephron is more effective than a single agent. Spironolactone (Aldactone) is an effective diuretic, even in patients with severe ascites. Spironolactone is also an antagonist of aldosterone and is potassium sparing. Other potassium-sparing diuretics include amiloride (Midamor) and triamterene (Dyrenium). A high-potency loop diuretic (e.g., furosemide [Lasix]), is often used in combination with a potassiumsparing drug. Tolvaptan (Samsca), a vasopressin-receptor antagonist, can correct hyponatremia, a common problem in patients with cirrhosis. It causes an increase in water excretion, resulting in an increase in serum sodium concentration. A paracentesis is a sterile procedure in which a catheter is used to withdraw fluid from the abdominal cavity. This procedure can diagnose a medical condition or relieve pain, pressure, or difficulty breathing. In the patient with cirrhosis, this procedure is done for the person with impaired respiration or abdominal discomfort caused by severe ascites who does not respond to diuretic therapy. It is only a temporary measure of palliation because the fluid tends to reaccumulate rapidly.12 TIPS (discussed later in this section) is used to treat ascites that does not respond to diuretics. A peritoneovenous shunt is a surgical procedure that provides continuous reinfusion of ascitic fluid into the venous system. It is rarely used due to the high rate of complications.

Esophageal and Gastric Varices The main therapeutic goal for esophageal and gastric varices is to prevent bleeding and variceal rupture by reducing portal pressure. The patient who has esophageal and/or gastric varices should avoid alcohol, aspirin, and nonsteroidal antiinflammatory drugs (NSAIDs). All patients with cirrhosis should have an upper endoscopy (esophagogastroduodenoscopy [EGD]) to screen for varices. Patients with varices at risk for bleeding are often started on a nonselective βblocker (nadolol [Corgard] or propranolol [Inderal]) to reduce the risk

of hemorrhage. β-Blockers decrease high portal pressure, which decreases the risk for rupture. When variceal bleeding occurs, the first step is to stabilize the patient and manage the airway. IV therapy is started and may include giving blood products. Care then moves toward stopping the bleeding, identifying the source, and applying interventions to prevent further bleeding. Management that involves a combination of drug therapy and endoscopic therapy is more successful than either approach alone. Drug therapy for bleeding varices may include the somatostatin analog octreotide (Sandostatin) or vasopressin. Both produce vasoconstriction of the splanchnic arterial bed, decrease portal blood flow, and decrease portal hypertension. Currently, octreotide is used more often because it has fewer side effects than vasopressin. At the time of endoscopy, band ligation or sclerotherapy of varices may be used to prevent rebleeding. Endoscopic variceal ligation (EVL, or “banding”) is done by placing a small rubber band (elastic O-ring) around the base of the varix (enlarged vein). Sclerotherapy involves injecting a sclerosing solution into the swollen veins through a needle placed through the endoscope. Balloon tamponade is an option when endoscopy does not control acute esophageal or gastric variceal hemorrhage. Balloon tamponade controls the hemorrhage by mechanical compression of the varices. Several types of tubes are available. The Sengstaken-Blakemore tube has 2 balloons, gastric and esophageal, with 3 lumens: 1 for the gastric balloon, 1 for the esophageal balloon, and 1 for gastric aspiration. Two other types of balloons are the Minnesota tube (a modified Sengstaken-Blakemore tube with an esophageal suction port above the esophageal balloon) and the Linton-Nachlas tube.

Safety Alert Balloon Tamponade

• Label each lumen to avoid confusion. • Secure the tube to prevent movement of the tube that could result in occlusion of the airway. • Deflate balloons for 5 minutes every 8 to 12 hr per agency policy to prevent tissue necrosis. Supportive measures during an acute variceal bleed include giving fresh frozen plasma and packed RBCs, vitamin K, and proton pump inhibitors (PPIs; e.g., pantoprazole). Lactulose and rifaximin (Xifaxan) may be given to prevent hepatic encephalopathy from breakdown of blood and the release of ammonia in the intestine. Antibiotics are given to prevent bacterial infection. Because of the high incidence of recurrent bleeding with each bleeding episode, continued therapy is necessary. Long-term management of patients who have had an episode of bleeding includes nonselective β-blockers, repeated band ligation of the varices, and portosystemic shunts in patients who develop recurrent bleeding.

Shunting Procedures Nonsurgical and surgical methods of shunting blood away from the varices are available. Shunting procedures tend to be done more after a second major bleeding episode than during an initial bleeding episode. Transjugular intrahepatic portosystemic shunt (TIPS) is a nonsurgical procedure in which a tract (shunt) between the systemic and portal venous systems is created to redirect portal blood flow. A catheter is placed in the jugular vein and then threaded through the superior and inferior vena cava to the hepatic vein. The wall of the hepatic vein is punctured, and the catheter is directed to the portal vein. Stents are positioned along the passageway, overlapping in the liver tissue and extending into both veins. This procedure reduces portal venous pressure and decompresses the varices, thus controlling bleeding. TIPS does not interfere with a future liver transplantation. Limitations of TIPS include the increased risk for hepatic encephalopathy (toxin-containing blood bypasses the liver) and stenosis of the stent. TIPS is contraindicated in patients with

severe hepatic encephalopathy, liver cancer, severe hepatorenal syndrome, and portal vein thrombosis.

FIG. 43.9 Portosystemic shunts. A, Portacaval shunt. The portal vein is anastomosed to the inferior vena cava, diverting blood from the portal vein to the systemic circulation. B, Distal splenorenal shunt. The splenic vein is anastomosed to the renal vein. The portal venous flow stays intact while esophageal varices are selectively decompressed. (The short gastric veins are decompressed.) The spleen conducts blood from the high pressure of the esophageal and gastric varices to the low-pressure renal vein.

Various surgical shunting procedures can decrease portal hypertension by diverting some of the portal blood flow while allowing adequate liver perfusion. Currently, the surgical shunts most often used are the portacaval shunt and the distal splenorenal shunt (Fig. 43.9).

Hepatic Encephalopathy The goal of management of hepatic encephalopathy is to reduce ammonia formation. Lactulose, a drug that traps ammonia in the gut, reduces ammonia formation in the intestines. We can give it orally, as an enema, or through a nasogastric (NG) tube. The drug’s laxative effect expels the ammonia from the colon. Antibiotics, such as rifaximin, also may be given, especially in patients who do not respond to lactulose. Regular and frequent bowel movements are necessary to minimize the ammonia buildup, so use measures to prevent constipation. Control of hepatic encephalopathy also involves treatment of precipitating causes (Table 43.10). This includes lowering dietary protein intake, preventing and controlling GI bleeds, and, in the case of a bleed, removing the blood promptly from the GI tract to decrease the protein accumulation in the gut.

Drug Therapy There is no specific drug therapy for cirrhosis. However, several drugs are used to treat symptoms and complications of advanced liver disease (Table 43.14).

Nutritional Therapy

The diet for the patient who has cirrhosis without complications is high in calories (3000 cal/day). It is high in carbohydrate content with moderate to low levels of fat. Protein restriction may be needed for some patients right after a severe flare of symptoms (i.e., episodic hepatic encephalopathy). However, protein restriction is rarely needed in patients with cirrhosis and persistent hepatic encephalopathy. For many, malnutrition is a more serious clinical problem than hepatic encephalopathy.3

TABLE 43.14 Drug TherapyCirrhosis

A patient with alcoholic cirrhosis often has protein-calorie malnutrition. Oral nutritional supplements containing protein from branched-chain amino acids that are metabolized by the muscles may be needed. These supplements provide protein that the liver can more easily metabolize. Parenteral nutrition or EN are used with severe cases of malnutrition (see Chapter 39). The patient with ascites and edema is placed on a low-sodium diet. The degree of sodium restriction depends on the patient’s condition. Teach the patient and caregiver about the degree of restriction. Table salt is a well-known source of sodium. Other foods high in sodium

include canned soups and vegetables, many frozen foods, salted snacks (e.g., potato chips), nuts, smoked meats and fish, crackers, breads, baking soda, olives, pickles, ketchup, and beer. Teach the patient to read labels for sodium content (see Fig. 34.5). Offer suggestions about how to make the diet more palatable. Seasonings, like garlic, parsley, onion, lemon juice, and spices may make food more appetizing. Collaborate with a dietitian about dietary strategies.

Nursing Management: Cirrhosis Nursing Assessment Subjective and objective data that should be obtained from a person with cirrhosis are outlined in Table 43.15.

Nursing Diagnoses Nursing diagnoses for the patient with cirrhosis may include: • Impaired nutritional status • Ineffective tissue perfusion • Activity intolerance • Fluid imbalance Additional information on nursing diagnoses and interventions for the patient with cirrhosis is presented in eNursing Care Plan 43.2 available on the website for this chapter.

Planning The overall goals are that the patient with cirrhosis will (1) have relief of discomfort, (2) have minimal to no complications (ascites, esophageal varices, hepatic encephalopathy), and (3) return to as normal a lifestyle as possible.

Nursing Implementation Health Promotion Common risk factors for cirrhosis include alcohol use, malnutrition, viral hepatitis, biliary obstruction, obesity, and right-sided heart failure. Prevention and early treatment of cirrhosis focus on reducing or eliminating these risk factors. Urge patients to abstain from alcohol.

Encourage those with chronic alcohol use to enroll in support programs that help patients maintain sobriety. (The treatment of alcohol use is discussed in Chapter 10.) Adequate nutrition, especially for the person who uses alcohol and other people at risk for cirrhosis, is essential to promote normal liver regeneration. Identify and treat acute hepatitis early so that it does not progress to chronic hepatitis and cirrhosis. Bariatric surgery for morbidly obese persons reduces the incidence of NAFLD.

Acute Care Nursing care for the patient with cirrhosis focuses on conserving the patient’s strength while maintaining muscle strength and tone. When the patient needs complete bed rest, implement measures to prevent pneumonia, thromboembolic problems, and pressure injuries. Modify the activity and rest schedule according to signs of improvement (e.g., decreasing jaundice, improvement in liver function studies).

TABLE 43.15 Nursing AssessmentCirrhosis

Subjective Data Important Health Information Past health history: Viral, toxic, or idiopathic hepatitis. Alcohol use, metabolic syndrome, chronic biliary obstruction and infection, severe right-sided heart failure Medications: Adverse reaction to any medication. Use of anticoagulants, aspirin, NSAIDs, acetaminophen

Functional Health Patterns Health perception–health management: Chronic alcohol use. Weakness, fatigue

Nutritional-metabolic: Anorexia, weight loss, dyspepsia, nausea and vomiting, gingival bleeding. Dry, yellow skin, bruising Elimination: Dark urine, decreased urine output, light-colored or black stools, flatulence, change in bowel habits. Cognitive-perceptual: Dull, right upper quadrant or epigastric pain. Numbness, tingling of extremities. Itching Sexuality-reproductive: Impotence, amenorrhea

Objective Data General Fever, cachexia, wasting of extremities

Integumentary Icteric sclera, jaundice, petechiae, ecchymoses, spider angiomas, palmar erythema, alopecia, loss of axillary and pubic hair, peripheral edema

Respiratory Shallow, rapid respirations. Epistaxis

Gastrointestinal Abdominal distention, ascites, distended abdominal wall veins, palpable liver and spleen, foul breath. Hematemesis. Black, tarry stools. Hemorrhoids

Neurologic

Altered mentation, asterixis

Reproductive Gynecomastia, testicular atrophy, and impotence (men); loss of libido (men and women); amenorrhea or heavy menstrual bleeding (women)

Possible Diagnostic Findings Anemia, thrombocytopenia; leukopenia. ↓ Serum albumin, potassium. Abnormal liver function studies. ↑ INR, ↓ platelets, ↑ ammonia, ↑ bilirubin levels. Abnormal abdominal ultrasound, CT, or MRI Anorexia, nausea and vomiting, pressure from ascites, and poor eating habits all interfere with adequate intake of nutrients. Oral hygiene before meals may improve the patient’s taste sensation. Make between-meal snacks available so that the patient can eat them at times when food is best tolerated. Offer preferred foods whenever possible. Explain the reason for any dietary restrictions to the patient and caregiver. Nursing assessment and care should include the patient’s physical status. Is jaundice present? Where is it seen—sclera, skin, hard palate? What is the progression of jaundice? If the pruritis accompanies jaundice, use measures to relieve itching. Cholestyramine or hydroxyzine (Atarax) may help. Other measures to relieve itching include baking soda or moisturizing bath oils (Alpha Keri), lotions containing calamine, antihistamines, soft or old linens, and control of the temperature (not too hot and not too cold). Keep the patient’s nails short and clean. Teach patients to rub with their knuckles rather than scratch with their nails when they cannot resist scratching.

TABLE 43.16 Nursing ManagementCare of the

Patient Undergoing Paracentesis

Preprocedure • Have the patient void or insert an indwelling catheter. • Obtain baseline vital signs and pulse oximetry. Weigh patient, inspect and palpate abdomen, and assess abdominal girth. Assess bladder for distention and determine last voiding. • Assess baseline laboratory values (e.g., CBC, electrolytes, coagulation studies). • Give any sedation or analgesia, if ordered. • Teach patient to remain immobile during the procedure. • Help the patient to a high-Fowler (sitting) position with feet on the floor.

Postprocedure • Perform assessment and compare to baseline: vital signs, pulse oximetry, abdominal girth, abdominal pain. Note any signs of hypovolemia. • Have the patient sit on the side of the bed or place in highFowler’s position. • Label and send the fluid for laboratory analysis. • Check the dressing for bleeding and/or leakage of ascitic fluid. • Give IV fluid and/or albumin as ordered. • Measure any drainage and describe the collected fluid. • Reweigh the patient and monitor intake and output. • Maintain bedrest per agency protocol. Note the color of urine and stools and assess for improvement or

normalization of color. When jaundice is present, the urine is often dark brown, and the stool is gray or tan. Edema and ascites require your assessment and intervention. Accurate calculation and recording of intake and output, daily weights, and measurements of extremities and abdominal girth help in the ongoing assessment of the location and extent of the edema. Mark the abdomen with a permanent marker so that you measure the girth at the same location each time. Immediately before a paracentesis, have the patient void to prevent puncturing of the bladder during the procedure. Other nursing care associated with a paracentesis is outlined in Table 43.16. Dyspnea is a frequent problem for the patient with severe ascites and can lead to pleural effusions. A semi-Fowler’s or Fowler’s position allows for maximal respiratory efficiency. Use pillows to support the arms and chest to increase the patient’s comfort and ability to breathe. Meticulous skin care is essential because the edematous tissues are prone to breakdown. Use an alternating-air pressure mattress or other special mattress. A turning schedule (minimum of every 2 hours) must be adhered to rigidly. Support the abdomen with pillows. If the abdomen is taut, cleanse it gently. The patient will tend to avoid moving because of abdominal discomfort and dyspnea. Range-ofmotion exercises are helpful. Implement measures such as coughing and deep breathing to prevent respiratory problems. The lower extremities may be elevated. If scrotal edema is present, a scrotal support gives some comfort. When the patient is taking diuretics, monitor serum sodium, potassium, chloride, and bicarbonate levels. Monitor renal function (blood urea nitrogen [BUN], serum creatinine) routinely and with any change in the diuretic dosage. Observe for signs of fluid and electrolyte imbalance, especially hypokalemia. Dysrhythmias, hypotension, tachycardia, and generalized muscle weakness may occur with hypokalemia. Muscle cramping, weakness, lethargy, and confusion may be present with hyponatremia from water excess. Observe for and provide nursing care for any hematologic

problems. These include bleeding tendencies, anemia, and increased susceptibility to infection. Assess the patient’s response to altered body image resulting from jaundice, spider angiomas, palmar erythema, ascites, and gynecomastia. The patient may have anxiety and embarrassment about these changes. Explain these phenomena and be a supportive listener. Provide nursing care with concern and encouragement to help the patient maintain his or her self-esteem.

Check Your Practice You are caring for a 69-yr-old male patient with advanced cirrhosis who just underwent banding for esophageal varices. The UAP tells you that the patient’s BP is 80/60 mm Hg and he is hard to arouse. • What is your concern? • What would you do?

Bleeding Varices If the patient has esophageal or gastric varices, observe for any signs of bleeding from the varices, such as hematemesis and melena. If hematemesis occurs, assess the patient for hemorrhage, call the HCP, and be ready to transfer the patient to the endoscopy suite and/or assist with equipment to control the bleeding. Maintain the patient’s airway. Patients with bleeding varices are usually admitted to the intensive care unit (ICU). Balloon tamponade is an option for patients who have bleeding that is unresponsive to band ligation or sclerotherapy. When balloon tamponade is used, explain to the patient and caregiver the use of the tube and how the balloon is inserted. Check the balloons for patency. It is usually the HCP’s responsibility to insert the tube by either the nose or mouth. Then the gastric balloon is inflated with 250 mL of air, and the tube is retracted until resistance (lower esophageal sphincter)

is felt. The tube is secured by placing a piece of sponge or foam rubber at the nostrils (nasal cuff). For continued bleeding, the esophageal balloon is then inflated. A sphygmomanometer is used to measure and maintain the desired pressure at 20 to 40 mm Hg. An x-ray verifies the balloon’s position. Nursing care includes monitoring for complications of rupture or erosion of the esophagus, regurgitation and aspiration of gastric contents, and occlusion of the airway by the balloon. If the gastric balloon breaks or is deflated, the esophageal balloon will slip upward, obstructing the airway and causing asphyxiation. If this happens, cut the tube or deflate the esophageal balloon. Keep scissors at the bedside. Minimize regurgitation by oral and pharyngeal suctioning and by keeping the patient in a semi-Fowler’s position. The patient is unable to swallow saliva because the inflated esophageal balloon occludes the esophagus. Encourage the patient to expectorate and provide an emesis basin and tissues. Frequent oral and nasal care offers relief from the taste of blood and irritation from mouth breathing.

Ethical/Legal Dilemmas Rationing

Situation T.H., a 43-yr-old female patient with cirrhosis of the liver, is frequently admitted to the hospital. She has been told that her continued alcohol use will inevitably lead to her death. She now has GI bleeding and needs blood transfusions. She has a rare blood type that is hard to match. Should you ask for an ethics consultation?

Ethical/Legal Points for Consideration • Rationing, or the controlled distribution of scarce resources, is a difficult ethical problem. The needs of an individual patient or group of patients are weighed against the needs of many

patients, who may have a greater chance of recovery, and the availability of the necessary resources. • Health interests can supersede the interests or rights of a person. For example, in anticipation of an anthrax attack, the government could confiscate all relevant antibiotics and restrict their use to treat the disease. • Two individual rights that must be considered regarding rationing are the (1) constitutional right to privacy and (2) right to consent to or refuse medical procedures and therapy. • The competent adult is the only person who may consent to or refuse treatment for his or her health care problems. • If T.H. consents to a blood transfusion, an intervening party may be allowed to refuse that treatment only given substantial intervening circumstances and not as a threat to compel adherent future behavior. • If involved parties cannot reach an agreement, legal intervention by way of a court order may become necessary.

Discussion Questions 1. Do you think patients with diseases that have a behavioral component, like substance use, deserve aggressive treatment? 2. Would you request an ethics committee consultation in T.H.’s case?

Hepatic Encephalopathy Nursing care of the patient with hepatic encephalopathy focuses on maintaining a safe environment, sustaining life, and assisting with measures to reduce the formation of ammonia. Patients with hepatic encephalopathy may be confused and at risk for falls or other injuries. Assess the patient’s (1) level of responsiveness (e.g., reflexes, pupillary reactions, orientation), (2) sensory and motor abnormalities (e.g., hyperreflexia, asterixis, motor coordination), (3) fluid and electrolyte

imbalances, (4) acid-base imbalances, and (5) response to treatment measures. Assess the neurologic status, including an exact description of the patient’s behavior, at least every 2 hours. Plan your care of the patient based on the severity of the encephalopathy. In patients with altered levels of consciousness or whose airway may become compromised, have emergency equipment readily available. Any GI bleeding may worsen encephalopathy. Institute measures to prevent falls or injuries. . Control factors known to precipitate encephalopathy as much as possible, including anything that may cause constipation (e.g., dehydration, opioid drugs). Measures to minimize constipation are important to reduce ammonia production. Give drugs, laxatives, and enemas as ordered. Encourage fluids, if not contraindicated. Assess the patient taking lactulose for diarrhea and excessive fluid and electrolyte losses.

Ambulatory Care The patient with cirrhosis may be faced with a prolonged course and the chance of life-threatening problems and complications. The patient and caregiver need to understand the importance of continual health care and medical supervision. Supportive measures include proper diet, rest, avoiding potentially hepatotoxic OTC drugs, such as acetaminophen in high doses, and abstaining from alcohol. Abstinence from alcohol is important and results in improvement in most patients. However, some patients find abstinence extremely hard and need emotional support. Explore your own attitude toward the patient whose cirrhosis is from chronic alcohol use. Always provide care without being condescending or judgmental. Treat patients with respect and concern for their well-being (see Chapter 10).

TABLE 43.17 Patient & Caregiver

TeachingCirrhosis When teaching the patient and caregiver about management of cirrhosis, do

the following: 1. Explain that cirrhosis is a chronic illness and requires continual health care. 2. Teach the symptoms of complications and when to seek medical attention to enable prompt treatment. 3. Teach the patient to avoid potentially hepatotoxic over-thecounter drugs, because the diseased liver is unable to metabolize them. 4. Encourage abstinence from alcohol because continued use increases the rate of liver disease progression and risk for liver complications. 5. Teach the patient with esophageal or gastric varices to avoid aspirin and NSAIDs to prevent hemorrhage. 6. Teach the patient with portal hypertension and varices that straining at stool, coughing, sneezing, and retching and vomiting may increase the risk for variceal hemorrhage. Cirrhosis is a chronic disease, and people can live many years with symptoms and complications from cirrhosis. The patient is affected not only physically but also psychologically, socially, and economically. Major lifestyle changes may be needed, especially if chronic alcohol use is the primary cause. Provide information about community support programs, such as Alcoholics Anonymous, for help with chronic alcohol use. Teach the patient and caregiver about complications and when to seek medical attention (Table 43.17). Include instructions about adequate rest periods, how to detect early signs of complications, skin care, drug therapy side effects, observation for bleeding, and protection from infection. Referral to a community or home health nurse may help ensure patient adherence to prescribed therapy. Home care for the patient with cirrhosis focuses on helping the patient with activities of daily living while maintaining the highest level of wellness possible.

Evaluation Expected outcomes are that the patient with cirrhosis will • Maintain food and fluid intake adequate to meet nutritional needs • Maintain skin integrity with relief of edema and itching • Have normal fluid and electrolyte balance • Acknowledge and get treatment for a substance use problem

Acute Liver Failure Acute liver failure, or fulminant hepatic failure, is a potentially lifethreatening clinical syndrome.3 It is characterized by a rapid onset of severe liver dysfunction in someone with no history of liver disease. It is often accompanied by hepatic encephalopathy. The most common cause of acute liver failure is drugs, usually acetaminophen. Other drugs that can cause acute liver failure include isoniazid, sulfa-containing drugs, and anticonvulsants. Drugs can cause hepatocyte damage by disrupting essential intracellular processes or causing an accumulation of toxic metabolic products. Other causes can include viral hepatitis, especially HBV. Hepatitis A is a less common cause. Outcomes depend on the cause. Cerebral edema, cerebellar herniation, and brainstem compression are the most common causes of death. Treatment of cerebral edema is described in Chapter 56. Liver transplantation is associated with a significant survival benefit in patients with a low probability of spontaneous recovery.

Clinical Manifestations and Diagnostic Studies Manifestations of acute liver failure include jaundice, coagulation abnormalities, and encephalopathy. Changes in cognitive function are often the first clinical sign. Patients are susceptible to a wide variety of complications, including cerebral edema, renal failure, hypoglycemia, metabolic acidosis, sepsis, and multiorgan failure. Serum bilirubin is high, and the PT time is prolonged. Liver enzyme levels (AST, ALT) are often markedly increased. Other laboratory tests include blood chemistries (especially glucose, since hypoglycemia may be present and need correction), complete blood count (CBC), acetaminophen level, screening for other drugs and toxins, viral hepatitis serology (especially HAV and HBV), serum ceruloplasmin (enzyme synthesized in liver) and α1-antitrypsin levels, iron levels, ammonia levels, and autoantibodies (ANAs and ASMAs).

CT or MRI can provide information about the liver size and contour, presence of ascites or tumors, and patency of the blood vessels.

Interprofessional and Nursing Care Since acute liver failure may progress rapidly, with hour-by-hour changes in consciousness, the patient is usually transferred to the ICU once the diagnosis is made. Planning for transfer to a transplant center should begin in patients with grade 1 or 2 encephalopathy because they may worsen rapidly. Early transfer is important because the risks involved with patient transport may increase or even prevent transfer if stage 3 or 4 encephalopathy develops (Table 43.12). Renal failure is a frequent complication of liver failure. It may be due to dehydration, hepatorenal syndrome, or acute tubular necrosis. The frequency of renal failure may be even greater with acetaminophen overdose or other toxins with which direct renal toxicity occurs. Although few patients die of renal failure alone, it often increases the mortality risk and may worsen the prognosis. Protect renal function by maintaining adequate fluid balance, avoiding nephrotoxic agents (e.g., aminoglycosides, NSAIDs), and promptly identifying and treating infection. Monitoring and management of hemodynamic and renal function, as well as glucose, electrolytes, and acid-base status, are critical. Conduct frequent neurologic evaluations for signs of increased intracranial pressure. Position the patient with the head elevated at 30 degrees. Avoid excessive patient stimulation. Maneuvers that cause straining or Valsalva-like movements may increase intracranial pressure (ICP). ICP monitoring is discussed in Chapter 56. Assess the patient regularly for baseline level of consciousness and orientation and report any changes to the HCP. Avoid the use of any sedatives due to their effects on mental status. The effects can be confused with worsening encephalopathy. Only minimal doses of benzodiazepines should be used due to their delayed metabolism by the failing liver. Closely observe the patient to prevent injuries and pad bedrails to avoid injury from possible seizures. Monitor intake

and output for renal function and provide good skin and oral care to avoid breakdown and infection. Changes in level of consciousness may compromise nutritional intake. Many patients receive vitamin supplementation. Other factors, such as coagulation problems, may influence whether EN is started. An NG tube may be irritating to the nasal and esophageal mucosa and cause bleeding.

Liver Cancer Primary liver cancer starts in the liver. The most common types of liver cancer are hepatocellular carcinoma (HCC) (75% of cases) and intrahepatic cholangiocarcinoma (bile duct cancer). In 2018 there were about 40,710 cases of HCC and 28,920 HCC deaths in the United States. Worldwide liver cancer is the fifth most common cancer and second most common cause of cancer death.13 Liver cancer is the most common cause of death in patients with cirrhosis. Cirrhosis caused by hepatitis C is the most common cause of HCC in the United States, followed by NAFLD. About 2% of patient with cirrhosis develop liver cancer each year. In primary liver cancer, lesions may be singular or numerous and nodular or diffusely spread over the entire liver. Some tumors infiltrate other organs, such as the gallbladder, or move into the peritoneum or the diaphragm. Primary liver cancer often metastasizes to the lung. Metastatic cancer in the liver is more common than primary liver cancer (Fig. 43.10). The liver is a common site of metastatic growth because of its high rate of blood flow and extensive capillary network. Cancer cells in other parts of the body are often carried to the liver via the portal circulation.

FIG. 43.10 Multiple hepatic metastases from a primary colon cancer. A, Gross specimen showing outside of liver. B, Liver section showing metastatic lesions. A, From Kumar V, Abbas AK, Fausto N: Robbins and Cotran pathologic basis of disease, ed 7, Philadelphia, 2005, Saunders. B, From Kumar V, Abbas AK, Aster JC, et al: Robbins and Cotran pathologic basis of disease, ed 8, Philadelphia, 2010, Saunders.

Clinical Manifestations and Diagnostic Studies The manifestations of early liver cancer can be absent or subtle. They are often a result of the underlying cirrhosis rather than from the actual liver tumor(s). The patient may present with hepatomegaly, splenomegaly, fatigue, peripheral edema, ascites, and other complications from portal hypertension. In late stages, patients will often have fever/chills, jaundice, anorexia, weight loss, palpable mass, and right upper quadrant pain. Diagnostic and screening for liver cancer are ultrasound, CT, and MRI. Recent advancements in MRI scanning have allowed for accurate diagnosis of liver cancers without the need for a percutaneous biopsy.13 Sometimes, a biopsy may be done when the results of diagnostic imaging studies are inconclusive or tissue is needed to guide treatment. Risks of a biopsy include bleeding and potential tumor cell seeding along the needle tract. Therefore a biopsy is generally not done unless a diagnosis cannot be made by CT or MRI and clinical presentation. Serum α-fetoprotein (AFP) levels combined with ultrasound have a high rate of detection of early-stage HCC. (AFP is discussed in Chapter 15.)

Interprofessional and Nursing Care Prevention of liver cancer focuses on identifying and treating chronic hepatitis B and C viral infections. Treatment of chronic alcohol use may lower the risk for liver cancer. Screening for at-risk patients (e.g., those with cirrhosis) usually involves a combination of serum AFP and CT, MRI, or ultrasound imaging of the liver. Treatment of liver cancer depends primarily on the stage of cancer:

number, size, and location of tumors; involvement of any blood vessels; patient age and overall health; and extent of underlying liver disease. Surgical liver resection (partial hepatectomy) offers the best chance for a cure. However, only about 15% of people have enough healthy liver tissue for this to be an option. The underlying cirrhosis and portal hypertension often compromise liver function and may cause liver failure after surgery. Furthermore, many patients are diagnosed at an advanced stage of cancer when surgery is not an option. For those patients who have early-stage liver cancer and impaired liver function, liver transplantation offers a good prognosis. Nonsurgical therapies include percutaneous ablation, chemoembolization, radioembolization, and sorafenib (Nexavar) oral therapy.13 In ablation, a thin needle is inserted into the core of the tumor. Then various substances can be injected (ethanol, acetic acid) and the temperature of the probe (radiofrequency, microwave, cryotherapy) can be altered to destroy the tumor. This procedure can be done percutaneously, laparoscopically, or through an open incision. It is typically limited by the number, size, and location of liver tumors. It is usually offered to patients with early-stage liver cancer. Although complications are not common, they can include infection, bleeding, dysrhythmias, and skin burn. In patients with multinodular HCC or intermediate-stage liver cancer, embolization of the tumors is another intervention. There are 2 options typically used: transarterial chemoembolization (TACE) or transarterial radioembolization (TARE). TACE and TARE are minimally invasive procedures done by interventional radiologists. A catheter is placed via the femoral artery or radial artery and advanced to the arterial blood supply of the tumors in the liver. Either a chemotherapy drug (TACE) or radioactive beads (TARE) along with embolizing agents are then injected into the arteries of the tumor(s) region. TACE works by shutting off the blood supply to the tumors and exposing liver tumor cells to the chemotherapy agent. TARE destroys the tumor(s) by slowly releasing radioactive material directly to the site of the tumor. It can take up to 3 months for complete results.

In patients with advanced HCC, sorafenib (Nexavar) is typically the first-line treatment. It is a kinase inhibitor, a type of targeted therapy, that blocks certain proteins (kinases) that play a role in tumor growth and cancer progression (see Table 15.13). This drug has the potential to slow tumor progression and prolong life. Nursing interventions focus on keeping the patient as comfortable as possible. Since these patients have the same problems as any patient with advanced liver disease, the nursing interventions discussed for cirrhosis of the liver apply to these patients (see p. 987). Although the prognosis for patients with liver cancer is poor, it is improving with early screening and surveillance programs for those with chronic hepatitis and/or cirrhosis. The cancer often progresses rapidly, with patients having complications from the advancing cancer and declining liver function. Without treatment, death may occur within 6 to 12 months, most often from hepatic encephalopathy or massive blood loss from GI bleeding.

Liver Transplantation Liver transplantation has become an option for many people with end-stage liver disease or localized HCC. Liver disease related to chronic viral hepatitis is the leading reason for liver transplantation. Other reasons include congenital biliary abnormalities (biliary atresia), inborn errors of metabolism, sclerosing cholangitis, acute liver failure, and chronic end-stage liver disease. In 2018, 11,514 patients were listed for a liver transplant in the United States with 8250 patients undergoing a transplant.3 Liver transplant candidates must go through a rigorous transplant evaluation prior to being placed on the transplant list. This is done to confirm the diagnosis of end-stage liver disease and to assess for other co-morbid conditions (e.g., cardiovascular disease, chronic kidney disease) that may affect the patient’s surgical outcome. The evaluation includes physical examination, laboratory tests (CBC, liver function tests), cardiac and pulmonary evaluations, endoscopy, CT scan, and psychologic testing. Potential recipients receive counseling about cigarette smoking and alcohol abstinence. Contraindications for liver transplant include severe extrahepatic disease, advanced HCC or other cancer, ongoing drug or chronic alcohol use, and inability to understand or adhere with the rigorous posttransplant care. Liver transplantation is done using both deceased (cadaver) and live donor livers. The live donor liver transplant was first developed for children whose parents wanted to serve as donors. Today, some liver transplant centers are performing live liver transplant procedures for adults. In this procedure, the living person donates a part of his or her liver to another. However, live liver donation poses potential risks to the donor, including biliary problems, hepatic artery thrombosis, wound infection, postoperative ileus, and pneumothorax. Because of the limited number of donor livers, when a liver becomes available for transplant it may be divided into 2 parts (split liver transplant) and implanted into 2 recipients. The decision to use a split donor liver is based on the donor’s size and health. The recipients

of the split liver generally are smaller than the donor. The success rate associated with split liver transplantation is somewhat lower than that associated with whole organ transplantation. Postoperative complications of liver transplant include bleeding, infection, and rejection. However, the liver is subject to a less aggressive immunologic attack than other organs, like the kidneys. Transplants and immunosuppressive therapy are discussed in Chapter 13. Immunosuppressive therapy generally involves a combination of corticosteroids, a calcineurin inhibitor (cyclosporine or tacrolimus), and an antiproliferative agent (e.g., azathioprine). Tacrolimus is superior to cyclosporine in liver transplantation. Standard immunosuppressive regimens often change over the course of the recipient’s life. Corticosteroid withdrawal may be done and is relatively safe to do in liver transplant recipients. About 80% of patients live more than 5 years after liver transplant. Long-term survival depends on the cause of liver failure (e.g., localized HCC, chronic hepatitis B or C, biliary disease). Patients who have liver disease from hepatitis B or C often have reinfection of the transplanted liver. For patients with hepatitis B, treatment after surgery with IV HBIG and a nucleoside or nucleotide analog (used to treat HBV infection) has reduced the rates of reinfection of the transplanted liver. For patients with HCV, treatment with the new direct-acting antivirals (DAAs) that can cure HCV infection has provided the opportunity to use HCV-positive liver grafts. The need for liver transplant may decrease in the HCV population. Research is ongoing to decide if DAAs should be started before or after transplant. The patient who had a liver transplant needs highly skilled nursing care, either in an ICU or other specialized unit. Postoperative nursing care includes assessing neurologic status; monitoring for signs of hemorrhage; preventing pulmonary complications; electrolyte levels, and urine output; and monitoring for manifestations of infection and rejection. Common respiratory problems are pneumonia, atelectasis, and pleural effusions. To prevent these complications, encourage the

patient to cough, deep breathe, use incentive spirometry, and frequently reposition. Measure the drainage from the Jackson-Pratt drain, NG tube, and T tube and note the color and consistency of the drainage at regular intervals. The first 2 months after surgery are critical for monitoring for infection. Causes of infection can be viral, fungal, or bacterial. Fever may be the only sign of infection. Adhering to the medication regimen can be hard, especially in the beginning. Emotional support and teaching for the patient and caregiver are essential to the success of the patient with a liver transplant.

Gerontologic Considerations: Liver Disease in the Older Adult The incidence of liver disease increases with age. The liver’s size and metabolic breakdown of drugs decrease, and hepatobiliary function is changed. The liver has a decreased capacity to respond to injury. This especially applies to regeneration after injury. Transplanted livers take longer to regenerate in the older adult compared with the younger adult. Older adults are particularly vulnerable to drug-induced liver injury. This is due to several factors, including the increased use of multiple prescription and OTC drugs, which can lead to drug interactions and potential drug toxicity. Age-related decreases in liver function result in decreased drug metabolism and a decreased ability to recover from drug-induced injury. A growing number of older adults have chronic hepatitis C and the resulting cirrhosis. Antibodies to HCV and elevated liver enzymes may be found during a routine health assessment in asymptomatic patients. Lifetime health behaviors may influence the development of chronic liver disease in the older adult. Chronic alcohol use and obesity can contribute to cirrhosis, fatty liver inflammation (NASH), and liver failure. Because of many older adults’ concomitant cardiovascular and lung diseases and possible anticoagulant therapy, variceal bleeding

can cause significant morbidity and mortality and needs immediate medical intervention. In the older adult with liver disease, hepatic encephalopathy is sometimes misdiagnosed as dementia and often overlooked. Because older adults tend to have more co-morbid conditions, transplantation may have more risks for complications. Therefore older adults may not be good candidates for liver transplants.

Disorders of The Pancreas Acute Pancreatitis Acute pancreatitis is an acute inflammation of the pancreas. Spillage of pancreatic enzymes into surrounding pancreatic tissue causes autodigestion and severe pain. The degree of inflammation varies from mild edema to severe hemorrhagic necrosis.

Etiology and Pathophysiology Many factors can cause injury to the pancreas. In the United States, the most common cause is gallbladder disease (gallstones), which is more common in women. The second most common cause is chronic alcohol use. This is more common in men. Other less common causes include drug reactions, pancreatic cancer, and hypertriglyceridemia (serum levels over 1000 mg/dL).14 Biliary sludge and microlithiasis, which is a mix of cholesterol crystals and calcium salts, can be present in patients with acute pancreatitis. The most common pathogenic mechanism in acute pancreatitis is autodigestion of the pancreas (Fig. 43.11). The causative factors injure pancreatic cells or activate the pancreatic enzymes in the pancreas rather than in the intestine. This may be due to reflux of bile acids into the pancreatic ducts through an open or distended sphincter of Oddi. This reflux may be caused by blockage created by gallstones. Obstruction of pancreatic ducts results in pancreatic ischemia. The exact mechanism by which chronic alcohol use predisposes a person to pancreatitis is not known. We think that alcohol increases the production of digestive enzymes in the pancreas. The pathophysiologic involvement of acute pancreatitis is classified as either mild pancreatitis (also known as edematous or interstitial pancreatitis) or severe pancreatitis (also called necrotizing pancreatitis) (Fig. 43.12). In severe pancreatitis, about half the patients have permanent decreases in pancreatic endocrine and exocrine function. Patients with severe pancreatitis are at high risk for developing

pancreatic necrosis, organ failure, and septic complications, resulting in an overall fatality rate of 5%.14

FIG. 43.11 Pathogenic process of acute pancreatitis.

FIG. 43.12 In acute pancreatitis, the pancreas appears edematous and is often hemorrhagic (H). From Stevens A, Lowe J: Pathology: Illustrated review in colour, ed 2, London, 2000, Mosby.

Clinical Manifestations Abdominal pain is the main manifestation of acute pancreatitis. The pain is due to distention of the pancreas, peritoneal irritation, and obstruction of the biliary tract. The pain is usually in the left upper quadrant, but it may be mid-epigastric. It often radiates to the back due to the retroperitoneal location of the pancreas. The pain has a sudden onset. It is described as severe, deep, piercing, and continuous or steady. Eating worsens the pain. It often starts when the patient is recumbent. Pain is not relieved by vomiting and may be accompanied by flushing, cyanosis, and dyspnea. The patient may assume various positions involving flexion of the spine to try to relieve the severe pain. Other manifestations include nausea and vomiting, low-grade fever, leukocytosis, hypotension, tachycardia, and jaundice. Abdominal tenderness with muscle guarding is common. Bowel sounds may be decreased or absent. Paralytic ileus may occur and causes marked abdominal distention. The lungs are often involved with crackles present. Intravascular damage from circulating trypsin (a proteolytic enzyme) may cause areas of cyanosis or greenish to yellow-brown discoloration of the abdominal wall. Other areas of ecchymoses are the flanks (Grey Turner’ spots or sign, a bluish flank discoloration) and the periumbilical area (Cullen’s sign, a bluish periumbilical discoloration). These result from seepage of bloodstained exudate from the pancreas and may occur in severe cases. Shock may occur from hemorrhage into the pancreas, toxemia from the activated pancreatic enzymes, or hypovolemia due to fluid shift into the retroperitoneal space (massive fluid shifts).

Complications

The severity of acute pancreatitis depends on the extent of pancreatic destruction. Acute pancreatitis can be life threatening. Some patients recover completely, others have recurring attacks, and others develop chronic pancreatitis. Two significant local complications of acute pancreatitis are pseudocyst and abscess. A pancreatic pseudocyst is an accumulation of fluid, pancreatic enzymes, tissue debris, and inflammatory exudates surrounded by a wall next to the pancreas. Manifestations are abdominal pain, palpable epigastric mass, nausea, vomiting, and anorexia. The serum amylase level is often high. CT, MRI, and endoscopic ultrasound (EUS) may detect a pseudocyst. The cysts usually resolve spontaneously within a few weeks but may perforate, causing peritonitis or rupture into the stomach or the duodenum. Treatment options include surgical drainage, percutaneous catheter placement and drainage, and endoscopic drainage. When a pseudocyst gets infected, a pancreatic abscess results from extensive necrosis in the pancreas. It may rupture or perforate into adjacent organs. Manifestations of an abscess include upper abdominal pain, abdominal mass, high fever, and leukocytosis. Pancreatic abscesses need prompt surgical drainage to prevent sepsis. The main systemic complications of acute pancreatitis are cardiovascular and pulmonary (pleural effusion, atelectasis, pneumonia, and acute respiratory distress syndrome [ARDS]). The pulmonary complications are due to the passage of exudate containing pancreatic enzymes from the peritoneal cavity through transdiaphragmatic lymph channels. Enzyme-induced inflammation of the diaphragm occurs, with the result being atelectasis caused by reduced diaphragm movement. Trypsin can activate prothrombin and plasminogen, increasing the patient’s risk for intravascular thrombi, pulmonary emboli, and DIC. Hypotension can occur from fluid shifts and sepsis. Tetany, which can be caused by hypocalcemia, is a sign of severe disease. It is due in part to the combining of calcium and fatty acids during fat necrosis. We do not understand the exact mechanisms of how or why hypocalcemia occurs. Patients with severe acute

pancreatitis are at risk for abdominal compartment syndrome from intraabdominal hypertension and edema.

Diagnostic Studies The primary diagnostic tests for acute pancreatitis are serum amylase and lipase (Table 43.18). The serum amylase level is usually high early and stays high for 24 to 72 hours. Serum lipase level, which is high in acute pancreatitis, is an important test because other disorders (e.g., mumps, cerebral trauma, renal transplantation) may increase serum amylase levels. Other serum findings include an increase in liver enzymes, triglycerides, glucose, and bilirubin and a decrease in calcium.

TABLE 43.18 Diagnostic FindingsAcute

Pancreatitis Laboratory Test Serum amylase

Abnormal Finding ↑

Serum lipase



Urinary amylase



Blood glucose



Serum calcium



Serum triglycerides



TABLE 43.19 Interprofessional CareAcute

Pancreatitis

Diagnostic Assessment

• History and physical examination • Serum amylase and lipase • Blood glucose • Serum calcium • Serum triglycerides • Flat plate of the abdomen • Abdominal ultrasound • Endoscopic ultrasound (EUS) • MRCP • ERCP • Contrast-enhanced CT of pancreas • Chest x-ray

Management • NPO with NG tube to suction • Albumin (if shock present) • IV calcium gluconate (10%) (if tetany present) • Lactated Ringer’s solution

Drug Therapy • Pain medication (e.g., morphine) • PPI (e.g., omeprazole [Prilosec]) • Antibiotics (if necrotizing pancreatitis) Diagnostic evaluation of acute pancreatitis is directed at determining the cause. An abdominal ultrasound, x-ray, or contrastenhanced CT scan may identify pancreatic problems. CT scan is the best imaging test for pancreatitis and related complications, such as pseudocysts and abscesses. ERCP is an option (although ERCP can

cause acute pancreatitis), along with EUS, magnetic resonance cholangiopancreatography (MRCP), and angiography. Chest x-rays may show atelectasis and pleural effusions.

Interprofessional Care Goals of interprofessional care for acute pancreatitis include (1) relief of pain, (2) prevention or alleviation of shock, (3) reduction of pancreatic secretions, (4) correction of fluid and electrolyte imbalances, (5) prevention or treatment of infections, and (6) removal of the precipitating cause, if possible (Table 43.19).

Conservative Therapy Treatment of acute pancreatitis is focused on supportive care, including aggressive hydration, pain management, management of metabolic complications, and minimization of pancreatic stimulation. Treatment and control of pain are very important. IV opioid analgesics may be given. Pain medications may be combined with an antispasmodic agent. Atropine and other anticholinergic drugs are avoided when paralytic ileus is present because they can decrease GI mobility, making the problem worse. Other drugs that relax smooth muscles (spasmolytics), such as nitroglycerin or papaverine, may be used. Supplemental O2 is used to maintain O2 saturation greater than 95%. In patients with severe pancreatitis, serum glucose levels are closely monitored for hyperglycemia. If shock is present, blood volume replacements are used. Plasma or plasma volume expanders, such as dextran or albumin, may be given. Lactated Ringer’s solution or other electrolyte solutions can correct fluid and electrolyte problems. Central venous pressure readings can help determine fluid replacement requirements. Vasoactive drugs, such as dopamine, may be needed to increase systemic vascular resistance in those with hypotension.

Check Your Practice

You are a nurse working in the emergency department. Your patient is a 45-yr-old woman who reports acute abdominal pain in her left upper quadrant. She is diagnosed with acute pancreatitis. She tells you, “I’ve been waiting in this emergency room for 8 hours and I’m starving. Why can’t I get something to eat? My pain is so bad; I think it’s becoming worse because you won’t give me food.” • How would you respond? • What information and teaching would you give her? It is important to reduce or suppress pancreatic enzymes to decrease stimulation of the pancreas and allow it to rest. This is achieved in several ways. First, the patient is NPO. Second, NG suction may be used to reduce vomiting and gastric distention and to prevent gastric acidic contents from entering the duodenum. Certain drugs are given to suppress gastric acid secretion (Table 43.20). With resolution of the pancreatitis, the patient resumes oral intake. For the patient with severe acute pancreatitis who does not resume oral intake, EN support may be started. The inflamed and necrotic pancreatic tissue is a good medium for bacterial growth. In patients with acute necrotizing pancreatitis, infection is the leading cause of morbidity and mortality. Therefore it is important to prevent infections. Because many of the organisms come from the intestine, enteral feeding reduces the risk for necrotizing pancreatitis. Monitor the patient closely so that antibiotic therapy can be started early if necrosis and infection occur. Endoscopic- or CT-guided percutaneous aspiration with Gram stain and culture may be done.

Surgical Therapy When the acute pancreatitis is related to gallstones, an urgent ERCP plus endoscopic sphincterotomy (severing of the muscle layers of the sphincter of Oddi) may be done. Laparoscopic cholecystectomy may follow ERCP to reduce the potential for recurrence. Surgical intervention may be needed when the diagnosis is uncertain and for

patients who do not respond to conservative therapy. Those with severe acute pancreatitis may need drainage of necrotic fluid collections. This is done surgically, under CT guidance, or endoscopically. Percutaneous drainage of a pseudocyst can be done, and a drainage tube left in place.

Drug Therapy Several different drugs are used to prevent and treat problems associated with pancreatitis (Table 43.20). Currently, there are no drugs that cure pancreatitis.

TABLE 43.20 Drug TherapyAcute and Chronic

Pancreatitis

Nutritional Therapy Initially, the patient with acute pancreatitis is on NPO status to reduce pancreatic secretion. Depending on the severity of the pancreatitis, EN is started. Because of infection risk, parenteral nutrition is reserved for patients who cannot tolerate EN (see Chapter 39). If IV lipids are given, monitor blood triglyceride levels. In cases of moderate to severe pancreatitis, the patient may need enteral feeding via a jejunal feeding

tube. When food is allowed, small, frequent feedings are given. The diet is high in carbohydrate content because that is the least stimulating to the exocrine part of the pancreas. Suspect intolerance to oral foods when the patient reports pain, has increasing abdominal girth, or has increased serum amylase and lipase levels. Supplemental fat-soluble vitamins may be given.

Nursing Management: Acute Pancreatitis Nursing Assessment Subjective and objective data that should be obtained from a person with acute pancreatitis are outlined in Table 43.21.

Nursing Diagnoses Nursing diagnoses for the patient with acute pancreatitis may include: • Acute pain • Fluid imbalance • Electrolyte imbalance • Impaired nutritional intake Additional information on nursing diagnoses and interventions for the patient with acute pancreatitis is presented in eNursing Care Plan 43.3 available on the website for this chapter.

Planning The overall goals are that the patient with acute pancreatitis will have (1) relief of pain, (2) normal fluid and electrolyte balance, (3) minimal to no complications, and (4) no recurrent attacks.

TABLE 43.21 Nursing AssessmentAcute

Pancreatitis

Subjective Data Important Health Information

Past health history: Biliary tract disease, alcohol use, abdominal trauma, duodenal ulcers, infection, metabolic disorders Medications: Thiazides, NSAIDs Surgery or other treatments: Surgical procedures on the pancreas, stomach, duodenum, or biliary tract. Endoscopic retrograde cholangiopancreatography (ERCP)

Functional Health Patterns Health perception–health management: Chronic alcohol use, fatigue Nutritional-metabolic: Nausea and vomiting, anorexia Activity-exercise: Dyspnea Cognitive-perceptual: Severe midepigastric or left upper quadrant pain that may radiate to the back, worsened by food and alcohol intake, unrelieved by vomiting

Objective Data General Restlessness, anxiety, low-grade fever

Integumentary Flushing, diaphoresis, discoloration of abdomen and flanks, cyanosis, jaundice. Decreased skin turgor, dry mucous membranes

Respiratory Tachypnea, basilar crackles

Cardiovascular Tachycardia, hypotension

Gastrointestinal Abdominal distention, tenderness, and muscle guarding. Decreased bowel sounds

Possible Diagnostic Findings ↑ Serum amylase and lipase, leukocytosis, hyperglycemia, hypocalcemia, abnormal ultrasound and CT scans of pancreas, abnormal ERCP or MRCP

Nursing Implementation Health Promotion The major factors involved in health promotion are (1) assessing the patient for predisposing and etiologic factors and (2) encouraging early treatment of these factors to prevent acute pancreatitis. Encourage the patient to cease alcohol intake, especially if they have had pancreatitis before. Recurrent attacks of pancreatitis may become milder or disappear if alcohol use is stopped. Encourage early diagnosis and treatment of biliary tract disease, such as gallstones.

Acute Care During the acute phase, it is important to monitor vital signs. Hypotension, fever, and tachypnea may compromise hemodynamic stability. Monitor the response to IV fluids. Closely monitor fluid and electrolyte balance. Frequent vomiting, along with gastric suction, may result in decreased chloride, sodium, and potassium levels. Respiratory failure may develop in the patient with severe acute

pancreatitis. Assess respiratory function (e.g., lung sounds, O2 saturation levels). If ARDS develops, the patient may need intubation and mechanical ventilation support.

Safety Alert Respiratory Distress in Acute Pancreatitis • Assess for respiratory distress in the patient with severe acute pancreatitis. • Listen to lung sounds and monitor O2 saturation on a regular basis. Because hypocalcemia can occur, observe for symptoms of tetany, including jerking, irritability, and muscular twitching. Numbness or tingling around the lips and in the fingers is an early sign of hypocalcemia. Assess the patient for a positive Chvostek’s sign or Trousseau’s sign (see Fig. 16.15). Give calcium gluconate (as ordered) to treat symptomatic hypocalcemia. Monitor serum magnesium levels since hypomagnesemia may develop. Because abdominal pain is a primary symptom of pancreatitis, a major focus of your care is pain relief. Pain and restlessness can increase the metabolic rate and contribute to hemodynamic instability. Opioids may be used for pain relief. Assess and document the duration of pain relief. Comfortable positioning, frequent changes in position, and relief of nausea and vomiting help reduce the restlessness that usually accompanies the pain. Assuming positions that flex the trunk and draw the knees up to the abdomen may decrease pain. A side-lying position with the head elevated 45 degrees decreases tension on the abdomen and may help ease the pain. For the patient who is on NPO status or has an NG tube, provide frequent oral and nasal care to relieve the dryness of the mouth and nose. Oral care is essential to prevent parotitis. If the patient is taking

anticholinergics to decrease GI secretions, the mouth will be especially dry. If the patient is taking antacids to neutralize gastric acid secretion, they should be sipped slowly or inserted in the NG tube. Observe for fever and other manifestations of infection in the patient with acute pancreatitis. Respiratory tract infections are common, which causes the patient to take shallow, guarded abdominal breaths. Measures to prevent respiratory tract infections include turning, coughing, deep breathing, and assuming a semiFowler’s position. Other important assessments are observation for signs of paralytic ileus, renal failure, and mental changes. Determine the blood glucose level to assess damage to the β cells of the islets of Langerhans in the pancreas. If patients have surgery to drain necrotic fluid or treat a cyst, they may need special wound care for an anastomotic leak or a fistula. To prevent skin irritation, use skin barriers (e.g., Stomahesive, Karaya Paste), pouching, and drains. In addition to protecting the skin, pouching allows a more accurate determination of fluid and electrolyte losses and increases patient comfort. Sterile pouching systems are available. Consult with a clinical specialist or wound, ostomy, and continence nurse (WOCN).

Ambulatory Care After acute pancreatitis, the patient may need home care follow-up. Because of loss of physical and muscle strength, physical therapy may be needed. Continued care to prevent infection and detect any complications is important. Counseling about abstinence from alcohol is important to prevent the patient from experiencing future attacks of acute pancreatitis and development of chronic pancreatitis. Because nicotine can stimulate the pancreas, smoking should be avoided. Teach the patient and caregiver about the treatment plan, including the importance of taking the required medications and following the recommended diet. Dietary teaching should include fat restriction because fats stimulate the secretion of cholecystokinin, which then stimulates the pancreas. Encourage carbohydrates as they are less

stimulating to the pancreas. Teach the patient to avoid crash and binge dieting because they can precipitate attacks. Teach the patient and caregiver to recognize and report symptoms of infection, diabetes, or steatorrhea (foul-smelling, fatty stools). These changes indicate ongoing destruction of pancreatic tissue and pancreatic insufficiency. The patient may need exogenous enzyme supplementation.

Evaluation The expected outcomes are that the patient with acute pancreatitis will • Have adequate pain control • Maintain adequate fluid and electrolyte balance • Be knowledgeable about the treatment plan to restore health • Get help for alcohol use and smoking cessation (if needed)

Chronic Pancreatitis Chronic pancreatitis is a continuous, prolonged, inflammatory, and fibrosing process of the pancreas. The pancreas is progressively destroyed as it is replaced by fibrotic tissue. Strictures and calcifications may occur in the pancreas.

Etiology and Pathophysiology Chronic pancreatitis can be due to chronic alcohol use; obstruction caused by gallstones, tumor, pseudocysts, or trauma; and systemic diseases (e.g., systemic lupus erythematosus), autoimmune pancreatitis, and cystic fibrosis. Some patients may not have an identifiable risk factor (idiopathic pancreatitis). Chronic pancreatitis may follow acute pancreatitis, but it may also occur in the absence of any history of an acute condition. The most common cause of obstructive pancreatitis is inflammation of the sphincter of Oddi associated with gallstones. Cancer of the ampulla of Vater, duodenum, or pancreas can also cause this type of chronic pancreatitis. The most common cause of nonobstructive pancreatitis (the most common type of chronic pancreatitis) is chronic alcohol use. There is inflammation and sclerosis, mainly in the head of the pancreas and around the pancreatic duct. In some people who drink alcohol, a genetic factor may predispose them to the direct toxic effect of the alcohol on the pancreas.

Clinical Manifestations As with acute pancreatitis, a major manifestation of chronic pancreatitis is abdominal pain. The patient may have episodes of acute pain, but it usually is chronic (recurrent attacks at intervals of months or years). The attacks may become more frequent until they are almost constant, or they may decrease as pancreatic fibrosis

develops. The pain is found in the same areas as in acute pancreatitis, but is usually described as a heavy, gnawing feeling or sometimes as burning and cramp-like. Food or antacids do not relieve the pain. Other manifestations include symptoms of pancreatic insufficiency, including malabsorption with weight loss, constipation, mild jaundice with dark urine, steatorrhea, and diabetes. The steatorrhea may become severe, with voluminous, foul-smelling, fatty stools. Some abdominal tenderness may be present. Chronic pancreatitis is associated with a variety of complications. These include pseudocyst formation, bile duct or duodenal obstruction, pancreatic ascites or pleural effusion, splenic vein thrombosis, pseudoaneurysms, and pancreatic cancer.

Diagnostic Studies Confirming the diagnosis of chronic pancreatitis can be hard. The diagnosis is based on the patient’s signs and symptoms, laboratory studies, and imaging. In chronic pancreatitis, serum amylase and lipase levels may be increased slightly or not at all, depending on the degree of pancreatic fibrosis. Serum bilirubin and alkaline phosphatase levels may be increased. There is usually mild leukocytosis and a high sedimentation rate. ERCP can visualize the pancreatic and common bile ducts. Imaging studies, such as CT, MRI, MRCP, abdominal ultrasound, and EUS, can show a variety of changes, including calcifications, ductal dilation, pseudocysts, and enlargement of the pancreas. Stool samples are examined for fecal fat content. Deficiencies of fatsoluble vitamins and cobalamin, glucose intolerance, and diabetes may occur in those with chronic pancreatitis. A secretin stimulation test can assess the degree of pancreatic dysfunction.

Interprofessional and Nursing Care When the patient with chronic pancreatitis has an acute attack, the therapy is identical to that for acute pancreatitis. At other times, the focus is on prevention of further attacks, relief of pain, and control of

pancreatic exocrine and endocrine insufficiency. It sometimes takes frequent doses of analgesics (morphine, fentanyl patch [Duragesic]) to relieve the pain if dietary measures and enzyme replacement are not effective. Diet, pancreatic enzyme replacement, and control of diabetes are ways to control the pancreatic insufficiency. Small, bland, frequent meals that are low in fat content are recommended to decrease pancreatic stimulation. Smoking is associated with accelerated progression of chronic pancreatitis. Teach the patient not to consume alcohol and caffeinated beverages. If the patient is dependent on alcohol, refer the patient to other resources as needed (see Chapter 10). Pancreatic enzyme products, such as pancrelipase (Pancrease, Zenpep, Creon, Viokace), contain amylase, lipase, and trypsin. They are used to replace the deficient pancreatic enzymes. The enzymes are usually enteric coated to prevent their breakdown or inactivation by gastric acid. They are usually taken with meals and snacks. Teach the patient and caregiver to monitor stools for steatorrhea to help determine the effectiveness of the enzymes. Bile salts may be given to help with fat-soluble vitamin (A, D, E, and K) absorption and prevent further fat loss. If diabetes develops, it is controlled with insulin (most often) or oral hypoglycemic agents. Teach the patient about testing blood glucose levels and drug therapy (see Chapter 48). While acid-neutralizing drugs (e.g., antacids) and acid-inhibiting drugs (e.g., H2 receptor blockers, PPIs) may be given to control gastric acidity, they have little overall effect on patient outcomes. Antidepressants can reduce any neuropathic pain associated with chronic pancreatitis. Treatment of chronic pancreatitis sometimes requires endoscopic therapy or surgery. When biliary disease is present or obstruction or pseudocyst develops, surgery may be needed. Surgical procedures can divert bile flow or relieve ductal obstruction. A choledochojejunostomy diverts bile around the ampulla of Vater, where there may be spasm or hypertrophy of the sphincter. In this procedure, the common bile duct is anastomosed into the jejunum.

Another type of surgical diverting procedure is the Roux-en-Y pancreatojejunostomy, in which the pancreatic duct is opened and an anastomosis made with the jejunum. Pancreatic drainage procedures can relieve ductal obstruction and are often done with ERCP. Some patients may have an ERCP with sphincterotomy and/or stent placement at the site of obstruction. These patients need follow-up procedures, such as ERCP, to either exchange or remove the stent.

Pancreatic Cancer There is a high mortality rate of pancreatic cancer with the incidence almost equal to the mortality rates. The median age at diagnosis is around 71 years of age.15 Most pancreatic tumors are adenocarcinomas that begin in the epithelium of the ductal system. More than half of the tumors occur in the head of the pancreas. As the tumor grows, the common bile duct becomes obstructed and obstructive jaundice develops. Tumors starting in the body or the tail often remain silent until their growth is advanced. Most cancers have metastasized at the time of diagnosis. The signs and symptoms of pancreatic cancer are similar to those of chronic pancreatitis. The prognosis of a patient with cancer of the pancreas is poor. Most patients die within 5 to 12 months of diagnosis. The 5-year survival rate is only 8%.15

Etiology and Pathophysiology The cause of pancreatic cancer is unknown. Risk factors for pancreatic cancer include chronic pancreatitis, diabetes, age, cigarette smoking, family history of pancreatic cancer, high-fat diet, and exposure to chemicals, such as benzidine. Blacks have a higher incidence of pancreatic cancer than whites. The most established risk factor is cigarette smoking. Smokers are 2 to 3 times more likely to develop pancreatic cancer than nonsmokers. The risk is related to both the duration and number of cigarettes smoked.

Clinical Manifestations Common manifestations include abdominal pain (dull, aching), anorexia, rapid and progressive weight loss, nausea, and jaundice. The most common manifestations with cancer of the head of the pancreas are pain, jaundice, and weight loss. In general, pain is common and is related to the cancer’s location. The pain is often in the

upper abdomen or left hypochondrium and often radiates to the back. It is often related to eating and occurs at night. Extreme, unrelenting pain is related to extension of the cancer into the retroperitoneal tissues and nerve plexuses. Pruritus may accompany obstructive jaundice. Weight loss is due to poor digestion and absorption caused by lack of digestive enzymes from the pancreas.

Diagnostic Studies Abdominal ultrasound or EUS, spiral CT scan, ERCP, MRI, and MRCP are the most often used diagnostic imaging techniques for pancreatic diseases, including cancer. EUS involves imaging the pancreas with the use of an endoscope positioned in the stomach and duodenum. EUS also allows for fine-needle aspiration of the tumor for pathologic examination. CT scan is often the first study and gives information on metastasis and vascular involvement of the tumor. ERCP allows visualization of the pancreatic duct and biliary system. With ERCP, pancreatic secretions and tissue can be obtained for biopsy and analysis of tumor markers. MRI, PET, PET/CT scans and MRCP may be done to confirm a cancer diagnosis and determine staging. They can also monitor progress and response to therapy. Tumor markers are used both for diagnosing pancreatic cancer and monitoring the response to treatment. Cancer-associated antigen 19-9 (CA 19-9) is increased in pancreatic cancer. It is the most commonly used tumor marker. However, CA 19-9 also can be increased in gallbladder cancer or in benign conditions, such as acute and chronic pancreatitis, hepatitis, and biliary obstruction.

Interprofessional Care Surgery is the most effective treatment for pancreatic cancer. Only 15% to 20% of patients have resectable tumors at the time of diagnosis. With the use of neoadjuvant chemotherapy (treatment before surgery), more patients can eventually become surgical candidates. The type of surgery depends on the size and location of the tumor. Pancreatic head tumors require the classic Whipple procedure or

pancreaticoduodenectomy (Fig. 43.13). In the Whipple surgery, the proximal pancreas (proximal pancreatectomy), along with duodenum (duodenectomy), distal segment of the common bile duct and distal part of the stomach (partial gastrectomy) are removed together followed by a surgical anastomosis of the pancreatic duct, common bile duct, and stomach to the jejunum. Pancreatic body and/or tail tumors require a distal pancreatectomy procedure. Sometimes, a total pancreatectomy is done. It causes diabetes and the patient is dependent on exogenous insulin and pancreatic enzyme supplementation for life. If the pancreatic tumor cannot be removed surgically, palliative measures, such as a cholecystojejunostomy, to relieve biliary obstruction and/or endoscopically placed biliary stents, can be done. Radiation therapy alone has little effect on survival but may be effective for pain relief. External radiation is most common, but implantation of internal radiation seeds into the tumor has been used. The current role of chemotherapy is limited and can have a significant side effect profile. Chemotherapy usually consists of fluorouracil and gemcitabine (Gemzar) either alone or in combination with agents such as capecitabine (Xeloda), paclitaxel (Abraxane), erlotinib (Tarceva), or irinotecan (Onivyde). Erlotinib is a targeted therapy drug (see Chapter 15).

FIG. 43.13 Whipple procedure or radical pancreaticoduodenectomy. This surgical procedure involves resecting the proximal pancreas, adjoining duodenum, distal part of the stomach, and distal part of the common bile duct. An anastomosis of the pancreatic duct, common bile

duct, and stomach to the jejunum is done. From Butcher GP: Gastroenterology: An illustrated colour text, London, 2004, Churchill Livingstone.

Nursing Management: Pancreatic Cancer Because the patient with pancreatic cancer has many of the same problems as the patient with pancreatitis, nursing care includes many of the same measures (see sections on acute and chronic pancreatitis on pp. 995 and 996). Provide symptomatic and supportive nursing care. This includes giving medications and providing comfort measures to relieve pain. Psychologic support is essential, especially during times of anxiety or depression. Adequate nutrition is an important part of the nursing care plan. Frequent and supplemental feedings may be needed. Include measures to stimulate the appetite as much as possible and to manage anorexia, nausea, and vomiting. If the patient is undergoing radiation therapy, observe for adverse reactions, such as anorexia, nausea, vomiting, and skin irritation. The prognosis for a patient with pancreatic cancer is poor. A significant part of the nursing care is helping the patient and caregiver cope with the diagnosis and prognosis. Chapter 9 provides information on palliative and end-of-life care.

Disorders of The Biliary Tract Cholelithiasis and Cholecystitis The most common disorder of the biliary system is cholelithiasis (stones in the gallbladder) (Fig. 43.14). The gallstones may lodge in the neck of the gallbladder or in the cystic duct. Cholecystitis (inflammation of the gallbladder wall) is usually associated with gallstones. They usually occur together, although a person can have gallstones without cholecystitis. Cholecystitis may present acutely or chronically. Gallbladder disease is a common health problem in the United States. Up to 10% of American adults have cholecystitis caused by gallstones. The actual number is not known because many persons with stones are asymptomatic. Cholecystectomy (removal of the gallbladder) is among the most common surgical procedures done in the United States. Gallstones are more common in women, especially multiparous women and women over 40 years of age. Postmenopausal women on estrogen replacement therapy and younger women on oral contraceptives are at an increased risk for gallbladder disease. Oral contraceptives affect cholesterol production and increase gallbladder cholesterol saturation. Other factors that increase the occurrence of gallbladder disease are a sedentary lifestyle, a familial tendency, and obesity. Obesity causes increased secretion of cholesterol in bile. The incidence of gallbladder disease is especially high in the Native American population.

FIG. 43.14 Cholesterol gallstones in a gallbladder that was removed. From Kumar V, Abbas AK, Aster JC, et al: Robbins and Cotran pathologic basis of disease, ed 8, Philadelphia, 2010, Saunders.

Gender Differences Cholelithiasis

Men • Incidence is lower in men than in women. • Gender differences in incidence decrease after age 50.

Women

• Pregnancy is the greatest risk factor for increased prevalence in women. • Obesity increases the risk, especially for women.

Etiology and Pathophysiology Cholelithiasis The cause of gallstones is unknown. They develop when the balance that keeps cholesterol, bile salts, and calcium in solution is changed so that these substances precipitate. Conditions that upset this balance include infection and changes in cholesterol metabolism. In patients with gallstones, the bile secreted by the liver is supersaturated with cholesterol (lithogenic bile). The bile in the gallbladder then becomes supersaturated with cholesterol and precipitation of cholesterol occurs in the gallbladder. Other components of bile that precipitate into stones are bile salts, bilirubin, calcium, and protein. Mixed cholesterol stones, which are mainly cholesterol, are the most common gallstones. Changes in the composition of bile are significant in gallstone formation. Bile stasis leads to progression of the supersaturation and changes in the chemical composition of the bile (biliary sludge). Immobility, pregnancy, and inflammatory or obstructive lesions in the biliary system decrease bile flow. Hormonal factors during pregnancy may cause delayed emptying of the gallbladder, resulting in bile stasis. The stones may stay in the gallbladder or migrate to the cystic duct or the common bile duct. They cause pain as they pass through the ducts, and they may lodge in the ducts and cause an obstruction. Small stones are more likely to move into a duct and cause obstruction. Table 43.22 describes the changes and manifestations that occur when the stones obstruct the common bile duct. If the blockage occurs in the cystic duct, the bile can continue to flow into the duodenum directly from the liver. However, when the bile in the gallbladder cannot escape, this stasis of bile may lead to cholecystitis.

Cholecystitis Cholecystitis is most often associated with obstruction caused by gallstones or biliary sludge. Cholecystitis in the absence of obstruction (acalculous cholecystitis) occurs most often in older adults and in patients who are critically ill. Acalculous cholecystitis is also associated with prolonged immobility and fasting, prolonged parenteral nutrition, and diabetes. We think the main cause of this illness is bile stasis. Critically ill patients are more predisposed because of increased bile viscosity due to fever and dehydration and because of prolonged absence of oral feeding resulting in a decrease or absence of cholecystokinin-induced gallbladder contraction. Other risk factors include adhesions, cancer, anesthesia, and opioids.

TABLE 43.22 Manifestations of Obstructed Bile

Flow Manifestation Bleeding tendencies Clay-colored stools

Etiology Lack of or ↓ absorption of vitamin K, resulting in ↓ production of prothrombin No bilirubin reaching small intestine to be converted to urobilinogen

Dark amber to brown urine, which foams when shaken

↑ Water-soluble (conjugated) bilirubin elimination in urine

Fever and chills

Bacterial reflux from biliary tract to systemic circulation

Intolerance for fatty foods

No bile in small intestine for fat digestion

Jaundice

No bile flow into duodenum, bilirubin accumulates in blood

Pruritus

Deposition of bile salts in skin tissues

Steatorrhea

Undigested fatty components of food are eliminated in stool. Occurs because no bile in small intestine, thus preventing emulsion, digestion, and absorption of fat No bilirubin reaching small intestine to be converted to urobilinogen

Urobilinogen absent in urine

Once acalculous cholecystitis is present, secondary infection with enteric pathogens, including E. coli, Enterococcus faecalis, Klebsiella, Pseudomonas, and Proteus, is common. Perforation occurs in severe cases. Inflammation is the major pathophysiologic condition. It may be confined to the mucous lining or involve the entire wall of the gallbladder. During an acute attack of cholecystitis, the gallbladder is edematous and hyperemic, and it may be distended with bile or pus. The cystic duct is also involved and may become occluded. The wall of the gallbladder becomes scarred after an acute attack. Decreased functioning will occur if large amounts of tissue become fibrotic.

Clinical Manifestations Gallstones may produce a range of symptoms. The severity depends on whether the stones are stationary or mobile and whether obstruction is present. When a stone is lodged in the ducts or when stones are moving through the ducts, spasms may result in response to the stone. This sometimes causes severe pain, which is termed biliary colic, even though the pain is rarely colicky. The pain is more often steady. The pain can be excruciating and accompanied by tachycardia, diaphoresis, and prostration. The severe pain may last up to an hour, and when it subsides, there is residual tenderness in the right upper quadrant. The attacks of pain often occur 3 to 6 hours after a high-fat meal or when the patient lies down. When total obstruction occurs, symptoms related to bile blockage occur (Table 43.22). If the common bile duct is obstructed, no bilirubin will reach the small intestine to be converted to urobilinogen. Thus the kidneys will excrete bilirubin, causing dark amber to brown urine. Manifestations of cholecystitis vary from indigestion to moderate to severe pain, fever, chills, and jaundice. Initial symptoms of acute cholecystitis include indigestion and acute pain and tenderness in the right upper quadrant. Pain may be referred to the right shoulder and scapula. The pain may be accompanied by nausea and vomiting, restlessness, and diaphoresis. Inflammation results in leukocytosis and fever. Physical findings include right upper quadrant or

epigastrium tenderness and abdominal rigidity. Chronic cholecystitis may present with a history of fat intolerance, dyspepsia, heartburn, and flatulence.

Complications Complications of gallstones and cholecystitis include gangrenous cholecystitis, subphrenic abscess, pancreatitis, cholangitis (inflammation of biliary ducts), biliary cirrhosis, fistulas, and rupture of the gallbladder, which can cause bile peritonitis. In older adults and those with diabetes, gangrenous cholecystitis and bile peritonitis are the most common complications of cholecystitis. Choledocholithiasis (stone in the common bile duct) may occur, producing symptoms of obstruction.

Diagnostic Studies Ultrasound is often used to diagnose gallstones (see Table 38.11). It is especially useful for patients with jaundice (because it does not depend on renal function) and for patients who are allergic to contrast medium. ERCP allows for visualization of the gallbladder, cystic duct, common hepatic duct, and common bile duct. Bile taken during ERCP is sent for culture to identify possible infecting organisms. Percutaneous transhepatic cholangiography is the insertion of a needle directly into the gallbladder duct followed by injection of contrast materials. It is generally done after ultrasound shows a bile duct blockage. Laboratory tests may reveal an increased WBC count because of inflammation. Serum enzymes (e.g., alkaline phosphatase, ALT, and AST), direct and indirect bilirubin levels, and urinary bilirubin levels may be increased if an obstructive process is present (Table 43.3). Serum amylase is increased if there is pancreatic involvement.

Interprofessional Care Once gallstones become symptomatic, definitive surgical intervention with cholecystectomy is usually needed. However, in some cases,

conservative therapy may be considered.

Conservative Therapy Cholelithiasis The treatment of gallstones depends on the stage of disease. Bile acids (cholesterol solvents), such as ursodeoxycholic acid (Ursodiol) and chenodeoxycholic acid (Chenodiol), are used to dissolve stones. However, the gallstones may recur. We usually do not treat gallstones with drugs because of the high use and success of laparoscopic cholecystectomy. ERCP with endoscopic sphincterotomy (papillotomy) may be used to remove stones (Fig. 43.15). ERCP allows for visualization of the biliary system, dilation (balloon sphincteroplasty), and placement of stents and sphincterotomy. Special catheters with wire baskets or inflatable balloon tip may be used for stone removal.16 When a stent is placed, it is generally removed or changed after a few months. Extracorporeal shock-wave lithotripsy (ESWL) is an alternative treatment used when endoscopic approaches cannot remove stones. In ESWL, a lithotripter uses high-energy shock waves to disintegrate gallstones. It usually takes 1 to 2 hours to disintegrate the stones. After they are broken up, the fragments pass through the common bile duct and into the small intestine. Usually ESWL and oral dissolution therapy are used together.

FIG. 43.15 During endoscopic sphincterotomy, an endoscope is advanced through the mouth and stomach until its tip sits in the duodenum opposite the common bile duct. Inset, After widening the duct mouth by incising the sphincter muscle, the HCP advances a basket attachment into the duct and snags the stone.

TABLE 43.23 Interprofessional

CareCholelithiasis and Acute Cholecystitis

Diagnostic Assessment

• History and physical examination • Ultrasound • ERCP • Percutaneous transhepatic cholangiography • Liver function tests • White blood cell count • Serum bilirubin

Management Conservative Therapy • IV fluid • NPO with NG tube, later progressing to low-fat diet • Antiemetics • Analgesics • Fat-soluble vitamins (A, D, E, and K) • Anticholinergics (antispasmodics) • Antibiotics (for secondary infection) • Transhepatic biliary catheter • ERCP with sphincterotomy (papillotomy) • Extracorporeal shock-wave lithotripsy

Dissolution Therapy • ursodeoxycholic acid (ursodiol [Actigall])

Surgical Therapy • Laparoscopic cholecystectomy • Incisional (open) cholecystectomy

Cholecystitis During an acute episode of cholecystitis, treatment focuses on pain control, control of infection with antibiotics, and maintaining fluid and electrolyte balance (Table 43.23). Treatment is supportive and focused on symptom management. If nausea and vomiting are severe, NG tube insertion and gastric decompression may be used to prevent further gallbladder stimulation. A cholecystostomy may be used to drain purulent material from the obstructed gallbladder. Opioids are given for pain management. Anticholinergics may be used to decrease GI secretions and counteract smooth muscle spasms.

Surgical Therapy Laparoscopic cholecystectomy is the treatment of choice for symptomatic gallstones. About 90% of cholecystectomies are done laparoscopically. In this procedure, the gallbladder is removed through 1 to 4 small punctures in the abdomen. The HCP makes a small cut below the umbilicus and inserts a needle into the area. CO2 gas is passed into the abdomen to expand the area, which allows the HCP to see the organs more clearly and gives more room to work. A laparoscope, which has a camera attached, and grasping forceps are inserted into the abdomen through the punctures. Using closed-circuit monitors to view the abdominal cavity, the HCP retracts and dissects the gallbladder and removes it with grasping forceps. This is a safe and routine procedure with minimal morbidity and quick recovery time. Most patients have minimal postoperative pain and are discharged the day of surgery or the day after. They can usually resume normal activities and return to work within 1 week. The main complication is injury to the common bile duct. The few contraindications to laparoscopic cholecystectomy include peritonitis, cholangitis, gangrene or perforation of the gallbladder, portal hypertension, and serious bleeding disorders. Some patients may need an incisional (open) cholecystectomy. This involves removing the gallbladder through a right subcostal incision. A T tube may be inserted into the common bile duct during surgery

when a common bile duct exploration is part of the surgical procedure (Fig. 43.16). This ensures patency of the duct until the edema from the trauma of exploring and probing the duct has subsided. It also allows excess bile to drain while the small intestine is adjusting to receiving a continuous flow of bile.

Transhepatic Biliary Catheter The transhepatic biliary catheter can be used preoperatively in biliary obstruction and in hepatic dysfunction from obstructive jaundice. It also can be inserted for palliative care when inoperable liver, pancreatic, or bile duct cancer obstructs bile flow. The catheter is used when endoscopic drainage has been unsuccessful. The catheter is inserted percutaneously and allows for decompression of obstructed extrahepatic bile ducts so that bile can flow freely. After placement of the catheter into the obstructed duct internally, the external catheter is connected to a drainage bag. Encourage patients to replace fluids lost in the drainage bag with electrolyte-rich drinks. Cleanse the skin around the catheter insertion site daily with an antiseptic. Observe for bile leakage at the insertion site and any signs or symptoms of sudden abdominal pain, nausea, fever, or chills that may signal an occluded or malfunctioning drain.

FIG. 43.16 Placement of T tube. Dotted lines show parts removed.

Drug Therapy The most common drugs used in the treatment of gallbladder disease are analgesics, anticholinergics (antispasmodics), fat-soluble vitamins, and bile salts. Morphine may be used initially for pain management. Anticholinergics, such as atropine and other antispasmodics, may be used to relax the smooth muscle and decrease ductal tone. The patient with chronic gallbladder disease or any biliary tract

obstruction may need fat-soluble vitamin (A, D, E, and K) replacement. Bile salts may be given to help digestion and vitamin absorption. Cholestyramine may provide relief from pruritus. Cholestyramine is a resin that binds bile salts in the intestine, increasing their excretion in the feces. It comes in powder form that is mixed with milk or juice. Side effects include nausea, vomiting, diarrhea or constipation, and skin reactions. Cholestyramine may bind with other medications, so check drug-to-drug interactions.

Nutritional Therapy People have fewer gallbladder problems if they eat smaller, more frequent meals with some fat at each meal to promote gallbladder emptying. If obesity is a problem, a reduced-calorie diet is indicated. The diet should be low in saturated fats (e.g., butter, shortening, lard) and high in fiber and calcium. Rapid weight loss should be avoided because it can promote gallstone formation. After a laparoscopic cholecystectomy, teach the patient to have liquids for the rest of the day and eat light meals for a few days. After an incisional cholecystectomy, the patient will progress from liquids to a regular diet once bowel sounds have returned. The amount of fat in the postoperative diet depends on the patient’s tolerance of fat. A low-fat diet may be helpful if the flow of bile is reduced (usually only in the early postoperative period) or if the patient is overweight. Sometimes the patient must restrict fats for 4 to 6 weeks. Otherwise, no special diet is needed other than to eat nutritious meals and avoid excess fat intake.

Nursing Management: Gallbladder Disease Nursing Assessment Subjective and objective data that should be obtained from a person with gallbladder disease are outlined in Table 43.24.

Nursing Diagnoses Nursing diagnoses for the patient with gallbladder disease treated surgically may include: • Acute pain • Lack of knowledge

Planning The overall goals are that the patient with gallbladder disease will have (1) relief of pain and discomfort, (2) no complications postoperatively, and (3) no recurrent attacks of cholecystitis or gallstones.

TABLE 43.24 Nursing AssessmentCholecystitis or

Cholelithiasis

Subjective Data Important Health Information Past health history: Obesity, multiparity, infection, cancer, extensive fasting, pregnancy Medications: Estrogen or oral contraceptives

Surgery or other treatments: Abdominal surgery

Functional Health Patterns Health perception–health management: Positive family history, sedentary lifestyle Nutritional-metabolic: Weight loss, anorexia, indigestion, fat intolerance, nausea and vomiting, dyspepsia, chills Elimination: Clay-colored stools, steatorrhea, flatulence. Dark urine Cognitive-perceptual: Moderate to severe pain in right upper quadrant that may radiate to the back or scapula. Itching

Objective Data General Fever, restlessness

Integumentary Jaundice, icteric sclera, diaphoresis

Respiratory Tachypnea, splinting during respirations

Cardiovascular Tachycardia

Gastrointestinal

Palpable gallbladder, abdominal guarding, and distention

Possible Diagnostic Findings ↑ Serum liver enzymes, alkaline phosphatase, and bilirubin. Absence of urobilinogen in urine, ↑ urinary bilirubin, leukocytosis. Abnormal gallbladder ultrasound

Nursing Implementation Health Promotion Be aware of predisposing factors for gallbladder disease in general health screening. Teach patients from ethnic groups in which the disease is more common, such as Native Americans, the early manifestations and to see their HCP if these manifestations occur. Patients with chronic cholecystitis may not have acute symptoms and may not seek help until jaundice and biliary obstruction occur. Earlier detection in these patients is important so that they can be managed with a low-fat diet and monitored more closely.

Acute Care Nursing goals for the patient undergoing conservative therapy include (1) treat pain, (2) relieve nausea and vomiting, (3) provide comfort and emotional support, (4) maintain fluid and electrolyte balance and nutrition, and (5) observe for complications. The patient with acute cholecystitis or gallstones often has severe pain. Give the drugs ordered to relieve the pain as needed before pain becomes severe. Observe for side effects of the drugs as part of the continued assessment. Nursing comfort measures, such as a clean bed, comfortable positioning, and oral care, are appropriate. Some patients have more severe nausea and vomiting than others. For these patients, an NG tube and gastric decompression may be ordered. Eliminating intake of food and fluids prevents further stimulation of the gallbladder. Oral hygiene, care of nares, accurate

intake and output measurements, and maintaining suction should be a part of the nursing care plan. For patients with less severe nausea and vomiting, antiemetics are usually adequate. When the patient is vomiting, provide comfort measures, such as frequent mouth rinses. Remove any vomitus at once from the patient’s view. If itching occurs with jaundice, use measures to relieve itching. These can include antihistamines or other treatments as previously discussed. Assess for progression of the symptoms and development of complications. Observe for signs of obstruction of the ducts by stones. These include jaundice; clay-colored stools; dark, foamy urine; steatorrhea; fever; and increased WBC count. When manifestations of obstruction are present (Table 43.22), bleeding may result from decreased prothrombin production by the liver. Common sites to observe for bleeding are the mucous membranes of the mouth, nose, gingivae, and injection sites. When giving injections, use a small-gauge needle and apply gentle pressure after the injection. Know the patient’s PT time and use it as a guide in the assessment process. Assessment for infections includes monitoring vital signs. A temperature elevation with chills and jaundice may indicate choledocholithiasis. Your care of the patient after ERCP with papillotomy includes assessment to detect complications, such as pancreatitis, perforation, infection, and bleeding. Monitor the patient’s vital signs. Abdominal pain, fever, and increasing amylase and lipase may indicate acute pancreatitis. The patient should be on bed rest for several hours and should be NPO until the gag reflex returns. Teach the patient the need for follow-up if the stent is to be removed or changed.

Postoperative Care Postoperative nursing care after a laparoscopic cholecystectomy includes monitoring for complications, such as bleeding, making the patient comfortable, and preparing the patient for discharge. Patients may report referred pain to the shoulder because of the CO2 that the HCP uses to inflate the abdominal cavity during surgery. It may not

be released or absorbed by the body. The CO2 can irritate the phrenic nerve and diaphragm, causing some difficulty in breathing. Placing the patient in the Sims’ position (on left side with right knee flexed) helps move the gas pocket away from the diaphragm. Encourage deep breathing along with movement and ambulation. NSAIDs or codeine can usually relieve pain. The patient is allowed clear liquids and can walk to the bathroom to void. Most patients go home the same day. Postoperative nursing care for incisional cholecystectomy focuses on adequate ventilation and prevention of respiratory complications. Other nursing care is the same as general postoperative nursing care (see Chapter 19). If the patient has a T tube (Fig. 43.16), maintain the system and monitor T-tube function and drainage. The T tube is usually connected to a closed gravity drainage system. If the Penrose or Jackson-Pratt drain or the T tube is draining large amounts of bile, it is helpful to use a sterile pouching system to protect the skin. Encourage the patient to replace any lost fluids and electrolytes.

Ambulatory Care When the patient has conservative therapy, nursing management depends on the patient’s symptoms and on whether surgical intervention is planned. Dietary teaching is usually needed. The diet is usually low in fat. The patient may need to take fat-soluble vitamin supplements. If needed, review a weight-reduction diet. Teach the patient signs and symptoms of obstruction (e.g., stool and urine changes, jaundice, itching). Explain the importance of continued health care follow-up.

TABLE 43.25 Patient & Caregiver

TeachingPostoperative Laparoscopic Cholecystectomy Postoperative teaching should include:

1. Remove the bandages on the puncture sites the day after surgery and you can shower. 2. Notify your HCP if any of the following signs and symptoms occurs: • Redness, swelling, bile-colored drainage or pus from any incision • Severe abdominal pain, nausea, vomiting, fever, chills 3. You can gradually resume normal activities. 4. Return to work within 1 wk of surgery. 5. You can resume your usual diet, but a low-fat diet is usually better tolerated for several weeks after surgery. The patient who undergoes a laparoscopic cholecystectomy is discharged soon after the surgery, so home care and teaching are important (Table 43.25). After an incisional cholecystectomy, tell the patient to avoid heavy lifting for 4 to 6 weeks. Usual sexual activities, including intercourse, can be resumed as soon as the patient feels ready, unless otherwise instructed by the HCP. Sometimes the patient needs to remain on a low-fat diet for 4 to 6 weeks. If so, an individualized dietary teaching plan is needed. A weight-reduction program may be helpful if the patient is overweight. Most patients tolerate a regular diet with no problems but should avoid excess fats.

Evaluation The overall expected outcomes are that the patient with gallbladder disease will • Appear comfortable and have pain relief • State knowledge of activity level and dietary restrictions

Gallbladder Cancer Gallbladder cancer is the sixth most common GI cancer in the United States.17 Most gallbladder cancers are adenocarcinomas. They are often found incidentally as the patient is asymptomatic. The majority have advanced disease at the time of diagnosis. The early symptoms are insidious and similar to those of chronic cholecystitis and gallstones, which makes the diagnosis difficult. Later symptoms are usually those of biliary obstruction. Diagnosis and staging of gallbladder cancer are done using EUS, abdominal ultrasound, CT, MRI, and/or MRCP. Unfortunately, gallbladder cancer often is not detected until the disease is advanced. When it is found early, surgery can be curative. Several factors influence successful surgical outcomes, including the depth of cancer invasion, extent of liver involvement, venous or lymphatic invasion, and lymph node metastasis. Extended cholecystectomy with lymph node dissection has improved outcomes for those with gallbladder cancer. When surgery is not an option, endoscopic stenting of the biliary tract can reduce obstructive jaundice. Adjuvant therapies, including radiation therapy and chemotherapy, may be used depending on the disease state. Overall, gallbladder cancer has a poor prognosis. Nursing management involves palliative care with special attention to nutrition, hydration, skin care, and pain relief. Nursing care measures used for patients with cholecystitis and gallstones and for the patient with cancer (see Chapter 15) are appropriate.

Case Study Cirrhosis of the Liver

© sbeagle/iStock/Thinkstock.

Patient Profile M.B., a 58-yr-old male rancher who lives in rural Wyoming, is admitted with a diagnosis of cirrhosis of the liver. He has been vomiting for 2 days and noticed blood in the toilet when he vomited. He lives 40 miles from the nearest hospital. He had one of his ranch hands drive him to the hospital. His medical history includes chronic hepatitis C, depression, and stage II chronic kidney disease.

Subjective Data • Has been estranged from his 2 children since his divorce 3 years ago

• Has had cirrhosis for 12 yrs • Acknowledges that he had been drinking heavily for 20 yrs but has been sober for the past 2 yrs • Reports experiencing anorexia, nausea, and abdominal discomfort

Objective Data Physical Examination • Has moderate ascites • Has jaundice of sclera and skin • Has 4+ pitting edema of the lower extremities • Liver and spleen are palpable

Laboratory Values • Total bilirubin: 15 mg/dL (257 mmol/L) • AST: 190 U/L (3.2 µkat/L) • ALT: 210 U/L (3.5 µkat/L) • Platelets: 45,000/µL • eGFR: 62 mL/min • ECG is below:

Discussion Questions 1. What are possible causes of cirrhosis? What type of cirrhosis does M.B. likely have? 2. Describe the pathophysiologic changes that occur in the liver as cirrhosis develops. 3. List M.B.’s clinical manifestations of liver failure. For each manifestation, explain the pathophysiologic basis. 4. Explain the significance of the results of his laboratory values and ECG findings. 5. If M.B. begins to show signs and symptoms of hepatic encephalopathy, what would you monitor? What measures would be used to control or decrease the encephalopathy? 6. What are possible causes of his GI bleeding? 7. Priority Decision: Based on the assessment data, what are the priority nursing diagnoses? Are there any collaborative problems? 8. Priority Decision: What are the priority nursing interventions for a patient at this stage of his illness? 9. Evidence-Based Practice: M.B. discusses his prognosis with you. He says, “There is no hope. I might as well keep drinking.” How would you respond to his statement? 10. Safety: Given M.B.’s bleeding history and current laboratory values, identify areas of injury risk and specify actions you will take to ensure patient safety. 11. Develop a conceptual care map for M.B. Answers and corresponding conceptual care map available at evolve.elsevier.com/Lewis/medsurg.

Case Study Managing Care of Multiple Patients

You are working on the medical-surgical unit and have been assigned to care for the following 5 patients. You have 1 LPN and 1 UAP who are assigned to help you.

Discussion Questions

1. Priority Decision: After receiving report, which patient should you see first? Provide a rationale for your decision. 2. Collaboration: Which tasks could you delegate to the LPN? (select all that apply) a. Administer a bolus enteral tube feeding to M.S. b. Assess L.C.’s dressing, pain level, and bowel sounds. c. Administer a scheduled dose of oral lactulose solution to M.B. d. Because she speaks Vietnamese, teach F.H.’s wife about his disease. e. Perform bedside glucometer reading and administer oral medications to S.R. 3. Priority Decision: Which diagnostic finding should you report to the health care provider immediately? a. Hemoglobin 7.9 g/dL and hematocrit 25% for F.H. b. Serum albumin 2.7 g/dL and prealbumin 11.2 g/dL for M.S. c. Cholesterol 250 mg/dL and triglycerides 202 mg/dL for S.R. d. Total bilirubin 3.2 mg/dL with positive urine bilirubin for M.B. 4. Priority Decision: As you are assessing M.B., the LPN informs you that F.H. just vomited a large amount of bright red blood. What initial action would be most appropriate? a. Have the LPN administer an antiemetic to F.H. b. Ask the LPN to notify F.H.’s health care provider. c. Leave M.B.’s room to perform a focused assessment on F.H. d. Ask the UAP to obtain a unit of packed RBCs from the blood bank.

Case Study Progression When you enter F.H.’s room, he tells you that his pain actually feels somewhat relieved since he vomited. However, you note that his skin is cool and clammy, his BP is 90/54 mm Hg, and his heart rate is 116

bpm. You notify his HCP. 4. Which interventions would you expect the HCP to order for F.H.? (select all that apply) a. Stat hemoglobin and hematocrit b. Emergent endoscopy with band ligation c. Discontinue the pantoprazole (Protonix) infusion d. Start a second IV site and administer a 500 mL normal saline bolus e. Contact HCP and notify operating room that patient is unstable and needs surgery 5. Priority Decision: After giving a bolus feeding of enteral nutrition to M.S., it would be most important to a. assess for gastric residual. b. obtain an abdominal x-ray. c. keep head of bed elevated 30 to 45 degrees. d. record the total amount of fluid administered. 6. Which intervention to treat ascites would you expect the HCP to order for M.B.? (select all that apply) a. Paracentesis b. 2 g sodium diet c. Diuretic therapy d. 1800 mL/day fluid restriction e. Shunt insertion from peritoneum to heart 7. Management Decision: As you enter the nurse’s station, you overhear derogatory comments made by the UAP to the LPN about S.R.’s weight. Which response would be most appropriate? a. Report the incident to charge nurse for follow-up. b. Talk to the UAP to discuss a possible HIPAA violation. c. Talk to S.R. about the impact of UAP’s bias on the patient’s self-image. d. Set up an in-service to teach staff members to recognize obesity as a disease process.

Answers and rationales available at http://evolve.elsevier.com/Lewis/medsurg.

Bridge to Nclex Examination The number of the question corresponds to the same-numbered outcome at the beginning of the chapter.

1. A patient with hepatitis A is in the acute phase. The nurse plans care for the patient based on the knowledge that a. itching is a common problem with jaundice in this phase. b. the patient is most likely to transmit the disease during this phase. c. gastrointestinal symptoms are not as severe in hepatitis A as they are in hepatitis B. d. extrahepatic manifestations of glomerulonephritis and polyarteritis are common in this phase. 2. A patient with acute hepatitis B is being discharged. The discharge teaching plan should include instructions to a. avoid alcohol for the first 3 weeks. b. use a condom during sexual intercourse. c. have family members get an injection of immunoglobulin. d. follow a low-protein, moderate-carbohydrate, moderatefat diet. 3. A patient has been told that she has elevated liver enzymes caused by nonalcoholic fatty liver disease (NAFLD). The nursing teaching plan should include a. having genetic testing done. b. recommending a heart-healthy diet.

c. the necessity to reduce weight rapidly. d. avoiding alcohol until liver enzymes return to normal. 4. The patient with advanced cirrhosis asks why his abdomen is so swollen. The nurse’s response is based on the knowledge that a. a lack of clotting factors promotes the collection of blood in the abdominal cavity. b. portal hypertension and hypoalbuminemia cause a fluid shift into the peritoneal space. c. decreased peristalsis in the GI tract contributes to gas formation and distention of the bowel. d. bile salts in the blood irritate the peritoneal membranes, causing edema and pocketing of fluid. 5. In planning care for a patient with metastatic liver cancer, the nurse should include interventions that a. focus primarily on symptomatic and comfort measures. b. reassure the patient that chemotherapy offers a good prognosis. c. promote the patient’s confidence that surgical excision of the tumor will be successful. d. provide information needed for the patient to make decisions about liver transplantation. 6. Nursing management of the patient with acute pancreatitis includes (select all that apply) a. administering pain medication. b. checking for signs of hypocalcemia. c. providing a diet low in carbohydrates.

d. giving insulin based on a sliding scale. e. monitoring for infection, particularly respiratory tract infection. 7. A patient with pancreatic cancer is admitted to the hospital for evaluation of treatment options. The patient asks the nurse to explain the Whipple procedure that the surgeon has described. The explanation includes the information that a Whipple procedure involves a. creating a bypass around the obstruction caused by the tumor by joining the gallbladder to the jejunum. b. resection of the entire pancreas and the distal part of the stomach, with anastomosis of the common bile duct and the stomach into the duodenum. c. removal of part of the pancreas, part of the stomach, the duodenum, and the gallbladder, with joining of the pancreatic duct, the common bile duct, and the stomach into the jejunum. d. removal of the pancreas, the duodenum, and the spleen, and attachment of the stomach to the jejunum, which requires oral supplementation of pancreatic digestive enzymes and insulin replacement therapy. 8. The nurse caring for a patient with suspected acute cholecystitis would anticipate (select all that apply) a. ordering a low-sodium diet. b. administration of IV fluids. c. monitoring of liver function tests. d. administration of antiemetics for patients with nausea. e. insertion of an indwelling catheter to monitor urinary

output. 9. Teaching in relation to home management after a laparoscopic cholecystectomy should include a. keeping the bandages on the puncture sites for 48 hours. b. reporting any bile-colored drainage or pus from any incision. c. using over-the-counter antiemetics if nausea and vomiting occur. d. emptying and measuring the contents of the bile bag from the T tube every day. 1. a, 2. b, 3. b, 4. b, 5. a, 6. a, b, e, 7. c, 8. b, c, d, 9. b For rationales to these answers and even more NCLEX review questions, visit evolve.elsevier.com/Lewis/medsurg.

Evolve Website/Resources List evolve.elsevier.com/Lewis/medsurg

Review Questions (Online Only) Key Points Answer Keys for Questions • Rationales for Bridge to NCLEX Examination Questions • Answer Guidelines for Case Study on p. 1003 • Answer Guidelines for Managing Care of Multiple Patients Case Study (Section 9) on p. 1006 Student Case Studies • Patient With Acute Pancreatitis and Septic Shock • Patient With Cholelithiasis/Cholecystitis • Patient With Cirrhosis

• Patient With Hepatitis Nursing Care Plans • eNursing Care Plan 43.1: Patient With Acute Viral Hepatitis • eNursing Care Plan 43.2: Patient With Cirrhosis • eNursing Care Plan 43.3: Patient With Acute Pancreatitis Conceptual Care Map Creator • Conceptual Care Map for Case Study on p. 1003 Audio Glossary Content Updates

References 1. Centers for Disease Control and Prevention: Viral hepatitis—Hepatitis A information—United States. Retrieved from www.cdc.gov/hepatitis/hav/index.htm. 2. Centers for Disease Control and Prevention: Viral hepatitis—Hepatitis B information—United States. Retrieved from www.cdc.gov/hepatitis/hbv/index.htm. 3. Friedman LS, Martin P: Handbook of liver disease, ed 4, Philadelphia, 2018, Elsevier. 4. Centers for Disease Control and Prevention: Viral hepatitis—Hepatitis C information—United States. Retrieved from www.cdc.gov/hepatitis/hcv/index.htm. 5. Barr R: Shear wave liver elastography, Abdom Radiol 43:800, 2018. American Association for the Study of Liver Diseases: Recommendations for testing, managing, and treating hepatitis C— United States. Retrieved from www.hcvguidelines.org/full-

report/initial-treatment-hcv-infection. Terrault N, Lok A, McMahon B, et al: Update on prevention, diagnosis, and treatment of chronic hepatitis B: AASLD 2018 hepatitis B guidance, Hepatology 67:4, 2018.

8. Liberal R, de Boer YS, Andrade RJ, et al: Expert clinical management of autoimmune hepatitis in the real world, Aliment Pharmacol Ther 45:723, 2017. 9. Kathawala M, Hirschfield GM: Insights into the management of Wilson’s disease, Therap Adv Gastroenterol 10:889, 2017. 10. Lazaridis N, Tsochatzis E: Current and future treatment options in non-alcoholic steatohepatitis, Expert Rev Gastroenterol Hepatol 11:4 357, 2017. Garcia-Tsao G: Current management of the complications of cirrhosis and portal hypertension: Variceal hemorrhage, ascites, and spontaneous bacterial peritonitis, Dig Dis 34:382, 2016.

12. Tsochatzis E, Gerbes A: Hepatology snapshot: Diagnosis and treatment of ascites, J Hepatol 67:184, 2017. Heimbach J, Kulik L, Finn R, et al: AASLD guidelines for the treatment of hepatocellular carcinoma, Hepatology 67:358, 2018. Crockett S, Wani S, Gardner T, et al: American Gastroenterological Association Institute guideline on initial management of acute pancreatitis, Gastroenterol 154: 1096, 2018.

15. Munoz A, Chakravarthy D, Gong J, et al: Pancreatic cancer: Current status and challenges, Curr Pharm Rep 3:396, 2017. Doshi B, Yasuda I, Ryozawa S, et al: Current endoscopic strategies for managing large bile duct stones, Dig Endosc 30:59, 2018.

17. Rahman R, Simoes E, Schmaltz C, et al: Trend analysis and survival of primary gallbladder cancer in the United States: A 1973–2009 population-based

study, Cancer Med 6:874, 2017.

SECTION TEN

Problems of Urinary Function OUTLINE 44. Assessment: Urinary System 45. Renal and Urologic Problems 46. Acute Kidney Injury and Chronic Kidney Disease

44

Assessment Urinary System Teresa Turnbull

LEARNING OUTCOMES 1. Identify the anatomic location and functions of the kidneys, ureters, bladder, and urethra. 2. Explain the physiologic events involved in the formation and passage of urine from glomerular filtration to voiding. 3. Obtain significant subjective and objective data related to the urinary system from a patient. 4. Link the age-related changes of the urinary system to the differences in assessment findings. 5. Perform a physical assessment of the urinary system using appropriate techniques. 6. Distinguish normal from abnormal findings of a physical assessment of the urinary system. 7. Describe the purpose, significance of results, and nursing responsibilities related to diagnostic studies of the urinary system. 8. Evaluate findings of a urinalysis.

KEY TERMS costovertebral angle (CVA), p. 1015 creatinine, p. 1018 cystoscopy, Table 44.11, p. 1019 glomerular filtration rate (GFR), p. 1009 glomerulus, p. 1008 nephron, p. 1008 renal biopsy, Table 44.11, p. 1020 urinalysis, p. 1018 Wherever there is a human being, there is an opportunity for a kindness. Seneca http://evolve.elsevier.com/Lewis/medsurg

Conceptual Focus Elimination Fluids and Electrolytes Adequate kidney function is essential to health. If a person has complete kidney failure and treatment is not provided, death is inevitable. This chapter discusses the structures and functions, assessment, and diagnostic studies of the urinary system.

Structures and Functions of Urinary System The upper urinary system consists of 2 kidneys and 2 ureters. The lower

urinary system consists of a urinary bladder and urethra (Fig. 44.1). Urine is formed in the kidneys, drains through the ureters to be stored in the bladder, and then passes out of the body through the urethra.

Kidneys The kidneys are the principal organs of the urinary system. The primary functions of the kidneys are to (1) regulate the volume and composition of extracellular fluid (ECF) and (2) excrete waste products from the body. The kidneys also function to control BP, make erythropoietin, activate vitamin D, and regulate acid-base balance.

Macrostructure The paired kidneys are bean-shaped organs located retroperitoneally (behind the peritoneum) on either side of the vertebral column at about the level of the twelfth thoracic (T12) vertebra to the third lumbar (L3) vertebra. Each kidney weighs 4 to 6 oz (113 to 170 g) and is about 5 in (12.5 cm) long. The right kidney, positioned at the level of the twelfth rib, is lower than the left. An adrenal gland lies on top of each kidney. Each kidney is surrounded by a considerable amount of fat and connective tissue that cushions, supports, and helps the kidney maintain its position. A thin, smooth layer of fibrous membrane called the capsule covers the surface of each kidney. The capsule protects the kidney and serves as a shock absorber if this area is traumatized from a sudden force or strike. The hilus on the medial side of the kidney serves as the entry site for the renal artery and nerves and as the exit site for the renal vein and ureter.

FIG. 44.1 Organs of the urinary system. A, Upper urinary tract in relation to other anatomic structures. B, Male urethra in relation to

other pelvic structures. C, Female urethra.

The parenchyma is the actual tissue of the kidney (Fig. 44.2). The outer layer of the parenchyma is the cortex, and the inner layer is the medulla. The medulla consists of a number of pyramids. The apices (tops) of these pyramids are the papillae, through which urine passes to enter the calyces. The minor calyces widen and merge to form major calyces, which form a funnel-shaped sac called the renal pelvis. The minor and major calyces transport urine to the renal pelvis, from there it drains through the ureter to the bladder. The renal pelvis can store a small volume of urine (3 to 5 mL).

Microstructure The nephron is the functional unit of the kidney. Each kidney has around 1 million nephrons. Each nephron is composed of the glomerulus, Bowman’s capsule, and a tubular system. The tubular system consists of the proximal convoluted tubule, loop of Henle, distal convoluted tubule, and collecting tubules (Fig. 44.3). The glomerulus, Bowman’s capsule, proximal tubule, and distal tubule are in the cortex of the kidney. The loop of Henle and collecting tubules are in the medulla. Several collecting tubules join to form a single collecting duct. The collecting ducts eventually merge into a pyramid that empties via the papilla into a minor calyx.

Blood Supply Blood flow to the kidneys, around 1200 mL/min, accounts for 20% to 25% of the cardiac output. Blood reaches the kidneys via the renal artery, which arises from the aorta and enters the kidney through the hilus. The renal artery divides into secondary branches and then into still smaller branches, each of which forms an afferent arteriole. The afferent arteriole divides into a capillary network, the glomerulus, which is a collection of up to 50 capillaries (Fig. 44.3). The capillaries of the glomerulus unite in the efferent arteriole. This efferent arteriole splits to form a capillary network, the peritubular capillaries, which surround the tubular system. All peritubular capillaries drain into the

venous system. The renal vein empties into the inferior vena cava.

FIG. 44.2 Longitudinal section of the kidney.

FIG. 44.3 The nephron is the basic functional unit of the kidney. This illustration of a single nephron unit shows the surrounding blood vessels. Modified from Thibodeau GA, Patton KT: The human body in health and disease, ed 4, St Louis, 2005, Mosby.

Physiology of Urine Formation Urine formation is the outcome of a complex, multistep process of filtration, reabsorption, secretion, and excretion of water, electrolytes, and metabolic waste products. Although urine formation is the result of this process, the primary functions of the kidneys are to filter the

blood and maintain the body’s internal homeostasis.

Glomerular Function Urine formation begins at the glomerulus, where blood is filtered. The glomerulus is a semipermeable membrane that allows filtration (Fig. 44.3). The hydrostatic pressure of the blood within the glomerular capillaries causes a portion of blood to be filtered across the semipermeable membrane into Bowman’s capsule. There, the filtered portion of the blood (glomerular filtrate) begins to pass down to the tubule. Filtration is more rapid in the glomerulus than in ordinary tissue capillaries because the glomerular membrane is porous. The glomerular filtrate is similar in composition to blood except that it lacks blood cells, platelets, and large plasma proteins. Under normal conditions, capillary pores are too small to allow the loss of these large blood components. However, in many kidney diseases, capillary permeability increases, which allows plasma proteins and blood cells to pass into the urine. The amount of blood filtered each minute by the glomeruli is expressed as the glomerular filtration rate (GFR). The normal GFR is about 125 mL/min. The peritubular capillary network reabsorbs most of the glomerular filtrate before it reaches the end of the collecting duct. Therefore only 1 mL/min (on average) is excreted as urine.

Tubular Function The tubules and collecting ducts are responsible for the reabsorption of essential materials and excretion of nonessential ones (Table 44.1). They carry out these functions by reabsorption and secretion. Reabsorption is the passage of a substance from the lumen of the tubules through the tubule cells and into the capillaries. This process involves both active and passive transport mechanisms. Tubular secretion is the passage of a substance from the capillaries through the tubular cells into the lumen of the tubule. Reabsorption and secretion cause many changes in the composition of the glomerular filtrate as it moves through the entire length of the tubule. In the proximal convoluted tubule, about 80% of the electrolytes are

reabsorbed. Normally, this includes all glucose, amino acids, and small proteins. As reabsorption continues in the loop of Henle, water is conserved, which is important for concentrating the filtrate. The descending loop is permeable to water and moderately permeable to sodium, urea, and other solutes. In the ascending limb, chloride ions (Cl−) are actively reabsorbed, followed by passive reabsorption of sodium ions (Na+). About 25% of the filtered sodium is reabsorbed in the ascending limb. Two important functions of the distal convoluted tubules are final regulation of water balance and acid-base balance. Antidiuretic hormone (ADH) is needed for water reabsorption in the kidney and is important in water balance. ADH makes the distal convoluted tubules and collecting ducts permeable to water. This allows water to be reabsorbed into the peritubular capillaries and eventually returned to the circulation.

TABLE 44.1 Functions of Nephron Segments

Osmoreceptors in the anterior hypothalamus detect decreases in plasma osmolality. These osmoreceptors send neural input to superoptic nuclei cells in the hypothalamus. These superoptic nuclei cells have neuronal axons that end in the posterior pituitary gland and act to inhibit secretion of ADH. In the absence of ADH, the tubules are essentially impermeable to water. Thus any water in the tubules

leaves the body as urine. Aldosterone (released from the adrenal cortex) acts on the distal tubule to cause reabsorption of Na+ and water. In exchange for Na+, potassium ions (K+) are excreted. The secretion of aldosterone is influenced by both circulating blood volume and plasma concentrations of Na+ and K+. Acid-base regulation involves reabsorbing and conserving most of the bicarbonate (HCO3−) and secreting excess hydrogen ions (H+). The distal tubule has different ways to keep the pH of ECF within a range of 7.35 to 7.45 (see Chapter 16). Myocyte cells in the right atrium secrete a hormone, atrial natriuretic peptide (ANP), in response to atrial distention from an increase in plasma volume. ANP acts on the kidneys to increase sodium excretion. At the same time, ANP inhibits renin, ADH, and the action of angiotensin II on the adrenal glands, thereby suppressing aldosterone secretion. These combined effects of ANP result in the production of a large volume of dilute urine. ANP also causes relaxation of the afferent arteriole, thus increasing the GFR. The renal tubules are also involved in calcium balance. The parathyroid gland releases parathyroid hormone (PTH) in response to low serum calcium levels. PTH maintains serum calcium levels by causing increased tubular reabsorption of calcium ions (Ca2+) and decreased tubular reabsorption of phosphate ions (PO42−). In kidney disease the effects of PTH may have a major effect on bone metabolism. Vitamin D is a hormone that we obtain in the diet or synthesize by the action of ultraviolet radiation on cholesterol in the skin. These forms of vitamin D are inactive and go through 2 more steps to become metabolically active. The first step occurs in the liver; the second step occurs in the kidneys. Active vitamin D is essential for the absorption of calcium from the gastrointestinal (GI) tract. The patient with kidney failure (also called renal failure) will have a deficiency of the active metabolite of vitamin D and problems with calcium and phosphate balance (see Chapter 47).

In summary, the basic function of nephrons is to cleanse blood plasma of unnecessary substances. After the glomerulus has filtered the blood, the tubules select the unwanted from the wanted portions of tubular fluid. Essential constituents are returned to the blood, and dispensable substances pass into urine.

Other Functions of Kidneys The kidneys participate in red blood cell (RBC) production and BP regulation. Erythropoietin is a hormone made in the kidneys and secreted in response to hypoxia and decreased renal blood flow. Erythropoietin stimulates RBC production in the bone marrow. A deficiency of erythropoietin occurs in kidney failure, leading to anemia. Renin is important in the regulation of BP. Renin is made and secreted by the kidney’s juxtaglomerular cells (Fig. 44.4). Renin is released into the bloodstream in response to decreased renal perfusion, decreased arterial BP, decreased ECF, decreased serum Na+ concentration, and increased urinary Na+ concentration. The plasma protein angiotensinogen (from the liver) is activated to angiotensin I by renin. Angiotensin I is then converted to angiotensin II by angiotensin-converting enzyme (ACE). ACE is found on the inner surface of all blood vessels, with especially high levels in the vessels of the lungs. Angiotensin II stimulates the release of aldosterone from the adrenal cortex. This causes Na+ and water retention, leading to increased ECF volume. Angiotensin II also causes increased peripheral vasoconstriction. An elevated BP inhibits renin release. Excessive renin production caused by impaired renal perfusion may be a contributing factor in causing hypertension (see Chapter 32).

FIG. 44.4 Renin-angiotensin-aldosterone system. Modified from Herlihy B, Maebius N: The human body in health and disease, ed 4, Philadelphia, 2011, Saunders.

Most body tissues synthesize prostaglandins (PGs) from the precursor arachidonic acid in response to appropriate stimuli. (See Chapter 11 and Fig. 11.2 for a more detailed discussion of PGs.) In the kidney, PG synthesis (mainly PGE2 and PGI2) occurs primarily in the medulla. These PGs have a vasodilating action, thus increasing renal blood flow and promoting Na+ excretion. They counteract the vasoconstrictive effect of substances such as angiotensin and norepinephrine. Renal PGs may have a systemic effect in lowering BP by decreasing systemic vascular resistance. The significance of renal PGs is related to the kidneys’ role in causing hypertension. In renal failure with a loss of functioning tissue, these renal vasodilator factors are also lost, which may contribute to hypertension (see Chapter 46).

Ureters The ureters are tubes that carry urine from the renal pelvis to the bladder (Fig. 44.1). Each ureter is about 10 to 12 inches (25 to 30.5 cm) long and 0.08 to 0.3 inches (0.2 to 0.8 cm) in diameter. Arranged in a meshlike outer layer, circular and longitudinal smooth muscle fibers

contract to promote the peristaltic, 1-way flow of urine through the ureters. Distention, neurologic and endocrine influences, and drugs can affect these muscle contractions. The narrow area where each ureter joins the renal pelvis is the ureteropelvic junction (UPJ). Subsequently, the ureters insert into either side of the bladder base at the ureterovesical junctions (UVJs). Because the ureteral lumens are narrowest at these junctions, the UPJ and UVJ are often sites of obstruction. The narrow ureteral lumens can be easily obstructed internally (e.g., urinary stones) or externally (e.g., tumors, adhesions, inflammation). Sympathetic and parasympathetic nerves, along with the vascular supply, surround the mucosal lining of the ureters. Stimulation of these nerves during passage of a stone may cause acute, severe pain, termed renal colic. Because the renal pelvis holds only 3 to 5 mL of urine, kidney damage can result from a backflow of more than that amount of urine. The UVJ relies on the ureter’s angle of bladder insertion and muscle fiber attachments with the bladder to prevent the backflow (reflux) of urine, which predisposes a person to an ascending infection. The distal ureter enters the bladder laterally at its base, courses along obliquely through the bladder wall for about 1.5 cm and intermingles with muscle fibers of the bladder base. Circular and longitudinal bladder muscle fibers adjacent to the imbedded ureter help secure it. When bladder pressure rises (e.g., during voiding or coughing), muscle fibers that the ureter shares with the bladder base contract first, promoting ureteral lumen closure. Next, the bladder contracts against its base, ensuring UVJ closure and prevention of urine reflux through the junction.

Bladder The urinary bladder is located behind the symphysis pubis and anterior to the vagina and rectum (Fig. 44.5). Its primary functions are to serve as a reservoir for urine and to eliminate waste products from the body. Like the stomach, the bladder is a stretchable, saclike organ that contracts when it is empty. The trigone is the triangular area formed by the 2 ureteral openings

and bladder neck at the base of the bladder. The trigone is attached to the pelvis by many ligaments and does not change its shape during bladder filling or emptying. The bladder muscle (detrusor) is composed of layers of intertwined smooth muscle fibers. These fibers are capable of considerable distention during bladder filling and contraction during emptying. It is attached to the abdominal wall by an umbilical ligament, the urachus. Because of this attachment, as the bladder fills it rises toward the umbilicus. The dome and the anterior and lateral aspects of the bladder expand and contract.

FIG. 44.5 Male urinary bladder. Modified from Thibodeau GA, Patton KT: Anatomy and physiology, ed

6, St Louis, 2007, Mosby.

Normal adult urine output is around 1500 mL/day, which varies with food and fluid intake. The volume of urine at night is less than half of that formed during the day because of hormonal influences (e.g., ADH). This diurnal pattern of urination is normal. Typically, a person will urinate 5 or 6 times during the day and occasionally at night. On average, 200 to 250 mL of urine in the bladder cause moderate distention and the urge to urinate. When the quantity of urine reaches 400 to 600 mL, the person feels uncomfortable. Bladder capacity varies with the person, but generally ranges from 600 to 1000 mL. Evacuation of urine is termed urination, micturition, or voiding. The bladder has the same mucosal lining as that of the renal pelvises, ureters, and bladder neck. The bladder is lined by transitional cell epithelium referred to as the urothelium. Unique to the urinary tract, the urothelium is resistant to absorption of urine. This means that after waste products (made by the kidneys) have left the kidneys, they cannot be reabsorbed in the urinary system. Microscopically, urothelium is only several cells deep. However, as urine enters the bladder, these cells can stretch to accommodate filling. As the bladder empties, the urothelium resumes its multicellular layer formation. Transitional cell cancers in one section of the urinary tract can easily metastasize to other urinary tract areas given that the mucosal lining throughout the urinary tract is the same. Cancer cells may move down from upper urinary tract cancers and embed in the bladder, or large bladder tumors can invade the ureter. Cancer recurrence within the bladder is common.

Urethra The urethra is a small tube that incorporates the smooth muscle of the bladder neck and extends to the striated muscle of the external meatus. The urethra’s primary functions are to (1) control voiding and (2) serve as a conduit for urine from the bladder to the outside of the

body during voiding. The female urethra is 1 to 2 in (2.5 to 5 cm) long and lies behind the symphysis pubis but anterior to the vagina (Fig. 44.1, C). The male urethra, which is about 8 to 10 in (20 to 25 cm) long, starts at the bladder neck and extends the length of the penis (Fig. 44.1, B).

Urethrovesical Unit Together, the bladder, urethra, and pelvic floor muscles form the urethrovesical unit. Voluntary control of this unit is defined as continence. Stimulating and inhibiting impulses are sent from the brain through the thoracolumbar (T11 to L2) and sacral (S2 to S4) areas of the spinal cord to control voiding. Bladder distention stimulates stretch receptors within the bladder wall. Impulses are transmitted to the sacral spinal cord and then to the brain, causing a desire to urinate. If you cannot void at a given time, inhibitor impulses in the brain are stimulated and transmitted back through the thoracolumbar and sacral nerves innervating the bladder. In a coordinated fashion, the detrusor muscle accommodates to the pressure (does not contract) while the sphincter and pelvic floor muscles tighten (contract) to resist bladder pressure. If you can void, cerebral inhibition is voluntarily suppressed. Impulses are transmitted via the spinal cord for the bladder neck, sphincter, and pelvic floor muscles to relax and for the bladder to contract. The sphincter closes, and the detrusor muscle relaxes when the bladder is empty. Any disease or trauma that affects the function of the brain, spinal cord, or nerves that directly innervate the bladder, bladder neck, external sphincter, or pelvic floor can affect bladder function. These conditions include diabetes, multiple sclerosis, paraplegia, and tetraplegia (quadriplegia). Drugs affecting nerve transmission can affect bladder function.

Gerontologic Considerations: Effects of

Aging on Urinary System Anatomic changes in the aging kidney include a 20% to 30% decrease in size and weight between ages 30 and 90 years. By the seventh decade of life, 50% of glomeruli have lost their function.1 Atherosclerosis accelerates the decrease of renal size with age. Physiologic changes in the aging kidney include decreased renal blood flow, due in part to atherosclerosis, resulting in a decreased GFR. Changes in hormone levels (including ADH, aldosterone, ANP) result in decreased urinary concentrating ability and changes in the excretion of water, sodium, potassium, and acid. Despite these changes, older adults maintain homeostasis unless they encounter diseases or other physiologic stressors. After abrupt changes in blood volume, acid load, or other insults, the kidney may not be able to function effectively because much of its renal reserve has been lost.1 Physiologic changes occur in the aging urethra and bladder. The female urethra, bladder, vagina, and pelvic floor undergo a loss of elasticity and muscle support. Consequently, older women are more prone to bladder infections and incontinence. The prostate surrounds the proximal urethra. As men age, the prostate enlarges and may affect urinary patterns, causing hesitancy, retention, slow stream, and bladder infections. Constipation, often experienced by older adults, can affect urination. Partial urethral obstruction may occur because of the rectum’s close proximity to the urethra. Age-related changes in the urinary system and differences in assessment findings are outlined in Table 44.2.

TABLE 44.2 Gerontologic Assessment

DifferencesUrinary System

Assessment of Urinary System Subjective Data Important Health Information Past Health History Ask the patient about the presence or history of kidney disease or other urologic problems. Note specific urinary problems, such as cancer, infections, benign prostatic hyperplasia (BPH), and stones. Ask about other health problems that may affect kidney function, including hypertension, diabetes, gout, connective tissue disorders (e.g., systemic lupus erythematosus), hepatitis, human immunodeficiency virus (HIV) infection, neurologic conditions (e.g., stroke, back injury), and trauma.2

Medications An assessment of the patient’s current and past use of medications is important. Include over-the-counter drugs, prescription drugs, and herbal therapies. Drugs affect the urinary tract in several ways. Many drugs can be nephrotoxic (Table 44.3). Certain drugs may alter the quantity and character of urine output (e.g., diuretics). Several drugs change the color of urine. Phenazopyridine (Pyridium) turns urine

orange. Nitrofurantoin (Macrodantin) turns urine dark yellow to brown. Anticoagulants may cause hematuria. Many antidepressants, calcium channel blockers, antihistamines, and drugs used for neurologic and musculoskeletal disorders affect the ability of the bladder or sphincter to contract or relax normally.

Surgery or Other Treatments Ask the patient about hospitalizations related to renal or urologic diseases and all urinary problems during past pregnancies. Inquire about the duration, severity, and patient’s perception of any problem and its treatment. Document

TABLE 44.3 Potentially Nephrotoxic Agents

Case Study Patient Introduction

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A.K. is a 28-yr-old black man who comes to the emergency department (ED) in acute distress with severe abdominal pain. The pain began about 6 hours ago after he finished a 10-mile run as part of his training for a marathon. He says that the pain has steadily

increased and he is nauseous. His urine is a dark, smoky color.

Discussion Questions 1. What are the possible causes of A.K.’s abdominal pain, nausea, and urine color? 2. What type of assessment would be most appropriate for A.K.: comprehensive, focused, or emergency? On what basis did you make that decision? 3. What assessment questions will you ask him? You will learn more about A.K. and his condition as you read through this assessment chapter. (See p. 1015 for more information on A.K.) Answers available at http://evolve.elsevier.com/Lewis/medsurg. past surgeries, especially pelvic surgeries, and urinary tract instrumentation (e.g., catheterization). Ask the patient about any radiation or chemotherapy treatment for cancer.

Functional Health Patterns Key questions to ask a patient with problems related to the renal system are listed in Table 44.4.

Health Perception–Health Management Pattern Ask about the patient’s general health. Abnormal kidney function may be suspected if the patient reports changes in weight or appetite, excess thirst, fluid retention, headache, pruritus, blurred vision, or “feeling tired all the time.” An older adult may report malaise and nonlocalized abdominal discomfort as the only symptoms of a urinary tract infection (UTI). In older adults with a UTI, family members may report the patient is disoriented, has fallen, or has increased confusion. Obtain a smoking history. Cigarette smoking is a major risk factor for bladder and kidney cancer. Smokers who also work with cancer-

causing chemicals have an especially high risk for bladder cancer.

TABLE 44.4 Health HistoryUrinary System

Health Perception–Health Management • How is your energy level compared with 1 yr ago? • Do you notice any visual changes?∗ • Have you ever smoked? If yes, how many packs per day? • Tell me about the types of jobs you have had.

Nutritional-Metabolic • How is your appetite? • Has your weight changed over the past year?∗ • Do you take vitamins, herbs, or any other supplements?∗ • How much and what kinds of fluids do you drink daily? • How many dairy products and how much meat do you eat? • Do you drink coffee? Colas? Tea? • Do you spice your food heavily?∗

Elimination • Are you able to sit through a 2-hr meeting or ride in a car for 2 hr without urinating? • Do you awaken at night with the desire to urinate? If so, how many times does this occur during an average night? • Do you ever notice blood in your urine?∗ If so, at what point in the urination does it occur? • Have you noticed any change in the color or smell of your urine?∗

• Do you ever pass urine when you do not intend to? When? • Do you use special devices or supplies for urine elimination or control?∗ • How often do you move your bowels? • Do you ever have constipation or diarrhea?∗ • Do you ever have problems controlling your bowels?∗

Activity-Exercise • Have you noticed any changes in your ability to perform your usual daily activities?∗ • Do certain activities worsen your urinary problem?∗ • Has your urinary problem caused you to alter or stop any activity or exercise?∗ • Do you need help moving or getting to the bathroom?∗

Sleep-Rest • Do you awaken at night from an urge to urinate?∗ How does this disturb your sleep? • Do you awaken at night from pain or other problems and urinate as a matter of routine before returning to sleep?∗ • Do you have daytime sleepiness and fatigue because of nighttime urination?∗

Cognitive-Perceptual • Do you ever have pain when you urinate?∗ If so, where is the pain?

Self-Perception–Self-Concept • How does your urinary problem make you feel about yourself? • Do you perceive your body differently since you have developed a urinary problem?

Role-Relationship • Does your urinary problem interfere with your relationships with family or friends?∗ • Has your urinary problem caused a change in your job status or affected your ability to carry out job-related responsibilities?∗

Sexuality-Reproductive • Has your urinary problem caused any change in your sexual pleasure or performance?∗ • Do hygiene concerns interfere with sexual activities?

Coping–Stress Tolerance • Do you feel able to manage the problems associated with your urinary problem? If not, explain. • What strategies are you using to cope with your urinary problem?

Values-Beliefs • Has your present illness affected your belief system?∗ • Are your treatment decisions related to your urinary problem in

conflict with your value system?∗



If yes, describe.

Exposure to certain chemicals can affect the urinary system. Aromatic amines and some organic chemicals increase the risk for bladder cancer. Phenol and ethylene glycol are examples of nephrotoxic chemicals. Obtain an occupational history. Machinists, painters, hairdressers, printers, and truck drivers have an increased incidence of bladder cancer.3 Information about places where a patient has lived is important. Persons living in the Southeast part of the United States have the highest incidence of urinary stones. This may be caused by the higher mineral content of the soil and water.4 A person living in Middle Eastern countries or Africa can acquire certain parasites that can cause cystitis or bladder cancer.

Genetic Risk Alert • Polycystic kidney disease and congenital urinary tract abnormalities (e.g., Alport syndrome [congenital nephritis]) are genetic disorders. • A family history of certain renal or urologic problems increases the chance of similar problems occurring in the patient. • For any disease reported in the health history, ask if other family members also have/had the same or similar diseases.

Nutritional-Metabolic Pattern The usual quantity and types of fluid a patient drinks are important in relation to urinary tract disease. Dehydration may contribute to UTIs,

stone formation, and kidney failure. Large intake of specific foods, such as dairy products or foods high in proteins, may lead to stone formation. Asparagus may cause the urine to smell musty. Red urine caused by beet ingestion may be mistaken for bloody urine. Caffeine, alcohol, carbonated beverages, some artificial sweeteners, or spicy foods often worsen urinary inflammatory diseases. Green tea and some herbal teas cause diuresis. An unexplained weight gain may be the result of fluid retention from a kidney problem. Anorexia, nausea, and vomiting can dramatically affect fluid status and require careful monitoring.

Elimination Pattern Questions about urine elimination patterns are the cornerstone of the health history in the patient with a lower urinary tract disorder. Begin with asking how the patient manages urine elimination. Ask about daytime (diurnal) voiding frequency and the frequency of nocturia. Pelvic organ prolapses, particularly advanced anterior vaginal prolapse, may cause suprapubic pressure, frequency, urgency, and incontinence from urinary retention. Ask about other bothersome lower urinary tract symptoms, including urgency, incontinence, or urinary retention. Table 44.5 lists some common manifestations of urinary tract disorders.

TABLE 44.5 Manifestations of Urinary System

Disorders

Changes in the color and appearance of urine are often significant and need evaluated. If blood is visible in the urine, determine if it occurs at the beginning of, throughout, or at the end of urination. This is harder for the female patient. Assess bowel function. Problems with fecal incontinence may signal neurologic causes for bladder problems because of shared nerve pathways. Constipation and fecal impaction can partially obstruct the urethra, causing inadequate bladder emptying, overflow incontinence, and infection. Determine the patient’s method of managing a urinary problem. A patient may already be using a catheter or collection device. Sometimes a patient must assume a specific position to urinate or perform maneuvers, such as pressing on the lower abdomen (Credé’s method) or straining (Valsalva maneuver), to empty the bladder.

Activity-Exercise Pattern Assess the patient’s level of activity. A sedentary person is more likely to have stasis of urine than an active person and thus be predisposed to infection and stones. Demineralization of bones in a person with limited physical activity can cause increased urine calcium precipitation. An active person may find that increasing activity worsens the urinary problem. The patient who has had prostate surgery or who has weakened pelvic floor muscles may leak urine when trying certain activities, such as running. Some men develop chronic inflammatory prostatitis or epididymitis after heavy lifting or long-distance driving.

Sleep-Rest Pattern Nocturia is a common and a particularly bothersome symptom that often leads to sleep deprivation, daytime sleepiness, and fatigue. It occurs in multiple problems affecting the lower urinary tract, including urinary incontinence, urinary retention, and interstitial cystitis. Nocturia may be related to polyuria from kidney disease,

poorly controlled diabetes, alcohol use, excess fluid intake, liver disease, heart failure, or obstructive sleep apnea. When assessing nocturia, determine whether the need to urinate causes the person to arise from sleep or whether pain or other symptoms interrupt sleep. Ask if the person urinates as a matter of habit before returning to bed. Up to 1 episode of nocturia is considered normal in younger adults, and up to 2 episodes are acceptable in adults ages 65 years or older. If an older adult has more than 2 episodes during the night, assess the amount and timing of fluid intake. This information will help determine whether further investigation is needed.

Cognitive-Perceptual Pattern Assess the level of mobility, visual acuity, and dexterity. These are important factors to evaluate in a patient with urologic problems, especially when urine retention or incontinence is a problem. Determine if the patient is alert, understands instructions, and can recall instructions when needed. If urinary incontinence is present, ask how the patient is managing the problem. Recognize that incontinence is often distressing and embarrassing. Discuss the problem with the patient with sensitivity in a nonjudgmental manner. A frequent symptom of renal and urologic problems is pain, including dysuria, groin pain, costovertebral pain, and suprapubic pain. Assess pain and document the location, character, and duration. The absence of pain when other urinary symptoms exist is significant. Many urinary tract cancers are painless in the early stages.

Self-Perception–Self-Concept Pattern Problems associated with the urinary system, such as incontinence, urinary diversion procedures, and chronic fatigue (may occur with anemia), can result in loss of self-esteem and a negative body image.

Role-Relationship Pattern

Urinary problems can affect many aspects of a person’s life, including the ability to work and relationships with others. These factors have important implications for future treatment and management of the patient’s condition. Urinary system problems may be serious enough to cause problems in job-related and social situations. Chronic dialysis therapy often makes regular employment or management of home and family responsibilities difficult. Concurrent poor health and negative body image can seriously affect existing roles.

Sexuality-Reproductive Pattern Assess the effect of renal problems on the patient’s sexual satisfaction. Problems related to personal hygiene and fatigue can negatively affect sexual relationships. Although urinary incontinence is not directly associated with sexual dysfunction, it often has a devastating effect on self-esteem and social and intimate relationships. Counseling both the patient and partner may be needed.

Objective Data Physical Examination Inspection Assess for changes in the following: • Skin: Pallor, yellow-gray cast, excoriations, changes in turgor, bruises, texture (e.g., rough, dry skin) (see Table 22.9 for assessment of dark-skinned persons) • Mouth: Stomatitis, ammonia breath odor • Face and extremities: Generalized edema, peripheral edema • Abdomen: Abdominal contour for midline mass in lower abdomen (may indicate bladder distention and urinary retention) or unilateral mass (sometimes seen in adults, indicating kidney enlargement from large tumor or polycystic kidney)

Case Study—cont’d Subjective Data

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A focused subjective assessment of A.K. revealed the following information: Past Medical History: History of 1 isolated incidence of gout 6 years ago. He stopped drinking alcohol with no further occurrence. Appendectomy 12 years ago.

Medications: None. Health Perception–Health Management: A.K. states that he is usually healthy. He does not smoke or drink alcohol. He has never had this type of pain before. Describes the pain as being sharp and colicky (coming in waves). Rates the pain as 9 on a scale of 0 to 10. Nutritional-Metabolic: A.K. is currently on a high-protein diet as he trains for the marathon. He eats a lot of chicken, beef, and seafood. He drinks milk-based protein shakes and water after exercising but admits that he does not think he drinks enough to replace fluid loss from perspiration. He drinks coffee for energy but denies eating chocolate or other sweets. He avoids sodas. Elimination: Denies any history of problems with urination, constipation, or diarrhea. This is the first time he has ever noticed a change of color in his urine. Activity-Exercise: Prides himself on his ability to exercise and run without difficulty. Sleep-Rest: Does not awaken at night to urinate. Cognitive-Perceptual: Denies pain on urination. Self-Perception–Self-Concept: Believes he can monitor himself and maintain a healthy lifestyle. Coping–Stress Tolerance: Worried that this pain may interfere with his marathon training.

Discussion Questions 1. Which subjective assessment findings are of most concern to you? 2. What would be your priority assessment of A.K.? 3. What should be included in the physical assessment? What would you be looking for? You will learn more about the physical examination of the urinary system in the next section. (See p. 1016 for more information on A.K.) Answers available at http://evolve.elsevier.com/Lewis/medsurg.

• Weight: Weight gain from edema. Weight loss and muscle wasting in kidney failure • General state of health: Fatigue, lethargy, and decreased alertness

Palpation The kidneys are posterior organs protected by the abdominal organs, ribs, and heavy back muscles. A landmark useful in locating the kidneys is the costovertebral angle (CVA) formed by the rib cage and the vertebral column. The normal-sized left kidney is rarely palpable because the spleen lies directly on top of it. Occasionally the lower

pole of the right kidney is palpable. To palpate the right kidney, place your left (anterior) hand behind and support the patient’s right side between the rib cage and the iliac crest (Fig. 44.6). Elevate the right flank with the left hand. Use your right hand to palpate deeply for the right kidney. The lower pole of the right kidney may be felt as a smooth, rounded mass that descends on inspiration. If the kidney is palpable, note its size, contour, and tenderness. Kidney enlargement is suggestive of cancer or other serious renal pathologic conditions. The urinary bladder is normally not palpable unless it is distended with urine. If the bladder is full, it may be felt as a smooth, round, firm organ and is sensitive to palpation.

FIG. 44.6 Palpating the right kidney. From Brundage DJ: Renal disorders, St Louis, 1992, Mosby.

FIG. 44.7 A, Costovertebral angle. B, Indirect fist percussion of the costovertebral angle (CVA). To assess the kidney, place one hand over the twelfth rib at the CVA on the back. Thump that hand with the ulnar edge of the other fist. From Jarvis C: Physical examination and health assessment, ed 7, St Louis, 2016, Saunders.

Percussion

Tenderness in the flank area may be detected by fist percussion (kidney punch). This technique is performed by striking the fist of one hand against the dorsal surface of the other hand, which is placed flat along the posterior CVA margin (Fig. 44.7). Normally this type of percussion should not elicit pain. If CVA tenderness and pain are present, it may indicate a kidney infection or polycystic kidney disease.5 A bladder does not percuss until it contains at least 150 mL of urine. If the bladder is full, dullness is heard above the symphysis pubis. A distended bladder may be percussed as high as the umbilicus.

Auscultation Use the diaphragm of the stethoscope to auscultate bowel sounds, since the bowels can affect the urinary system.

Focused Assessment Urinary System Use this checklist to ensure that the key assessment steps have been done.

Subjective Ask the patient about any of the following and note responses.

Painful urination

Y

N

Changes in color of urine (blood, cloudy)

Y

N

Change in characteristics of urination (decreased, excessive)

Y

N

Problems with frequent nighttime urination (nocturia)

Y

N

Objective: Diagnostic Check the following laboratory results for critical values.

Blood urea nitrogen



Serum creatinine



Urinalysis



Urine culture and sensitivity



Objective: Physical Examination Inspect

Abdomen



Urinary meatus for inflammation or discharge



Palpate ✓

Abdomen for bladder distention, masses, or tenderness

Percuss

Costovertebral angle for tenderness



TABLE 44.6 Normal Physical Assessment of

Urinary System • No costovertebral angle tenderness • Nonpalpable kidney and bladder • No palpable masses Table 44.6 shows how to record the normal physical assessment findings of the urinary system. Table 44.7 describes assessment abnormalities of the urinary system. Assessment findings may vary in the older adult. Table 44.2 presents the age-related changes in the urinary system and differences in assessment findings. Use a focused

assessment to evaluate the status of previously identified urinary system problems and to monitor for signs of new problems. A focused assessment of the urinary system is outlined in the box on this page.

Case Study—cont’d Objective Data: Physical Examination

© iStockphoto/Thinkstock.

A focused assessment of A.K. reveals the following: A.K. is lying with his knees bent and drawn to his abdominal area. He appears restless and keeps moving from back to side to reduce his discomfort. Vital signs are as follows: BP 156/70, apical pulse 108,

respiratory rate 24, temperature 37.4° C, O2 saturation 96% on room air. Awake, alert, and oriented × 3. Lungs are clear to auscultation. Apical pulse is regular. Abdomen nondistended with + bowel sounds in all 4 quadrants. No rebound tenderness. Positive left costovertebral tenderness. Voiding small amounts of dark, smoky urine.

Discussion Questions 1. Which physical assessment findings are of most concern to you? 2. Based on the results of the subjective and physical assessment findings, what diagnostic studies do you think may be ordered for A.K.? You will learn more about diagnostic studies related to the urinary system in the next section. (See p. 1022 for more information on A.K.) Answers available at http://evolve.elsevier.com/Lewis/medsurg.

TABLE 44.7 Assessment AbnormalitiesUrinary

System Finding Anuria

Description Possible Etiology and Significance Technically no urination (24-hr Acute kidney injury, end-stage renal disease, urine output 60 yr

Prevention and Management Prevent insult or injury to kidneys

Cardiovascular disease

Institute aggressive risk factor reduction

Diabetes

Achieve optimal glycemic control

Ethnic minority (e.g., black, Native American)

Teach about ↑ risk and assist with appropriate screening (BP measurement, urinalysis)

Exposure to nephrotoxic drugs

Limit exposure and give sodium bicarbonate as treatment

Family history of CKD

Teach about ↑ risk and assist with appropriate screening

Hypertension

Maintain BP in normal range with ACE inhibitors or ARBs

TABLE 46.7 Stages of Chronic Kidney Disease

Source: Alseiari M, Meyer KB, Wong JB: Evidence underlying KDIGO (Kidney Disease: Improving Global Outcomes) guideline recommendations: A systematic review, Am J Kidney Dis 67:417, 2016. Over half a million Americans are receiving treatment (dialysis, transplant) for ESRD. Despite all the technologic advances in lifesustaining treatment with dialysis, patients with ESRD have a high mortality rate. As the stage of kidney disease progresses, the mortality rate increases. Mortality rates are as high as 19% to 24% for patients with ESRD on dialysis.14,16 The prognosis and course of CKD are highly variable depending on the cause, patient’s condition and age, and adequacy of health care follow-up. Some people live normal, active lives with kidney disease, while others may rapidly progress to ESRD (stage 5). Since 1972, the United States has covered most of the costs of providing dialysis through Medicare benefits. Under Title XVIII of the Social Security Act, ESRD was recognized as a disability. Medicare pays for 80% of eligible charges. The state, private insurance, or patient covers the rest.16

Promoting Health Equity Chronic Kidney Disease

• Has a high incidence in minority populations, especially blacks and Native Americans • Hypertension and diabetes are more common in blacks and Native Americans

Blacks • The risk for CKD as a complication of hypertension is significantly higher in blacks • Have the highest rate of CKD, nearly 4 times that of whites

Native Americans • Have a rate of CKD twice that of whites • Rate of CKD is 6 times higher among Native Americans with diabetes than among other ethnic groups with diabetes

Hispanics • Rate of CKD in Hispanics is 1.5 times higher than in nonHispanic whites

Clinical Manifestations As kidney function deteriorates, all body systems become affected. The manifestations result from retained urea, creatinine, phenols, hormones, electrolytes, and water. Uremia is a syndrome in which kidney function declines to the point that symptoms may develop in multiple body systems (Fig. 46.2). It often occurs when the GFR is 15 mL/min or less. The manifestations of uremia vary among patients depending on the cause of the kidney disease, co-morbid conditions, age, and degree of adherence to the prescribed medical regimen. Many patients are tolerant of the changes caused by declining kidney

function because they occur gradually.

Urinary System In the early stages of CKD, patients usually do not report any change in urine output. Since diabetes is the primary cause of CKD, polyuria may be present, but not necessarily from kidney disease. As CKD progresses, patients have increasing difficulty with fluid retention and need diuretic therapy. After a period on dialysis, patients may develop anuria.

Metabolic Disturbances Waste Product Accumulation As the GFR decreases, the BUN and serum creatinine levels increase. The BUN increase is not only from kidney disease but also protein intake, fever, corticosteroids, and catabolism. For this reason, serum creatinine clearance determinations (calculated GFR) are considered more accurate indicators of kidney function than BUN or creatinine (Table 46.8). Significant increases in BUN contribute to nausea, vomiting, lethargy, fatigue, impaired thought processes, and headaches.

Altered Carbohydrate Metabolism Impaired glucose metabolism, resulting from cellular insensitivity to the normal action of insulin, causes defective carbohydrate metabolism. Mild to moderate hyperglycemia and hyperinsulinemia may occur. Insulin and glucose metabolism may improve (but not to normal values) after starting dialysis. Patients with diabetes who needed insulin before starting dialysis may need less insulin therapy when they start dialysis and their kidney disease progresses. Patients with diabetes who develop uremia may need less insulin than before the onset of CKD. Insulin, which depends on the kidneys for excretion, stays in the circulation longer. Insulin dosing must be individualized,

and glucose levels monitored carefully.

Check Your Practice You are working in a community-based dialysis unit. One of your patients is a 56-yr-old woman who has been on HD for 3 weeks. You are reviewing her medications with her and she is surprised that her dose of glargine insulin has been decreased. She tells you, “I have been a diabetic for 30 years, and this is the first time ever that my dose of insulin has been decreased.” • How would you respond?

FIG. 46.2 Possible manifestations of CKD.

TABLE 46.8 Indicators of Kidney Function This example shows why serum creatinine alone is a poor indicator of kidney function. Calculation of GFR is considered the best index to estimate kidney function as shown by the following example.

Cr, Creatinine; GFR, glomerular filtration rate; MDRD, modification of diet in renal disease. ∗

Cockcroft-Gault GFR = (140 − Age) × (Weight in kilograms) × (0.85 if female)/(72 × Cr).



GFR as estimated by MDRD equation calculator can be accessed at www.mdrd.com .

Elevated Triglycerides Hyperinsulinemia stimulates hepatic production of triglycerides. Many patients with uremia develop dyslipidemia, with increased very-low-density lipoproteins (VLDLs), increased low-density lipoproteins (LDLs), and decreased high-density lipoproteins (HDLs). The altered lipid metabolism is related to decreased levels of the enzyme lipoprotein lipase, which is important in the breakdown of lipoproteins. Most patients with CKD die from CVD.17

Electrolyte and Acid-Base Imbalances Potassium Hyperkalemia is a serious electrolyte disorder associated with CKD. Fatal dysrhythmias can occur when the serum potassium level reaches 7 to 8 mEq/L (7 to 8 mmol/L). Hyperkalemia results from the decreased excretion of potassium by the kidneys, the breakdown of cellular protein, bleeding, and metabolic acidosis. Potassium may come from foods, dietary supplements, drugs, and IV infusions.

Sodium Sodium may be high, normal, or low in kidney disease. Because of impaired sodium excretion, sodium is retained with water. If large quantities of water are retained, dilutional hyponatremia occurs. Sodium retention can contribute to edema, hypertension, and HF. Sodium intake is patient specific but is generally restricted to 2 g/day.

Calcium and Phosphate Calcium and phosphate changes are discussed in the section on the musculoskeletal system on pp. 1068–1069.

Magnesium Magnesium is primarily excreted by the kidneys. Hypermagnesemia is generally not a problem unless the patient is ingesting magnesium (e.g., Milk of Magnesia, magnesium citrate, antacids containing magnesium). Manifestations can include absent reflexes, decreased mental status, dysrhythmias, hypotension, and respiratory failure.

Metabolic Acidosis Metabolic acidosis results from the kidneys’ impaired ability to excrete excess acid and from defective reabsorption and regeneration of HCO3−. The average adult makes 80 to 90 mEq of acid per day. This acid is normally buffered by HCO3−. In kidney disease, plasma HCO3−, which is an indirect measure of acidosis, usually falls to a new steady state at around 16 to 20 mEq/L (16 to 20 mmol/L). The decreased plasma HCO3− reflects its use in buffering metabolic acids. The HCO3− level generally does not progress below this level because hydrogen ion production is usually balanced by buffering from demineralization of the bone (the phosphate buffering system).

Hematologic System Anemia A normocytic, normochromic anemia is associated with CKD. Anemia in CKD is due to decreased production of the hormone erythropoietin by the kidneys. Erythropoietin normally stimulates precursor cells in the bone marrow to make RBCs (erythropoiesis). Other factors contributing to anemia are nutritional deficiencies, decreased RBC life span, increased hemolysis of RBCs, frequent blood samplings, and GI bleeding. For patients receiving maintenance HD, blood loss in the

dialyzer can contribute to the anemic state. Increased parathyroid hormone (PTH) (made to compensate for low serum calcium levels) can inhibit erythropoiesis, shorten survival of RBCs, and cause bone marrow fibrosis, which can result in decreased numbers of hematopoietic cells. We need sufficient iron stores for erythropoiesis. Many patients with kidney disease are iron deficient and need iron supplementation. Oral iron supplements may not be effective for the person with CKD. GI side effects can cause adherence difficulties. Medications, such as proton pump inhibitors or phosphate binders, decrease absorption. Patients on dialysis may need IV iron to restore iron levels. Folic acid, essential for RBC maturation, is dialyzable because it is water soluble. Many patients receive supplemental folic acid (1 mg/day).18

Bleeding Tendencies The most common cause of bleeding in uremia is a qualitative defect in platelet function. This dysfunction is caused by impaired platelet aggregation and impaired release of platelet factor III. Changes in the coagulation system occur due to increased concentrations of both factor VIII and fibrinogen. The altered platelet function, hemorrhagic tendencies, and GI bleeding susceptibility can usually be corrected with regular HD or PD.

Infection Patients with advanced CKD have an increased susceptibility to infection. This is due to changes in WBC function and altered immune response and function. Both cellular and humoral immune responses are suppressed. Other factors contributing to the increased risk for infection include hyperglycemia and external trauma (e.g., catheters, needle insertions into vascular access sites).

Cardiovascular System The most common cause of death in patients with CKD is CVD. Leading causes of death are myocardial infarction (MI), ischemic heart

disease, peripheral arterial disease, HF, cardiomyopathy, and stroke.17 CVD and CKD are so closely linked that if patients develop cardiac events (e.g., MI, HF), kidney function is evaluated. Traditional CVD risk factors, such as hypertension and increased lipids, are common in CKD patients. CVD may be related to vascular calcification and arterial stiffness. Calcium deposits in the vascular medial layer are associated with stiffening of the blood vessels. The mechanisms involved are multifactorial. They include (1) vascular smooth muscle cells changing into chondrocytes or osteoblast-like cells, (2) high total body amount of calcium and phosphate resulting from abnormal bone metabolism, (3) impaired renal excretion, and (4) drug therapies to treat the bone disease (e.g., calcium-phosphate binders).19 Hypertension, which is prevalent in patients with CKD, is both a cause and a consequence of CKD. Hypertension is worsened by sodium retention and increased ECF volume.20 In some people, increased renin production contributes to hypertension. Hypertension and diabetes are contributing risk factors for vascular complications.19 Long-standing hypertension, ECF volume overload, and anemia contribute to development of left ventricular hypertrophy that may eventually lead to cardiomyopathy and HF. Hypertension can cause retinopathy, encephalopathy, and nephropathy. Because of the many effects of hypertension, BP control is one of the most important therapeutic goals in the management of CKD.20 Patients with CKD are susceptible to dysrhythmias from hyperkalemia and decreased coronary artery perfusion. Uremic pericarditis can develop and sometimes progresses to pericardial effusion and cardiac tamponade. Pericarditis typically presents with a friction rub, chest pain, and low-grade fever.

Respiratory System With severe acidosis, the respiratory system may try to compensate with Kussmaul breathing, which results in increased CO2 removal by exhalation (see Chapter 16). Dyspnea may occur because of fluid

overload, pulmonary edema, uremic pleuritis (pleurisy), pleural effusions, and respiratory infections (e.g., pneumonia).

Gastrointestinal System Stomatitis with exudates and ulcerations, a metallic taste in the mouth, and uremic fetor (a urinous odor of the breath) often occur in CKD. Anorexia, nausea, and vomiting may develop if CKD progresses to ESRD and is not treated with dialysis. Weight loss and malnutrition may occur. Diabetic gastroparesis (delayed gastric emptying) can compound the effects of malnutrition for patients with diabetes. GI bleeding is a risk because of mucosal irritation and the platelet defect. Constipation may be due to ingesting iron salts or calciumcontaining phosphate binders. Limitations on fluid intake and physical inactivity can increase the risk for constipation.

Neurologic System Neurologic changes are expected as kidney disease progresses. They are the result of increased nitrogenous waste products, electrolyte imbalances, metabolic acidosis, and atrophy and demyelination of nerve fibers. The central nervous system (CNS) becomes depressed, resulting in lethargy, apathy, decreased ability to concentrate, fatigue, irritability, and altered mental ability. Seizures and coma may result from a rapidly increasing BUN and hypertensive encephalopathy. Peripheral neuropathy initially manifests as a slowing of nerve conduction to the extremities. The patient may describe paresthesias in the feet and legs as a burning sensation. Eventually, motor involvement may lead to bilateral foot drop, muscular weakness and atrophy, and loss of deep tendon reflexes. Muscle twitching, jerking, asterixis (hand-flapping tremor), and nocturnal leg cramps may occur. In patients with diabetic neuropathy, uremic neuropathy can compound symptoms.21 Those with advanced stage 5 CKD may develop restless legs syndrome (see Chapter 58). Dialysis should improve general CNS manifestations and may slow or halt the progression of neuropathies. Motor neuropathy may not be

reversible. The treatment for neurologic problems is dialysis or transplantation. Altered mental status, a late manifestation of CKD stage 5, rarely occurs unless the patient has chosen not to have RRT.

Musculoskeletal System CKD mineral and bone disorder (CKD-MBD) develops as a systemic disorder of mineral and bone metabolism caused by progressive deterioration in kidney function (Fig. 46.3). Activated vitamin D is necessary to optimize absorption of calcium from the GI tract. As kidney function deteriorates, less vitamin D is converted to its active form, resulting in decreased serum levels. Low levels of active vitamin D result in decreased serum calcium levels.19

FIG. 46.3 Mechanisms of CKD-MBD. GFR, Glomerular filtration rate; PTH, parathyroid hormone.

Serum calcium levels are regulated primarily by PTH. When hypocalcemia occurs, the parathyroid gland secretes PTH, which stimulates bone demineralization, releasing calcium from the bones. Phosphate is also released, leading to high serum phosphate levels. Hyperphosphatemia results from decreased phosphate excretion by the kidneys. It decreases serum calcium levels and further reduces the kidneys’ ability to activate vitamin D.

Low serum calcium, increased phosphate, and decreased vitamin D contribute to the stimulation of the parathyroid gland and excretion of PTH. PTH acts on the bone to increase remodeling and increase serum calcium levels. The accelerated rate of bone remodeling causes a weakened bone matrix and places the patient at a higher risk for fractures. Normally plasma calcium is found ionized or free (physiologically active form) or bound to protein. Low ionized calcium levels can lead to tetany (see Chapter 16). However, in CKD, it is unusual for hypocalcemia to be symptomatic. In the acidotic state associated with CKD, more calcium is in the ionized form than is bound to protein. CKD-MBD is a common complication of CKD and results in skeletal complications, vascular and soft tissue (extraskeletal) complications. Skeletal complications include (1) osteomalacia (results from demineralization from slow bone turnover and defective mineralization of newly formed bone) and (2) osteitis fibrosa (decalcification of the bone and replacement of bone tissue with fibrous tissue). Soft tissue complications result from vascular calcifications. Vascular calcifications are a significant contributing factor to CVD. Irritation from calcium deposits in the eye can cause “uremic red eye.” Intracardiac calcifications can disrupt the conduction system and cause cardiac arrest.

Integumentary System A small number of patients develop refractory pruritus that can have a devastating impact on their well-being and quality of life. Pruritus has multiple causes, including dry skin, calcium-phosphate deposition in the skin, and sensory neuropathy. It is more common in patients receiving dialysis than in the earlier stages of CKD. The itching may be so intense that it can lead to bleeding or infection from scratching. Uremic frost is an extremely rare condition in which urea crystallizes on the skin. This is usually seen only when BUN levels are extremely high (e.g., over 200 mg/dL).

Reproductive System Both men and women can have infertility and a decreased libido. Women usually have low levels of estrogen, progesterone, and luteinizing hormone, causing anovulation and menstrual changes (usually amenorrhea). Menses and ovulation may return after starting dialysis. Men have loss of testicular consistency, decreased testosterone levels, and low sperm counts. Sexual dysfunction may be caused by anemia, which causes fatigue and decreased libido. Peripheral neuropathy can cause impotence in men and anorgasmia in women. Other factors that may cause changes in sexual function are psychologic problems (e.g., anxiety, depression), physical stress, and medication side effects. Sexual function may improve with maintenance dialysis and become normal with successful transplantation. Patients who become pregnant while receiving dialysis have been able to carry a fetus to term, but there is significant risk to the mother and infant. Pregnancy in patients with a kidney transplant is more common, but there is still considerable risk to both the mother and fetus.

Psychologic Changes Personality and behavioral changes, emotional lability, withdrawal, and depression often occur in patients with CKD. Fatigue and lethargy contribute to the feeling of illness. The changes in body image caused by edema, integumentary changes, and access devices (e.g., fistulas, catheters) may lead to anxiety and depression. Decreased ability to concentrate and slowed mental activity can give the appearance of dullness and disinterest in the environment. The patient must deal with significant changes in lifestyle, occupation, family responsibilities, and financial status. Long-term survival depends on medications, dietary restrictions, dialysis, and possibly transplantation. The patient grieves the loss of kidney function and independence.

Diagnostic Studies Persistent proteinuria is usually the first sign of kidney damage. Screening for CKD involves a dipstick evaluation of protein in the urine or evaluation for albuminuria, which is not detected with routine urinalysis. The urine of patients with diabetes must be examined for albuminuria if no protein is present on routine urinalysis. A person with persistent proteinuria (1+ protein on standard dipstick testing 2 or more times over a 3-month period) should have further assessment of risk factors and a diagnostic workup with blood and urine tests to evaluate for CKD. A urinalysis can detect RBCs, WBCs, protein, casts, and glucose. A renal ultrasound is usually done to detect any obstructions and determine the size of the kidneys. Other diagnostic studies (Table 46.9) help establish the diagnosis and cause of CKD. A kidney biopsy may be necessary to provide a definitive diagnosis. Serum creatinine alone poorly reflects kidney function. GFR is the preferred measure to determine kidney function. Several GFR calculators are available. The equations used most often to estimate GFR are the Cockcroft-Gault formula and Modification of Diet in Renal Disease (MDRD) Study equation (Table 46.8). MDRD is the preferred method.22

TABLE 46.9 Interprofessional CareChronic

Kidney Disease

Diagnostic Assessment • History and physical examination • Identification of reversible kidney disease • Renal ultrasound, renal scan, CT scan • Renal biopsy • BUN, serum creatinine, and creatinine clearance levels

• Serum electrolytes • Lipid profile • Urinalysis • Protein-to-creatinine ratio in first morning voided specimen • Hematocrit and hemoglobin levels

Management • Correction of extracellular fluid volume overload or deficit • RRT (dialysis, kidney transplant) • Nutritional therapy (Tables 46.10 and 16.6) • Measures to lower potassium (Table 46.5)

Drug Therapy • Calcium supplementation, phosphate binders, or both • Antihypertensive therapy • ACE inhibitors or ARBs • Erythropoietin therapy • Lipid-lowering drugs • Adjustment of drug dosages to degree of renal function

Interprofessional Care The overall goals of CKD therapy are to preserve existing kidney function, reduce the risks for CVD, prevent complications, and provide for the patient’s comfort. Early recognition, diagnosis, and treatment can prevent the progression of kidney disease. It is important that patients with CKD receive appropriate referral to a nephrologist early in the course of the disease. Every effort is made to detect and treat potentially reversible causes of kidney failure (e.g., HF, dehydration, infections, nephrotoxins, urinary tract obstruction,

glomerulonephritis, renal artery stenosis). Patients with CKD have a high incidence of CVD. More patients die from CVD than live to need dialysis. When a patient has CKD, therapy is aimed at treating CVD in addition to slowing the progression of kidney disease (Table 46.9). A focus on stages 1 through 4 (Table 46.7) before the need for dialysis (stage 5) includes the control of hypertension, hyperparathyroidism, CKD-MBD, anemia, and dyslipidemia. The next section focuses primarily on the drug and nutritional aspects of care.

Drug Therapy Hyperkalemia Multiple strategies are used to manage hyperkalemia (Table 46.5). These include restricting high-potassium foods and drugs. Acute hyperkalemia may need treatment with IV glucose and insulin or IV 10% calcium gluconate. Sodium polystyrene sulfonate, a cation-exchange resin, is often given to lower potassium levels in stage 4 CKD. Sodium polystyrene sulfonate has an osmotic laxative action and ensures evacuation of the potassium from the bowel. Tell the patient to expect some diarrhea. Never give sodium polystyrene sulfonate to a patient with a hypoactive bowel (paralytic ileus) because fluid shifts could lead to bowel necrosis. Since sodium polystyrene sulfonate exchanges sodium ions for potassium ions, observe the patient for sodium and water retention. If changes appear in the ECG, such as peaked T waves and widened QRS complexes, dialysis may be needed to remove excess potassium. Patiromer (Veltassa) is an oral suspension that binds potassium in the GI tract. It is used to treat hyperkalemia in persons with CKD. It should not be used in emergency situations to treat hyperkalemia because of its delayed onset of action. Because this drug can bind other oral medications, it needs to be taken at least 6 hours before or 6 hours after other oral medications.

Hypertension For some, the progression of CKD can be delayed by controlling hypertension.20 Treatment of hypertension includes (1) weight loss (if indicated), (2) therapeutic lifestyle changes (e.g., exercise, avoidance of alcohol, smoking cessation), (3) diet recommendations (DASH Diet), and (4) antihypertensive drugs. Most patients need 2 or more drugs to reach target BP. The treatment of hypertension is discussed in Chapter 32. Prescribed medications depend on whether the patient with CKD has diabetes. ACE inhibitors and ARBs are given to patients with diabetes and those with nondiabetic proteinuria. They decrease proteinuria and may delay the progression of CKD. They must be used with caution as they can further decrease the GFR and increase serum potassium levels. Measure the BP with the patient in the supine, sitting, and standing positions to monitor the effect of antihypertensive drugs. Teach the patient and caregiver how to monitor the BP at home and what readings require immediate intervention.

CKD-MBD It is hard to determine what type of bone disease a patient may have by just looking at the serum levels of calcium, phosphorus, PTH, and alkaline phosphatase. The gold standard for diagnosis is a bone biopsy. Interventions for CKD-MBD include limiting dietary phosphorus, giving phosphate binders, supplementing vitamin D, and controlling hyperparathyroidism.19 Phosphate intake is not usually restricted until the patient needs RRT. At that time, phosphate is usually limited to about 1 g/day, but dietary control alone is usually inadequate. Phosphate binders include calcium-based binders, calcium acetate, and calcium carbonate. They bind phosphate in the bowel and then excrete it in the stool. Giving calcium may increase the calcium load and place the patient at increased risk for vascular calcifications. So, when calcium levels are increased or there is evidence of existing vascular or soft tissue calcifications, non–calcium-based phosphate

binders may be used. These include lanthanum carbonate (Fosrenol); sevelamer carbonate (Renvela;, and iron-based, calcium-free phosphate binders, such as sucroferric oxyhydroxide (Velphoro) and ferric citrate (Auryxia). To be most effective, give phosphate binders with each meal. Constipation is a frequent side effect of phosphate binders. Stool softeners may be needed. Because bone disease (osteomalacia) is associated with excess aluminum, aluminum preparations should be used with caution in patients with kidney disease. Do not use magnesium-containing antacids (e.g., Maalox, Mylanta) because magnesium depends on the kidneys for excretion. Hypocalcemia is a problem in the later stages of CKD due to the inability of the GI tract to absorb calcium in the absence of active vitamin D. If hypocalcemia persists even if the serum phosphate levels are normal, supplemental calcium and vitamin D should be given. Assess vitamin D levels to determine the need for supplementation. If the levels are low (serum values less than 30 ng/mL), vitamin D is given in the form of cholecalciferol. Treatment of secondary hyperparathyroidism in ESRD patients requires the activated form of vitamin D because the kidneys cannot activate vitamin D. Active vitamin D is available as oral or IV calcitriol (Rocaltrol), IV paricalcitol (Zemplar), or oral or IV doxercalciferol (Hectorol). Their use can reduce the high PTH levels. Cinacalcet (Sensipar), a calcimimetic agent, is used to control secondary hyperparathyroidism. Calcimimetics mimic calcium and increase the sensitivity of the calcium receptors in the parathyroid glands. As a result, the parathyroid glands detect calcium at lower serum levels and decrease PTH secretion. If parathyroid disease becomes severe, a subtotal or total parathyroidectomy may be done to decrease the synthesis and secretion of PTH. In most cases, a total parathyroidectomy is done and parathyroid tissue transplanted into the forearm. The transplanted cells make PTH as needed. If PTH production becomes excessive, some cells can be removed from the forearm.

Hypercalcemia may occur with calcium and vitamin D supplementation. If hypercalcemia occurs, vitamin D may be withheld, and calcium-based phosphate binders replaced with non– calcium-based phosphate binders.

Anemia Anemia in CKD is caused by a decreased production of erythropoietin by the kidneys. Exogenous erythropoietin (EPO) is used to treat anemia. It is available as epoetin alfa (Epogen, Procrit), which can be given IV or subcutaneously, usually 2 or 3 times per week. Darbepoetin alfa (Aranesp) is longer acting and can be given weekly or biweekly. Hemoglobin and hematocrit levels may take 2 to 3 weeks to increase. Higher hemoglobin levels (more than 12 g/dL) and higher doses of EPO are associated with a higher rate of thromboembolic events and increased risk for death from serious CV events (MI, HF, stroke). The recommendation is to use the lowest possible dose of EPO to treat anemia. Treatment of CKD-related anemia is patient specific with the goal being to reduce the need for blood transfusions. There is no target hemoglobin or widely accepted EPO dosing strategy. Teach people who are prescribed EPO about the risks and benefits and allow them to decide about their treatment plan. EPO can increase BP and is contraindicated in uncontrolled hypertension. The underlying mechanism is related to the hemodynamic changes (e.g., increased whole blood viscosity) that occurs as the anemia is corrected. EPO therapy may lead to iron deficiency from the increased demand for iron to support erythropoiesis. Iron supplementation is recommended if the plasma ferritin concentrations fall below 100 ng/mL. Most CKD patients receive iron supplementation. Although iron can be given by mouth or IV, the enteral route is limited due to GI side effects, which decrease patient adherence. Oral iron should not be taken at the same time as phosphate binders because calcium binds the iron, preventing its absorption. Tell the

patient that iron may make the stool dark in color. Most patients receiving HD are prescribed IV iron sucrose (Venofer) or sodium ferric gluconate complex (Ferrlecit). Supplemental folic acid (1 mg/day) is usually given because it is needed for RBC formation and is removed by dialysis. Blood transfusions are avoided unless the patient has an acute blood loss or has symptomatic anemia (i.e., dyspnea, excess fatigue, tachycardia, palpitations, chest pain). Transfusions increase the development of antibodies, thus making it harder to find a compatible donor for kidney transplantation. Multiple blood transfusions may lead to iron overload because each unit of blood has about 250 mg of iron.

Dyslipidemia Dyslipidemia, a risk factor for CVD, is a common problem in CKD. Statins (HMG-CoA reductase inhibitors), such as atorvastatin (Lipitor), are used to lower LDL cholesterol levels (see Table 33.6). Statins should be used in patients with CKD, especially those with diabetes, not yet on dialysis. 23 Fibrates (fibric acid derivatives), such as gemfibrozil (Lopid), are used to lower triglyceride levels (see Table 33.6) and can increase HDLs. Specific drugs used in these classes depend on the individual patient response and HCP recommendation.

Complications of Drug Therapy The kidneys partially or totally excrete many drugs. CKD causes decreased elimination that leads to an accumulation of drugs and the potential for drug toxicity. Drug doses and frequency of administration are adjusted based on the severity of the kidney disease. Increased sensitivity may result as drug levels increase in the blood and tissues. Drugs of particular concern include digoxin, diabetic agents (metformin, glyburide), antibiotics (e.g., vancomycin, gentamicin), and opioid drugs.

Nutritional Therapy

Protein Restriction The current diet for the person with CKD is designed to maintain good nutrition (Table 46.10). Calorie-protein malnutrition is a potential and serious problem that results from altered metabolism, anemia, proteinuria, anorexia, and nausea. Other factors leading to malnutrition include depression and complex diets that restrict protein, phosphorus, potassium, and sodium. Frequent monitoring of laboratory parameters, especially serum albumin, prealbumin, and ferritin, and anthropometric measurements are necessary to evaluate nutritional status. All patients with CKD should be referred to a dietitian for nutritional teaching. For the patient undergoing dialysis, protein is not routinely restricted. For CKD stages 1 through 4, many HCPs encourage a diet with normal protein intake. Teach patients to avoid high-protein diets and supplements because they may overburden the diseased kidneys.24 Dietary protein guidelines for PD differ from those for HD because of protein loss through the peritoneal membrane. During PD, protein intake must be high enough to compensate for the losses so that the nitrogen balance is maintained. The recommended protein intake is at least 1.2 g/kg of ideal body weight (IBW) per day. This can be increased depending on the patient’s needs. For patients with malnutrition or inadequate caloric or protein intake, commercially prepared products that are high in protein but low in sodium and potassium are available (e.g., Nepro, Amin-Aid). As an alternative, liquid or powder breakfast drinks may be bought at the grocery store.

Fluid Restriction Water and any other fluids are not routinely restricted in patients with CKD stages 1 to 5 who are not receiving HD. To reduce fluid retention, diuretics are often used. Patients on HD have a more restricted fluid intake than patients receiving PD. For those receiving HD, as their urine output decreases, fluids are restricted. Recommended fluid intake depends on the daily urine output.

Generally, 600 mL (from insensible loss) plus an amount equal to the previous day’s urine output is allowed for a patient receiving HD.

TABLE 46.10 Nutritional TherapyChronic

Kidney Disease

Foods that are liquid at room temperature (e.g., gelatin, ice) are counted as fluid intake. Space fluid allotment throughout the day so that the patient does not become thirsty. Teach patients to limit fluid intake so that weight gains are no more than 1 to 3 kg between dialyses (interdialytic weight gain).

Sodium and Potassium Restriction Teach patients with CKD to restrict sodium. Sodium-restricted diets may vary from 2 to 4 g/day. Teach the patient to avoid high-sodium foods, such as cured meats, pickled foods, canned soups and stews, frankfurters, cold cuts, soy sauce, and salad dressings (see Table 34.8). Potassium restriction depends on the kidneys’ ability to excrete potassium. Salt substitutes should be avoided in potassium-restricted diets because they contain potassium chloride. Dietary restrictions for potassium range from about 2000 to 3000 mg (39 mg = 1 mEq). Teach patients receiving HD which foods are high in

potassium and to avoid them (see Table 16.6). Patients using PD do not usually need potassium restrictions. They may need oral potassium supplementation because of the loss of potassium with dialysis exchanges.

Phosphate Restriction As kidney function deteriorates, phosphate elimination by the kidneys is decreased and the patient begins to develop hyperphosphatemia. By the time a patient reaches ESRD, phosphate is limited to around 1 g/day. Foods that are high in phosphate include meat and dairy products (e.g., milk, ice cream, cheese, yogurt, pudding). Many foods that are high in phosphate are also high in protein. Since patients on dialysis are encouraged to eat a diet containing protein, phosphate binders are essential to control the phosphate level.

Nursing Management: Chronic Kidney Disease Nursing Assessment Obtain a complete history of any existing kidney disease or family history of kidney disease. Some kidney disorders, including Alport syndrome and polycystic kidney disease, have a genetic component. Other disorders that can lead to CKD are diabetes, hypertension, and SLE. Because many drugs are potentially nephrotoxic, ask the patient about both current and past use of prescription and OTC drugs and herbal preparations. Decongestants and antihistamines that contain pseudoephedrine and phenylephrine cause vasoconstriction and lead to an increase in BP. Magnesium and aluminum from antacids can accumulate in the body because they cannot be excreted. Some antacids have high levels of salt, contributing to hypertension. NSAIDs (aspirin, ibuprofen, naproxen) can contribute to the development of AKI and progression of CKD, especially when taken

in higher doses than recommended. If taken as prescribed, these analgesics are usually considered safe. Assess the patient’s dietary habits and discuss any problems with intake. Measure the patient’s height and weight and evaluate any recent weight changes. The chronicity of kidney disease and the long-term treatment affect virtually every area of a person’s life, including family relationships, social and work activities, self-image, and emotional state. Assess the patient’s support systems. The choice of treatment modality may be related to support systems available.

Nursing Diagnoses Nursing diagnoses for patients with CKD include: • Fluid imbalance • Electrolyte imbalance • Impaired nutritional status • Difficulty coping More information on nursing diagnoses and interventions for the patient with CKD is presented in eNursing Care Plan 46.1, available on the website for this chapter.

Planning The overall goals are that a patient with CKD will (1) show knowledge of and ability to adhere to the therapeutic plan, (2) take part in decision making for the plan of care and future treatment modality, (3) have effective coping strategies, and (4) continue with activities of daily living within physiologic limitations.

Nursing Implementation Health Promotion

Identify those at risk for CKD. At-risk persons include those diagnosed with diabetes or hypertension and people with a history (or a family history) of kidney disease or repeated urinary tract infections (UTIs). They should have regular checkups that include a routine urinalysis and calculation of the estimated GFR. People with diabetes need to have their urine checked for albuminuria if routine urinalysis is negative for protein. Teach patients with diabetes to report any changes in urine appearance (color, odor), frequency, or volume to the HCP. If a patient needs a potentially nephrotoxic drug, it is important to monitor kidney function with serum creatinine, BUN, and GFR. Those at risk must take measures to prevent or delay the progression of CKD. Most important are measures to reduce the risk or progression of CVD. These include glycemic control for patients with diabetes (see Chapter 48), BP control (see Chapter 32), and lifestyle modifications, including smoking cessation.

TABLE 46.11 Patient & Caregiver

TeachingChronic Kidney Disease Include the following information in the teaching plan for the patient and caregiver: 1. Dietary (sodium, potassium, phosphate) and fluid restrictions. 2. Common problems patient will encounter in modifying diet and fluid intake. 3. Signs and symptoms of electrolyte imbalance, especially high potassium. 4. Alternative ways of reducing thirst, such as sucking on ice cubes, lemon, or hard candy. 5. Reasons for prescribed drugs and common side effects. Examples: • Phosphate binders (including calcium supplements used as phosphate barriers) should be taken with

meals. • Take calcium supplements prescribed to treat hypocalcemia on an empty stomach, but not at the same time as iron supplements. • Iron supplements should be taken between meals. 6. The importance of reporting any of the following: weight gain >4 lb (2 kg), increasing BP, shortness of breath, edema, increasing fatigue or weakness, or confusion or lethargy 7. Need for support and encouragement. Share concerns about lifestyle changes, living with a chronic illness, and decisions about type of dialysis or transplantation.

Promoting Population Health Prevention and Detection of Chronic Kidney Disease • Early detection and treatment are the primary methods for reducing CKD. • Ensure proper diagnosis and treatment of diabetes as it is the leading cause of CKD. • Monitor BP to detect elevations so that treatment can be started early. • Treat hypertension appropriately and aggressively as it is the second leading cause of CKD.

Acute Care Most of the care of the patient with CKD occurs on an outpatient basis. In-hospital care is needed for management of complications and for kidney transplantation (if applicable).

Ambulatory Care

Encourage patients to take part in their care. Teach the patient and caregiver about the diet, drugs, and follow-up medical care (Table 46.11). The patient needs to understand the drugs and common side effects. Because patients with CKD take many medications, a pillbox organizer or a list of the drugs and the times of administration may be helpful. Tell the patient to avoid OTC medications, such as NSAIDs and aluminum- and magnesium-based laxatives and antacids. Teach the patient to take daily BP readings and watch for signs and symptoms of fluid overload, hyperkalemia, and other electrolyte imbalances. The dietitian should meet with the patient and caregiver on a regular basis for diet planning. A diet history and consideration of cultural variations help with diet planning and adherence. The rate of progression of CKD is dependent on the type of kidney disease and presence of other co-morbid conditions. The patient can complete an evaluation for a kidney transplant prior to the need to start dialysis. Patients may receive a transplant before ever having to start dialysis. Even though transplantation offers the best therapeutic management for many ESRD patients, the critical shortage of donor organs limits this option for many patients. Most patients need either PD or HD. Most patients use HD. Explain to the patient and caregiver what is involved in PD or HD and home HD modalities, transplantation, and palliative care. Offer information about all treatment options so that the patient can be involved in the decision-making process, giving a sense of control over life-altering decisions. Tell the patient that even while on dialysis, transplant is still an option. Let the patient know that if a transplanted organ fails, the patient can return to dialysis. It is important to respect the patient’s choice to not receive treatment. Patients themselves often start the conversation about palliative care. Focus the discussion on moving from the curative approach to promotion of comfort care and consideration of hospice care. Listen to the patient and caregiver, allowing them to do most of the talking and pay special attention to their hopes and fears. (Palliative and end-of-life care is discussed in Chapter 9.)

Evaluation The expected outcomes are that the patient with CKD will maintain • Fluid and electrolyte levels within normal ranges • An acceptable weight with no more than a 10% weight loss

Dialysis Dialysis is the movement of fluid and molecules across a semipermeable membrane from one compartment to another. Clinically, dialysis is a technique in which substances move from the blood through a semipermeable membrane and into a dialysis solution (dialysate). It corrects fluid and electrolyte imbalances and removes waste products in kidney failure. It also can be used to treat drug overdoses. The 2 methods of dialysis available are peritoneal dialysis (PD) and hemodialysis (HD) (Table 46.12). In PD the peritoneal membrane acts as the semipermeable membrane. In HD an artificial membrane (usually made of cellulose-based or synthetic materials) is used as the semipermeable membrane and is in contact with the patient’s blood. Dialysis is begun when the patient’s uremia can no longer be adequately treated with conservative medical management. Generally, this is when the GFR is less than 15 mL/min/1.73 m2. This criterion can vary widely in different clinical situations. The nephrologist determines when to start dialysis based on the patient’s clinical status. Certain uremic complications, including encephalopathy, neuropathies, uncontrolled hyperkalemia, pericarditis, and accelerated hypertension, indicate a need for immediate dialysis. Most patients with ESRD are treated with dialysis because (1) there is a lack of donated organs, (2) some patients are physically or mentally unsuitable for transplantation, or (3) some patients do not want transplants. An increasing number of people, including older adults and those with complex medical problems, are receiving

maintenance dialysis. A patient’s age is not a factor in determining candidacy for dialysis.

TABLE 46.12 Comparison of Peritoneal Dialysis

and Hemodialysis

General Principles of Dialysis Solutes and water move across the semipermeable membrane from the blood to the dialysate or from the dialysate to the blood per concentration gradients. The principles of diffusion, osmosis, and ultrafiltration are involved in dialysis (Fig. 46.4). Diffusion is the movement of solutes from an area of greater concentration to an area of lesser concentration. In kidney failure, urea, creatinine, uric acid, and electrolytes (potassium, phosphate) move from the blood to the dialysate with the net effect of lowering their concentration in the blood. RBCs, WBCs, and plasma proteins are too large to diffuse through the pores of the membrane. Small-molecular-weight substances can pass from the dialysate into a patient’s blood, so the

purity of the water used for dialysis is monitored and controlled. Osmosis is the movement of fluid from an area of lesser concentration to an area of greater concentration of solutes. Glucose is added to the dialysate and creates an osmotic gradient across the membrane, pulling excess fluid from the blood. Ultrafiltration (water and fluid removal) results when there is an osmotic gradient or pressure gradient across the membrane. In PD, excess fluid is removed by increasing the osmolality of the dialysate (osmotic gradient) with the addition of glucose. In HD, the gradient is created by increasing pressure in the blood compartment (positive pressure) or decreasing pressure in the dialysate compartment (negative pressure). ECF moves into the dialysate because of the pressure gradient. The excess fluid is removed by creating a pressure differential between the blood and the dialysate solution with a combination of positive pressure in the blood compartment and negative pressure in the dialysate compartment.

FIG. 46.4 Osmosis and diffusion across a semipermeable membrane.

Peritoneal Dialysis Although PD was first used in 1923, it did not come into widespread use for chronic treatment until the 1970s with the development of soft, pliable peritoneal solution bags and the introduction of the concept of continuous PD. In the United States, about 12% of patients receiving dialysis treatments are on PD.

Catheter Placement Peritoneal access is obtained by inserting a catheter through the anterior abdominal wall (Fig. 46.5). The catheter is about 24 in (60 cm) long and has 1 or 2 Dacron cuffs. The cuffs act as anchors and prevent the migration of microorganisms into the peritoneum. Within a few weeks, fibrous tissue grows into the Dacron cuff, holding the catheter in place and preventing bacterial penetration into the peritoneal cavity. The tip of the catheter rests in the peritoneal cavity. It has many perforations spaced along the distal end of the tubing, allowing fluid movement through the catheter. The technique for catheter placement varies. It is usually placed surgically so that the catheter can be seen directly, minimizing potential complications. Patient preparation for catheter insertion includes emptying the bladder and bowel, weighing the patient, and obtaining a signed consent form. After placement, PD may be started at once with low-volume exchanges or delayed for 2 weeks pending healing and sealing of the exit site. Once the catheter incision site is healed, the patient may shower and then pat the catheter and exit site dry.25 Daily catheter care varies. Some patients just wash with soap and water and go without a dressing (Fig. 46.6). Others need daily dressing changes. Showering is preferred to bathing.

FIG. 46.5 Peritoneal dialysis showing peritoneal catheter inserted into peritoneal cavity.

FIG. 46.6 Peritoneal catheter exit site. Courtesy Mary Jo Holechek, Baltimore, MD.

In PD it is critical to maintain aseptic technique to avoid peritonitis. Several tubing connections and devices are commercially available to help maintain an aseptic system. Teach all patients to examine their catheter site for signs of infection.

Dialysis Solutions and Cycles PD is done by putting dialysis solution into the peritoneal space. The 3 phases of the PD cycle are inflow (fill), dwell (equilibration), and drain. Together, the 3 phases are an exchange. For manual PD, a period of about 30 to 50 minutes is needed to complete an exchange. During inflow, a prescribed amount of solution, usually 2 L, is infused through an established catheter over about 10 minutes. The flow rate may be decreased if the patient has pain. After the solution has been infused, the inflow clamp is closed. The next part of the cycle is the dwell phase, or equilibration, during which diffusion and osmosis occur between the patient’s blood and

peritoneal cavity. The duration of the dwell time is usually between 4 and 6 hours. Drain time takes 15 to 30 minutes. It may be facilitated by gently massaging the abdomen or changing position. The cycle starts again with the infusion of another 2 L of solution. PD solutions vary. The choice of the exchange volume is primarily determined by the size of the peritoneal cavity. An average-size person typically uses a 2-L exchange. A larger person may need a 3-L exchange volume. Smaller exchange volumes are used for patients with a smaller body, pulmonary compromise (the added pressure of the large volume may cause respiratory problems), or inguinal hernias.

FIG. 46.7 Automated PD that can be used while the patient is sleeping.

Ultrafiltration (fluid removal) during PD depends on osmotic forces. Dextrose is the most commonly used osmotic agent in PD solutions. It

is relatively safe and inexpensive. It is associated with high rates of peritoneal glucose absorption, leading to problems with hypertriglyceridemia, hyperglycemia, and long-term peritoneal membrane dysfunction. Alternatives to dextrose PD solution include icodextrin and amino acid solutions. Icodextrin is a commercially available iso-osmolar preparation. It induces ultrafiltration by its oncotic effect. Amino acid PD solutions are available and used mainly for patients who need nutritional supplementation.

Peritoneal Dialysis Systems Automated Peritoneal Dialysis Automated peritoneal dialysis (APD) is the most popular form of PD because it allows patients to do dialysis while they sleep. An automated device called a cycler delivers the dialysate for APD (Fig. 46.7). The size of a cycler is similar to a DVD player. The automated cycler times and controls the fill, dwell, and drain phases. The machine cycles 4 or more exchanges per night with 1 to 2 hours per exchange. Alarms and monitors are built into the system to make it safe for the patient to sleep while dialyzing. The patient disconnects from the machine in the morning and usually leaves fluid in the abdomen during the day. It is hard to achieve the required solute and fluid clearance solely with nighttime APD. One or 2 daytime manual exchanges may be prescribed to ensure adequate dialysis.

Continuous Ambulatory Peritoneal Dialysis Continuous ambulatory peritoneal dialysis (CAPD) is done every few hours during the day. The patient may perform an exchange of 2 L of peritoneal dialysate 4 times daily, with dwell times averaging 4 hours. A common schedule includes exchanges at 7 AM, 12 noon, 5 PM, and 10 PM. In CAPD, the person instills 2 to 3 L of dialysate from a plastic bag into the peritoneal cavity through a disposable administration line.

The bag and line are then disconnected. After the equilibration period, the line is reconnected to the catheter, the dialysate (effluent) is drained from the peritoneal cavity, and a new 2- to 3-L bag of dialysate solution is infused.

Complications of Peritoneal Dialysis Exit Site Infection Infection of the peritoneal catheter exit site is most often caused by Staphylococcus aureus or Staphylococcus epidermidis (from skin flora). Manifestations include redness at the site, tenderness, and drainage. Superficial exit site infections caused by these organisms generally resolve with antibiotic therapy. If not treated immediately, subcutaneous tunnel infections may progress and may cause peritonitis, necessitating catheter removal.

Peritonitis Peritonitis results from contact contamination or an exit site or tunnel infection. Most often it occurs because of improper technique when connections for exchanges are contaminated. Peritonitis is usually caused by S. aureus or S. epidermidis. It rarely results from bacteria in the intestine crossing into the peritoneal cavity. The main manifestations are abdominal pain, rebound tenderness, and cloudy peritoneal effluent with a WBC count greater than 100 cells/µL (more than 50% neutrophils) or bacteria in the peritoneal effluent shown by Gram stain or culture. GI manifestations may include diarrhea, vomiting, abdominal distention, and hyperactive bowel sounds. Fever may or may not be present. To determine if the peritoneal effluent is cloudy, drain the effluent and place the drained bag on reading material, such as a newspaper. If you cannot read the print through the effluent, it is cloudy. Cultures, Gram stain, and a WBC differential of the peritoneal effluent are used to confirm the diagnosis of peritonitis. Antibiotics can be given orally, IV, or intraperitoneally. In most cases, the patient is treated on an outpatient basis.

The formation of adhesions in the peritoneum can result from repeated infections and interferes with the peritoneal membrane’s ability to act as a dialyzing surface. Repeated infections may require the removal of the peritoneal catheter and a temporary or permanent change of modality to HD.

Hernias Increased intraabdominal pressure from the dialysate volume can cause hernias to develop in predisposed persons, such as multiparous women and older men. After hernia repair, PD often can be resumed after several days using small dialysate volumes and keeping the patient supine.

Lower Back Problems Increased intraabdominal pressure can cause or worsen lower back pain. The lumbosacral curvature is increased by intraperitoneal infusion of dialysate. Orthopedic binders and a regular exercise program for strengthening the back muscles are helpful for some patients.

Bleeding After peritoneal catheter placement, it is common for the PD effluent drained after the first few exchanges to be pink or slightly bloody from trauma associated with catheter insertion. Bloody effluent over several days or the new appearance of blood in the effluent can indicate active intraperitoneal bleeding. If this occurs, check the BP and hematocrit. Blood may be present in the effluent of women who are menstruating or ovulating. This requires no intervention.

Pulmonary Complications Atelectasis, pneumonia, and bronchitis may occur from repeated upward displacement of the diaphragm, resulting in decreased lung expansion. Longer dwell times increase the risk for pulmonary problems. Frequent repositioning and deep-breathing exercises can

help. When the patient is lying in bed, elevate the head of the bed to prevent these problems.

Protein Loss The peritoneal membrane is permeable to plasma proteins, amino acids, and polypeptides. These substances are lost in the dialysate fluid. The amount of loss is usually about 0.5 g/L of dialysate drainage, but it can be as high as 10 to 20 g/day. This loss may increase to as much as 40 g/day during episodes of peritonitis as the peritoneal membrane becomes more permeable. Unresolved peritonitis is associated with excessive protein loss that can result in malnutrition. PD may need to stop temporarily or sometimes permanently.

Effectiveness of Chronic Peritoneal Dialysis Mortality rates are similar between in-center HD patients and PD patients for the first few years. After about 2 years, mortality rates for patients receiving PD increase, especially for the older person with diabetes and patients with a prior history of CVD.25 The primary advantage of PD is its simplicity and that it is a homebased program, increasing patient participation in their care. Learning the self-management skills needed to do PD usually involves a 3- to 7day training program. There is no need for special water systems. Equipment setup is relatively simple.

Hemodialysis Vascular Access Sites HD requires a very rapid blood flow and access to a large blood vessel. Obtaining vascular access is one of the hardest problems associated with HD. Enough time is needed for evaluation and consideration of the best arteriovenous (AV) access for HD. The types of vascular access include AV fistulas (AVFs), AV grafts (AVGs), and

temporary vascular access.26

Arteriovenous Fistulas and Grafts A subcutaneous arteriovenous fistula (AVF) is usually created in the forearm or upper arm with an anastomosis between an artery and a vein (usually cephalic or basilic) (Figs. 46.8, A, and 46.9). The fistula allows arterial blood to flow through the vein. The vein becomes “arterialized,” increasing in size and developing thicker walls. The arterial blood flow is essential to provide the rapid blood flow needed for HD. As the fistula matures, it is more amenable to repeated venipunctures. Maturation may take 6 weeks to months. AVF should be placed at least 3 months before starting HD. A fistula is the preferred access for HD.26 Normally, a thrill (buzzing sensation) can be felt by palpating the fistula, and a bruit (rushing sound) can be heard with a stethoscope. The thrill and bruit are created by arterial blood moving at a high velocity through the vein.

Check Your Practice You are rotating to the inpatient dialysis unit today. It is your first time working with HD patients. You are helping a hemodialysis tech “hook-up” a 56-yr-old man to HD. He has been on HD for 5 years due to polycystic kidney disease. You take his vital signs, palpate his AV fistula, and then use your stethoscope to auscultate the AV fistula. You are concerned because you feel a super-strong pulse and hear a very loud “whoosh” sound. The patient turns to you and just smirks, “I bet you have never had a thrill like that.” • You are very flustered and not sure how to respond. What should you say to him? AVFs are harder to create in patients with a history of severe

peripheral vascular disease (e.g., people with diabetes), those with prolonged IV drug use, and obese women. These persons may need a synthetic graft. Arteriovenous grafts (AVGs) are made of synthetic materials (polytetrafluoroethylene [PTFE, Teflon]) and form a “bridge” between the arterial and venous blood supplies. Grafts are placed under the skin and are surgically anastomosed between an artery (usually brachial) and a vein (usually antecubital) (Fig. 46.8, B). An interval of 2 to 4 weeks is usually needed to allow the graft to heal, but it may be used earlier. Because grafts are made of artificial materials, they are more likely than AVFs to become infected and tend to form clots. When AVG infections occur, they may need surgical removal, since it is hard to completely resolve the infection from the synthetic material.

FIG. 46.8 Vascular access for hemodialysis. A, AVF. B, AVG. C, HeRO Graft.

A common problem in patients on HD is central venous stenosis (CVS) or occlusion. CVS is serious and has a greater impact than peripheral venous stenosis because the central veins are the final pathway for blood flow to the heart. As CVS progresses, vascular access for HD is often lost. HeRO (Hemodialysis Reliable Outflow) Graft is a special bridge access used in patients when other access options are exhausted. It consists of 2 pieces: a reinforced tube to bypass blockages in veins and a dialysis graft anastomosed to an artery to be accessed for HD (Fig. 46.8, C). The HeRO Graft is placed under the skin, like both a fistula and standard graft. The HeRO Graft bypasses the venous system and provides blood flow directly from a target artery to the heart. It may be harder to auscultate the bruit or feel the thrill in this type of access because of the absence of a venous anastomosis. Surgical creation of AV access for HD has several risks. These include distal ischemia (steal syndrome) and pain because too much arterial blood is being shunted or “stolen” from the distal extremity. Manifestations of steal syndrome are pain distal to the access site, numbness or tingling of fingers that may worsen during dialysis, and poor capillary refill. Aneurysms can develop in the AV access and can rupture if left untreated.

FIG. 46.9 AVF created by anastomosing an artery and a vein. Courtesy Dr. Stephen Van Voorst, MD.

FIG. 46.10 Temporary double-lumen vascular access catheter for acute hemodialysis. A, Soft, flexible double-lumen tube is attached to a Y hub. B, The distance between the arterial intake lumen and the venous return lumen typically provides recirculation rates of 5% or less. A, Courtesy Quinton Instrument Co., Seattle, WA.

Safety Alert AV Fistulas and Grafts • Never perform BP measurements, IV line insertion, or venipuncture in an extremity with AV access.

• These special precautions are taken to prevent infection and clotting of the vascular access. • When a patient is hospitalized, place signs in patient’s room and label the arm with a band that says, “No BP, blood draws, or IV in this arm.”

Temporary Vascular Access When immediate vascular access is needed, catheterization of the internal jugular or femoral vein is done. A flexible catheter inserted at the bedside into 1 of these large veins gives access to the circulation without surgery (Fig. 46.10). The catheters usually have a double external lumen with an internal septum separating the 2 internal segments. One lumen is used for blood removal and the other for blood return (Fig. 46.11, A and B). Temporary catheters have high rates of infection, dislodgment, and malfunction. A patient should not be discharged from the hospital with a temporary catheter in place.

FIG. 46.11 A, Right internal jugular placement for a tunneled, cuffed semipermanent catheter. B, Temporary hemodialysis catheter in place. C, Long-term cuffed hemodialysis catheter. B and C, Courtesy Dr. Stephen Van Voorst, MD.

Long-term cuffed HD catheters are often used for temporary vascular access. These catheters give temporary access while the patient is waiting for fistula placement or as long-term access when other forms of access have failed. They exit on the upper chest wall and are tunneled subcutaneously to the internal or external jugular vein (Fig. 46.11, C). The catheter tip rests in the right atrium. It has 1 or 2 subcutaneous Dacron cuffs that prevent infection from tracking along the catheter and anchor the catheter, eliminating the need for sutures.

FIG. 46.12 Parts of a hemodialysis system. Blood is removed via a needle inserted in a fistula or via catheter lumen. It is propelled to the dialyzer by a blood pump. Heparin is infused either as a predialysis bolus or through a heparin pump continuously to prevent clotting. Dialysate is pumped in and flows in the opposite direction of the blood. The dialyzed blood is returned to the patient through a second needle or catheter lumen. Old dialysate and ultrafiltrate are drained and discarded.

Dialyzers

The HD dialyzer is a plastic cartridge that has thousands of parallel hollow tubes or fibers. The fibers are semipermeable membranes made of cellulose-based or other synthetic materials. The blood is pumped into the top of the cartridge and dispersed into all the fibers. Dialysis fluid (dialysate) is pumped into the bottom of the cartridge and bathes the outside of the fibers. Ultrafiltration, diffusion, and osmosis occur across the pores of this semipermeable membrane. When the dialyzed blood reaches the end of the thousands of semipermeable fibers, it converges into a single tube that returns it to the patient. Dialyzers differ in surface area, membrane composition and thickness, clearance of waste products, and removal of fluid.

Procedure for Hemodialysis The needles used for HD are large bore, usually 14 to 16 gauge. They are inserted into the fistula or graft to obtain vascular access. One needle is placed to pull blood from the circulation to the HD machine, and the other needle is used to return the dialyzed blood to the patient. The needles are attached via tubing to dialysis lines. If a patient has a catheter, the 2 blood lines are attached to the 2 catheter lumens. The needle closer to the fistula (red catheter lumen) pulls blood from the patient to the dialyzer using a blood pump. Blood is returned from the dialyzer to the patient through the second needle (blue catheter lumen).27 When blood comes in contact with a foreign material, such as the dialyzer, it tends to clot. Heparin is added to the blood to prevent clotting. In addition to the dialyzer, a dialysate delivery and monitoring system is used (Fig. 46.12). This system pumps the dialysate through the dialyzer, countercurrent to the blood flow. To end the treatment, a saline solution is used to return the blood in the extracorporeal circuit back to the patient through the vascular access. The needles are removed from the patient, and firm pressure is applied to the venipuncture sites until the bleeding stops.

FIG. 46.13 Home hemodialysis is growing in popularity, and machines are more compact. From NxStage Medical, Inc, Lawrence, MA.

Before beginning treatment, assess fluid status (weight, BP, peripheral edema, lung and heart sounds), condition of vascular access, and temperature. The difference between the last postdialysis weight and the present predialysis weight determines the ultrafiltration or the amount of weight (from fluid) to be removed. While the patient is on dialysis, take vital signs at least every 30 to 60 minutes because rapid BP changes may occur.

Settings and Schedules for Hemodialysis Most HD patients are treated in a community-based center and dialyze for 3 to 4 hours 3 days per week. Most people sleep, read, talk,

or watch television during HD. Other schedule options for HD are short daily HD and long nocturnal HD. The patient receiving long nocturnal HD has the advantage of sleeping while dialyzing. Each nocturnal treatment lasts 6 to 8 hours, and the patient dialyzes up to 6 times per week. In addition to in-center HD, home HD is available (Fig. 46.13). The use of home HD often depends on a patient’s family support. One of the main advantages of home HD is that it allows greater freedom in choosing dialysis times. In short daily HD, the patient dialyzes for 2½ to 3 hours per session 5 to 6 days per week. Short daily HD is usually done at home. Patients who choose daily dialysis or nocturnal dialysis may have fewer uremic symptoms, tend to need fewer medications, and have fewer dialysis-related side effects (e.g., hypotension, cramps). In addition, they have more autonomy. Although daily home HD offers the potential of significant health benefits, only about 2% of HD patients dialyze at home.

Complications of Hemodialysis Hypotension Hypotension that occurs during HD primarily results from rapid removal of vascular volume (hypovolemia), decreased cardiac output, and decreased systemic vascular resistance. The drop in BP may cause light-headedness, nausea, vomiting, seizures, vision changes, and chest pain from cardiac ischemia. The usual treatment for hypotension includes decreasing the volume of fluid removed and infusing 0.9% saline solution.

Muscle Cramps We do not completely understand the cause of muscle cramps in HD. Factors associated with developing muscle cramps include hypotension, hypovolemia, high ultrafiltration rate, and low-sodium dialysis solution. Treatment includes reducing the ultrafiltration rate and giving fluids (saline, glucose, mannitol). Hypertonic saline is not

recommended since the sodium load can be problematic. Hypertonic glucose is preferred.

Loss of Blood Blood loss may result from blood not being completely rinsed from the dialyzer, accidental separation of blood tubing, dialysis membrane rupture, or bleeding after removing the needles at the end of HD. If a patient has received too much heparin or has clotting problems, postdialysis bleeding can occur. It is essential to rinse back all blood, avoid excess anticoagulation, and hold firm but nonocclusive pressure on access sites until the risk for bleeding has passed.

Hepatitis Hepatitis B used to have an unusually high prevalence in dialysis patients, but the incidence today is low. Lower transfusion requirements, screening, and recommendations for vaccinations have lowered the incidence. Outbreaks of hepatitis B still occur, likely from breaks in infection control practices. To prevent transmission, all patients and personnel in dialysis units receive hepatitis B vaccine. Currently, hepatitis C virus (HCV) causes most cases of hepatitis in dialysis patients. (Hepatitis is discussed in more detail in Chapter 43.) About 10% of patients undergoing dialysis in the United States are positive for anti-HCV, which indicates a previous infection. Infection control precautions are mandated in caring for the patient with hepatitis C to protect the patient and staff (see Chapter 14). Currently no vaccine is available for hepatitis C.

Effectiveness of Hemodialysis HD is still an imperfect therapy for management of ESRD. It cannot fully replace the normal biologic functions of the kidneys. It can ease many of the symptoms of CKD and, if started early, can prevent certain complications. It does not alter the accelerated rate of CVD and the related high mortality rate. The yearly death rate of patients receiving maintenance HD is

around 19% to 24%. CVD (stroke, MI) causes most deaths. Infectious complications are the second leading cause of death.27 Adaptation to maintenance HD varies considerably. At first, many patients feel positive about the dialysis because it makes them feel better and keeps them alive, but there is often great ambivalence about whether it is worthwhile. Dependence on a machine is a reality. In response to their illness, dialysis patients may be nonadherent or depressed and show suicidal tendencies. The primary nursing goals are to (1) help the patient to maintain a healthy self-image and (2) return the patient to the highest level of function possible, including returning to work.

Continuous Renal Replacement Therapy Continuous renal replacement therapy (CRRT) is a method for treating AKI. It provides a means by which uremic toxins and fluids are removed while acid-base status and electrolytes are adjusted slowly and continuously in a hemodynamically unstable patient. The principle of CRRT is to dialyze patients in a more physiologic way (over 24 hours), just like the kidneys. CRRT is contraindicated if a patient has life-threatening manifestations of uremia (hyperkalemia, pericarditis) that need rapid treatment. CRRT can be used in conjunction with HD. Several types of CRRT are available (Table 46.13). CRRT often uses the venovenous approaches of continuous venovenous hemofiltration (CVVH), continuous venovenous hemodialysis (CVVHD), and continuous venovenous hemodiafiltration (CVVHDF). Vascular access for CRRT is achieved by using a double-lumen catheter (as used in HD [Fig. 46.10]) placed in the jugular or femoral vein. A blood pump propels the blood through the circuit. A highly permeable, hollow-fiber hemofilter removes plasma water and nonprotein solutes, which are collectively termed ultrafiltrate. The ultrafiltration rate (UFR) may range from 0 to 500 mL/hr. Under the

influence of hydrostatic pressure and osmotic pressure, water and nonprotein solutes pass out of the filter into the extracapillary space and drain through the ultrafiltrate port into a collection device (drainage bag) (Fig. 46.14). The remaining fluid continues through the filter and returns to the patient via the return port of the doublelumen catheter.

TABLE 46.13 Continuous Renal Replacement

Therapies

FIG. 46.14 Basic schematic of continuous venovenous therapies. A blood pump is required to pump blood through the circuit. Replacement ports are used for instilling replacement fluids and can be given prefilter or postfilter. Dialysate port is used for infusing dialysis solution. Regardless of modality, ultrafiltrate is drained via the ultrafiltration drain port.

As ultrafiltrate drains out of the hemofilter, fluid and electrolyte replacements can be infused through a port found before or after the filter as the blood returns to the patient. Replacement fluid is designed to replace volume and solutes, such as sodium, chloride, HCO3−, and glucose. The infusion rate of replacement fluid is determined by the degree of fluid and electrolyte imbalance. Replacement fluid infused into the infusion port before the hemofilter allows for greater clearance of urea and can decrease filter clotting. An infusion port after the filter dilutes intravascular fluid and decreases the

concentration of unwanted solutes, such as BUN, creatinine, and potassium. Anticoagulants are given to prevent blood clotting. They may be infused as a bolus at the initiation of CRRT or through an infusion port before the hemofilter. The type of CRRT can be customized to the patient’s needs. Some types involve the introduction of replacement fluids. CVVHD and CVVHDF use dialysate. Dialysis fluid is attached to the distal end of the hemofilter, and the fluid is pumped countercurrent to the blood flow (Fig. 46.14). As in hemodialysis, diffusion of solutes and ultrafiltration via hydrostatic pressure and osmosis occur. This is an ideal treatment for a patient who needs both fluid and solute control but cannot tolerate the rapid fluid shifts associated with HD. Several features of CRRT differ from HD: • The blood pump in CRRT runs at a slower (150 mL/min average) rate. This may improve hemodynamic stability. • Continuous rather than intermittent. Fluid volume can be removed over days (24 hours to more than 2 weeks) versus hours (3 to 4 hours). • Solute removal can occur by convection (no dialysate required) in addition to osmosis and diffusion. • Causes less hemodynamic instability (e.g., hypotension) • Does not need constant monitoring by a specialized HD nurse but does require a trained ICU nurse • Does not require complicated HD equipment CRRT can be continued as long as 30 to 40 days. The hemofilter should be changed every 24 to 48 hours because of loss of filtration efficiency or potential for clotting. The ultrafiltrate should be clear yellow. Specimens may be obtained for serum chemistries. If the ultrafiltrate becomes bloody or blood tinged, suspect a rupture in the filter membrane. Stop treatment to prevent blood loss. Specific nursing interventions include obtaining weights and monitoring and documenting laboratory values daily to ensure adequate fluid and electrolyte balance. Assess hourly intake and

output, vital signs, and hemodynamic status. Although reductions in central venous pressure and pulmonary artery pressure are expected, there should be little change in mean arterial pressure or cardiac output. Assess and maintain the patency of the CRRT system. Care for the patient’s vascular access site to prevent infection. Once the patient’s AKI is resolved or there is a decision to withdraw treatment, CRRT is stopped and the needle(s) removed.

Wearable Artificial Kidney The wearable artificial kidney (WAK) has recently been developed and is approved for use to improve the quality of life of an ESRD patient. The WAK is a miniaturized dialysis machine that can be worn on the body. The carrier resembles a tool belt. The device connects to a patient via a catheter. Like conventional dialysis machines, it is designed to filter the blood of ESRD patients. Unlike current portable or stationary dialysis machines, it can run continuously on batteries. The present version weighs about 10 lb, but future modifications could make it lighter and more streamlined.28

Kidney Transplantation Major advances have been made in kidney transplantation since the first live donor kidney transplant was done in 1954 between identical twins. These advances include organ procurement and preservation, surgical techniques, tissue typing and matching, immunosuppressant therapy, and prevention and treatment of graft rejection. A general discussion of organ transplantation is in Chapter 13. Even though kidney transplantation is the best treatment option available to patients with ESRD, fewer than 4% ever receive a transplant. This is due to the large disparity between the supply and demand for kidneys. Every year thousands are waiting for kidney transplants (more than 100,000 are currently on the list), yet only about 17,000 transplants take place every year. Most die while waiting. Transplants from a deceased (cadaveric) donor usually

require a prolonged waiting period, with differences in waiting time depending on age, gender, and race. Average wait times in the United States for a deceased kidney usually range from 2 to 5 years.29-31 Kidney transplantation is very successful, with 1-year graft survival rates over 90% for deceased donor transplants and 95% for live donor transplants.30 An advantage of kidney transplantation when compared with dialysis is that it reverses many of the pathophysiologic changes associated with renal disease. It eliminates the dependence on dialysis and the accompanying dietary and lifestyle restrictions. Transplantation is less expensive than dialysis after the first year.

Recipient Selection Appropriate recipient selection is important for a successful outcome. Candidacy is determined by a variety of medical and psychosocial factors that vary among transplant centers. Some transplant programs exclude patients who are morbidly obese or who continue to smoke despite smoking cessation interventions. A careful evaluation is done to identify and minimize potential complications after transplantation. Certain patients, particularly those with CVD and diabetes, are considered high risk. They must be carefully evaluated and then monitored closely after transplantation. For a small number of patients who are approaching ESRD, a preemptive transplant (before dialysis is required) is possible if they have a living donor. This approach is best for patients with diabetes, who have a much higher mortality rate on dialysis than nondiabetics. Contraindications to transplantation include advanced cancer, refractory or untreated heart disease, chronic respiratory failure, extensive vascular disease, chronic infection, and unresolved psychosocial disorders (e.g., nonadherence to medical regimens, alcohol use, drug use). Being HIV-positive or having hepatitis B or C infection is not a contraindication to transplantation. Surgical procedures may be done before transplantation based on the results of the recipient evaluation. Coronary artery bypass or

coronary angioplasty may be needed for advanced coronary artery disease. Cholecystectomy may be necessary for patients with a history of gallstones, biliary obstruction, or cholecystitis. On rare occasions, bilateral nephrectomies are done for patients with refractory hypertension, recurrent UTIs, or grossly enlarged kidneys from polycystic kidney disease. In general, the recipient’s own kidneys are not removed before receiving a kidney transplant.

Histocompatibility Studies Histocompatibility studies, including human leukocyte antigen (HLA) testing and crossmatching, are discussed in Chapter 13 on p. 205.

Donor Sources Kidneys for transplantation are obtained from compatible blood-type deceased donors, blood relatives, emotionally related (close and distant) living donors (e.g., spouses, distant cousins,), and altruistic living donors who are known (friends) or unknown to the recipient. Living donation accounts for around 27% of all kidney transplants in the United States. Most transplant centers regard them as the preferred donation modality. 31

Ethical/Legal Dilemmas Allocation of Resources

Situation T.H., a transplant nurse coordinator, is considering her feelings about 2 patients who are being evaluated for placement on the deceased kidney transplant waiting list. One patient is a 40-yr-old black schoolteacher. She is married and has 2 children. The other patient is a 22-yr-old unemployed white man. He misses 3 or 4 dialysis treatments per month and does not take his antihypertensive drugs

consistently.

Ethical/Legal Points for Consideration • Ethical principles that are important in the allocation of human organs include utility and justice. • Allocation policies based on utility require we use standardized outcome measures to give a rough estimate about which allocation would produce the greatest good. Factors considered include patient survival, quality of life, availability of alternative treatments, and age. • We must give equal respect and concern to each patient. Allocation based on social characteristics (e.g., race, socioeconomic class, gender) conflict with the principle of justice and violate constitutional law. • Constitutional laws prohibit discrimination based on race, gender, religion, and ethnic background. It is highly unlikely that these standard prohibitions will change. It is possible that definitions of unhealthy behavior, such as substance use, alcohol use, smoking, and obesity, may be used to screen out candidates. • Nurses are concerned about social justice because of their health advocacy role. Today the situation is immensely more complex because of the cost and availability of care.

Discussion Questions 1. What does the American Nurses Association Code of Ethics say about how you as a nurse should view patients? 2. What are your thoughts about which patient should receive the next available kidney transplant? 3. Can you assign value to the lives of various patients? Who is worth more?

Live Donors

Live donors undergo an extensive evaluation to ensure that they are in good health and have no history of disease that would place them at risk for developing kidney disease or operative complications. Crossmatches are done at the time of the evaluation and about a week before the transplant to ensure that no antibodies to the donor are present or that the antibody titer is below the allowed level. Advantages of a live donor kidney include (1) better patient and graft survival rates regardless of histocompatibility match, (2) immediate organ availability, (3) immediate function due to minimal cold time (kidney out of body and not getting blood supply), and (4) the opportunity to have the recipient in the best possible medical condition because the surgery is elective. The potential donor sees a nephrologist for a complete history and physical examination and laboratory and diagnostic studies. Laboratory studies include a 24-hour urine study for creatinine clearance and total protein, complete blood count, and chemistry and electrolyte profiles. Hepatitis B and C, HIV, and cytomegalovirus (CMV) testing is done to assess for transmitted diseases. An ECG and chest x-ray are done. A renal ultrasound and renal arteriogram or 3dimensional CT scan is done to ensure that the blood vessels supplying each kidney are adequate and that no anomalies exist and to determine which kidney will be used in the transplant. A transplant psychologist or social worker determines if the person is emotionally stable and able to deal with the issues related to organ donation. All donors must be informed about the risks and benefits of donation, the potential short- and long-term complications, and what to expect during the hospitalization and recovery phases. Kidney donation is considered safe without any long-term health consequences. Although the recipient’s insurance covers the costs of the evaluation and surgery, no compensation is available for lost wages during the posthospitalization recovery period. This period can last 6 weeks or longer. When there is ABO incompatibility between a donor and recipient, paired donor exchange is a viable alternative. Paired organ donation, in which one donor/recipient pair who are incompatible or poorly

matched with each other find another donor/recipient pair with whom they can exchange kidneys. Thus a spouse (person A) who wants to donate a kidney to his wife (person B) but is incompatible is paired with another donor/recipient pair involving a son with ESRD (person C) and his mother (person D). In this example, person A would donate his kidney to person C, and person D would donate her kidney to person B. Paired organ donation is the practice of matching biologically incompatible donor/recipient pairs to permit transplantation of both candidates with a well-matched organ. Another option for ABO incompatibility or a positive crossmatch between the donor and recipient is to use plasmapheresis to remove antibodies from the recipient. This allows transplant candidates to receive kidneys from live donors with blood types that we have traditionally considered incompatible. After the transplant, the patient undergoes more plasmapheresis treatments.

Deceased Donors Deceased (cadaver) kidney donors are relatively healthy persons who have an irreversible brain injury and are declared brain dead. The most common causes of injury are cerebral trauma from motor vehicle accidents or gunshot wounds, intracerebral or subarachnoid hemorrhage, and anoxic brain damage caused by cardiac arrest. The brain-dead donor must have effective CV function and be supported on a ventilator to preserve the organs. Even if the donor carried a signed donor card, permission from the donor’s legal next of kin is still requested after brain death has been declared. That is why it is important for you to talk with your family about your wishes before losing the capacity to convey your desires. In deceased kidney donation, the kidneys are removed and preserved. They can be preserved for up to 72 hours. Most transplant surgeons prefer to transplant kidneys before the cold time (time outside of the body when being transported from the deceased donor to the recipient) reaches 24 hours. Prolonged cold time increases the chance that the kidney will not function immediately, and ATN may develop.

The United Network for Organ Sharing (UNOS) distributes deceased donor kidneys using an objective computerized point system. A new kidney allocation system (KAS) started in early 2015 after several years of refinement. All donor kidneys receive a kidney donor profile index (KDPI). The KDPI includes 10 donor factors that evaluate the risk for a kidney transplant failure. The KDPI can help predict how long a kidney may function. Each kidney transplant candidate gets an individual Estimated Post-Transplant Survival (EPTS) score. This score ranges from 0 to 100 percent. The score is related to how long a candidate will need a functioning kidney transplant when compared with other candidates. For example, a person with an EPTS score of 20% is likely to need a kidney longer than 80% of other candidates. The EPTS score is based on age, length of time on dialysis, previous transplants, and having diabetes.32 When a donor becomes available, the donor’s key information is compared with the data of all patients awaiting transplantation locally and nationwide. When a kidney arrives at the recipient’s transplant center, a final crossmatch is done. It must be negative for the deceased donor transplantation to proceed. The only exception is if a patient needs an emergency transplant or if a donor and recipient match on all 6 HLA antigens (zero antigen mismatch). The patient meeting either of these criteria goes to the top of the list. Emergency transplants receive priority because the patient is facing imminent death if not transplanted. If a zero antigen mismatch patient is found nationally, since statistically these grafts have better survival rates, one of the donor kidneys must be sent to that recipient’s transplant center regardless of location.

Surgical Procedure Live Donor A transplant surgeon performs the live donor nephrectomy. The donor’s surgery begins 1 to 2 hours before the recipient’s surgery. The recipient is surgically prepared for the kidney transplant in a nearby operating room.

Laparoscopic donor nephrectomy is the most common technique for removing a kidney in a living donor. (Laparoscopic nephrectomy is discussed in Chapter 45.) After the kidney is removed, it is flushed with a chilled, sterile electrolyte solution and prepared for immediate transplant into the recipient. The use of a laparoscopic donor nephrectomy procedure is minimally invasive, with fewer risks and shorter recovery time than an open procedure. The laparoscopic approach significantly decreases hospital stay, pain, operative blood loss, debilitation, and length of time off work. For these reasons, the number of people willing to donate a kidney has increased significantly. For an open (conventional) nephrectomy, the donor is placed in the lateral decubitus position on the operating table so that the flank is exposed laterally. An incision is made at the level of the eleventh rib. The rib may have to be removed to give adequate visualization of the kidney.

Kidney Transplant Recipient The transplanted kidney is usually placed extraperitoneally in the iliac fossa. The right iliac fossa is preferred to facilitate anastomoses of the blood vessels and ureter and minimize the occurrence of paralytic ileus. A urinary catheter is placed into the bladder, and an antibiotic solution is instilled to distend the bladder and decrease the risk for infection. A crescent-shaped incision is made extending from the iliac crest to the symphysis pubis (Fig. 46.15).

FIG. 46.15 A, Surgical incision for a renal transplant. B, Surgical placement of transplanted kidney.

Rapid revascularization is critical to prevent ischemic injury to the kidney. The donor artery is anastomosed to the recipient’s internal iliac (hypogastric) or external iliac artery. The donor vein is anastomosed to the recipient’s external iliac vein. When the anastomoses are complete, the clamps are released, and blood flow to the kidney is reestablished. The kidney should become firm and pink. Urine may begin to flow from the ureter at once. The donor ureter is then tunneled through the bladder submucosa before entering the bladder cavity and being sutured in place. This approach is called ureteroneocystostomy. This allows the bladder wall to compress the ureter as it contracts for micturition, thereby preventing reflux of urine up the ureter into the transplanted kidney. Transplant surgery takes about 3 to 4 hours.

Nursing Management: Kidney Transplant Recipient Preoperative Care Nursing care of the patient in the preoperative phase includes emotional and physical preparation for surgery. Because the patient and caregiver may have been waiting years for the kidney transplant, a review of the operative procedure and what can be expected in the immediate postoperative recovery period is necessary. Stress that there is a chance the kidney may not function at once, and dialysis may be needed for days to weeks. Review the need for immunosuppressive drugs and measures to prevent infection. To ensure the patient is in the best physical condition for surgery, an ECG, chest x-ray, and laboratory studies are done. Dialysis may be needed before surgery for fluid overload or hyperkalemia. Because dialysis may be needed after transplantation, the patency of the vascular access must be maintained. Label the vascular access

extremity “dialysis access, no procedures” to prevent use of that extremity for BP measurement, blood drawing, or IV infusions. A patient on PD must empty the peritoneal cavity of all dialysate solution before going to surgery and have the PD catheter capped.

Postoperative Care Live Donor Postoperative care for the donor is similar to that after open (conventional) or laparoscopic nephrectomy (see Chapter 45). Closely monitor renal function to assess for impairment and the hematocrit to assess for bleeding. Donors usually have more pain than the recipient. Donors who had an open surgical approach may have more pain than those after a laparoscopic approach. Donors who had an open approach are usually discharged from the hospital in 4 or 5 days and return to work in 6 to 8 weeks. With a laparoscopic approach, donors are discharged from the hospital in 2 to 4 days and return to work in 4 to 6 weeks. The surgeon sees the donor 1 to 2 weeks after discharge. Nurses caring for the living donor must acknowledge the precious gift that this person has given. The donor has taken physical, emotional, and financial risks to help the recipient. It is vital that the donor is not forgotten after surgery. The donor will need support if the donated organ does not work at once or for some reason fails.

Kidney Transplant Recipient The priority during the postoperative period is maintaining fluid and electrolyte balance. Kidney transplant recipients require close monitoring and spend the first 12 to 24 hours in the ICU. Large volumes of urine may be made soon after the blood supply to the transplanted kidney is reestablished. This diuresis is due to the (1) new kidney’s ability to filter BUN, which acts as an osmotic diuretic; (2) abundance of fluids given during the surgery; and (3) initial renal tubular dysfunction, which inhibits the kidney from concentrating urine normally. Urine output during this phase may be as high as 1

L/hr and gradually decreases as the BUN and serum creatinine levels return toward normal. Urine output is replaced with fluids milliliter for milliliter hourly for the first 12 to 24 hours. Central venous pressure readings are essential for monitoring fluid status. Dehydration must be avoided to prevent renal hypoperfusion and renal tubular damage. Electrolyte monitoring to assess for hyponatremia and hypokalemia often associated with rapid diuresis is critical. Treatment with potassium supplements or infusion of 0.9% normal saline may be needed. IV sodium bicarbonate may be given if the patient develops metabolic acidosis from a delay in the return of kidney function. ATN in the transplanted kidney can occur because of prolonged cold times causing ischemic damage or the use of marginal cadaveric donors (those who are medically suboptimal). While the patient is in ATN, dialysis is needed to maintain fluid and electrolyte balance. Some patients have high-output ATN with the ability to excrete fluid but not metabolic wastes or electrolytes. Other patients have oliguric or anuric ATN. These patients are at risk for fluid overload in the immediate postoperative period and must be assessed closely for the need for dialysis. ATN can last from days to weeks, with gradually improving kidney function. Most patients with ATN are discharged from the hospital on dialysis. This is extremely discouraging for the patient, who needs reassurance that renal function usually improves. Dialysis is discontinued when urine output increases and serum creatinine and BUN begin to normalize. A sudden decrease in urine output in the early postoperative period is a cause for concern. It may be due to dehydration, rejection, a urine leak, or obstruction. A common cause of early obstruction is a blood clot in the urinary catheter. Catheter patency must be maintained since the catheter stays in the bladder for 3 to 5 days to allow the ureter-bladder anastomosis to heal. If you suspect blood clots, gentle catheter irrigation (if ordered) can reestablish patency. With a hospital length of stay averaging 4 to 5 days, identify and address discharge planning and teaching needs early. Patient teaching ensures a smooth transition from the hospital to home. Include how to

recognize signs of rejection, infection, and any complications of surgery. Frequent blood tests and clinic visits help to detect rejection early.

Immunosuppressive Therapy The goal of immunosuppression is to adequately suppress the immune response to prevent rejection of the transplanted kidney while maintaining sufficient immunity to prevent overwhelming infection. Immunosuppressive therapy is discussed in Chapter 13.

Complications of Transplantation Complications of PD, HD, and kidney transplantation are compared in Table 46.14.

Rejection Rejection is one of the major problems after kidney transplantation. Rejection can be hyperacute, acute, or chronic. The types of rejection are discussed in Chapter 13 on p. 206. Patients with chronic rejection may be placed on the transplant list to be retransplanted before dialysis is required.

Infection Infection is a significant cause of morbidity and mortality after transplantation.32 The transplant recipient is at risk for infection because of suppression of the body’s normal defense mechanisms by surgery, immunosuppressive drugs, and the effects of ESRD. Underlying systemic illness, such as diabetes or SLE, malnutrition, and older age, can further compound the negative effects on the immune response. The signs and symptoms of infection can be subtle. You must be astute in your assessment of kidney transplant recipients because prompt diagnosis and treatment of infection improves patient outcomes.

TABLE 46.14 Complications of Dialysis and

Transplantation

The common infections seen in the first month after transplantation are like those of any postoperative patient. These include pneumonia, wound infections, UTIs, and IV line and drain infections. Fungal and viral infections are common due to the patient’s immunosuppressed state. Fungal infections include Candida, Cryptococcus, and Aspergillus organisms and Pneumocystis jiroveci. Fungal infections are hard to treat, require prolonged treatment periods, and often involve the administration of nephrotoxic drugs. Transplant recipients usually receive prophylactic antifungal drugs to prevent these infections, such as clotrimazole, fluconazole (Diflucan), and trimethoprim/sulfamethoxazole (Bactrim). Viral infections, including CMV, Epstein-Barr virus, herpes simplex virus (HSV), varicella-zoster virus, and polyomavirus (e.g., BK virus), can be primary infections or reactivations of existing disease. Primary infections occur as new infections after transplantation from an exogenous source such as the donated organ or a blood transfusion. Reactivation occurs when a virus exists in a patient and becomes reactivated after transplantation because of immunosuppression. CMV is one of the most common viral infections. If a recipient has

never had CMV and receives an organ from a donor with a history of CMV, antiviral prophylaxis will be needed (e.g., ganciclovir, valganciclovir [Valcyte]). To prevent HSV infections, oral acyclovir (Zovirax) is given for several months after the transplant.

Cardiovascular Disease CVD is the leading cause of death after renal transplantation.32 Transplant recipients have an increased incidence of atherosclerotic vascular disease. Hypertension, dyslipidemia, diabetes, smoking, rejection, infections, and increased homocysteine levels (many of which existed prior to the transplant) can all contribute to CVD. Immunosuppressants can worsen hypertension and dyslipidemia. Teach the patient to control risk factors, such as high cholesterol, triglycerides, and blood glucose and weight gain. Adherence to the prescribed antihypertensive regimen is essential to prevent CV events and damage to the new kidney.

Cancers The overall incidence of cancer in kidney transplant recipients is greater than in the general population, primarily because of immunosuppressive therapy. Not only do immunosuppressants suppress the immune system to prevent rejection, they also suppress the ability to fight infection and the production of abnormal cells, including cancer cells. The most common types of cancer after transplant are (1) skin cancers—basal and squamous cell cancers and melanoma—and (2) posttransplant lymphoproliferative disorder (PTLD). Most PTLDs are of Bcell origin, associated with Epstein-Barr virus (EBV), and cause aggressive lymphomas (Hodgkin’s and non-Hodgkin’s lymphoma). Most cases of PTLD occur within the first year of transplant. Patients are also at risk for cancers of the colorectum, breast, cervix, liver, stomach, oropharynx, anus, vulva, and penis. Regular screening for cancer is an important part of the transplant recipient’s preventive care. Teach the patient to avoid sun exposure by using protective clothing and sunscreens to minimize the incidence of skin cancers.

Recurrence of Original Kidney Disease Recurrence of the original disease that destroyed the native kidneys occurs in some kidney transplant recipients. It is most common with certain types of glomerulonephritis, immunoglobulin A (IgA) nephropathy, diabetic nephropathy, and focal segmental sclerosis. Disease recurrence can result in the loss of a functioning kidney transplant. Patients must be advised before transplantation if they have a disease known to recur.

Corticosteroid-Related Complications Aseptic necrosis of the hips, knees, and other joints can result from chronic corticosteroid therapy and renal osteodystrophy. Other significant problems related to corticosteroids include peptic ulcer disease, diabetes, cataracts, dyslipidemia, infections, and cancers. The use of tacrolimus and other immunosuppressants has allowed corticosteroid doses to be much lower than they were in the past. Many transplant programs have started corticosteroid-free drug regimens because of the problems of long-term corticosteroid use. Other centers withdraw patients from corticosteroids after transplantation. For patients who stay on corticosteroids, vigilant monitoring for side effects and prompt treatment is essential. Corticosteroid therapy as immunosuppression is discussed in Chapter 13 on p. 207.

Gerontologic Considerations: Chronic Kidney Disease The incidence of CKD in the United States is increasing most rapidly in older adults. The most common diseases leading to renal disease in older adults are hypertension and diabetes.33 The care of older patients is particularly challenging, not only because of the normal physiologic changes of aging but also because of the disabilities, chronic diseases, and co-morbid conditions that occur with aging. Physiologic changes include decreased

cardiopulmonary function, bone loss, immunodeficiency, altered protein synthesis, impaired cognition, and altered drug metabolism. Malnutrition is common in these patients for a variety of reasons, including lack of mobility, social isolation, physical disability, and impaired cognitive function. When conservative therapy for CKD is no longer effective, the older patient needs to consider the best treatment modality based on physical and emotional health, personal preferences, and availability of support. Quality-of-life measures show no justification for excluding the older adult from dialysis programs. Rationing dialysis based on age alone is not a reasonable decision for health care professionals to make. Older adults have successfully used dialysis, especially PD. Many choose treatment with in-center HD due to a lack of help in the home and reluctance to manage the technology of home HD or PD. Establishing vascular access for HD may be difficult because of atherosclerotic changes. Although transplantation is an option, older adults must be carefully screened to ensure that the benefits of transplantation outweigh the risks.34 Although a living donor is preferable, this may not be an option for many older patients. The most common cause of death in older ESRD patients is CVD (MI, stroke), followed by withdrawal from dialysis. If a competent patient decides to withdraw from dialysis, it is essential to support the patient and family. Ethical issues (see the Ethical/Legal Dilemmas box) to consider in this situation include patient competency, benefit versus burden of treatment, and futility of treatment. Withdrawal from treatment is not a failure if the patient is well informed and comfortable with the decision.

Ethical/Legal Dilemmas Withdrawing Treatment

Situation

L.R., a 70-yr-old patient with diabetes and ESRD, has been on dialysis for 10 years. He tells you that he wants to stop his dialysis. His quality of life has diminished during the past 2 years since his wife died. He is not a transplant candidate.

Ethical/Legal Points for Consideration • Informed consent includes the legal right to refuse treatment. However, the right to refuse may be more difficult if (1) it is contrary to the wishes of family and friends, (2) the treatment still appears to have effectiveness, and (3) the treatment has been in place for some time. • Quality-of-life decisions often outweigh the benefit against the burden of treatment. When a treatment becomes too burdensome, the patient, if competent, may request to withdraw the treatment. • It must be determined whether some other treatable problem, such as depression, may be clouding the patient’s judgment. • Although there is no ethical or legal difference between withdrawing treatment and withholding treatment, withdrawing treatment feels different because it requires an action. • Some health care professionals become conflicted when asked to withdraw treatment, since they may think they are contributing to the patient’s premature death. • If a decision is made to withdraw treatment, the interprofessional care team, patient, and family should develop a follow-up plan that includes palliative care and hospice support.

Discussion Questions 1. How should you respond to L.R.’s request? 2. What is the American Nurses Association’s position on withdrawing or withholding treatment that no longer benefits the patient or causes suffering?

Case Study Chronic Kidney Disease

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Patient Profile M.B. is a 56-yr-old black college professor. He is seen by his primary care provider for a routine physical examination. He has not seen an HCP in a little over a year. He reports generalized malaise, frequent urination, and “increasing thirst.” His medical history is significant for borderline hypertension and dyslipidemia. He smokes 1 pack of cigarettes per day. His efforts to quit have been unsuccessful.

Subjective Data • Family history: father died of an MI at age 62, brother had coronary artery bypass graft (CABG) at age 50, mother died from complications of diabetes • Becomes “winded” when walking from his car to his office at the university • Wakes up at night to urinate and has more frequent urination • Increasing thirst

Objective Data Laboratory Data • Calculated creatinine clearance using the MDRD equation: 42 mL/min/1.73 m2 • Serum creatinine 2.5 mg/dL • BUN 35 mg/dL • Serum glucose 264 mg/dL • Hgb 13 g/dL • Serum cholesterol 236 mg/dL

Physical Examination • Weight 220 lb, height 5 ft, 11 in

• BP 168/104 mm Hg

Discussion Questions 1. What do you think caused M.B.’s kidney disease? 2. What stage of chronic kidney disease does he have? 3. Identify the abnormal diagnostic study results and why each would occur. 4. Priority Decision: Based on the assessment data provided, what are the priority nursing diagnoses? Are there any collaborative problems? 5. What are the most important treatment measures that the interprofessional team can provide for M.B.? 6. Patient-Centered Care: What are the nursing interventions that would help promote M.B.’s self-management of his disease process? 7. Collaboration: How can the interprofessional team work together with M.B. to decide on the best form of renal replacement therapy? 8. Evidence-Based Practice: M.B. tells you that he has not been taking his BP medications regularly. When he asks you how important they are, what will you tell him? Answers available at http://evolve.elsevier.com/Lewis/medsurg.

Case Study Managing Care of Multiple Patients You are working on the medical-surgical unit and have been assigned to care for the following 4 patients. You are also assigned to receive the next new admission to the clinical unit. You have 1 UAP on your team to help you.

Discussion Questions 1. Priority Decision: After receiving report, which patient should you see first? Second? Provide a rationale for your decision. 2. Collaboration: Which tasks could you delegate to the UAP (select all that apply)? a. Obtain vital signs on M.B. b. Strain A.K.’s voided urine. c. Report D.M.’s potassium level to the HCP. d. Measure D.M.’s urine output and report the results to the RN.

e. Assess S.U. for manifestations of sepsis and diabetic ketoacidosis. 3. Priority Decision: As you are assessing D.M., the UAP tells you that M.B.’s BP is 190/96. He is asymptomatic. Additionally, the charge nurse tells you that you will be receiving a patient with heart failure from the ED within the next 20 minutes. Which action would be most appropriate? a. Ask the charge nurse to assign the new admission to someone else. b. Have the UAP admit the new patient while you administer M.B.’s IV metoprolol. c. Call the ED and have them hold the new admission until after you have assessed all your patients. d. Ask the charge nurse to give M.B.’s IV metoprolol while you complete your assessment of D.M. and S.U.

Case Study Progression As you complete your assessment of D.M., you note her apical pulse is irregular. She has 1+ pitting edema in her lower extremities. Her BP is 160/90 mm Hg, heart rate 108 beats/min, and respiratory rate 28/min. Auscultation of her lungs reveals crackles in the bases and O2 saturation is 92% on room air. You notify her HCP. 4. Which interventions would you expect the HCP to order for D.M.? (select all that apply) a. Administer IV Kayexalate. b. Obtain arterial blood gas levels. c. Administer 40 mg of furosemide IV push. d. Prepare her for hemodialysis and notify her family. e. Obtain a 12-lead ECG and start continuous ECG monitoring. 5. Priority Decision: Which concern has the highest priority when planning care for A.K.? a. Acute pain b. Infection risk

c. Risk for injury d. Difficulty coping 6. Priority Decision: You begin S.U.’s scheduled infusion of IV ceftriaxone. Which parameters are the most important to monitor while she is receiving this drug? a. PT and INR b. BUN and creatinine c. CBC with differential d. Liver function studies 7. Which statement would be most appropriate when teaching S.U. about her kidney infection? a. “The damage to your kidneys will likely require dialysis.” b. “You will need to be in the hospital for a 2-week course of IV antibiotics.” c. “It is very important that you maintain adequate hydration to flush your kidneys.” d. “You will not need further antibiotics once you are discharged from the hospital.” 8. Collaboration: As the UAP prepares the room for the patient being admitted from the ED, you overhear her telling a coworker that she does all your work for you. What is your best initial action? a. Report the incident to the charge nurse for follow-up. b. Ask the UAP to discuss her concerns with you in private. c. Tell the UAP how much you appreciate and value her input on your team. d. Immediately clarify the situation by telling the UAP all the tasks you are completing. Answers available at http://evolve.elsevier.com/Lewis/medsurg.

Bridge to Nclex Examination

The number of the question corresponds to the same-numbered outcome at the beginning of the chapter.

1. RIFLE defines the first 3 stages of AKI based on changes in a. blood pressure and urine osmolality. b. fractional excretion of urinary sodium. c. estimation of GFR with the MDRD equation. d. serum creatinine or urine output from baseline. 2. During the oliguric phase of AKI, the nurse monitors the patient for (select all that apply) a. hypotension. b. ECG changes. c. hypernatremia. d. pulmonary edema. e. urine with high specific gravity. 3. If a patient is in the diuretic phase of AKI, the nurse must monitor for which serum electrolyte imbalances? a. Hyperkalemia and hyponatremia b. Hyperkalemia and hypernatremia c. Hypokalemia and hyponatremia d. Hypokalemia and hypernatremia 4. A patient is admitted to the hospital with chronic kidney disease. The nurse understands that this condition is characterized by a. progressive irreversible destruction of the kidneys. b. a rapid decrease in urine output with an elevated BUN. c. an increasing creatinine clearance with a decrease in urine output.

d. prostration, somnolence, and confusion with coma and imminent death. 5. Nurses can screen patients at risk for developing chronic kidney disease. Those considered to be at increased risk include (select all that apply) a. older black patients. b. patients more than 60 years old. c. those with a history of pancreatitis. d. those with a history of hypertension. e. those with a history of type 2 diabetes. 6. Patients with chronic kidney disease have an increased incidence of cardiovascular disease related to (select all that apply) a. hypertension. b. vascular calcifications. c. a genetic predisposition. d. hyperinsulinemia causing dyslipidemia. e. increased high-density lipoprotein levels. 7. Nutritional support and management are essential across the entire continuum of chronic kidney disease. Which statements are true related to nutritional therapy? (select all that apply) a. Sodium and salt may be restricted in someone with advanced CKD. b. Fluid is not usually restricted for patients receiving peritoneal dialysis. c. Decreased fluid intake and a low-potassium diet are part

of the diet for a patient receiving hemodialysis. d. Decreased fluid intake and a low-potassium diet are part of the diet for a patient receiving peritoneal dialysis. e. Decreased fluid intake and a diet in protein-rich foods are part of a diet for a patient receiving hemodialysis. 8. An ESRD patient receiving hemodialysis is considering asking a relative to donate a kidney for transplantation. In helping the patient decide about treatment, the nurse informs the patient that a. successful transplantation usually provides better quality of life than that offered by dialysis. b. if rejection of the transplanted kidney occurs, no further treatment for the renal failure is available. c. hemodialysis replaces the normal functions of the kidneys, and patients do not have to live with the continual fear of rejection. d. the immunosuppressive therapy after transplantation makes the person ineligible to receive other treatments if the kidney fails. 9. To assess the patency of a newly placed arteriovenous graft for dialysis, the nurse should (select all that apply) a. monitor the BP in the affected arm. b. irrigate the graft daily with low-dose heparin. c. palpate the area of the graft to feel a normal thrill. d. listen with a stethoscope over the graft to detect a bruit. e. assess the pulses and neurovascular status distal to the graft. 10. A kidney transplant recipient has had fever, chills, and

dysuria over the past 2 days. What is the first action that the nurse should take? a. Assess temperature and initiate workup to rule out infection. b. Reassure the patient that this is common after transplantation. c. Provide warm covers to the patient and give 1 gram oral acetaminophen. d. Notify the nephrologist that the patient has manifestations of acute rejection. 1. d, 2. b, d, 3. c, 4. a, 5. a, b, d, e, 6. a, b, d, 7. a, b, c, 8. a, 9. c, d, e, 10. a For rationales to these answers and even more NCLEX review questions, visit http://evolve.elsevier.com/Lewis/medsurg.

Evolve Website http://evolve.elsevier.com/Lewis/medsurg

Review Questions (Online Only) Key Points Answer Keys for Questions • Rationales for Bridge to NCLEX Examination Questions • Answer Guidelines for Case Study on p. 1085 • Answer Guidelines for Managing Care of Multiple Patients Case Study (Section 10) on p. 1088 Student Case Studies • Patient With Glomerulonephritis and Acute Kidney Injury

• Patient With Kidney Transplant Nursing Care Plan • eNursing Care Plan 46.1: Patient With Chronic Kidney Disease Conceptual Care Map Creator Audio Glossary Content Updates

References Moriama N, Saito S, Ishihara S, et al: Early development of acute kidney injury is an independent predictor of in-hospital mortality in patients with acute myocardial infarction, J Cardiol 69:1, 2017.

2. Thornburg B: Acute kidney injury, Nursing 46:24, 2016. 3. Bevc S, Ekart R, Hois R: The assessment of acute kidney injury in critically ill patients, Eur J Int Med 45:54, 2017. Omotoso BA, Abdel-Rahman EM, Xin W, et al: Dialysis requirement, long-term major adverse cardiovascular events (MACE) and allcause mortality in hospital acquired acute kidney injury (AKI): A propensity-matched cohort study, J Nephrol 29:847, 2016. Nash DM, Przech S, Wald R, et al: Systematic review and metaanalysis of renal replacement therapy modalities for acute kidney injury in the intensive care unit, J Crit Care 41:138, 2017. Abdel-Basset E, Walid A, Maha A, et al: Early versus delayed initiation of continuous renal replacement therapy in critically ill patients with acute kidney injury, Egy J Hosp Med 69:2219, 2017. Perez-Fernandez X, Sabater-Riera J, Sileanu F, et al: Renal: Clinical variables associated with poor outcome from sepsis-associated acute kidney injury and the relationship with timing of initiation of

renal replacement therapy, J Crit Care 40:154, 2017. Greer R, Yang L, Crews D, et al: Hospital discharge communications during care transitions for patients with acute kidney injury: A cross-sectional study, BMC Health Serv Res 16:449, 2016. Zarbock A, Gerb J, Van Aken H, et al: Early versus late initiation of renal replacement therapy in critically ill patients with acute kidney injury, JAMA 148:558, 2016. Izawa J, Uchino S, Takinami M: A detailed evaluation of the new acute kidney injury criteria by KDIGO in critically ill patients, J Anesthesiol 30:215, 2016.

11. Loiselle M: Decisional needs assessment to help patients with advanced chronic kidney disease make better dialysis choices, Nephrol Nurs J 43:463, 2016. Alseiari M, Meyer KB, Wong JB: Evidence underlying KDIGO guideline recommendations: A systematic review, Am J Kidney Dis, 67:417, 2016. Flack JM, Calhoun D, Schifrin EL: The new ACC/AHA hypertension guidelines for the prevention, detection, evaluation, and management of high blood pressure in adults, Am J Hypertension 31:133, 2018. Galbraith L, Jacobs C, Hemmelgarn B, et al: Chronic disease management interventions for people with chronic kidney disease in primary care: a systematic review and meta-analysis, Neph Dialysis Transpl 33:112, 2017.

15. National Institute of Diabetes and Digestive and Kidney Diseases: US Renal Data System: 2017 annual data report: Epidemiology of kidney disease in the US. Retrieved from www.usrds.org/adr.aspx. 16. US Department of Health and Human Services: ESRD: General information. Retrieved from www.cms.gov/Medicare/End-Stage-RenalDisease/ESRDGeneralInformation/index.html. Ettehad D, Emdin CA, Kiran A, et al: Blood pressure lowering for

prevention of cardiovascular disease and death: A systematic review and meta-analysis, Lancet 387:10022, 2016.

18. Coyne D, Goldsmith D, Macdougall L: New options for the anemia of chronic kidney disease, Kidney Int 7:157, 2017. Ketteler M, Block GA, Evenepoel P: Executive summary of the 2017 KDIGO CKD-MBD guideline update: What’s changed and why it matters, Kidney Int 92:26, 2017. Malhotra R, Nguyen H, Benevente, et al: Association between more intensive versus less intensive blood pressure lowering and risk of mortality in chronic kidney disease stages 3-5: A systematic review and meta-analysis, JAMA Int Med 177:1498, 2017. Natale P, Ruospo M, Saglimbene VM, et al: Interventions for improving sleep quality with chronic kidney disease. Cochrane Database Syst Rev, CD012625, 2017.

22. Saran R, Robinson B, Abbott KC, et al: US Renal Data System 2016 annual data report: Epidemiology of kidney disease in the United States, Am J Kidney Dis 69:S688, 2017. 23. National Kidney Foundation: NKF Kidney Disease Outcomes Quality Initiative. Retrieved from www.kidney.org/professionals/guidelines/guidelines_commentaries Perez-Torres A, Garcia EG, Garcia-Llana H, et al: Improvement in nutritional status in patients with chronic kidney disease by a nutritional program with no impact on renal function and determined by male sex. J Renal Nutrition 27:303, 2017.

25. National Kidney and Urologic Diseases Information Clearinghouse: Treatment methods for kidney disease: Peritoneal dialysis. Retrieved from http://kidney.niddk.nih.gov/health-information/kidneyfailure/peritoneal-dialysis. 26. Debus ES, Grundmann RT: Evidence-based therapy in

vascular surgery, New York, 2017, Springer. 27. National Kidney and Urologic Diseases Information Clearinghouse: Treatment methods for kidney disease: hemodialysis. Retrieved from http://kidney.niddk.nih.gov/health-information/kidneydisease/kidney-failure/hemodialysis. 28. Lee CJ, Rossi PJ: Portable and wearable dialysis devices for the treatment of patients with ESRD. In: Shalhub S, Dua A, Shin S, eds: Hemodialysis access: Fundamentals and advanced management, Basel, Switzerland, 2017, Springer. 29. Hart A, Smith JM, Skeans MA, et al: OPTN/SRTR 2016 annual data report: Kidney, Amer J Transplant 18:18, 2018. Neuberger JM, Bechstein WO, Kuypers DR, et al: Practical recommendations for long term management of modifiable risk factors in kidney and liver transplant recipients: A guidance report and clinical checklist on managing modifiable risk in transplantation, Transplantation 101:S1, 2017. Mathur AK, Chang YH, Steidley DE, et al: Patterns of care and outcomes in cardiovascular disease after kidney transplantation in the United States, Transplant Direct 3:e26, 2017.

32. Organ procurement and transplant network kidney allocation system. Retrieved from https://optn.transplant.hrsa.gov/learn/professionaleducation/kidney-allocation-system/. Wongrakpanich S, Susantitaphong P, Isaranuwatchai S, et al: Dialysis therapy and conservative management of advanced chronic kidney disease in the elderly: A systematic review, Nephron 137:178, 2017.

34. O’Hare AM, Song MK, Moss AH: Research priorities for palliative care for older adults with advanced kidney disease, J Palliative Med 20:453, 2017.

∗Evidence-based information for clinical practice.

SECTION ELEVEN

Problems Related to Regulatory and Reproductive Mechanisms OUTLINE 47. Assessment: Endocrine System 48. Diabetes Mellitus 49. Endocrine Problems 50. Assessment: Reproductive System 51. Breast Disorders 52. Sexually Transmitted Infections 53. Female Reproductive Problems 54. Male Reproductive Problems

47

Assessment Endocrine System Julia A. Hitch

LEARNING OUTCOMES 1. Describe the common characteristics and functions of hormones. 2. Identify the locations of the endocrine glands. 3. Describe the functions of hormones secreted by the pituitary, thyroid, parathyroid, and adrenal glands and the pancreas. 4. Describe the locations and roles of hormone receptors. 5. Obtain significant subjective and objective assessment data related to the endocrine system from a patient. 6. Perform a physical assessment of the endocrine system using the appropriate techniques. 7. Link age-related changes in the endocrine system to differences in assessment findings. 8. Distinguish normal from common abnormal findings of a physical assessment of the endocrine system. 9. Describe the purpose, significance of results, and nursing responsibilities related to diagnostic studies of the endocrine system.

KEY TERMS aldosterone, p. 1095 antidiuretic hormone (ADH), p. 1093 catecholamines, p. 1094 circadian rhythm, p. 1090 corticosteroid, p. 1095 cortisol, p. 1095 hormones, p. 1089 insulin, p. 1095 negative feedback, p. 1090 positive feedback, p. 1090 thyroxine (T4), p. 1094 triiodothyronine (T3), p. 1094 tropic hormones, p. 1093 Our compassion and acts of selflessness take us to the deeper truths. Amma http://evolve.elsevier.com/Lewis/medsurg

Conceptual Focus Homeostasis Hormonal Regulation Reproduction Stress

Structures and Functions of Endocrine System Glands Endocrine glands include the hypothalamus, pituitary, thyroid, parathyroids, adrenals, pancreas, ovaries, testes, and pineal gland (Fig. 47.1). These glands make and release special chemical messengers called hormones. The endocrine system has 5 general functions: (1) a role in reproductive and central nervous system (CNS) development in the fetus, (2) stimulating growth and development during childhood and adolescence, (3) sexual reproduction, (4) maintaining homeostasis, and (5) responding to emergency demands.1

Hormones Hormones are chemical substances made by endocrine glands that control and regulate the activity of certain target cells or organs. Many are made in one part of the body and control and regulate the activity of certain cells or organs in another part of the body. The thyroid gland makes the hormone thyroxine, which affects many body tissues when released directly into the circulation. Other hormones act locally on cells where they are released and never enter the bloodstream. We call this local effect paracrine action. The action of sex steroids on the ovary is an example of paracrine action. Most hormones have common characteristics, including (1) secretion in small amounts at variable but predictable rates, (2) regulation by feedback systems, and (3) ability to bind to specific target cell receptors. Table 47.1 reviews the major hormones, the glands or tissues that make the hormones, their target organs or tissues, and their functions.

FIG. 47.1 Location of the major endocrine glands. The parathyroid glands lie on the posterior surface of the thyroid gland. Modified from Patton KT, Thibodeau GA: Anatomy and physiology, ed 8, St Louis, 2013, Mosby.

There is a strong connection between the endocrine system and nervous system. Catecholamines (e.g., epinephrine), secreted by the adrenal gland, travel through the bloodstream and affect multiple organ systems. These same substances, when secreted by nerve cells in the brain and peripheral nervous system, act as neurotransmitters, sending important impulses across nerve synapses.1 Organs can act as endocrine glands by secreting hormones. For example, the kidneys secrete erythropoietin, a substance that stimulates red blood cell production. The heart secretes atrial natriuretic peptide (ANP). The gastrointestinal (GI) tract secretes many peptide hormones (e.g., gastrin), that aid in digestion. These hormones are discussed in their respective assessment chapters.

Hormone Receptors Hormones exert their effects by recognizing their target tissues and attaching to receptor sites in a “lock-and-key” type of mechanism. This means a hormone will act only on cells that have a receptor specific for that hormone (Fig. 47.2).

Lipid-Soluble and Water-Soluble Hormones We classify hormones by their chemical structure as either lipid soluble or water soluble. The differences in solubility become important in understanding how the hormone interacts with the target cell (Fig. 47.3). Lipid-soluble hormones (steroids, thyroid) are bound to plasma proteins as they travel to target cells. They cross the cell membrane by simple diffusion. Water-soluble hormones (insulin, growth hormone, prolactin) circulate freely in the blood and act directly on target tissues.

Regulation of Hormonal Secretion Specific mechanisms control endocrine activity by either stimulating

or inhibiting hormone synthesis and secretion. These include positive and negative feedback, nervous system control, and physiologic rhythms.

Simple Feedback Negative feedback relies on the blood level of a hormone or other chemical compound regulated by the hormone (e.g., glucose). It is the most common type of endocrine feedback system. It results in the gland increasing or decreasing the release of a hormone. Negative feedback functions like a thermostat. Cold air in a room activates the thermostat to release heat. Warm air signals the thermostat to turn off the heater. An example of negative feedback is calcium and parathyroid hormone (PTH) regulation. Low blood levels of calcium stimulate the parathyroid gland to release PTH. PTH acts on the bone, intestine, and kidneys to increase blood calcium levels. The increased blood calcium level then inhibits further PTH release (Fig. 47.4). With positive feedback, increasing hormone levels cause another gland to release a hormone that then stimulates further release of the first hormone. Something must stop the release of the first hormone (e.g., follicle death) or its release will continue. The ovarian hormone estradiol works by this type of feedback. Increased levels of estradiol made by the follicle during the menstrual cycle result in the production and release of follicle-stimulating hormone (FSH) by the anterior pituitary. FSH causes further increases in estradiol until the death of the follicle. This results in a drop of FSH serum levels.

Nervous System Control Nervous system activity directly affects some endocrine glands. Pain, fear, sexual excitement, and other stressors can stimulate the nervous system to control hormone secretion. For example, when the CNS senses or perceives stress, the sympathetic nervous system (SNS) secretes catecholamines (e.g., epinephrine), which maximize heart and lung function and vision to deal with the stress more effectively. Chronic exposure to some stressors can cause persistent increases in heart rate and BP and changes in the endocrine system. This puts

patients at risk for chronic disease, such as hypertension and heart disease. Stress-related effects are discussed in Chapter 6.

Rhythms A common physiologic rhythm is the circadian rhythm. It is a 24-hour rhythm that is driven by sleep-wake or dark-light 24-hour (diurnal) cycles. Hormone levels and the responsiveness of target tissues fluctuate predictably during these cycles. Cortisol, made by the adrenal cortex, rises early in the day, declines toward evening, and rises again toward the end of sleep to peak by morning (Fig. 47.5). Growth hormone, thyroid-stimulating hormone, and prolactin levels peak during sleep. Reproductive cycles are often longer than 24 hours (ultradian). An example is the menstrual cycle. These rhythms are important to consider when interpreting laboratory results for hormone levels.

Hypothalamus Although many refer to the pituitary gland as the “master gland” of the endocrine system, most of its functions rely on its interrelationship with the hypothalamus, which lies next to the pituitary gland. The hypothalamus releases substances that either stimulate or inhibit the production and release of hormones from the pituitary gland (Table 47.2). Examples of these hormones include corticotropin-releasing hormone and thyrotropin-releasing hormone. Somatostatin inhibits growth hormone release.

Table 47.1 Endocrine Glands and Hormones

FIG. 47.2 The target cell concept. Hormones act only on cells that have receptors specific to that hormone, since the shape of the receptor determines which hormone can react with it. This is an example of the lock-and-key model of biochemical reactions.

FIG. 47.3 A, Lipid-soluble hormones (e.g., steroid hormones) penetrate the cell membrane and interact with intracellular receptors. B, Water-soluble hormones (e.g., protein hormones) bind to receptors in the cell membrane. The hormone-receptor interaction stimulates various cell responses. Modified from McCance KL, Huether SE: Pathophysiology: The biologic basis for disease in adults and children, ed 6, St Louis, 2010, Mosby.

Neurons in the hypothalamus receive input from the CNS, including the brainstem, limbic system, and cerebral cortex. These neurons create a circuit that helps coordinate the endocrine system

and autonomic nervous system (ANS). The hypothalamus also coordinates the expression of complex behavioral responses, such as anger, fear, and pleasure.

FIG. 47.4 Feedback mechanism between PTH and calcium.

FIG. 47.5 Circadian rhythm of cortisol secretion.

TABLE 47.2 Hormones of the Hypothalamus The following hormones from the hypothalamus target the anterior pituitary:

Releasing Hormones • Corticotropin-releasing hormone (CRH) • Thyrotropin-releasing hormone (TRH) • Growth hormone–releasing hormone (GHRH) • Gonadotropin-releasing hormone (GnRH) • Prolactin-releasing factor (PRF)

Inhibiting Hormones • Somatostatin (inhibits growth hormone release) • Prolactin-inhibiting factor (PIF)

Pituitary The pituitary gland (hypophysis) is in the sella turcica under the hypothalamus at the base of the brain above the sphenoid bone (Fig. 47.1). The infundibular (hypophyseal) stalk connects the pituitary and hypothalamus. This stalk relays information between the hypothalamus and pituitary, creating a strong neuroendocrine connection. The pituitary consists of 2 major parts, the anterior lobe (adenohypophysis) and posterior lobe (neurohypophysis). A smaller intermediate lobe makes melanocyte-stimulating hormone (MSH).

FIG. 47.6 Relationship between the hypothalamus, pituitary, and target organs. The hypothalamus communicates with the anterior pituitary via a capillary system and with the posterior pituitary via nerve tracts. The anterior and posterior pituitary hormones are shown with their target tissues. Modified from Patton KT, Thibodeau GA: Anatomy and physiology, ed 8, St Louis, 2013, Mosby.

Anterior Pituitary The anterior lobe of the pituitary accounts for 80% of the gland by weight. The hypothalamus regulates the anterior lobe through releasing and inhibiting hormones. These hypothalamic hormones reach the anterior pituitary through a network of capillaries known as the hypothalamus-hypophyseal portal system. These releasing and inhibiting hormones in turn affect the secretion of 6 hormones from the anterior pituitary (Fig. 47.6). We refer to several hormones secreted by the anterior pituitary as

tropic hormones. Tropic hormones control the secretion of hormones by other glands. Thyroid-stimulating hormone (TSH) stimulates the thyroid gland to secrete thyroid hormones. Adrenocorticotropic hormone (ACTH) stimulates the adrenal cortex to secrete corticosteroids. FSH stimulates secretion of estrogen and the development of ova in women and sperm in men. Luteinizing hormone (LH) stimulates ovulation in women and secretion of sex hormones in both men and women. Growth hormone (GH) affects the growth and development of all body tissues. It has many biologic actions, including a role in protein, fat, and carbohydrate metabolism. Prolactin, or lactogenic hormone, stimulates the breast development needed for lactation after childbirth.

Posterior Pituitary The posterior pituitary is composed of nerve tissue and is essentially an extension of the hypothalamus. Communication between the hypothalamus and posterior pituitary occurs through nerve tracts. The hormones secreted by the posterior pituitary, antidiuretic hormone (ADH) and oxytocin, are made in the hypothalamus. These hormones travel down the nerve tracts from the hypothalamus to the posterior pituitary and are stored there until stimuli trigger their release (Fig. 47.6).

FIG. 47.7 Relationship of plasma osmolality to ADH release and action.

The major physiologic role of ADH (also called arginine vasopressin) is to regulate fluid volume. It causes the renal tubules to reabsorb water, making the urine more concentrated. A rise in plasma osmolality or hypovolemia causes specialized neurons in the hypothalamus, known as osmoreceptors, to stimulate ADH release from

the posterior pituitary (Fig. 47.7). When ADH release is inhibited, renal tubules do not reabsorb water, resulting in a more dilute urine. Volume receptors in large veins, heart atria, and carotid arteries that sense pressure changes (from hypovolemia) also contribute to ADH control. ADH is also a potent vasoconstrictor.

FIG. 47.8 Thyroid and parathyroid glands. Note the surrounding structures. From Thibodeau GA, Patton KT: The human body in health and disease, ed 4, St Louis, 2005, Mosby.

Pineal Gland The pineal gland is in the brain. It is composed of photoreceptive cells. Its primary function is the secretion of the hormone melatonin. Melatonin secretion increases in response to exposure to the dark and decreases in response to light exposure. The gland helps to regulate

circadian rhythms and the reproductive system at the onset of puberty.

Thyroid Gland The thyroid gland is in the anterior part of the neck in front of the trachea. It consists of 2 encapsulated lateral lobes connected by a narrow isthmus (Fig. 47.8). The thyroid gland is highly vascular. Its size is related to TSH secretion by the anterior pituitary. The 3 hormones made and secreted by the thyroid gland are thyroxine (T4), triiodothyronine (T3), and calcitonin.

Thyroxine and Triiodothyronine Thyroxine (T4) accounts for 90% of thyroid hormone made by the thyroid gland. However, triiodothyronine (T3) is much more potent and has greater metabolic effects. The thyroid gland directly secretes about 20% of circulating T3. The rest comes from the conversion of T4 after its release into the bloodstream. Iodine is required for the synthesis of both T3 and T4. Both hormones affect metabolic rate, caloric requirements, O2 consumption, carbohydrate and lipid metabolism, growth and development, brain function, and other nervous system activities. More than 99% of thyroid hormones are bound to plasma proteins, especially thyroxine-binding globulin made by the liver. Only the unbound “free” hormones are biologically active. TSH from the anterior pituitary gland stimulates thyroid hormone production and release. When circulating levels of thyroid hormone are low, the hypothalamus releases thyrotropin-releasing hormone (TRH). TRH causes the anterior pituitary to release TSH. High circulating thyroid hormone levels inhibit the secretion of both TRH from the hypothalamus and TSH from the anterior pituitary gland.

Calcitonin Calcitonin is made by C cells (parafollicular cells) of the thyroid gland

in response to high circulating calcium levels. Calcitonin lowers serum calcium levels by (1) inhibiting the transfer of calcium from the bone to blood, (2) increasing calcium storage in bone, and (3) increasing renal excretion of calcium and phosphorus. Calcitonin and PTH regulate calcium balance.

FIG. 47.9 The adrenal gland is composed of the adrenal cortex and the adrenal medulla.

Parathyroid Glands There are usually 2 pairs of parathyroid glands lying behind each

thyroid lobe (Fig. 47.8). Although there are usually 4 glands, their number may range from 2 to 6.

Parathyroid Hormone The parathyroid glands secrete parathyroid hormone (PTH), also called parathormone. Its major role is to regulate serum calcium levels. PTH increases serum calcium levels by acting on bone, the kidneys, and indirectly on the GI tract. PTH stimulates the transfer of calcium from the bone into the blood. In the kidney, PTH promotes calcium reabsorption (moving calcium from the renal tubules back into the bloodstream) and phosphate excretion. PTH stimulates the renal conversion of vitamin D to its most active form (1,25dihydroxyvitamin D3). This form of vitamin D promotes calcium and phosphorus absorption in the GI tract. PTH secretion is regulated by a negative feedback system. When serum calcium or magnesium levels are low, PTH secretion increases. When serum calcium or active vitamin D levels are high, PTH secretion falls.

Adrenal Glands The adrenal glands are small, paired, highly vascular glands located on the upper part of each kidney. Each gland consists of 2 parts: medulla and cortex (Fig. 47.9). Each part has distinct functions and act independently from the other.

Adrenal Medulla The adrenal medulla is the inner part of the adrenal gland. It consists of sympathetic postganglionic neurons. The medulla secretes the catecholamines epinephrine (adrenaline), norepinephrine (noradrenaline), and dopamine. We consider catecholamines neurotransmitters when they are secreted by neurons and hormones when they are secreted by the adrenal medulla. They are an essential part of the SNS’s “fight or flight” response.

Adrenal Cortex

The adrenal cortex is the outer part of the adrenal gland. It secretes several steroid hormones, including glucocorticoids, mineralocorticoids, and androgens. Cholesterol is the precursor for steroid hormone synthesis. Glucocorticoids (e.g., cortisol) are named for their effects on glucose metabolism. They inhibit the inflammatory response and are considered antiinflammatory. Mineralocorticoids (e.g., aldosterone) are essential for maintaining fluid and electrolyte balance. The term corticosteroid refers to both glucocorticoids and mineralocorticoids.

Cortisol Cortisol, the most abundant and potent glucocorticoid, is necessary to maintain life and protect the body from stress. It is secreted in a diurnal pattern (Fig. 47.5). A negative feedback mechanism controls cortisol secretion. The release of corticotropin-releasing hormone (CRH) from the hypothalamus stimulates the secretion of ACTH by the anterior pituitary. A major function of cortisol is regulating blood glucose concentration by stimulating hepatic glucose formation (gluconeogenesis). Cortisol inhibits peripheral glucose use in the fasting state, inhibits protein synthesis, and stimulates the mobilization of glycerol and free fatty acids. It helps maintain vascular integrity and fluid volume through its action on mineralocorticoid receptors. Cortisol decreases the inflammatory response by stabilizing the membranes of cellular lysosomes and preventing increased capillary permeability. Stress, burns, infection, fever, acute anxiety, and hypoglycemia increase cortisol levels.

Aldosterone Aldosterone is a potent mineralocorticoid that maintains extracellular fluid volume. It acts on the renal tubule to promote renal reabsorption of sodium and excretion of potassium and hydrogen ions. Hyponatremia, hyperkalemia, and angiotensin II stimulate aldosterone synthesis and secretion. ANP and hypokalemia inhibit aldosterone synthesis and release.

Adrenal Androgens The adrenal cortex secretes small amounts of androgens. They are converted to sex steroids in peripheral tissues: testosterone in men and estrogen in women. The most common adrenal androgens are dehydroepiandrosterone (DHEA) and androstenedione. Because they are precursors to other sex steroids, their actions are like those of testosterone and estrogen. In postmenopausal women, the major source of estrogen is the peripheral conversion of adrenal androgens to estrogen.

Pancreas The pancreas is a long, tapered, lobular, soft gland located behind the stomach and anterior to the first and second lumbar vertebrae. The pancreas has both exocrine and endocrine functions. The hormonesecreting part of the pancreas is the islets of Langerhans. The islets account for less than 2% of the gland. They consist of 4 types of hormone-secreting cells: α, β, delta, and F cells. The α cells make and secrete the hormone glucagon. The β cells make and secrete insulin and amylin. Delta cells make and secrete somatostatin. F (or PP) cells secrete pancreatic polypeptide.

Glucagon Pancreatic α cells release glucagon in response to low blood glucose levels, protein ingestion, and exercise. Glucagon increases blood glucose, providing fuel for energy by stimulating glycogenolysis (breakdown of glycogen into glucose), gluconeogenesis (formation of glucose from noncarbohydrate molecules), and ketogenesis. Glucagon and insulin function in a reciprocal manner to maintain normal blood glucose levels.

Insulin Insulin is the main regulator of metabolism and storage of ingested carbohydrates, fats, and proteins. Insulin facilitates glucose transport into cells, transport of amino acids across muscle membranes, and the

synthesis of amino acids into protein in the peripheral tissues. However, the brain, nerves, lens of the eye, hepatocytes, erythrocytes, and cells in the intestinal mucosa and kidney tubules are not dependent on insulin for glucose uptake. After a meal, insulin is responsible for how we use and store nutrients (anabolism). An increased blood glucose level is the major stimulus for insulin synthesis and secretion. Low blood glucose levels, glucagon, somatostatin, hypokalemia, and catecholamines usually inhibit insulin secretion.

TABLE 47.3 Gerontologic Assessment

DifferencesEndocrine System

Gerontologic Considerations: Effects of Aging on Endocrine System Normal aging has many effects on the endocrine system (Table 47.3).

These include (1) decreased hormone production and secretion, (2) altered hormone metabolism and biologic activity, (3) decreased responsiveness of target tissues to hormones, and (4) changes in circadian rhythms. Assessing the effects of aging on the endocrine system may be difficult because the subtle changes of aging may mimic manifestations of endocrine disorders. Endocrine problems may manifest differently in an older adult than in a younger person. Older adults may have multiple co-morbidities and take medications that change the body’s usual response to endocrine function. Symptoms of endocrine problems, such as fatigue, constipation, or mental impairment, may be attributed to aging, resulting in delayed treatment.

Assessment of Endocrine System Endocrine problems generally result from too much or too little of a specific hormone. The onset of symptoms is often gradual. Subtle or vague symptoms are often attributed to other physiologic or psychologic causes. Patients may present with fluid and electrolyte imbalances, altered tissue perfusion, inadequate coping mechanisms, changes in heart rhythm, or changes in skin integrity that can be interpreted as many other conditions. Alternatively, patients may present with acute symptoms that are life threatening and demand immediate intervention.

Case Study Patient Introduction

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L.M. is a 35-yr-old Hispanic woman who comes to the clinic saying she is “just not feeling well.” Her husband, H.M., is with her. L.M. states that she has gained a lot of weight despite trying to watch her diet and just seems to be getting more and more tired. H.M. voices concerns about the changes in his wife’s energy level.

Discussion Questions 1. What are the possible causes of L.M.’s weight gain, fatigue, and irritability?

2. What would be your priority assessment of L.M.? 3. What questions would you ask L.M.? You will learn more about L.M. and her condition as you read through this assessment chapter. (See p. 1098 for more information on L.M.) Answers available at http://evolve.elsevier.com/Lewis/medsurg.

Subjective Data Information obtained from the patient can provide important clues as to the functioning of the endocrine system. You will need to obtain a thorough history from the patient and/or a caregiver if the patient’s mental acuity is compromised.

Important Health Information Past Health History Patients with endocrine disorders often present with nonspecific complaints. The chief complaint may relate to not just one but a group of symptoms. The most common presenting problems include fatigue, weakness, menstrual irregularities, and weight changes. It is important to determine if the onset of symptoms has been gradual or sudden and what the patient has done about them. Because some of the more general signs of problems are the easiest to overlook, you must evaluate any reported or observed changes in weight, appetite, skin, libido, mental acuity, emotional stability, or energy levels.

Medications Ask about the use of all medications (both prescription and over-thecounter), herbs, and dietary supplements. Ask about the reason for taking the drug, the dosage, and the length of time the drug has been taken. In particular, ask about the use of hormone replacements. Knowing that the patient is currently taking hormone replacements,

such as insulin, thyroid hormone, or corticosteroids (e.g., prednisone), should alert you to potential adverse drug events. For example, corticosteroids may increase blood glucose levels and cause bone loss with long-term use. Thyroid preparations may cause tachycardia or dysrhythmias. Drug-to-drug interactions and adverse effects of nonhormonal medications can contribute to endocrine problems.

Surgery or Other Treatments Ask about past medical, surgical, and obstetric history, including number of pregnancies and live births. Assess growth patterns and stages of physical and emotional development. For example, knowing about radiation therapy to the head and neck is important when you suspect thyroid or pituitary problems.

Functional Health Patterns Key questions to ask the patient with an endocrine problem are outlined in Table 47.4.

Health Perception–Health Management Pattern Heredity plays a key role in the development of endocrine problems. Ask about first-degree relatives with diabetes, thyroid disease, or endocrine gland cancers, since these conditions have a familial tendency. A genetic assessment of family members may be needed.

Genetic Risk Alert Pituitary • Nephrogenic diabetes insipidus can be inherited as a sex-linked or autosomal disorder.

Thyroid

• Genetics has a role in many cases of hypothyroid and hyperthyroid disorders. • Hashimoto’s thyroiditis, the most common cause of hypothyroidism, and Graves’ disease, a cause of hyperthyroidism, are autoimmune disorders. Both likely result from a combination of genetic and environmental factors.2

Multiple Endocrine Neoplasia • Multiple endocrine neoplasia (MEN) involves tumors in 2 or more different endocrine glands. • There are several types of MEN. Mutations of MEN1, RET, and CDKN1B genes determine the type. • The features of MEN are relatively consistent within a family. • A common tumor associated with MEN type 2 is medullary thyroid cancer.2

Diabetes • Genetics has a strong role in the development of type 1 and type 2 diabetes.

Nutritional-Metabolic Pattern Changes in appetite and weight can indicate an endocrine problem. Ask about a history of weight distribution and changes. Weight loss with increased appetite may occur with hyperthyroidism or diabetes. Weight gain may occur with hypothyroidism or hypocortisolism. Obese persons are more likely to develop type 2 diabetes. Ask if there have been problems with nausea, vomiting, or diarrhea. An enlarged thyroid gland can cause difficulty swallowing or a change in neck size. Increased SNS activity, including nervousness, palpitations, sweating, and tremors, may occur with thyroid problems

or a rare tumor of the adrenal medulla (pheochromocytoma). Heat or cold intolerance occur with hyperthyroidism or hypothyroidism, respectively. Ask about changes in the patient’s skin, especially on the face, neck, hands, or body creases. Changes in skin texture and skin that seems thicker or drier may suggest an endocrine problem. A patient with hypothyroidism or excess GH may have skin that feels coarse or leathery. Ask if the patient has noticed any change in the distribution of hair anywhere on the body.

TABLE 47.4 Health HistoryEndocrine System

Health Perception–Health Management • What is your usual day like? • Have you noticed any changes in your ability to perform your usual activities compared with last year? 5 years ago?∗

Nutritional-Metabolic • What are your weight and height? • How much do you want to weigh? • Have there been any changes in your appetite or weight?∗ • Have you noticed any changes in the distribution of the hair anywhere on your body? ∗ • Have you noticed any changes in the color of your skin, especially on your face, neck, hands, or body creases? ∗ • Has the texture of your skin changed? For example, does it seem thicker and drier than it used to?∗ • Have you noticed any difficulty swallowing, throat pain, or hoarseness? Is the top button on your shirt or blouse hard to

button?∗ • Do you feel more nervous than you used to? Do you notice your heart pounding or that you sweat when you do not think you should be sweating? • Do you have difficulty holding things because of shakiness of your hands?∗ • Do you feel that most rooms are too hot or too cold? Do you often have to put on a sweater, or feel as though you need to open windows when others in the room seem comfortable?∗ • Do you have, or have you had any wounds that were slow to heal?∗

Elimination • Do you have to get up at night to urinate? If so, how many times? Do you keep water by your bed at night? • Have you ever had a kidney stone?∗ • Describe your usual bowel pattern. Have you noted any bowel changes?∗ • Do you use anything, such as laxatives, to help you move your bowels?∗

Activity-Exercise • What is your usual activity pattern during a typical day? • Do you have a planned exercise program? If yes, what is it and have you had to make any changes in this routine lately? If so, why, and what kinds of changes? • Do you have fatigue with or without activity?∗ • Have you had any trouble with breathing?∗

Sleep-Rest • How many hours do you sleep at night? Do you feel rested on awakening? • Are you ever awakened by sweating during the night?∗ • Do you have nightmares?∗

Cognitive-Perceptual • How is your memory? Have you noticed any changes?∗ • Have you had any blurring or double vision?∗ • When was your last eye examination?

Self-Perception–Self-Concept • Have you noticed any changes in your physical appearance or size?∗ • Are you concerned about your weight?∗ • Do you feel you are able to do what you think you can do? If not, why not? • Does your health problem affect how you feel about yourself?∗

Role-Relationship • Do you have a support system or partner? Are you married? Do you have any children? Do you think you are able to take care of your family and home? If not, why not? • Where do you work? What kind of work do you do? Are you able to do what is expected of you and what you expect of yourself? • Are you retired? What type of work did you do before you

retired? How do you spend your time now that you have retired?

Sexuality-Reproductive Women • When did you start to menstruate? Was this earlier or later than other women in your family? • When was your last menstrual period? Do you have scant, heavy, or irregular menstrual flows? • How many children have you had? How much did they weigh at birth? Were you told you had diabetes during any pregnancy?∗ • Are you menopausal? If so, for how long? • Are you trying to get pregnant but cannot?∗ • Are you postmenopausal? If so, do you have any bleeding from your uterus?

Men • Have you noticed any changes in your ability to get and maintain an erection?∗ • Are you trying to have children but cannot?∗

Coping–Stress Tolerance • What kind of stressors do you have? • How do you deal with stress or problems? • What is your support system? To whom do you turn when you have a problem?

Value-Belief

• Do you think medicine should still be taken even though you feel okay? • Do any of your prescribed therapies cause any conflict in your value-belief system?∗



If yes, describe.

Elimination Pattern Because maintaining fluid balance is a major role of the endocrine system, questions related to fluid intake and elimination patterns may uncover endocrine problems. For example, increased thirst and urination can indicate diabetes (pancreas disorder) or diabetes insipidus (pituitary disorder). Ask about the frequency and consistency of bowel movements. Diarrhea can occur with hyperthyroidism or thyroid cancer. Constipation occurs with hypothyroidism, hypoparathyroidism, and hypopituitarism.

Activity-Exercise Pattern Determine if there are any acute or gradual changes in energy level or persistent fatigue. A patient with chronic fatigue secondary to hypothyroidism, hypocortisolism, or diabetes may report changes in activity level.

Sleep-Rest Pattern Ask the patient how many hours they typically sleep, and if they feel rested on awakening. Sleep problems can result from nocturia, nightmares, anxiety, depression, or insomnia that occur with diabetes or thyroid problems.

Cognitive-Perceptual Pattern Memory deficits may occur with hypothyroidism and changes in sodium levels. Inappropriate secretion of antidiuretic hormone

(SIADH) or pituitary tumors can cause hyponatremia. These issues can occur gradually. Gathering information from patient and family about memory, cognitive abilities, and balance can increase the chances of an earlier diagnosis.

Self-Perception–Self-Concept Pattern Many endocrine disorders may affect a patient’s self-esteem because of associated changes in physical appearance. For example, weight gain associated with hypothyroidism or exophthalmos and goiter associated with hyperthyroidism can cause problems related to body image.

Role-Relationship Pattern Questions related to roles and relationships can highlight depression, chronic fatigue, and sleep problems. With chronic fatigue, depression, and anxiety, patients and their families will have stressed relationships. Questions related to home life and the patients’ ability to fulfill their role in the family will aid in identifying problems.

Sexuality-Reproductive Pattern The endocrine system regulates GH, prolactin, LH, FSH, testosterone, and estrogen. Therefore, menstrual problems, hirsutism, infertility, decreased libido, and growth disorders can be a result of endocrine disorders. Some women develop hypothyroidism during or after menopause. Other patients begin to develop type 2 diabetes during middle age when sex hormones are changing. Document the presence of abnormal secondary sex characteristics, such as facial hair (hirsutism) in women. Obtain a detailed history of menstruation and pregnancy. Menstrual problems can occur with disorders of the ovaries and pituitary, thyroid, and adrenal glands. A history of largebirth-weight babies or gestational diabetes increases the risk for developing type 2 diabetes later in life. Male sexual problems may include impotence, infertility, or the lack of development of secondary sexual characteristics. Retrograde ejaculation can occur in diabetes.

Coping–Stress Tolerance Pattern Because stress worsens some endocrine conditions, ask patients about their stress level and usual coping patterns. Patients with adrenal insufficiency have difficulty dealing with stress. These patients are at risk for developing hypotension and fluid and electrolyte imbalance.

Value-Belief Pattern Determining a patient’s ability to make lifestyle changes is an important nursing function. Identify the patient’s value-belief patterns so that you can help to determine appropriate treatment plans. This is especially important in a condition such as diabetes, which may require major lifestyle changes. Other disorders, such as hypothyroidism or hypocortisolism, may be managed with medications but need lifelong monitoring.

Case Study—cont’d Subjective Data

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A focused subjective assessment of L.M. revealed the following information: • Past Medical History: Denies any medical or surgical history. Has not seen an HCP for 8 yr. • Medications: None. • Health Perception–Health Management: L.M. works as a receptionist for a local law firm and says it is all she can do to make it through the work day. She often wakes up with a

headache and goes to bed with the same headache, describing it as a dull, throbbing ache between her eyes. She does not have the energy she had 5 yr ago or even 6 mo ago. She used to enjoy gardening and going out with friends but now can barely manage work and coming home. • Nutritional-Metabolic: L.M. reports a steady weight gain over the past 6 mo, mainly in her abdominal area. She feels as if she looks pregnant but knows that is not possible. Her appetite has decreased, but she is not able to lose any weight. She says she feels “bloated.” She reports growth of facial hair and notices she is bruising easily. L.M. denies difficulty with swallowing, hoarseness, palpitations, or tremors. • Elimination: Denies any changes or problems with urination or bowel movements. • Activity-Exercise: L.M. states that she has no ambition to exercise. She is just too tired at the end of the workday and has no energy on the weekends either. She reports leg cramps with walking. • Sleep-Rest: Sleeps 10+ hr at night but does not feel rested on awakening. • Cognitive-Perceptual: L.M. is worried she is going crazy. She finds herself easily angered and irritable, often snapping at coworkers and her husband. She says this is not her usual self. At first, she thought it was because she was dealing with a constant, dull headache. Lately, she has noticed that her vision is blurry and that is making work and life more stressful. She says her headache hurts between her eyes. She rates the pain as a 4 on a scale of 0 to 10 and states that ibuprofen does not ease the pain. The pain is typically worse on arising in the morning. It slowly decreases during the day. • Self-Perception–Self-Concept: L.M. hates the way she looks. She says when she looks in the mirror, she cannot believe what she sees. She feels as if she has aged 10 yr over the past 6 mo and has gained weight in her face, neck, and trunk. She is concerned that

her scalp hair is thinning, and she is growing a beard. She tells you she feels “old and ugly”! • Coping–Stress Tolerance: L.M. states that she is finding it harder to cope with the stresses of her job, her relationship with her husband, and life in general. She believes her emotions are very “raw and labile,” so different from the easy-going, smiling person she had once prided herself in being.

Discussion Questions 1. Which subjective assessment findings are of most concern to you? 2. Based on the subjective assessment findings, what should you include in the physical assessment? What would you be looking for? You will learn more about the physical examination of the endocrine system in the next section. (See p. 1099 for more information on L.M.) Answers available at http://evolve.elsevier.com/Lewis/medsurg.

Objective Data Except the thyroid and testes, most endocrine glands are inaccessible to direct examination. Assessment can be accomplished using objective data from the physical examination and diagnostic tests. It is essential to understand the actions of hormones in order to assess the function of a gland by monitoring the target tissue.

Physical Examination Use the following general examination when evaluating endocrine function.3 Specific clinical findings for the various endocrine problems are discussed in Chapters 48 and 49. Endocrine disorders may cause changes in mental and emotional status. Throughout the examination,

assess the patient’s orientation, alertness, memory, cognitive abilities, affect, personality, and appropriateness of their behavior. Take a full set of vital signs at the beginning of the examination. Variations in temperature, heart rate, and BP can occur with a variety of endocrine-related problems. Obtain height and weight. Calculate body mass index (BMI) to assess nutritional status.

Integument Assess the color and texture of the skin, hair, and nails. Note the overall skin color as well as pigmentation and bruising. Decreased skin pigmentation can occur in hypopituitarism, hypothyroidism, and hypoparathyroidism. Hyperpigmentation, or “bronzing” of the skin, especially on knuckles, elbows, knees, genitalia, and palmar creases, is a classic finding in a form of adrenal insufficiency known as Addison’s disease. Palpate the skin for texture and moisture. Examine hair distribution on the head, face, trunk, and extremities. Assess the hair’s appearance and texture. Hair loss, excess hair growth, or dull, brittle hair may suggest endocrine problems. Assess for delayed wound healing.

FIG. 47.10 Posterior palpation of the thyroid gland. From Jarvis C: Physical examination and health assessment, ed 6, St Louis, 2012, Saunders.

Head Inspect the size and contour of the head. Facial features should be symmetric. Hyperreflexia and facial muscle contraction upon percussion of the facial nerve (Chvostek’s sign) may occur in hypoparathyroidism. Inspect the eyes for position, symmetry, and shape. Large and protruding eyes (exophthalmos) are associated with hyperthyroidism. Assess visual acuity using a Snellen eye chart. Visual field loss may occur with a pituitary tumor. In the mouth, inspect the buccal mucosa, condition of teeth, and tongue size. Note hair distribution on the scalp and face. Hearing loss is common in acromegaly from excess GH.4

Neck The thyroid gland is not usually visible during inspection. A feature

that distinguishes the thyroid from other masses in the neck is its upward movement on swallowing. Inspect the neck while the patient swallows a sip of water. The neck should appear symmetric without lumps or bulging. Palpate the thyroid for its size, shape, symmetry, and tenderness and for any nodules. Goiter, an enlarged thyroid gland, can occur with hyperthyroidism or hypothyroidism. Be careful not to press too hard or massage an enlarged thyroid gland. This can cause a sudden release of thyroid hormone into an already overloaded system. An experienced clinician should perform palpation in patients with a known diagnosis of hyperthyroidism. Perform palpation using a posterior or anterior approach. For anterior palpation, stand in front of the patient, with the patient’s neck flexed. Place your thumb horizontally with the upper edge along the lower border of the cricoid cartilage. Then move your thumb over the isthmus as the patient swallows water. Place your fingers laterally to the anterior border of the sternocleidomastoid muscle and palpate each lateral lobe before and while the patient swallows water. For posterior palpation, stand behind the patient (Fig. 47.10). With the thumbs of both hands resting on the nape of the patient’s neck, use your index and middle fingers of both hands to feel for the thyroid isthmus and for the anterior surfaces of the lateral lobes. To relax the neck muscles, ask the patient to flex the neck slightly forward and to the right. Displace the thyroid cartilage to the right with your left hand and fingers. Palpate with your right hand after placing the thumb deep and behind the sternocleidomastoid muscle with the index and middle fingers in front of it. Ask the patient to swallow water and feel for the thyroid to move up. In a normal person, the thyroid is often not palpable. If palpable, it usually feels smooth with a firm consistency. It is not tender with gentle pressure.5 If nodules, enlargement, asymmetry, or hardness (abnormal findings) are present, refer the patient for further evaluation. Auscultate the lateral lobes of an enlarged thyroid gland with the stethoscope bell to hear a bruit, a soft swishing sound that can occur with a goiter or hyperthyroidism.

Thorax Inspect the thorax for shape and characteristics of the skin. Note the presence of breast gynecomastia in men. Auscultate lung sounds and heart sounds. Note any adventitious lung sounds (wheezing, decreased sounds) or extra heart sounds. Signs of fluid overload or heart failure may be present in patients with SIADH or hypothyroidism.

Abdomen Inspect the contour of the abdomen and note the symmetry and color. Cushing syndrome (hypercortisolism) causes the skin to be fragile, resulting in purple-blue striae across the abdomen. Note general obesity or truncal obesity. Auscultate bowel sounds.

Extremities Assess the size, shape, symmetry, and general proportion of hands and feet. Patients with acromegaly from pituitary tumors may have large hands and feet. Inspect the skin for changes in pigmentation, lesions, and edema. Assess muscle strength and deep tendon reflexes. In the upper extremities, assess for tremors by placing a piece of paper on the outstretched fingers, palm down. Muscular spasms of the hand elicited on application of an occlusive BP cuff for 3 minutes (Trousseau’s sign) may occur in hypoparathyroidism.

Genitalia Inspect the genital hair distribution pattern, since it may be changed with hormone problems. Assessment abnormalities related to the endocrine system are outlined in Table 47.5. A focused assessment of the endocrine system is shown on p. 1101.

Case Study—cont’d

Objective Data: Physical Examination A focused assessment of L.M. reveals the following:

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L.M. is sitting on the edge of the examination table. She appears somewhat anxious. Her BP is 190/80, heart rate 84, respiratory rate 20, temp 98.6° F (37° C). Her weight is 160 lb, and she is 5 ft, 4 in tall. L.M.’s face is reddened and puffy. She appears to have a lump on the

back of her neck and shoulders. There is some acne on her face, along with some hair growth on her upper lip and chin area. Her abdomen is protruding, but her arms and legs are thin. She has +1 edema in her ankles bilaterally. There are several bruises on her upper and lower extremities, as well as purple stretch marks on her abdomen.

Discussion Questions 1. Which physical assessment findings are of most concern to you? 2. Based upon the subjective and objective assessment data presented so far, what are 3 priority nursing diagnoses? 3. What diagnostic studies would you expect to be ordered? You will learn more about diagnostic studies related to the endocrine system in the next section. (See p. 1106 for more information on L.M.) Answers available at http://evolve.elsevier.com/Lewis/medsurg.

TABLE 47.5 Assessment AbnormalitiesEndocrine

System

Focused Assessment Endocrine System Use this checklist to ensure the key assessment steps have been done.

Subjective Ask the patient about any of the following and note responses.

Excessive or increased thirst

Y

N

Excess or decreased urination

Y

N

Excessive hunger

Y

N

Heat or cold intolerance

Y

N

Excessive sweating

Y

N

Recent weight gain or loss

Y

N

Objective: Diagnostic Check the following laboratory results for critical values.

Potassium



Glucose



Sodium



Glycosylated hemoglobin (A1C)



Thyroid studies: TSH, T3, T4



Serum osmolality



Objective: Physical Examination Inspect/Measure Body temperature



Height and weight



Alertness and emotional state



Skin for changes in color and texture





Hair for changes in color, texture, and distribution

Auscultate Heart rate, BP



Palpate Extremities for edema



Skin for texture and temperature



Neck for thyroid size, shape



Diagnostic Studies of Endocrine System Diagnostic studies of the endocrine system are shown in Tables 47.6 and 47.7. Pertinent findings from the history and physical examination guide the selection of diagnostic studies. Imaging studies can identify pituitary tumors, thyroid nodules, or adrenal tumors. Laboratory studies may include direct measurement of the hormone level or an indirect measure of gland function by evaluating blood or urine components affected by the hormone, such as glucose or electrolytes. We can also measure the releasing or stimulating hormone. For example, we can evaluate thyroid function by measuring TSH. We can assess hormones with constant basal levels, such as T4, with a single measurement. Note the time of the sample collection on the laboratory slip. Information about night shift work is important for hormones with circadian or sleep-related secretion (e.g., cortisol). Evaluating other hormones may require multiple blood samplings, such as in suppression tests (e.g., dexamethasone) and stimulation tests (e.g., glucose tolerance). In these situations, it is often necessary

to obtain IV access to give the testing medication and fluids and draw multiple blood samples. Pituitary gland problems can manifest in a wide variety of ways because of the number of hormones produced. Many diagnostic studies evaluate these hormones either directly or indirectly. Several tests are available to evaluate thyroid function. The most sensitive and accurate laboratory test is the measurement of TSH. Thus it is often the first diagnostic test done to evaluate thyroid function.6 Follow-up tests ordered when the TSH level is abnormal include total T4, free T4, and total T3. Free T4 is the unbound thyroxine and more accurately reflects thyroid function than total T4. The only hormone secreted by the parathyroid glands is PTH. Because PTH regulates serum calcium and phosphate levels, these levels reflect abnormalities in PTH secretion. For this reason, diagnostic tests for the parathyroid gland typically include PTH, serum calcium, and serum phosphate levels. Tests associated with the adrenal cortex function focus on measuring blood plasma and urine levels of the 3 types of hormones secreted: glucocorticoids, mineralocorticoids, and androgens. Urine studies often require a 24-hour urine collection to eliminate the impact of short-term fluctuations in plasma hormone levels. The tests used to evaluate glucose metabolism are important in the diagnosis and management of diabetes. See Chapter 48 for information about diagnostic studies for diabetes.

TABLE 47.6 Serology and Urine StudiesEndocrine

System

TABLE 47.7 Radiologic StudiesEndocrine System

Case Study—cont’d Objective Data: Diagnostic Studies

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The HCP orders the following initial diagnostic studies to be drawn in the morning after an 8-hr fast: • CBC, basic metabolic panel (electrolytes, BUN, creatinine) • Fasting blood glucose (FBG) • TSH, free T4 • Plasma cortisol levels • Plasma ACTH levels

CBC results reveal a WBC of 12,200/µL and a decreased lymphocyte count at 800 cells/µL. The rest of the CBC is within normal limits (WNL). The FBG is 130 mg/dL. The plasma cortisol and ACTH levels are high. Thyroid studies are WNL.

Discussion Questions 1. Which diagnostic study results are of most concern to you? 2. Do you expect the HCP to order any other diagnostic studies for L.M.? 3. What are the interprofessional team’s priorities for L.M. at this time? Answers available at http://evolve.elsevier.com/Lewis/medsurg.

Bridge to Nclex Examination The number of the question corresponds to the same-numbered outcome at the beginning of the chapter.

1. A characteristic common to all hormones is that they a. circulate in the blood bound to plasma proteins. b. influence cellular activity of specific target tissues. c. accelerate the metabolic processes of all body cells. d. enter a cell and change the cell’s metabolism or gene expression. 2. A patient is receiving radiation therapy for cancer of the kidney. The nurse monitors the patient for signs and symptoms of damage to the a. pancreas. b. thyroid gland. c. adrenal glands.

d. posterior pituitary gland. 3. A patient has a serum sodium level of 152 mEq/L (152 mmol/L). The normal hormonal response to this situation is a. release of ADH. b. release of ACTH. c. secretion of aldosterone. d. secretion of corticotropin-releasing hormone. 4. All cells in the body are believed to have intracellular receptors for a. insulin. b. glucagon. c. growth hormone. d. thyroid hormone. 5. When obtaining subjective data from a patient during assessment of the endocrine system, the nurse asks specifically about a. energy level. b. intake of vitamin C. c. employment history. d. frequency of sexual intercourse. 6. An appropriate technique to use during physical assessment of the thyroid gland is a. asking the patient to hyperextend the neck during palpation. b. percussing the neck for dullness to define the size of the thyroid.

c. having the patient swallow water during inspection and palpation of the gland. d. using deep palpation to determine the extent of a visibly enlarged thyroid gland. 7. Endocrine disorders often go unrecognized in the older adult because a. symptoms are often attributed to aging. b. older adults rarely have identifiable symptoms. c. endocrine disorders are relatively rare in the older adult. d. older adults usually have subclinical endocrine disorders that minimize symptoms. 8. Abnormal findings during an endocrine assessment include (select all that apply) a. excess facial hair on a woman. b. blood pressure of 100/70 mm Hg. c. soft, formed stool every other day. d. 3-lb weight gain over last 6 months. e. hyperpigmented coloration in lower legs. 9. A patient has a total serum calcium level of 3 mg/dL (1.5 mEq/L). If this finding reflects hypoparathyroidism, the nurse would expect further diagnostic testing to reveal a. decreased serum PTH. b. increased serum ACTH. c. increased serum glucose. d. decreased serum cortisol levels. 1. b, 2. c, 3. a, 4. d, 5. a, 6. c, 7. a, 8. a, e, 9. a For rationales to these answers and even more NCLEX review questions, visit http://evolve.elsevier.com/Lewis/medsurg.

Evolve Website/Resources List http://evolve.elsevier.com/Lewis/medsurg

Review Questions (Online Only) Key Points Answer Keys for Questions • Rationales for Bridge to NCLEX Examination Questions • Answer Guidelines for the Case Study on pp. 1096, 1098, 1099, and 1106 Conceptual Care Map Creator Audio Glossary Supporting Media • Animations • Overview of the Endocrine System • Thyroid and Parathyroid Glands • Thyroid Secretion Supporting Media Content Updates

References 1. Huether SE, McCance K: Understanding pathophysiology, ed 6, St Louis, 2017, Elsevier. 2. Stratakis CA: Genetics of endocrine disorders, St Louis, 2017, Elsevier. 3. Jarvis C: Physical examination and health assessment, ed 7, St Louis, 2016, Saunders.

Vilar L, Vilar CF, Lyra R, et al: Acromegaly: Clinical features at diagnosis, Pituitary 20:22, 2017.

5. Parsa AA, Gharib H: Thyroid nodules, New York, 2018, Humana. 6. Pagana K, Pagana T, Pagana TN: Mosby’s manual of diagnostic and laboratory tests, ed 13, St Louis, 2017, Mosby. American Diabetes Association: Standards of medical care in diabetes —2018, Diabetes Care 41:S13, 2018. ∗Evidence-based information for clinical practice.

48

Diabetes Mellitus Jane K. Dickinson

LEARNING OUTCOMES 1. Describe the pathophysiology and clinical manifestations of diabetes mellitus. 2. Distinguish between type 1 and type 2 diabetes mellitus. 3. Describe the interprofessional care of a patient with diabetes. 4. Describe the role of nutrition and exercise in managing diabetes mellitus. 5. Discuss the nursing management of a patient with newly diagnosed diabetes mellitus. 6. Describe the nursing management of a patient with diabetes mellitus in the ambulatory and home care settings. 7. Relate the pathophysiology of acute and chronic complications of diabetes mellitus to the clinical manifestations. 8. Explain the interprofessional care and nursing management of a patient with acute and chronic complications of diabetes mellitus.

KEY TERMS basal-bolus plan, p. 1113

dawn phenomenon, p. 1118 diabetes mellitus (DM), p. 1108 diabetes-related ketoacidosis (DKA), p. 1130 diabetes-related nephropathy, p. 1137 diabetes-related neuropathy, p. 1137 diabetes-related retinopathy, p. 1136 hyperosmolar hyperglycemia syndrome (HHS), p. 1133 impaired fasting glucose (IFG), p. 1111 impaired glucose tolerance (IGT), p. 1111 insulin resistance, p. 1111 prediabetes, p. 1111 self-monitoring of blood glucose (SMBG), p. 1123 Somogyi effect, p. 1117 Wherever a man turns he can find someone who needs him. Albert Schweitzer http://evolve.elsevier.com/Lewis/medsurg

Conceptual Focus Glucose Regulation Infection Nutrition Self-Management Sensory Perception This chapter discusses the pathophysiology, manifestations, complications, and management of diabetes. The long-term complications associated with diabetes can make it a devastating

disease. Diabetes is the leading cause of adult blindness, end-stage renal disease, and nontraumatic lower limb amputations. It is a major contributing factor to heart disease and stroke. Managing diabetes requires daily decisions about food intake, blood glucose monitoring, medication, and exercise. You play a vital role in promoting the patient’s self-management of diabetes through providing comprehensive patient and caregiver education.

Diabetes Mellitus Diabetes mellitus (DM), most often referred to as diabetes, is a chronic multisystem disease characterized by hyperglycemia from abnormal insulin production, impaired insulin use, or both. Diabetes is a serious health problem throughout the world. Its prevalence is rapidly increasing. Currently in the United States, an estimated 29.1 million people, or 9.3% of the population, have diabetes. 86 million more people have prediabetes.1 About 8.1 million people with diabetes have not been diagnosed and are unaware that they have the disease. Diabetes is the seventh leading cause of death in the United States.2 Adults with diabetes have heart disease death rates and risk for strokes that are 2 to 4 times higher than adults without diabetes. In addition, more than half of adults with diabetes have hypertension and high cholesterol levels.2

Etiology and Pathophysiology Current theories link the causes of diabetes, singly or in combination, to genetic, autoimmune, and environmental factors (e.g., virus, obesity). Regardless of its cause, diabetes is primarily a disorder of glucose metabolism related to absent or insufficient insulin supply and/or poor use of the available insulin. The American Diabetes Association (ADA) recognizes 4 different classes of diabetes. The 2 most common are type 1 and type 2 diabetes (Table 48.1). The 2 other classes are gestational diabetes and other specific types of diabetes with various causes.

Normal Glucose and Insulin Metabolism Insulin is a hormone made by the β cells in the islets of Langerhans of the pancreas. Under normal conditions, insulin is continuously released into the bloodstream in small amounts, with increased release when food is ingested (Fig. 48.1). Insulin lowers blood glucose and facilitates a stable, normal glucose range of about 74 to 106 mg/dL

(4.1 to 5.9 mmol/L). The amount of insulin secreted daily by an adult is about 40 to 50 U, or 0.6 U/kg of body weight.

TABLE 48.1 Comparison of Type 1 and Type 2

Diabetes

FIG. 48.1 Normal endogenous insulin secretion. After meals, insulin concentrations rise rapidly in blood and peak at about 1 hour. Then insulin concentrations promptly decline toward preprandial values as carbohydrate absorption from the GI tract declines. After carbohydrate absorption from the GI tract is complete and during the night, insulin concentrations are low and fairly constant, with a slight increase at dawn.

Insulin promotes glucose transport from the bloodstream across the cell membrane to the cytoplasm of the cell (Fig. 48.2). Cells break down glucose to make energy. Liver and muscle cells store excess glucose as glycogen. The rise in plasma insulin after a meal inhibits gluconeogenesis, enhances fat deposition of adipose tissue, and increases protein synthesis. For this reason, insulin is an anabolic, or storage, hormone. The fall in insulin level during normal overnight fasting promotes the release of stored glucose from the liver, protein from muscle, and fat from adipose tissue. Skeletal muscle and adipose tissue have specific receptors for insulin and are considered insulin-dependent tissues. Insulin is required to “unlock” these receptor sites, allowing the transport of glucose into the cells to be used for energy. Other tissues (e.g., brain, liver, blood cells) do not directly depend on insulin for glucose transport but require an adequate glucose supply for normal function. Although liver cells are not considered insulin-dependent tissue, insulin receptor sites on the liver facilitate uptake of glucose and its conversion to glycogen.

FIG. 48.2 Normal glucose metabolism. Insulin binds to receptors along the cell walls of muscle, adipose, and liver cells. Glucose transport proteins (GLUT 4s) then attach to the cell wall and allow glucose to enter the cell, where it is either stored or used to make energy.

Other hormones (glucagon, epinephrine, growth hormone [GH], cortisol) work against the effects of insulin. They are counterregulatory hormones. These hormones increase blood glucose levels by (1) stimulating glucose production and release by the liver and (2) decreasing the movement of glucose into the cells. The counterregulatory hormones and insulin work together to maintain blood glucose levels within the normal range by regulating the release of glucose for energy during food intake and periods of fasting.

Insulin is synthesized from its precursor, proinsulin. Enzymes split proinsulin to form insulin and C-peptide, and the 2 substances are released in equal amounts. Therefore measuring C-peptide in serum and urine is a useful clinical indicator of pancreatic β-cell function and insulin levels.

Genetics in Clinical Practice Type 1 and Type 2 Diabetes and Maturity-Onset Diabetes of the Young (MODY)

Type 1 Diabetes Type 1 diabetes, formerly known as juvenile-onset diabetes or insulindependent diabetes mellitus (IDDM), accounts for about 5% to 10% of all people with diabetes. Type 1 diabetes generally affects people under 40 years of age, although it can occur at any age.3

Etiology and Pathophysiology

Type 1 diabetes is an autoimmune disorder in which the body develops antibodies against insulin and/or the pancreatic β cells that make insulin. This eventually results in not enough insulin for a person to survive. A genetic predisposition and exposure to a virus are factors that may contribute to the development of immune-related type 1 diabetes.

Genetic Link Predisposition to type 1 diabetes is related to human leukocyte antigens (HLAs) (see Chapter 13). In theory, when a person with certain HLA types is exposed to a viral infection, the β cells of the pancreas are destroyed, either directly or through an autoimmune process. The HLA types associated with an increased risk for type 1 diabetes include HLA-DR3 and HLA-DR4. Idiopathic diabetes is a form of type 1 diabetes that is strongly inherited and not related to autoimmunity. It only occurs in a small number of people with type 1 diabetes, most often of Hispanic, African, or Asian ancestry.3 Latent autoimmune diabetes in adults (LADA), a slowly progressing autoimmune form of type 1 diabetes. It occurs in adults and is often mistaken for type 2 diabetes.

Onset of Disease In type 1 diabetes, the islet cell autoantibodies responsible for β-cell destruction are present for months to years before the onset of symptoms. Manifestations develop when the person’s pancreas can no longer make enough insulin to maintain normal glucose. Once this occurs, the onset of symptoms is usually rapid. Patients often are initially seen with impending or actual ketoacidosis. The patient usually has a history of recent and sudden weight loss and the classic symptoms of polydipsia (excessive thirst), polyuria (frequent urination), and polyphagia (excessive hunger). The person with type 1 diabetes requires insulin from an outside source (exogenous insulin) to sustain life. Without insulin, the patient will develop diabetes-related ketoacidosis (DKA), a life-threatening

condition resulting in metabolic acidosis. Newly diagnosed patients may have a remission, or “honeymoon period,” for 3 to 12 months after starting treatment. During this time, the patient needs little injected insulin because β-cell insulin production is still sufficient for healthy blood glucose levels. Eventually, as more β cells are destroyed and blood glucose levels increase, the honeymoon period ends and the patient will require insulin on a permanent basis.

Type 2 Diabetes Type 2 diabetes, formerly known as adult-onset diabetes or non–insulindependent diabetes mellitus (NIDDM), accounts for about 90% to 95% of people with diabetes.2 Many risk factors contribute to the development of type 2 diabetes. These include being overweight or obese, being older, and having a family history of type 2 diabetes. Although the disease is seen less often in children, the incidence is increasing due to the increasing prevalence of childhood obesity. Type 2 diabetes is more prevalent in some ethnic populations. Blacks, Asian Americans, Hispanics, Native Hawaiians or other Pacific Islanders, and Native Americans have a higher rate of type 2 diabetes than whites.2

Promoting Health Equity Diabetes • Native Americans and Alaska Natives have highest prevalence for both men (14.9%) and women (15.3%). • Pima Indians in Arizona have the highest rate of diabetes in the world (50% of adults). • Native American and Alaska Native women are twice as likely to die from diabetes as white women. • Rates are higher among blacks (12.7%) and Hispanics (12.1%) than among whites (7.4%) and Asians (8.0%).

• Blacks are twice as likely as whites to die from diabetes.

Etiology and Pathophysiology Type 2 diabetes is characterized by a combination of inadequate insulin secretion and insulin resistance. The pancreas usually makes some endogenous (self-made) insulin. However, the body either does not make enough insulin or does not use it effectively, or both. The presence of endogenous insulin is a major distinction between type 1 and type 2 diabetes. In type 1 diabetes, there is an absence of endogenous insulin.

Genetic Link Although we do not fully understand the genetics of type 2 diabetes, it is likely multiple genes are involved. We have found genetic mutations that lead to insulin resistance and a higher risk for obesity in many people with type 2 diabetes. Persons with a first-degree relative with the disease are 10 times more likely to develop type 2 diabetes. Metabolic abnormalities have a role in the development of type 2 diabetes (Fig. 48.3). The first factor is insulin resistance, a condition in which body tissues do not respond to the action of insulin because insulin receptors are unresponsive, are insufficient in number, or both. Most insulin receptors are located on skeletal muscle, fat, and liver cells. When insulin is not properly used, the entry of glucose into the cell is impeded, resulting in hyperglycemia. In the early stages of insulin resistance, the pancreas responds to high blood glucose by producing greater amounts of insulin (if β cell function is normal). This creates a temporary state of hyperinsulinemia that coexists with hyperglycemia.

FIG. 48.3 Altered mechanisms in type 1 and type 2 diabetes.

A second factor in the development of type 2 diabetes is a marked decrease in the ability of the pancreas to make insulin, as the β cells become fatigued from the compensatory overproduction of insulin or when β-cell mass is lost. The underlying basis for the failure of β cells to adapt is unknown. It may be linked to the adverse effects of chronic hyperglycemia or high circulating free fatty acids. In addition, the α cells of the pancreas increase production of glucagon. This leads to a third factor, which is inappropriate glucose production by the liver. Instead of properly regulating the release of glucose in response to blood levels, the liver does so in a haphazard way that does not correspond to the body’s needs at the time. A fourth factor is altered production of hormones and cytokines by adipose tissue (adipokines). Adipokines secreted by adipose tissue appear to play a role in glucose and fat metabolism and are likely to contribute to the development of type 2 diabetes.4 We think adipokines cause chronic inflammation, a factor involved in insulin resistance, type 2 diabetes, and cardiovascular disease (CVD). The 2 main adipokines thought to affect insulin sensitivity are adiponectin and leptin. Finally, the brain, kidneys, and gut have roles in the development of type 2 diabetes. We are continuously learning more about metabolic factors in the development of type 2 diabetes.4 People with metabolic syndrome have an increased risk for developing type 2 diabetes. Metabolic syndrome has 5 components: increased glucose levels, abdominal obesity, high BP, high levels of triglycerides, and decreased levels of high-density lipoproteins (HDLs) (see Table 40.12). A person with 3 of the 5 components is considered to have metabolic syndrome.5 Overweight persons with metabolic syndrome can reduce their risk for diabetes through a program of weight loss and regular physical activity. See Chapter 40 for more about metabolic syndrome.

Onset of Disease The disease onset in type 2 diabetes is usually gradual. The person

may go for many years with undetected hyperglycemia and few, if any, symptoms. Many people are diagnosed on routine laboratory testing or when they undergo treatment for other conditions, and elevated glucose or glycosylated hemoglobin (A1C) levels are found. The signs and symptoms of hyperglycemia develop when about 50% to 80% of β cells are no longer secreting insulin. At the time of diagnosis, the average person has had type 2 diabetes for 6½ years.

Prediabetes Persons diagnosed with prediabetes are at increased risk for developing type 2 diabetes. Prediabetes is defined as impaired glucose tolerance (IGT), impaired fasting glucose (IFG), or both. It is an intermediate stage between normal glucose homeostasis and diabetes, in which the blood glucose levels are elevated but not high enough to meet the diagnostic criteria for diabetes.6 A diagnosis of IGT is made if the 2-hour oral glucose tolerance test (OGTT) values are 140 to 199 mg/dL (7.8 to 11.0 mmol/L). IFG is diagnosed when fasting blood glucose levels are 100 to 125 mg/dL (5.56 to 6.9 mmol/L). Persons with prediabetes usually do not have symptoms. However, long-term damage to the body, especially the heart and blood vessels, may already be occurring. It is important for patients to undergo screening and to understand risk factors for diabetes. People with prediabetes can take action to prevent or delay the development of type 2 diabetes. Encourage those with prediabetes to have their blood glucose and A1C checked regularly and monitor for symptoms of diabetes, such as fatigue, frequent infections, or slow-healing wounds. Maintaining a healthy weight, exercising regularly, and making healthy food choices reduce the risk for developing overt type 2 diabetes in people with prediabetes.

Gestational Diabetes Gestational diabetes develops during pregnancy and occurs in about 2% to 10% of pregnancies in the United States.7 Women with gestational diabetes have a higher risk for cesarean delivery, and their babies have increased risk for perinatal death, birth injury, and neonatal

complications. Women who are at high risk for gestational diabetes are screened at the first prenatal visit. Those at high risk include women who are obese, are of advanced maternal age, or have a family history of diabetes. Women with an average risk for gestational diabetes are screened using an OGTT at 24 to 28 weeks of gestation. Most women with gestational diabetes have normal glucose levels within 6 weeks postpartum. Women with a history of gestational diabetes have up to a 63% chance of developing type 2 diabetes within 16 years.7 Gestational diabetes and managing the pregnant patient with diabetes are specialized areas not covered in detail in this chapter. Consult an obstetric text for more information.

Other Specific Types of Diabetes Diabetes occurs in some people because of another medical condition or treatment of a medical condition that causes abnormal blood glucose levels. Conditions that may cause diabetes can result from injury to, interference with, or destruction of the β-cell function in the pancreas. These include Cushing syndrome, hyperthyroidism, recurrent pancreatitis, cystic fibrosis, hemochromatosis, and parenteral nutrition. Common drugs that can induce diabetes include corticosteroids (prednisone), thiazides, phenytoin (Dilantin), and atypical antipsychotics (e.g., clozapine [Clozaril]). Diabetes caused by medical conditions or drugs can resolve when the underlying condition is treated or the drug is discontinued.

Clinical Manifestations Type 1 Diabetes Because the onset of type 1 diabetes is rapid, the first manifestations are usually acute. The classic symptoms are polyuria, polydipsia, and polyphagia. The osmotic effect of excess glucose in the bloodstream causes polydipsia and polyuria. Polyphagia is a result of cellular malnourishment when insulin deficiency prevents cells from using glucose for energy. Weight loss may occur because the body cannot get glucose and instead breaks down fat and protein to try to make

energy. Weakness and fatigue may result because body cells lack needed energy from glucose. Ketoacidosis, a complication most common in those with untreated type 1 diabetes, is associated with additional manifestations. It is discussed later in this chapter.

Type 2 Diabetes The manifestations of type 2 diabetes are often nonspecific. It is possible a person with type 2 diabetes will have classic symptoms associated with type 1 diabetes, including polyuria, polydipsia, and polyphagia. Some of the more common manifestations associated with type 2 diabetes are fatigue, recurrent infections, recurrent vaginal yeast or candida infections, prolonged wound healing, and vision problems.

Diagnostic Studies The diagnosis of diabetes is made using 1 of the following 4 methods: 1. A1C of 6.5% or higher 2. Fasting plasma glucose (FPG) level of 126 mg/dL (7.0 mmol/L) or greater. Fasting is defined as no caloric intake for at least 8 hours 3. A 2-hour plasma glucose level of 200 mg/dL (11.1 mmol/L) or greater during an OGTT, using a glucose load of 75 g 4. In a patient with classic symptoms of hyperglycemia (polyuria, polydipsia, unexplained weight loss) or hyperglycemic crisis, a random plasma glucose level of 200 mg/dL (11.1 mmol/L) or greater If a patient is seen with a hyperglycemic crisis or clear symptoms of hyperglycemia (polyuria, polydipsia, polyphagia) with a random plasma glucose level of 200 mg/dL or greater, repeat testing is not needed. Otherwise, criteria 1 through 3 require confirmation by repeat testing to rule out laboratory error. It is preferable for the repeat test to be the same test used initially. For example, if a random elevated

blood glucose is used for the initial measurement, that same measure should be used to confirm a diagnosis. The accuracy of laboratory results depends on adequate patient preparation and attention to the many factors that may influence the results. For example, factors that can falsely elevate values include recent severe restrictions of dietary carbohydrate, acute illness, drugs (e.g., contraceptives, corticosteroids), and restricted activity, such as bed rest. A patient with impaired gastrointestinal (GI) absorption or who has recently taken acetaminophen may have false-negative results. A1C measures the amount of glycosylated hemoglobin (Hgb) as a percentage of total Hgb. For example, A1C of 6.5% means that 6.5% of the total Hgb has glucose attached to it. The amount of glycosylated Hgb depends on the blood glucose level. When blood glucose levels are elevated over time, the amount of glucose attached to Hgb increases. This glucose stays attached to the red blood cell (RBC) for the life of the cell (about 120 days). Therefore, A1C provides a measurement of blood glucose levels over the previous 2 to 3 months, with increases in the Hb A1C reflecting elevated blood glucose levels. The A1C has several advantages over the FPG, including greater convenience, since fasting is not needed. Diseases affecting RBCs (e.g., iron deficiency anemia, sickle cell anemia) can influence the A1C and should be considered when interpreting results. A1C results can be converted to the same units (mg/dL or mmol/L) that patients use in blood glucose measurements. An estimated average glucose (eAG) can be determined from the A1C. The eAG = 28.7 × A1C − 46.7. For example, an A1C of 8.0% is equivalent to a glucose level of 183 mg/dL. Teach patients with diabetes and prediabetes to have their A1C monitored regularly to determine how well the current treatment plan is working and make changes in the plan if glycemic goals are not achieved. The ADA identifies an A1C goal for patients with diabetes of less than 7.0%. The American College of Endocrinology recommends an A1C of less than 6.5%. When the A1C is maintained at near-normal levels, the risk for developing microvascular and

macrovascular complications is greatly reduced. For people with prediabetes, monitoring the A1C can detect overt diabetes and provide feedback on efforts to prevent diabetes. Fructosamine is another way to assess glucose levels. It is formed by a chemical reaction of glucose with plasma protein. It reflects glycemia in the previous 1 to 3 weeks. Fructosamine levels may show a change in blood glucose levels before A1C does. It is used for people with hemoglobinopathies, or for short-term measurement of glucose levels, for instance, after a change in medication or during pregnancy. Islet cell autoantibody testing is primarily done to help distinguish between autoimmune type 1 diabetes and diabetes from other causes. Autoantibodies can develop to 1 or several autoantigens, including GAD65, IA-2, or insulin.

Interprofessional Care The goals of diabetes management are to reduce symptoms, promote well-being, prevent acute complications related to hyperglycemia and hypoglycemia, and prevent or delay the onset and progression of long-term complications. These goals are most likely to be met when the patient maintains blood glucose levels as near to normal as possible. Patient teaching, which enables the patient to become the most active participant in their own care, is essential to achieve glycemic goals. Nutrition therapy, drug therapy, exercise, and selfmonitoring of blood glucose are the tools used in managing diabetes (Table 48.2). The 3 major types of glucose-lowering agents (GLAs) used in the treatment of diabetes are insulin, oral agents (OAs), and noninsulin injectable agents. All persons with type 1 diabetes require insulin. For some people with type 2 diabetes, a healthy eating plan, regular physical activity, and maintaining a healthy body weight are enough to attain optimal blood glucose levels. Eventually, most people will need medication management because type 2 diabetes is a progressive disease.

Drug Therapy: Insulin Exogenous (injected) insulin is needed when a patient has inadequate insulin to meet specific metabolic needs. People with type 1 diabetes require exogenous insulin to survive. They often use multiple daily injections of insulin (often 4 or more) or continuous insulin infusion via an insulin pump to adequately manage blood glucose levels. People with type 2 diabetes may need exogenous insulin during periods of severe stress, such as illness or surgery. Since type 2 diabetes is a progressive disease, over time, the combination of nutrition therapy, exercise, OAs, and noninsulin injectable agents may no longer adequately manage blood glucose levels. At that point, exogenous insulin is added as part of the management plan. People with type 2 diabetes may also need up to 4 injections per day to adequately maintain their blood glucose levels. Insulin pumps also can be used for patients with type 2 diabetes.

TABLE 48.2 Interprofessional CareDiabetes

Diagnostic Assessment • History and physical examination • Blood tests, including fasting blood glucose, postprandial blood glucose, A1C, fructosamine, lipid profile, BUN and serum creatinine, electrolytes, islet cell autoantibodies • Urine for complete urinalysis, albuminuria, and acetone (if indicated) • BP • ECG (if indicated) • Funduscopic examination (dilated eye examination) • Dental examination • Neurologic examination, including monofilament test for sensation to lower extremities

• Ankle-brachial index (ABI) (if indicated) (see Table 37.3) • Foot (podiatric) examination • Monitoring of weight

Management • Patient and caregiver teaching and follow-up programs • Nutrition therapy (Table 48.8) • Exercise therapy (Tables 48.9 and 48.10) • Self-monitoring of blood glucose (SMBG) (Table 48.11)

Drug Therapy • Insulin (Fig. 48.3 and Tables 48.3 and 48.4) • OAs and noninsulin injectable agents (Table 48.7) • Enteric-coated aspirin (81–162 mg/day) • ACE inhibitors (see Table 32.6) • Angiotensin II receptor blockers (ARBs) (see Table 32.6) • Antihyperlipidemic drugs (see Table 33.6)

Types of Insulin Today, people use only genetically engineered human insulin made in laboratories. The insulin is derived from common bacteria (e.g., Escherichia coli) or yeast cells using recombinant deoxyribonucleic acid (DNA) technology. In the past, insulin was extracted from beef and pork pancreases. These forms of insulin are no longer available. Insulins differ by their onset, peak action, and duration (Fig. 48.4). They are categorized as rapid-acting, short-acting, intermediateacting, and long-acting insulin (Table 48.3).

Insulin Plans

Examples of insulin plans are shown in Table 48.4. The insulin approach that most closely mimics endogenous insulin production is the basal-bolus plan (often called intensive or physiologic insulin therapy). It consists of multiple daily insulin injections (or an insulin pump) together with frequent self-monitoring of blood glucose (or a continuous glucose monitoring system). Injections include rapid- or short-acting (bolus) insulin before meals and intermediate- or longacting (basal) background insulin once or twice a day. The goal is to achieve a glucose level as close to normal as possible, as much of the time as possible. This is referred to as “time in range.” Other, less intense plans can promote healthy blood glucose levels for some people. Ideally, the patient and the HCP will work together to choose a plan. Selection criteria are based on the desired and feasible blood glucose levels and the patient’s lifestyle, food choices, and activity patterns. If a less intense plan is not giving the person optimal results, the HCP may encourage a more intense approach.

Mealtime Insulin (Bolus) To manage postprandial blood glucose levels, the timing of rapid- and short-acting insulin in relation to meals is crucial. Rapid-acting synthetic insulin analogs, which include aspart (NovoLog), glulisine (Apidra), and lispro (Humalog), have an onset of action of about 15 minutes. They should be injected within 15 minutes of mealtime. The rapid-acting analogs most closely mimic natural insulin secretion in response to a meal. Short-acting regular insulin has an onset of action of 30 to 60 minutes. It is injected 30 to 45 minutes before a meal to ensure that the insulin is working at the same time as meal absorption. Because timing an injection 30 to 45 minutes before a meal is hard for some people to do with their lifestyles, the flexibility that rapid-acting insulins offer is preferred by those taking insulin with their meals.8 Short-acting insulin is more likely to cause hypoglycemia because of a longer duration of action.

Long- or Intermediate-Acting (Basal) Background Insulin

In addition to mealtime insulin, people with type 1 diabetes use a long- or intermediate-acting basal (background) insulin to maintain blood glucose levels in between meals and overnight. Without 24hour background insulin, people with type 1 diabetes are more prone to developing DKA. Many people with type 2 diabetes who use OAs will need basal insulin to adequately manage blood glucose levels. The long-acting insulins include degludec (Tresiba), detemir (Levemir), and glargine (Lantus, Toujeo, Basaglar).This type of insulin is released steadily and continuously. For most people, it does not have a peak of action. The action time for long-acting insulin varies (Fig. 48.4). Although they can be given once daily, detemir is often given twice daily. Because they lack peak action time, the risk for hypoglycemia from this type of insulin is greatly reduced. Glargine and detemir must not be diluted or mixed with any other insulin or solution in the same syringe. If OAs and long-acting insulin are not adequate to achieve glycemic goals, mealtime insulin may be added.

FIG. 48.4 Commercially available insulin preparations showing onset, peak, and duration of action. Individual patient responses to each type of insulin are different and affected by many different factors.

TABLE 48.3 Drug TherapyTypes of Insulin



These numbers refer to percentages of each type of insulin.

Intermediate-acting insulin (NPH) can be used as a basal insulin. It has a duration of 12 to 18 hours. The disadvantage of NPH is that it has a peak ranging from 4 to 12 hours, which can result in hypoglycemia. NPH can be mixed with short- and rapid-acting insulins. It should never be given IV.

Check Your Practice You are preparing your patient’s order for NPH insulin. When you look at the vial, you notice that it is cloudy. You are thinking that you should throw away the vial because has become contaminated. • Before you take this action, what should you do? All insulins are clear solutions except NPH, lispro protamine, and aspart protamine. They are cloudy because they contain a protein called protamine, which makes them work longer. These insulins must be gently agitated before administration.

Combination Insulin Therapy

For those who want to use only 1 or 2 injections per day, a short- or rapid-acting insulin is mixed with intermediate-acting insulin in the same syringe. This allows the patient to have both mealtime and basal coverage without having to give 2 separate injections. Although this may be more appealing to the patient, most patients achieve optimal blood glucose levels with basal-bolus therapy. Patients may mix the 2 types of insulin themselves or use a commercially premixed formula or pen (Table 48.3). Premixed formulas offer convenience to patients, who do not have to draw up and mix insulin from 2 different vials. This is especially helpful to those who lack the visual, manual, or cognitive skills to mix insulin themselves. However, the convenience of these formulas limits the potential for optimal blood glucose levels because there is less opportunity for flexible dosing based on need.

TABLE 48.4 Drug TherapyInsulin Regimens

Rapid-acting (lispro, aspart, glulisine) insulin. Short-acting (regular) insulin. Intermediate-acting (NPH) or long-acting (glargine, detemir, degludec) insulin.

Storage of Insulin As a protein, insulin has special storage considerations. Extreme temperatures alter the insulin molecule and can make it less effective.

Insulin vials and pens in use may be left at room temperature for up to 4 weeks unless the room temperature is higher than 86° F (30° C) or below freezing (less than 32° F [0° C]). Teach patients to avoid prolonged exposure to direct sunlight. A patient who is traveling in hot climates may store insulin in a thermos or cooler to keep it cool (not frozen). Store unopened insulin vials and pens in the refrigerator. Patients who are traveling or caregivers of patients who are sight impaired or who lack the manual dexterity to fill their own syringes may prefill insulin syringes. Prefilled syringes with 2 different insulins are stable for up to 1 week when stored in the refrigerator. Syringes with only 1 type of insulin are stable up to 30 days. Teach patients to store syringes in a vertical position with the needle pointed up to avoid clumping of suspended insulin in the needle. Before injection, gently roll prefilled syringes between the palms 10 to 20 times to warm the insulin and resuspend the particles. Some insulin combinations cannot be prefilled and stored because the mixture can alter the onset, action, and/or peak times of either insulin. Consult a reference as needed when mixing and prefilling different types of insulin.

Administration of Insulin Routine doses of insulin are given by subcutaneous injection. Regular insulin can be given IV when immediate onset of action is desired. Insulin is not taken orally because it is inactivated by gastric fluids. Teach patients to avoid injecting insulin IM because rapid and unpredictable absorption could result in hypoglycemia.

Insulin Injection The steps in giving a subcutaneous insulin injection are outlined in Table 48.5. Teach this technique to new insulin users and review it periodically with long-term users. Never assume that because the patient already uses insulin, they know and practice the correct insulin injection technique. The patient may not have understood prior instructions, or changes in eyesight may result in inaccurate preparation.9 The patient may not see air bubbles in the syringe or

may improperly read the scale on the syringe. The patient receiving mixed insulins in the same syringe needs to learn the proper technique for combining them if commercially prepared premixed insulins are not used.

TABLE 48.5 Patient & Caregiver

TeachingPreparing an Insulin Injection Include the following instructions when teaching the patient and caregiver about insulin therapy: 1. Wash hands thoroughly. 2. Always inspect insulin bottle before using it. Make sure that it is the proper type and concentration, expiration date has not passed, and top of bottle is in perfect condition. Insulin solutions (except for NPH, lispro protamine, aspart protamine) should look clear and colorless. Discard if it appears discolored or if you see particles in the solution. 3. For intermediate-acting insulins (which are normally cloudy), gently roll the insulin bottle between the palms of hands to mix the insulin. Clear insulins do not need to be agitated. 4. Choose proper injection site (Fig. 48.5). 5. Ensure that the site is clean and dry. 6. Push the needle straight into the skin (90-degree angle). If you are very thin, muscular, or using an 8- or 12-mm needle, you may need to pinch the skin and/or use a 45-degree angle. 7. Push the plunger all the way down, leave needle in place for 5 sec to ensure that all insulin has been injected, and then remove needle. 8. Destroy and dispose of single-use syringe safely. The speed with which peak serum concentrations are reached varies with the injection site. The fastest subcutaneous absorption is from the abdomen, followed by the arm, thigh, and buttock. Although the

abdomen is often the preferred injection site, other sites work well (Fig. 48.5). Caution the patient about injecting into a site that is to be exercised. For example, injecting into the thigh and then going jogging could increase body heat and circulation. This could increase the rate of insulin absorption and speed the onset of action, resulting in hypoglycemia. Teach patients to rotate the injection within and between sites. This allows for better insulin absorption. It may be helpful to think of the abdomen as a checkerboard, with each ½-in square representing an injection site. Injections are rotated systematically across the board, with each injection site at least ½ to 1 inch away from the previous injection site. It can be helpful to inject fast-acting insulin into fasterabsorbing sites and slow-acting insulin into slower absorbing sites. Most commercial insulin is available as U100. This means that 1 mL contains 100 U of insulin. U100 insulin must be used with a U100marked syringe. Disposable plastic insulin syringes are available in a variety of sizes, including 1.0, 0.5, and 0.3 mL. The 0.5-mL size may be used for doses of 50 U or less. The 0.3-mL syringe can be used for doses of 30 U or less. The 0.5- and 0.3-mL syringes are in 1-unit increments. This provides more accurate delivery when the dose is an odd number. The 1.0-mL syringe is necessary for patients who inject more than 50 U of insulin. The 1.0-mL syringe is in 2-unit increments. When patients change from a 0.3- or a 0.5-mL to a 1.0-mL syringe, tell them of the dose increment difference. Insulin syringe needles come in 3 lengths: 6 mm (½ in), 8 mm (5⁄16 in), and 12.7 mm (½ in).10 Needle gauges vary among syringes. The needle gauges available are 28, 29, 30, and 31. The higher the gauge number, the smaller the diameter, thus resulting in a more comfortable injection. Only the person using the syringe should recap the needle; never recap a needle used for a patient. To prepare the site, routine hygiene, such as washing with soap and rinsing with water, is adequate. This applies primarily to patient self-injection technique. When injection occurs in a health care agency, policy usually mandates site preparation with alcohol to prevent health care– associated infection (HAI).

FIG. 48.5 Injection sites for insulin.

FIG. 48.6 Parts of insulin pen.

Insulin injections are typically given at a 90-degree angle. For extremely thin or muscular patients in the hospital, perform injections at a 45-degree angle. At home, patients inject at a 90-degree angle using the shortest needle desired. Pinching up of the skin to avoid IM injection is no longer done because of the use of short needles. An insulin pen is a compact portable device loaded with an insulin cartridge that serves the same function as a needle and syringe (Fig. 48.6). Pen needles are available in lengths of 4 mm (5⁄32 in), 5 mm (3⁄16 in), 8 mm (5⁄16 in), and 12.7 mm (½ in) and in 3 gauges: 29, 31, and 32. Insulin pens offer convenience and flexibility. They are portable and compact, are more discreet than using a vial and syringe, and provide consistent and accurate dosing. For patients with poor vision, the pen is a better option, since they can hear the clicks of the pen as the dose is selected. Insulin pens come packaged with printed instructions, including pictures of the steps to take when using the pen. These instructions are helpful when teaching new users and reviewing technique with current users of a pen.

Insulin Pump An insulin pump delivers a continuous subcutaneous insulin infusion through a small device worn on the belt, in a pocket, or under clothing. Insulin pumps use rapid-acting insulin. It is loaded into a reservoir or cartridge and connected via plastic tubing to a catheter inserted into the subcutaneous tissue. Insulet Corporation has an insulin pump that is a tubing-free system (Fig. 48.7). All insulin pumps are programmed to deliver a continuous infusion of rapidacting insulin 24 hours a day, known as the basal rate. Basal insulin can be temporarily increased or decreased based on carbohydrate intake, activity changes, or illness. Pump users need different basal rates at different times of the day.

FIG. 48.7 A, OmniPod Insulin Management System. The Pod holds and delivers insulin. B, The Personal Diabetes Manager (PDM) wirelessly programs insulin delivery via the Pod. The PDM has a builtin glucose meter. Courtesy of Insulet Corporation.

At mealtime, the user programs the pump to deliver a bolus infusion of insulin appropriate to the amount of carbohydrate ingested and an additional amount, if needed, to bring down or “correct” high preprandial blood glucose. The infusion set is changed every 2 to 3 days and placed in a new site to avoid infection and promote good insulin absorption. Insulin pump users check their blood glucose level at least 4 times per day and/or use a continuous glucose monitoring system. Monitoring 8 times or more per day is common. A major advantage of the insulin pump is the potential for keeping blood glucose levels in a tighter range with a goal of eliminating both high and low glucose. With careful programming and constant monitoring, this is possible because insulin delivery is similar to the normal physiologic pattern. Pumps offer users more flexibility with meal and activity patterns. Potential challenges of insulin pump therapy include infection at the insertion site, an increased risk for DKA if the insulin infusion is disrupted, the cost of the pump and supplies, and being attached to a device.11

Problems With Insulin Therapy Problems associated with insulin therapy include hypoglycemia, allergic reactions, lipodystrophy, hypertrophy, and the Somogyi effect. Hypoglycemia is discussed in detail later in this chapter. Guidelines for assessing patients treated with insulin and other GLAs are outlined in Table 48.6.

Allergic Reactions Local inflammatory reactions to insulin may occur, such as itching, erythema, and burning around the injection site. Local reactions may be self-limiting within 1 to 3 months or may improve with a low dose of antihistamine. A true insulin allergy, which is rare, is manifested by a systemic response with urticaria and possibly anaphylactic shock. Preservative in the insulin and the latex or rubber stoppers on the vials have been implicated in allergic reactions.

Lipodystrophy and Hypertrophy Lipodystrophy (loss of subcutaneous fatty tissue) may occur if the same injection sites are used frequently. The use of human insulin has significantly reduced the risk for lipodystrophy. Atrophy, which is uncommon, is the wasting of subcutaneous tissue and presents as indentations in injection sites. Hypertrophy happens more often and is a thickening of the subcutaneous tissue. It eventually regresses if the patient does not use the site for at least 6 months. Injecting into a hypertrophied site may result in erratic insulin absorption.

TABLE 48.6 Assessing the Patient Treated With

Glucose-Lowering Agents

Somogyi Effect and Dawn Phenomenon Hyperglycemia in the morning may be due to the Somogyi effect. A high dose of insulin causes a decline in blood glucose levels during the night. As a result, counterregulatory hormones (e.g., glucagon, epinephrine, GH, cortisol) are released. They stimulate lipolysis, gluconeogenesis, and glycogenolysis, which in turn cause rebound hyperglycemia. The danger of this effect is that when blood glucose levels are measured in the morning, hyperglycemia is apparent and the patient (or the HCP) may increase the insulin dose. If a patient has morning hyperglycemia, checking blood glucose levels between 2:00 and 4:00 AM for hypoglycemia will help determine if the cause is the Somogyi effect. The patient may report headaches on awakening and recall having night sweats or nightmares. The dawn phenomenon is also characterized by hyperglycemia that is present on awakening. Two counterregulatory hormones (GH and cortisol), which are excreted in increased amounts in the early morning hours, may be the cause of this phenomenon. The dawn phenomenon affects many people with diabetes and tends to be most severe when GH is at its peak in adolescence and young adulthood. Careful assessment is needed to diagnose the Somogyi effect or

dawn phenomenon because the treatment for each differs. The treatment for Somogyi effect is a bedtime snack, reducing the dose of insulin, or both. The treatment for dawn phenomenon is an increase in insulin or an adjustment in administration time. Your assessment must include insulin dose, injection sites, and variability in the time of meals or insulin administration. Ask the patient to measure and document bedtime, nighttime (between 2:00 and 4:00 AM), and morning fasting blood glucose levels on several occasions. If the predawn levels are less than 60 mg/dL (3.3 mmol/L) and signs and symptoms of hypoglycemia are present, the insulin dosage should be reduced. If the 2:00 to 4:00 AM blood glucose is high, the insulin dosage should be increased. Counsel the patient on appropriate bedtime snacks.

Inhaled Insulin Afrezza is a rapid-acting inhaled insulin. It is given at the beginning of each meal or within 20 minutes after starting a meal. Afrezza must be used in combination with long-acting insulin in patients with type 1 diabetes. It should not be used to treat diabetic ketoacidosis. Patients with chronic lung disease, such as asthma or COPD, or who smoke, should not use Afrezza because bronchospasm can occur. Other common adverse reactions are hypoglycemia, cough, and throat pain or irritation.

Drug Therapy: Oral and Noninsulin Injectable Agents OAs and noninsulin injectable agents work to improve the mechanisms by which the body makes and uses insulin and glucose. These drugs primarily work on 3 defects of type 2 diabetes: (1) insulin resistance, (2) decreased insulin production, and (3) increased hepatic glucose production (Fig. 48.8). These drugs may be used in combination with agents from other classes or with insulin to achieve blood glucose goals. OAs and noninsulin injectable agents are listed in Table 48.7.

Biguanides The most widely used OA is metformin. It is the only drug in the biguanide class available in the United States. Metformin is the most effective first-line treatment for type 2 diabetes.8 Forms of metformin include Glucophage (immediate release), Glucophage XR (extended release), Fortamet (extended release), and Riomet (liquid). The primary action of metformin is to reduce glucose production by the liver. It enhances insulin sensitivity at the tissue level and improves glucose transport into the cells. It also has beneficial effects on plasma lipids. Because it may cause moderate weight loss, metformin may be useful for people with type 2 diabetes and prediabetes who are overweight or obese. It is also used to prevent type 2 diabetes in those with prediabetes who are younger than age 60 and have risk factors, such as hypertension or a history of gestational diabetes.

FIG. 48.8 Sites and mechanisms of action of type 2 diabetes drugs. DDP-4, Dipeptidyl peptidase; GLP-1, glucagon-like peptide-1; SGLT, sodium-glucose co-transporter.

TABLE 48.7 Drug TherapyOral Agents and

Noninsulin Injectable Agents

Patients who are undergoing surgery or radiologic procedures that involve the use of a contrast medium need to temporarily discontinue metformin before surgery or the procedure. This reduces the risk of contrast-induced kidney injury (CIN) (see Chapter 44). They should not resume the metformin until 48 hours afterward, once their serum creatinine has been checked and is normal.

Drug Alert Metformin • Do not use in patients with kidney disease, liver disease, or heart failure. Lactic acidosis is a rare complication of metformin accumulation. • IV contrast media that contain iodine pose a risk for CIN, which could worsen metformin-induced lactic acidosis. • To reduce risk for CIN, discontinue metformin 2 days before the procedure. • May be resumed 48 hours after the procedure, assuming kidney function is normal. • Do not use in people who drink excess amounts of alcohol. • Take with food to minimize GI side effects.

Sulfonylureas Sulfonylureas include glimepiride (Amaryl), glipizide (Glucotrol,

Glucotrol XL), and glyburide (DiaBeta, Glynase). The primary action of sulfonylureas is to increase insulin production by the pancreas. Therefore hypoglycemia is the major side effect.

Meglitinides Like sulfonylureas, nateglinide (Starlix) and repaglinide (Prandin) increase insulin production by the pancreas. However, because they are more rapidly absorbed and eliminated than sulfonylureas, they are less likely to cause hypoglycemia. When taken just before meals, pancreatic insulin production increases during and after the meal, mimicking the normal response to eating. Teach patients to take meglitinides any time from 30 minutes before each meal right up to the time of the meal. These drugs should not be taken if a meal is skipped.

α-Glucosidase Inhibitors These drugs, also known as “starch blockers,” work by slowing down carbohydrate absorption in the small intestine. Acarbose (Precose) and miglitol (Glyset) are the available drugs in this class. Taken with the first bite of each main meal, they are most effective in lowering postprandial blood glucose. Their effectiveness is measured by checking 2-hour postprandial glucose levels.

Thiazolidinediones Thiazolidinediones, sometimes called “insulin sensitizers,” include pioglitazone (Actos) and rosiglitazone (Avandia). They are most effective for people who have insulin resistance. These agents improve insulin sensitivity, transport, and use at target tissues. Because they do not increase insulin production, they do not cause hypoglycemia when used alone. However, these drugs are rarely used today because of their adverse effects. Rosiglitazone is associated with adverse cardiovascular events (e.g., myocardial infarction [MI]) and can be obtained only through restricted access programs. Pioglitazone can worsen heart failure (HF) and is associated with an increased risk for

bladder cancer.

Dipeptidyl Peptidase-4 (DPP-4) Inhibitors Normally, the intestines release incretin hormones throughout the day. When glucose levels are normal or elevated, incretins increase insulin synthesis and release from the pancreas and decrease hepatic glucose production. Levels increase in response to a meal. The 2 main incretin hormones are gastric inhibitory peptide [GIP] and glucagonlike peptide-1 [GLP-1]). They are quickly inactivated by the enzyme dipeptidyl peptidase-4 (DPP-4). DPP-4 inhibitors (also known as gliptins) come in pill form. They include alogliptin (Nesina), linagliptin (Tradjenta), saxagliptin (Onglyza), and sitagliptin (Januvia). DPP-4 inhibitors block the action of DPP-4, which inactivates incretin hormones. The result is an increase in insulin release, decrease in glucagon secretion, and decrease in hepatic glucose production. Since the DPP-4 inhibitors are glucose dependent, they lower the potential for hypoglycemia. The main benefit of these drugs over other medications with similar effects is the absence of weight gain as a side effect.

Sodium-Glucose Co-Transporter 2 (SGLT2) Inhibitors Normally, sodium glucose transporters reabsorb glucose from the kidneys back into the blood stream. Sodium-glucose co-transporter 2 (SGLT2) inhibitors work by blocking the reabsorption of glucose by the kidney, increasing urinary glucose excretion. Drugs in this class include canagliflozin (Invokana), dapagliflozin (Farxiga), and empagliflozin (Jardiance).

Dopamine Receptor Agonist Bromocriptine (Cycloset) is a dopamine receptor agonist that improves glucose levels. The mechanism of action is unknown. We think patients with type 2 diabetes have low levels of dopamine activity in the morning. These low dopamine levels may interfere with the body’s ability to control blood glucose. Bromocriptine increases

dopamine receptor activity. It can be used alone or as an add-on to another type 2 diabetes treatment.

Combination Oral Therapy Many combination drugs are currently available (Table 48.7). These drugs combine 2 different classes of medications to treat diabetes. One advantage of combination therapy is that the patient takes fewer pills, thus improving medication taking.

Glucagon-Like Peptide-1 Receptor Agonists Albiglutide (Tanzeum), dulaglutide (Trulicity), exenatide (Byetta), exenatide extended-release (Bydureon), liraglutide (Victoza), and lixisenatide (Adlyxin) simulate GLP-1 (an incretin hormone), which is decreased in people with type 2 diabetes. These drugs increase insulin synthesis and release from the pancreas, inhibit glucagon secretion, slow gastric emptying, and reduce food intake by increasing satiety. These drugs may be used as monotherapy or adjunct therapy for patients with type 2 diabetes who have not achieved optimal glucose levels on OAs. These drugs are given using a subcutaneous injection in a prefilled pen. Byetta is given twice daily. Liraglutide is given once daily. Albiglutide, dulaglutide, and Bydureon are given once every 7 days. The delayed gastric emptying that occurs with these drugs may affect the absorption of oral medications. Advise patients to take fastacting oral medications at least 1 hour before injecting a GLP-1 agonist drug.

Drug Alert Exenatide (Byetta) • Acute pancreatitis and kidney problems have been associated with its use.

Drug Alert Liraglutide (Victoza) and Dulaglutide (Trulicity) • Do not use in patients with a personal or family history of medullary thyroid cancer. • Acute pancreatitis has been associated with its use.

Amylin Analogs Pramlintide (Symlin) is the only available amylin analog. Amylin, a hormone secreted by the β cells of the pancreas in response to food intake, slows gastric emptying, reduces glucagon secretion, and increases satiety. Pramlintide is used in addition to mealtime insulin in patients with type 1 or type 2 diabetes who have elevated blood glucose levels on insulin therapy. It is only used concurrently with insulin and is not a replacement for insulin. Pramlintide is given before meals subcutaneously into the thigh or abdomen. It cannot be injected into the arm because absorption from this site is too variable. The drug cannot be mixed in the same syringe with insulin. The concurrent use of pramlintide and insulin increases the risk for severe hypoglycemia during the 3 hours after injection, especially in patients with type 1 diabetes. Teach patients to eat a meal with at least 250 calories and keep a form of fast-acting glucose on hand in case hypoglycemia develops. When pramlintide is used, the bolus dose of insulin should be reduced.

Drug Alert Pramlintide (Symlin) • Can cause severe hypoglycemia when used with insulin.

Other Drugs Affecting Blood Glucose Levels Both the patient and the HCP must be aware of drug interactions that can potentiate hypoglycemia and hyperglycemia effects. For example, β-adrenergic blockers can mask symptoms of hypoglycemia and prolong the hypoglycemic effects of insulin. Thiazide and loop diuretics can worsen hyperglycemia by inducing potassium loss, although low-dose thiazide therapy is usually considered safe.

Nutrition Therapy Individualized nutrition therapy, consisting of counseling, education, and ongoing monitoring, is a cornerstone of care for people with diabetes and prediabetes.12 Changing eating habits can be challenging for many people. Achieving nutrition goals requires a coordinated team effort that considers the person’s behavioral, cognitive, socioeconomic, cultural, and religious backgrounds and preferences. Because of these complexities, it is recommended that a dietitian with expertise in diabetes management work with the person who has diabetes. The dietitian starts with a nutrition assessment and develops an individualized food plan. Other team members may include nurses, certified diabetes educators (CDEs), clinical nurse specialists, social workers, and other HCPs. Guidelines from the ADA state that, within the context of an overall healthy eating plan, a person with diabetes can eat the same foods as a person who does not have diabetes. This means that the same principles of healthy nutrition that apply to the general population also apply to the person with diabetes. Table 48.8 describes nutrition guidelines for patients with diabetes. According to the ADA, the overall goal of nutrition therapy is to help people with diabetes make healthy food choices that will lead to achieving and/or maintaining safe and healthy blood glucose levels. Additional specific goals include: • Maintain blood glucose levels as close to normal as safely possible to prevent or reduce the risk for complications of

diabetes. • Achieve lipid profiles and BP levels that reduce the risk for CVD. • Prevent or slow the rate of development of chronic complications of diabetes by modifying nutrient intake and lifestyle. • Address individual nutrition needs while considering personal and cultural preferences and respecting the person’s willingness or ability to change eating and dietary habits. • Maintain the pleasure of eating by encouraging a variety of healthy food choices.

TABLE 48.8 Nutrition TherapyDiabetes

Source: American Diabetes Association: Lifestyle management: Standards of medical care in diabetes, Diabetes Care 41:S38, 2018.

Type 1 Diabetes People with type 1 diabetes base their meal planning on usual food intake and preferences balanced with insulin and exercise patterns. The patient coordinates insulin dosing with eating habits and activity pattern in mind. Day-to-day consistency in timing and amount of food eaten makes it much easier to manage blood glucose levels, especially

for those using conventional, fixed insulin regimens. Patients using rapid-acting insulin can adjust the dose before each meal based on the current blood glucose level and the carbohydrate content of the meal. Intensified insulin therapy, such as multiple daily injections or the use of an insulin pump, allows considerable flexibility in food selection and can be adjusted for changes from usual eating and exercise habits. This does not diminish or replace the need for healthy food choices and a well-balanced diet.

Type 2 Diabetes Nutrition therapy in type 2 diabetes emphasizes achieving glucose, lipid, and BP goals. Modest weight loss has been associated with improved insulin sensitivity. Therefore weight loss is recommended for all persons with diabetes who are overweight or obese.13 There is no one proven strategy or method. A nutritionally adequate meal plan with appropriate serving sizes, a reduction of saturated and trans fats, and low carbohydrates can decrease calorie consumption. Spacing meals is another strategy that spreads nutrient intake throughout the day. A weight loss of 5% to 7% of body weight often improves blood glucose levels, even if desirable body weight is not achieved. Weight loss is best achieved by a moderate decrease in calories and an increase in caloric expenditure. Regularly exercising and adopting new behaviors and attitudes can promote long-term lifestyle changes. Monitoring blood glucose levels, A1C, lipids, and BP gives feedback on how well the goals of nutrition therapy are being met.

Food Composition A healthy balance of nutrients is essential to maintain blood glucose levels and overall health. Energy from food intake can be balanced with the patient’s energy output. Teach patients to plan their individual meal plan with their lifestyle and health goals in mind. The following are general recommendations for nutrient balance.

Carbohydrate

Carbohydrates include sugars, starches, and fiber. They are an important source of energy, fiber, vitamins, and minerals and needed by all people, including those with diabetes. Foods containing carbohydrate from whole grains, fruits, vegetables, and low-fat dairy are part of a healthy meal plan. The ADA recommends individualizing carbohydrate intake as there is no ideal amount for all people with diabetes. All persons benefit from including dietary fiber as part of a healthy meal plan. The current recommendation for the general population is 25 to 30 g/day.13 Nutritive and nonnutritive sweeteners may be included in a healthy meal plan in moderation. Nonnutritive sweeteners include the sugar substitutes saccharine, aspartame, sucralose, stevia, neotame, and acesulfame-K.

Fat Dietary fat provides energy, transports fat-soluble vitamins, and provides essential fatty acids. The ADA recommends individualizing saturated fat intake. Less than 200 mg/day of cholesterol and limited trans fats are recommended as part of a healthy meal plan. Decreasing fat and cholesterol intake helps reduce the risk for CVD. Healthy fats are those that come from plants, such as olives, nuts, and avocados.

Protein The amount of daily protein in the diet for people with diabetes and normal renal function is the same as for the general population. The ADA recommends individualizing protein intake. Teach patients to choose lean protein whenever possible.

Alcohol Alcohol inhibits gluconeogenesis (breakdown of glycogen to glucose) by the liver. This can cause severe hypoglycemia in patients on insulin or OAs that increase insulin secretion. Create a trusting environment in which patients feel comfortable being honest about their alcohol

use because its use can make blood glucose harder to manage. Moderate alcohol consumption can be safely incorporated into the meal plan if the person is monitoring blood glucose levels and not at risk for other alcohol-related problems. Moderate consumption is defined as 1 drink per day for women and 2 drinks per day for men. A patient can reduce the risk for alcohol-induced hypoglycemia by eating carbohydrates when drinking alcohol. On the other hand, mixed drinks often contain sweetened mixers and can increase blood glucose levels. To decrease the carbohydrate content, recommend using sugar-free mixes and drinking dry, light wines.

Patient Teaching Related to Nutrition Therapy Most often, the dietitian initially teaches the principles of nutrition management. Whenever possible, work with dietitians as part of an interprofessional diabetes care team. Some patients who have limited insurance coverage or live in remote areas do not have access to a dietitian. In these cases, you may need to assume responsibility for teaching basic nutrition principles to patients with diabetes. Carbohydrate counting is a meal planning technique used to keep track of the amount of carbohydrate eaten with each meal and per day. Teach patients to keep carbohydrate intake within a healthy range. The amount of total carbohydrate per day depends on blood glucose levels, age, weight, activity level, patient preference, and prescribed medications. A serving size of carbohydrate is 15 g. A typical adult usually starts with 45 to 60 g of carbohydrate per meal. For some patients, insulin doses are tailored to the amount of carbohydrate foods that a patient will consume at the meal, with a set number of units of insulin given per gram of carbohydrate (e.g., 1 U/15 g carbohydrate, 2 U/25 g carbohydrate). Teach the patient about the foods that contain carbohydrate, how to read food labels, and appropriate serving sizes. Diabetes exchange lists are another method for meal planning. Instead of counting carbohydrate, the person is given a meal plan with specific numbers of helpings from a list of exchanges for each meal and snack. The exchanges are starches, fruits, milk, meats, vegetables,

fats, and free foods. The patient chooses foods from the various exchanges based on the prescribed meal plan. This method may be easier for some patients than carbohydrate counting. It also encourages a well-balanced meal plan. Another advantage is that this approach helps the patient limit portion sizes and overall food intake, an important part of weight management. MyPlate was developed by the U.S. Department of Agriculture (USDA) to represent national nutrition guidelines for people with or without diabetes. This simple method helps the patient see the amount of vegetables, starch, and meat that fills a 9-in plate. The recommendation is that each meal has half of the plate filled with nonstarchy vegetables, one fourth filled with a starch, and one fourth filled with a protein (www.diabetes.org/food-and-fitness/food/planningmeals/create-your-plate). An 8-oz glass of nonfat milk and a small piece of fresh fruit complete the meal.12 Whenever possible, include family members and caregivers in nutrition education and counseling, especially the person who cooks for the household. However, the responsibility for maintaining a healthy eating plan still belongs to the person with diabetes. Reliance on another person to make health decisions interferes with the patient’s ability to develop self-care skills, which are essential in managing diabetes. Foster independence, even in patients with visual or cognitive impairment. It is important to discuss traditional foods with the patient. Individualize food choices considering the patient’s preferences and culturally appropriate foods.

Exercise Regular, consistent exercise is an essential part of diabetes and prediabetes management.14 The ADA recommends that people with diabetes engage in at least 150 min/wk (30 minutes, 5 days/week) of a moderate-intensity aerobic physical activity (Table 48.9). The ADA encourages people with type 2 diabetes to perform resistance training 3 times a week unless contraindicated.15

TABLE 48.9 Activities That Affect Caloric

Expenditure

Exercise decreases insulin resistance and can have a direct effect on lowering blood glucose levels. It contributes to weight loss, which further decreases insulin resistance. The therapeutic benefits of regular physical activity may result in a decreased need for diabetes medications to reach target blood glucose goals in people with type 2 diabetes. Regular exercise may also help reduce triglyceride and lowdensity lipoprotein (LDL) cholesterol levels, increase HDL, reduce BP, and improve circulation. Encourage patients to be active every day and to seek medical clearance before starting a new or more intensive exercise program. Patients start slowly with gradual progression toward the desired goal. Patients who use insulin, sulfonylureas, or meglitinides are at increased risk for hypoglycemia when they increase physical activity, especially if they exercise at the time of peak drug action or eat too little to maintain adequate blood glucose levels. This can also occur if a normally sedentary patient with diabetes has an unusually active day. The glucose-lowering effects of exercise can last up to 48 hours after the activity, so it is possible for hypoglycemia to occur long after the activity. Patients who use drugs that can cause hypoglycemia should exercise about 1 hour after a meal or have a 10- to 15-g carbohydrate snack and check their blood glucose before exercising. It is preferable

not to increase caloric intake for exercise. If needed, they can eat small carbohydrate snacks every 30 minutes during exercise to prevent hypoglycemia. Patients using drugs that place them at risk for hypoglycemia should always carry a fast-acting source of carbohydrate, such as glucose tablets or hard candies, when exercising. If they have frequent lows from exercise, the medication dose may need to be lowered. Table 48.10 describes exercise guidelines for patients with diabetes.

TABLE 48.10 Patient & Caregiver

TeachingExercise for Patients With Diabetes Include the following information in the exercise teaching plan for the patient and caregiver: 1. Exercise does not have to be vigorous to be effective. The blood glucose-reducing effects of exercise can be reached with activity such as brisk walking. 2. Choose exercises that are enjoyable to foster regularity. 3. Use properly fitting footwear to avoid rubbing or injury. 4. The exercise session includes a warm-up period and a cooldown period. Start the exercise program gradually and increase slowly. 5. Exercise is best done after meals, when the blood glucose level is rising. 6. Exercise plans are patient specific and monitored by the HCP. 7. Monitor blood glucose levels before, during, and after exercise to determine the effect exercise has on blood glucose levels at specific times of the day. 8. Before exercise, if blood glucose ≤100 mg/dL, eat a 15-g carbohydrate snack. After 15 to 30 min, recheck blood glucose levels. Delay exercise if 9 lb. Chronic pancreatitis, Cushing syndrome, acromegaly, family history of type 1 or type 2 diabetes Medications: Use of insulin or OAs, corticosteroids, diuretics, phenytoin (Dilantin) Surgery or other treatments: Any recent surgery

Functional Health Patterns Health perception–health management: Positive family history, malaise Nutrition-metabolic: Obesity, weight loss (type 1), weight gain (type 2). Thirst, hunger, nausea and vomiting. Poor healing (especially involving the feet), eating habits Elimination: Constipation or diarrhea, frequent urination, frequent bladder infections, nocturia, urinary incontinence Activity-exercise: Muscle weakness, fatigue Cognitive-perceptual: Abdominal pain, headache, blurred vision,

numbness or tingling of extremities, pruritus Sexuality-reproductive: ED, frequent vaginal infections, vaginal dryness or pain, ↓ libido Adaptation: Depression, irritability, apathy Value-belief: Health beliefs, commitment to lifestyle changes involving food, medication, and activity patterns

Objective Data Eyes Soft, sunken eyeballs.∗ History of vitreal hemorrhages, cataracts

Integumentary Dry, warm, inelastic skin. Pigmented lesions (on legs), ulcers (especially on feet), loss of hair on toes, acanthosis nigricans

Respiratory Rapid, deep respirations (Kussmaul respirations)∗

Cardiovascular Hypotension.∗ Weak, rapid pulse∗

Gastrointestinal Dry mouth, vomiting.∗ Fruity breath∗

Neurologic

Altered reflexes, restlessness, confusion, stupor, coma∗

Musculoskeletal Muscle wasting∗

Possible Findings Serum electrolyte abnormalities. Fasting blood glucose level ≥126 mg/dL. OGTT >200 mg/dL, random glucose ≥200 mg/dL. Leukocytosis. ↑ BUN, creatinine, triglycerides, cholesterol, LDL, VLDL. ↓ HDL. A1C >6.0% (A1C >7.0% in those with diagnosed diabetes), glycosuria, ketonuria, albuminuria. Acidosis



Indicates manifestations of diabetes-related ketoacidosis (DKA).

Nursing Diagnoses Nursing diagnoses related to diabetes may include: • Lack of knowledge • Hyperglycemia • Hypoglycemia • Risk for injury • Impaired peripheral neurovascular function Additional information on nursing diagnoses and interventions for the patient with diabetes is presented in eNursing Care Plan 48.1 available on the website.

Planning

The overall goals are for the patient with diabetes to (1) engage in selfcare behaviors to actively manage diabetes, (2) have few or no hyperglycemia or hypoglycemia emergencies, (3) maintain blood glucose levels at normal or near-normal levels, (4) reduce the risk for chronic complications from diabetes, and (5) adjust lifestyle to accommodate the diabetes plan with minimum stress. The goal is for the patient with diabetes to safely and effectively fit diabetes into life, rather than living life around diabetes.

Nursing Implementation Health Promotion Your role in health promotion is to identify, monitor, and teach the patient at risk for diabetes. Obesity is the main risk factor for type 2 diabetes. The ADA recommends routine screening for type 2 diabetes for all adults who are overweight or obese (BMI 25 kg/m2 or greater) or have 1 or more risk factors. For people who do not have risk factors for diabetes, begin screening at age 45. Table 48.13 provides criteria to screen for prediabetes and diabetes. If results are normal, repeat screening at 3-year intervals.3 Many other factors put a person at an increased risk for diabetes. These include age, ethnicity (being Native American, Hispanic, black, Asian, Pacific Islander), having a baby that weighed more than 9 lb at birth, history of gestational diabetes, and a family history of diabetes. A diabetes risk test is available at www.diabetes.org/risk-test.jsp. The diabetes risk test determines if the person is at risk for prediabetes or diabetes based on the number of risk factors present.

TABLE 48.13 Screening for Diabetes in

Asymptomatic, Undiagnosed Persons

Who to Screen

1. Consider screening all adults who are overweight (BMI >25 kg/m2) and have additional risk factors: • First-degree relative with diabetes • Physically inactive • Members of a high-risk ethnic population (e.g., black, Hispanic, Native American, Asian American,∗ Pacific Islander) • Women who delivered a baby weighing >9 lb or were diagnosed with gestational diabetes • Hypertensive (≥140/90 mm Hg) or on therapy for hypertension • HDL cholesterol level ≤35 mg/dL (0.90 mmol/L) and/or a triglyceride level ≥250 mg/dL (2.82 mmol/L) • Women with polycystic ovary syndrome • A1C ≥5.7%, IGT, or IFG on previous screening • Other conditions associated with insulin resistance (e.g., acanthosis nigricans) 2. In the absence of the above criteria, screening for diabetes should begin at age 45 yr. 3. If results are normal, repeat screening at least every 3 years, with more frequent screening depending on initial results and risk status.

What Measurements Are Used To screen for diabetes or to assess risk of future diabetes, A1C, FPG, or 2-hour OGTT is appropriate.



Consider screening Asian Americans with a BMI of 23 kg/m2 or higher. Source: American Diabetes Association: Standards of medical care in diabetes, Diabetes Care 41:S15, 2018.

Primary prevention is a cost-effective approach. Current recommendations for primary prevention include lifestyle modifications for at-risk people. A modest weight loss of 5% to 7% of body weight and 150 minutes of physical activity a week lowered the risk for developing type 2 diabetes by 34% to 58%.17

Promoting Population Health Preventing Diabetes • Increase level of exercise by aiming for 150 minutes of moderate activity each week. • Maintain a healthy weight through a nutritionally balanced diet. • If overweight, lose weight and take part in a regular exercise program. • Follow a diet low in fat, total calories, and processed foods and high in whole grains, fruits, and vegetables. • If overweight and over age 45, get screened for diabetes yearly. • Avoid cigarette smoking or tobacco products. • Limit consumption of alcohol to moderate levels. • Follow the prescribed treatment plan for hypertension.

Acute Care Acute situations involving the patient with diabetes include hypoglycemia, DKA, and hyperosmolar hyperglycemic syndrome (HHS). Nursing management for these situations is discussed in more detail later in this chapter. Other areas of acute care relate to management during acute illness and surgery.

Acute Illness and Surgery Both emotional and physical stress can increase the blood glucose level and result in hyperglycemia. Because stress is unavoidable,

certain situations may require more intense treatment, such as extra insulin and more frequent blood glucose monitoring, to maintain glycemic goals and avoid hyperglycemia. Acute illness, injury, and surgery may evoke a counterregulatory hormone response, resulting in hyperglycemia. Even common illnesses, such as a viral upper respiratory tract infection or the flu, can cause this response. Encourage patients with diabetes to check blood glucose at least every 4 hours during times of illness. Teach acutely ill patients with type 1 diabetes and a blood glucose greater than 240 mg/dL (13.3 mmol/L) to check urine for ketones every 3 to 4 hours. Teach patients to contact the HCP when glucose levels are over 300 mg/dL twice in a row or urine ketone levels are moderate to high. A patient with type 1 diabetes may need an increase in insulin to prevent DKA. Elevated blood glucose levels can lead to poor healing and infection. Insulin therapy may be needed for a patient with type 2 diabetes to prevent or treat hyperglycemia symptoms and avoid an acute hyperglycemia emergency. In critically ill patients, insulin therapy may be started if the blood glucose is persistently greater than 180 mg/dL. These patients have a higher targeted blood glucose goal, which is usually 140 to 180 mg/dL. Food intake is important during times of stress and illness, when the body needs extra energy. If patients can eat normally, they can continue with their regular meal plan while increasing the intake of noncaloric fluids, such as water, sugar-free gelatin, and other decaffeinated beverages, and continue taking OAs, noninsulin injectable agents, and insulin as prescribed. When illness causes patients to eat less than normal, they can continue to take OAs, noninsulin injectable agents, and/or insulin as prescribed while supplementing food intake with carbohydrate-containing fluids. Examples include low-sodium soups, juices, and regular, sugarsweetened decaffeinated soft drinks. It is important to tell the patient to contact an HCP if they are unable to keep down food or fluid. During the intraoperative period, adjustments in the diabetes plan can be made to ensure safe and healthy blood glucose levels. The patient is given IV fluids and insulin (if needed) just before, during,

and after surgery when there is no oral intake. Explain to the patient with type 2 diabetes who has been on OAs that this is a temporary measure, not a sign of worsening diabetes. When caring for an unconscious surgical patient receiving insulin, be alert for signs of hypoglycemia, such as sweating, tachycardia, and tremors. Frequent monitoring of blood glucose can prevent episodes of severe hypoglycemia.

Ambulatory Care Successful diabetes management involves ongoing interaction among the patient, caregiver, and interprofessional team. It is important that a CDE be involved in the care of the patient and family. Because diabetes is a complex chronic condition, a great deal of patient contact takes place in outpatient and home settings. The major goal of patient care in these settings is to enable the patient (with the help of a caregiver as needed) to reach an optimal level of independence in selfcare activities. Unfortunately, many patients face challenges in reaching these goals. Diabetes increases the risk for other chronic conditions that can affect self-care activities. These include visual impairment, lower extremity problems that affect mobility, and other functional limitations related to a stroke. An important nursing function is to assess the ability of patients and caregivers in performing activities such as SMBG and insulin injection. Assistive devices for self-administration of insulin include syringe magnifiers, vial stabilizers, and dosing aids for the visually impaired. In some cases, referrals are made to help the patient achieve the self-care goal. These may include an occupational therapist, a social worker, a home care nurse, a home health aide, or a dietitian. A diagnosis of diabetes affects the patient in many profound ways. Self-management of the disease is demanding. Patients with diabetes continually face lifestyle choices that affect the foods they eat, their activities, and demands on their time and energy. The requirements of scheduled meals, SMBG, medication, and insulin management may interfere with the patient’s other responsibilities. Any change in the daily routine can be hard. In addition, they face the challenge of

preventing or dealing with the devastating complications of diabetes. Careful assessment of what it means to the patient to have diabetes is a good starting point for teaching. The goals of teaching are mutually determined by the patient and you, based on individual needs and therapeutic requirements. Identify the patient’s support system, and include them in planning, teaching, and counseling. When family members and other persons close to the patient are included, they can support the patient’s self-care behaviors. They can also provide care if self-care is not possible. Encourage the family and caregivers to provide emotional support and encouragement as the patient deals with the reality of living with a chronic disease.

Insulin Therapy Nursing responsibilities for the patient receiving insulin include proper administration, assessment of the patient’s response to insulin therapy, and teaching the patient about administration, storage, and side effects of insulin (Table 48.5). Table 48.6 lists guidelines for assessing a patient using GLAs, including insulin and OAs.

Evidence-Based Practice Interactive Self-Management and Diabetes A.Y. is a 62-yr-old woman with a history of poorly controlled type 2 diabetes. She knows the importance of keeping blood glucose levels close to normal to prevent long-term complications. A.Y. tells you she wants to be more involved in her care. You see she is motivated and wants to learn how to better manage her diabetes.

Making Clinical Decisions Best Available Evidence. The delivery of education and skills related to diabetes self-management includes a variety of formats. These include the use of electronic messages transmitted by phone or the Web and behavioral change

techniques, such as goal-setting, problem-solving, and action planning. Evidence supports multiple benefits from using interactive self-management interventions. These include improved glycemic control as measured by A1C levels, increased knowledge and self-efficacy, and reduced diabetesrelated distress. Clinician Expertise. You know interactive self-management strategies are effective in helping patients improve glycemic control. You are aware that several options, such as text messaging and Web-based programs, can be useful for delivering information to and from patients with diabetes who manage their own care. Patient Preferences and Values. A.Y. shows a strong interest in taking more control of her diabetes and wishes to receive information on physical activity, blood glucose monitoring, and diet.

Implications for Nursing Practice 1. What options for interactive self-management of her diabetes will you offer A.Y.? 2. As you empower A.Y. to initially manage her care, why is it important for you to assess A.Y.’s knowledge and skills? 3. What parameters will you use to assess if she is able to manage her own care?

Reference for Evidence Cheng L, Sit J.W.H, Choi K.-C, et al. Effectiveness of interactive selfmanagement interventions in individuals with poorly controlled type 2 diabetes: a meta-analysis of randomized controlled trials. Worldviews Evid Based Nurs. 2017;14:65. Assessment of the patient who is a new user of insulin includes

evaluating their ability to safely manage this therapy. This includes the ability to understand the interaction of insulin, food, and activity and to recognize and treat the symptoms of hypoglycemia appropriately. If the patient does not have the cognitive skills to do these things, identify and teach another responsible person. The patient or caregiver must have the cognitive and manual skills needed to prepare and inject insulin. Otherwise, additional resources will be needed to assist the patient. For patients with cognitive, physical, and other barriers, consider referral to a CDE. A CDE has the specialized knowledge and skills to promote self-care behaviors for these patients. Many patients are fearful when they first begin using insulin. Some find it hard to self-inject because they are afraid of needles or the pain associated with an injection. Others may think that they do not need insulin or that they will be hypoglycemic after an injection. Explore the patient’s underlying fears before beginning the teaching. Assessing the patient’s beliefs and concerns about starting insulin will guide the teaching, counseling, and plan of care. Having open discussion with patients, providing educational materials and programs, and working with a CDE are all beneficial for patients starting insulin. Follow-up assessment of the patient who has been using insulin therapy includes inspecting injection sites for signs of lipodystrophy and other reactions, reviewing insulin preparation and injection technique, taking a history of the occurrence of hypoglycemia, and assessing how the patient managed hypoglycemia. A review of the patient’s recorded blood glucose readings is vital in assessing how the patient is doing and making any needed adjustments.

Oral and Noninsulin Injectable Agents Your responsibilities for the patient taking OAs and noninsulin injectable agents are similar to those for the patient taking insulin. Proper administration, assessment of the patient’s use of and response to these drugs, and teaching the patient and family are all essential nursing actions. Your assessment is valuable in determining the most appropriate

drug for a patient. Factors such as the patient’s mental status, eating habits, home environment, learning ability, resources, attitude toward diabetes, and medication history all play a significant role in determining the most appropriate drug. For example, frail older adults who live alone are at high risk for severe hypoglycemia because low blood glucose is often undetected or untreated. This is especially true if the patient has cognitive impairment. In these cases, an OA that does not cause hypoglycemia, or a shorter-acting OA, would be most appropriate. Patient teaching is essential. Some patients may assume that their diabetes is not a serious condition if they are only taking a pill to treat it. Teach the patient that OAs will help manage blood glucose and help prevent serious long- and short-term complications of diabetes. Discuss how OAs and noninsulin injectable agents are used in addition to food choices and activity as therapy for diabetes and the importance of following their meal and activity plans. Teach patients not to take extra pills if they have overeaten. If the patient uses sulfonylureas and metformin, teach the patient about the prevention, recognition, and management of hypoglycemia.

Personal Hygiene The potential for infection requires diligent skin and dental hygiene practices. Because of the susceptibility to periodontal disease, encourage daily brushing and flossing and regular dental visits. When having dental work done, have the patient tell the dentist they have diabetes. Routine care includes regular bathing, with an emphasis on foot care. Advise patients to inspect their feet daily, avoid going barefoot, and wear shoes that are supportive and comfortable. If cuts, scrapes, or burns occur, treat them promptly and monitor them carefully. Wash the area and apply a nonabrasive or nonirritating antiseptic ointment. Cover the area with a dry, sterile pad. Teach patients to notify the HCP at once if the injury does not begin to heal within 24 hours or if signs of infection develop.

Medical Identification and Travel Teach the patient to always carry medical identification indicating that they have diabetes. Police, paramedics, and many private citizens are aware of the need to look for this identification when working with sick or unconscious persons. An identification card (Fig. 48.11) can supply valuable information, such as the name of the HCP; the type of diabetes; and the type and dosage of insulin, noninsulin injectable agents, or OAs. Travel for a patient with diabetes requires planning. Being sedentary for long periods may raise the person’s glucose level. Encourage the patient to get up and walk at least every 2 hours to lower the risk for deep vein thrombosis and prevent elevation of glucose levels. Teach the patient to have a full set of diabetes care supplies in the carry-on luggage when traveling by plane, train, or bus. This includes blood glucose monitoring equipment, insulin, noninsulin injectable agents, OAs, and syringes or insulin pens and pen needles.

FIG. 48.11 Medical alerts. A patient with diabetes should carry a card and wear a bracelet or necklace that indicates diabetes. If the patient with diabetes is unconscious, these measures will ensure prompt and appropriate attention.

Nursing Management Caring for the Patient With Diabetes You will need to collaborate with many health care team members to deliver, delegate, and coordinate care based on the patient’s status. • Assess for risk factors for prediabetes and type 1 and type 2 diabetes. • Teach the patient and caregiver about diabetes management, including SMBG, insulin, noninsulin injectables, OAs, nutrition, physical activity, and managing hypoglycemia. • Develop a plan to avoid hypoglycemia or hyperglycemia in a patient with DM who is acutely ill or having surgery. • Assess for acute complications and implement appropriate actions for hypoglycemia, DKA, and HHS. • In patients having acute complications, perform or directly supervise actions, including IV fluid and insulin administration. • Assess for chronic complications, including CVD, retinopathy, nephropathy, neuropathy, and foot complications. • Teach the patient and caregiver about prevention and management of chronic complications related to diabetes. • Oversee LPN/VNs, and in some states and settings UAP, administer insulin, noninsulin injectable agents, and OAs to stable patients.

Collaborate With Other Team Members Dietitian • Obtain a diet history from the patient. • Work with patient and caregiver to create an individualized meal plan. • Provide instructions for meal plan as needed.

Physical Therapist • Assess patient’s current level of fitness. • Develop an exercise plan with the patient.

Occupational Therapist • Teach with patient with vision impairment how to use devices to draw up and measure insulin. • Provide teaching on how to use a talking blood glucose monitor or use any blood glucose monitor one handed. • Develop protective techniques for activities that involve exposure to heat, cold, and sharp objects.

Social Worker • Aid the patient in finding resources to meet medical and financial needs. • Help with coping with diabetes, including managing problems within the family or workplace. Best practices for traveling with diabetes supplies and equipment change frequently. Encourage patients to check TSA guidelines before traveling at www.diabetes.org/living-with-diabetes/know-yourrights/discrimination/public-accommodations/air-travel-and-diabetes/. Notify screeners if an insulin pump is used so that they can inspect it while it is on the body, rather than removing it. For patients who use insulin or OAs that can cause hypoglycemia, keep snack items and a quick-acting carbohydrate source for treating hypoglycemia in the carry-on luggage. Keep extra insulin available in case a bottle breaks or is lost. For longer trips, carry a full day’s supply of food in case of canceled flights, delayed meals, or closed

restaurants. If the patient is planning a trip out of the country, it is wise to have a letter from the HCP explaining that the patient has diabetes and requires all the materials, especially syringes, for ongoing health care. When travel involves time changes, such as traveling coast to coast or across the International Date Line, the patient can contact the HCP to plan an appropriate insulin schedule. During travel, most patients find it helpful to keep watches set to the time of the city of origin until they reach their destination. The key to travel when taking insulin is to know the type of insulin being taken, its onset of action, the anticipated peak time, and mealtimes.

Patient and Caregiver Teaching The goals of diabetes self-management education are to match the level of self-management to the patient’s individual ability so that they can become the most active participant possible. Patients who actively manage their diabetes care have better outcomes than those who do not. For this reason, an educational approach that facilitates informed decision making by the patient is advocated. We call this the empowerment approach to education. The empowerment approach includes eliminating messages that are judgmental and negative and replacing them with empowering, person-centered, and strengths-based language. An example includes referring to a patient as a person with diabetes versus calling them a diabetic. This places the emphasis on the person versus the disease. Other examples of words that may be perceived as negative or judgmental include compliant, uncontrolled, and poorly controlled.”18 Research has shown that people with diabetes feel the impact of negative language and would trust their HCPs more if they used empowering language and made them feel like a partner in their care.

Complementary & Alternative Therapies

Herbs and Supplements That May Affect Blood Glucose

Scientific Evidence Herbs and supplements that may lower blood glucose include aloe, ginger, cinnamon, St. John’s wort, garlic, and ginseng. However, many studies have been small and not well designed. Further research is needed.

Nursing Implications • Teach patients to use herbs and supplements with caution since they may affect blood glucose. • Encourage patients with diabetes to talk with their HCP before using herbs or nutritional supplements. • Teach patients who use herbs to regularly monitor their blood glucose levels. Source: Gupta RC, Chang D, Nammi S, et al: Interactions between antidiabetic drugs and herbs: an overview of mechanisms of action and clinical implications, Diabetol Metab Syndr 9:59, 2017.

Informatics in Practice Patient Teaching Using Smart Phone Apps • Teaching is a critical part of nursing care for patients with diabetes. Put some fun into patient teaching by using smart phone applications. • Apps offer convenient, quick access to up-to-date information. • Introduce patients to a variety of smart phone apps for healthy living and managing diabetes. • Sample apps include Glooko, Health2Sync, Glucosio, MyNetDiaryPRO, Diabetes Tracker, mySugr, and BeatO.

Source: Based on a list provided by Healthline. Retrieved from www.healthline.com/health/diabetes/top-iphone-android-apps. Unfortunately, patients can encounter a variety of physical, psychologic, and emotional barriers when it comes to effectively managing their diabetes. These barriers may include feelings of inadequacy about one’s own abilities, unwillingness to make behavioral changes, ineffective coping strategies, and cognitive deficits. If the patient is not able to manage the disease, a family member may be able to assume part of this role. If the patient or caregiver cannot make decisions related to diabetes management, consider a referral to a CDE, social worker, or other resources within the community. These resources can help the patient and family in outlining a feasible treatment program that meets their capabilities. An assessment of the patient’s knowledge of diabetes and lifestyle preferences is useful in planning a teaching program. Tables 48.14 and 48.15 present guidelines to use for patient and caregiver teaching. Assess the patient’s knowledge base frequently so that gaps in knowledge or incorrect or inaccurate ideas can be corrected. The ADA offers resources for patients in the form of pamphlets, booklets, books, and a monthly magazine called Diabetes Forecast. Affiliates of the ADA are found in all states. Most can be reached by dialing 1-800-DIABETES (800-342-2383). The ADA publishes materials and sponsors conferences for health care professionals concerned with diabetes education, research, and management of patients. The ADA website (www.diabetes.org) has extensive information for the public and health care professionals. The ADA also recognizes education programs that meet the national standards of diabetes education and can provide a list of these programs. Most drug companies manufacturing diabetes-related products have free educational materials for patients and HCPs. It is critical that you stay current in your diabetes knowledge so that you can effectively teach and support patients with diabetes.

Evaluation

The expected outcomes are that the patient with diabetes will • State key elements of the treatment plan • Describe self-care measures that may prevent or slow progression of chronic complications • Maintain a balance of nutrition, activity, and insulin availability that results in stable, safe, and healthy blood glucose levels • Have no injury from decreased sensation in the feet • Implement measures to increase peripheral circulation

Acute Complications of Diabetes The acute complications of diabetes arise from events associated with hyperglycemia and hypoglycemia. Hyperglycemia (high blood glucose) occurs when there is not enough insulin working. Hypoglycemia (low blood glucose) occurs when there is too much insulin working. Many signs and symptoms of hyperglycemia and hypoglycemia overlap. It is important for the HCP to distinguish between them because hypoglycemia worsens rapidly and is a serious threat if action is not immediately taken. Table 48.16 compares the manifestations, causes, management, and prevention of hyperglycemia and hypoglycemia.

TABLE 48.14 Patient & Caregiver

TeachingManagement of Diabetes Include the following instructions when teaching the patient and caregiver how to manage diabetes:

Diabetic Ketoacidosis Etiology and Pathophysiology Diabetes-related ketoacidosis (DKA) is caused by a profound deficiency of insulin. It is characterized by hyperglycemia, ketosis, acidosis, and dehydration. It is most likely to occur in people with type 1 diabetes. DKA may be seen in people with type 2 diabetes in conditions of severe illness or stress in which the pancreas cannot meet the extra demand for insulin. Precipitating factors include illness; infection; inadequate insulin dosage; undiagnosed type 1 diabetes; lack of education, understanding, or resources; and neglect.

TABLE 48.15 Patient & Caregiver

TeachingInstructions for Patients With Diabetes Include the following essential instructions for diabetes management for the patient and caregiver:

Blood Glucose • Monitor your blood glucose at home and record results in a log. • Take your insulin, OA, and/or noninsulin injectable agent as prescribed. • Take insulin consistently, especially when you are sick. • Keep an adequate supply of insulin on hand at all times. • Obtain A1C blood test every 3–6 mo as an indicator of your longterm blood glucose levels. • Be aware of symptoms of hypoglycemia and hyperglycemia. • Always carry a form of rapid-acting glucose so that you can treat hypoglycemia quickly. • Teach family members how and when to use glucagon if patient becomes unresponsive because of hypoglycemia.

Exercise • Learn how exercise and food affect your blood glucose levels. • Remember that exercise will usually lower your blood glucose level. • Begin an exercise program after approval from HCP.

Food • Work with a dietitian to create a patient specific meal plan. • Make healthy food choices and eat regular meals at regular times. • Choose foods low in saturated and trans fat. Know your cholesterol level. • Limit the amount of alcohol you drink. • Be aware that excess amounts of alcohol may lead to unpredictable low blood glucose events. • Avoid fad diets. • Limit regular soda and fruit juice.

Other Guidelines • Obtain an annual eye examination by an ophthalmologist. • Obtain annual urine monitoring for protein. • Examine your feet at home. • Wear comfortable, well-fitting shoes to help prevent foot injury. Break in new shoes gradually. • Always carry identification that says you have diabetes. • Have other medical problems treated, especially high BP and high cholesterol. • Have a yearly influenza vaccination. • Quit or never start smoking cigarettes or using nicotine products.

• Avoid applying heat or cold directly to your feet. • Avoid going barefoot. • Keep skin moisturized by applying cream to surfaces of feet, but not between toes. When the circulating supply of insulin is insufficient, glucose cannot be properly used for energy. The body compensates by breaking down fat stores as a secondary source of fuel (Fig. 48.12). Ketones are acidic by-products of fat metabolism that can cause serious problems when they become excessive in the blood. Ketosis alters the pH balance, causing metabolic acidosis to develop. Ketonuria is a process that occurs when ketone bodies are excreted in the urine. During this process, electrolytes that are cations are also excreted with the anionic ketones to try to maintain electrical neutrality. Insulin deficiency impairs protein synthesis and causes excessive protein degradation. This results in nitrogen losses from the tissues. Insulin deficiency stimulates the production of glucose from amino acids (from proteins) in the liver and leads to further hyperglycemia. Because of the insulin deficiency, the additional glucose cannot be used and the blood glucose level rises further, adding to the osmotic diuresis.

TABLE 48.16 Comparison of Hyperglycemia and

Hypoglycemia

FIG. 48.12 Metabolic events leading to diabetic ketoacidosis. Modified from Kumar V, Abbas AK, Aster JC, et al: Robbins and Cotran pathologic basis of disease, ed 8, Philadelphia, 2010, Saunders.

If not treated, the patient will develop severe depletion of sodium, potassium, chloride, magnesium, and phosphate. Vomiting caused by the acidosis results in more fluid and electrolyte losses. Eventually, hypovolemia, followed by shock, will ensue. Renal failure, which may eventually occur from hypovolemic shock, causes the retention of ketones and glucose, and the acidosis progresses. Untreated, the patient becomes comatose from dehydration, electrolyte imbalance, and acidosis. If the condition is not treated, death is inevitable.

Clinical Manifestations Dehydration occurs in DKA with manifestations of dry mucous membranes, tachycardia, and orthostatic hypotension. Early symptoms may include lethargy and weakness. As the patient becomes severely dehydrated, the skin becomes dry and loose, and the eyes become soft and sunken. Abdominal pain may be present and accompanied by anorexia, nausea, and vomiting. Acetone is noted on the breath as a sweet, fruity odor. Kussmaul respirations (rapid, deep breathing associated with dyspnea) are the body’s attempt to reverse metabolic acidosis through the exhalation of excess CO2. (See Chapter 16 for a discussion of respiratory compensation of metabolic acidosis.) Laboratory findings include a blood glucose level of 250 mg/dL (13.9 mmol/L) or greater, arterial blood pH less than 7.30, and serum bicarbonate level less than 16 mEq/L (16 mmol/L). Moderate to large ketones are present in the urine or serum.

Interprofessional Care Before we had SMBG, patients with DKA needed hospitalization for treatment. Today, hospitalization may not be needed. If fluid and electrolyte imbalances are not severe and blood glucose levels can be safely monitored at home, DKA can be managed on an outpatient

basis (Table 48.17). Other factors to consider when deciding where the patient is managed include the presence of fever, nausea, vomiting, and diarrhea; altered mental status; the cause of the ketoacidosis; and availability of frequent communication with the HCP (every few hours). Patients with DKA who have an illness such as pneumonia or a urinary tract infection (UTI) usually need admitted to the hospital.

TABLE 48.17 Interprofessional CareDiabetes-

Related Ketoacidosis (DKA) and Hyperosmolar Hyperglycemia Syndrome (HHS)

Diagnostic Assessment • History and physical examination • Blood studies, including blood glucose, CBC, pH, ketones, electrolytes, BUN, arterial or venous blood gases • Urinalysis, including specific gravity, glucose, acetone

Management • Administration of IV fluids • IV administration of short-acting insulin • Electrolyte replacement • Assessment of mental status • Recording of intake and output • Central venous pressure monitoring (if indicated) • Assessment of blood glucose levels • Assessment of blood and urine for ketones • ECG monitoring • Assessment of cardiovascular and respiratory status

DKA is a serious condition that proceeds rapidly and must be treated promptly. Refer to Table 48.18 for the emergency management of a patient with DKA. Because fluid imbalance is potentially life threatening, the first goal of therapy is to establish IV access and begin fluid and electrolyte replacement. Typically, the initial fluid therapy involves an IV infusion of 0.45% or 0.9% NaCl at a rate to raise BP and restore urine output to 30 to 60 mL/hr. When blood glucose levels approach 250 mg/dL (13.9 mmol/L), 5% to 10% dextrose is added to prevent hypoglycemia and a sudden drop in glucose that can be associated with cerebral edema. Overzealous rehydration, especially with hypotonic IV solutions, can cause cerebral edema. The aim of fluid and electrolyte therapy is to replace extracellular and intracellular water and to correct deficits of sodium, chloride, bicarbonate, potassium, phosphate, and magnesium. Monitor patients with renal or cardiac compromise for fluid overload. Obtain a serum potassium level before starting insulin. If the patient is hypokalemic, giving insulin will further decrease potassium levels, making early potassium replacement essential. Although initial serum potassium may be normal or high, levels can rapidly decrease once therapy starts as insulin drives potassium into the cells, leading to life-threatening hypokalemia. IV insulin therapy is given to correct hyperglycemia and hyperketonemia. It is important to prevent rapid drops in serum glucose to avoid cerebral edema. A blood glucose reduction of 36 to 54 mg/dL/hr (2 to 3 mmol/L/hr) will avoid complications. Insulin allows water and potassium to enter the cell along with glucose and can lead to a depletion of vascular volume and hypokalemia, so monitor the patient’s fluid balance and potassium levels.

Check Your Practice A 22-yr-old female patient admitted with DKA has a blood glucose level of 554 mg/dL. You are trying to regulate her IV rate. You know that giving IV fluids too rapidly and quickly lowering of serum

glucose can lead to cerebral edema. You also know that incorrect fluid replacement, especially with hypotonic fluids, can cause a sudden fall in serum sodium that can cause cerebral edema. • What are the best clinical indicators of successful treatment of DKA? • What is your role as a nurse in caring for this patient?

TABLE 48.18 Emergency ManagementDiabetes-

Related Ketoacidosis

Hyperosmolar Hyperglycemia Syndrome Hyperosmolar hyperglycemia syndrome (HHS) is a life-threatening syndrome that can occur in the patient with diabetes who is able to make enough insulin to prevent DKA, but not enough to prevent severe hyperglycemia, osmotic diuresis, and extracellular fluid depletion (Fig. 48.13). HHS is less common than DKA (Table 48.17). It often occurs in patients over 60 years of age with type 2 diabetes. Common causes of HHS are UTIs, pneumonia, sepsis, any acute illness, and newly diagnosed type 2 diabetes. HHS is often related to impaired thirst sensation and/or a functional inability to replace fluids. There is usually a history of inadequate fluid intake, increasing mental depression or cognitive impairment, and polyuria.

FIG. 48.13 Pathophysiology of hyperosmolar hyperglycemic syndrome. Modified from Urden LD, Stacy KM, Lough ME: Critical care nursing: Diagnosis and management, ed 6, St Louis, 2010, Mosby.

The main difference between HHS and DKA is that the patient with HHS usually has enough circulating insulin so that ketoacidosis does not occur. Because HHS has fewer symptoms in the earlier stages, blood glucose levels can climb quite high before the problem is recognized. The higher blood glucose levels increase serum osmolality and cause more severe neurologic manifestations, such as somnolence, coma, seizures, hemiparesis, and aphasia. Since these manifestations resemble a stroke, immediate determination of the glucose level is critical for correct diagnosis and treatment. Laboratory values in HHS include a blood glucose level greater than 600 mg/dL (33.33 mmol/L) and a marked increase in serum osmolality. Ketone bodies are absent or minimal in both blood and urine.

Interprofessional Care HHS is a medical emergency. It has a high mortality rate. The management of HHS is similar to DKA. It includes immediate IV administration of insulin and either 0.9% or 0.45% NaCl. HHS usually requires large volumes of fluid replacement. This should be done slowly and carefully. Patients with HHS are often older and may have cardiac or renal compromise, requiring hemodynamic monitoring to avoid fluid overload during fluid replacement. When blood glucose levels fall to about 250 mg/dL (13.9 mmol/L), IV fluids containing dextrose are given to prevent hypoglycemia. Electrolytes are monitored and replaced as needed. Hypokalemia is not as significant in HHS as it is in DKA, although fluid losses may result in milder potassium deficits that require replacement. Assess vital signs, intake and output, laboratory values, and cardiac monitoring to check the efficacy of fluid and electrolyte replacement. This includes monitoring serum osmolality and frequently assessing cardiac, renal, and mental status. Once the patient is stabilized, begin

attempts to detect and correct the underlying cause.

Nursing Management: DiabetesRelated Ketoacidosis and Hyperosmolar Hyperglycemia Syndrome Closely monitor the hospitalized patient with appropriate blood and urine tests. You are responsible for monitoring blood glucose and urine for output and ketones and using laboratory data to determine appropriate patient care. Monitor the administration of (1) IV fluids to correct dehydration, (2) insulin therapy to reduce blood glucose and serum ketone levels, and (3) electrolytes given to correct electrolyte imbalance. Assess renal status and cardiopulmonary status related to hydration and electrolyte levels. Monitor the level of consciousness. Assess for signs of potassium imbalance resulting from low levels of insulin and osmotic diuresis (see Chapter 16). When insulin treatment is started, serum potassium levels may decrease rapidly as potassium moves into the cells once insulin is available. This movement of potassium into and out of extracellular fluid influences cardiac functioning. Cardiac monitoring is useful in detecting characteristic changes of potassium excess or deficit that are observable on ECG tracings (see Fig. 16.14). Assess vital signs often to identify fever, hypovolemic shock, tachycardia, and Kussmaul respirations.

Hypoglycemia Hypoglycemia, or low blood glucose, occurs when there is too much insulin in proportion to available glucose in the blood. This causes the blood glucose level to drop to less than 70 mg/dL (3.9 mmol/L). When glucose drops below 70 mg/dL, counterregulatory hormones are released and the autonomic nervous system is activated. Suppression of insulin secretion and production of glucagon and epinephrine provide a defense against hypoglycemia. Epinephrine release causes manifestations that include shakiness, palpitations, nervousness, diaphoresis, anxiety, hunger, and pallor. Because the brain needs a constant supply of glucose in sufficient quantities to function properly, hypoglycemia can affect mental functioning. These “neuroglycopenia” manifestations are difficulty speaking, visual changes, stupor, confusion, and coma. Manifestations of hypoglycemia can mimic alcohol intoxication. Untreated hypoglycemia can progress to loss of consciousness, seizures, coma, and death. Hypoglycemia unawareness is a condition in which a person does not have the warning signs and symptoms of hypoglycemia until the glucose level reaches a critical point. Then the person may become incoherent and combative or lose consciousness. This is often a result of diabetes-related autonomic neuropathy that interferes with the secretion of counterregulatory hormones that cause these symptoms. Patients at risk for hypoglycemia unawareness include those who have had repeated episodes of hypoglycemia, older adults, and patients who use β-adrenergic blockers. Using intensive treatment to lower blood glucose levels in patients who have or are at risk for hypoglycemia unawareness may not be an appropriate goal. These patients usually keep blood glucose levels somewhat higher than those who can detect and manage the onset of hypoglycemia. Causes of hypoglycemia are often related to a mismatch in the timing of food intake and the peak action of insulin or OAs that increase endogenous insulin secretion. The balance between blood

glucose and insulin can be disrupted by giving too much insulin or medication, ingesting too little food, delaying the time of eating, and performing unusual or unexpected exercise. Hypoglycemia can occur at any time, but most often occurs when the OA or insulin is at its peak of action or when the patient’s daily routine is disrupted without adequate adjustments in diet, drugs, and activity. Although hypoglycemia is most common with insulin therapy, it can occur with noninsulin injectable agents and OAs and may persist for an extended time because of the longer duration of action of these drugs. Symptoms of hypoglycemia may occur when a very high blood glucose level falls too rapidly (e.g., a blood glucose level of 300 mg/dL [16.7 mmol/L] falling quickly to 150 mg/dL [10 mmol/L]). Although the blood glucose level is above normal by definition and measurement, the sudden metabolic shift can cause hypoglycemia symptoms. Aggressively managing blood glucose levels, lowering high blood glucose levels for the first time, or lowering blood glucose with insulin after a long period of hyperglycemia can cause this situation.

Nursing and Interprofessional Management: Hypoglycemia Hypoglycemia can usually be quickly reversed with effective treatment. At the first sign of hypoglycemia, check the blood glucose, if possible. If it is less than 70 mg/dL (3.9 mmol/L), immediately begin treatment for hypoglycemia. If the blood glucose is greater than 70 mg/dL, investigate other possible causes of the signs and symptoms. If the patient has manifestations of hypoglycemia and monitoring equipment is not available or the patient has a history of fluctuating blood glucose levels, assume hypoglycemia, and start treatment. Follow the “Rule of 15” to treat hypoglycemia (Table 48.19). A blood glucose value less than 70 mg/dL is treated by ingesting 15 g of a simple (fast-acting) carbohydrate, such as 4 to 6 oz of fruit juice or a regular soft drink. Commercial products, such as gels or tablets containing specific amounts of glucose, are convenient for carrying in a purse or pocket to be used in such situations. Recheck the blood glucose 15 minutes later. If the value is still less than 70 mg/dL, ingest 15 g more of carbohydrate and recheck the blood glucose in 15 minutes. If no significant improvement occurs after 2 or 3 doses of 15 g of simple carbohydrate, contact the HCP. After an acute episode of hypoglycemia, the patient may need a snack with carbohydrate and protein if the next meal is more than an hour away or if they are being active.

TABLE 48.19 Emergency

ManagementHypoglycemia

Avoid treatment with carbohydrates that contain fat, such as candy bars, cookies, whole milk, and ice cream. The fat in those foods will slow the absorption of the glucose and delay the response to treatment. Do not overtreat with large quantities of quick-acting carbohydrates because a rapid fluctuation to hyperglycemia can occur. In an acute care setting, patients with hypoglycemia may be given 20 to 50 mL of 50% dextrose IV. If the patient is not alert enough to swallow and no IV access is available, another option is to give 1 mg of glucagon by IM or subcutaneous injection. An IM injection in a site such as the deltoid muscle will result in a quicker response. Glucagon stimulates a strong hepatic response to convert glycogen to glucose and makes glucose rapidly available. Nausea is a common reaction after glucagon injection. To prevent aspiration if vomiting occurs, turn the patient on the side until they are alert. Patients with minimal glycogen stores will not respond to glucagon. This includes patients with alcohol-related hepatic disease, starvation, and adrenal insufficiency. Teach family members and others likely to be present if severe hypoglycemia occurs when and how to inject glucagon. Once the acute hypoglycemia is reversed, explore with the patient the reasons why the situation developed. This assessment may indicate the need for further patient teaching to avoid future episodes

of hypoglycemia.

Chronic Complications Associated with Diabetes Angiopathy Chronic complications associated with diabetes are primarily those of end-organ disease from damage to blood vessels (angiopathy) from chronic hyperglycemia (Fig. 48.14). Angiopathy is a leading cause of diabetes-related deaths, with about 68% of deaths caused by CVD and 16% caused by strokes for those ages 65 or older.19 These chronic blood vessel dysfunctions are divided into 2 categories: macrovascular complications and microvascular complications. Several theories exist as to how and why chronic hyperglycemia damages cells and tissues. Possible causes include (1) the accumulation of damaging by-products of glucose metabolism, such as sorbitol, which is associated with damage to nerve cells; (2) the formation of abnormal glucose molecules in the basement membrane of small blood vessels, such as those that circulate to the eyes and kidneys; and (3) a derangement in RBC function that leads to a decrease in oxygenation to the tissues. The Diabetes Control and Complications Trial (DCCT), a landmark study in diabetes management, showed the risk for microvascular complications could be significantly reduced in patients with type 1 diabetes by keeping blood glucose levels as near to normal as possible for as much of the time as possible (tight or intensive therapy).20 Those who maintained tight glucose levels reduced their risk for developing retinopathy and nephropathy, common microvascular complications. Based on these findings, the ADA issued recommendations for diabetes management that included treatment goals to maintain blood glucose levels as near to normal as possible. Specific targets for individual patients must consider the risk for severe or undetected hypoglycemia as a side effect of intensive management.

FIG. 48.14 Long-term complications of diabetes. From Kumar V, Abbas AK, Aster JC, et al: Robbins and Cotran pathologic basis of disease, ed 8, Philadelphia, 2010, Saunders.

The United Kingdom Prospective Diabetes Study (UKPDS) showed that intensive treatment of type 2 diabetes significantly lowered the risk for developing diabetes-related eye, kidney, and neurologic problems. The findings included a 25% reduction of microvascular disease and a 16% reduction in the risk for MI in those who maintained long-term blood glucose levels.21 Because of the devastating effects of long-term complications, patients with diabetes need scheduled and ongoing monitoring for the detection and prevention of chronic complications. The ADA recommendations for ongoing evaluation are shown in Table 48.20. It is essential that patients understand the importance of regular followup visits.

Macrovascular Complications Macrovascular complications are diseases of the large and medium-size

blood vessels that occur with greater frequency and with an earlier onset in people with diabetes. Macrovascular diseases include cerebrovascular, cardiovascular, and peripheral vascular disease. Women with diabetes have a 4 to 6 times increased risk for CVD. Men with diabetes have a 2 to 3 times increased risk for CVD compared with those without diabetes.2

TABLE 48.20 Monitoring for Long-Term

Complications Related to Diabetes



If patients have a history of foot ulcers, loss of sensation in their feet, or other foot abnormalities, the recommendation is to have a foot examination at every visit.

Source: American Diabetes Association: Standards of medical care in diabetes, Diabetes Care 41:S86, 2018. Patients with diabetes can decrease several risk factors associated with macrovascular complications, such as obesity, smoking, hypertension, high fat intake, and sedentary lifestyle. The ADA recognizes that diabetes alone is a CVD risk factor. The ADA recommends yearly screening for CVD risk factors in people with diabetes.22 Insulin resistance is important in the development of CVD and implicated in the pathogenesis of essential hypertension and

dyslipidemia. We do not completely understand the role of insulin resistance in the pathogenesis of CVD. It seems to combine with dyslipidemia in contributing to greater risk for CVD in patients with diabetes. Optimizing BP control in patients with diabetes is significant in preventing CVD and renal disease. Treating hypertension in those with diabetes results in a decrease in macrovascular and microvascular complications. Hypertension in people with diabetes causes an increase in mortality greater than for those with hypertension without diabetes. The ADA recommends BP screening at every visit for people with diabetes. They recommend lifestyle counseling for BP greater than 130/80 mm Hg and treatment to achieve a target BP of less than 140/90 mm Hg for most patients with diabetes.22 Hypertension is discussed in Chapter 32, and coronary artery disease is discussed in Chapter 33.) Patients with diabetes have an increase in lipid abnormalities that contribute to their increased risk for CVD. The ADA recommends screening all adults for dyslipidemia at the time diabetes is diagnosed and starting statin therapy as needed. Dosing is based on the presence of age and other CVD risk factors. The ADA advocates treating hyperlipidemia with lifestyle interventions, including nutrition therapy, exercise, weight loss, and smoking cessation. Smoking, which is detrimental to health in general, is especially dangerous for people with diabetes. It significantly increases their risk for blood vessel and CVD, stroke, and lower extremity amputation.

Microvascular Complications Microvascular complications result from thickening of the vessel membranes in the capillaries and arterioles (small vessels) in response to conditions of chronic hyperglycemia. Although microangiopathy can be found throughout the body, the areas most noticeably affected are the eyes (retinopathy), kidneys (nephropathy), and nerves (neuropathy). Microvascular changes are present in some patients with type 2 diabetes at the time of diagnosis.

Retinopathy Etiology and Pathophysiology Diabetes-related retinopathy refers to the process of microvascular damage to the retina because of chronic hyperglycemia, nephropathy, and hypertension in patients with diabetes. Diabetes-related retinopathy is the leading cause of new cases of adult blindness.2 We classify retinopathy as nonproliferative or proliferative. In nonproliferative retinopathy, the most common form, partial occlusion of the small blood vessels in the retina causes microaneurysms to develop in the capillary walls. The walls of these microaneurysms are so weak that capillary fluid leaks out, causing retinal edema and eventually hard exudates or intraretinal hemorrhages. This may cause mild to severe vision loss, depending on which parts of the retina are affected. If the center of the retina (macula) is affected, vision loss can be severe. Proliferative retinopathy, the most severe form, involves the retina and vitreous. When retinal capillaries become occluded, the body compensates by forming new blood vessels to supply the retina with blood, a pathologic process known as neovascularization. These new vessels are extremely fragile and hemorrhage easily, producing vitreous contraction. Eventually light is prevented from reaching the retina as the vessels break and bleed into the vitreous cavity. The patient sees black or red spots or lines. If these new blood vessels pull the retina while the vitreous contracts, causing a tear, partial or complete retinal detachment will occur. If the macula is involved, vision is lost. Without treatment, more than half of patients with proliferative diabetic retinopathy will be blind. Persons with diabetes are prone to other visual problems. Glaucoma occurs because of the occlusion of the outflow channels from neovascularization. This type of glaucoma is hard to treat and often results in blindness. Cataracts develop at an earlier age and progress more rapidly in people with diabetes.

Interprofessional Care The earliest and most treatable stages of diabetes-related retinopathy often cause no changes in the vision. Therefore teach patients with type 2 diabetes to have a dilated eye examination by an ophthalmologist or a specially trained optometrist at the time of diagnosis and annually thereafter for early detection and treatment. Those with type 1 diabetes need to have a dilated eye examination within 5 years after the onset of diabetes and then annually. The best approach to managing diabetes-related eye disease is to prevent it by maintaining healthy blood glucose levels and managing hypertension. Laser photocoagulation therapy can reduce the risk for vision loss in patients with proliferative retinopathy or macular edema and, sometimes, nonproliferative retinopathy. Laser photocoagulation destroys the ischemic areas of the retina that make growth factors that encourage neovascularization. A patient who develops vitreous hemorrhage and retinal detachment of the macula may need to undergo vitrectomy. Vitrectomy is the aspiration of blood, membrane, and fibers from the inside of the eye through a small incision just behind the cornea. (Photocoagulation and vitrectomy are discussed in Chapter 20.) A fluocinolone acetonide intravitreal implant (Iluvien) is used to treat retinopathy. It is an injectable microinsert that provides sustained treatment through continuous delivery of corticosteroid fluocinolone acetonide for 36 months. Iluvien is injected in the back of the patient’s eye with an applicator that uses a 25-gauge needle, which allows for a self-sealing wound. Vascular endothelial growth factor (VEGF) plays a key role in the development of diabetes-related retinopathy. We are currently studying drugs injected into the eye that block the action of VEGF and reduce inflammation for their effectiveness in treating retinopathy.23

Nephropathy Diabetes-related nephropathy is a microvascular complication associated with damage to the small blood vessels that supply the glomeruli of the kidney. It is the leading cause of ESRD in the United States and seen in 20% to 40% of people with diabetes. Risk factors include hypertension, genetic predisposition, smoking, and chronic hyperglycemia. Keeping blood glucose levels in a healthy range is critical in the prevention and delay of diabetes-related nephropathy.21 Patients are screened for nephropathy annually with a random spot urine collection to assess for albuminuria and measure the albuminto-creatinine ratio. Serum creatinine is measured to give an estimate of the glomerular filtration rate and the degree of kidney function. Patients with diabetes who have albuminuria receive either ACE inhibitor drugs (e.g., lisinopril [Prinivil, Zestril]) or angiotensin II receptor blockers (e.g., losartan [Cozaar]). Both classifications of these drugs are used to treat hypertension and delay the progression of nephropathy in patients with diabetes. Hypertension significantly accelerates the progression of nephropathy. Therefore aggressive BP management is indicated for all patients with diabetes. See Chapter 32 for a discussion of hypertension and Chapter 46 for a discussion of renal failure.

Neuropathy Diabetes-related neuropathy is nerve damage that occurs because of the metabolic imbalances associated with diabetes. About 60% to 70% of patients with diabetes have some degree of neuropathy.2 The most common type affecting persons with diabetes is sensory neuropathy. This can lead to the loss of protective sensation in the lower extremities. Coupled with other factors, it significantly increases the risk for complications that result in a lower limb amputation. More than 60% of nontraumatic amputations in the United States occur in people with diabetes.2 Screening for neuropathy begins at the time of diagnosis in patients with type 2 diabetes and 5 years after diagnosis in patients with type 1 diabetes.3

Etiology and Pathophysiology We do not completely understand the pathophysiologic processes of diabetes-related neuropathy. Theories include metabolic, vascular, and autoimmune factors. The prevailing theory is that persistent hyperglycemia leads to an accumulation of sorbitol and fructose in the nerves that causes damage. How they cause damage is unknown. The result is reduced nerve conduction and demyelination. Ischemic damage by chronic hyperglycemia in blood vessels that supply the peripheral nerves is implicated in the development of diabetes-related neuropathy. Neuropathy can precede, accompany, or follow the diagnosis of diabetes.

Classification The 2 major categories of diabetes-related neuropathy are sensory neuropathy, which affects the peripheral nervous system, and autonomic neuropathy. Each type has several forms.

Sensory Neuropathy

The most common form of sensory neuropathy is distal symmetric polyneuropathy, which affects the hands and/or feet bilaterally. This is sometimes called stocking-glove neuropathy. Characteristics include loss of sensation, abnormal sensations, pain, and paresthesias. The pain, which patients describe as burning, cramping, crushing, or tearing, is usually worse at night and may occur only at that time. The paresthesias may be associated with tingling, burning, and itching sensations. The patient may report a feeling of walking on pillows or numb feet. The skin can become so sensitive (hyperesthesia) that the patient cannot tolerate even light pressure from bed sheets. Complete or partial loss of sensitivity to touch and temperature is common. Foot injury and ulcerations can occur without the patient ever having pain (Fig. 48.15). Neuropathy can cause atrophy of the small muscles of the hands and feet, causing deformity and limiting fine movement. Managing blood glucose is the only treatment for diabetes-related neuropathy. It is effective in many, but not all, cases. Drug therapy may be used to treat neuropathic symptoms, especially pain. At the start of therapy, symptoms usually increase, followed by relief of pain in 2 to 3 weeks. Drugs commonly used include topical creams (e.g., capsaicin [Zostrix]), tricyclic antidepressants (e.g., amitriptyline), selective serotonin and norepinephrine reuptake inhibitors (e.g., duloxetine [Cymbalta]), and antiseizure drugs (e.g., gabapentin [Neurontin], pregabalin [Lyrica]). Capsaicin is a moderately effective topical cream made from chili peppers. It depletes the accumulation of painmediating chemicals in the peripheral sensory neurons. The cream is applied 3 or 4 times a day. Tricyclic antidepressants are moderately effective in treating diabetes-related neuropathy. They work by inhibiting the reuptake of norepinephrine and serotonin, which are neurotransmitters thought to play a role in the transmission of pain through the spinal cord. We think duloxetine relieves pain by increasing the levels of serotonin and norepinephrine, which improves the body’s ability to regulate pain. Antiseizure drugs decrease the release of neurotransmitters that transmit pain.24

Autonomic Neuropathy Autonomic neuropathy can affect nearly all body systems and lead to hypoglycemia unawareness, bowel incontinence and diarrhea, and urinary retention. Gastroparesis (delayed gastric emptying) is a complication of autonomic neuropathy that can cause anorexia, nausea, vomiting, gastroesophageal reflux, and persistent feelings of fullness. Gastroparesis can trigger hypoglycemia by delaying food absorption. Cardiovascular abnormalities associated with autonomic neuropathy are postural hypotension, resting tachycardia, and painless MI. Assess patients with diabetes for postural hypotension to determine if they are at risk for falls. Teach the patient with postural hypotension to change from a lying or sitting position slowly. Diabetes can affect sexual function in men and women. Erectile dysfunction (ED) in men with diabetes is well recognized and common, often being the first manifestation of autonomic neuropathy. ED is associated with other factors, including vascular disease, elevated blood glucose levels, endocrine disorders, psychogenic factors, and medications. Decreased libido is a problem for some women with diabetes. Candida and nonspecific vaginitis are common. ED or sexual dysfunction requires sensitive therapeutic counseling for both the patient and the patient’s partner. See Chapter 55 for more about ED.

FIG. 48.15 Neuropathy: Neurotrophic ulceration.

A neurogenic bladder may develop as the sensation in the inner bladder wall decreases, causing urinary retention. A patient with retention has infrequent voiding, difficulty voiding, and a weak stream of urine. Emptying the bladder every 3 hours in a sitting position helps prevent stasis and infection. Tightening the abdominal muscles during voiding and using the Credé maneuver (mild massage downward over the lower abdomen and bladder) may help with complete bladder emptying. Cholinergic agonist drugs, such as bethanechol (Urecholine), may be used. The patient may need to learn self-catheterization (see Chapter 45).

Complications of Feet and Lower Extremities People with diabetes are at high risk for foot ulcerations and lower extremity amputations. The development of diabetes-related foot complications can be the result of a combination of microvascular and macrovascular diseases that place the patient at risk for injury and serious infection (Fig. 48.16). Sensory neuropathy and peripheral artery disease (PAD) are risk factors for foot complications. In addition, clotting abnormalities, impaired immune function, and autonomic neuropathy have a role. Smoking has a negative effect on the health of lower extremity blood vessels and increases the risk for amputation. Sensory neuropathy is a major risk factor for lower extremity amputation in the person with diabetes. Loss of protective sensation (LOPS) often prevents the patient from being aware that a foot injury has occurred. Improper footwear and injury from stepping on foreign objects while barefoot are common causes of undetected foot injury in the person with LOPS. Because the primary risk factor for lower extremity amputation is LOPS, annual screening using a monofilament is important.25 This is done by applying a thin, flexible filament to several spots on the plantar surface of the foot and asking the patient to report if it is felt. Insensitivity to a monofilament greatly increases the risk for foot ulcers that can lead to amputation.

FIG. 48.16 The necrotic toe developed as a complication of diabetes. A, Before amputation. B, After amputation. From Chew SL, Leslie D: Clinical endocrinology and diabetes: An illustrated colour text, Edinburgh, 2006, Churchill Livingstone.

PAD increases the risk for amputation by causing a reduction in blood flow to the lower extremities. With decreased blood flow, oxygen, white blood cells (WBCs), and vital nutrients are not available to the tissues. Wounds take longer to heal, and the risk for infection increases. Signs of PAD include intermittent claudication, pain at rest, cold feet, loss of hair, delayed capillary filling, and dependent rubor (redness of the skin that occurs when the extremity is in a dependent position). PAD is diagnosed by history, ankle-brachial index (ABI), and angiography. Management includes reduction of risk factors, especially smoking, cholesterol intake, and hypertension. Bypass or graft surgery is indicated in some patients. PAD is discussed in Chapter 37. If the patient has LOPS or PAD, aggressive measures must be taken

to teach the patient how to prevent foot ulcers. These measures include choosing proper footwear, including protective shoes. Teach the patient to carefully avoid injury to the foot, practice diligent skin and nail care, inspect the foot thoroughly each day, and treat small problems promptly. Guidelines for patient teaching are listed in Table 48.21. Proper care of a foot ulcer is critical for wound healing. Several forms of treatment can be used. Casting can redistribute the weight on the plantar surface of the foot. Wound care for the ulcer can include debridement, dressings, advanced wound healing products (becaplermin [Regranex]), vacuum-assisted closure, ultrasound, hyperbaric O2, and skin grafting.

Table 48.21 Patient & Caregiver Teaching∗ Foot

Care Include the following instructions when teaching the patient and caregiver about foot care: 1. Wash feet daily with a mild soap and warm water. First test water temperature with elbow. 2. Pat feet dry gently, especially between toes. 3. Examine feet daily for cuts, blisters, swelling, and red, tender areas. Do not depend on feeling sores. If eyesight is poor, have others inspect feet. 4. Use lanolin on feet to prevent skin from drying and cracking. Do not apply between toes. 5. Use mild foot powder on sweaty feet. 6. Do not use commercial remedies to remove calluses or corns. 7. Cleanse cuts with warm water and mild soap, covering with clean dressing. Do not use iodine, rubbing alcohol, or strong adhesives. 8. Report skin infections or nonhealing sores to HCP at once. 9. Cut toenails evenly with rounded contour of toes. Do not cut

down corners. The best time to trim nails is after a shower or bath. 10. Separate overlapping toes with cotton or lamb’s wool. 11. Avoid open-toe, open-heel, and high-heel shoes. Leather shoes are preferred to plastic ones. Wear slippers with soles. Do not go barefoot. Inspect feet, socks and shoes for foreign objects before putting on. 12. Wear clean, absorbent (cotton or wool) socks or stockings that have not been mended. Colored socks must be colorfast. 13. Do not wear clothing that leaves impressions, hindering circulation. 14. Do not use hot water bottles or heating pads to warm feet. Wear socks for warmth. 15. Guard against frostbite. 16. Exercise feet daily either by walking or by flexing and extending feet in suspended position. Avoid prolonged sitting, standing, and crossing of legs.



This teaching guide is also appropriate for patients with peripheral vascular problems.

Neuropathic arthropathy, or Charcot’s foot, results in ankle and foot changes that lead to joint dysfunction and footdrop. These changes occur gradually and promote an abnormal distribution of weight over the foot. This increases the chances of developing a foot ulcer as new pressure points appear. Foot deformity should be recognized early, and proper footwear fitted before ulceration occurs.

Skin Complications Up to two thirds of persons with diabetes develop skin problems. Diabetes-related dermopathy, the most common skin lesion, is characterized by reddish brown, round or oval patches. They initially are scaly, then they flatten out and become indented. The lesions appear most often on the shins but can occur on the front of the thighs, forearm, side of the foot, scalp, and trunk. Acanthosis nigricans is a manifestation of insulin resistance. It can appear as a velvety light brown to black skin thickening, mainly on flexures, axillae, and the neck. Necrobiosis lipoidica diabeticorum usually appears as red-yellow lesions, with atrophic skin that becomes shiny and transparent, revealing tiny blood vessels under the surface (Fig. 48.17). This condition is uncommon. It occurs more often in young women. It may appear before other signs and symptoms of diabetes. Because the thin skin is prone to injury, special care must be taken to protect affected areas from injury and ulceration.

Infection A person with diabetes is more susceptible to infections because of a defect in the mobilization of WBCs and an impaired phagocytosis by neutrophils and monocytes. Recurring or persistent infections, such as Candida albicans, boils, and furuncles in the undiagnosed patient often lead the HCP to suspect diabetes. Loss of sensation (neuropathy) may delay the detection of an infection. Persistent glycosuria may predispose patients to bladder infections, especially patients with a neurogenic bladder. Decreased circulation resulting from angiopathy can prevent or delay the immune response. Antibiotic therapy has prevented infection from being a major cause of death in patients with diabetes. The treatment of infections must be prompt and vigorous. Teach patients to prevent infection by practicing good hand hygiene, avoiding exposure to persons who have a communicable illness, and getting an annual influenza vaccine and pneumococcal vaccine. (Guidelines for pneumococcal vaccine are shown in Table 27.5.)

FIG. 48.17 Necrobiosis lipoidica diabeticorum. From Chew SL, Leslie D: Clinical endocrinology and diabetes: An illustrated colour text, Edinburgh, 2006, Churchill Livingstone.

Psychologic Considerations Patients with diabetes have high rates of depression, anxiety, and eating disorders. Depression contributes to diminished diabetes selfcare, feelings of helplessness related to chronic illness, and poor outcomes.9 Diabetes distress is different from depression and encompasses the stress, fear, and burden of living with and managing a demanding chronic disease. Assess patients for manifestations of depression and/or diabetes distress. Disordered eating behaviors (DEBs) can occur in people with both type 1 and type 2 diabetes. DEBs include anorexia, bulimia, binge eating, excessive restriction of calories, and intense exercise. The greatest incidence of eating disorders is seen in females. Adolescent girls with diabetes are more than twice as likely to develop DEB than those who do not have diabetes.26 Patients may intentionally decrease their dose of insulin or omit the dose. This is called “diabulimia.” It leads to weight loss, hyperglycemia, and glycosuria because the food ingested cannot be used for energy without adequate insulin. Insulin omission and DEBs can have serious consequences, including retinopathy, neuropathy, lipid abnormalities, DKA, and death.26 Open communication is critical to identify these behaviors early. Refer patients with eating disorders to a mental health professional with expertise in eating disorders and an understanding of diabetes management.

Gerontologic Considerations: Diabetes Diabetes is present in more than 25% of persons over 65 years of age. This age-group is the fastest-growing segment of the population developing diabetes.2 Older people with diabetes have higher rates of premature death, functional disability, and coexisting illnesses, such as hypertension and stroke, than those without diabetes. The prevalence of diabetes increases with age. A major reason for this is that the process of aging is associated with a reduction in β-cell

function, decreased insulin sensitivity, and altered carbohydrate metabolism. Aging is also associated with conditions that are more likely to be treated with drugs that impair insulin action (e.g., corticosteroids, antihypertensives, phenothiazines). Undiagnosed and untreated diabetes is more common in older adults, partly because many of the normal physiologic changes of aging resemble those of diabetes, such as low energy levels, falls, dizziness, confusion, and chronic UTIs. Several factors affect setting glycemic goals for an older adult. One is that hypoglycemia unawareness is more common in older adults, making them more likely to have adverse consequences from blood glucose–lowering therapy. They may have delayed psychomotor function that could interfere with the ability to treat hypoglycemia. Other factors include the patient’s desire for treatment and coexisting medical problems, such as cognitive impairment. Compounding the challenge, diabetes increases the rate of decline of cognitive function. Although it is generally agreed that treatment is indicated to prevent complications, intensive diabetes management may be hard and dangerous to achieve, especially in older adults.

Ethical/Legal Dilemmas Durable Power of Attorney for Health Care

Situation G.V., a 64-yr-old woman, is admitted to the intensive care unit with HF. She has many complications from a long-term history of type 1 diabetes and hypertension, including a right leg above-the-knee amputation and blindness related to retinopathy. She severed ties with her family 30 years ago. She has a life partner of 35 years whom she chose as her proxy in her signed Durable Power of Attorney. She has said many times that she would rather die than have renal dialysis. She has been sedated and intubated for 3 days. The HCP plans to extubate her and resuscitate her so that she can start dialysis.

Her brother shows up at the hospital and supports the HCP’s decision. Her partner disagrees with the decision. The HCP refuses to recognize her partner as proxy because she is not a blood relative.

Ethical/Legal Points for Consideration The Patient Self-Determination Act (1990) requires all health care facilities receiving Medicare and Medicaid funding to make available advance directives allowing persons to state their preferences or refusals of health care in the event that they are incapable of consenting for themselves. Durable Power of Attorney for health care is one type of advance directive in which people, when they are competent, identify someone else to make decisions for them, should they lose their decision-making ability in the future (see Table 9.6). The Living Will, another type of advance directive, permits people to state their own preferences and refusals. Many HCPs mistakenly think that proxies must be family members or blood relatives. Lesbian, gay, bisexual, and transgender (LGBT) persons often have difficulty having their partnership recognized as valid, especially if the patient’s family disputes their rights. Some families are deeply divided on decisions for their loved ones. Sometimes difficulties occur when money and property are also disputed. The passage of time may be an issue where the original documents were executed and then changes occurred (e.g., divorce, death or disability of the proxy, inability to contact the proxy, inability to find a valid original of the advance directive). Within your scope of nursing practice, you need to know the decision-making laws and regulations in your own state and make advance directive documents available to patients. In addition, you need to (1) teach patients and their families about advance directives, (2) make sure that HCPs are aware of and follow advance directives, (3) assist the patient and family in communicating with the HCPs when a “No Code” order is requested, and (4) assist a conflicted family in obtaining appropriate counseling whenever needed. Counsel LGBT patients on the importance of having a health care proxy and a will to legally protect their end-of-life choices.

Discussion Questions 1. How would you handle a situation in which the family and surrogate decision maker disagree? 2. How can you assess the patient and family’s understanding of durable power of attorney and assist them in understanding their role in decision making? 3. What should you do when an HCP orders dialysis to be started when you know that this goes against the patient’s advance directive? Meal planning and exercise are recommended therapy for older adults with diabetes. Consider functional limitations that may interfere with physical activity and the ability to prepare meals. Because of the physiologic changes that occur with aging, the therapeutic outcome for the older adult who receives OAs may be altered. Assess renal function and creatinine clearance in those over 80 years of age taking metformin. Monitor those taking sulfonylurea drugs (e.g., glipizide) for hypoglycemia and renal and liver dysfunction. Insulin therapy may be started if OAs are not effective. However, older adults are more likely to have limitations in the manual dexterity and visual acuity necessary for accurate insulin administration. Insulin pens may be a safer alternative. Patient education issues include those related to altered vision, mobility, cognitive status, and functional ability. Plan patient teaching based on individual needs, using a slower pace with simple printed or audio materials in patients with cognitive and functional limitations. Include the family or caregivers in the teaching. Consider the patient’s financial and social situation and the effect of multiple drugs, eating habits, and quality-of-life issues.

Case Study

Diabetes-Related Ketoacidosis

© katrinaelena/iStock/Thinkstock.

Patient Profile N.B., a 48-yr-old farmer, was admitted to the emergency department after he was found unconscious by his wife in their barn. They live 40 miles from the nearest health care facility. He has a medical history of type 1 diabetes, hypertension, and diabetic neuropathy.

Subjective Data (Provided by Wife)

• Diagnosed with type 1 diabetes 15 years ago • Takes 40 U/day of insulin via insulin pump: 5 U of lispro insulin bolus with breakfast, 5 U bolus with lunch, and 10 U bolus with dinner plus 20 U of basal insulin • Has history of gastroenteritis for 1 wk with vomiting and anorexia • Stopped taking meal time boluses 2 days ago when he was unable to eat • Has not changed his infusion set in 5 days

Objective Data Physical Examination • Respirations deep with rate 36 breaths/min • Fruity acetone smell on breath • Skin flushed and dry • Heart rate 118 beats/min; BP 98/60 mm Hg

Diagnostic Studies • Blood glucose level 730 mg/dL (40.5 mmol/L) • Blood pH 7.26

Discussion Questions 1. Briefly explain the pathophysiology behind N.B.’s diabetesrelated ketoacidosis (DKA). 2. What factors precipitated his developing DKA? 3. What clinical manifestations of DKA does this patient exhibit? 4. What distinguishes this case history from one of hyperosmolar hyperglycemia syndrome (HHS) or hypoglycemia?

5. Priority Decision: Based on the assessment data presented, what are the priority nursing diagnoses? Are there any collaborative problems? 6. Priority Decision: What is the priority nursing intervention for N.B.? 7. Priority Decision: What is the priority teaching for this patient and his family? 8. Evidence-Based Practice: N.B.’s wife asks you if she should have given her husband insulin when he got sick. How would you respond? 9. Collaboration: How can the interprofessional team be most effective in caring for N.B? 10. Quality Improvement: What outcomes would indicate that the interprofessional team was effective in caring for N.B.? 11. Develop a conceptual care map for N.B. Answers and a corresponding concept map are available at http://evolve.elsevier.com/Lewis/medsurg.

Bridge to Nclex Examination The number of the question corresponds to the same-numbered outcome at the beginning of the chapter.

1. Polydipsia and polyuria related to diabetes are primarily due to a. the release of ketones from cells during fat metabolism. b. fluid shifts resulting from the osmotic effect of hyperglycemia. c. damage to the kidneys from exposure to high levels of glucose. d. changes in RBCs resulting from attachment of excess glucose to hemoglobin. 2. Which statement would be correct for a patient with type 2 diabetes who was admitted to the hospital with pneumonia? a. The patient must receive insulin therapy to prevent ketoacidosis. b. The patient has islet cell antibodies that have destroyed the pancreas’s ability to make insulin. c. The patient has minimal or absent endogenous insulin secretion and requires daily insulin injections. d. The patient may have enough endogenous insulin to prevent ketosis but is at risk for hyperosmolar hyperglycemia syndrome. 3. Analyze the following diagnostic findings for your patient with type 2 diabetes. Which result will need further

assessment? a. A1C 9% b. BP 126/80 mmHg c. FBG 130 mg/dL (7.2 mmol/L) d. LDL cholesterol 100 mg/dL (2.6 mmol/L) 4. Which statement by the patient with type 2 diabetes is accurate? a. “I will limit my alcohol intake to 1 drink each day.” b. “I am not allowed to eat any sweets because of my diabetes.” c. “I cannot exercise because I take a blood glucoselowering medication.” d. “The amount of fat in my diet is not important. Only carbohydrates raise my blood sugar.” 5. You are caring for a patient with newly diagnosed type 1 diabetes. What information is essential to include in your patient teaching before discharge from the hospital? (select all that apply) a. Insulin administration b. Elimination of sugar from diet c. Need to reduce physical activity d. Use of a portable blood glucose monitor e. Hypoglycemia prevention, symptoms, and treatment 6. What is the priority action for the nurse to take if the patient with type 2 diabetes reports blurred vision and irritability? a. Call the provider.

b. Give insulin as ordered. c. Assess for other neurologic symptoms. d. Check the patient’s blood glucose level. 7. A patient with diabetes has a serum glucose level of 824 mg/dL (45.7 mmol/L) and is unresponsive. After assessing the patient, the nurse suspects diabetes-related ketoacidosis rather than hyperosmolar hyperglycemia syndrome based on the finding of a. polyuria. b. severe dehydration. c. rapid, deep respirations. d. decreased serum potassium. 8. Which are appropriate therapies for patients with diabetes? (select all that apply) a. Use of statins to reduce CVD risk b. Use of diuretics to treat nephropathy c. Use of ACE inhibitors to treat nephropathy d. Use of serotonin agonists to decrease appetite e. Use of laser photocoagulation to treat retinopathy 1. b, 2. d, 3. a, 4. a, 5. a, d, e, 6. d, 7. c, 8. a, c, e For rationales to these answers and even more NCLEX review questions, visit http://evolve.elsevier.com/Lewis/medsurg.

Evolve Website/Resources List http://evolve.elsevier.com/Lewis/medsurg

Review Questions (Online Only) Key Points

Answer Keys for Questions • Rationales for Bridge to NCLEX Examination Questions • Answer Guidelines for Case Study on p. 1141 Student Case Studies • Patient With Type 1 Diabetes Mellitus and DiabetesRelated Ketoacidosis • Patient With Type 2 Diabetes Mellitus and Hyperosmolar Hyperglycemia Syndrome Nursing Care Plans • eNursing Care Plan 48.1: Patient With Diabetes Mellitus Conceptual Care Map Creator • Conceptual Care Map for Case Study on p. 1141 Audio Glossary Supporting Media • Animation • Insulin Function Content Updates

References 1. American Diabetes Association: Statistics about diabetes. Retrieved from www.diabetes.org/diabetesbasics/statistics. 2. Centers for Disease Control and Prevention: 2017 National diabetes statistics report. Retrieved from www.cdc.gov/diabetes/pdfs/data/statistics/nationaldiabetes-statistics-report.pdf.

American Diabetes Association: Diagnosis and classification of diabetes mellitus, Diab Care 41:S13, 2018.

4. Bouzid T, Hamel FG, Lim JY: Role of adipokines in controlling insulin signaling pathways in type-2 diabetes and obesity, Int J Diabetes Res 5:75, 2016. 5. Ben-Shmuel S, Rostoker R, Scheinman EJ, et al: Metabolic syndrome, type 2 diabetes, and cancer: Epidemiology and potential mechanisms, Handb Exp Pharmacol 233:355, 2016. 6. Kawada T: Risk factors for developing prediabetes, J Diabetes Res Clin Metab 135:232, 2018. 7. Centers for Disease Control and Prevention: Gestational diabetes. Retrieved from www.cdc.gov/diabetes/basics/gestational.html. Chamberlain JJ, Herman WH, Leal S, et al. Pharmacologic therapy for type 2 diabetes: Synopsis of the 2017 ADA standards of medical care in diabetes, Ann Intern Med 166:572, 2017.

9. American Association of Diabetes Educators: The art and science of self-management education desk reference, ed 4, Chicago, 2017, The Association. 10. BD Diabetes: Syringe and needle sizes. Retrieved from www.bd.com/en-us/offerings/capabilities/diabetescare/insulin-syringes. 11. Joslin Diabetes Center: The advantages and disadvantages of an insulin pump. Retrieved from www.joslin.org/info/the_advantages_and_disadvantages_of_an_insul American Diabetes Association: Lifestyle management: Standards of medical care in diabetes, Diabetes Care 41:S38, 2018.

13. American Diabetes Association: Food and fitness: Create your plate. Retrieved from www.diabetes.org/food-and-fitness/food. US Department of Health and Human Services: Physical Activity

Guidelines Advisory Committee report. Retrieved from www.cdc.gov/nccdphp/sgr/contents.htm. American Diabetes Association: Fitness. Retrieved from www.diabetes.org/food-and-fitness/fitness.

16. Wood A, O’Neal D, Furler J, et al: Continuous glucose monitoring: A review of the evidence, opportunities for future use and ongoing challenges, Internal Med J 48:499, 2018. 17. American Diabetes Association: Prevention or delay of type 2 diabetes, Diab Care 40:S44, 2017. Dickinson JK, Guzman SJ, Maryniuk MD, et al: The use of language in diabetes care and education, Diab Care 40:1790, 2017.

19. Boucher J, Hurrell D: Cardiovascular disease and diabetes, Diab Spect 21:154, 2008. (Classic) Diabetes Control and Complications Trial Research Group: The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus, N Engl J Med 329:977, 1993. (Classic) UK Prospective Diabetes Study (UKPDS) Group: Intensive bloodglucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes, Lancet 352:837, 1998. (Classic)

22. American Diabetes Association: Cardiovascular disease and risk management: Standards of medical care in diabetes, Diab Care 41:S86, 2018. 23. Bahrami B, Hong T, Gilles MC, et al: Anti-VEGF therapy for diabetic eye diseases, Asia Pac J Ophthalmol 6:535, 2017. Waldfogel JM, Nesbit SA, Dy SM, et al: Pharmacotherapy for diabetic peripheral neuropathy: A systematic review, Neurology 88:1958, 2017. American Diabetes Association: Microvascular complications and foot

care: Standards of medical care in diabetes, Diab Care 41:S105, 2018.

26. Doyle EA, Quinn SM, Ambrosino JM, et al: Disordered eating behaviors in emerging adults with type 1 diabetes: A common problem for both men and women, J Pediatr Health Care 31:327, 2017. ∗Evidence-based information for clinical practice.

49

Endocrine Problems Ann Crawford

CONCEPTUAL FOCUS Coping Fluids and Electrolytes Hormonal Regulation Nutrition Perfusion Reproduction Thermoregulation Tissue Integrity LEARNING OUTCOMES 1. Explain the pathophysiology, clinical manifestations, and interprofessional and nursing management of the patient with an imbalance of hormones made by the anterior pituitary gland. 2. Describe the pathophysiology, clinical manifestations, and interprofessional and nursing management of the patient with an imbalance of hormones made by the posterior pituitary gland. 3. Explain the pathophysiology, clinical manifestations, and interprofessional and nursing management of the patient with thyroid dysfunction. 4. Describe the pathophysiology, clinical manifestations, and interprofessional and nursing management of the patient with

parathyroid dysfunction. 5. Identify the pathophysiology, clinical manifestations, and interprofessional and nursing management of the patient with an imbalance of hormones made by the adrenal cortex. 6. Describe the pathophysiology, clinical manifestations, and interprofessional and nursing management of the patient with an excess of hormones made by the adrenal medulla. 7. List the side effects of corticosteroid therapy.

KEY TERMS acromegaly, p. 1144 Addison’s disease, p. 1165 Cushing syndrome, p. 1161 diabetes insipidus (DI), p. 1148 exophthalmos, p. 1150 goiter, p. 1149 Graves’ disease, p. 1150 hyperaldosteronism, p. 1167 hyperparathyroidism, p. 1159 hyperthyroidism, p. 1150 hypoparathyroidism, p. 1161 hypopituitarism, p. 1145 hypothyroidism, p. 1156 myxedema, p. 1156 pheochromocytoma, p. 1168 syndrome of inappropriate antidiuretic hormone (SIADH), p. 1147 thyroid cancer, p. 1158

thyroiditis, p. 1149 thyrotoxicosis, p. 1150 The best way to cheer yourself up is to try to cheer somebody else up. Mark Twain http://evolve.elsevier.com/Lewis/medsurg The endocrine system is made up of several organs and glands that are involved in the synthesis and secretion of hormones that affect every body system. Because hormones have a wide range of action, problems with their regulation are associated with homeostatic changes that can affect many aspects of a person’s life. The severity varies widely. There may be adverse effects on perfusion, metabolism, and nutrition. Regulating fluid and electrolyte balance, skin integrity, and temperature may be difficult. The patient may have problems with growth and fertility and reproductive processes since these are hormone dependent. There may be a wide range of psychologic responses, including anxiety and depression.

Disorders of Anterior Pituitary Gland The pituitary gland is considered the master gland of the endocrine system. The anterior pituitary gland secretes growth hormone (GH), prolactin, and tropic hormones, adrenocorticotropic hormone (ACTH), thyroid-stimulating hormone (TSH), follicle-stimulating hormone (FSH), and luteinizing hormone (LH). These hormones affect growth, sexual maturation, reproduction, metabolism, stress response, and fluid balance. As a result, pituitary gland disorders manifest in a variety of ways. Tumors of the pituitary gland account for 5% to 20% of primary intracranial tumors.1 The most common, a pituitary adenoma, is a slow-growing, benign tumor. It often occurs in adults between 40 and 60 years of age. Hypersecretory pituitary adenomas secrete an excess of a specific hormone causing manifestations related to the action of

that hormone. The most common are prolactinomas and GH- and ACTH-secreting adenomas.1

Acromegaly Acromegaly is a rare condition characterized by an overproduction of GH. Around 4 of every 1 million adults in the United States are diagnosed annually.2 It affects both genders equally. The mean age at the time of diagnosis is 40 to 45 years old.

Etiology and Pathophysiology Acromegaly most often occurs because of a benign GH-secreting pituitary adenoma. The excess GH results in an overgrowth of soft tissues and bones in the hands, feet, and face. Because the problem develops after epiphyseal closure, the bones of the arms and legs do not grow longer.

Clinical Manifestations The changes resulting from excess GH in adults can occur slowly, over many years, and may go unnoticed by the person, family, and friends. Thickening and enlargement of the bony and soft tissues on the face, feet, and head occur (Fig. 49.1). Patients may have proximal muscle weakness and joint pain that can range from mild to crippling. Carpal tunnel syndrome and peripheral neuropathy may be present. Tongue enlargement results in dental and speech problems. The voice deepens because of hypertrophy of the vocal cords. Sleep apnea may occur because of upper airway narrowing and obstruction from increased amounts of pharyngeal soft tissues. The skin becomes thick, leathery, and oily with acne outbreaks. Vision changes may occur from pressure on the optic nerve from a pituitary adenoma. Headaches are common. Since GH antagonizes the action of insulin, glucose intolerance and manifestations of diabetes may occur, including polydipsia (increased thirst) and polyuria

(increased urination). The life expectancy of those with acromegaly is reduced by 5 to 10 years. They are prone to cardiovascular disease (CVD), diabetes, and colorectal cancer.3 Even if patients are cured or the disease is well controlled, manifestations such as joint pain and deformities often remain.

Diagnostic Studies In addition to the history and physical examination, a diagnosis requires evaluating plasma insulin-like growth factor-1 (IGF-1) levels and GH response to an oral glucose tolerance test (OGTT). IGF-1 mediates the peripheral actions of GH. As GH levels rise, so do IGF-1 levels. Since GH is released in a pulsatile fashion, several samples are needed to obtain an accurate assessment. Serum IGF-1 levels are more constant, giving a more reliable diagnostic measure of acromegaly. During an OGTT, GH concentration normally falls because glucose inhibits GH secretion. In acromegaly, GH levels do not fall and in some cases GH levels rise.

FIG. 49.1 Progressive development of facial changes associated with

acromegaly. Courtesy Linda Haas, Seattle, WA.

MRI or high-resolution CT scan with contrast media can detect pituitary adenomas. A complete eye examination, including visual fields, is done because a tumor may cause pressure on the optic chiasm or optic nerves.

Interprofessional and Nursing Care The patient’s prognosis depends on the age at onset, age when treatment started, and tumor size. The overall goal is to return the patient’s GH levels to normal. Treatment consists of surgery, radiation therapy, drug therapy, or a combination of these therapies. Treatment can stop bone growth and reverse tissue hypertrophy. However, sleep apnea, diabetes, and cardiac problems may persist. Surgery (hypophysectomy) is the treatment of choice. It offers the best chance for a cure and optimal symptom management, especially for smaller pituitary tumors.4 Surgery results in an immediate reduction in GH levels. IGF-1 levels fall within a few weeks. Patients with larger tumors or those with GH levels greater than 45 ng/mL may need adjuvant radiation or drug therapy. Surgery and radiation therapy for pituitary tumors are discussed later in this chapter on p. 1145. Drug therapy is an option for patients whose surgery did not result in a cure and/or in combination with radiation therapy. The main drug used is octreotide (Sandostatin), a somatostatin analog. It reduces GH levels to normal in many patients. Octreotide is given by subcutaneous injection 3 times a week. Long-acting somatostatin analogs, octreotide (Sandostatin LAR), pasireotide (Signifor), and lanreotide SR (Somatuline Depot), are available as IM injections given every 4 weeks. GH levels are measured every 2 weeks to guide drug dosing and then every 6 months until the desired response is achieved. Dopamine agonists (e.g., bromocriptine, cabergoline) may be given alone or with somatostatin analogs if complete remission has not been

achieved after surgery. These drugs reduce the secretion of GH from the tumor. GH antagonists (e.g., pegvisomant [Somavert]) reduce the effect of GH in the body by blocking liver production of IGF-1. Most patients taking this drug achieve normal IGF-1 levels with symptom improvement.3 Serial photographs showing improvement in appearance may be helpful to the patient’s recovery. Psychosocial effects of acromegaly include body image problems, sexual problems, and depression. Fatigue and sleep problems may persist after surgery. Patients will need strategies for dealing with these symptoms. Referral to a support group may be helpful.

Excesses of Other Tropic Hormones Excess secretion of prolactin or the tropic hormones (e.g., ACTH, TSH) by the anterior pituitary gland will cause other endocrine glands to overproduce certain hormones. An excess of these hormones (discussed later in the chapter) can cause significant problems in metabolism and general health. A prolactin-secreting adenoma is known as a prolactinoma. They account for about 40% of pituitary tumors.5 Women with prolactinomas may have galactorrhea, anovulation, infertility, infrequent or absent menses, decreased libido, and hirsutism. In men, impotence, decreased sperm density, and libido may result. Compression of the optic chiasm can cause vision changes and signs of increased intracranial pressure, including headache, nausea, and vomiting. Because prolactinomas do not typically progress in size, drug therapy is usually the first-line treatment. The dopamine agonists cabergoline and bromocriptine are given to block the release of prolactin. Surgery may be an option, depending on the extent and size of the tumor. Radiation therapy can reduce the risk for tumor recurrence for patients with large tumors.

Hypofunction of Pituitary Gland Hypopituitarism is a rare disorder that involves a decrease in 1 or more of the pituitary hormones. A deficiency of only 1 pituitary hormone is called selective hypopituitarism. Total failure of the pituitary gland results in deficiency of all pituitary hormones—a condition referred to as panhypopituitarism. The most common hormone deficiencies associated with hypopituitarism involve GH and gonadotropins (e.g., LH, FSH).

Etiology and Pathophysiology The usual cause of pituitary hypofunction is a pituitary tumor. Autoimmune disorders, infections, pituitary infarction (Sheehan syndrome), or destruction of the pituitary gland (from trauma, radiation, or surgical procedures) can also cause hypopituitarism. Blacks have a higher incidence of pituitary tumors than other ethnic groups.6 Anterior pituitary hormone deficiencies can lead to end-organ failure. TSH and ACTH deficiencies are life threatening. ACTH deficiency can lead to acute adrenal insufficiency and hypovolemic shock from sodium and water depletion. Acute adrenal insufficiency is discussed later in this chapter on pp. 1165–1166.

Clinical Manifestations and Diagnostic Studies The manifestations vary with the type and degree of dysfunction. Early manifestations associated with a space-occupying lesion include headaches, vision changes (decreased visual acuity or decreased peripheral vision), loss of smell, nausea and vomiting, and seizures. Manifestations associated with hyposecretion of the target glands vary widely (Table 49.1). In addition to a history and physical examination, diagnostic studies such as MRI and CT can identify a pituitary tumor. Laboratory tests generally involve the direct measurement of pituitary hormones (e.g., TSH) or an indirect determination of the target organ hormones

(e.g., triiodothyronine [T3], thyroxine [T4]). (See Chapter 47 for more information about diagnostic studies.)

Interprofessional and Nursing Care The treatment for hypopituitarism often consists of surgery or radiation therapy followed by lifelong hormone therapy. Surgery and radiation therapy for pituitary tumors are discussed in the next section. Appropriate hormone therapy is used (e.g., GH, corticosteroids, thyroid hormone). Hormone therapies for thyroid hormone and corticosteroids are discussed later in this chapter on p. 1156 and p. 1167.

TABLE 49.1 Manifestations of Hypopituitarism

Somatropin (Genotropin, Humatrope, Omnitrope), recombinant human GH, is used for long-term hormone therapy in adults with GH deficiency. These patients respond well to GH replacement. They have increased energy, increased lean body mass, a feeling of well-being, and improved body image. Mild to moderate side effects of GH include fluid retention with swelling in the feet and hands, myalgia, joint pain, and headache. GH is given daily as a subcutaneous injection (preferably in the evening). The dosing is variable and adjusted based on symptoms, IGF-1 levels, and the presence of adverse effects.

Although gonadal deficiency is not life threatening, hormone therapy will improve sexual function and general well-being. It is contraindicated in those with certain medical conditions, such as phlebitis, pulmonary embolism, breast cancer in women, and prostate cancer in men. Estrogen and progesterone replacement therapy may be given to hypogonadal women to treat hot flashes, vaginal dryness, and decreased libido. (Hormone therapy for women is discussed in Chapter 53.) Testosterone is used to treat men with gonadotropin deficiency. The benefits achieved with testosterone therapy include a return of male secondary sex characteristics; improved libido; and increased muscle mass, bone mass, and bone density. (Hormone therapy for men is discussed in Chapter 54.)

Pituitary Surgery A hypophysectomy is the surgical removal of the pituitary gland. It is the treatment of choice for tumors in the pituitary area, especially smaller pituitary adenomas. Most surgeries are done by an endoscopic transsphenoidal approach (Fig. 49.2). When the entire pituitary gland is removed, there is permanent loss of all pituitary hormones. The patient will need lifelong replacement therapy of thyroid hormone, sex hormones, and glucocorticoids. Radiation therapy can reduce the size of a tumor before surgery. It is also used when surgery does not produce a cure or when patients are poor candidates for surgery. Its full effects may not be noted for months to years. Radiation therapy may lead to hypopituitarism, which then requires lifelong hormone replacement therapy. Stereotactic radiosurgery (gamma knife surgery, proton beam, linear accelerator) is an option for small, surgically inaccessible pituitary tumors or in place of conventional radiation.

FIG. 49.2 Surgery on the pituitary gland is most often done by a transsphenoidal approach. An incision is made in the inner aspect of the upper lip and gingiva. The sella turcica is entered through the floor of the nose and sphenoid sinuses.

Nursing Management: Pituitary Surgery After surgery, assess the patient for the formation of a hematoma compressing the optic nerve or optic chiasma. Monitor peripheral vision, visual acuity, extraocular movements, and pupillary response. Report changes at once because prompt intervention may prevent visual deterioration from becoming permanent (Table 49.2).

Cerebrospinal fluid (CSF) leaks and epistaxis are other common complications after surgery.7 The HCP may place a petroleum jelly– coated ribbon of gauze or a balloon-tipped catheter (like an indwelling urinary catheter) in the sphenoid sinus. It is usually removed after 24 hours. It can be left in for 2 to 3 days if there is concern for bleeding or CSF leak. It is important that the patient does not blow the nose for at least 48 hours after surgery and avoids vigorous coughing, sneezing, and straining at stool. Monitor the “moustache” dressing regularly for any drainage. Check any clear drainage with a urine dipstick for glucose and protein. If present, notify the HCP of a possible CSF leak. A sample can be sent to the laboratory. A glucose level greater than 30 mg/dL (1.67 mmol/L) indicates CSF leakage from an open connection with the brain. If this happens, the patient is at increased risk for meningitis. A persistent and severe generalized or supraorbital headache may indicate CSF leakage into the sinuses. A CSF leak usually resolves within 72 hours when treated with head elevation and bed rest. If the leak persists, daily spinal taps may be done to reduce pressure to below-normal levels. Other measures include elevating the head of the patient’s bed at all times to a 30-degree angle. This avoids pressure on the sella turcica and decreases headaches. Monitor the pupillary response, speech patterns, and extremity strength to detect neurologic complications. Gentle mouth care every 4 hours is essential to keep the surgical area clean and free of debris. Have the patient avoid tooth brushing for at least 10 days to protect the suture line.

TABLE 49.2 Nursing ManagementCare of the

Patient After Pituitary Surgery • Monitor vital signs. Assess peripheral pulses and watch for orthostatic hypotension.

• Monitor neurologic/cognitive status (e.g., level of consciousness, orientation, speech) hourly for the first 24 hr and then every 4 hr. • Assess extremity strength and reflexes. • Monitor field of vision, visual acuity, extraocular movements, and pupillary response. Notify HCP of any changes. • Assess dressing for type and amount of drainage. Notify HCP for excessive bleeding or CSF drainage. • Maintain strict intake and output and monitor fluid balance. Assess for DI or SIADH. • Keep head of bed elevated at least 30 degrees at all times. • Encourage deep breathing exercises and incentive spirometer use. • Monitor for pain and give analgesic medications as prescribed. • Encourage high-fiber diet to decrease potential for constipation. • Perform oral care every 4 hr. • Teach the patient to: • Avoid vigorous coughing, sneezing, and blowing the nose • Avoid bending over at the waist or straining at stool (Valsalva maneuver) due to potential increased intracranial pressure • Avoid use of toothbrushes until incision heals • Follow replacement hormone therapy plan Fluid and electrolyte problems can occur from the development of diabetes insipidus (DI).8 Transient DI may occur because of the loss of antidiuretic hormone (ADH), which is stored in the posterior lobe of the pituitary gland, or cerebral edema related to manipulation of the pituitary during surgery. DI may be permanent after surgery. To assess for DI, closely monitor urine output and measure specific gravity. Report a urine output of more than 200 mL/hr for more than 3 consecutive hours or a specific gravity level of 90% of cases Nervousness, irritability, weight loss, heat intolerance, warm moist skin Present in >90% of cases

Ophthalmopathy Exophthalmos (Fig. 49.6) present in 20%–40% of cases Cardiac features Tachycardia and palpitations common, but without heart failure

Older Adult Graves’ disease or toxic nodular goiter Anorexia, weight loss, apathy, lassitude, depression, confusion Present in about 50% of cases Exophthalmos less common Angina, dysrhythmia (especially atrial fibrillation with rapid ventricular response), heart failure may occur

In acute thyrotoxicosis, all the symptoms of hyperthyroidism are prominent and severe. Manifestations include severe tachycardia, heart failure, shock, hyperthermia (up to 106°F [41.1°C]), agitation, delirium, seizures, abdominal pain, vomiting, diarrhea, and coma.

Diagnostic Studies The primary laboratory findings used to confirm the diagnosis of hyperthyroidism are low or undetectable TSH levels (17 mo). These problems may be irreversible. • Teach the patient to immediately report decreased visual acuity. • Monitor for signs of deep vein thrombosis, pulmonary embolism, and stroke, including shortness of breath, leg cramps, and weakness. Aromatase inhibitors Aromatase inhibitor drugs interfere with the anastrozole enzyme

aromatase, which is needed for the synthesis of estrogen. These drugs include anastrozole, letrozole (Femara), and exemestane (Aromasin). They are used in the treatment of breast cancer in postmenopausal women. Aromatase inhibitors do not block the production of estrogen by the ovaries. Thus they are of little benefit and may be harmful in premenopausal women. Aromatase inhibitors have different side effects than tamoxifen. They rarely cause blood clots and do not cause endometrial cancer. Because they block the production of estrogen in postmenopausal women, osteoporosis and bone fractures may occur. These drugs have been associated with night sweats, nausea, arthralgias, and myalgias. Estrogen receptor modulator and others Raloxifene (Evista) is a selective ER modulator that has both estrogenagonistic effects on bone and estrogen-antagonistic effects on breast tissue. (Raloxifene is discussed in the section on osteoporosis in Chapter 63.) Less common drugs that may be used to suppress hormone-dependent breast tumors include megestrol acetate, diethylstilbestrol, and fluoxymesterone.

Immunotherapy and Targeted Therapy As more is known about the genetic changes in breast cancer, we have developed drugs that specifically target cells that have altered gene expression. One of these genetic changes is the overexpression of HER-2. Tumors that overexpress the HER-2 protein tend to be more aggressive and are more likely to recur. Trastuzumab (Herceptin) is a monoclonal antibody to HER-2. After the antibody attaches to the antigen, blocks signals that tell the cancer cells to proliferate. It can be used alone or in combination with chemotherapy agents. The most common side effects are flu-like symptoms (fever, chills, myalgia), nausea and vomiting, diarrhea, and infusion reactions. Another possible, but more serious side effect, is heart damage. Trastuzumab-qyyp (Trazimera) and trastuzumab-pkrb (Herzuma) are newly approved biosimiliars of trastuzamab.

Drug Alert Trastuzumab (Herceptin) • Use with caution in women with preexisting heart disease. • Monitor for signs of ventricular dysfunction and heart failure. Other drugs that target HER-2 include pertuzumab (Perjeta) and ado-trastuzumab emtansine (Kadcyla). Kadcyla is trastuzumab connected to a chemotherapy drug called DM1. Lapatinib (Tykerb) works inside the cell by blocking the function of the HER-2 protein. Nerotinib (Nerlynx) is an option for extended adjuvant therapy for some high-risk women. Using 2 of these agents together for neoadjuvant therapy can increase the number of tumors that become undetectable and can improve survival when used for adjuvant therapy. Other drugs that target HER-2 include pertuzumab (Perjeta), trastuzumab-qyyp (Trazimera), trastuzumab-pkrb (Herzuma), and ado-trastuzumab emtansine (Kadcyla). Kadcyla is trastuzumab connected to a chemotherapy drug called DM1. Lapatinib (Tykerb) works inside the cell by blocking the function of the HER-2 protein. Using 2 of these agents together for neoadjuvant therapy can increase the number of tumors that become undetectable. Drugs in other classes that are used to treat breast cancer include everolimus (Afinitor) and the CDK 4 and 6 inhibitors palbociclib (Ibrance), ribociclib (Kisquali), and abemaciclib (Verzenio). Everolimus works by blocking mTOR, a protein that normally promotes cell growth and division. CDK 4 and 6 inhibitors prevent cells from dividing, thus slowing cancer growth. (The use of immunotherapy and targeted therapy is discussed in Chapter 15.)

Culturally Competent Care: Breast Cancer Differences exist in the incidence, mortality rates, and care issues among diverse racial and ethnic groups related to breast cancer (see

Promoting Health Equity box on this page). In addition, cultural differences may involve gender roles, health beliefs, religion, family structure, socioeconomic factors (e.g., poverty) and lack of health insurance. Lack of education may influence disparities related to access to health care and having recommended surveillance examinations.17,18

Promoting Health Equity Breast Cancer • White and black women have the highest incidence of breast cancer. • Black women have lower survival rates from breast cancer than white women, even when diagnosed at an early stage. • Hispanic and black women are more likely to be diagnosed at a later stage of breast cancer than white women. • Triple-negative breast cancer has a higher incidence in black and Hispanic women. • Mortality rates are lower among Hispanic and Asian/Pacific Islander women than among white and black women. • Breast cancer is the most common diagnosed cancer among Hispanic women. • Indian/Alaskan native women have the lowest rate of breast cancer screening of any ethnic group. Cultural values strongly influence how a person responds to and copes with breast cancer and treatment. Diverse cultural norms influence health beliefs and behaviors. Breast cancer screening, diagnosis, and treatment are affected by the cultural values and meanings (body image, sexuality, modesty, motherhood) associated with the breasts. Women may delay screening or treatment for

varying reasons, including an acceptance of disease as inevitable fate or “God’s will,” a mistrust of Western medicine, lack of health care benefits, fear, or the stigma of a cancer diagnosis.

Nursing Management: Breast Cancer Nursing Assessment You must consider many factors when assessing a patient with a breast problem. The history of the breast disorder helps establish a diagnosis. Investigate the presence of nipple discharge, pain, rate of growth of the lump, breast asymmetry, and correlation with the menstrual cycle. Carefully record the size and location of the lump or lumps. Assess the physical characteristics of the lesion, including consistency, mobility, and shape. If nipple discharge is present, note the color and consistency and whether it occurs from 1 or both breasts. Subjective and objective data to obtain from a person suspected of having or diagnosed with breast cancer are outlined in Table 51.9.

Nursing Diagnoses Nursing diagnoses related to the care of a patient diagnosed with breast cancer vary. After diagnosis and before a treatment plan has been selected, the following nursing diagnoses would apply: • Difficulty coping • Lack of knowledge • Disturbed body image If surgery is planned, the nursing diagnoses and interventions may include those in eNursing Care Plan 51.1 (available on the website for this chapter).

Planning

The overall goals are that the patient with breast cancer will (1) actively take part in the decision-making process related to treatment, (2) adhere to the therapeutic plan, (3) communicate about and manage the side effects of adjuvant therapy, (4) access and benefit from the support provided by significant others and HCPs, and (5) adhere to recommended follow-up and surveillance after treatment.

Nursing Implementation Health Promotion Review the risk factors in Table 51.2. People can reduce their risk factors by maintaining a healthy weight, exercising regularly, limiting alcohol, eating nutritious food, and never smoking (or quitting if currently smoking). Encourage people to adhere to the breast cancer screening guidelines shown on pp. 1190–1191. A person at high risk needs to develop a personalized plan with the HCP. Early detection can decrease the morbidity and mortality associated with breast cancer.

TABLE 51.9 Nursing AssessmentBreast Cancer

Subjective Data Important Health Information Past health history: Benign breast disease with atypical changes. Previous unilateral breast cancer. Menstrual history (early menarche with late menopause), pregnancy history (nulliparity or first full-term pregnancy after age 30). Endometrial, ovarian, or colon cancer. Hyperestrogenism and testicular atrophy (in men) Medicines: Hormones, especially as postmenopausal hormone therapy and in oral contraceptives. Infertility treatments Surgery or other treatments: Exposure to therapeutic radiation (e.g.,

Hodgkin’s lymphoma or thyroid radiation)

Functional Health Patterns Health perception–health management: Family history of breast cancer (young age at diagnosis). History of abnormal mammogram or atypical prior biopsy. Palpable change found on BSE. Known BRCA mutation carrier, first-degree relative of BRCA carrier (but untested) Nutritional-metabolic: Obesity; unexplained severe weight loss (may indicate metastasis) Activity-exercise: Level of usual activity Cognitive-perceptual: Changes in cognition, headache, bone pain (may indicate metastasis) Sexuality-reproductive: Unilateral nipple discharge (clear, milky, bloody). Change in breast contour, size, or symmetry Coping–stress tolerance: Psychologic stress Self-perception–self-concept: Anxiety about threat to self-esteem

Objective Data General Axillary and supraclavicular lymphadenopathy

Integumentary Hard, irregular, nonmobile breast lump most often in upper, outer sector, possibly fixated to fascia or chest wall. Thickening of breast. Nipple inversion or retraction, erosion. Edema (“peau d’orange”), erythema, induration, infiltration, or dimpling (in later stages). Firm, discrete nodules at mastectomy site (may indicate local recurrence). Peripheral edema (may indicate metastasis)

Respiratory Pleural effusions (may indicate metastasis)

Gastrointestinal Hepatomegaly, jaundice, ascites (may indicate liver metastasis)

Possible Diagnostic Findings Finding of mass or change in tissue on breast examination. Abnormal mammogram, ultrasound, or breast MRI. Positive results of FNA or surgical biopsy; similar results with a needle biopsy Along with these lifestyle choices, there are other risk-reduction options for people at high risk. Genetic testing for BRCA and other gene mutations is available. People with a strong family history of breast cancer should talk with their HCP about the possibility of genetic testing. There is no reason for routine screening for genetic abnormalities in women without evidence of a strong family history of breast cancer. In women with an abnormal BRCA1 or BRCA2 gene, prophylactic oophorectomy may reduce their risk for developing breast cancer and ovarian cancer. In deciding whether and when to undergo this surgical procedure, women should receive counseling about the risks and benefits of prophylactic oophorectomy, including fertility issues. Prophylactic surgery decisions require a great deal of thought, patience, and discussion with the HCP, genetic counselor, and family. Patients need to consider these options and make decisions with which they feel comfortable. Removing both breasts and ovaries at a young age does not eliminate the risk for breast cancer. A small risk exists that cancer can develop in the areas where the breasts used to

be. Close follow-up is necessary even after prophylactic surgery.

Acute Care The times of waiting for the initial biopsy results and waiting for the HCP to make treatment recommendations are difficult for patients and their families. Even after the HCP has discussed treatment options, the patient often relies on you to clarify and expand on these options. During this stressful time, the patient may not be coping effectively. Appropriate nursing interventions are to explore the patient’s usual decision-making processes, help to evaluate the advantages and disadvantages of the options, provide information relevant to the decision, clarify unresolved issues with the HCP, and support the patient and family once the decision is made. Provide the patient with enough information to ensure informed consent. Some patients seek extensive, detailed information to maintain a sense of control. Others avoid information to decrease anxiety and fear. Be sensitive to the person’s need for and preferred type of information. These include (1) instructions on pain control and what to expect after surgery (e.g., dressing and drain care, turning, coughing, deep breathing), (2) a review of mobility restrictions and postoperative exercises, and (3) an explanation of the recovery period. The woman who has breast-conserving surgery usually has an uncomplicated postoperative course with variable pain intensity. Pain depends primarily on the extent of the lymph node sampling procedure. If an ALND has been done or if the patient had a mastectomy, drains are generally left in place and patients are discharged home with them. Teach the patient and family, with a return demonstration, how to manage the drains at home. Most patients are discharged from the hospital 24 to 48 hours after a mastectomy, depending on if reconstructive surgery was done. Restoring arm function on the affected side after breast cancer surgery is a key nursing goal. Arm and shoulder exercises, which are started gradually, may begin prior to discharge (Fig. 51.8). These exercises are designed to prevent contractures and muscle shortening, maintain muscle tone, and improve lymph and blood circulation. The difficulty

and pain encountered in performing what used to be simple tasks may cause frustration and depression. The goal of all exercise is a gradual return to full range of motion. Discomfort can be minimized by giving analgesics regularly when the patient is in pain and about 30 minutes before starting exercises. When the patient can shower, the warm water on the involved shoulder often relaxes the muscle and reduces joint stiffness. Explain the specific follow-up plan to the patient and emphasize the importance of ongoing monitoring and self-care. After surgery, teach the patient to report symptoms, such as fever, inflammation at the surgical site, erythema, and unusual swelling. Other changes to report are new back pain, weakness, shortness of breath, and change in mental status, including confusion.

FIG. 51.8 Postoperative exercises for the patient with a mastectomy or lumpectomy with axillary lymph node sampling and/or dissection.

For women who have had a mastectomy without breast reconstruction, a variety of products are available. Your role is to present the choices and resources. Options include garments such as camisoles with soft breast prosthetic inserts or a fitted prosthesis with bra. Should the woman choose a breast prosthesis, a certified fitter can help her choose a comfortable, more permanent weighted prosthesis and bra. This is generally done 4 to 8 weeks after surgery.

Lymphedema Upper extremity lymphedema can occur at any point after treatment for breast cancer. Teach the patient ways to prevent and reduce lymphedema. These include no BP readings, venipunctures, or injections on the affected arm, if possible. The affected arm should not be dependent for long periods. Caution should be used to prevent infection, burns, or compromised circulation on the affected side. Encourage exercise and maintaining a normal weight. If trauma to the arm occurs, the area should be washed thoroughly with soap and water and observed. A topical antibiotic ointment and a bandage or other sterile dressing may be applied. When lymphedema is acute (Fig. 51.6), complete decongestive therapy will be recommended. This therapy is performed by specially trained professionals. It consists of a massage-like technique to mobilize the subcutaneous accumulation of fluid. This may be followed by use of compression bandaging and an intermittent pneumatic compression sleeve. The sleeve applies mechanical massage to the arm and helps move lymph drainage up toward the heart. Elevating the arm so that it is level with the heart and performing isometric exercises reduce the fluid in the arm. To maintain maximum volume reduction, the patient may need to wear a fitted compression sleeve during waking hours and preventively during air travel.

Psychosocial Support

Throughout history, the female breast has been a symbol of beauty, femininity, sexuality, and motherhood. The potential loss of a breast, or part of a breast, may be devastating for many women because of the significant psychologic, social, sexual, and body image implications associated with it. For men diagnosed with breast cancer, isolation and embarrassment related to the diagnosis can occur. You must be aware of resources for men (www.malebreastcancer.org). As hard as it is to predict which patients will develop physical effects of treatment, it can be even more difficult to foresee the psychosocial effects of treatment. In some cases, psychosocial concerns may increase the physical effects of cancer, such as pain, fatigue, sleep problems, fear of recurrence, and cognitive changes. Screening all cancer patients for psychosocial distress is a Commission on Cancer accreditation requirement.19 From the time of diagnosis through treatment, survivorship, or metastatic disease, the patient may have signs of distress or tension (e.g., tachycardia, increased muscle tension, sleep problems, restlessness, changes in appetite or mood). Assess the patient’s body language and affect during periods of high stress and indecision so that you can begin appropriate interventions, including referral to a mental health provider. Remain sensitive to the complex psychologic impact that a diagnosis of cancer and breast surgery can have on patients and their families. With an accepting attitude and the offer of resources, you can help the patient cope with feelings of fear, anger, anxiety, and depression. You can help to: • Provide a safe environment for the expression of feelings. • Identify sources of support and strength, such as the partner, family, and spiritual or religious practices. • Encourage the patient to identify and learn personal coping strengths. • Promote communication among the patient, family, and friends. • Answer questions about the disease, treatment options, and

reproductive, fertility, or lactation issues (if appropriate). • Make resources available for mental health counseling. • Offer information about local and national community resources. Referring patients to support resources, such as www.Breastcancer.org, the Cancer Support Community, or local breast cancer organizations, is valuable. The ACS and National Cancer Institute can provide excellent materials to help you in meeting the special needs of patients with breast cancer. In addition to in-person and online support programs, multiple free smart phone applications are available through national cancer organizations that provide reliable and current information for the patient and his or her family. How the loss of part or all of the breast and cancer affect the patient’s sexual identity, body image, and relationships can vary. Many HCPs do not adequately address sexual concerns. If you are comfortable, begin a discussion of sexuality by inviting questions about relationships or intimacy concerns. Often the patient’s partner and/or family members need help dealing with their emotional reactions to the diagnosis and surgery before they can provide effective support for the patient. There are no physical reasons why a mastectomy would prevent sexual satisfaction. A woman taking hormone therapy may have a decreased sexual

Complementary & Alternative Therapies Supportive Care Many women use complementary and integrative therapies as supportive care during cancer treatment to improve quality of life and manage treatment-related side effects.

Scientific Evidence • There is strong evidence that practicing meditation and relaxation

decreases anxiety and depression and improves quality of life. • Stress management, yoga, massage, music therapy, and meditation decrease stress, fatigue, anxiety, and depression and improve quality of life.

Nursing Implications • Women use a variety of integrative therapies during breast cancer treatment. • Meditation, yoga, relaxation, stress management, massage, music therapy, and energy conservation may be especially helpful in managing symptoms and improving quality of life during treatment.

Reference for Evidence Greenlee H, DuPont-Reyes M.J, Balneaves L, et al. Clinical practice guidelines on the evidence-based use of integrative therapies during and after breast cancer treatment. CA Cancer J Clin. 2017;67:1954. drive or vaginal dryness. She may need to use lubrication to prevent discomfort during intercourse. If difficulty in adjustment or other problems develop, single or couples counseling may be useful to deal with the emotional side of a diagnosis of cancer. Depression and anxiety may occur with the continued stress and uncertainty of a cancer diagnosis. A patient’s self-esteem and identity may be threatened. The support of family and friends and taking part in a cancer support group and/or counseling are important aspects of care that may improve the patient’s quality of life.

Survivorship Almost 3 million breast cancer survivors are alive in the United States,

making this population the largest group of cancer survivors. We expect this number to grow due to an aging population and improved methods for early detection and treatment. After treatment for breast cancer, the patient will have ongoing survivorship care.19,20 A history and physical examination is recommended 1 to 4 times per year as clinically appropriate for 5 years, then annually thereafter. In addition, teach breast cancer survivors to perform monthly BSE and chest wall self-examination and report any changes to their HCP. Local recurrence of breast cancer is usually at the surgical site. Breast cancer survivors should have an annual mammogram. Other breast imaging studies, such as a breast ultrasound or breast MRI, should be done only as an adjunct to mammography and not for annual routine surveillance. Cancer survivorship is discussed in Chapter 15 on p. 264.

Evaluation Expected outcomes are that the patient after breast cancer surgery will • Identify activities that can reduce postoperative edema and improve mobility • Show effective use of coping strategies • Discuss feelings about and the meaning of changes in physical appearance • Identify community and online resources, personal counseling resources, and support groups

Gerontologic Considerations: Breast Cancer A major risk for breast cancer is increasing age. More than half of all breast cancers occur in women who are age 65 or older.1 Older women are less likely to have mammograms. Screening and treatment decisions for breast cancer should be based on a woman’s general health status rather than biologic age, since health status has a greater influence on tolerance to treatment and long-term prognosis. In addition to medical co-morbidities and life expectancy, treatment

decisions for the older woman with breast cancer should be based on an assessment of nutritional and functional status; vision, gait, and balance; and the presence of delirium, dementia, or depression. Breast cancer treatment is similar for older and younger patients, including the use of surgery, radiation therapy, and drug therapy. For healthy older women, breast cancer survival rates are similar to those of younger women when matched by cancer stage.

Mammoplasty Mammoplasty is the surgical change in the size or shape of the breast. It may be done electively for cosmetic purposes to either enlarge or reduce the size of the breasts. It also may be done to reconstruct the breast after a mastectomy. A professional, nonjudgmental attitude and clear information about surgical breast options are most useful for women engaged in decision making about mammoplasty. The desire to change the appearance of the breasts has special significance for each woman as she attempts to change or recreate her body image. Be aware of the cultural value that the woman places on the breast. Help the patient set realistic expectations about what mammoplasty can achieve and possible complications (e.g., hematoma formation, hemorrhage, infection). If an implant is involved, capsular contracture and loss of the implant are possible.

Breast Reconstruction Breast reconstructive surgery is a type of surgery for women who have had all or part of a breast removed. It is done to achieve symmetry and to restore or preserve body image. It may be done simultaneously with a mastectomy or some time afterward. The timing of reconstructive surgery is personalized based on the patient’s physical and psychologic needs.21

Indications

The main indication for breast reconstruction is to improve a woman’s self-image, regain a sense of normalcy, and assist in coping with the loss of the breast. It restores the contour of the breast without the use of an external prosthesis. Reconstruction techniques cannot restore lactation, nipple sensation, or erectility. Although the breast will not fully resemble its premastectomy appearance, the reconstructed appearance usually is an improvement over the mastectomy scar (Fig. 51.9).

Types of Reconstruction Breast Implants and Tissue Expansion Implants have a silicone shell filled with either silicone gel or saline.22 Some newer types use a cohesive gel, which is a thicker silicone gel. Implant surgery can be done in 1 or 2 stages. In the 1-stage procedure, the implant is placed at the same time as the mastectomy. The implant is usually placed under the pectoralis muscle. In the 2-stage procedure, a tissue expander is inserted after the mastectomy. The expander stretches the skin and muscle at the mastectomy site before inserting permanent implants (Fig. 51.10). It is placed in a pocket under the pectoralis muscle, which protects the implant and provides soft tissue coverage. The expander is minimally inflated, then gradually filled by weekly injections of sterile saline solution. This procedure stretches the skin and muscle and can be painful. A small magnet embedded in most expanders helps locate the port where the fluid is injected. A woman should not have an MRI with a magnet in place.

FIG. 51.9 A, Appearance of chest after bilateral mastectomy. B, Breast reconstruction before nipple-areolar reconstruction. C, Breast reconstruction after nipple-areolar reconstruction. Courtesy Brian Davies, MD. From Fortunato N, McCullough S, eds: Plastic and reconstructive surgery, St Louis, 1998, Mosby.

FIG. 51.10 A, Tissue expander with gradual expansion. B, Tissue expander in place after mastectomy.

The expander can be (1) surgically removed and a permanent implant is inserted or (2) remain in place to become the implant, thus eliminating the need for a second surgical procedure. Tissue expansion does not work well in those with extensive scar tissue from surgery or radiation therapy. The body’s natural response to the presence of a foreign substance is the formation of a fibrous capsule around the implant. If excessive capsular formation occurs because of infection, hematoma, trauma, or reaction to a foreign body, a contracture can develop, resulting in deformity. Although HCPs differ in their approaches to the prevention of contracture formation, gentle manual massage around the implant is routine. Other adverse outcomes include wrinkling,

scarring, asymmetry, pain, and infection at the incision site. There is a small chance of anaplastic large cell lymphoma occurring. This has mostly been associated with textured implants.19

Tissue Flap Procedures Another type of breast reconstruction uses autologous (person’s own) tissue to recreate a breast mound. In autologous reconstruction, tissue from the abdomen, back, thighs, or buttocks is used to create a reconstructed breast. The most common types of tissue flap procedures are transverse rectus abdominis musculocutaneous (TRAM) flap, deep inferior epigastric artery perforator (DIEP) flap, and latissimus dorsi flap. The TRAM flap is a common flap surgery. The rectus abdominis muscles are paired flat muscles running from the rib cage down to the pubic bone. Arteries running inside the muscles provide branches at many levels, and these branches supply the fat and skin across a large expanse of the abdomen. There are 2 different types of TRAM flaps: pedicle and free. In a pedicle flap, the tissue stays attached to the rectus muscle and is tunneled under the skin to the patient’s chest (Fig. 51.11). In a free flap, the tissue is completely separated from the muscle and its blood supply and moved to the new place on the patient’s chest. The tissue is molded and fashioned to form a breast. The abdominal incision is closed, giving the patient a result that is similar to having an abdominoplasty (“tummy tuck”). The procedure can last 6 to 8 hours with recovery taking 6 to 8 weeks. Some patients have report pain and fatigue for up to 3 months. Complications include bleeding, seroma, hernia, infection, and low back pain. Perforator flaps are a type of free flap (a perforator artery connects a superficial artery with a deep one) that do not use muscle tissue. A DIEP flap is the type done most often. With the DIEP flap, only the skin and fat are taken from the same lower abdominal area as the TRAM flap. Patients may have less pain and restriction of movement with this procedure. The superficial inferior epigastric artery perforator (SIEAP) is another option using the abdominal area.

The latissimus dorsi flap is a pedicle flap. In this type of flap, a block of skin and muscle from the patient’s back replaces tissue removed during mastectomy. A small implant may be needed under the flap to gain reasonable breast shape and size. A disadvantage of this technique is a scar on the back. Less often, flaps are taken from the buttocks, hips, or thighs. The transverse upper gracilis flap, or inner thigh flap, is one type of free flap. Tissue, including the gracilis muscle, is taken from the bottom fold of the buttock extending into the inner thigh. The inferior or superior gluteal artery perforators are used for flaps taken from the buttocks.

Nipple-Areolar Reconstruction Many patients undergoing breast reconstruction also have nippleareolar reconstruction. Nipple reconstruction gives the reconstructed breast a much more natural appearance (Fig. 51.9, C). Nipple-areolar reconstruction is usually done a few months after breast reconstruction. Tissue to construct a nipple may be taken from the opposite breast or from a small flap of tissue on the reconstructed breast mound. Most often, the areola is tattooed with a permanent pigmented dye. Improved techniques now allow skilled tattoo artists to create a complete 3D nipple-areola complex. Polyurethane removable nipples are also available.

Breast Augmentation In augmentation mammoplasty (procedure to enlarge the breasts), an implant is placed in a surgically created pocket between the capsule of the breast and pectoral fascia, or ideally under the pectoralis muscle. (Implants are discussed on p. 1207.)

FIG. 51.11 Transverse rectus abdominis musculocutaneous (TRAM) flap. A, TRAM flap is planned. B, The abdominal tissue, while attached to the rectus muscle, nerve, and blood supply, is tunneled through the abdomen to the chest. C, The flap is trimmed to shape the breast. The lower abdominal incision is closed. D, Nipple and areola are reconstructed after the breast is healed.

Breast Reduction For some women, large breasts can be a source of physical and psychologic discomfort. They can interfere with normal daily activities, such as walking, using a computer, and driving a car. The weight of large breasts can lead to back, shoulder, and neck problems, including degenerative nerve changes. Overly large breasts can interfere with self-esteem, self-image, and comfort in wearing some clothing. Reducing breast size can have positive effects on the patient’s psychologic and physical health. Reduction mammoplasty is done by resecting wedges of tissue from the upper and lower quadrants of the breast. The excess skin is removed, and the areola and nipple are relocated on the breast. Lactation usually can be accomplished if massive amounts of tissue are not removed and the nipples are left connected during surgery.

Nursing Management: Breast Augmentation and Reduction Breast augmentation and breast reduction may be done in the

outpatient surgical area or involve overnight hospitalization. General anesthesia is used. Drains are generally placed in the surgical site to prevent hematoma formation and then removed when drainage is under 20 to 30 mL/day. Examine drainage for color and odor to detect infection or hemorrhage. Monitor the temperature. Change dressings as needed using sterile technique. After surgery, assure the woman that the breast’s appearance will improve when healing is complete. Depending on HCP preference, the patient may be told to wear a bra that provides good support continuously for 2 or 3 days after breast reduction or augmentation. Depending on the extent of the surgery, most women resume normal activities within 2 to 3 weeks. Strenuous exercise must often be avoided for several weeks.

Case Study Breast Cancer

© XiXinXing/iStock/Thinkstock.

Patient Profile A.K., a 68-yr-old married Asian American woman, has been diagnosed with a 1.3-cm estrogen- and progesterone-positive, HER-2– negative breast cancer. She is scheduled in the morning for a lumpectomy and sentinel lymph node biopsy (SLNB) with possible axillary node dissection.

Interprofessional Care

Preoperative • When she is seen in the clinic 1 week before surgery, she is crying uncontrollably and says, “My husband does not want to look at me anymore. He is afraid of what I am going to look like with a flat chest.” • She says, “I cannot sleep, and I just pace the floor at night.” • “My mother died of breast cancer when she was 60, and my sister got it when she was 40.” • Expresses concern that her 2 daughters (34 and 32) and their daughters are going to get “this horrible disease.”

Operative Procedure • Lumpectomy and SLNB are done • Tumor was removed with clear margins • No cancer cells in her sentinel lymph nodes • 4 lymph nodes are removed • Tissue specimen sent for a 21-gene recurrence score genomic test

Postoperative • Does not want to leave hospital and refuses to get out of bed • Swelling and restricted range of motion in right arm • Pain not controlled well with pain medication

Follow-Up Findings and Treatment • 21-Gene recurrence score is 11, low risk • Scheduled for external radiation and a consult with medical oncologist to discuss hormone therapy

Discussion Questions 1. What in A.K.’s breast cancer experience with her family members may influence her coping response? 2. Patient-Centered Care: How will you include cultural preferences in A.K.’s plan of care? 3. What complication did she develop after her surgery? 4. Which common exercises will A.K. need to practice after her surgery? 5. What information is important for you to provide to A.K. about her radiation treatment and hormonal therapy? 6. Safety: Describe specific nursing interventions aimed at minimizing risk for harm for A.K. 7. Patient-Centered Care: What information would you provide to A.K. about her surgery and why the 21-gene recurrence test was done? 8. What information is important for you to provide to A.K. and her daughters? What early detection measures are important for them to know? 9. Evidence-Based Practice: A.K. wants to know what the psychologic benefit may be for her daughters if they decide on a breast cancer genetic risk assessment. 10. Collaboration: What types of referrals may be indicated for A.K.? 11. Collaboration: What community resources are available to help A.K. and her family adjust to the change in her body and cope with the diagnosis of cancer? 12. Quality Improvement: What outcomes would indicate nursing interventions were successful for A.K.? 13. Develop a conceptual care map for A.K. Answers and a corresponding conceptual care map available at http://evolve.elsevier.com/Lewis/medsurg.

Bridge to Nclex Examination The number of the question corresponds to the same-numbered outcome at the beginning of the chapter.

1. You are a community health nurse planning a program on breast cancer screening guidelines for women in the neighborhood. Which recommendations you would include? (select all that apply) a. Women over age 55 may have biennial screening. b. Screening should end when the women reaches age 65. c. Women aged 45 to 54 years should be screened annually. d. Regular screening mammography should start at age 45 years. e. Clinical breast examinations can be used if the woman has average risk. 2. You are caring for a young woman who has painful fibrocystic breast changes. Management of this patient would include a. scheduling a biopsy to rule out the presence of breast cancer. b. teaching that symptoms will subside if she stops using oral contraceptives. c. preparing her for surgical removal of the lumps, since they will become larger and more painful. d. explaining that restricting coffee and chocolate and supplementing with vitamin E may relieve some discomfort. 3. When discussing risk factors for breast cancer with a group

of women, you emphasize that the greatest known risk factor for breast cancer is a. being a woman over age 60. b. experiencing menstruation for 30 years or more. c. using hormone therapy for 5 years for menopausal symptoms. d. having a paternal grandmother with postmenopausal breast cancer. 4. A patient with breast cancer has a lumpectomy with sentinel lymph node biopsy that is positive for cancer. You explain that, of the other tests done to determine the risk for cancer recurrence or spread, the results that support the more favorable prognosis are (select all that apply) a. well-differentiated tumor. b. estrogen receptor–positive tumor. c. overexpression of HER-2 cell marker. d. involvement of two to four axillary nodes. e. aneuploidy status from cell proliferation studies. 5. You are caring for a patient with breast cancer following a simple mastectomy. Postoperatively, to restore arm function on the affected side, you would a. apply heating pads or blankets to increase circulation. b. place daily ice packs to minimize the risk for lymphedema. c. teach passive exercises with the affected arm in a dependent position. d. emphasize regular exercises for the affected shoulder to increase range of motion.

6. Preoperatively, to meet the psychologic needs of a woman scheduled for a simple mastectomy, you would a. discuss the limitations of breast reconstruction. b. include her significant other in all conversations. c. promote an environment for expression of feelings. d. explain the importance of regular follow-up screening. 7. To prevent capsular formation after breast reconstruction with implants, teach the patient to a. gently massage the area around the implant. b. bind the breasts tightly with elastic bandages. c. avoid strenuous exercise until the implant has healed. d. exercise the arm on the affected side to promote drainage. 1. a, c, d, 2. d, 3. a, 4. a, b, 5. d, 6. c, 7. a For the rationale for these answers and even more NCLEX review questions, visit http://evolve.elsevier.com/Lewis/medsurg.

Evolve Website/Resources List http://evolve.elsevier.com/Lewis/medsurg

Review Questions (Online Only) Key Points Answer Keys for Questions • Rationales for Bridge to NCLEX Examination Questions • Answer Guidelines for Case Study on p. 1209 Student Case Study • Patient With Breast Cancer

Nursing Care Plan • eNursing Care Plan 51.1: Patient After Breast Surgery Conceptual Care Map Creator • Conceptual Care Map for Case Study on p. 1209 Audio Glossary Content Updates

References 1. American Cancer Society: Cancer facts and figures 2017. Retrieved from www.cancer.org/content/dam/cancer-org/research/cancerfacts-and-statistics/annual-cancer-facts-andfigures/2017/cancer-facts-and-figures-2017.pdf. American Cancer Society: ACS recommendations for early detection of breast cancer. Retrieved from www.cancer.org/cancer/breastcancer/screening-tests-and-early-detection/american-cancer-societyrecommendations-for-the-early-detection-of-breast-cancer.html. National Comprehensive Cancer Network: NCCN guidelines, version1, 017: Breast cancer screening and diagnosis. Retrieved from www.nccn.org/professionals/physician_gls/pdf/breast-screening.pdf.

4. Liu J, Jacobs L: The management of benign breast disease. In: Cameron J, Cameron A: Current surgical therapy, ed 12, Atlanta, 2017, Elsevier. 5. Nordqviist C. Mastitis: Treatment, causes, and symptoms. Retrieved from www.medicalnewstoday.com/articles/163876.php. 6. Bland KI, Copeland EM, Klimberg VS, et al: The breast comprehensive management of benign and malignant diseases, ed 5, Philadelphia, 2018, Elsevier.

7. Smith R: Fibrocystic breast changes. In: Netter’s obstetrics and gynecology, ed 3, Philadelphia, 2018, Elsevier. American College of Obstetricians and Gynecologists: Practice bulletin: Diagnosis and management of benign breast disorders, Obstet & Gynecol 127:e141, 2016.

9. American Cancer Society: Breast cancer: Risk factors and prevention. Retrieved from www.cancer.org/cancer/breast-cancer/risk-andprevention.html. 10. National Cancer Institute: Genetics and breast and gynecologic cancers PDQ®—Health professional version. Retrieved from www.cancer.gov/types/breast/hp/breastovarian-genetics-pdq. 11. National Comprehensive Cancer Network: NCCN guidelines, version 2, 2017: Genetic/familial high-risk assessment: Breast and ovarian. Retrieved from www.nccn.org/professionals/physician_gls/pdf/genetics_screening.pd 12. Breastcancer.org: Gene testing. Retrieved from www.breastcancer.org/symptoms/testing/genetic. 13. Guiliano AE, Connelly JL, Edge SB, et al: Breast cancer—Major changes in the American Joint Committee on Cancer 8th edition cancer staging manual, Cancer J Clin 67:290, 2017. National Comprehensive Cancer Network: NCCN guidelines, version 2, 2017: Breast cancer. Retrieved from www.nccn.org/professionals/physician_gls/pdf/breast.pdf.

15. About OncotypeDX breast DCIS score. Retrieved from www.oncotypeiq.com/en-US/breast-cancer/patientsand-caregivers/stage-0-dcis/about-the-test. 16. Post-breast therapy pain syndrome. Retrieved from www.cancersupportivecare.com/neuropathicpain.php.

17. Who gets triple negative breast cancer? Retrieved from www.breastcancer.org/symptoms/diagnosis/trip_neg/who_gets Koç H, O’Donnell O, Van Ourti T: What explains education disparities in screening mammography in the United States? A comparison with the Netherlands, Int J Environ Res Public Health 15:1961, 2018.

19. American College of Surgeons Commission on Cancer: Cancer program standards 2016 edition: Ensuring survivor-centered care. Retrieved from www.facs.org/ ∼/media/files/quality%20programs/cancer/coc/2016%20coc%20stan 20. Runowicz CD, Leach CR, Henry LH. et al: ACS/American Society of Clinical Oncology breast cancer survivorship care guideline, J Clin Oncol 34:611, 2016. 21. American Cancer Society: Breast reconstructive surgery. Retrieved from www.cancer.org/cancer/breastcancer/reconstruction-surgery.html. 22. Food and Drug Administration: Breast implants. Retrieved from www.fda.gov/MedicalDevices/ProductsandMedicalProcedures/Implan ∗Evidence-based information for clinical practice.

52

Sexually Transmitted Infections Daniel P. Worrall

LEARNING OUTCOMES 1. Identify factors contributing to sexually transmitted infections (STIs) in the United States. 2. Describe the etiology, clinical manifestations, complications, and diagnostic studies for chlamydia, gonorrhea, trichomoniasis, genital herpes, genital warts, and syphilis. 3. Compare and contrast primary genital herpes with recurrent genital herpes. 4. Explain the interprofessional care and treatment of chlamydia, gonorrhea, trichomoniasis, genital herpes, genital warts, and syphilis. 5. Discuss the nursing assessment for patients who have an STI. 6. Describe the nursing management of patients with STIs. 7. Summarize the nursing role in the prevention and control of STIs.

KEY TERMS chlamydial infections, p. 1213 genital herpes, p. 1217

genital warts, p. 1218 gonorrhea, p. 1215 sexually transmitted infections (STIs), p. 1212 syphilis, p. 1220 trichomoniasis, p. 1216 The meaning of life is to find your gift. The purpose of life is to give it away. Pablo Picasso http://evolve.elsevier.com/Lewis/medsurg

Conceptual Focus Infection Pain Reproduction Sexuality Sexually transmitted infections (STIs) are infectious diseases that are spread through sexual contact with the penis, vagina, anus, mouth, or sexual fluids of an infected person. Many do not view STIs as a serious health threat because they are easily treated. However, the complications are serious and can include infertility and cancer. Having an STI can affect persons’ well-being, their relationships, and their sexual lives. Patient education, counseling, and referral are essential nursing roles for promoting health and optimal sexual wellbeing. Mucosal tissues in the genitals (urethra in men, vagina in women), rectum, and mouth are especially susceptible to the bacteria and viruses that cause STIs. A list of common STIs is shown in Table 52.1. Some STIs, such as genital human papillomavirus (HPV), can spread

from direct skin-to-skin contact with an infected person. Other STIs, such as human immunodeficiency virus (HIV), may be contracted via blood or blood products or be transmitted from mother to baby during pregnancy or labor and delivery. Some STIs can spread through autoinoculation (spread of infection by touching or scratching an infected area and transferring it to another part of the body). STIs cannot typically be transmitted from casual contact or inanimate objects.

Factors Affecting Incidence of Stis STIs are quite common. There are nearly 20 million new STIs diagnosed in the United States each year, resulting in an estimated 16 billion in health care costs.1 More than 110 million Americans are infected with an STI at any given time. Having 1 STI increases the risk for getting another. A person can have more than 1 STI at the same time. All STIs have an incubation period. It is the time from initial infection to the time when symptoms first appear or screening tests for the infection are positive. This can lead to the transmission of disease from an asymptomatic (but infected) person to another person, even before any symptoms or signs begin. In the United States, all cases of gonorrhea, chlamydia, and syphilis must be reported to public health authorities for surveillance purposes for federally funded control programs and partner notification. Surveillance and partner notification are a major part of the effort to prevent and control the spread of STIs. Nurses and other HCPs play a vital role, as they are mandated to report these STIs to public health authorities. Despite this requirement, only a small number of infections are reported. This is especially important when considering that the more than 2 million cases of gonorrhea, chlamydia, and syphilis reported in the United States annually do not represent the actual number of infections.

TABLE 52.1 Causes of Sexually Transmitted

Infections (STIs)

TABLE 52.2 Risk Factors for STIs

High-Risk Behaviors • Alcohol or drug use (inhibits judgment) • Having new or multiple sexual partners • Having more than 1 sexual partner • Having sexual partners who have/have had multiple partners • Inconsistent or incorrect use of condoms or other barrier methods • Sharing needles used to inject drugs

High-Risk Medical History • Having 1 STI is a risk factor for getting another • Not being vaccinated for STIs or other infections that may be transmitted through some forms sexual activity (HPV, hepatitis A

and B) • Receiving multiple courses of nonoccupational postexposure prophylaxis for HIV infection

High-Risk Populations • Adolescents and young adults (age 90 mm Hg, MAP >85) • Administer IV fluids • Insert NG tube and attach to suction. • Assessment and management of nutrition • Maintain normal body temperature • Indwelling urinary catheter • Pain management • VTE prophylaxis • Pressure injury prevention • Stress ulcer prophylaxis • Bowel and bladder care and training • Mobilization once spine stabilized • Physical, occupational, speech therapy and physiatrist consults

Rehabilitation and Home Care • Physical therapy (ROM, mobility, strength, equipment) • Occupational therapy (splints, ADLs training) • Speech therapy (swallow and cognition) • Pain management • Spasticity management • Bowel and bladder training

• Autonomic dysreflexia prevention • Pressure injury prevention • Recreational therapy • Patient and caregiver teaching

Nursing Management: Spinal Cord Injury Nursing Assessment Subjective and objective data you should obtain from a patient with recent SCI are outlined in Table 60.5.

TABLE 60.5 Nursing AssessmentSpinal Cord

Injury

Subjective Data Important Health Information Past health history: Motor vehicle crash, sports injury, industrial incident, gunshot or stabbing injury, falls

Functional Health Patterns Health perception–health management: Use of alcohol or recreational drugs. Risk-taking behaviors Activity-exercise: Loss of strength, movement, and sensation below level of injury. Dyspnea, inability to breathe adequately (“air hunger”) Cognitive-perceptual: Tenderness, pain at or above level of injury. Numbness, tingling, burning, twitching of extremities

Coping–stress tolerance: Fear, denial, anger, depression

Objective Data General Poikilothermia (unable to regulate body heat)

Integumentary Warm, dry skin below level of injury (neurogenic shock)

Respiratory Injury at C1-3: Apnea, inability to cough Injury at C4: Poor cough, diaphragmatic breathing, hypoventilation Injury at C5-T6: ↓ Respiratory reserve

Cardiovascular Injury above T6: Bradycardia, hypotension, postural hypotension, absence of vasomotor tone

Gastrointestinal ↓ Or absent bowel sounds (paralytic ileus in injuries above T5), abdominal distention, constipation, fecal incontinence, fecal impaction

Urinary

Retention (for injuries at T1-L2), flaccid bladder (acute stages), spasticity with reflex bladder emptying (later stages)

Reproductive Priapism, altered sexual function

Neurologic Complete: Areflexic, flaccid paralysis and anesthesia below level of injury resulting in tetraplegia (injuries above C8) or paraplegia (injuries below C8), hyperactive deep tendon reflexes and bilaterally positive Babinski test (after resolution of spinal shock) Incomplete: Mixed loss of voluntary motor activity and sensation

Musculoskeletal Muscle atony (in flaccid state), contractures (in spastic state)

Pain Neuropathic, musculoskeletal, and/or visceral

Possible Diagnostic Findings Location of level and type of bony involvement on spinal x-ray. Injury, edema, compression on CT scan and MRI; positive finding on myelogram

Nursing Diagnoses

Nursing diagnoses for the patient with SCI depend on the severity of the injury and level of dysfunction. Nursing diagnoses for a patient with SCI may include: • Impaired breathing • Impaired nutritional status • Ineffective tissue perfusion • Impaired tissue integrity • Impaired urinary system function • Constipation • Difficulty coping Additional information on nursing diagnoses and interventions for the patient with complete cervical SCI is presented in eNursing Care Plan 60.1 (available on the website for this chapter).

Planning Overall goals are that the patient with an SCI will (1) maintain an optimal level of neurologic functioning; (2) have minimal or no complications of immobility; (3) learn new skills, gain new knowledge, and acquire new behaviors to be able to care for self or direct others to do so; and (4) return home at an optimal level of functioning.

Nursing Implementation Health Promotion Nursing interventions for the prevention of SCI include identifying high-risk persons and providing teaching. Support measures to combat distracted and impaired driving. Teach people to use child safety seats and helmets for motorcyclists and bicyclists. Promote programs for older adults (e.g., STEADI) aimed at preventing accidental death and injury.15 Emphasize the importance of health promotion and screening

behaviors after SCI. Health-promoting behaviors after SCI can have significant impact on the general health and well-being of the person with SCI. Nursing interventions include (1) teaching and counseling; (2) referring to programs such as smoking cessation classes, recreation programs, and alcohol treatment programs; and (3) performing routine physical examinations for non-neurologic problems. Promotion and screening programs must be accessible to and accommodate people with SCI. Nurses should advocate for wheelchair-accessible examination rooms, adjustable-height examination tables, and appointment scheduling that allows extra time if needed.

Acute Care High cervical cord injury caused by flexion-rotation is the most complex SCI. It is the focus of this section. Interventions for this type of injury can be modified for patients with less severe injuries.

Immobilization To restrict spinal motion, maintain the neck in a neutral position. For cervical injuries, closed reduction with skeletal traction is used for early realignment (reduction) of the injury. Crutchfield (Fig. 60.6) or Gardner-Wells tongs or halo (halo ring) can provide this type of traction. A rope extends from the center of the device over a pulley to weights attached at the end. Traction must be maintained at all times. Possible displacement of the skull pins is a disadvantage of tongs. If pin displacement occurs, hold the patient’s head in a neutral position and get help. Immobilize the head while the HCP reinserts the tongs.

Safety Alert Cervical Spine Injuries • Always keep the patient’s body in correct alignment.

• Turn the patient as a unit (e.g., logrolling) to prevent movement of the spine. No specific guidelines address the maximum weight for traction. The HCP may start with 10 lb and add 5 lb for each level to the injury. The goal is spinal reduction. Awake patients are monitored with x-ray and neurologic and pain assessment. Comatose patients need serial xrays to evaluate the effects of traction. The need for surgery is determined after the spine is reduced. After cervical fusion or other stabilization surgery, the patient may have a hard cervical collar or sternal-occipital-mandibular immobilizer brace (Fig. 60.7). Some patients with spinal fractures with or without acute SCI may not be able to have surgery but still need immobilization for their cervical fracture. In these patients, the halo frame can be attached to a special vest (Halo vest) (Fig. 60.8). This allows the patient to move and ambulate while cervical bones fuse. Surgery is used instead of the halo if the patient has ligament instability from the injury; has severe cervical deformity; or is morbidly obese, older, cachectic, or noncompliant. Infection at the tong or pin insertion sites is a potential problem. Preventive care is based on agency protocol. A common protocol involves cleansing sites twice a day with chlorhexidine. Antibiotic ointment is then applied to act as a mechanical barrier to the entrance of bacteria. Patient and caregiver teaching for a patient with a halo vest is outlined in Table 60.6. Patients with stable thoracic or lumbar spine injuries may be immobilized with a custom thoracolumbar sacral orthosis (TLSO or body jacket) to limit spinal flexion, extension, and rotation. A Jewett brace may be used instead to restrict forward flexion. Unstable injuries may require surgical decompression and fusion in addition to the TLSO or lumbosacral orthotic (LSO).

FIG. 60.6 Cervical traction is attached to tongs inserted in the skull. Courtesy Michael S. Clement, MD, Mesa, AZ.

FIG. 60.7 Sternal-occipital-mandibular immobilizer brace.

FIG. 60.8 Halo vest. The halo traction brace immobilizes the cervical spine, which allows the patient to ambulate and take part in self-care. Modified from Urden LD, Stacy KM, Lough ME: Priorities in critical care nursing, ed 6, St Louis, 2012, Mosby.

TABLE 60.6 Patient & Caregiver TeachingHalo

Vest Care

Include the following instructions when teaching the patient and caregiver management of a halo vest: 1. Inspect the pins on the halo traction ring. Report to HCP if pins are loose or signs of infection are present, including redness, tenderness, swelling, or drainage at insertion sites. 2. Clean around pin sites carefully with chlorhexidine, water, or half-strength peroxide on a cotton swab as directed. 3. Apply antibiotic ointment as prescribed. 4. For skin care, have patient lie down with the head resting on a pillow to reduce pressure on the brace. Loosen 1 side of the vest. Gently wash the skin under the vest with soap and water, rinse area, and then dry it thoroughly. At the same time, check the skin for pressure points, redness, swelling, bruising, or chafing. Close the open side and repeat the procedure on the other side. 5. If the vest becomes wet or damp, carefully dry it with a blow dryer. 6. Encourage patient to use assistive device (e.g., cane, walker) to improve balance; encourage use of flat shoes. 7. Teach patient to turn the entire body, not just the head and neck, when trying to look sideways. 8. In case of an emergency, always keep a set of wrenches close to the halo vest. 9. Mark the vest strap to maintain consistent buckling and fit. 10. Avoid grabbing bars or vest to help the patient. 11. Keep sheepskin pad under vest. Change and wash pad at least weekly. 12. If perspiration or itching is a problem, encourage patient to wear a cotton T-shirt under the sheepskin. The T-shirt can be modified with a Velcro seam closure on one side. The effects of immobility can be great. Thorough skin care is important because decreased sensation and circulation increase the risk for skin breakdown. Remove the patient’s backboard as soon as

possible. Replace it with other forms of immobilization to prevent skin breakdown in the coccygeal and occipital areas. Fit cervical collars properly. Carefully assess areas under any device used for immobilization. We often place patients on special beds (Fig. 60.9). Kinetic therapy involves continuous side-to-side rotation of a patient to 40 degrees or more to help prevent lung complications. This lateral rotation also redistributes pressure, helping prevent pressure injuries.

FIG. 60.9 The RotoRest Therapy System helps prevent and treat lung

complications for immobile patients, including those with unstable cervical, thoracic, and lumbar fractures. Kinetic therapy, the continual side-to-side bilateral rotation of the patient, redistributes pulmonary blood flow and mobilizes secretions to improve ventilation and perfusion matching. The therapy system helps to prevent pressure injuries. Courtesy Arjo Huntleigh, Addison, IL.

Respiratory Dysfunction Respiratory complications are the leading acute and chronic causes of morbidity and mortality in SCI.16 Respiratory dysfunction is present in up to 65% of patients with cervical SCI. During the first 48 hours after injury, spinal cord edema may increase the level of dysfunction, and respiratory distress may occur. Injury at or above C4 affects the phrenic nerve, which leads to the diaphragm, and breathing can stop. Monitor the patient carefully for respiratory compromise and be prepared for quick action if arrest occurs. Regularly assess (1) breath sounds, (2) arterial blood gases (ABGs), (3) tidal volume, (4) vital capacity, (5) skin color, (6) breathing patterns (especially use of accessory muscles), (7) subjective comments about the ability to breathe, and (8) amount and color of sputum. A PaO2 greater than 60 mm Hg and a PaCO2 less than 45 mm Hg are acceptable values in a patient with uncomplicated tetraplegia. A patient who is unable to count to 20 aloud without taking a breath needs immediate attention. In addition to ongoing assessment, intervene to maintain ventilation. Apply O2 and provide appropriate ventilatory support until ABGs stabilize. If the patient is exhausted from labored breathing or ABGs show inadequate oxygenation or ventilation, endotracheal intubation or tracheostomy and mechanical ventilation is needed. Patients who have chest trauma or difficulty weaning from the ventilator may need a tracheostomy for airway management. Clearing secretions is vital in reducing the risk for lung complications and possible respiratory failure.16 Perform tracheal suctioning if crackles or coarse breath sounds are present. Chest physiotherapy and assisted (augmented) coughing can help. Perform assisted coughing either manually, by placing the heels of both hands

just below the xiphoid process and exert firm upward pressure to the area timed with the patient’s efforts to cough (see Fig. 67.6), or mechanically with an insufflation-exsufflation device. Encourage the use of incentive spirometry. The older adult has more difficulty responding to hypoxia and hypercapnia. Thus aggressive chest physiotherapy, adequate oxygenation, and proper pain management are essential to maximize respiratory function and gas exchange.

Cardiovascular Instability Heart rate is slowed, often to less than 60 beats/min, because of unopposed vagal response. Any increase in vagal stimulation, as occurs with turning or suctioning, can cause cardiac arrest. Loss of SNS tone in peripheral vessels results in chronic low BP with potential orthostatic hypotension. The lack of muscle tone to aid venous return can cause sluggish blood flow and predispose the patient to VTE. Dysrhythmias may occur. Frequently assess vital signs. If bradycardia is symptomatic, give an anticholinergic drug, such as atropine. A temporary or permanent pacemaker may be inserted in some patients. Maintain SBP greater than 90 mm Hg and keep MAP between 85 and 90 mm Hg for the first 7 days after SCI. Manage hypotension with fluid replacement and a vasopressor agent, such as phenylephrine or norepinephrine. Maintain a normal blood volume. If blood loss has occurred from other injuries, monitor hemoglobin and hematocrit and give blood according to protocol. Assess the patient for signs of hypovolemic shock from hemorrhage. Orthostatic hypotension is likely to occur in the patient with injury at T6 and above. The patient may have light headedness, dizziness, and nausea. Assess orthostatic BP when mobilizing the patient. Some lose consciousness when moved from the bed to a chair. For symptomatic patients, use an abdominal binder and graduated compression stockings to promote venous return. Drugs used to increase intravascular volume include salt tablets and fludrocortisone. Midodrine may be given to promote blood vessel contraction and

increase venous return. Consider the effects of aging on the cardiovascular system of the older adult. The older patient is less able to manage the stress of traumatic injury because heart contractions weaken, and cardiac output is reduced. Maximum heart rate is reduced. The older adult may also have cardiovascular disease. Use LMWH or low-dose heparin in combination with intermittent pneumatic compression devices or graduated compression stockings to promote venous return and reduce the risk for VTE. Remove stockings every 8 hours for skin care. Assess thighs and calves every shift for signs of VTE. Regularly perform range-of-motion (ROM) exercises and stretching. Continue VTE prophylaxis for 3 months after injury.

Fluid and Nutritional Management During the first 48 to 72 hours after the injury, the GI tract may stop functioning (paralytic ileus). A nasogastric (NG) tube must be inserted if ileus occurs. Because the patient cannot have oral intake, monitor fluid and electrolyte status. Nutrition should be started within the first 72 hours after injury. Specific solutions and additives are determined by individual requirements. Due to severe catabolism, a high-protein, high-calorie diet is needed for energy and tissue repair. If the patient cannot be fed through the GI system, either orally or through EN, PN should be started to reduce nitrogen losses that occur during the hypermetabolic state. Once bowel sounds are present or flatus is passed, and the patient is not receiving mechanical ventilation, a formal swallow evaluation is done. If no risk for aspiration is identified, gradually introduce oral food and fluids. If the patient fails the swallow evaluation or is unable to eat due to an endotracheal tube or tracheostomy, a more secure feeding tube may be placed in the stomach or jejunum (see Chapter 39).

Check Your Practice You are working in the spinal cord unit. Your 28-yr-old male patient with SCI at T6 weighs 168 lb. When he was admitted 3 weeks ago he weighed 186 lb. He asks you, “Well, what is my weight? Are you gonna make me eat now? You know you can’t do that.” • What assessment data are important for you to obtain? • What interventions would help him avoid further weight loss and regain lean body mass? Patients may have anorexia due to depression, boredom with agency food, or discomfort at being fed (often by a hurried person). Some patients have a normally small appetite. Sometimes refusal to eat is a way of asserting control. If the patient is not eating adequately, assess the cause. Based on assessment findings, make a contract with the patient with mutual goal setting for the diet. This contract gives the patient increased control and often results in improved nutritional intake. General measures also may be effective. For example, provide a pleasant eating environment, allow adequate time to eat (including any self-feeding the patient can achieve), encourage the family to bring in special foods, and plan social rewards for eating. Consult a dietitian to ensure evaluation of the appropriate laboratory markers and develop the treatment plan. Keep a calorie count and record the patient’s daily weight to evaluate progress. If possible, the patient should take part in recording calorie intake. Dietary supplements may be needed to meet nutritional goals. Include increased dietary fiber to promote bowel function.

Bladder and Bowel Management Immediately after the injury, urine retention occurs because of the loss of autonomic and reflex control of the bladder and sphincter (neurogenic bladder). Because there is no sensation of fullness,

overdistention of the bladder can result in reflux into the kidney and cause renal failure. Bladder overdistention may even result in rupture of the bladder. Thus an indwelling catheter may be inserted soon after injury. Ensure patency of the catheter by frequent inspection and irrigation, if needed. In some agencies, an HCP’s order is required for this procedure. Strict aseptic technique for catheter care is essential to prevent infection. During the period of indwelling catheterization, encourage a large fluid intake. Check the catheter to prevent kinking and ensure free flow of urine. Catheter-acquired urinary tract infection (CAUTI) is a common problem. The best way to prevent CAUTI is regular and complete bladder drainage. Once the patient is stabilized, assess the best means of managing long-term urinary function. Clean intermittent catheterization (CIC) is the preferred method for emptying the bladder. CAUTI and CIC are discussed in Chapter 45. CIC should be done 4 to 6 times daily to prevent bacterial overgrowth from urinary stasis. Keep urine residuals under 500 mL to prevent bladder distention. If the urine is cloudy or has a strong odor or if the patient develops symptoms of a urinary tract infection (UTI) (e.g., chills, fever, malaise), send a specimen for culture. Consider age-related changes in renal function. The older adult is more likely to develop renal stones. Older men may have benign prostatic hyperplasia, which may interfere with urinary flow and complicate management of urinary problems. It can affect the ability to complete CIC. Start a bowel program to combat constipation from neurogenic bowel. This involves inserting a rectal stimulant (suppository or small-volume enema) daily at a regular time, followed by gentle digital stimulation or manual evacuation until evacuation is complete. At first, the program may be done in bed with the patient in the sidelying position. However, as soon as the patient has resumed sitting, the patient should be in the upright position on a padded bedside commode chair. These programs typically take 30 to 60 minutes to complete. Measures to reduce constipation include adequate fluid intake, a diet high in fiber and vegetables, and increased activity and

exercise.

Temperature Control Monitor the environment closely to maintain an appropriate temperature. Regularly assess the patient’s body temperature. Do not use excess covers or unduly expose the patient (e.g., during bathing). If an infection with high fever develops, more aggressive methods for temperature control may be needed (e.g., a cooling blanket).

Stress Ulcers Stress ulcers can occur in the patient with SCI because of the physiologic response to severe trauma and psychologic stress. Peak incidence of stress ulcers is 6 to 14 days after injury. Test stool and gastric contents daily for blood. Monitor the hematocrit for a slow drop. Histamine (H2)-receptor blockers (e.g., ranitidine) or proton pump inhibitors (e.g., pantoprazole, omeprazole) given prophylactically decreases the secretion of HCl acid and prevents ulcers.

Sensory Deprivation To prevent sensory deprivation, compensate for the patient’s absent sensations by stimulating the patient above the level of injury. Conversation, music, and interesting foods can be a part of the nursing care plan. If the head of the bed must stay flat, provide prism glasses to help the patient read and watch television. Help the patient avoid withdrawing from the environment. Promote adequate rest and sleep. Assess for changes in mood. Depression is common (discussed later in chapter on p. 1418).

Pain Management Musculoskeletal nociceptive pain can develop from injuries to bones, muscles, and ligaments. The pain is worse with movement or palpation. Antiinflammatory drugs, such as ibuprofen (Motrin), may help with pain. Opioids may be used to manage nociceptive pain.

Visceral nociceptive pain is a dull, tender, or cramping pain in the thorax, abdomen, or pelvis. It may originate in the bladder or bowel. Assess the patient’s bowel and bladder function to avoid bladder distention or constipation. Other causes of nociceptive pain include UTI and renal stones. Notify the HCP if the patient has persistent pain despite treatment. Diagnostic imaging may be needed to determine the cause. Neuropathic pain in the initial phase is usually at the level of SCI. It may occur on 1 or both sides of the body within the affected dermatome and up to 3 levels below. The patient will describe hot, burning, tingling, shooting, electric pain. Pregabalin (Lyrica) is used to reduce symptoms. Neuropathic pain can occur months or years after SCI, become chronic, and negatively affect sleep. The patient’s mood, sudden noise, constipation, and infection can affect the pain. Teach the patient and caregiver about possible pain triggers and offer relaxation therapy. Other modes of treatment may include tricyclic antidepressants, intrathecal drugs, antiseizure drugs, epidural stimulation, and destructive surgical intervention.

Skin Care The most common long-term complication in SCI is pressure injury (PI) formation. Healthy skin requires adequate blood circulation. Constant pressure in 1 position can compress blood vessels and limit blood supply, causing cell death and PI. Little evidence addresses interventions for prevention and treatment of PI in SCI.17 Factors associated with increased risk for PI formation include heart and renal disease, smoking, alcohol or drug use, diabetes, hypoxia, hypotension, and pneumonia, UTI, and other infections.18 Prevention of PI requires diligent nursing care. Perform a risk assessment for PI formation with a daily comprehensive visual and tactile examination of the skin. Areas most vulnerable to breakdown include the sacrum, ischia, trochanters, and heels. Assess surgical incisions for healing and skin integrity under collars and braces. Regularly assess nutritional status. Both weight loss and gain can

contribute to skin breakdown. Teach the patient and caregiver about the causes and risk factors for PI development.19 A consult with the wound, ostomy, continence nurse (WOCN) can assist with prevention and management strategies (e.g., surface overlays).19 Monitor incontinence and implement appropriate neurogenic bowel and bladder management interventions. Apply skin barrier creams. Carefully position and reposition the patient at least every 2 hours. Gradually increase the times between turns if no redness over bony prominences is seen when turning. While the patient is supine in bed, float the heels to reduce pressure. Consider prophylactic dressings to prevent sacral and heel wounds. Move the patient carefully during turns and transfers to avoid stretching and folding of soft tissues (shear) or abrasion. Many patients are placed on specialty mattresses.17 When the patient is moved to a chair or wheelchair, use pressure-relieving cushions. Pressure relief should be scheduled every 15 to 20 minutes when the patient is in a chair and should last 30 to 60 seconds each time.

Reflexes Once spinal cord shock is resolved, return of reflexes may complicate rehabilitation. Lacking control from the higher brain centers, reflexes are often hyperactive and have exaggerated responses. Penile erection can occur from a variety of stimuli, causing embarrassment and discomfort. Spasms ranging from mild twitches to convulsive movements below the level of injury may occur. The patient or caregiver may interpret this reflex activity as a return of function. Tactfully explain the reason for the activity. Tell the patient of the positive use of these reflexes in sexual, bowel, and bladder retraining. Antispasmodic drugs, such as baclofen (Lioresal), dantrolene (Dantrium), and tizanidine (Zanaflex), may help control spasms. Botulism toxin injections may be given to treat severe spasticity.

Autonomic Dysreflexia

The return of reflexes after the resolution of spinal shock means patients with injury at T6 or higher may develop autonomic dysreflexia. Autonomic dysreflexia (AD) is a massive, uncompensated cardiovascular reaction mediated by the SNS. It involves stimulation of sensory receptors below the level of the SCI. The intact SNS below the level of injury responds to the stimulation with a reflex arteriolar vasoconstriction that increases BP. The parasympathetic nervous system is unable to directly counteract these responses via the injured spinal cord. Baroreceptors in the carotid sinus and aorta sense the hypertension and stimulate the parasympathetic system. This causes a decrease in heart rate. Visceral and peripheral vessels do not dilate because efferent impulses cannot pass through the injured spinal cord. It most often presents in the chronic phase after SCI.20 The most common precipitating cause of AD is a distended bladder or rectum. However, any sensory stimulation, including contraction of the bladder or rectum, stimulation of the skin, or stimulation of pain receptors can cause AD. AD is a life-threatening condition that requires immediate resolution. Proper identification and elimination of the inciting stimulus for AD can resolve the event. If uncorrected, it can lead to status epilepticus, stroke, myocardial infarction, and even death. Manifestations include hypertension, throbbing headache, marked diaphoresis above the level of injury, bradycardia (30 to 40 beats/min), piloerection from pilomotor spasm, flushing of the skin above the level of injury, blurred vision or spots in the visual fields, nasal congestion, anxiety, and nausea. Measure BP when a patient with SCI reports a headache. Suspect AD in adults with SBP elevation of 20 to 40 mm Hg above baseline.20 Immediate nursing interventions include elevating the head of the bed 45 degrees or sitting the patient upright (to lower the BP) and determining the cause (bowel impaction, urinary retention, UTI, PI, tight clothing). Notify the HCP. The most common cause is bladder irritation. Immediate catheterization to relieve bladder distention may be needed. Instill lidocaine jelly in the urethra before catheterization.

If a catheter is already in place, check it for kinks or folds. If it is plugged, perform small-volume irrigation slowly and gently to open the catheter or insert a new catheter. Stool impaction can cause AD. Apply an anesthetic ointment to avoid increasing symptoms, then perform a digital rectal examination (if trained). Remove all skin stimuli, such as constrictive clothing and tight shoes. Monitor BP often during the episode. If symptoms persist after the source has been relieved, give a rapid-onset and shortduration agent, such as nitroglycerin, nitroprusside, or hydralazine. Continue careful monitoring until vital signs stabilize. Teach the patient and caregiver to recognize causes and symptoms of AD (Table 60.7). They must understand the life-threatening nature of AD, know how to relieve the cause, and activate the ERS, if needed.

Rehabilitation and Home Care Rehabilitation of the person with SCI is complex. With physical and psychologic care and intensive and specialized rehabilitation, the patient with SCI can learn to function at the highest level of wellness. All patients with a new SCI should receive comprehensive inpatient rehabilitation in a rehabilitation unit or center that specializes in SCI rehabilitation.2 Rehabilitation is an interprofessional team effort. Team members include rehabilitation nurses, HCPs, physical therapists, occupational therapists, speech therapists, vocational counselors, psychologists, therapeutic recreation specialists, prosthetists, orthotists, case managers, social workers, and dietitians.

TABLE 60.7 Patient & Caregiver

TeachingAutonomic Dysreflexia For a patient at risk for autonomic dysreflexia, include the following information in the teaching plan for the patient and caregiver: 1. Signs and symptoms • Sudden onset of acute headache.

• Elevation in BP and/or reduction in pulse rate. • Flushed face and upper chest (above level of injury) and pale extremities (below level of injury). • Sweating above level of injury. • Nasal congestion. • Feeling of apprehension. • Immediate interventions. • Raise the person to a sitting position. • Remove the noxious stimulus (fecal impaction, kinked urinary catheter, tight clothing). • Call the HCP if above actions do not relieve the signs and symptoms. 2. Measures to decrease the incidence of autonomic dysreflexia • Maintain regular bowel function. • If manual rectal stimulation is used to promote bowel function, use a local anesthetic to prevent autonomic dysreflexia. • Monitor urine output. • Teach the patient to wear a Medic Alert bracelet indicating a history of risk for autonomic dysreflexia. Many of the problems that begin in the acute period become chronic and continue throughout life. Rehabilitation focuses on retraining physiologic processes as well as extensive patient and caregiver teaching about how to manage the physiologic and life changes resulting from the injury (Fig. 60.10). Rehabilitation care is organized around the patient’s goals and needs. The patient is expected to be involved in therapies and learn self-care for several hours each day. Such intensive work at a time when the patient is dealing with the sudden change in health and function can be stressful. Progress may be slow. The rehabilitation nurse has a key role in providing encouragement, specialized nursing care, and patient and caregiver teaching and in helping to coordinate efforts of the rehabilitation team.

Respiratory Rehabilitation The patient with mechanical ventilation will need around-the-clock caregivers who are knowledgeable about respiratory hygiene and tracheostomy care. The rehabilitation nurse and respiratory therapist should teach patients and caregivers about home ventilator and tracheostomy care. The patient may need chest percussion or postural drainage to manage secretions to lower the risk for atelectasis and pneumonia. Refer to appropriate community agencies as needed. Some patients with high cervical SCI have improved respiratory function with phrenic nerve stimulators or electronic diaphragmatic pacemakers.21 These devices are not appropriate for all ventilatordependent patients but are safe and effective for those with an intact phrenic nerve. Some ventilators are portable, allowing ventilatordependent patients with tetraplegia to be mobile and less dependent. If the patient was weaned from the ventilator during hospitalization, downsizing (gradual decrease in size) and removal of the tracheostomy will be done during rehabilitation. Teach assisted coughing, regular use of incentive spirometry, and breathing exercises to the patient who is not ventilator dependent. They should limit exposure to persons with fever, cold, and cough. Adhering to swallowing precautions (e.g., proper positioning of head and neck) and diet recommendations can prevent aspiration.

FIG. 60.10 A spinal cord injury has a major effect on a person’s physical, emotional, and psychologic health.

TABLE 60.8 Types of Neurogenic Bladder

Neurogenic Bladder Types of neurogenic bladder are described in Table 60.8. The type of bladder dysfunction determines management options. After the patient’s overall condition is stable and assessment shows return of neurologic reflexes, urodynamic testing (see Table 44.11) and a urine culture may be done. Diagnostic and interprofessional care of neurogenic bladder is described in Table 60.9. The patient with SCI and a neurogenic bladder needs a comprehensive program to manage bladder function. The goal is to improve quality of life and safety through preserving renal function, minimizing UTI and bladder stones, and developing a plan for urinary continence. Many factors are considered when selecting a bladder management strategy. These include patient preference, upper extremity function, and caregiver availability. For the selected strategy, teach the patient and caregiver successful self-management. Teach them about the various management techniques, how to obtain supplies, care of supplies and equipment, and when to seek health care. Various drugs can be used to treat patients with a neurogenic bladder. Anticholinergic drugs (e.g., oxybutynin, tolterodine [Detrol]) may be used to suppress bladder contraction. α-Adrenergic blockers (e.g., terazosin, doxazosin [Cardura]) can relax the urethral sphincter. Antispasmodic drugs (e.g., baclofen) may decrease spasticity of pelvic

floor muscles. Botulinum toxin is an effective alternative in patients with neurogenic detrusor overactivity who cannot tolerate or had an inadequate response to anticholinergic drugs.22 Numerous drainage methods are possible. These include bladder reflex retraining (if partial voiding control remains), indwelling catheter, CIC, and external catheter (condom catheter). Evaluate longterm use of an indwelling catheter because of the associated high incidence of CAUTI, fistula formation, and diverticula. However, this is the best option for some patients. Patients with indwelling catheters need to have adequate fluid intake (at least 3 to 4 L/day). Regularly check the patency of the indwelling catheter. Frequency of routine catheter changes ranges widely depending on the type of catheter used and agency policy.

TABLE 60.9  Interprofessional CareNeurogenic

Bladder

Diagnostic Assessment • History and physical examination, including neurologic and pelvic examinations • Laboratory: Urinalysis, urine culture and sensitivity, blood urea nitrogen, serum creatinine, creatinine clearance • Urodynamic testing (postvoid residual, cystometric testing, EMG, urethral pressure profile)

Management • Patient teaching • Voiding diary • Bladder retraining: time voiding, manual expression, intermittent catheterization

• Fluid schedule: intake of 1800–2000 mL/day • Indwelling urinary catheter

Drug Therapy • Tricyclic antidepressants • Anticholinergic drugs • α-Adrenergic blockers • Antispasmodics • Botulinum toxin injection into bladder wall

Bladder and/or Urethral Surgical Therapy • Bladder augmentation • Sphincter resection or removal (sphincterotomy) • Electrode placement for electrical stimulation • Urinary diversion • Urethral stents and balloon dilation • Artificial urinary sphincter CIC is recommended as the first-line option for bladder management (see Chapter 45). Nursing assessment is important in selecting the time interval between catheterizations. At first, catheterization is done every 4 hours. Measure bladder volume before catheterization using a bladder ultrasound machine. If less than 200 mL of urine is present, the time interval until catheterization may be extended. If more than 500 mL of urine is present, the time interval is shortened. CIC is usually done 4 to 6 times daily.

TABLE 60.10 Patient & Caregiver TeachingBowel

Management After Spinal Cord Injury For the patient with a spinal cord injury, include the following information about bowel management in the teaching plan for the patient and caregiver: 1. Optimal nutritional intake includes the following: • 3 well-balanced meals each day • 2 servings from the milk group • 2 or more servings from the meat group, including beef, pork, poultry, eggs, fish • 4 or more servings from the vegetable and fruit groups • 4 or more servings from the bread and cereal group 2. Fiber intake should be about 20–30 g/day. Increase the amount of fiber eaten gradually over 1–2 wk. 3. Consume at least 2–3 L of fluid per day unless contraindicated. Drink water or fruit juices (fluid softens hard stools). Limit caffeinated beverages, such as coffee, tea, and cola (caffeine stimulates fluid loss through urination). 4. Avoid foods that produce gas (e.g., beans) or upper GI upset (e.g., spicy foods). 5. Timing: Follow a regular schedule for bowel elimination. A good time is 30 min after the first meal of the day. 6. Position: If possible, an upright position with feet flat on the floor or on a step stool enhances bowel evacuation. Staying on the toilet, commode, or bedpan for longer than 20–30 min may cause skin breakdown. Based on stability, someone may need to stay with the patient. 7. Activity: Exercise is important for bowel function. In addition to improving muscle tone, it increases appetite and GI transit time. Exercise muscles, including stretching, ROM, position changing, and functional movement. 8. Drug treatment: Suppositories may be needed to stimulate a bowel movement. Manual stimulation of the rectum may be helpful in starting defecation. Use stool softeners as needed to regulate stool consistency. Use oral laxatives only if necessary.

Suprapubic catheters are a safe option in select patients. Because of personal preference or the inability to catheterize due to neurologic dysfunction, 30% of patients with SCI use indwelling urethral or suprapubic catheters. The incidence of bacteriuria after catheter introduction is 5% to 10% per day. Traditional bladder management options include urinary diversion surgery for the recurrent UTI patient with renal involvement or repeated stones. Surgical treatment of neurogenic bladder includes bladder neck revision (sphincterotomy), bladder augmentation (augmentation cystoplasty), perineal ureterostomy, cystotomy, vesicostomy, and anterior urethral transplantation. Placement of a sacral cord stimulator, penile prosthesis, or artificial sphincter is possible. Urinary diversion procedures are discussed in Chapter 45.

Neurogenic Bowel Careful management of bowel evacuation is necessary in the patient with SCI because voluntary control may be lost. Usual measures for preventing constipation include high-fiber diet and adequate fluid intake (see Table 42.10). Patient and caregiver teaching is needed to promote successful independent bowel management. Guidelines related to bowel management are outlined in Table 60.10. These measures may not be adequate to stimulate evacuation. Suppositories (e.g., bisacodyl [Dulcolax], glycerin) or small-volume enemas and digital stimulation (done 20 to 30 minutes after suppository insertion) by the nurse or patient may be needed. In the patient with an upper motor neuron injury, digital stimulation can relax the external sphincter to promote defecation. A stool softener, such as docusate sodium (Colace), can help regulate stool consistency. Oral stimulant laxatives should be used only if absolutely necessary and not on a regular basis. Valsalva maneuver and manual stimulation are useful in patients with lower motor neuron injuries. Because the Valsalva maneuver requires intact abdominal muscles, it is used in patients with injuries below T12. In general, a bowel movement every other day is considered adequate. However, consider preinjury patterns. Fecal

incontinence can result from too much stool softener or a fecal impaction. Timing of defecation is important. Planning bowel evacuation for 30 to 60 minutes after the first meal of the day may enhance success by taking advantage of the gastrocolic reflex induced by eating. This reflex may also be stimulated by drinking a warm beverage right after the meal. Discuss timing of the bowel program among the interprofessional team so there are no interruptions when the patient is doing therapy (e.g., swimming pool therapy). Record all bowel movements, including amount, time, and consistency. Consider using the International Spinal Cord Injury Bowel Function Data Set. This is a 16-item, comprehensive, standardized format for assessing bowel function in the patient with SCI.23

Spasticity Spasticity can be both beneficial and undesirable. It aids with mobility, especially for the patient with incomplete SCI. Spasticity improves circulation by promoting venous return, decreasing orthostatic hypotension and the risk for VTE. Unfortunately, the patient with marked spasticity and tone may have difficulty with positioning and mobility from spasms. Spasms can cause significant pain and make activities of daily living (ADLs) difficult for the patient. The Ashworth and Modified Ashworth Scales are used to evaluate spasticity. Treatment includes ROM exercises to prevent muscle and joint tightness and reduce the risk for contracture. Antispasmodic drugs, such as baclofen or tizanidine, may be given. Botulinum toxin injection is useful for specific muscle involvement.

Skin Care Prevention of PI is part of the lifelong treatment plan after SCI. Nurses in rehabilitation are responsible for teaching the patient and caregiver about daily skin care. PI may not be noticed until severe damage has occurred. Include information on the importance of adequate

nutrition to skin condition. Anticipatory guidance about potential risks is essential. Patient and caregiver teaching related to skin care is outlined in Table 60.11.

Pain Management The acute pain of the initial injury may persist during the first few weeks of rehabilitation. Chronic pain can result from overuse of muscles in the shoulders and arms for movement and repositioning. Pain often disrupts sleep. Assess, evaluate, and treat pain routinely. Use analgesics and interventions, such as massage and repositioning, to help the patient during therapy. Patients may benefit from referral to a pain management specialist.

Sexuality Sexuality is an important issue regardless of the patient’s age or sex. Open discussion with the patient about sexual rehabilitation is essential. A nurse or other rehabilitation professional trained in sexual counseling should provide support for the patient and the partner. Alternative methods of obtaining sexual satisfaction, such as oralgenital sex, may be suggested. Explicit films may help, such as a film showing sexual activities of a patient with paraplegia and a nondisabled partner. Use graphics cautiously because they may focus too much on the mechanics of sex rather than on the relationship.

TABLE 60.11 Patient & Caregiver TeachingSkin

Care After Spinal Cord Injury To prevent skin breakdown in a patient with spinal cord injury, include the following instructions when teaching the patient and caregiver:

Change Position Frequently • If in a wheelchair, lift self and shift weight every 15–30 min. • If in bed, change position with a regular turning schedule (at least

every 2 hr) that includes sides, back, and abdomen. • Use pressure-reducing mattresses and wheelchair cushions (not eggcrate). • Use pillows to protect bony prominences when in bed.

Monitor Skin Condition • Inspect skin often for areas of redness, swelling, and breakdown. • If a wound develops, follow standard wound care procedures.

Protect Skin • Do not sit too close to fires, space heaters, or other sources of heat. • Use sunscreen liberally when outdoors. • Keep fingernails trimmed to avoid scratches and abrasions. • Do not wear clothes that are too tight or too loose. • Dress warmly in cold weather to prevent frostbite. • Do not put hot foot in your lap without protection. Knowledge of the level and completeness of injury is needed to understand the male patient’s potential for orgasm, erection, and fertility, and the patient’s capacity for sexual satisfaction. Men normally have 2 types of erections: psychogenic and reflex. The process of psychogenic erection begins in the brain with sexual thoughts. Signals from the brain are sent through the nerves of the spinal cord to the T10-L2 levels. The signals are then relayed to the penis and trigger an erection. Men with low-level incomplete injuries are more likely to have psychogenic erection than men with higher level incomplete injuries. Men with complete injuries are less likely to have psychogenic erection.24 A reflex erection occurs with direct physical contact to the penis or

other erotic areas. This short lived, uncontrolled, erection is involuntary and does not require sexually stimulating thoughts. Most men with SCI can have a reflex erection with physical stimulation if the S2-S4 nerve pathways are not damaged. Treatment for erectile dysfunction includes drugs, vacuum devices, and surgical procedures. Phosphodiesterase inhibitors (e.g., sildenafil [Viagra]) have become the first-line treatment in men with SCI between T6 and L5. Sexual stimulation is needed to get an erection after taking the medication. Penile injection of vasoactive substances (papaverine, alprostadil, or a combination) is another medical treatment. Risks include scarring, bruising, and infection. Use may lead to priapism. Vacuum suction devices use negative pressure to encourage blood flow into the penis. Erection is maintained by a constriction band placed at the base of the penis. The main surgical option is implantation of a penile prosthesis.24 (Erectile dysfunction is discussed in Chapter 54.) SCI affects male fertility, causing poor sperm motility and ejaculatory dysfunction. Recent advances in methods of sperm retrieval include penile vibratory stimulation and rectal probe electroejaculation. Surgical removal of sperm is a last resort for sperm retrieval. Once retrieved, sperm can be directly injected into an egg via intracytoplasmic sperm injection (ICSI). These techniques have changed the prognosis for men with SCI to father children from unlikely to a reasonable chance of successful outcomes.24 The effect of SCI on female sexual response is less clear. A woman of childbearing age with SCI usually stays fertile. The injury does not affect the ability to become pregnant or deliver normally through the birth canal. Menses may cease for as long as 6 months after injury. If sexual activity is resumed, protection against unplanned pregnancy is needed. Pregnancy is associated with increased risk for diabetes and UTI and higher rates of AD, PI, increased spasticity, and catheterrelated issues. Labor and delivery have high rates of complications.25 Care should be taken not to dislodge an indwelling catheter during sexual activity. A patient with an external catheter should refrain from fluids and remove the catheter before sexual activity. Teach patients

about the risk for AD. The bowel program should include evacuation the morning of sexual activity. Encourage the patient to tell the partner that incontinence is always possible. The woman may need a water-soluble lubricant to supplement decreased vaginal secretions and ease vaginal penetration. Women with some residual pelvic innervation can achieve normal orgasm. Use of the Eros device may help with orgasmic dysfunction.25

Grief and Depression Depression after SCI is common and disabling. Patients with SCI may feel an overwhelming sense of loss. They may temporarily lose control over everyday activities as they depend on others for ADLs and for life-sustaining measures. Patients may feel they are useless and burdens to their families. At a life stage when independence is of great importance, they may be totally dependent on others. Working through grief is a hard, lifelong process for which the patient needs support and encouragement. Table 60.12 outlines the grief response to SCI and appropriate nursing interventions. Your role in grief work is to support the patient and family and to allow mourning as part of the rehabilitation process. Maintaining hope is important during the grieving process and should not be interpreted as denial. With recent advances in rehabilitation, the patient is often independent physically and discharged from the rehabilitation center before completing the grief process. The goal of recovery is related more to adjustment than to acceptance. Adjustment implies the ability to go on with living with certain limitations. Problem-based strategies are effective in supporting positive adjustment. When the patient accepts the current new normal, levels of coping and adjustment are improved. Nonacceptance is more predictive of psychologic distress, disengagement, denial, fantasy, and dependence on drugs and alcohol. When the patient is depressed, be patient. Sympathy is not helpful. Treat the patient as an adult and encourage participation in care planning.26 A primary nurse relationship is helpful. To adjust, the

patient needs continual support throughout the rehabilitation process in the form of acceptance, affection, and caring. Be attentive when the patient needs to talk and sensitive to needs at various stages of the grief process. Although depression during the grief process usually lasts days to weeks, some patients become clinically depressed and need treatment for depression. Evaluation by a psychiatric nurse or psychiatrist is recommended. Treatment may include drugs and therapy. Treatment is maximized when the patient’s personal preferences are identified, and care is tailored to patient needs.

Ethical/Legal Dilemmas Right to Refuse Treatment

Situation R.D., a 25-yr-old man, had a SCI to C7-8 after a motorcycle accident. He was diagnosed with anterior cord syndrome and has motor paralysis, which may prevent him from riding motorcycles again. He has become extremely depressed and no longer wishes to live. Because of his emotional state, R.D. is now refusing to eat. Can he be forced to receive EN?

Ethical/Legal Points for Consideration • Withholding treatment in a newly injured but otherwise healthy young adult may present an ethical dilemma for some nurses. They may consider it assisted suicide and believe that it violates the ethical principles of beneficence and nonmaleficence. • A competent adult has the right to consent to or refuse medical treatment under the right to privacy, the Fourteenth Amendment of the Constitution, and case law.∗ • Case law has supported the concept that forced treatment is battery (unlawful use of force on somebody). A mentally

competent, physically incapacitated adult can refuse EN. The health agency must follow the patient’s wishes.† • To be competent to take part in informed consent or refusal, an adult must be able to understand the information provided about the procedure or treatment, consider choices among available alternatives, and make a choice based on his values and preferences. Depression may not be a factor in determining competency to make informed treatment choices. • If, after adequate evaluation and treatment for pain, depression, or other medical conditions, the patient persists in his refusal, his wishes must be respected. • Refusal to eat or drink has never been upheld as illegal, and the alternative—forced eating and drinking—is clearly a violation of patient rights and the criminal act of battery.

Discussion Questions 1. What are your feelings about requests to withhold treatment in a young person with a newly acquired disability? 2. What resources are available to help R.D., his family, and nursing staff deal with this emotionally charged and ethically complex situation?



Cruzan v. Director, Missouri Department of Health, 497 U.S. 261, 1990. Retrieved from www.supreme.justia.com/cases/federal/us/497/261. † Bouvia v. Superior Court, 1986. Retrieved from http://law.justia.com/cases/california/calapp3d/179/1127.html. Caregivers need counseling to avoid promoting dependency in the patient through guilt or misplaced sympathy. They have intense grieving. A support group of family members and friends of patients with SCI can help them increase their participation and knowledge of

the grieving process, physical problems, rehabilitation plan, and meaning of the disability.

Evaluation Expected outcomes are that the patient with SCI will • Maintain adequate ventilation and have no signs of respiratory distress • Maintain adequate circulation and BP • Maintain intact skin over bony prominences • Maintain adequate nutrition • Establish a bowel management program based on neurologic function and personal preference • Establish a bladder management program based on neurologic function, caregiver status, and lifestyle choices • Have no episodes of AD

TABLE 60.12 Grief Response in Spinal Cord

Injury

Gerontologic Considerations: Spinal Cord Injury Because of increased work and recreational activities among older adults, more of them have SCI (Fig. 60.11). Falls are the leading cause of SCI for people age 65 and older. Older adults with traumatic injuries have more complications than younger patients, are hospitalized longer, and have higher mortality rates. Chronic illnesses associated with aging can have a serious impact on older adults living with SCI. As patients with SCI age, both individual aging changes and length of time since injury can affect functional ability. For example, bowel and bladder dysfunction can increase with the duration and severity of SCI. Health promotion and screening are important for the older patient with SCI. Daily skin inspections and UTI prevention measures are critical. Regular breast examinations for women and prostate cancer screening for men are recommended. Heart disease is the most common cause of morbidity and mortality among older adults with SCI. The lack of sensation, including chest pain, in persons with high-

level injuries may mask acute myocardial ischemia. Altered autonomic nervous system function and decreases in physical activity can place patients at risk for heart problems, including hypertension. Rehabilitation for the older adult with SCI may take longer because of preexisting conditions and poorer health status at the time of initial injury. An interprofessional approach to rehabilitation is essential in preventing secondary complications.

FIG. 60.11 An increasing number of older adults are living with a chronic spinal cord injury. © WavebreakmediaLtd/WavebreakMedia/Thinkstock.

FIG. 60.12 Types of spinal cord tumors.

Spinal Cord Tumors Spinal cord tumors can have a devastating impact due to spinal compression and neurologic dysfunction. Tumors are classified as primary (arising from some part of spinal cord, dura, nerves, or vessels) or secondary (from primary growths in other places in the body that have metastasized to the spinal cord).

Etiology and Pathophysiology Spinal cord tumors are either extradural (outside the dura), intradural-

extramedullary (between the spinal cord and dura), and intramedullary (within the substance of spinal cord itself) (Fig. 60.12 and Table 60.13). Extradural tumors include metastatic cancer and benign schwannomas. Many patients with cancer will have metastasis to the spine. Metastatic lesions can invade intradurally and compress the spinal cord. Tumors that often metastasize to the spinal epidural space are those that spread to bone, such as prostate, breast, lung, and kidney cancer. Intradural-extramedullary lesions include meningiomas that develop in the arachnoid membrane, schwannomas and neurofibromas that extend from the nerve root, and ependymomas found at the end of the spinal cord. Intramedullary tumors arise from glial or ependymal cells found throughout the entire spinal cord. The most common lesions are astrocytes and ependymomas.27 Many spinal cord tumors are slow growing. Their symptoms are due to the mechanical effects of slow compression and irritation of nerve roots, displacement of the spinal cord, or gradual obstruction of the blood supply. The slowness of growth does not cause secondary injury as in traumatic SCI. Thus complete functional restoration may be possible when the tumor is removed.

Clinical Manifestations Both sensory and motor problems may result, with the location and extent of the tumor determining the severity and extent of the problem. The most common early symptom of a spinal cord tumor is back pain or pain radiating along the compressed nerve route.28 Location of the pain depends on the level of compression. Pain may worsen with activity, coughing, straining, and/or lying down. There may be slowly increasing clumsiness, weakness, and spasticity. Paralysis can develop. Sensory disruption occurs as coldness, numbness, and tingling in 1 or more extremities. Neurogenic bowel and bladder are marked by incontinence, constipation, and urgency with difficulty in starting the flow, progressing to retention with overflow incontinence.

TABLE 60.13 Classification of Spinal Cord

Tumors

Interprofessional and Nursing Care Extradural tumors can be seen on routine spinal x-rays. Intradural extramedullary and intramedullary tumors require MRI, CT scan, or CT myelogram for detection. CSF analysis may reveal tumor cells. Patients with tumors suspicious for metastatic disease need an oncology referral and further diagnostic testing to identify the primary cancer.27 Spinal cord compression is an emergency. Relief of ischemia related to the compression is the goal of therapy. Corticosteroids (e.g., dexamethasone) are generally given immediately to relieve tumorrelated edema.29 Indications for surgery depend on the type of tumor and neurologic deficit. Emergency surgery may be needed to decompress the spinal cord, obtain tissue for biopsy, and help to determine appropriate treatment.27 Primary spinal tumors may be removed with the goal of cure. In patients with metastatic tumors, treatment is mainly palliative. The goal is to restore or preserve neurologic function, stabilize the spine, and alleviate pain. Radiation and/or chemotherapy may be used to treat the tumor.

Relieving pain and maximizing neurologic function are the ultimate goals of treatment. Assess the patient’s neurologic status before and after treatment. Giving analgesia as needed is an important nursing responsibility. Depending on the amount of neurologic dysfunction, care of the patient may be similar to that of a patient recovering from SCI.

Cranial Nerve Disorders Cranial nerve disorders are often classified as peripheral neuropathies. The 12 pairs of cranial nerves are considered the peripheral nerves of the brain. The disorders usually involve the motor and/or sensory branches of a single nerve (mononeuropathies). Causes of cranial nerve problems include tumors, trauma, infection, inflammatory processes, and idiopathic (unknown) causes. The 2 cranial nerve disorders discussed here are trigeminal neuralgia and Bell’s palsy.

Trigeminal Neuralgia Trigeminal neuralgia (TN) (tic douloureux) is characterized by sudden, usually unilateral, severe, brief, stabbing, recurrent episodes of pain in the distribution of the trigeminal nerve. It occurs in about 12 per 100,000 Americans each year. TN affects more women than men. It occurs most often in people over age 50. We classify TN as classic (TN 1) or atypical (TN 2). Patients may have both types. The pain intensity and lifestyle disruption that accompany TN can cause marked physical and psychologic dysfunction.

Etiology and Pathophysiology The trigeminal nerve, the fifth cranial nerve (CN V), has both motor and sensory branches. TN most often affects the sensory (afferent) branches of the second and third division (maxillary and mandibular branches) of CN V (Fig. 60.13).

FIG. 60.13 A, Trigeminal (fifth cranial) nerve and its 3 main divisions: ophthalmic, maxillary, and mandibular nerves. B, Cutaneous innervation of the head. Modified from Patton KT, Thibodeau GA: Anatomy and physiology, ed 8, St Louis, 2013, Mosby.

Most cases result from vascular compression of the trigeminal nerve root by an abnormal loop of the superior cerebellar artery. This artery

compresses the nerve as it exits the brainstem. Constant compression appears to lead to chronic injury, causing flattening and atrophy of the nerve and damage to the myelin sheath.30 In some cases, TN may be related to underlying pathology, such as multiple sclerosis, shingles, or masses in the cerebellum or brainstem.

Clinical Manifestations The first episode of TN is sudden with a memorable onset. In TN 1, the patient has an abrupt onset of waves of excruciating pain. It is described as a burning, knifelike, or lightning-like shock in the lips, upper or lower gums, cheek, forehead, or side of the nose.31 Facial twitching, grimacing, and frequent blinking and tearing of the eye can occur during the acute attack (giving rise to the term tic douloureux). Some patients may have facial sensory loss. Attacks are usually brief, lasting only seconds to 2 or 3 minutes. Frequency ranges from 1 to over 50 times a day.31 Pain episodes are usually started by a triggering mechanism of light touch at a specific point (trigger zone) along the distribution of the nerve branches. Precipitating stimuli include chewing, brushing the teeth, feeling a hot or cold blast of air on the face, washing the face, yawning, or even talking. As a result, the patient may eat improperly, neglect hygienic practices, wear a cloth over the face, and withdraw from interaction with others. The patient may sleep excessively as a means of coping with pain. TN 2 manifests as constant aching, burning, crushing, or stabbing pain. The pain has a lower intensity and does not subside completely.32 The distinct attacks associated with TN 1 do not occur in TN 2.

Diagnostic Studies Diagnosis is based almost entirely on history, along with results from physical and neurologic examinations. Other disorders that cause facial pain should be ruled out before TN is diagnosed. MRI may be

used to assess for sinusitis, cancer, multiple sclerosis, or masses in the cerebellopontine angle. 3D reconstruction and angiography MRI are helpful with seeing the specific brain anatomy, nerve roots, and vasculature involved. A complete neurologic assessment is required along with consulting other subspecialties, such as neurology, neuroradiology, neurosurgery, dentistry, maxillofacial surgery, and pain management.

Interprofessional Care Once a diagnosis is made, the goal is relief of pain with either medical or surgical treatment (Tables 60.14 and 60.15). Electrical stimulation of the nerves and nerve blocks with local anesthetics or botulinum toxin are options.

Drug Therapy Antiseizure drug therapy may reduce pain by stabilizing the neuronal membrane and blocking nerve firing. These drugs are usually effective in treating TN 1 but less effective in TN 2. First-line drugs include carbamazepine (Tegretol) and oxcarbazepine (Trileptal). Topiramate (Topamax), clonazepam (Klonopin), phenytoin (Dilantin), lamotrigine (Lamictal), gabapentin, and valproic acid are other options.30 Tricyclic antidepressants, such as amitriptyline or nortriptyline, can help treat the constant burning or aching pain. Analgesics or opioids are usually not effective in controlling pain in TN 1 but may help with pain in TN 2.30

Surgical Therapy If a conservative approach is ineffective or the patient is unable to tolerate adverse effects of medications, surgical therapy is available (Table 60.15). In percutaneous procedures, affected nerve fibers are damaged to eliminate pain. Although most patients are pain-free after any of the procedures, pain relief lasts longest with microvascular decompression. About half of treated patients develop recurrent pain

within 12 to 15 years.30

Nursing Management: Trigeminal Neuralgia Patients usually receive outpatient treatment. Assess the attacks in detail, including triggering factors, characteristics, frequency, and pain management techniques. This information helps you to plan patient care. Evaluate the degree of pain and its effects on the patient’s lifestyle, drug use, emotional state, and suicidal tendencies. Note behavior (including withdrawal).

TABLE 60.14 Interprofessional CareTrigeminal

Neuralgia

Diagnostic Assessment • History and physical examination (including neurologic examination) • MRI

Management • Drug therapy • Antiseizure drugs (e.g., carbamazepine, oxcarbazepine [Trileptal], gabapentin [Neurontin]) • Tricyclic antidepressants (e.g., amitriptyline) • Local nerve block • Surgical therapy (Table 60.15) Monitor the patient’s response to drug therapy and note any side

effects. Discuss complementary pain management measures, such as acupuncture, biofeedback, and yoga. Environmental assessment is essential during an acute period to decrease triggering stimuli. The room should be kept at an even, moderate temperature and free of drafts. The patient may prefer to complete all self-care activities, fearing someone else will inadvertently cause injury. Assess the patient’s nutritional status and hygiene (especially oral). Teach the patient about the importance of nutrition, hygiene, and oral care. Convey understanding if oral neglect is apparent. A small, softbristled toothbrush or a warm mouthwash helps promote oral care. Hygiene activities are best done when analgesia is at its peak.

TABLE 60.15 Surgical Therapy for Trigeminal

Neuralgia

Encourage food that is high in protein and calories and easy to chew. Food should be served lukewarm and offered frequently. If oral intake is sharply reduced and the patient’s nutritional status is

compromised, an NG tube can be inserted on the unaffected side for EN. Appropriate teaching related to surgical procedures depends on the type of procedure planned (e.g., percutaneous). The patient needs to know they will be awake during local procedures in order to cooperate when corneal and ciliary reflexes and facial sensations are checked. After the procedure, compare the patient’s pain with the preoperative intensity. Evaluate the corneal reflex, extraocular muscles, hearing, sensation, and facial nerve function often (see Chapter 55). If the corneal reflex is impaired, take special care to protect the eyes. This includes using artificial tears or eye shields. After a percutaneous radiofrequency procedure, apply an ice pack to the jaw on the operative side for 3 to 5 hours. To avoid injuring the mouth, the patient should not chew on the operative side until sensation has returned. If intracranial surgery was done, general postoperative nursing care after a craniotomy is appropriate. (Nursing care related to craniotomy is discussed in Chapter 56.) Plan for regular follow-up care. Teach the patient about any medications. Although pain may be relieved, encourage the patient to keep environmental stimuli to a moderate level and to use stress management techniques. Long-term management after surgical intervention depends on residual effects of the procedure. If anesthesia is present or the corneal reflex is altered, teach the patient to (1) chew on the unaffected side; (2) avoid hot foods or beverages, which can burn the mucous membranes; (3) check the oral cavity after meals to remove food particles; (4) practice meticulous oral hygiene and continue with semiannual dental visits; (5) protect the face against extremes of temperature; (6) use an electric razor; (7) wear a protective eye shield and avoid rubbing eyes; and (8) examine eye regularly for symptoms of infection or irritation.

FIG. 60.14 Glycerol rhizotomy for the treatment of trigeminal neuralgia. A, Patient with trigeminal neuralgia having needle placed. B, HCP injecting glycerol. Courtesy Joe Rothrock, Media, PA.

Bell’s Palsy Bell’s palsy is an acute, usually temporary, facial paresis (or palsy) resulting from damage or trauma of the facial nerve (CN VII). It usually affects only 1 side of the face, but both sides can be affected. Bell’s palsy is the most common facial nerve disorder.33 Each year about 40,000 Americans are diagnosed with Bell’s palsy. It occurs equally between men and women and can affect any age-group. The peak incidence is between ages 15 and 60 years. There is a high incidence during pregnancy and in persons with upper respiratory tract conditions (e.g., flu, colds), obesity, diabetes, and hypertension.33

Etiology and Pathophysiology We do not know the exact cause. Several theories exist. Some think it is a reactivation of herpes simplex virus isoform (HSV-1) and/or herpes zoster virus (HZV). The viral infection causes inflammation, leading to nerve compression and the subsequent clinical features (Fig. 60.15). Another cause may be acute demyelination similar to what happens in Guillain-Barré syndrome. The prognosis for persons with Bell’s palsy is generally very good. The extent of nerve damage determines the extent of recovery. Most begin to get better within 2 weeks after the onset and recover some or all facial function within 6 months. In some cases, there may be residual effects, including facial asymmetry or abnormal facial movements.

Clinical Manifestations CN VII is a mixed cranial nerve with motor, sensory, and autonomic function, which accounts for the manifestations. The key feature of Bell’s palsy is the acute onset of unilateral lower motor facial weakness. 50% to 60% have pain around and behind the ear and neck. Other manifestations include drooping of the eyelid and corner of the mouth, drooling, facial twitching, dryness of the eye or mouth, facial

numbness, altered taste, hearing loss, and excessive tearing in 1 eye.33 Most often these symptoms begin suddenly and reach their peak within 48 to 72 hours. Quality of life is often decreased due to problems with eating, swallowing, speech, and taste. Patients may have psychologic withdrawal because of changes in appearance, malnutrition, dehydration, mucous membrane trauma, corneal abrasions, muscle stretching, and facial spasms and contractures.

FIG. 60.15 Facial characteristics of a person with Bell’s palsy. © Jo Ann Snover/123RF Stock Photo/123rf.com.

Diagnostic Studies Bell’s palsy is a clinical diagnosis. No definitive diagnostic test exists. The diagnosis and prognosis are indicated by clinical examination and observing the typical pattern of onset. Current guidelines do not

support routine laboratory, imaging, or neurophysiologic testing at first presentation of Bell’s palsy. If indicated, MRI and CT can eliminate other causes for facial paralysis. Blood tests can diagnose infections or other diseases. Electromyography (EMG) can confirm the presence of nerve damage. Patients should be referred to a neurologist or otolaryngologist as soon as possible to exclude other neurologic conditions.

Interprofessional Care The patient with Bell’s palsy is treated as an outpatient. Care focuses on relieving symptoms, preventing complications, and protecting the eye on the affected side. Treatment is often started to try to improve the chance of a complete recovery. Oral corticosteroid therapy to reduce inflammation and swelling should be started within 72 hours of onset.34 Some patients should receive an antiviral agent, such as acyclovir (Zovirax), in addition to the steroid therapy. Surgical decompression of the facial nerve is controversial but is considered in refractory cases.

Nursing Management: Bell’s Palsy Mild analgesics can relieve pain. Moist heat can reduce discomfort and aid circulation. Electrical stimulation of the nerve, facial massage, and physical therapy help maintain muscle tone and ease pain. A facial sling may be helpful to support affected muscles, improve lip alignment, and facilitate eating. The facial sling is usually made and fitted by a physical or occupational therapist. When function begins to return, active facial muscle exercises are done several times a day. Tell the patient to protect the face from cold and drafts because trigeminal hyperesthesia (extreme sensitivity to pain or touch) may occur.

Check Your Practice You are working in the outpatient neurology clinic. Your patient is a 68-yr-old woman with Bell’s palsy. Her main problem today is dry eyes. When you are doing an assessment, she tells you, “I hate the way I look. I cannot go anywhere, and I am afraid to leave the house. I am ugly and scary looking.” • How can you help her cope with her disorder? • What can you suggest to increase moisture in the affected eye? Eye protection is important. The patient may wear dark glasses for protective and cosmetic reasons. Artificial tears (methylcellulose) should be instilled often during the day to prevent drying of the cornea. Ointment and an impermeable eye shield can be used at night to retain moisture. In some patients, taping the lids closed at night may be needed. Teach the patient to report ocular pain, drainage, or discharge. Maintaining good nutrition is important. Teach the patient to chew on the unaffected side of the mouth to avoid trapping food and to enjoy the taste of food. Thorough oral hygiene must be done after each meal to prevent parotitis, caries, and periodontal disease from accumulated residual food. The change in physical appearance from Bell’s palsy can be devastating. Reassure the patient that a stroke did not occur and that chances for a full recovery are good. Enlisting support from family and friends is important. Tell the patient most people recover within 3 to 6 months after onset of symptoms.

Polyneuropathies Guillain-Barré Syndrome Guillain-Barré syndrome (GBS) is an autoimmune process that occurs a few days or weeks after a viral or bacterial infection. GBS is

rare, affecting about 1 person in every 100,000.35 It can occur at any age, but those over age 50 are at greatest risk.36 The most common type of GBS is acute inflammatory demyelinating polyneuropathy (AIDP). Other types include acute motor axonal neuropathy (AMAN) and acute motor sensory axonal neuropathy (AMSAN). AMAN is more common in children.

Etiology and Pathophysiology The cause of GBS is unknown. Both cellular and humoral immune responses likely play a role in AIDP. Humoral responses appear to cause AMAN.36 Following an infection, immune responses cause injury to either the myelin sheath (AIDP) or the nerve axon itself (AMAN). There is edema and inflammation of affected nerves. The result is segmental loss of the myelin sheath with exposed nerve membranes in nerve terminals and the nodes of Ranvier. Transmission of nerve impulses is stopped or slowed. This leads to flaccid paralysis with muscle denervation and atrophy. In the recovery phase, remyelination occurs slowly. Neurologic function returns in a proximal-to-distal pattern. Most cases of GBS follow a viral or bacterial infection of the GI or upper respiratory tract. Cytomegalovirus is the most common viral cause. Campylobacter jejuni gastroenteritis is the most common bacterial cause, especially for AMAN. Other related infections include Epstein-Barr virus, Mycoplasma pneumoniae, Haemophilus influenza, hepatitis (A, B, E), and Zika virus.35 Surgery and trauma may trigger GBS.

Clinical Manifestations and Complications The main features of GBS include acute, ascending, rapidly progressive, symmetric weakness of the limbs. The first symptoms are weakness, paresthesia (numbness and tingling), and hypotonia (reduced muscle tone) of the limbs. Reflexes in the affected limbs are weak or absent. Maximal weakness is reached in 4 weeks. Autonomic nervous system dysfunction occurs with AIDP and

AMSAN, causing orthostatic hypotension, hypertension, and abnormal vagal responses (bradycardia, heart block, asystole). Other autonomic dysfunction effects include bowel and bladder dysfunction, facial flushing, and diaphoresis. Cranial nerve involvement manifests as facial weakness and paresthesia, extraocular eye movement problems, and dysphagia. Pain is common. It can include paresthesia, muscular aches and cramps, and hyperesthesia. It is often worse at night. Pain may contribute to decreased appetite and interfere with sleep. The most serious complication of GBS is respiratory failure. It occurs if the paralysis progresses to nerves that innervate the thoracic area. Frequently assess the respiratory system by checking respiratory rate and depth to determine the need for immediate intervention, including intubation and mechanical ventilation. Respiratory infection or UTI may occur. Immobility from paralysis can cause paralytic ileus, muscle atrophy, VTE, PIs, orthostatic hypotension, and nutritional deficiencies.37

Diagnostic Studies Diagnosis is based mainly on the patient’s history and clinical signs. Clinical features required for diagnosis include progressive weakness of more than 1 limb and decreased or absent reflexes. Electrolyte levels, liver function tests, creatinine phosphokinase, and erythrocyte sedimentation rates are evaluated. Cerebrospinal fluid (CSF) analysis helps exclude other causes. In GBS the CSF has more protein than normal.37 Results of EMG and nerve conduction studies (NCS) are used after 2 weeks to confirm the diagnosis. NCS allow the HCP to diagnose the subtype. NCS in AIDP show demyelination. This information helps with prognosis, as patients with demyelination often need mechanical ventilation and have a poorer outcome.38

Interprofessional and Nursing Care The management of GBS is supportive. Ventilatory support is critical during the acute phase. Patients may be in ICU for hemodynamic

monitoring. Immunomodulating treatments, such as plasma exchange (PE) (plasmapheresis) or high-dose IV immunoglobulin (IVIG), are most effective if used within the first 2 weeks of symptom onset. They are equally effective. PE removes antibodies and other immune factors. It is used 5 times either daily or every other day in the first 2 weeks. (PE is discussed in Chapter 13.) IVIG interferes with antigen presentation. It is given over 5 days. It is readily available and is the preferred treatment in many centers.39 After 4 weeks past disease onset, PE and IVIG therapies have little value. Corticosteroids have little effect on the prognosis or duration of the disease. Assessment is the most important aspect of nursing care during the acute phase. During the neurologic assessment, evaluate motor and sensory function. Report changes in motor function (e.g., ascending paralysis), reflexes, cranial nerve function (gag, cornea, swallow), and level of consciousness. Carefully assess respiratory and cardiac function. Monitor ABGs and vital capacity. Closely monitor BP and cardiac rate and rhythm during the acute phase because dysrhythmias, orthostatic hypotension, and increased or decreased BP and heart rate may occur. Vasopressor agents and volume expanders may be needed to treat the low BP. If fever develops, obtain sputum and blood cultures to identify the pathogen. Appropriate antibiotic therapy is then started. Nutritional needs must be met despite possible problems associated with delayed gastric emptying, paralytic ileus, and potential for aspiration if the gag reflex is lost. In addition to testing for the gag reflex, note drooling and other problems with secretions that may indicate an inadequate gag reflex. EN or PN may be used to ensure adequate caloric intake. Throughout the course of the illness, provide support and encouragement to the patient and caregivers. Early referrals should be made for physical, occupational, and speech therapy. Counseling may help the patient adjust to the sudden disabling syndrome and dependence on others. Most patients with GBS will start to recover spontaneously at about 28 days. 80% of patients walk independently at 6 months with 60%

making a full recovery in 1 year. GBS patients who have a GI infection, are older in age, have a rapid clinical onset, have a hospital length of stay longer than 11 days, have poor upper extremity motor strength, or need mechanical ventilation have a poorer prognosis.39

Chronic Inflammatory Demyelinating Polyneuropathy Chronic inflammatory demyelinating polyneuropathy (CIDP) is a motor and sensory neuropathy. CIDP is a rare autoimmune disorder, affecting 1 to 2 persons per 100,000.40 CIDP is more common in those in their 50s and 60s and in men more than women.41 Like GBS, there are different types of CIDP. CIDP differs from GBS in that symptoms gradually occur over 8 weeks and there is not an acute onset. CIDP is not self-limiting (with an end to the acute phase). Early recognition and treatment can help the patient avoid significant disability.

Etiology and Pathophysiology We do not know the exact cause of CIDP. There is evidence to support the theory that like GBS, it has an autoimmune basis.40 CIDP seems to be associated with infection, HIV, hepatitis C, Sjögren’s syndrome, inflammatory bowel disease, melanoma, lymphoma, and diabetes.

Clinical Manifestations and Diagnostic Studies It is important to recognize the differences between CIPD and GBS to prevent incorrect or delayed treatment. The classic presentation of patients with CIPD includes progressive symptoms lasting over 2 months, more weakness than sensory deficits, symmetric weakness in the arms and legs, impaired sensation (from distal to proximal), paresthesia and dysesthesia, and absent or decreased reflexes in all extremities. Tremors, facial weakness, and papilledema may be

present. Sensory ataxia and impaired vibration and pinprick sensation occur more often in CIDP. CIDP diagnostic tests are similar to those for GBS. CSF shows high protein levels. MRI may show changes. Key identifying features of CIDP include nerve conduction block and slowed conduction velocity, possibly due to demyelination. Nerve biopsy is done when other studies do not confirm a diagnosis.41

Interprofessional and Nursing Care Early recognition and diagnosis of CIDP are key to reducing permanent disability. The goal of treatment is to halt the immune response and stop nerve inflammation and demyelination. Use of IVIG, high-dose corticosteroids, or plasma exchange are all effective treatments.41 Patients continue therapy until maximum clinical improvement is achieved or until they reach a clinical plateau. Patients will need maintenance therapy to prevent relapse or progression. Appropriate referrals to rehabilitation should be made early in the patient’s care to promote maximum recovery. Therapy may improve muscle strength, function, and mobility while minimizing muscle atrophy and joint distortion.40

Tetanus Tetanus (lockjaw) is a severe infection of the nervous system affecting spinal and cranial nerves. In the United States, because of widespread immunization and careful wound care, there are only about 30 cases per year.42 The annual worldwide incidence is between 500,000 and 1 million cases.43 Tetanus results from the effects of a potent neurotoxin (tetanospasmin) released by the anaerobic bacillus Clostridium tetani. The spores of the bacillus are present in soil, garden mold, and manure. Tetanospasmin binds to motor nerves and enters the axons. From there it can travel to the brain and spinal cord and stop the

release of inhibitory neurotransmitters. The result is sustained muscle contraction. If the toxin reaches the blood or lymph system, many different muscles can be affected.42 C. tetani enters the body through a wound that provides an appropriate low-O2 environment for the organisms to mature and make toxin. Examples of such wounds include IV drug use injection sites, human and animal bites, puncture wounds from stepping on a nail, gardening injuries, burns, frostbite, open fractures, and gunshot wounds. The incubation period is typically 4 to 14 days. The shorter the period, the more severe the symptoms. The hallmark feature of generalized tetanus is muscle rigidity and spasms. Patients may have muscle soreness, cramping, or difficulty swallowing. Facial muscles are affected first with stiffness in the jaw (trismus). Patients may have a sardonic smile (risus sardonicus) due to facial muscle contractions. As the disease progresses, the neck muscles, back, abdomen, and extremities become increasingly rigid. In severe forms, continuous tonic seizures may occur with opisthotonos (extreme arching of the back and retraction of the head).42 Laryngeal and respiratory spasms cause apnea and anoxia. The slightest noise, jarring motion, or bright light can set off a painful seizure. Tetanus prevention and immunizations, which are the most important factors influencing incidence, are outlined in Table 68.6. Adults should receive a tetanus and diphtheria toxoid booster every 10 years.43 Teach the patient that immediate, thorough cleansing of all wounds with soap and water is important to prevent tetanus. If an open wound occurs and the patient has not been immunized within 5 years, contact the HCP so that a tetanus booster can be given. Tetanus is a medical emergency that requires hospitalization. Patients are given immediate treatment with tetanus immune globulin (TIG). It provides temporary immunity by directly providing antitoxin.43 Drugs to control spasms are essential. Diazepam (Valium) or barbiturates are given to promote sedation and skeletal muscle relaxation. In severe cases, neuromuscular blocking agents (e.g., vecuronium) are given to paralyze skeletal muscles. Opioid analgesics, such as morphine or fentanyl, are used for pain

management. A 10- to 14-day course of penicillin, metronidazole (drug of choice), tetracycline, or doxycycline is recommended to inhibit further growth of C. tetani. Because of laryngospasm and the potential need for neuromuscular blocking drugs, the patient is placed on mechanical ventilation. Sedative agents and opioid analgesics are given to all patients who are pharmacologically paralyzed. IV fluids are needed for proper hydration due to sustained muscle contraction. Any wound should be debrided or abscess drained. Antibiotics may be given to prevent secondary infections.

Botulism Botulism is a rare, but the most serious type, of food poisoning. It is caused by GI absorption of a neurotoxin made by Clostridium botulinum. This organism is found in the soil, and the spores are hard to destroy. It can grow in any food contaminated with the spores. Improper home canning of foods is often the cause. We think the neurotoxin destroys or inhibits the neurotransmission of acetylcholine at the myoneural junction, resulting in disturbed muscle innervation. Neurologic manifestations can develop rapidly or evolve over several days. They include a descending paralysis with muscle incoordination and weakness, difficulty swallowing, and seizures. Respiratory muscle weakness can quickly lead to respiratory and/or cardiac arrest. The manifestations, prevention, and treatment are described in Table 41.24. Patient and caregiving teaching related to food poisoning are outlined in Table 41.25. Nursing care during the acute illness is like that for GBS. Supportive nursing interventions include rest, activities to maintain respiratory function, adequate nutrition, and preventing loss of muscle mass.

Case Study

Spinal Cord Injury

© ComstockImages/Stockbyte/Thinkstock.

Patient Profile Acute Phase S.W., an 18-yr-old white woman, is admitted to the ED with the diagnosis of a cervical spinal cord injury (SCI). S.W. was swimming at a neighbor’s backyard pool. She dove into the shallow end, striking her head on the bottom of the pool. Her friends noticed she did not resurface. They rescued her and brought her to the side of the pool.

They maintained neck immobilization until the rescue crews arrived.

Subjective Data • Awake and alert • Reporting neck pain • Anxious and asking why she cannot move her legs • Asking to see her family

Objective Data Physical Examination • Weak elbow flexion (biceps) movement bilaterally • No triceps movement bilaterally • Gross shoulder movement present bilaterally • No movement in bilateral lower extremities • Decreased sensation from the shoulders down • No bladder or bowel control • BP 85/50 mm Hg; pulse 56 beats/min; respirations 32 breaths/min and labored

Diagnostic Studies • CT C-spine shows C5 subluxation and compression fracture • MRI C-spine shows severe spinal cord compression at C5-6

Interprofessional Care • Intubated in the ED • Started on mechanical ventilation • Placed in tongs and traction on arrival to the ICU

Discussion Questions (Acute Phase) 1. Priority Decision: What nursing activities would be a priority on S.W.’s arrival in the ICU? 2. What physiologic problems are causing S.W. to have hypotension and bradycardia? 3. What would be the initial treatment for S.W.’s hypotension and bradycardia? 4. Safety: What signs and symptoms would indicate respiratory distress? What physiologic problem would cause respiratory distress in S.W.’s injury state? 5. Collaboration: What can the interprofessional team do to decrease S.W.’s anxiety? 6. Priority Decision: Based on the assessment data provided, what are the priority nursing diagnoses? What are the collaborative problems? 7. Collaboration: Identify activities that can be delegated to unlicensed assistive personnel (UAP).

Patient Profile Rehabilitation Phase S.W. is now 1-month postinjury and has been admitted to a local inpatient SCI rehabilitation agency. She has been extubated and uses a wheelchair to mobilize. She eats 3 meals a day with help and is on a strict bowel and bladder program.

Subjective Data • Awake and alert but anxious • Reporting a severe headache, blurred vision, and nausea

Objective Data Physical Examination

• Flushed and diaphoretic above the level of injury • No bowel movement for 2 days • BP 235/106 mm Hg, pulse 32 beats/min, respirations 30 breaths/min and labored

Discussion Questions (Rehabilitation Phase) 1. Priority Decision: What initial priority nursing interventions would be appropriate? 2. What physiologic problem is causing S.W.’s hypertension and bradycardia? 3. Once the HCP has been notified, what other interventions would be appropriate? 4. Quality Improvement: What outcomes would indicate that nursing interventions were successful? 5. Patient-Centered Care: Patient and caregiver involvement in the rehabilitation process is vital. What teaching will you provide about bowel management? 6. Evidence-Based Practice: S.W. and her family are concerned about the risk for autonomic dysreflexia. What effective strategies to prevent autonomic dysreflexia would you discuss with them? Answers available at http://evolve.elsevier.com/Lewis/medsurg.

Bridge to Nclex Examination The number of the question corresponds to the same-numbered outcome at the beginning of the chapter.

1. During rehabilitation, a patient with spinal cord injury begins to ambulate with long leg braces. Which level of injury does the nurse associate with this degree of

recovery? a. L1-2 b. T6-7 c. T1-2 d. C7-8 2. A patient with a T4 spinal cord injury has neurogenic shock due to sympathetic nervous system dysfunction. What would the nurse recognize as characteristic of this condition? a. Tachycardia b. Hypotension c. Increased cardiac output d. Peripheral vasoconstriction 3. A patient with spinal cord injury has severe neurologic deficits. What is the most likely mechanism of injury for this patient? a. Compression b. Hyperextension c. Flexion-rotation d. Extension-rotation 4. A patient undergoing rehabilitation for a C7 spinal cord injury tells the nurse he must have the flu because he has a bad headache and nausea. The nurse’s first priority is to a. call the health care provider. b. check the patient’s temperature. c. measure the patient’s blood pressure. d. elevate the head of the bed to 90 degrees.

5. The most common early symptom of a spinal cord tumor is a. urinary incontinence. b. back pain that worsens with activity. c. paralysis below the level of involvement. d. impaired sensation of pain, temperature, and light touch. 6. During assessment of the patient with trigeminal neuralgia, the nurse should (select all that apply) a. inspect all aspects of the mouth and teeth. b. assess the gag reflex and respiratory rate and depth. c. lightly palpate the affected side of the face for edema. d. test for temperature and sensation perception on the face. e. ask the patient to describe factors that initiate an episode. 7. During routine assessment of a patient with Guillain-Barré syndrome, the nurse finds the patient is short of breath. The patient’s respiratory distress is caused by a. elevated protein levels in the CSF. b. immobility resulting from ascending paralysis. c. degeneration of motor neurons in the brainstem and spinal cord. d. paralysis ascending to the nerves that stimulate the thoracic area. 8. A nurse is caring for a patient newly diagnosed with chronic inflammatory demyelinating polyneuropathy (CIDP). Which statement can the nurse accurately use to

teach the patient about CIDP? a. “Corticosteroids have little effect on this disease.” b. “Maintenance therapy will be needed to prevent relapse.” c. “You will go into remission in approximately eight weeks.” d. “You should be able to walk without help within three months.” 1. a, 2. b, 3. c, 4. c, 5. b, 6. a, d, e, 7. d, 8. b. For rationales to these answers and even more NCLEX review questions, visit http://evolve.elsevier.com/Lewis/medsurg.

Evolve Website/Resources List http://evolve.elsevier.com/Lewis/medsurg

Review Questions (Online Only) Key Points Answer Keys for Questions • Rationales for Bridge to NCLEX Examination Questions • Answer Guidelines for Case Study on p. 1426 Student Case Study • Patient With Spinal Cord Injury Nursing Care Plan • eNursing Care Plan 60.1: Patient With a Spinal Cord Injury Conceptual Care Map Creator Audio Glossary

Content Updates

References 1. The National SCI Statistical Center: Spinal cord injury (SCI) facts and figures at a glance. Retrieved from www.nscisc.uab.edu/Public/Facts%202016.pdf. Fehlings MG, Tetreault LA, Wilson JR, et al: A clinical practice guideline for the management of acute spinal cord injury: Introduction, rationale, and scope, AOspine 7:845, 2017.

3. Hachem LD, Ahuja CS, Fehling MG: Assessment and management of acute spinal cord injury: From point of injury to rehabilitation, J Spinal Cord Med 40:665, 2017. 4. Ulndreaj A, Chio JC, Ahuja CS, et al : Modulating the immune response in spinal cord injury, Expert Re Neurother 16:1127, 2016. 5. Ruiz IA, Squair JW, Phillips AA, et al: Incidence and natural progression of neurogenic shock after traumatic spinal cord injury, J Neurotrauma 35:461, 2018. 6. Dave S, Cho JJ: Shock: Neurogenic shock, Treasure Island, FL, 2018, StatPearls Publishing. Retrieved from www.ncbi.nlm.nih.gov/books/NBK459361/. 7. Roberts TT, Leonard GR, Cepela DJ : Classifications in brief: ASIA Impairment Scale, Clin Orthop Relat Res 475:1499, 2017. 8. Stein DM, Knight WA: Emergency neurological life support: Traumatic spine injury, Neurocrit Care 27:S170, 2017. Neseyo U, Santiago-Lastra Y: Long-term complications of the neurogenic bladder, Ur Clin N Am 44:355, 2017.

10. Martinez L, Neshatican L, Khavari R: Neurogenic bowel dysfunction in patients with neurogenic bladder, Curr Bladder Dysfunct Rep 11:334, 2017. Felleiter P, Krebs J: Post-traumatic changes in energy expenditure and body composition in patients with acute spinal cord injury, J Rehabil Med 49:579, 2017. Fehlings MG, Tetreault LA, Jefferson RW, et al: A clinical practice guideline for management of patients with acute spinal cord injury: Recommendations on the type and timing of anticoagulant thromboprophylaxis, AOSpine 7:2125, 2017.

13. Yue JK, Winkler EA, Rick JW, et al: Update on critical care for acute spinal cord injury in the setting of polytrauma, Neurosurg Focus 43:E19, 2017. Evanie N, Belley-Cote EP, Falla N, et al: Methylprednisolone for the treatment of patients with acute spinal cord injuries: A systematic review and meta-analysis, J Neurotraum 33:468, 2016.

15. STEADI: Stopping elderly accidents, deaths and injuries. Retrieved from www.cdc.gov/steadi/index.html. Kumar N, Pieri-Davies S, Chowdury JR, et al: Evidence-based respiratory management strategies required to preen complications and improve outcome in acute spinal cord injury patients, Trauma 19:23, 2017. Atkinson RA, Cullum NA: Interventions for pressure ulcers: A summary of evidence for prevention and treatment, Spin Cord 56:186, 2017. Brienza D, Krishnan S, Karg P, et al: Predictors of pressure ulcer incidence following traumatic spinal cord injury: A secondary analysis of a prospective longitudinal study, Spin Cord 56:28, 2018. Wound, Ostomy and Continence Nurses Society: Guidelines for prevention and management of pressure ulcers, J Wound Ostomy Continence Nurs 44:241, 2017. Eldahan KC, Rabchevsky AG: Autonomic dysreflexia after spinal cord injury: Systemic pathophysiology and methods of management,

Auton Neurosci 209:59, 2018. Garara B, Wood A, Marcus HJ, et al: Intramuscular diaphragmatic stimulation for patient with traumatic high cervical injuries and ventilator dependent respiratory failure: A systematic review of safety and effectiveness, Injury 47:539, 2016. Cho YS, Kim KH: Botulinum toxin in spinal cord injury patients with neurogenic detrusor overactivity, J Exerc Rehabil 12:624, 2018.

23. Krogh K, Emmanuel A, Perrouin-Verbe B, et al: International Spinal Cord Bowel Function Basic Data Set (Version 2.0), Spin Cord 55:692, 2017. 24. Christopher & Dana Reeve Foundation Paralysis Resource Center: Sexual health for men. Retrieved from www.christopherreeve.org/living-withparalysis/health/sexual-health/sexual-health-for-men. 25. Christopher & Dana Reeve Foundation Paralysis Resource Center: Sexual health for women. Retrieved from www.christopherreeve.org/living-withparalysis/health/sexual-health/sexual-health-for-women. Kornhabe R, Mclean L, Betivas V, et al: Resilience and the rehabilitation of adult spinal cord injury survivors: A qualitative systematic review, J Adv Nurs 74:23, 2018.

27. Kretzer RM: Intradural spinal cord tumors, Spine 42:22, 2017. 28. American Association of Neurological Surgeons: Spinal tumors. Retrieved from www.aans.org/Patients/Neurosurgical-Conditions-andTreatments/Spinal-Tumors. 29. Kumar A, Weber MH, Gokaslan Z, et al: Metastatic spinal cord compression and steroid treatment, Clin Spine Surg 30:156, 2017. 30. National Institute of Health: Trigeminal neuralgia fact sheet. Retrieved from

www.ninds.nih.gov/Disorders/Patient-CaregiverEducation/Fact-Sheets/Trigeminal-Neuralgia-Fact-Sheet. Crucca G, Finnerup NB, Jensen TS, et al: Trigeminal neuralgia: New classification of diagnostic grading for practice and research, Am Acad Neurol 87:220, 2016. Spina A, Mortini P, Alemanno F, et al: Trigeminal neuralgia: Toward a multimodal approach, World Neurosurg 103:220, 2017.

33. National Institute of Neurologic Disorders and Stroke: Bell’s palsy information page. Retrieved from www.ninds.nih.gov/Disorders/All-Disorders/Bells-PalsyInformation-Page. Thielker J, Geibler K, Granitzka T, et al: Acute management of Bells palsy, Curr Otorhinolaryngol Rep 6:161, 2018.

35. National Institute of Neurologic Disorders and Stroke: Guillain-Barré fact sheet. Retrieved from www.ninds.nih.gov/Disorders/Patient-CaregiverEducation/Fact-Sheets/Guillain-Barr%C3%A9Syndrome-Fact-Sheet. 36. Centers for Disease Control and Prevention (CDC): Guillain-Barré syndrome. Retrieved from www.cdc.gov/campylobacter/guillain-barre.html. 37. Andary MT, Klein MJ: Guillain-Barré syndrome updated. Retrieved from https://emedicine.medscape.com/article/315632-overview. 38. Wilson HJ, Jacobs BC, van Doorn PA: Guillain-Barre syndrome, Lancet 388:717, 2016. 39. Verboon C, van Doorn PA, Jacobs BC. Treatment dilemma in Guillain-Barr syndrome, J Neurol Neurosurg Psychiatry 88:346, 2017. 40. National Institute of Neurologic Disorders and Stroke: Chronic inflammatory demyelinating polyneuropathy. Retrieved from

www.ninds.nih.gov/Disorders/All-Disorders/ChronicInflammatory-Demyelinating-Polyneuropathy-CIDPInformation-Page. 41. Daroff RB, Jankovic J, Mazziotta JC, et al: Bradley’s neurology in clinical practice, ed 7, St Louis, 2016, Elsevier. 42. Davis DP, Stoppler MC: Tetanus. Retrieved from www.emedicinehealth.com/tetanus/article_em.htm#facts_on_tetanus 43. Centers for Disease Control and Prevention (CDC): Tetanus. Retrieved from www.cdc.gov/tetanus/clinicians.html. ∗

Evidence-based information for clinical practice.

61

Assessment Musculoskeletal System Colleen Walsh

LEARNING OUTCOMES 1. Describe the gross and microscopic anatomy of bone. 2. Explain the classification system for joints and movements at synovial joints. 3. Describe the functions of cartilage, muscles, ligaments, tendons, fascia, and bursae. 4. Link age-related changes in the musculoskeletal system to the differences in assessment findings. 5. Obtain significant subjective and objective assessment data related to the musculoskeletal system from a patient. 6. Perform a physical assessment of the musculoskeletal system using appropriate techniques. 7. Distinguish normal from abnormal findings of a physical assessment of the musculoskeletal system. 8. Describe the purpose, significance of results, and nursing responsibilities related to diagnostic studies of the musculoskeletal system.

KEY TERMS ankylosis, Table 61.6, p. 1439 arthrocentesis, Table 61.9, p. 1442 arthroscopy, Table 61.9, p. 1442 atrophy, Table 61.6, p. 1439 bone remodeling, p. 1430 contracture, Table 61.6, p. 1439 crepitation, Table 61.6, p. 1439 isometric contractions, p. 1432 isotonic contractions, p. 1432 kyphosis, Table 61.6, p. 1439 lordosis, Table 61.6, p. 1439 range of motion (ROM), p. 1437 scoliosis, p. 1438 x-ray, p. 1440 It takes strength to be gentle and kind. Steven Morrissey http://evolve.elsevier.com/Lewis/medsurg

Conceptual Focus Functional Ability Mobility Safety The musculoskeletal system is composed of voluntary muscle and 6

types of connective tissue: bone, cartilage, ligaments, tendons, fascia, and bursae. The purpose of the musculoskeletal system is to protect body organs, provide support and stability for the body, store minerals, and allow coordinated movement. This chapter reviews the structure and function of the musculoskeletal system to facilitate nursing assessment and evaluation of the assessment findings.

Structures and Functions of Musculoskeletal System Bone Function The main functions of bone are support, protection of internal organs, voluntary movement, blood cell production, and mineral storage. Bones provide the supporting framework that keeps the body from collapsing. It allows the body to bear weight. Bones protect underlying vital organs and tissues. For example, the skull encloses the brain and vertebrae surround the spinal cord. The rib cage protects the lungs and heart. Bones serve as a point of attachment for muscles and ligaments. Muscles are connected to bones by tendons. Bones act as a lever for muscles. Movement occurs because of muscle contractions applied to these levers. Ligaments provide stability to joints. Bone marrow contains hematopoietic tissue responsible for making red and white blood cells. Bones serve as a storage site for inorganic minerals, including calcium and phosphorus. Bone is a dynamic tissue that continuously changes form and composition. It contains both organic material (collagen) and inorganic material (calcium, phosphate). The internal and external growth and remodeling of bone are ongoing processes.

Microscopic Structure Bone is classified according to structure as cortical (compact and

dense) or cancellous (spongy). In cortical bone, cylindrical structural units called osteons (Haversian systems) fit closely together to create a dense bone structure (Fig. 61.1, A). Within the systems, the Haversian canals run parallel to the bone’s long axis. They contain the blood vessels that travel to the bone’s interior from the periosteum. Surrounding each osteon are concentric rings known as lamellae, which indicate mature bone. Smaller canals (canaliculi) extend from the Haversian canals to the lacunae, where mature bone cells are embedded.

FIG. 61.1 Bone structure. A, Cortical bone showing numerous structural units called osteons. B, Anatomy of a long bone (tibia) showing cancellous and compact bone. A, From Herlihy B, Maebius N: The human body in health and illness, ed 4, Philadelphia, 2011, Saunders. B, From Patton KT, Thibodeau GA: Anatomy and physiology, ed 8, St Louis, 2013, Mosby.

Cancellous bone has a different structure than cortical bone. The lamellae are not arranged in concentric rings. Instead, they occur along the lines of maximum stress placed on the bone. Cancellous bone is filled with red or yellow marrow. Blood reaches the bone cells by passing through spaces in the marrow. The 3 types of bone cells are osteoblasts, osteocytes, and osteoclasts.1 Osteoblasts synthesize organic bone matrix (collagen) and are the basic bone-forming cells. Osteocytes are mature bone cells. Osteoclasts take part in bone remodeling by helping in the breakdown of bone tissue. Bone remodeling is the removal of old bone by osteoclasts (resorption) and the deposit of new bone by osteoblasts (ossification). The inner layer of bone is made mostly of osteoblasts with a few osteoclasts.

Gross Structure The anatomic structure of bone is best represented by a typical long bone, such as the tibia (Fig. 61.1, B). Each long bone consists of the epiphysis, diaphysis, and metaphysis. The epiphysis, the widened area at each end of a long bone, is made mostly of cancellous bone. The wide epiphysis allows greater weight distribution and provides stability for the joint. The epiphysis is a primary location of muscle attachment. Articular cartilage covers the ends of the epiphysis. It provides a smooth, low-friction surface for joint movement. The diaphysis is the main shaft of the long bone. It provides structural support and is composed of cortical bone. The tubular structure of the diaphysis allows it to withstand bending and twisting forces more easily. The metaphysis is the flared area between the epiphysis and diaphysis. Like the epiphysis, it is composed of cancellous bone. The epiphyseal plate (physis or growth plate) is the cartilaginous area

between the epiphysis and metaphysis. In skeletally immature children who still have open growth plates, the epiphyseal plate actively makes chondrocytes that become mature bone. Division of the chondrocytes causes longitudinal bone growth in children. Injury to the epiphyseal plate in a growing child can cause the formation of new bone to stop at the growth plate. This leads to a shorter extremity and may contribute to significant functional problems. In the adult, the metaphysis and epiphysis become joined when chondrocyte formation at the growth plate stops and bone formation is complete. The periosteum is composed of fibrous connective tissue that covers the bone. Tiny blood vessels penetrate the periosteum to bring nutrition to underlying bone. Musculotendinous fibers attach to the outer layer of the periosteum. Collagen bundles attach the inner layer of the periosteum to the bone. There is no periosteum on the articular surfaces of long bones. These bone ends are covered by articular cartilage. The medullary (marrow) cavity in the center of the diaphysis contains either red or yellow bone marrow.2 In adults, red marrow is found mainly in the flat bones, such as the pelvis, skull, sternum, cranium, ribs, vertebrae, and scapulae, and cancellous (“spongy”) bone at the epiphyseal ends of long bones, such as the femur and humerus. Red bone marrow is involved in blood cell production (hematopoiesis). In the adult, the medullary cavity of long bones contains yellow bone marrow (mainly adipose tissue). Yellow marrow is involved in hematopoiesis in times of great blood cell need.

Types The skeleton consists of 206 bones. They are classified according to shape as long, short, flat, or irregular. Long bones have a central shaft (diaphysis) and 2 widened ends (epiphyses) (Fig. 61.1, B). Examples include the femur, humerus, and tibia. Short bones are composed of cancellous bone covered by a thin layer of compact bone. Examples include the carpals in the hand and tarsals in the foot. Flat bones have 2 layers of compact bone separated by a layer of

cancellous bone. Examples include the ribs, skull, scapula, and sternum. The spaces in the cancellous bone contain bone marrow. Irregular bones appear in a variety of shapes and sizes. Examples include the sacrum, mandible, and ear ossicles.

Joints A joint (articulation) is a place where the ends of 2 bones are close and move in relation to each other. Joints are classified by the degree of movement that they allow (Fig. 61.2).

FIG. 61.2 Classification of joints. A to C, Synarthrotic (immovable) and amphiarthrotic (slightly movable) joints. D and E, Diarthrodial

(freely movable) joints.

The most common joint is the freely movable diarthrodial (synovial) type. Each joint is enclosed in a capsule of fibrous connective tissue, which joins the 2 bones together to form a cavity (Fig. 61.3). The capsule is lined by a synovial membrane, which secretes thick synovial fluid. This fluid lubricates the joint, reduces friction, and allows opposing surfaces to slide smoothly over each other. The end of each bone is covered with articular (hyaline) cartilage. Supporting structures (e.g., ligaments, tendons) reinforce the joint capsule. They provide limits and stability to joint movement. Types of diarthrodial joints are shown in Fig. 61.4.

Cartilage The 3 types of cartilage are hyaline, elastic, and fibrous. Hyaline cartilage is the most common. It has a moderate amount of collagen fibers. It is found in the trachea, bronchi, nose, epiphyseal plate, and articular surfaces of bones. Elastic cartilage, which has both collagen and elastic fibers, is more flexible than hyaline cartilage. It is found in the ear, epiglottis, and larynx. Fibrous cartilage (fibrocartilage) consists mostly of collagen fibers. It is a tough tissue that often functions as a shock absorber. Fibrous cartilage is found between the vertebral discs. It also forms a protective cushion between the bones of the pelvic girdle, knee, and shoulder. Cartilage in synovial joints serves as a support for soft tissue and provides the articular surface for joint movement. It protects underlying tissues. Because articular cartilage is avascular, it must receive nourishment by the diffusion of material from the synovial fluid. The lack of a direct blood supply contributes to the slow metabolism of cartilage cells and explains why healing and repair of cartilage tissue occur slowly. The cartilage in the epiphyseal plate is also involved in the growth of long bones before physical maturity is reached.

FIG. 61.3 Structure of diarthrodial (synovial) joint.

Muscle Types

The 3 types of muscle tissue are cardiac (striated, involuntary), smooth (nonstriated, involuntary), and skeletal (striated, voluntary) muscle. Cardiac muscle is found only in the heart. Its spontaneous contractions pump blood through the circulatory system. Smooth muscle is found in the walls of hollow structures, such as airways, arteries, gastrointestinal (GI) tract, urinary bladder, and uterus. Smooth muscle contraction is controlled by neuronal and hormonal influences. Skeletal muscle, which requires neuronal stimulation for contraction, accounts for about half of a human’s body weight. It is the focus of the following discussion.

Structure The skeletal muscle is enclosed by the epimysium, a continuous layer of deep fascia. The epimysium helps muscles slide over nearby structures. Connective tissue surrounding and extending into the muscle can be subdivided into fiber bundles (fasciculi). These bundles are covered by perimysium and an innermost connective tissue layer called the endomysium that surrounds each fiber (Fig. 61.5). The structural unit of skeletal muscle is the muscle cell or muscle fiber. It is highly specialized for contraction. Skeletal muscle fibers are long, multinucleated cylinders that contain many mitochondria to support their high metabolic activity. Muscle fibers are composed of myofibrils, which in turn are made up of protein contractile filaments. The sarcomere is the contractile unit of the myofibrils. Each sarcomere consists of myosin (thick) filaments and actin (thin) filaments. The arrangement of the thin and thick filaments causes the characteristic banding of muscle seen under a microscope. Muscle contraction occurs as thick and thin filaments slide past each other, causing the sarcomeres to shorten.

FIG. 61.4 Types of diarthrodial (synovial) joints.

Contractions Skeletal muscle contractions allow posture maintenance, body

movement, and facial expressions. Isometric contractions increase the tension within a muscle but do not produce movement. Isotonic contractions shorten a muscle to produce movement. Most contractions are a combination of tension generation (isometric) and shortening (isotonic). Repeated isometric and/or isotonic contractions provide stress to stimulate muscle growth. Muscular atrophy (decrease in size) occurs with the absence of contractions that results from immobility or decreased neuronal stimulation. Increased muscular activity leads to hypertrophy (increase in size). Skeletal muscle fibers are divided into 2 groups based on the type of activity they show. Slow-twitch muscle fibers support prolonged muscle activity, such as marathon running. Because they also support the body against gravity, they help in posture maintenance. Fast-twitch muscle fibers are used for rapid muscle contraction needed for activities, such as blinking the eye, jumping, or sprinting. Fast-twitch fibers tend to tire more quickly than slow-twitch fibers.

Neuromuscular Junction Skeletal muscle fibers require a nerve impulse to contract. A nerve fiber and the skeletal muscle fibers it stimulates are called a motor endplate. The junction between the axon of the nerve cell and the adjacent muscle cell is called the myoneural or neuromuscular junction (Fig. 61.6). Presynaptic neurons release acetylcholine. It diffuses across the neuromuscular junction to bind with receptors on the motor endplate of the muscle. In response to this stimulation, the sarcoplasmic reticulum releases calcium ions into the cytoplasm. The presence of calcium triggers the contraction in the myofibrils. When calcium is low, tetany (involuntary contractions of skeletal muscle) can occur.

Energy Source The direct energy source for muscle fiber contractions is adenosine triphosphate (ATP). ATP is synthesized by cellular oxidative metabolism in the numerous mitochondria found close to the myofibrils. It is rapidly depleted through conversion to adenosine

diphosphate (ADP) and must be rephosphorylated. Phosphocreatine provides a rapid source for the resynthesis of ATP, but it is, in turn, converted to creatine. Glycolysis can serve as a source of ATP when the O2 supply is inadequate for metabolic needs of the muscle tissue. In this process, 1 glucose molecule is broken down to 2 ATP molecules.

FIG. 61.5 Structure of a muscle. From Patton KT, Thibodeau GA, Douglas M: Essentials of anatomy and physiology, St Louis, 2012, Mosby.

Ligaments and Tendons Ligaments and tendons are composed of dense, fibrous connective tissue with bundles of closely packed collagen fibers arranged in the same plane for additional strength. Tendons attach muscles to bones as an extension of the muscle sheath that adheres to the periosteum. Ligaments connect bones to bones (e.g., tibia to femur at knee joint). They have a higher elastic content than tendons.3 Ligaments provide stability while allowing controlled movement at joints. Ligaments and tendons have a relatively poor blood supply. This can make tissue repair a slow process after injury. For example, the stretching or tearing of ligaments that occurs with a sprain may require a long time to mend.

Fascia Fascia refers to layers of connective tissue with intermeshed fibers that can withstand limited stretching. Superficial fascia lies right under the skin. Deep fascia is a dense, fibrous tissue that surrounds muscle bundles, nerves, and blood vessels. It also encloses individual muscles, allowing them to act independently and to glide over each other during contraction. In addition, fascia provides strength to muscle tissues.

Bursae Bursae are small sacs of connective tissue lined with synovial membrane and containing viscous synovial fluid. They are found at bony prominences or joints to relieve pressure and decrease friction between moving parts.4 For example, bursae are found between the (1) patella and skin (prepatellar bursae), (2) olecranon process of the elbow and skin (olecranon bursae), (3) head of the humerus and acromion process of the scapula (subacromial bursae), and (4) greater trochanter of the proximal femur and skin (trochanteric bursae). Bursitis is an inflammation of a bursa sac. The inflammation may be acute or chronic.

FIG. 61.6 Neuromuscular junction. From Patton KT, Thibodeau GA: Anatomy and physiology, ed 8, St Louis, 2013, Mosby.

Gerontologic Considerations: Effects of Aging on Musculoskeletal System Many functional problems experienced by the older adult are related to changes in the musculoskeletal system. Although some changes begin in early adulthood, obvious signs of musculoskeletal impairment may not appear until later adult years. Changes may affect the older adult’s ability to complete self-care tasks and pursue other usual activities. Effects of musculoskeletal changes may range from mild discomfort and decreased ability to perform ADLs to severe, chronic pain and immobility. The bone remodeling process changes in the aging adult. Increased bone resorption and decreased bone formation cause a loss of bone density. This contributes to the development of osteopenia and

osteoporosis (see Chapter 63). Muscle mass and strength decrease. Almost 30% of muscle mass is lost by age 70. A loss of motor neurons can cause problems with skeletal muscle movement. Tendons and ligaments become less flexible, making movement more rigid. Perform a musculoskeletal assessment with an emphasis on exercise practices. Obtain information on the type of exercise performed, including frequency and warm-up activities. Determine the impact of age-related changes of the musculoskeletal system on functional status. Specifically ask about changes in self-care habits and ability to be independent in the home environment. Functional limitations that are accepted by the older adult as a normal part of aging can often be addressed with appropriate preventive strategies (see Table 62.1). The risk for falls increases in the older adult due in part to loss of strength. Aging can also bring changes in the patient’s balance, making the person unsteady. Proprioception (awareness of self in relation to the environment) may be altered. Identify any musculoskeletal changes that increase the patient’s risk for falls. Discuss fall prevention strategies. Osteoarthritis is more likely to affect joints in the aging adult (see Chapter 64).5 Metabolic bone diseases involve the deterioration of bone tissue (osteoporosis) and destruction of cartilage (osteoarthritis). Carefully distinguish between expected changes and the effects of disease in the aging adult. Symptoms of disease can be treated in many cases, helping the older adult to return to a higher functional level. Age-related changes in the musculoskeletal system and differences in assessment findings are outlined in Table 61.1.

TABLE 61.1 Gerontologic Assessment

DifferencesMusculoskeletal System

Assessment of Musculoskeletal System Subjective Data Important Health Information Past Health History The most common manifestations of musculoskeletal impairment include pain, weakness, deformity, limitation of movement, stiffness, and joint crepitation (crackling sound). Ask the patient about changes in sensation or in the size of a muscle. Questions should focus on symptoms of arthritic and connective tissue diseases (e.g., gout, psoriatic arthritis, systemic lupus erythematosus [SLE]), osteomalacia, osteomyelitis, and fungal infection of bones or joints. Ask the patient about sources of a secondary bacterial infection, such as ears, tonsils, teeth, sinuses, lungs, or genitourinary tract. These infections can enter the bones, resulting in osteomyelitis or joint destruction. Get a detailed account of the course and treatment of any of these problems. Certain illnesses are known to affect the musculoskeletal system

directly or indirectly. Ask the patient about medical problems, such as tuberculosis, poliomyelitis, diabetes, parathyroid problems, hemophilia, rickets, soft tissue infection, and neuromuscular disability. Trauma to the musculoskeletal system is a common reason for seeking medical care. The patient who is a good historian can recount minor and major injuries of the musculoskeletal system. Record information chronologically and include:

Case Study Patient Introduction

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G.A. is a 58-yr-old black woman whose husband brought her to the

emergency department (ED) this morning after she awoke with a sudden onset of excruciating pain in her left great toe. She denies any injury to her foot. She says she has never had this type of pain before.

Discussion Questions 1. What are the possible causes for G.A.’s acute pain in her great toe? 2. Is this condition stable or an emergency? 3. What type of assessment would be most appropriate for G.A.: comprehensive, focused, or emergency? What is the basis for your decision? 4. What assessment questions will you ask G.A.? 5. How will you individualize the assessment based on her age, ethnic/cultural background, and condition? You will learn more about how to assess G.A.’s condition as you read through this chapter. See p. 1436 for more information on G.A. Answers available at http://evolve.elsevier.com/Lewis/medsurg. • Mechanism and circumstances of the injury (e.g., twist, crush, stretch) • Methods and duration of treatment • Current status related to the injury • Need for assistive devices • Interference with ADLs

Medications Ask the patient about prescription and over-the-counter drugs, herbal products, and nutritional supplements. Get detailed information about each treatment, including its name, dose and frequency, length of time it was taken, reason for use, and any possible side effects. Ask about the use of skeletal muscle relaxants, opioids, nonsteroidal antiinflammatory drugs, corticosteroids, and calcium and vitamin D

supplements. Review the use of drugs that can have detrimental effects on the musculoskeletal system. Some of these and their potential side effects include antiseizure drugs (osteomalacia), phenothiazines (gait changes), corticosteroids (avascular necrosis, decreased bone and muscle mass), and potassium-depleting diuretics (muscle cramps and weakness). Ask postmenopausal women about the use of hormone therapy.

Surgery or Other Treatments Ask about any hospitalizations related to a musculoskeletal problem. Document the reason for hospitalization; the date and duration; and the treatment, including ongoing rehabilitation. Record details of emergency treatment for musculoskeletal injuries. Get specific information about any surgical procedure, postoperative course, and complications. Ask the patient about past total knee or total hip replacement. If the patient had a period of prolonged immobilization, consider the possible development of disuse osteoporosis and muscle atrophy.

Functional Health Patterns Past or developing musculoskeletal problems can affect the patient’s overall health. The use of functional health patterns helps organize assessment data. Table 61.2 outlines specific questions to ask in relation to functional health patterns.

TABLE 61.2 Health HistoryMusculoskeletal

System

Health Perception–Health Management Pattern • Describe your usual daily activities. • Do you have any problems performing these activities?∗ Describe

what you do if you have trouble dressing, preparing meals and feeding yourself, performing basic hygiene, writing or using the phone, or maintaining your home. • Do you have to lift heavy objects? Do your work or exercise habits require repetitive motion or joint stress? Describe any special equipment you use or wear when you work or exercise that helps protect you from injury. • Do you take any drugs or herbal products to manage your musculoskeletal problem? If so, what are their names and what are the expected effects?

Nutritional-Metabolic Pattern • What is your usual daily intake of food and snacks? • Do you have problems preparing your food? • What dietary supplements do you take? Do you take calcium or vitamin D supplements? • What is your weight? Describe any recent weight loss or gain.

Elimination Pattern • Does your musculoskeletal problem make it hard for you to reach the toilet in time?∗ • Do you need any assistive devices or equipment to manage toileting?∗ • Do you have constipation related to decreased mobility or drugs taken for your musculoskeletal problem?∗

Activity-Exercise Pattern • Do you need help in completing your usual daily activities because of a musculoskeletal problem?∗

• Describe your usual exercise pattern. Do you have musculoskeletal symptoms before, during, or after exercising?∗ • Are you able to move all your joints comfortably through full range of motion? • Do you use any prosthetic or orthotic devices?∗

Sleep-Rest Pattern • Do you have any problems sleeping because of a musculoskeletal problem?∗ • Do you need frequent position changes at night?∗ • Do you wake up at night because of musculoskeletal pain?∗ • Do you use complementary and alternative therapies to help you sleep at night?∗

Cognitive-Perceptual Pattern • Describe any musculoskeletal pain you have. How do you manage your pain? Ask about adjunctive therapies, such as heat and cold, or complementary and alternative therapies, such as acupuncture.

Self-Perception–Self-Concept Pattern • Have changes in your musculoskeletal system (posture, walking, muscle strength) and decreased ability to do certain things affected how you feel about yourself?∗ • Have these changes affected your lifestyle?∗

Role-Relationship Pattern

• Do you live alone? • Describe how family, friends, or others help you with your musculoskeletal problem. • Describe the effect of your musculoskeletal problem on your work and your social relationships.

Sexuality-Reproductive Pattern • Describe any sexual concerns related to your musculoskeletal problem.

Coping–Stress Tolerance Pattern • Describe how you deal with problems such as pain, weakness, or immobility that have resulted from your musculoskeletal problem.

Value-Belief Pattern • Describe any cultural practices or religious beliefs that may influence the treatment of your musculoskeletal problem.



If yes, describe.

Health Perception–Health Management Pattern Ask about the patient’s health practices related to the musculoskeletal system. This includes maintaining normal body weight, avoiding excessive stress on muscles and joints, and using proper body mechanics when lifting objects. Ask the patient about tetanus, pertussis, and polio immunizations. Safety practices can affect the patient’s predisposition for certain

injuries and illnesses. Ask the patient about safety practices related to the work environment, home life, recreation, and exercise. For example, if the patient is a computer programmer, ask about ergonomic adaptations in the office that decrease the risk for carpal tunnel syndrome or low back pain. Identifying problems in this area will direct your plan for patient teaching. Get a family history of rheumatoid arthritis, SLE, ankylosing spondylitis, osteoarthritis, gout, osteoporosis, and scoliosis. A patient may have a genetic predisposition to these or other musculoskeletal disorders.

Nutritional-Metabolic Pattern The patient’s description of a typical day’s diet gives clues to areas of nutritional concern that can affect the musculoskeletal system. Adequate intake of vitamins C and D, calcium, and protein is essential for a healthy musculoskeletal system. Abnormal nutritional patterns can contribute to problems such as osteomalacia and osteoporosis. Maintaining normal weight is an important nutritional goal. Obesity places added stress on weight-bearing joints, such as the knees, hips, and spine. This increases the risk for cartilage deterioration and ligament instability.

Genetic Risk Alert Autoimmune Diseases • Many autoimmune diseases of the musculoskeletal system have a genetic basis involving human leukocyte antigens (HLAs). • These diseases include ankylosing spondylitis, rheumatoid arthritis, and SLE.

Osteoporosis

• Genetic factors contribute to osteoporosis by influencing bone mineral density, and bone size, quality, and turnover.

Osteoarthritis, Gout, and Scoliosis • A genetic predisposition is a contributing risk factor in all these diseases.

Muscular Dystrophy • The most common types of muscular dystrophy are X-linked recessive disorders.

Elimination Pattern Questions about the patient’s mobility may reveal problems with ambulating to the toilet. Ask the patient if an assistive device, such as an elevated toilet seat or a grab bar, is needed to manage toileting. Decreased mobility from a musculoskeletal problem can lead to constipation. Musculoskeletal problems can contribute to bowel or bladder incontinence when ambulation is a problem.

Activity-Exercise Pattern Many musculoskeletal problems can affect the patient’s activityexercise pattern. Get a detailed account of the type, duration, and frequency of exercise and recreational activities. Compare daily, weekend, and seasonal patterns because occasional exercise can be more of a problem than regular exercise. Ask the patient about clumsiness or limitations in movement, pain, weakness, crepitus, or any change in bones or joints that interferes with daily activities. Extremes of activity related to occupation can affect the musculoskeletal system. For example, a desk job can negatively affect muscle flexibility and strength. Jobs that require heavy lifting or pushing can lead to damage of joints and supporting structures.

Specifically ask the patient about work-related musculoskeletal injuries, including treatment and time lost from work.

Sleep-Rest Pattern The discomfort caused by musculoskeletal problems can interfere with the patient’s normal sleep pattern and lead to fatigue.6 Ask the patient about any changes in sleep patterns. If the patient describes poor sleep related to a musculoskeletal problem, ask about the type of bedding and pillows used, bedtime routine, sleeping partner, and sleeping positions.

Cognitive-Perceptual Pattern Fully discuss any pain reported by the patient due to a musculoskeletal problem. To give a baseline for later reassessment, ask the patient to describe the intensity of the pain on a numeric scale from 0 to 10 (0 = no pain, 10 = most severe pain imaginable). Reassessments over time help to determine the effectiveness of any treatment plan. Ask the patient about measures used to manage pain. Also ask about related problems, such as joint swelling or muscle weakness, and any adjustments that help with the problem. (Pain is discussed in Chapter 8.)

Self-Perception–Self-Concept Pattern Many chronic musculoskeletal problems lead to deformities and a reduction in activities. This can have a serious negative impact on the patient’s body image and sense of personal worth.6 Assess the patient’s feelings about these changes and any effect on interactions with family and friends.

Role-Relationship Pattern Impaired mobility and chronic pain from musculoskeletal problems can negatively affect the patient’s ability to perform in roles of spouse, parent, and/or employee. The ability to pursue and maintain meaningful social and personal relationships also can be affected by

musculoskeletal problems. Carefully ask the patient about role performance and relationships. If the patient lives alone, any musculoskeletal problem and rehabilitation may make it hard or impossible to continue to do so. Assess how much help is available from family, friends, and other caregivers. Find out if other resources are needed, such as physical therapy and home health care.

Sexuality-Reproductive Pattern Ask women about their menstrual history. Episodes of premenopausal amenorrhea can contribute to the development of osteoporosis.7 The pain of musculoskeletal problems can affect the patient’s ability to obtain sexual satisfaction. Explore this area in a sensitive and nonjudgmental way. Help the patient feel comfortable discussing any sexual problems related to pain, movement, and positioning. More information on obtaining patient data in this area is discussed in Chapter 50.

Coping–Stress Tolerance Pattern Mobility limitations and pain are serious potential stressors that challenge the patient’s coping resources. Recognize the potential for difficulty coping in the patient and family or significant other. Additional questions will help to determine if a musculoskeletal problem is causing difficulties in coping and adjusting.

Value-Belief Pattern Ask the patient about cultural or religious beliefs that may influence acceptance of treatment for the musculoskeletal problem. These may include recommendations for diet, exercise, medication, and lifestyle modifications.

Case Study—cont’d

Subjective Data

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A focused subjective assessment of G.A. revealed the following

information: Past Medical History: Hypertension for 6 years. Type 2 diabetes for 11 yr, 40-pack-yr smoking history. Medications: Metformin (Glucophage) 500 mg PO bid; glyburide (DiaBeta) 5 mg/day PO; hydrochlorothiazide 50 mg PO bid. Health Perception–Health Management: Currently smokes 1 pack of cigarettes per day. Is trying to quit but finding it difficult. Drinks alcohol at night. Nutritional-Metabolic: G.A. is 5 ft, 2 in tall and weighs 160 lb (BMI 29.3 kg/m2). Does not take any nutritional supplements and avoids milk and other dairy products because they make her “gassy.” Activity-Exercise: Minimally active; does not exercise. Able to perform ADLs without assistance. Denies any history of musculoskeletal problems. Cognitive-Perceptual: Rates toe pain at 8 on a scale of 0 to 10. Describes sharp, burning pain that increases in intensity with any movement. Coping–Stress Tolerance: Is asking for pain medicine “as strong as you can give me.”

Discussion Questions 1. What subjective assessment findings are of most concern to you? 2. Is this an appropriate time to talk with G.A. about her weight? 3. Based on these subjective findings, what should be included in the physical assessment? You will learn more about the physical assessment of the musculoskeletal system in the next section. See p. 1438 for more information on G.A. Answers available at http://evolve.elsevier.com/Lewis/medsurg.

Objective Data Physical Examination The basic musculoskeletal physical examination involves inspection, palpation, neurovascular assessment, and range of motion, strength, and reflex testing. Other special tests can be used to assess for specific conditions. Conduct a general overview. While obtaining a careful health history, choose areas to concentrate on during the local examination. Take specific measurements as indicated by the local examination.

Inspection A systematic inspection is done, starting at the head and neck then moving to the upper extremities, lower extremities, and trunk. The regular use of a systematic approach is important to avoid missing important aspects of the examination. Inspect the skin for general color, scars, or other overt signs of previous injury or surgery. Certain skin lesions require further investigation because they can indicate underlying disorders. For example, butterfly rash over the cheeks and nose is characteristic of SLE. Note the patient’s general posture and body build, muscle size and symmetry, and symmetry and contour of joints. Observe for any swelling, deformity, nodules or masses, and discrepancies in limb length or muscle size. Use the patient’s opposite body part for comparison when you suspect an abnormality. If the patient can move independently, assess posture and gait by watching the patient walk, stand, and sit. Musculoskeletal and neurologic problems can result in abnormal gait patterns.

Palpation As with inspection, palpation usually proceeds head to toe. Examine the neck, shoulders, elbows, wrists, hands, back, hips, knees, ankles, and feet. Warm your hands to prevent muscle spasm, which can interfere with identifying essential landmarks or soft tissue structures. Carefully palpate any specific areas of concern because of a subjective

report or abnormal appearance on inspection. Both superficial and deep palpation are usually done consecutively. Consider the underlying anatomy structures and landmarks you are palpating. Purposefully palpate both muscles and joints to evaluate skin temperature, local tenderness, swelling, and crepitation. Establish the relationship of adjacent structures. Evaluate the general contour, abnormal prominences, and local landmarks. Note the specific anatomic location of any abnormal findings.

Motion When assessing the patient’s joint mobility, carefully evaluate active and passive range of motion (ROM). ROM is the full movement potential of a joint. Measurements should be similar for active and passive maneuvers. Active ROM means the patient takes their own joints through all movements without assistance. Passive ROM occurs when someone else moves the patient’s joints without their assistance through the full ROM. Be careful in performing passive ROM because of the risk for injury to underlying structures. If pain or resistance occurs, stop at once. If you note deficits in active or passive ROM, assess functional ROM to determine if joint changes are affecting the ability to perform ADLs. Ask the patient if activities, such as eating, grooming, dressing, and bathing, require help or cannot be done at all. We use a goniometer to accurately assess ROM. It measures the angle of the joint (Fig. 61.7). We do not usually measure specific degrees of ROM of all joints. If a specific musculoskeletal problem has been identified, measure ROM of the affected joint. A less exact but valuable assessment method is simply to compare the ROM of 1 extremity with that on the opposite side. Common movements that occur at the synovial joints, including abduction, adduction, flexion, and extension, are described in Table 61.3.

Muscle-Strength Testing Grade the strength of individual muscles or groups of muscles during contraction on a 5-point scale (Table 61.4). Grade normal muscle

strength with full resistance to opposition as a 5/5 bilaterally. To test resistance to opposition, have the patient apply resistance as you exert a force. For example, have the patient try to extend the elbow while you try to flex it. Compare muscle strength with the strength of the opposite extremity. Note any subtle variations in muscle strength when comparing the patient’s dominant and nondominant sides. Variations in strength also exist when comparing people.

Measurement When limb length discrepancies or subjective problems are noted, measure limb length and circumferential muscle mass. For example, when gait disorders are observed, measure leg length between the anterosuperior iliac crest and the bottom of the medial malleolus. Then compare it with the similar measurement of the opposite extremity. Measure muscle mass circumferentially at the largest area of the muscle. When recording measurements, record the exact location at which the measurements were obtained (e.g., the left quadriceps muscle was measured 15 cm above the patella). This tells the next examiner of the exact area to measure and ensures consistency during reassessment.

FIG. 61.7 A, Goniometer. B, Measurement of joint ROM using a goniometer. A, From Wilson SF, Giddens JF: Health assessment for nursing practice, ed 5, St Louis, 2013, Mosby. B, From Barkauskas V, Baumann L, Stoltenberg-Allen K, et al: Health and physical assessment, ed 2, St Louis, 1998, Mosby.

TABLE 61.3 Synovial Joint Movements

Movement Abduction

Description Movement of part away from midline of body

Adduction

Movement of part toward midline of body

Circumduction Dorsiflexion

Circular motion of a body part from a combination of flexion, abduction, extension, and adduction Flexion of the ankle and toes toward the shin

Eversion

Turning of sole outward away from midline of body

Extension

Straightening of joint that ↑ angle between 2 bones

External rotation

Movement along longitudinal axis away from midline of body

Flexion

Bending of joint from muscle contraction that causes ↓ angle between 2 bones

Hyperextension Extension in which angle exceeds 180 degrees Movement along longitudinal axis toward midline of body Internal rotation Turning of sole inward toward midline of body Inversion

Pronation

Moving the first and fifth metacarpals anteriorly from a flattened palm (“cupping position”); makes it possible to hold objects between the thumb and fingers Flexion of the ankle and toes toward the plantar surface of the foot (“toes pointed”) Turning of palm downward

Supination

Turning of palm upward

Opposition Plantar flexion

TABLE 61.4 Muscle Strength Scale

0/5

No detection of muscular contraction

1/5

Barely detectable flicker or trace of contraction with observation or palpation

2/5

Active movement of body part with elimination of gravity

3/5

Active movement against gravity only and not against resistance

4/5

Active movement against gravity and some resistance

5/5

Active movement against full resistance without evident fatigue (normal muscle strength)

FIG. 61.8 A, Thoracic scoliosis. B, X-ray of same patient showing scoliosis greater than 90 degrees. From Hawary R, Chukwunyerenwa C: Update on evaluation and treatment of scoliosis, Pediatr Clin North Am 61:1223, 2014.

Other Note the patient’s use of an assistive device, such as a walker or cane. Assess the patient for proper fit while reviewing the safe and correct technique for using these devices. Regularly review with the patient the use of the assistive device to be sure it is still appropriate and safe. Ask the patient if the assistive device is used regularly. If not, determine possible reasons for inconsistent use.8 Scoliosis is a lateral S-shaped curvature of the thoracic and lumbar spine. Unequal shoulder and scapula height is usually noted when the patient is observed from the back (Fig. 61.8). Ask the patient to place the hands together above the head as if diving into a swimming pool and slowly bend forward at the waist, allowing assessment of thoracic rib prominence or paravertebral muscle prominence in the lumbar spine. Advanced scoliosis can impair lung and heart function. The straight-leg-raising test is done on the supine patient with sciatica or leg pain. Passively raise the patient’s leg 60 degrees or less. The test is positive if the patient reports pain along the distribution of the sciatic nerve. A positive test shows nerve root irritation from intervertebral disc prolapse and herniation, especially at level L4-5 or L5-S1. Assessment of reflexes is discussed in Chapter 55. Table 61.5 shows an example of how to record a normal physical assessment of the musculoskeletal system. Abnormal assessment findings of the musculoskeletal system are described in Table 61.6.

TABLE 61.5 Normal Physical Assessment of the

Musculoskeletal System • Ordinary spinal curvatures • No muscle atrophy or asymmetry • No joint swelling, deformity, or crepitation

• No tenderness on palpation of spine, joints, or muscles • Full ROM of all joints without pain or laxity • Muscle strength of 5/5 A focused assessment is used to evaluate previously identified musculoskeletal problems and to monitor for signs of new problems. See the Focused Assessment of the Musculoskeletal System box.

Case Study—cont’d Objective Data: Physical Examination

(© pixelheadphoto/iStock/Thinkstock.)

A focused assessment of G.A. reveals the following:

BP 128/94, heart rate 88, respiratory rate 26, temp 96.8° F, O2 saturation 98%. Alert and oriented × 3. Lungs are clear bilaterally. Left great toe is red and swollen. No open wounds. Tremendous pain on palpation and with any movement of the left great toe. +1 Pedal pulses bilaterally.

Discussion Questions 1. What physical assessment findings concern you most? 2. Based on results of the subjective and physical assessment, what diagnostic studies might you expect to be ordered for G.A.? You will learn more about diagnostic studies related to the musculoskeletal system in the next section. See p. 1442 for more information on G.A. Answers available at http://evolve.elsevier.com/Lewis/medsurg.

Focused Assessment Musculoskeletal System Use this checklist to be sure key assessment steps have been done.

Subjective Ask the patient about any of the following and note responses.

Joint pain or stiffness

Y

N

Muscle weakness

Y

N

Bone pain

Y

N

Objective: Diagnostic Check the results of the following diagnostic studies.

X-ray



MRI or CT scan



Bone scan



Objective: Physical Examination Inspect and Palpate Spine and extremities (compare sides) for alignment, contour, symmetry, size, gross deformities



Joints for ROM, tenderness or pain, heat, crepitus, swelling



Muscles (compare sides) for size, symmetry, tone, tenderness, or pain



Bones for tenderness or pain



TABLE 61.6 Assessment

AbnormalitiesMusculoskeletal System

Finding Achilles tendonitis Ankylosis Antalgic gait

Ataxic gait Atrophy Boutonnière deformity

Contracture

Possible Etiology and Significance Pain in ankle and posterior calf, initially Stress on Achilles tendon when running or walking. Can progress to over time causing pain at rest. inflammation. Stiffness and fixation of a joint. Chronic joint inflammation and destruction (e.g., rheumatoid arthritis). Shortened stride with minimal weight Pain or discomfort in the bearing on the affected side, resulting in a lower extremity on weight limp. bearing. Can be due to trauma or other disorders. Staggering, uncoordinated gait often with Neurogenic disorders (e.g., sway. spinal cord lesion). ↓ Size and strength of muscle leading to ↓ Muscle denervation, function and tone. contracture, prolonged disuse from immobilization. Finger abnormality, flexion of proximal Typical deformity of interphalangeal (PIP) joint and rheumatoid and psoriatic hyperextension of the distal interphalangeal arthritis caused by disruption (DIP) joint of the fingers (see Fig. 64.4, B). of extensor tendons over the fingers. Resistance of movement of muscle or joint Shortening of muscle or

Description

due to fibrosis of supporting soft tissues. Crepitation (crepitus) Frequent, audible crackling sound with palpable grating that accompanies movement. Separation of 2 bones from their normal Dislocation position within a joint. While walking, neck, trunk, and knees flex Festinating gait and the body is rigid. Delayed start with short, quick, shuffling steps. Speed may ↑ as if patient is unable to stop (festination). Small fluid-filled mass over a tendon sheath Ganglion cyst or joint, usually on dorsal surface of wrist or foot. Kyphosis (dowager’s Exaggerated thoracic curvature. hump)

Limited range of motion (ROM)

Dull ache along outer aspect of elbow, worsens with twisting and grasping motions. Joint does not achieve expected degrees of motion.

Lordosis (swayback)

Exaggerated lumbar curvature.

Muscle spasticity

↑ Muscle tone (rigidity) with sustained muscle contractions (spasms); stiffness or tightness may interfere with gait, movement, speech. General muscle tenderness and pain.

Lateral epicondylitis (tennis elbow)

Myalgia

Paresthesia

Numbness and tingling, often described as a “pins and needles” sensation.

Pes planus (flatfoot)

Abnormal flatness of the sole and arch of the foot.

Plantar fasciitis

Burning, sharp pain on heel and sole of foot. Worse in the morning with first step out of bed. Asymmetric elevation of shoulders, scapulae, and iliac crests with lateral spine curvature (Fig. 61.8).

Scoliosis

ligaments, tightness of soft tissue, incorrect positioning of immobilized extremity. Fracture, dislocation, temporomandibular joint dysfunction, osteoarthritis. Trauma, disorders of surrounding soft tissues. Neurogenic disorders (e.g., Parkinson’s disease). Inflammation of tissues around a joint, which can increase in size or disappear. Poor posture, tuberculosis, arthritis, osteoporosis, growth disturbance of vertebral epiphyses, vertebral fractures. Injury, inflammation, and/or partial tearing of tendon at its insertion on epicondyle. Injury, inflammation, contracture. Other spinal deformities, muscular dystrophy, obesity, flexion contracture of hip, congenital dislocation of hip. Neuromuscular disorders, such as multiple sclerosis (MS) or cerebral palsy. Chronic pain syndromes (e.g., fibromyalgia). Overuse, injury, or strain. May result from statin therapy. Compromised sensory nerves, often due to edema in a closed space (e.g., cast, bulky dressing). Spinal stenosis. Hereditary, muscle paralysis, mild cerebral palsy, early muscular dystrophy, injury to posterior tibial tendon. Chronic degenerative/reparative cycle resulting in inflammation. Idiopathic or congenital condition, neuromuscular, fracture or dislocation,

Short-leg gait

A limp, unless corrective footwear used.

osteomalacia. Leg length discrepancy ≥1 in, generally of structural origin (arthritis, fracture). Neurogenic (e.g., cerebral palsy, hemiplegia).

Short steps with dragging of foot. Jerky, uncoordinated, cross-knee (scissor) movement. ↑ Hip and knee flexion to clear the foot from Neurogenic disorders (e.g., Steppage gait the floor. Foot drop is evident, foot slaps peroneal nerve injury, down and along walking surface. paralyzed dorsiflexor muscles). Partial dislocation of joint. Instability of joint capsule Subluxation and supporting ligaments (e.g., trauma, arthritis). Hyperextension of the PIP joint with flexion Typical deformity of Swan neck deformity of the metacarpophalangeal (MCP) and DIP rheumatoid and psoriatic joints of the fingers (see Fig. 64.4, D). arthritis caused by contracture of muscles and tendons. Enlargement, often of a joint due to fluid Trauma or inflammation. Swelling collection. Usually leads to pain, stiffness. Superficial swelling, pain, and tenderness Inflammation that often Tenosynovitis along a tendon sheath. occurs with infection, injury, or overuse. Neck is rotated and laterally bent in Prolonged contraction of Torticollis (wryneck) unusual position to one side. neck muscles (congenital or acquired). Fingers drift to ulnar side of forearm (see Typical deformity of Ulnar deviation Fig. 64.4, A). rheumatoid arthritis due to (ulnar drift) tendon contracture. When knees are together and there is 1 in (2.5 cm) exists.

Arthritis, congenital deformity.

Diagnostic Studies of Musculoskeletal System Many diagnostic studies are used to assess the musculoskeletal system. Tables 61.7, 61.8, and 61.9 present the most common studies. Select studies are described in more detail next. The use of studies such as x-rays, MRI, and bone scans has greatly improved orthopedic care. The x-ray is the most common diagnostic

study used to assess musculoskeletal problems and to monitor treatment effectiveness. Because bones are denser than other tissues and contain calcium, most x-rays are absorbed by the bone tissue and do not penetrate it. Dense areas show as white on the standard x-ray. X-rays provide information about bone deformity, joint congruity, bone density, and calcification in soft tissue. X-rays are useful for diagnosing fractures. They also help evaluate genetic, developmental, infectious, inflammatory, malignant, metabolic, and degenerative disorders. Aspirated synovial fluid is assessed for volume, color, clarity, viscosity, and mucin clot formation. Normal synovial fluid is transparent and colorless or straw colored. It should be scant in amount and of low viscosity. Fluid from an infected joint may be purulent and thick or gray and thin. In gout, the fluid may be whitish yellow. Blood may be aspirated if there is hemarthrosis due to injury or a bleeding disorder. The mucin clot test indicates the character of the protein portion of the synovial fluid. Normally a white, ropelike mucin clot is formed. In the presence of inflammation, the clot fragments easily. The fluid is examined grossly for floating fat globules, which indicate bone injury. In septic arthritis, protein content is increased, and glucose is considerably decreased. Presence of uric acid crystals suggests a diagnosis of gout. A Gram stain and culture also may be done to assess for the presence and type of infection.

TABLE 61.7 Serology StudiesMusculoskeletal

System Test Aldolase

Reference Intervals 22–59 mU/L

30–120 U/L Alkaline phosphatase (0.5–2.0

Description and Purpose Useful in monitoring muscular dystrophy, dermatomyositis. Enzyme made by osteoblasts, needed for mineralization of organic bone matrix. ↑ Levels found with healing fractures, bone cancers, osteoporosis, osteomalacia, Paget’s disease.

µkat/L) Negative or Anticyclic citrullinated 24 hours) are at risk for O2 toxicity. • Target FIO2 levels are to maintain SpO2 >92% and PaO2 between 60 and 80 mm Hg. • Assess ABGs for evidence of excess O2. • Monitor patient for signs of O2 toxicity: uncontrolled coughing, chest pain, and dyspnea.

Positive Pressure Ventilation Positive pressure ventilation (PPV) is the main method used with acutely ill patients (Fig. 65.19). During inspiration the ventilator pushes air into the lungs under positive pressure. Unlike spontaneous

ventilation, intrathoracic pressure is raised during lung inflation rather than lowered. Expiration occurs passively as in normal expiration. There are 2 categories of PPV: volume and pressure ventilation.13

Volume Ventilation With volume ventilation, a predetermined VT is delivered with each inspiration. The amount of pressure needed to deliver the breath varies based on compliance and resistance factors of the patientventilator system. So, the VT is consistent from breath to breath, but airway pressures vary.

Pressure Ventilation With pressure ventilation, the peak inspiratory pressure is predetermined. The VT delivered to the patient varies based on the selected pressure and compliance and resistance factors of the patientventilator system. Careful attention must be given to the VT to prevent unplanned hyperventilation or hypoventilation. For example, when the patient breathes out of synchrony with the ventilator, the pressure limit may be reached quickly, and the volume of gas delivered may be small.

Settings of Mechanical Ventilators Mechanical ventilator settings regulate rate, VT, O2 concentration, and other characteristics of ventilation (Table 65.10, Fig. 65.20). Settings are based on the patient’s status (e.g., ABGs, ideal body weight, current physiologic state, level of consciousness, respiratory muscle strength). Settings are evaluated and adjusted until oxygenation and ventilation targets have been reached. It is important that you check that all ventilator alarms are always on. Alarms alert the staff to potentially dangerous situations, such as mechanical malfunction, apnea, unplanned extubation, or patient asynchrony with the ventilator (Table 65.11). On many ventilators, the

alarms can be temporarily suspended or silenced for up to 2 minutes for suctioning or testing while a staff member is in the room. After that time, the alarm system automatically turns back on.

Safety Alert Alarm Fatigue • Alarm fatigue can develop in those who hear an excess number of alarms, resulting in sensory overload. • This can cause a delayed response to alarms or dismissing them altogether and can lead to serious adverse events (e.g., patient death). • One way to reduce alarm fatigue includes customizing alarm parameters based on patient specific needs.23

FIG. 65.19 Patient receiving mechanical ventilation. Courtesy Draeger Medical, Houston, TX.

TABLE 65.10 Settings of Mechanical Ventilation

Adapted from Urden LD, Stacy, KM, Lough ME: Critical care nursing: Diagnosis and management, ed 8, St Louis, 2018, Elsevier.

Ventilator Alarms Mechanical ventilators may become disconnected or malfunction. Most deaths from accidental ventilator disconnection occur while the alarm is off. Most accidental disconnections are discovered by lowpressure alarms. The most frequent site for disconnection is between the tracheal tube and the adapter. Push connections together and then twist to secure more tightly. Be certain that alarms are always set and activated. Chart that this is the case. You can pause alarms (not inactivate) during suctioning or removal from the ventilator, but you must reactivate them before leaving the patient’s bedside.

Ventilator malfunction may occur. Although most agencies have emergency generators in case of a power failure and newer ventilators may have battery backup, power failure is always a possibility. Have a plan for manually ventilating all patients who depend on a ventilator. If, at any time, you decide the ventilator is malfunctioning (e.g., failure of O2 supply), disconnect the patient from the machine and manually ventilate with a BVM and 100% O2 until the ventilator is fixed or replaced.

FIG. 65.20 Ventilator control panel (Puritan Bennett 840). From Roberts JR: Roberts and Hedges’ clinical procedures in emergency medicine and acute care, ed 7 ed, St Louis, 2019, Elsevier.

Modes of Volume Ventilation The ways by which the patient and ventilator interact to deliver effective ventilation are called ventilator modes. The selected ventilator mode is based on how much WOB the patient should or can perform.

WOB is the inspiratory effort needed to overcome the elasticity and viscosity of the lungs along with the airway resistance. The mode is determined by the patient’s ventilatory status, respiratory drive, and ABGs. Generally, ventilator modes are controlled or assisted. With controlled ventilatory support, the ventilator does all the WOB for the patient. With assisted ventilatory support, the ventilator and patient share the WOB. Historically, volume modes, such as controlled mandatory ventilation (CMV), assist-control ventilation (ACV), and synchronized intermittent mandatory ventilation (SIMV), have been used to treat critically ill patients. Pressure modes, such as pressure support ventilation (PSV), pressure-control ventilation (PCV), and inverse ratio ventilation (PC-IRV) are becoming more common.24 Table 65.12 describes ventilator modes.

Assist-Control Ventilation With assist-control ventilation (ACV), the ventilator delivers a preset VT at a preset frequency. When the patient initiates a spontaneous breath, the ventilator senses a decrease in intrathoracic pressure and then delivers the preset VT. The patient can breathe faster than the preset rate but not slower. ACV has the advantage of allowing the patient some control over ventilation while providing some assistance. It is used in patients with a variety of conditions, including neuromuscular disorders (e.g., Guillain-Barré syndrome), pulmonary edema, and acute respiratory failure. With ACV, the patient has the potential for hyperventilation. The spontaneously breathing patient can easily be overventilated, resulting in hyperventilation. If the volume or minimum rate is set too low and the patient is apneic or weak, the patient can be hypoventilated. Thus these patients need vigilant assessment and monitoring of ventilatory status, including respiratory rate, ABGs, SpO2, and ScvO2 or SvO2. It is important that the sensitivity, or amount of negative pressure needed to start a breath, is appropriate to the patient’s condition. For example, if it is too hard for the patient to begin a breath, the WOB is increased and the patient may tire (i.e., the patient “rides” the ventilator) or develop ventilator dyssynchrony

(i.e., the patient “fights” the ventilator).

TABLE 65.11 Managing Mechanical Ventilation

Alarms

Adapted from Urden LD, Stacy KM, Lough ME: Critical care nursing: Diagnosis and management, ed 8, St Louis, 2018, Elsevier.

TABLE 65.12 Modes of Mechanical Ventilation

Modified from Wiegand DL: AACN procedure manual for high acuity, progressive, and critical care, ed 7, St Louis, 2017, Elsevier; and Urden LD, Stacy, KM, Lough ME: Critical care nursing: Diagnosis and management, ed 8, St Louis, 2018, Elsevier.

Synchronized Intermittent Mandatory Ventilation With synchronized intermittent mandatory ventilation (SIMV), the ventilator delivers a preset VT at a preset frequency in synchrony with the patient’s spontaneous breathing. Between ventilator-delivered breaths, the patient can breathe spontaneously through the ventilator circuit. Thus the patient receives the preset FIO2 during the spontaneous breaths but self-regulates the rate and VT of those breaths. SIMV is used during continuous ventilation and during weaning from the ventilator. It may be combined with PSV (described later). Potential benefits of SIMV include improved patient-ventilator synchrony, lower mean airway pressure, and prevention of muscle atrophy as the patient takes on more of the WOB. SIMV has disadvantages. If spontaneous breathing decreases when

the preset rate is low, ventilation may not be adequately supported. Only patients with regular, spontaneous breathing should use lowrate SIMV. Weaning with SIMV demands close monitoring and may take longer because the rate of breathing is gradually reduced. Patients being weaned with SIMV may have increased muscle fatigue associated with spontaneous breathing efforts.

Modes of Pressure Ventilation Pressure Support Ventilation With pressure support ventilation (PSV), positive pressure is applied to the airway only during inspiration and is used with the patient’s spontaneous respirations. The patient must be able to initiate a breath in this modality. The level of positive airway pressure is preset so that the gas flow rate is greater than the patient’s inspiratory flow rate. As the patient starts a breath, the machine senses the spontaneous effort and supplies a rapid flow of gas at the initiation of the breath and variable flow throughout the breath. With PSV, the patient determines inspiratory length, VT, and respiratory rate. VT depends on the pressure level and airway compliance. PSV is used with continuous ventilation and during weaning. It also may be used with SIMV during weaning. PSV is not often used as ventilatory support during acute respiratory failure because of the risk for hypoventilation and apnea. Advantages include increased patient comfort, decreased WOB (because inspiratory efforts are augmented), decreased O2 consumption (because inspiratory work is reduced), and increased endurance conditioning (because the patient is exercising respiratory muscles).

Pressure-Control and Pressure-Control Inverse Ratio Ventilation Pressure-control ventilation (PCV) provides a pressure-limited breath delivered at a set rate. It may permit spontaneous breathing. The VT is not set. It is determined by the pressure limit set. Pressure-control

inverse ratio ventilation (PC-IRV) combines pressure-limited ventilation with an inverse ratio of inspiration (I) to expiration (E). Some HCPs use PC without IRV. The I/E ratio is the ratio of duration of inspiration to the duration of expiration. This ratio is normally 1:2 or 1:3. With IRV, the I/E ratio begins at 1:1 and may progress to 4:1. Prolonged positive pressure is applied, increasing inspiratory time. IRV gradually expands collapsed alveoli. The short expiratory time has a PEEP-like effect, preventing alveolar collapse. Because IRV imposes a nonphysiologic breathing pattern, the patient needs sedation and often paralysis. PC-IRV is used for patients with acute respiratory distress syndrome (ARDS) who continue to have hypoxemia despite high levels of PEEP. Not all patients with poor oxygenation respond to PCIRV.

Airway Pressure Release Ventilation Airway pressure release ventilation (APRV) permits spontaneous breathing at any point during the respiratory cycle with a preset CPAP with short timed pressure releases. The CPAP level (pressure high, pressure low) is adjusted to keep oxygenation goals while the timed releases (time high, time low) are increased or decreased to meet ventilation goals.25 VT is not set. It varies depending on the CPAP level, the patient’s compliance and resistance, and spontaneous breathing effort. This mode is best for patients who need high pressure levels for alveolar recruitment (open collapsed alveoli). An advantage is that it allows for spontaneous respirations. This may reduce the need for deep sedation or paralytics.

Positive End-Expiratory Pressure Positive end-expiratory pressure (PEEP) is a ventilatory maneuver, or mechanical ventilator setting, in which positive pressure is applied to the airway during exhalation. Normally during exhalation, airway pressure drops to near 0, and exhalation occurs passively. With PEEP, exhalation is passive but pressure falls to a preset level, often 3 to 20

cm H2O. Lung volume during expiration and between breaths is greater than normal with PEEP. This increases FRC and often improves oxygenation by restoring the lung volume that normally remains at the end of passive exhalation. The mechanisms by which PEEP increases FRC and oxygenation include increased aeration of patent alveoli, aeration of previously collapsed alveoli, and prevention of alveolar collapse throughout the respiratory cycle. PEEP is titrated to the point that oxygenation improves without compromising hemodynamics. We call this optimal PEEP. Often 5 cm H2O PEEP (referred to as physiologic PEEP) is used prophylactically to replace the glottic mechanism, help maintain a normal FRC, and prevent alveolar collapse. PEEP of 5 cm H2O is used for patients with a history of alveolar collapse during weaning. PEEP improves gas exchange, vital capacity, and inspiratory force when used during weaning. In contrast, auto-PEEP is not purposely set on the ventilator but is a result of inadequate exhalation time. Auto-PEEP is more PEEP over what is set by the HCP. This added PEEP may result in increased WOB, barotrauma, and hemodynamic instability. Interventions to limit auto-PEEP include sedation and analgesia, large-diameter ET tube, bronchodilators, short inspiratory times, and decreased respiratory rates. Reducing water accumulation in the ventilator circuit by frequent emptying or use of heated circuits also limits autoPEEP. In patients with short exhalation times and early airway closure (e.g., asthma), setting PEEP above auto-PEEP can offset auto-PEEP effects by splinting the airway open during exhalation and preventing “air trapping.” FIO2 often can be reduced when PEEP is used. PEEP is generally indicated in all patients who are mechanically ventilated. The classic indication for PEEP therapy is ARDS (see Chapter 67). PEEP is used with caution in patients with increased ICP, low CO, and hypovolemia. In these cases, the adverse effects of high PEEP may outweigh the benefits.

Other Modes

Advances in ventilator technology have led to the development of other pressure modes. However, the names and features of these other options are manufacturer specific. The superiority of these modes has not been proven. Some examples include volume-assured pressure ventilation and adaptive support ventilation.

Check Your Practice You are caring for a 75-yr-old woman who was orally intubated yesterday for respiratory distress due to pneumonia and placed on ACV. Her ventilator settings are: VT 400, RR 14 (set), PEEP 5, and FIO2 40%. You respond to the ventilator alarm sounding and note audible air movement heard around her ET tube cuff as you suction her. The alarm panel shows “low exhaled tidal volume.” She appears anxious, with the following vital signs: HR 112, RR 26, and SpO2 89%. • What would be your next steps?

Other Methods to Improve Oxygenation and Ventilation Automatic Tube Compensation Automatic tube compensation (ATC) is an adjunct designed to overcome WOB through an artificial airway. It is currently available on many ventilators. ATC is increased during inspiration and decreased during expiration. It is set by entering the internal diameter of the patient’s airway and the desired number for compensation. ATC may be less effective in patients with excess secretions or who need longer term ventilation.

High-Frequency Oscillatory Ventilation High-frequency oscillatory ventilation (HFOV) involves delivery of a small VT (usually 1 to 5 mL/kg of body weight) at rapid respiratory

rates (100 to 300 breaths/min). The goals are to recruit (e.g., alveolar expansion) and maintain lung volume and reduce intrapulmonary shunting. While HFOV may be a useful mode for patients with lifethreatening hypoxia, it has not improved survival of patients with ARDS.26 Patients receiving HFOV must be sedated and may need to be paralyzed to suppress spontaneous respiration.

Nitric Oxide Nitric oxide (NO) is a gaseous molecule that is made intravascularly and takes part in the regulation of pulmonary vascular tone. Inhibiting NO production results in pulmonary vasoconstriction. Administering continuous inhaled NO results in pulmonary vasodilation. NO may be given through an ET tube, a tracheostomy, or a face mask. Currently, NO is used as a diagnostic screening tool for pulmonary hypertension and to improve oxygenation during mechanical ventilation in this patient population. The use of NO does not reduce mortality in patients with ARDS and may cause kidney injury.27

Prone Positioning Prone positioning is the repositioning of a patient from a supine or lateral position to a prone (on the stomach, face down) position. This repositioning improves lung recruitment through various mechanisms. Gravity reverses the effects of fluid in the dependent parts of the lungs as the patient is moved from supine to prone. The heart rests on the sternum, away from the lungs, contributing to an overall uniformity of pleural pressures. The prone position requires increased sedation and is nurse-intensive. It is an effective supportive therapy used in critically ill patients with severe ARDS to improve oxygenation.28

Extracorporeal Membrane Oxygenation Extracorporeal membrane oxygenation (ECMO) is an alternative form of pulmonary support for the patient with severe respiratory failure (Fig.

65.21).13 It is used most often in the pediatric and neonatal populations but is increasingly being used in adults. ECMO is a modification of cardiac bypass. It involves partially removing blood from a patient with large-bore catheters, infusing O2, removing CO2, and returning the blood to the patient. This intensive therapy requires systemic anticoagulation and is a time-limited intervention. A skilled team of specialists, including a perfusionist, must be continuously at the bedside.

FIG. 65.21 ECMO circuit. The circuit consists of a pump, oxygenator, and heating-cooling element. Circulatory access is typically obtained through the femoral vein and artery. From Mann DL, Zipes DP, Libby P, et al: Braunwald’s heart disease: A textbook of cardiovascular medicine, ed 11, St Louis, 2019, Saunders.

Informatics in Practice Importing Monitor and Ventilator Data • In many ICUs, monitor data (e.g., vital signs, hemodynamic pressures, core temperature, pulse oximetry) are directly imported into the electronic health record (EHR). Ventilator data also may be sent to the EHR. • Depending on the information technology system, this connectivity of monitoring devices and ventilators can help drive evidence-based practice. Trends can be readily noted, and prompts can link the user to protocols. • Some systems can send alarms or notifications to the HCP from the EHR. • Always verify that correct patient data were imported into the EHR when documenting. Delete artifact or false data according to your agency’s policy.

Complications of Positive Pressure Ventilation Although PPV may be essential to maintain ventilation and oxygenation, it can cause adverse effects. It may be hard to distinguish complications of mechanical ventilation from the underlying disease.

Cardiovascular System PPV can affect circulation because of the transmission of increased mean airway pressure to various structures in the thorax. Increased intrathoracic pressure compresses the thoracic vessels. This

compression causes decreased venous return to the heart, left ventricular end-diastolic volume (preload), and CO, resulting in hypotension. Mean airway pressure is further increased if PEEP is being titrated (greater than 5 cm H2O) to improve oxygenation. If the lungs are noncompliant (e.g., ARDS), airway pressures are not as easily transmitted to the heart and blood vessels. Thus effects of PPV on CO are reduced. Conversely, with compliant lungs (e.g., COPD), there is increased danger of transmission of high airway pressures and negative effects on hemodynamics. Hypovolemia (e.g., hemorrhage) and decreased venous tone (e.g., sepsis, spinal shock) can further compromise venous return. Restoring and maintaining the circulating blood volume are important in minimizing cardiovascular complications.

Pulmonary System Barotrauma As lung inflation pressures increase, risk for barotrauma increases. Barotrauma results when the increased airway pressure distends the lungs and possibly ruptures fragile alveoli or emphysematous blebs. Patients with noncompliant lungs (e.g., COPD) are at greatest risk for barotrauma. Patients with stiff lungs (e.g., ARDS) who are given high inspiratory pressures and high levels of PEEP (greater than 5 cm H2O) or have a lung abscess from necrotizing organisms (e.g., staphylococci) are also at risk. Air can escape into the pleural space from alveoli or the interstitium and become trapped. Pleural pressure increases and collapses the lung, causing a pneumothorax (see Chapter 27 for more about pneumothorax.) The lungs receive air during inspiration but cannot expel it during expiration. Respiratory bronchioles are larger on inspiration than expiration. They may close on expiration, and air becomes trapped. With PPV, a simple pneumothorax can become a life-threatening tension pneumothorax. The mediastinum and contralateral lung are compressed, reducing CO. Immediate treatment of the pneumothorax is required.

Pneumomediastinum usually begins with rupture of alveoli into the lung interstitium. Progressive air movement occurs into the mediastinum and subcutaneous neck tissue, and a pneumothorax often follows. New, unexplained subcutaneous emphysema is an indication for immediate chest x-ray. Pneumomediastinum and subcutaneous emphysema may be too small to detect on x-ray or clinically before the development of a pneumothorax.

Volutrauma The concept of volutrauma in PPV relates to the lung injury that occurs when a large VT is used to ventilate noncompliant lungs. Volutrauma results in alveolar rupture and movement of fluids and proteins into the alveolar spaces. Low-volume ventilation should be used in patients with ARDS to protect the lungs.

Alveolar Hypoventilation Alveolar hypoventilation can be caused by inappropriate ventilator settings, leakage of air from the ventilator tubing or around the ET tube or tracheostomy cuff, lung secretions or obstruction, and low ventilation/perfusion ratio. A low VT or respiratory rate decreases minute ventilation. This results in hypoventilation, atelectasis, and respiratory acidosis. A leaking cuff or tubing that is not secured may cause air leakage and lower VT. Mobilizing the patient, turning the patient at least every 2 hours, encouraging deep breathing and coughing, and suctioning (as needed) may limit lung secretions. Increasing the VT, adding small increments of PEEP, and adding a preset number of sighs to the ventilator settings (i.e., a deeper than normal breath incorporated into the respiratory cycle) can help reduce the risk for atelectasis.

Alveolar Hyperventilation Respiratory alkalosis can occur if the respiratory rate or VT is set too high (mechanical overventilation) or if the patient receiving assisted ventilation is hyperventilating. It is easy to overventilate a patient on

PPV. Especially at risk are patients with chronic alveolar hypoventilation and CO2 retention. For example, the patient with COPD may have a chronic PaCO2 elevation (acidosis) and compensatory bicarbonate retention by the kidneys. When the patient is ventilated, the patient’s “normal baseline” rather than the standard normal values is the therapeutic goal. If the COPD patient is returned to a standard normal PaCO2, the patient will develop alkalosis because of the retained bicarbonate. Such a patient could move from compensated respiratory acidosis to serious metabolic alkalosis. The presence of alkalosis makes weaning from the ventilator difficult. Alkalosis, especially if the onset is abrupt, can have serious consequences, including hypokalemia, hypocalcemia, and dysrhythmias. Usually the patient with COPD who is supported on the ventilator does better with a short inspiratory and longer expiratory time. If hyperventilation is spontaneous, it is important to determine the cause and treat it. Common causes include hypoxemia, pain, fear, anxiety, or compensation for metabolic acidosis. Patients who fight the ventilator or breathe out of synchrony may be anxious or in pain. If the patient is anxious and fearful, sitting with the patient and verbally coaching the patient to breathe with the ventilator or weaning the ventilator to a more appropriate setting may help. If these measures fail, manually ventilating the patient slowly with a BVM and 100% O2 may slow breathing enough to bring it in synchrony with the ventilator.

Ventilator-Associated Pneumonia The risk for HAI pneumonia is highest in patients requiring mechanical ventilation because the ET or tracheostomy tube bypasses normal upper airway defenses. Poor nutrition, immobility, and the underlying disease process (e.g., immunosuppression, organ failure) make the patient more prone to infection. Ventilator-associated pneumonia (VAP) is pneumonia that occurs 48 hours or more after ET intubation.29 It occurs in as many as 27% of all intubated patients.

Patients who develop VAP have significantly longer hospital stays and higher mortality rates than those who do not. Half of the patients develop early VAP (VAP that occurs within 96 hours of mechanical ventilation). In those with early VAP, sputum cultures often grow gram-negative bacteria (e.g., E coli, Klebsiella, Streptococcus pneumoniae, H influenzae). Organisms associated with late VAP include antibiotic-resistant organisms, such as Pseudomonas aeruginosa and oxacillin-resistant Staphylococcus aureus. These organisms are abundant in the hospital environment and the patient’s GI tract. They can spread in a number of ways, including contaminated respiratory equipment, inadequate hand washing, adverse environmental factors (e.g., poor room ventilation, high traffic flow), and decreased patient ability to cough and clear secretions. Colonization of the oropharynx tract by gramnegative organisms predisposes the patient to gram-negative pneumonia. Clinical signs that suggest VAP include fever, high white blood cell count, purulent or odorous sputum, crackles or wheezes on auscultation, and pulmonary infiltrates noted on chest x-ray. The patient is given antibiotics after appropriate cultures are taken by tracheal suctioning or bronchoscopy and when infection is evident. Guidelines for VAP prevention include (1) minimizing sedation, including daily spontaneous awakening trials (SATs) and daily spontaneous breathing trials (SBTs), (2) early exercise and mobilization, (3) use of ET tubes with subglottic secretion drainage ports for patients likely to be intubated greater than 48 to 72 hours, (4) HOB elevation at a minimum of 30 to 45 degrees unless medically contraindicated, (5) oral care with chlorhexidine, and (6) no routine changes of the patient’s ventilator circuit tubing.30 Other preventive measures include strict hand washing before and after suctioning, whenever ventilator equipment is touched, and after contact with any respiratory secretions (see Nursing Management: Artificial Airway earlier in this chapter). Always wear gloves when in contact with the patient and change gloves between activities (e.g., emptying urinary catheter drainage, hanging an IV drug). Last,

always drain the water that collects in the ventilator tubing away from the patient as it collects.

Safety Alert VAP Prevention Strategies • Practice good hand hygiene techniques before and after suctioning. • Wear gloves when providing oral hygiene. • Suction patients as needed for comfort. • Keep the HOB elevated >30 to 45 degrees. • Turn patient according to agency policy (e.g., side to side every 2 hours). • Initiate early mobilization. • Follow agency policy for limiting sedation with SAT. • Perform daily SBT unless contraindicated.31

Psychosocial Needs The patient receiving mechanical ventilation often has physical and emotional stress. In addition to the problems related to critical care patients discussed at the beginning of this chapter, the patient supported by a mechanical ventilator is unable to speak, eat, move, or breathe normally. Tubes and machines cause pain, fear, and anxiety. Usual activities, such as eating, elimination, and coughing, are extremely complicated. The ABCDEF Bundle is an evidence-based practice of providing care that strives to attain an environment in which all patients receiving mechanical ventilation are calm, delirium free, and able to express their needs for pain control, positioning, and reassurance. The ABCDEF Bundle ensures (1) Assessment, (2) Both SATs and SBTs are done, (3) correct Choice of analgesia and sedation, (4) Delirium

prevention and management, (5) Early mobility, and (6) Family engagement.32 Feeling safe is an overpowering need of patients on mechanical ventilation. Work to strengthen the various factors that affect feeling safe. Encourage hope, as appropriate, and build trusting relationships with both the patient and caregiver. Involve them in decision making as much as possible.19

Sedation and Analgesia Patients receiving PPV may need sedation (e.g., propofol) and/or analgesia (e.g., fentanyl) to help with optimal ventilation. Before starting sedation or analgesia in the mechanically ventilated patient who is agitated or anxious, identify the cause of distress. Common problems that can result in patient agitation or anxiety include PPV, nutritional deficits, pain, hypoxemia, hypercapnia, drugs, and environmental stressors (e.g., sleep deprivation). At times, the decision is made to paralyze the patient with a neuromuscular blocking agent (e.g., cisatracurium [Nimbex]) to provide more effective synchrony with the ventilator and improve oxygenation. Remember that the paralyzed patient can hear, see, and feel. It is essential to give IV sedation and analgesia concurrently when the patient is paralyzed. Sedated or paralyzed patients may be aware of their surroundings. You should always address them as if they were awake and alert. Monitoring patients receiving these drugs is challenging. Assess the patient using train-of-four (TOF) peripheral nerve stimulation, physiologic signs of pain or anxiety (e.g., changes in HR and BP), and ventilator synchrony. The TOF assessment involves using a peripheral nerve stimulator to deliver 4 successive stimulating currents to elicit muscle twitches (Fig. 65.22).33 The number of twitches varies with the amount of neuromuscular blockade. The usual goal is 1 or 2 twitches out of 4 currents. Noninvasive electroencephalogram technology (e.g., bispectral index monitoring [BIS]) can be used to guide sedative and analgesic therapy.34 Excess administration of neuromuscular blocking agents

may predispose the patient to prolonged paralysis and muscle weakness even after these agents are stopped.

Neurologic System In patients with head injury, PPV, especially with PEEP, can impair cerebral blood flow. The increased intrathoracic positive pressure impedes venous drainage from the brain. This results in jugular venous distention. The patient may have increases in ICP due to the impaired venous return and subsequent increase in cerebral volume. Elevating the HOB and keeping the patient’s head in alignment may reduce the harmful effects of PPV on ICP.

Sodium and Water Imbalance Progressive fluid retention often occurs after 48 to 72 hours of PPV, especially PPV with PEEP. Fluid retention is associated with decreased urine output and increased sodium retention. Fluid balance changes may be due to decreased CO, which causes decreased renal perfusion. This stimulates the release of renin with the subsequent production of angiotensin and aldosterone (see Chapter 44, Fig. 44.4). This results in sodium and water retention. It is possible that pressure changes within the thorax are associated with decreased release of atrial natriuretic peptide, which also causes sodium retention. Less insensible water loss occurs via the airway because ventilated delivered gases are humidified with body-temperature water. As a part of the stress response, release of antidiuretic hormone (ADH) and cortisol contributes to sodium and water retention.

FIG. 65.22 Placement of electrodes along ulnar nerve.

Gastrointestinal System Patients receiving PPV are stressed because of the serious illness, immobility, or discomforts associated with the ventilator. This places the patient at risk for developing stress ulcers and GI bleeding. Patients with a preexisting ulcer or those receiving corticosteroids have a higher risk. Any circulatory compromise, including reduced CO caused by PPV, may contribute to ischemia of the gastric and intestinal mucosa and increase the risk for translocation of GI bacteria. Stress ulcer prophylaxis includes giving histamine (H2)-receptor blockers (e.g., ranitidine), proton pump inhibitors (PPIs) (e.g.,

esomeprazole), or EN to decrease gastric acidity and reduce the risk for stress ulcer and hemorrhage. PPIs may increase the risk for Clostridium difficile infection.35 (This is discussed in Chapter 41 on p. 898.) Gastric and bowel dilation may occur because of gas accumulation in the GI tract from swallowed air. The irritation of an artificial airway may cause excessive air swallowing and gastric dilation. Gastric or bowel dilation may put pressure on the vena cava, decrease CO, and prohibit adequate diaphragmatic excursion during spontaneous breathing. Elevation of the diaphragm from a paralytic ileus or bowel dilation leads to compression of the lower lobes of the lungs. This may cause atelectasis and compromise respiratory function. Decompression of the stomach is done by inserting an OG or NG tube. Immobility, sedation, circulatory impairment, decreased oral intake, use of opioid pain medicines, and stress contribute to decreased peristalsis. The patient’s inability to exhale against a closed glottis may make defecation difficult. As a result, the ventilated patient is at risk for constipation. A bowel regimen should be started to help with motility.

Musculoskeletal System Maintaining muscle strength and preventing complications associated with immobility are important. Adequate analgesia and nutrition can enhance exercise tolerance. Plan for early and progressive mobility of appropriate patients receiving PPV.8 In collaboration with physical and occupational therapy, perform passive and active exercises to maintain muscle tone in the upper and lower extremities. Simple maneuvers, such as leg lifts, knee bends, or arm circles, are appropriate. Prevent contractures, pressure injuries, footdrop, and external rotation of the hip and legs by proper positioning and using specialized mattresses or beds. Use a portable ventilator or provide manual ventilation with a BVM and 100% O2 when ambulating patients who are mechanically ventilated.

Nutritional Therapy: Patient Receiving Positive Pressure Ventilation PPV and the hypermetabolism associated with critical illness can contribute to inadequate nutrition. Critical illness, trauma, and surgery are associated with hypermetabolism, anxiety, pain, and increased WOB, which greatly increase caloric expenditure. The presence of an ET tube eliminates the normal route for eating. Inadequate nutrition makes the patient receiving prolonged mechanical ventilation prone to poor O2 transport from anemia and to poor tolerance of minimal exercise. It can delay mechanical ventilation weaning, decrease resistance to infection, and slow recovery. Critically ill patients have frequent EN interruptions. We often hold feedings due to procedures and during routine nursing care. Poor nutrition and the disuse of respiratory muscles contribute to decreased respiratory muscle strength. Serum protein levels (e.g., albumin, prealbumin, transferrin, total protein) are usually decreased. Patients unlikely to be able to eat independently for 3 to 5 days should have a nutritional assessment and EN started within 24 to 48 hours of admission.9 EN is the preferred method to meet caloric needs of mechanically ventilated patients (see Chapter 39 for discussion of EN). Consult the dietitian to determine the caloric and nutrient needs of these patients. When eating with a tracheostomy tube in place, the patient should tilt the head slightly forward to assist with swallowing and to prevent aspiration. The diet may be restricted to soft foods (e.g., puddings, ice cream) and thickened liquids. Patients with a long-term tracheostomy will likely have a tube placed in the stomach (gastrostomy) or small bowel (jejunostomy) for nutritional support (see Chapter 39). Patients may be able to eat normally once the tracheostomy site heals and they meet criteria that will allow them to take oral intake. Swallowing studies and a speech therapy consultation are done to assess the patient’s readiness for oral intake.

Nursing Management Caring for the Patient Requiring Mechanical Ventilation In the critically ill patient who requires mechanical ventilation, the RN and RT provide most of the care. Some patients who need chronic mechanical ventilation may be in long-term care settings or at home. In these settings, the RN and RT assess the patient and plan and evaluate care, but implementation of some activities may be delegated. • Develop plan for communication with the patient who has an ET tube or tracheostomy. • Give sedatives, analgesics, and paralytic drugs as needed. • Teach patient and caregiver about mechanical ventilation and weaning procedures. • Auscultate breath sounds and respiratory effort, assessing for decreased ventilation or adventitious sounds. • Monitor ventilator settings and alarms. • Determine need for ET tube suctioning and suction patients as needed. • Reposition and secure ET tube (based on agency policy). • Monitor oxygenation level and signs of respiratory fatigue during weaning procedure. • Provide enteral nutrition. • Oversee UAP: • Obtain vital signs and report to the RN. • Provide personal hygiene, skin care, and oral care, as directed by RN. • Assist with frequent position changes, including ambulation, as directed by the RN. • Help to perform passive or active range-of-motion (ROM) exercises.

Collaborate With Respiratory Therapist (RT) • Auscultate breath sounds and respiratory effort, assessing for decreased ventilation or adventitious sounds. • Monitor ventilator settings and alarms. • Change ventilator settings as needed or ordered by HCP. • Maintain appropriate cuff inflation on ET tube. • Determine need for ET tube suctioning and suction patients as needed. • Reposition and secure ET tube (based on agency policy). • Monitor oxygenation level and signs of respiratory fatigue during weaning procedure.

Collaborate With Physical and Occupational Therapist • Perform ROM exercises. • Assist with early and progressive ambulation as directed by the RN.

Collaborate With Dietitian • Assess and monitor patient’s nutritional status. • Recommend formulations for enteral and/or parenteral nutrition as needed.

Collaborate With Speech Therapist • Perform swallowing studies. • Assess patient’s cognitive function and assist with communication.

• Provide teaching for patient with a long-term tracheostomy.

Collaborate With Social Worker • Work with the patient and caregiver to identify care needs. • Help the patient with transitions through the health care system. • Teach the patient the various levels of care and seek to optimize outcomes in a cost-effective manner.

Weaning From Positive Pressure Ventilation and Extubation Weaning is the process of reducing ventilator support and resuming spontaneous breathing. The weaning process differs for patients on short-term ventilation (up to 3 days) versus long-term ventilation (longer than 3 days). Those with short-term ventilation (e.g., after heart surgery) have a linear weaning process. Patients with prolonged PPV (e.g., patients with COPD who develop respiratory failure) often have a weaning process that consists of alternating gains and losses. Preparation for weaning begins when PPV is started and involves a team approach (e.g., HCP, RT, RN, patient). Weaning consists of 3 phases: the preweaning phase, the weaning process, and the outcome phase. The preweaning, or assessment phase, looks at the patient’s ability to breathe spontaneously. Assessment depends on a combination of respiratory and nonrespiratory factors (Table 65.13). Note the resolution of the primary problem that prompted patient admission. The patient’s lungs should be reasonably clear on auscultation and chest x-ray. Weaning assessment parameters should include criteria to assess muscle strength (negative inspiratory force) and endurance (spontaneous VT, vital capacity, minute ventilation, rapid shallow breathing index). There should be minimal secretions, the ability to cough and gag, and a cuff leak when the ET tube cuff is deflated. Nonrespiratory factors include the patient’s neurologic status;

hemodynamics; fluid, electrolytes, and acid-base balance; nutrition; and hemoglobin. It is important to have an alert, well-rested, and well-informed patient relatively free from pain and anxiety who can cooperate with the weaning plan. This does not mean complete withdrawal from sedatives or analgesics. Instead, drugs should be titrated to achieve comfort without causing excessive drowsiness.

TABLE 65.13 Indicators for Weaning

Weaning Readiness Patients receiving mechanical ventilation for respiratory failure should undergo a formal assessment of weaning potential if the following are satisfied∗: 1. Reversal of the underlying cause of respiratory failure 2. Adequate oxygenation • PaO2/FIO2 >150–200 • SpO2 ≥90% • PEEP ≤5–7 cm H2O • FIO2 ≤40%–50% • pH ≥7.25 3. Hemodynamically stabile • Absence of myocardial ischemia • Absence of clinically significant hypotension (low dose or no vasopressor therapy) 4. Patient ability to initiate respirations 5. Optional criteria • Hemoglobin ≥7–10 g/dL • Core temperature ≤100.4° F (38° C) to 101.3° F (38.5° C) • Mental status awake and alert or easily arousable



The decision to use these criteria are personalized to the patient. Adapted from Urden LD, Stacy, KM, Lough ME: Critical care nursing: Diagnosis and management, ed 8, St Louis, 2018, Elsevier. A SAT and an SBT are recommended in patients who meet a daily safety screen. A SAT should be done by stopping all sedatives and, in patients without active pain, all opioids. Sedation should be restarted at 50% of the previous dose in patients who “fail” the SAT and remain off in patients who “pass.”

Evidence-Based Practice Early Mobilization and Critically Ill Patients W.R. is a 68-yr-old man who has been in the ICU for 2 days. He is receiving mechanical ventilation, and weaning trials are planned. You have started passive exercises and dangling with W.R. You prepare to

discuss early mobilization with him and his partner.

Making Clinical Decisions Best Available Evidence. Implementing an early exercise and mobilization protocol for stable, mechanically ventilated patients is safe and well tolerated. Early mobilization improves patient outcomes (e.g., prevention of ICU-acquired weakness, maintenance of long-term function, preservation of quality of life) and reduces the length of hospital stays. Involving patients and families in decision-making around care (e.g., early mobilization) is an identified priority among this group. Clinician Expertise. Your unit has successfully implemented AACN’s ABCDEF bundle related to delirium, immobility, sedation/analgesia, and ventilator management in the ICU. You know that patients and their families often worry about ambulating with complex equipment attached to them. Patient Preferences and Values. W.R. writes on the computer that he does not want to get out of bed until his “breathing tube is out.” His partner tells you he is “afraid of falling.”

Implications for Nursing Practice 1. What will you tell W.R. and his partner about the benefits of and protocol for early mobilization? 2. How will you involve them in the decision to take part in the program?

Reference for Evidence McKenzie E, Potestio M.L, Boyd J.M, et al. Reconciling patient and provider priorities for improving the care of critically ill patients: a consensus method and qualitative analysis of decision making. Health Expect. 2017;20:1367.

An SBT should last at least 30 minutes but no more than 120 minutes.13 It may be done with low levels of PEEP, low levels of PSV, or FIO2. Tolerance of the trial may lead to extubation. Failure to tolerate an SBT should prompt a search for reversible or complicating factors and a return to a nonfatiguing ventilator modality. The SBT should be tried daily, unless contraindicated. All health care team members should be familiar with the weaning plan. The use of a weaning protocol decreases ventilator days.13 The ventilator settings are not as important as the use of a daily protocol to prevent delays in weaning. The patient receiving SIMV can have the ventilator breaths gradually reduced as ventilatory status permits. PEEP or PSV can be added to SIMV. PSV is thought to provide gentle, slow respiratory muscle conditioning. It may be especially beneficial for patients who are deconditioned or have heart problems. Weaning may be tried at any time of day. It is usually done after a period of time when the patient has been ventilated in a rest mode. The rest mode should be a stable, nonfatiguing, and comfortable form of support for the patient. It is important to allow the patient’s respiratory muscles to rest between weaning trials. Once the respiratory muscles become fatigued, they may need 12 to 24 hours to recover. The patient and caregiver need ongoing emotional support. Explain the weaning process to them to keep them informed of progress. Place the patient in a comfortable sitting or semirecumbent position. Obtain baseline vital signs and respiratory parameters. During the weaning trial, closely monitor the patient for signs and symptoms that may signal a need to end the trial (e.g., tachypnea, dyspnea, tachycardia, dysrhythmias, sustained desaturation [SpO2 less than 90%], hypertension or hypotension, agitation, diaphoresis, anxiety, sustained VT less than 5 mL/kg, changes in mental status). Record the patient’s tolerance throughout the weaning process. Include statements about the patient’s and the caregiver’s feelings. The weaning outcome phase is the period when the patient is ready for extubation or weaning is stopped because progress is not being made. The patient who is ready for extubation should receive

hyperoxygenation and suctioning (e.g., oropharynx, ET tube) prior to extubation. Loosen the ET tapes or commercial holder. Have the patient take a deep breath, and at the peak of inspiration, deflate the ET tube cuff and remove the tube in one motion. After removal, encourage the patient to deep breath and cough. Suction the oropharynx as needed. Have the patient say their name to assess vocalization. Give supplemental O2 and provide naso-oral care. Carefully monitor vital signs, respiratory status, and oxygenation immediately after extubation, within 1 hour, and per agency policy. If the patient does not tolerate extubation (e.g., decreased SpO2 levels, tachypnea or bradypnea, tachycardia, decreased level of consciousness, decrease in PaO2, increase in PaCO2), immediate reintubation or a trial of noninvasive ventilation may be needed.

Chronic Mechanical Ventilation Mechanical ventilators are now a part of long-term and home care. In some instances, terminally ill, ventilated patients may be discharged to hospice. The emphasis on controlling hospital costs has increased the number of patients discharged early from the acute care setting and the need to provide highly technical care, such as mechanical ventilation, in home settings. The success of home mechanical ventilation depends, in part, on careful predischarge assessment and planning for the patient and caregivers. Patients must first meet criteria to be discharged on mechanical ventilation (e.g., tracheostomy, stabile mechanical ventilator settings). Both negative pressure and positive pressure ventilators can be used in the home. Negative pressure ventilators do not require an artificial airway and are less complicated to use. Several types of small, portable (battery-powered) positive pressure ventilators are available. They can be attached to a wheelchair or placed on a bedside table. Settings and alarms on these ventilators are simpler to use than on the standard ICU ventilators. Home mechanical ventilation has advantages and disadvantages. Having the patient in the home eliminates the strain that the hospital

setting imposes on family dynamics. Caregivers may feel helpless when they first hear about the need for long-term mechanical ventilation. However, these feelings are often balanced by the opportunity to take part in the patient’s care in the home setting. At home, the patient may be able to take part in more activities of daily living around a personalized schedule. Because of the smaller size of the home ventilator, the patient may be more mobile. Another advantage is a lower risk for HAIs. Disadvantages include problems related to equipment, reimbursement, caregiver stress and fatigue, and the patient’s complex needs. Ventilated patients are usually dependent, requiring extensive nursing care, at least initially. Disposable products may not be reimbursable. Carefully assess financial resources when arranging home ventilation. Schedule a meeting with the interprofessional care team (e.g., social worker, home health care RN, RT) before starting a discharge teaching plan. Caregivers may seem enthusiastic about caring for their loved one in the home but may not understand the sacrifices they may have to make financially and in personal time and commitment. Encourage caregivers to consider respite care to periodically relieve their stress and fatigue.

TABLE 65.14 Cross-References to Critical Care

Content Topic Acute coronary syndrome (ACS)

Discussed in Chapter 33

Acute heart failure

34

Acute respiratory distress syndrome (ARDS)

67

Acute respiratory failure

67

Basic life support and CPR

Appendix A

Burns

24

Cardiac pacemakers

35

Cardiac surgery

33

Central venous access device (CVAD)

16

Continuous renal replacement therapy (CRRT)

46

Delirium

59

Dysrhythmias

35

Emergencies

68

End-of-life (EOL) care

9

Enteral nutrition (EN)

39

Head injury and ICP monitoring

56

Multiple organ dysfunction syndrome (MODS)

66

Myocardial infarction (MI)

33

Oxygen delivery

28

Pain management

8

Parenteral nutrition (PN)

39

Pulmonary edema

34

Renal dialysis

46

Shock

66

Stroke

57

Systemic inflammatory response syndrome (SIRS)

66

Tracheostomy

26

Trauma

68

Other Critical Care Content Table 65.14 lists critical care content discussed in other chapters of this book.

Case Study Critical Care and Mechanical Ventilation

(© Thinkstock.)

Patient Profile R.K. is a 72-yr-old white man who collapsed in his home. He was found by his daughter, and she activated the emergency response

system. He was unresponsive on admission to the emergency department and is still unresponsive on arrival to the ICU. He has an oral ET tube in place and is receiving mechanical ventilation. A largebore, peripheral IV has been placed and fluids are infusing.

Subjective Data None. Patient has no eye opening. He is intubated and is unresponsive to painful stimuli.

Objective Data Physical Examination • Noninvasive BP 100/75 mm Hg; apical-radial HR 128; temperature 102° F (38.8° C); SpO2 is 98% • ECG: atrial fibrillation with a rapid ventricular response • Purulent secretions suctioned from ET tube • Breath sounds: coarse crackles bilaterally, decreased breath sounds on the right • Weight: 168 lb. (76 kg)

Diagnostic Studies • Chest x-ray shows right lower lung consolidation • ABGs: pH 7.48; PaO2 94 mm Hg; PaCO2 30 mm Hg; HCO3 34 mEq/L • CT scan is positive for a hemorrhagic stroke

Interprofessional Care • Positive pressure ventilation settings: assist-control mode • Settings: FIO2 70%, VT 700 mL, respiratory rate 16 breaths/min,

PEEP 5 cm H2O • Orogastric tube. EN at 25 mL/hr, increase by 20 mL/hr every 2 hr with a goal of 80 mL/hr to start on day 2 • External condom catheter for urinary drainage and measurement • HOB elevated at 40 degrees • Reposition at least every 2 hr • Azithromycin (Zithromax) 500 mg IV q24hr • Cefotaxime 2 gram IV q6hr • NS at 75 mL/hr

Discussion Questions 1. Identify 2 reasons for intubating and providing mechanical ventilation for R.K. 2. What does R.K.’s ABG indicate, and which ventilator setting(s) should be changed to prevent barotrauma? 3. R.K.’s BP drops to 80 mm Hg. Despite increasing doses of vasopressors and fluid challenges, his BP is still low. A central venous catheter and an arterial line are inserted. Arterial pressure–based cardiac output (APCO) monitoring is started. What would be the purpose of hemodynamic monitoring in this patient? 4. Priority Decision: What are 2 priority nursing considerations for a patient with invasive monitoring? 5. R.K.’s pulmonary condition deteriorates. PaO2 drops to 60 mm Hg, and SpO2 is 89%. PEEP is increased to 7.5 cm H2O. What implications does this have for R.K. given his hemodynamic status? What other intervention could be done to improve oxygenation? 6. Collaboration: What patient care activities can you delegate to unlicensed assistive personnel? 7. Evidence-Based Practice: R.K.’s caregivers want to know why he is to receive tube feedings. What would you tell them? What

is the evidence to support the use of EN? 8. Patient-Centered Care: After 4 days, R.K. is still unresponsive and has developed renal failure. The HCP thinks the patient will not recover from his neurologic injury and wishes to discuss goals of care with the patient’s caregivers. What would be your role in this meeting? Answers available at http://evolve.elsevier.com/Lewis/medsurg.

Bridge to NCLEX Examination The number of the question corresponds to the same-numbered outcome at the beginning of the chapter.

1. Certification in critical care nursing (CCRN) by the American Association of Critical-Care Nurses indicates that the nurse a. is an advanced practice nurse who cares for acutely and critically ill patients. b. may practice independently to provide symptom management for the critically ill. c. has earned a master’s degree in the field of advanced acute and critical care nursing. d. has practiced in critical care and successfully completed a test of critical care knowledge. 2. What are appropriate nursing interventions for the patient with delirium in the ICU? (select all that apply) a. Use clocks and calendars to maintain orientation. b. Encourage round-the-clock presence of caregivers at the bedside. c. Silence all alarms, reduce overhead paging, and avoid

conversations around the patient. d. Sedate the patient with appropriate drugs to protect the patient from harmful behaviors. e. Identify physiologic factors that may be contributing to the patient’s confusion and irritability. 3. The critical care nurse recognizes that an ideal plan for caregiver involvement includes a. having a caregiver at the bedside at all times. b. allowing caregivers at the bedside at preset, brief intervals. c. a personally devised plan to involve caregivers with care and patient needs. d. restriction of visiting in the ICU because the environment is overwhelming to caregivers. 4. To establish hemodynamic monitoring for a patient, the nurse zeros the a. cardiac output monitoring system to the level of the left ventricle. b. pressure monitoring system to the level of the catheter tip in the patient. c. pressure monitoring system to the level of the atrium, or the phlebostatic axis. d. pressure monitoring system to the level of the atrium, or the midclavicular line. 5. The hemodynamic changes the nurse expects to find after successful initiation of intraaortic balloon pump therapy in a patient with cardiogenic shock include (select all that apply)

a. decreased SV. b. decreased SVR. c. decreased PAWP. d. increased diastolic BP. e. decreased myocardial O2 consumption. 6. The purpose of adding PEEP to positive pressure ventilation is to a. increase functional residual capacity and improve oxygenation. b. increase FIO2 to try to help wean the patient and avoid O2 toxicity. c. determine if the patient can be weaned and avoid pneumomediastinum. d. determine if the patient is in synchrony with the ventilator or needs to be paralyzed. 7. The nursing management of a patient with an artificial airway includes a. maintaining ET tube cuff pressure at 35 cm H2O. b. routine suctioning of the tube at least every 2 hours. c. observing for cardiac dysrhythmias during suctioning. d. preventing tube dislodgment by limiting mouth care to lubrication of the lips. 8. The nurse monitors the patient with positive pressure mechanical ventilation for a. paralytic ileus because pressure on the abdominal contents affects bowel motility. b. diuresis and sodium depletion because of increased

release of atrial natriuretic peptide. c. signs of cardiovascular insufficiency because pressure in the chest impedes venous return. d. respiratory acidosis in a patient with COPD because of alveolar hyperventilation and increased PaO2 levels. 1. d, 2. a, d, e, 3. c, 4. c, 5. b, c, d, e, 6. a, 7. c, 8. c For rationales to these answers and even more NCLEX review questions, visit http://evolve.elsevier.com/Lewis/medsurg.

Evolve Website/Resources List http://evolve.elsevier.com/Lewis/medsurg

Review Questions (Online Only) Key Points Answer Keys to Questions • Rationales for Bridge to NCLEX Examination Questions • Answer Guidelines for Case Study on p. 1563 Student Case Study • Patient With Pulmonary Embolism and Respiratory Failure Nursing Care Plan • eNursing Care Plan 65.1: Patient on Mechanical Ventilation Conceptual Care Map Creator Audio Glossary Supporting Media • Animation

• Endotracheal Intubation Content Updates

References 1. American Association of Critical-Care Nurses: AACN scope and standards for acute and critical care nursing. Retrieved from www.aacn.org/nursingexcellence/standards/aacn-scope-and-standards-for-acuteand-critical-care-nursing-practice. Tirkkonen J, Tamminen T, Skrifvars MB: Outcome of adult patients attended by rapid response teams: A systematic review of the literature, Resuscitation 112:43, 2017.

3. American Association of Critical-Care Nurses: Frequently asked questions about APRN Consensus Model—For nurse practitioners. Retrieved from www.aacn.org/wd/certifications/content/aprn-nurses-npfaqs.pcms?menu=certification. 4. Papathanassoglou ED, Hadjibalassi M, Miltiadous P, et al: Effects of an integrative nursing intervention on pain in critically ill patients, Amer J Crit Care 27:172, 2018. 5. Hariharan U, Garg R: Sedation and analgesia in critical care, J Anesth Crit Care Open Access 7:262, 2017. Boyko Y, Jennum P, Toft P: Sleep quality and circadian rhythm disruption in the intensive care unit: A review, Nat Sci Sleep 9:277, 2017. Kanova M, Sklienka P, Kula R, et al: Incidence and risk factors for delirium development in ICU patients. A prospective observational study, Biomedical Paper 161:187, 2017. Blair GJ, Mehmood T, Rudnick M, et al: Nonpharmacologic and

medication minimization strategies for the prevention and treatment of ICU delirium: A narrative review, J Intensive Care Med 34:183, 2019. McClave SA, Taylor BE, Martindale RG, et al: Guidelines for the provision and assessment of nutrition support therapy in the adult critically ill patient, J Parenter Enteral Nutr 40:159, 2016. Davidson JE, Aslakson RA, Long AC, et al: Guidelines for familycentered care in the neonatal, pediatric, and adult ICU, CCM 45:103, 2017.

11. Clark AP, Guzzetta CE: A paradigm shift for patient/family-centered care in intensive care units: Bring in the family, Crit Care Nurse 37:96, 2017. 12. Edwards Lifesciences: Hemodynamic monitoring. Retrieved from www.edwards.com/devices/hemodynamic-monitoring. Wiegand DL: AACN procedure manual for high acuity, progressive, and critical care, ed 7, St Louis, 2017, Elsevier.

14. Baird MB: Manual of critical care nursing, ed 7, St Louis, 2016, Elsevier. Cook JL, Colvin M, Francis GS, et al: Recommendations for the use of mechanical circulatory support. Ambulatory and community patient care. A scientific statement from the AHA, Circulation 135:e1, 2017.

16. Herritt B, Chaudhuri D, Thavorn K, et al: Early vs. late tracheostomy in intensive care settings: Impact on ICU and hospital costs, J Crit Care 44:285, 2018. 17. Dean C, Chapman E: Induction of anaesthesia, Anaesth Intensive Care, 19:383, 2018. Hampson J, Green C, Stewart J, et al: Impact of the introduction of an endotracheal tube attachment device on the incidence and severity of oral pressure injuries in the intensive care unit: A retrospective observational study, BMC Nursing 17:4, 2018. Holm A, Dreyer P: Intensive care unit patients’ experience of being

conscious during endotracheal intubation and mechanical ventilation, Nurs Crit Care 22:81, 2017.

20. Au G, Johnson JR, Chlan LL: Time for a paradigm shift: Assessing for anxiety in patients receiving mechanical ventilation, Heart & Lung 46:135, 2017. 21. Mohammed HM, Ali AA: Nursing issues of unplanned extubation in ICU, IJNSS 8:17, 2018. Sousa AS, Ferrito C, Paiva JA: Intubation-associated pneumonia: An integrative review, Intensive Crit Care Nurs 44:45, 2018. Allan SH, Doyle PA, Sapirstein A, et al: Data-driven implementation of alarm reduction interventions in a cardiovascular surgical ICU, Jt Comm J Qual Patient Saf 43:62, 2017.

24. Pham T, Brochard LJ, Slutsky AS: Mechanical ventilation: State of the art, Mayo Clin Proc 92:1382, 2017. 25. Bein T, Wrigge H: Airway pressure release ventilation (APRV): Do good things come to those who can wait? J Thorac Dis 10:667, 2018. 26. Ng J, Ferguson ND: High-frequency oscillatory ventilation: Still a role? Curr Opin Crit Care 23:175, 2017. Karam O, Gebistorf F, Wetterslev J, et al: The effect of inhaled nitric oxide in acute respiratory distress syndrome in children and adults: A Cochrane systematic review with trial sequential analysis, Anaesthesia 72:106, 2017. Fan E, Del Sorbo L, Goligher E, et al: An official American Thoracic Society/European Society of Intensive Care Medicine/Society of Critical Care Medicine Clinical Practice guideline: Mechanical ventilation in adult patients with acute respiratory distress syndrome, Amer J Resp Crit Care Med 195:1253, 2017.

29. Centers for Disease Control and Prevention (CDC): Pneumonia (ventilator-associated [VAP] and non-

ventilator-associated pneumonia [PNEU]) event. Retrieved from www.cdc.gov/nhsn/pdfs/pscmanual/6pscvapcurrent.pdf. American Association of Critical Care Nurses: Ventilator assisted pneumonia. Retrieved from www.aacn.org/clinical-resources/practicealerts/ventilator-associated-pneumonia-vap.

31. Larrow V, Klich-Heartt EI: Prevention of ventilatorassociated pneumonia in the intensive care unit: Beyond the basics, J Neuroscience Nurs 48:160, 2016. Marra A, Ely EW, Pandharipande PP, Patel MB: The ABCDEF bundle in critical care, Crit Care Clin 33:225, 2017.

33. Naguib M, Brull SJ, Johnson KB: Conceptual and technical insights into the basis of neuromuscular monitoring, Anaesthesia 72:16, 2017. 34. Faritous Z, Barzanji A, Azarfarin R, et al: Comparison of bispectral index monitoring with the critical-care pain observation tool in the pain assessment of intubated adult patients after cardiac surgery, Anesthesiol Pain Med 6:e38334, 2016. Watson T, Hickok J, Fraker S, et al: Evaluating the risk factors for hospital-onset Clostridium difficile infections in a large healthcare system. Clin Infect Dis 66:1957, 2018. ∗Evidence-based information for clinical practice.

66

Shock, Sepsis, and Multiple Organ Dysfunction Syndrome Helen Miley

LEARNING OUTCOMES 1. Relate the pathophysiology to the clinical manifestations of the different types of shock: cardiogenic, hypovolemic, distributive, and obstructive. 2. Compare the effects of shock, sepsis, systemic inflammatory response syndrome, and multiple organ dysfunction syndrome on the major body systems. 3. Compare the interprofessional care, drug therapy, and nursing management of patients with different types of shock. 4. Describe the interprofessional care and nursing management of a patient experiencing multiple organ dysfunction syndrome.

KEY TERMS anaphylactic shock, p. 1569 cardiogenic shock, p. 1566 hypovolemic shock, p. 1568 multiple organ dysfunction syndrome (MODS), p. 1584

neurogenic shock, p. 1568 obstructive shock, p. 1571 sepsis, p. 1569 septic shock, p. 1569 shock, p. 1566 systemic inflammatory response syndrome (SIRS), p. 1583 You have not lived until you have done something for someone who can never repay you. John Bunyen http://evolve.elsevier.com/Lewis/medsurg

Conceptual Focus Anxiety Fluids and Electrolytes Gas Exchange Immunity Perfusion Shock, systemic inflammatory response syndrome (SIRS), sepsis, and multiple organ dysfunction syndrome (MODS) are serious and interrelated problems (Fig. 66.1). Shock is a syndrome characterized by decreased tissue perfusion and impaired cellular metabolism. This results in an imbalance between the supply of and demand for O2 and nutrients. The exchange of O2 and nutrients at the cellular level is essential to life. When cells are hypoperfused, the demand for O2 and nutrients exceeds the supply at the microcirculatory level. Ischemia can occur, leading to cell injury and death. Thus shock of any cause is life-threatening. This chapter gives an overview of the different types of shock, SIRS, sepsis, and MODS and the related management of

each.

Shock Classification of Shock The 4 main categories of shock are cardiogenic, hypovolemic, distributive, and obstructive (Table 66.1). Although the cause, initial presentation, and management vary for each type, the physiologic responses of the cells to hypoperfusion are similar.

Cardiogenic Shock Cardiogenic shock occurs when either systolic or diastolic dysfunction of the heart’s pumping action results in reduced cardiac output (CO), stroke volume (SV), and BP. These changes compromise myocardial perfusion, further depress myocardial function, and decrease CO and perfusion. Causes of cardiogenic shock are shown in Table 66.1. Mortality rates for patients with cardiogenic shock are around 50%.1 It is the leading cause of death from acute myocardial infarction (MI).1 The heart’s inability to pump the blood forward is called systolic dysfunction. This inability results in a low CO (less than 4 L/min) and cardiac index (less than 2.5 L/min/m2). Systolic dysfunction primarily affects the left ventricle since systolic pressure is greater on the left side of the heart. The most common cause of systolic dysfunction is acute MI. When systolic dysfunction affects the right side of the heart, blood flow through the pulmonary circulation is reduced. Decreased filling of the heart results in decreased SV. Causes of diastolic dysfunction are shown in Table 66.1. Fig. 66.2 describes the pathophysiology of cardiogenic shock. Whether the first event is myocardial ischemia, a structural problem (e.g., valvular disorder, ventricular septal rupture), or dysrhythmias, the physiologic responses are similar. The patient has impaired tissue perfusion and cellular metabolism.

FIG. 66.1 Relationship of shock, systemic inflammatory response syndrome, and multiple organ dysfunction syndrome. (∗See Table 66.1 for causes of shock states.)

TABLE 66.1 Classification of Shock States

FIG. 66.2 The pathophysiology of cardiogenic shock. Modified from Urden LD, Stacy KM, Lough ME: Critical care nursing: Diagnosis and management, ed 6, St Louis, 2010, Mosby.

The early presentation of a patient with cardiogenic shock is similar to that of a patient with acute decompensated heart failure (HF) (see

Chapter 34). The patient may have tachycardia and hypotension. Pulse pressure may be narrowed due to the heart’s inability to pump blood forward during systole and increased volume during diastole. An increase in systemic vascular resistance (SVR) increases the workload of the heart. This increases myocardial O2 consumption. On assessment, the patient is tachypneic and has crackles on auscultation of breath sounds because of pulmonary congestion. The hemodynamic profile shows an increase in the pulmonary artery wedge pressure (PAWP), stroke volume variation (SVV), and pulmonary vascular resistance. Signs of peripheral hypoperfusion (e.g., cyanosis, pallor, diaphoresis, weak peripheral pulses, cool and clammy skin, delayed capillary refill) occur. Decreased renal blood flow results in sodium and water retention and decreased urine output. Anxiety, confusion, and agitation may develop with impaired cerebral perfusion. Tables 66.2 and 66.3 describe the laboratory findings and clinical presentation of a patient with cardiogenic shock.

Hypovolemic Shock Hypovolemic shock occurs from inadequate fluid volume in the intravascular space to support adequate perfusion (Table 66.1).2 The volume loss may be either an absolute or a relative volume loss. Absolute hypovolemia results when fluid is lost through hemorrhage, gastrointestinal (GI) loss (e.g., vomiting, diarrhea), fistula drainage, diabetes insipidus, or diuresis. In relative hypovolemia, fluid volume moves out of the vascular space into the extravascular space (e.g., intracavitary space). We call this type of fluid shift third spacing. One example of relative volume loss is fluid leaking from the vascular space to the interstitial space from increased capillary permeability, as seen in burns (see Chapter 24). Whether the loss of intravascular volume is absolute or relative, the physiologic consequences are similar. The reduced intravascular volume results in a decreased venous return to the heart, decreased preload, decreased SV, and decreased CO. A cascade of events results in decreased tissue perfusion and impaired cellular metabolism, the

hallmarks of shock (Fig. 66.3). The patient’s response to acute volume loss depends on several factors, including extent of injury, age, and general state of health. The clinical presentation of hypovolemic shock is consistent (Table 66.3). An overall assessment of physiologic reserves may indicate the patient’s ability to compensate. A patient may compensate for a loss of up to 15% of the total blood volume (around 750 mL). Further loss of volume (15% to 30%) results in a sympathetic nervous system (SNS)– mediated response.2 This response results in an increase in heart rate, CO, and respiratory rate and depth. The decreased circulating blood volume causes decreases in SV, central venous pressure (CVP), and PAWP.3 The patient may appear anxious. Urine output begins to decrease. If hypovolemia is corrected by crystalloid fluid replacement at this time, tissue dysfunction is generally reversible. If volume loss is greater than 30%, compensatory mechanisms may fail and immediate replacement with blood products should be started. Loss of autoregulation in the microcirculation and irreversible tissue destruction occur with loss of more than 40% of the total blood volume. Common laboratory studies and assessments that are done include serial measurements of hemoglobin and hematocrit levels, electrolytes, lactate, blood gases, mixed central venous O2 saturation (SvO2), and hourly urine outputs (Table 66.2).

Distributive Shock Neurogenic Shock Neurogenic shock is a hemodynamic phenomenon that can occur within 30 minutes of a spinal cord injury and last up to 6 weeks. Neurogenic shock related to spinal cord injuries is generally associated with a cervical or high thoracic injury. The injury results in a massive vasodilation without compensation because of the loss of SNS vasoconstrictor tone.4 This massive vasodilation leads to a pooling of blood in the blood vessels, tissue hypoperfusion, and

impaired cellular metabolism (Fig. 66.4). In addition to spinal cord injury, spinal anesthesia can block transmission of impulses from the SNS. Depression of the vasomotor center of the medulla from drugs (e.g., opioids, benzodiazepines) can decrease the vasoconstrictor tone of the peripheral blood vessels, resulting in neurogenic shock (Table 66.1). The classic manifestations are hypotension (from the massive vasodilation) and bradycardia (from unopposed parasympathetic stimulation).4 The patient may not be able to regulate body temperature. Combined with massive vasodilation, the inability to regulate temperature promotes heat loss. At first, the patient’s skin is warm due to the massive vasodilation. As the heat disperses, the patient is at risk for hypothermia. Later, the patient’s skin may be cool or warm depending on the ambient temperature (poikilothermia, taking on the temperature of the environment). In either case, the skin is usually dry. Tables 66.2 and 66.3 further describe the laboratory findings and clinical presentation of a patient with neurogenic shock.

TABLE 66.2 Diagnostic StudiesShock

ALT, Alanine aminotransferase; AST, aspartate aminotransferase; GGT, γ-glutamyl transferase; INR, international normalized ratio; PT, prothrombin time; PTT, partial thromboplastin time.

Although spinal shock and neurogenic shock often occur in the same patient, they are not the same disorder. Spinal shock is a transient condition that is present after an acute spinal cord injury (see Chapter 60). The patient with spinal shock has an absence of all voluntary and reflex neurologic activity below the level of the injury.

Anaphylactic Shock Anaphylactic shock is an acute, life-threatening hypersensitivity (allergic) reaction to a sensitizing substance (e.g., drug, chemical, vaccine, food, insect venom).5 The reaction quickly causes massive vasodilation, release of vasoactive mediators, and an increase in capillary permeability. As capillary permeability increases, fluid leaks from the vascular space into the interstitial space. Anaphylactic shock can lead to respiratory distress due to laryngeal edema or severe bronchospasm and circulatory failure from the massive vasodilation. The patient has a sudden onset of symptoms, including dizziness, chest pain, incontinence, swelling of the lips and tongue, wheezing, and stridor. Skin changes include flushing, pruritus, urticaria, and angioedema. The patient may be anxious and confused and have a sense of impending doom. A patient can have a severe allergic reaction, possibly leading to anaphylactic shock, after contact, inhalation, ingestion, or injection with an antigen (allergen) to which the person has previously been sensitized (Table 66.1). IV administration of the antigen (allergen) is the route most likely to cause anaphylaxis. However, oral, topical, and inhalation routes can cause anaphylactic reactions. Tables 66.2 and 66.3 describe the laboratory findings and clinical presentation of a patient in anaphylactic shock. Quick and decisive action is critical to prevent an allergic reaction from progressing to anaphylactic shock. (Anaphylaxis is discussed in Chapter 13.)

Septic Shock Sepsis is a life-threatening syndrome in response to an infection. It is characterized by a dysregulated patient response along with new organ dysfunction related to the infection (Table 66.4).6 In as many as 30% of patients with sepsis, the causative organism is not identified. Sepsis and septic shock have a high incidence worldwide, with a mortality rate of 25% or higher.7 Septic shock is a subset of sepsis. It has an increased mortality risk due to profound circulatory, cellular, and metabolic abnormalities.

Septic shock is characterized by persistent hypotension, despite adequate fluid resuscitation, and inadequate tissue perfusion that results in tissue hypoxia.6,7 The main organisms that cause sepsis are gram-negative and gram-positive bacteria. Parasites, fungi, and viruses can also cause sepsis and septic shock.6 Fig. 66.5 presents the pathophysiology of septic shock.

TABLE 66.3 Clinical Presentation of Types of

Shock



Also see Table 66.2.

When a microorganism enters the body, the normal immune or inflammatory responses are triggered. However, in sepsis and septic shock the body’s response to the microorganism is exaggerated. Both proinflammatory and antiinflammatory responses are activated,

coagulation increases, and fibrinolysis decreases.6 Endotoxins from the microorganism cell wall stimulate the release of cytokines. These include tumor necrosis factor (TNF), interleukin-1 (IL-1), and other proinflammatory mediators that act through secondary mediators, such as platelet-activating factor, IL-6, and IL-8.6 (See Chapter 11 for discussion of the inflammatory response.) The release of plateletactivating factor results in the formation of microthrombi and obstruction of the microvasculature. The combined effects of the mediators result in damage to the endothelium, vasodilation, increased capillary permeability, and neutrophil and platelet aggregation and adhesion to the endothelium.

FIG. 66.3 The pathophysiology of hypovolemic shock. Modified from Urden LD, Stacy KM, Lough ME: Critical care nursing: Diagnosis and management, ed 6, St Louis, 2010, Mosby.

Septic shock has 3 major pathophysiologic effects: vasodilation, maldistribution of blood flow, and myocardial depression. Patients may be euvolemic, but because of acute vasodilation and shifting of fluids out of the intravascular space, relative hypovolemia and

hypotension occur. Blood flow in the microcirculation is decreased, causing poor O2 delivery and tissue hypoxia. We think the combination of TNF and IL-1 has a role in sepsis-induced myocardial dysfunction. The ejection fraction (EF) is decreased for the first few days after the initial insult. Because of a decreased EF, the ventricles dilate to maintain the SV. The EF typically improves, and ventricular dilation resolves over 7 to 10 days. Persistent high CO and a low SVR beyond 24 hours is an ominous finding. It is often associated with an increased development of hypotension and MODS. Coronary artery perfusion and myocardial O2 metabolism are not primarily altered in septic shock. Respiratory failure is common. The patient initially hyperventilates as a compensatory mechanism, causing respiratory alkalosis. Once the patient can no longer compensate, respiratory acidosis develops. Respiratory failure develops in 85% of patients with sepsis, and 40% develop acute respiratory distress syndrome (ARDS) (see Chapter 67). These patients may need to be intubated and mechanically ventilated. Other signs of septic shock include changes in neurologic status, decreased urine output, and GI dysfunction, such as GI bleeding and paralytic ileus. Table 66.3 gives the clinical presentation of a patient with septic shock.

FIG. 66.4 The pathophysiology of neurogenic shock. Modified from Urden LD, Stacy KM, Lough ME: Critical care nursing: Diagnosis and management, ed 6, St Louis, 2010, Mosby.

Obstructive Shock Obstructive shock develops when a physical obstruction to blood flow occurs with a decreased CO (Fig. 66.6). This can be caused by restricted diastolic filling of the right ventricle from compression (e.g., cardiac tamponade, tension pneumothorax, superior vena cava syndrome). Other causes include abdominal compartment syndrome, in which increased abdominal pressures compress the inferior vena cava. This decreases venous return to the heart. Pulmonary embolism and right ventricular thrombi cause an outflow obstruction as blood leaves the right ventricle through the pulmonary artery. This leads to decreased blood flow to the lungs and decreased blood return to the left atrium. Patients have a decreased CO, increased afterload, and variable left ventricular filling pressures depending on the obstruction. Other signs include jugular venous distention and pulsus paradoxus. Rapid assessment and treatment are important to prevent further hemodynamic compromise and possible cardiac arrest (Fig. 66.6).

Stages of Shock In addition to understanding the underlying pathogenesis of the type of shock the patient has, management is guided by knowing where the patient is on the shock “continuum.” We categorize shock into 4 overlapping stages: (1) initial stage, (2) compensatory stage, (3) progressive stage, and (4) refractory stage.6

TABLE 66.4 Diagnostic Criteria for Sepsis Infection, documented or suspected, and some of the following:

General Variables • Altered mental status

• Fever (temperature >100.9°F [38.3°C]) • Heart rate >90 beats/min • Hyperglycemia (blood glucose >140 mg/dL) in the absence of diabetes • Hypothermia (core temperature 20 mL/kg over 24 hr) • Tachypnea (respiratory rate ≥22/min)

Inflammatory Variables • Leukocytosis (WBC count >12,000/µL) • Leukopenia (WBC count 10% immature forms (bands) • Elevated C-reactive protein • Elevated procalcitonin

Hemodynamic Variables • Arterial hypotension (SBP 4 mg/dL) • Ileus (absent bowel sounds)

• Serum creatinine increase >0.5 mg/dL • Thrombocytopenia (platelet count 1 mmol/L) • Mottling or decreased capillary refill FIO2, Fraction of inspired O2; INR, international normalized ratio; PaO2, partial pressure of arterial O2; PTT, partial thromboplastin time. Source: Singer M, Deutschman CS, Seymour CW, et al: The third international consensus definitions for sepsis and septic shock (Sepsis3), JAMA 315:801, 2016.

FIG. 66.5 The pathophysiology of septic shock. Modified from Urden LD, Stacy KM, Lough ME: Critical care nursing: Diagnosis and management, ed 6, St Louis, 2010, Mosby.

FIG. 66.6 The pathophysiology of obstructive shock.

Initial Stage The continuum begins with the initial stage of shock that occurs at a cellular level. This stage is usually not clinically apparent. Metabolism changes at the cellular level from aerobic to anaerobic, causing lactic acid buildup. Lactic acid is a waste product that is removed by the liver. However, this process requires O2, which is unavailable because of the decrease in tissue perfusion.

Compensatory Stage In the compensatory stage the body activates neural, hormonal, and biochemical compensatory mechanisms to try to overcome the increasing consequences of anaerobic metabolism and maintain homeostasis. The patient’s clinical presentation begins to reflect the body’s responses to the imbalance in O2 supply and demand (Table 66.5). A classic sign of shock is a drop in BP. This occurs because of a decrease in CO and a narrowing of the pulse pressure. The baroreceptors in the carotid and aortic bodies immediately respond by activating the SNS. The SNS stimulates vasoconstriction and the release of the potent vasoconstrictors epinephrine and norepinephrine. Blood flow to the heart and brain is maintained. Blood flow to the nonvital organs, such as kidneys, GI tract, skin, and lungs, is diverted or shunted. The myocardium responds to the SNS stimulation and the increase in O2 demand by increasing the heart rate and contractility. Increased contractility increases myocardial O2 consumption. The coronary arteries dilate to try to meet the increased O2 demands of the myocardium. Shunting blood away from the lungs has an important clinical effect in the patient in shock. Decreased blood flow to the lungs increases the patient’s physiologic dead space. Physiologic dead space is the anatomic dead space (the amount of air that will not reach gasexchanging units) and any inspired air that cannot take part in gas exchange. The clinical result of an increase in dead space ventilation is a ventilation-perfusion mismatch. Some areas of the lungs that are being ventilated will not be perfused because of the decreased blood flow to the lungs. Arterial O2 levels will decrease, and the patient will have a compensatory increase in the rate and depth of respirations (see Chapter 67). The shunting of blood from other organ systems results in clinically important changes. The decrease in blood flow to the GI tract results in impaired motility and a slowing of peristalsis. This increases the

risk for a paralytic ileus. Decreased blood flow to the skin results in the patient feeling cool and clammy. The exception is the patient in early septic shock who may feel warm and flushed because of a hyperdynamic state. Decreased blood flow to the kidneys activates the renin-angiotensin system. Renin stimulates angiotensinogen to make angiotensin I, which is then converted to angiotensin II (see Fig. 44.4). Angiotensin II is a potent vasoconstrictor that causes both arterial and venous vasoconstriction. The net result is an increase in venous return to the heart and an increase in BP. Angiotensin II stimulates the adrenal cortex to release aldosterone. This results in sodium and water reabsorption and potassium excretion by the kidneys. The increase in sodium reabsorption raises the serum osmolality and stimulates the release of antidiuretic hormone (ADH) from the posterior pituitary gland. ADH increases water reabsorption by the kidneys, further increasing blood volume. The increase in total circulating volume results in an increase in CO and BP. A multisystem response to decreasing tissue perfusion starts during the compensatory stage of shock. At this stage, the body can compensate for the changes in tissue perfusion. If the cause of the shock is corrected, the patient will recover with little or no residual effects. If the cause of the shock is not corrected and the body is unable to compensate, the patient enters the progressive stage of shock.

Progressive Stage The progressive stage of shock begins as compensatory mechanisms fail. Changes in the patient’s mental status are important findings in this stage. Patients must be moved to the intensive care unit (ICU), if not already there, for advanced monitoring and treatment. The cardiovascular system is profoundly affected in the progressive stage of shock. CO begins to fall, resulting in a decrease in BP and coronary artery, cerebral, and peripheral perfusion. Continued decreased cellular perfusion and resulting altered capillary permeability are the distinguishing features of this stage. Altered

capillary permeability allows fluid and protein to leak out of the vascular space into the surrounding interstitial space. In addition to the decrease in circulating volume, there is an increase in systemic interstitial edema. The patient may have anasarca (diffuse profound edema). Fluid leakage from the vascular space affects the solid organs (e.g., liver, spleen, GI tract, lungs) and peripheral tissues by further decreasing perfusion. Sustained hypoperfusion results in weak peripheral pulses, and ischemia of the distal extremities eventually occurs. Myocardial dysfunction from decreased perfusion results in dysrhythmias, myocardial ischemia, and possibly MI. The result is a complete deterioration of the cardiovascular system. The pulmonary system is often the first system to display signs of critical dysfunction. During the compensatory stage, blood flow to the lungs is already reduced. In response to the decreased blood flow and SNS stimulation, the pulmonary arterioles constrict, resulting in increased pulmonary artery (PA) pressure. As the pressure within the pulmonary vasculature increases, blood flow to the pulmonary capillaries decreases and ventilation-perfusion mismatch worsens.

TABLE 66.5 Manifestations of Stages of Shock∗

MVO2, myocardial O2 consumption.



The shock continuum begins with the initial stage of shock. This stage occurs at the cellular level and is usually not clinically apparent. Also see Table 66.2 and Table 66.3.

Another key response in the lungs is the movement of fluid from the pulmonary vasculature into the interstitial space. As capillary permeability increases, the movement of fluid to the interstitial spaces results in interstitial edema, bronchoconstriction, and a decrease in functional residual capacity. With further increases in capillary permeability, fluid moves into the alveoli, causing alveolar edema and a decrease in surfactant production. The combined effects of pulmonary vasoconstriction and bronchoconstriction are impaired gas exchange, decreased compliance, and worsening ventilation-perfusion mismatch. Clinically, the patient has tachypnea, crackles, and an overall increased work of breathing. The GI system is affected by prolonged decreased tissue perfusion. As the blood supply to the GI tract is decreased, the normally protective mucosal barrier becomes ischemic. This ischemia predisposes the patient to ulcers and GI bleeding (see Chapter 41). It increases the risk for bacterial migration from the GI tract to the blood and lungs. The decreased perfusion to the GI tract leads to a decreased ability to absorb nutrients. The effect of prolonged hypoperfusion on the kidneys is renal tubular ischemia. The resulting acute tubular necrosis may lead to acute kidney injury (AKI). This can be worsened by nephrotoxic drugs (e.g., certain antibiotics, anesthetics, diuretics) (see Chapter 46). The patient has decreased urine output and increased blood urea nitrogen (BUN) and serum creatinine. Metabolic acidosis occurs from the kidneys’ inability to excrete acids (especially lactic acid) and reabsorb bicarbonate. The sustained hypoperfusion in the progressive stage of shock greatly affects other organs. The loss of the functional ability of the liver leads to a failure of the liver to metabolize drugs and waste products (e.g., lactate, ammonia). Jaundice results from an accumulation of bilirubin. As the liver cells die, liver enzymes

increase. The liver loses its ability to function as an immune organ. Kupffer cells no longer destroy bacteria from the GI tract. Instead, they are released into the bloodstream, increasing the possibility of bacteremia. Dysfunction of the hematologic system adds to the complexity of the clinical picture. The patient is at risk for disseminated intravascular coagulation (DIC). The consumption of the platelets and clotting factors with secondary fibrinolysis results in clinically significant bleeding from many orifices. These include the GI tract, lungs, and puncture sites (see Chapter 30). Altered laboratory values in DIC are shown in Table 66.3. In this stage, aggressive interventions are needed to prevent the development of MODS.

Refractory Stage In the last stage of shock, the refractory stage, decreased perfusion from peripheral vasoconstriction and decreased CO worsen anaerobic metabolism. The accumulation of lactic acid contributes to increased capillary permeability and dilation. Increased capillary permeability allows fluid and plasma proteins to leave the vascular space and move to the interstitial space. Blood pools in the capillary beds due to the constricted venules and dilated arterioles. The loss of intravascular volume worsens hypotension and tachycardia and decreases coronary blood flow. Decreased coronary blood flow leads to worsening myocardial depression and a further decline in CO. Cerebral blood flow cannot be maintained and cerebral ischemia results. The patient in this stage of shock has profound hypotension and hypoxemia. The failure of the liver, lungs, and kidneys results in an accumulation of waste products, such as lactate, urea, ammonia, and CO2. The failure of 1 organ system affects several other organ systems. Recovery is unlikely in this stage. The organs are in failure and the body’s compensatory mechanisms are overwhelmed (Table 66.5).

Diagnostic Studies

There is no single diagnostic study to determine whether a patient is in shock. The diagnosis starts with a history and physical examination. Obtaining a thorough medical and surgical history and a history of recent events (e.g., surgery, chest pain, trauma) gives valuable data. Decreased tissue perfusion in shock leads to an increased lactate with a base deficit (the amount needed to bring the pH back to normal). These laboratory changes reflect an increase in anaerobic metabolism.8 Table 66.2 outlines laboratory findings seen in shock. Other diagnostic studies include a 12-lead electrocardiogram (ECG), continuous ECG monitoring, chest x-ray, continuous pulse oximetry, and invasive and noninvasive hemodynamic monitoring. Chapter 65 discusses hemodynamic monitoring)

Interprofessional Care Critical factors in the successful management of a patient in shock relate to the early recognition and treatment of the shock state. Prompt intervention in the early stages of shock may prevent the decline to the progressive or irreversible stage. Successful management of the patient in shock includes (1) identification of patients at risk for the development of shock; (2) integration of the patient’s history, physical examination, and clinical findings to establish a diagnosis; (3) interventions to control or eliminate the cause of the decreased perfusion; (4) protecting target and distal organs from dysfunction; and (5) providing multisystem supportive care. Table 66.6 provides an overview of the initial assessment findings and interventions for the emergency care of patients in shock. General management strategies begin with ensuring that the patient is responsive and has a patent airway. Once the airway is established, either naturally or with an endotracheal tube, O2 delivery must be optimized. Supplemental O2 and mechanical ventilation may be needed to maintain an arterial O2 saturation of 90% or more (PaO2 greater than 60 mm Hg) to avoid hypoxemia (see Chapter 65). The mean arterial pressure (MAP) and circulating blood volume are

optimized with fluid replacement and drug therapy.

Oxygen and Ventilation O2 delivery depends on CO, available hemoglobin, and arterial O2 saturation (SaO2). Methods to optimize O2 delivery are directed at increasing supply and decreasing demand. Supply is increased by (1) optimizing the CO with fluid replacement and/or drug therapy, (2) increasing the hemoglobin through transfusion of whole blood or packed red blood cells (RBCs), and/or (3) increasing the arterial O2 saturation with supplemental O2 and mechanical ventilation. Plan care to avoid disrupting the balance of O2 supply and demand. Space activities that increase O2 consumption (e.g., endotracheal suctioning, position changes) appropriately for O2 conservation. Intermittent or continuous monitoring of ScvO2 by a central venous catheter or mixed venous O2 saturation (SvO2) may be helpful. Both reflect the dynamic balance between O2 supply and demand. Assess these values along with related hemodynamic measures (e.g., arterial pressure–based cardiac output [APCO], O2 consumption, hemoglobin) to evaluate the patient’s response to treatments and activities (see Chapter 65).

TABLE 66.6 Emergency ManagementShock



See Table 66.1 for other causes of shock.

Fluid Resuscitation The cornerstone of therapy for septic, hypovolemic, and anaphylactic shock is volume expansion with administration of the appropriate fluid (Table 66.7). Fluid resuscitation should start using 1 or 2 largebore (e.g., 14- to 16-gauge) IV catheters, an intraosseous (IO) access device, or a central venous catheter.

Safety Alert Intraosseous (IO) Access • Use an IO access device for emergency resuscitation when IV access cannot be obtained. • Insertion sites include the sternum, proximal and distal tibia, and proximal and distal humerus. • Remove IO devices within 24 hours of insertion or as soon as

possible after peripheral or central IV access is obtained. • Monitor for complications: extravasation of drugs and fluids into the soft tissue, fractures caused during insertion, and osteomyelitis. The choice of resuscitation fluid is based on the type and volume of fluid lost and the patient’s clinical status. The ideal choice of fluid is controversial. Currently, normal saline is most often used in the initial resuscitation of shock. Large-volume resuscitation with normal saline can lead to hyperchloremic metabolic acidosis. Lactated Ringer’s solution can cause serum lactate levels to increase because the failing liver cannot convert lactate to bicarbonate.9 Transfusions of RBCs may be given to treat hypovolemic shock due to bleeding. Colloids (4% to 5%) have not been shown to improve patient outcomes.9 Fluid responsiveness is determined by clinical assessment. This includes vital signs, cerebral and abdominal perfusion pressures, capillary refill, skin temperature, and urine output. Hemodynamic parameters, such as SVV or CO, are also used. Monitor trends in BP with an automatic BP cuff or an arterial catheter to assess the patient’s response. Use an indwelling urinary catheter to monitor urine output during resuscitation. The goal for fluid resuscitation is to restore tissue perfusion. Although BP helps determine whether the patient’s CO is adequate, an assessment of end-organ perfusion (e.g., urine output, neurologic function, peripheral pulses) provides more relevant data.

Safety Alert Complications of Fluid Resuscitation • Warm crystalloid and colloid solutions during massive fluid resuscitation to prevent hypothermia. • When giving large volumes of packed RBCs, remember that they

do not contain clotting factors. • Replace clotting factors based on the clinical situation and laboratory studies.

Drug Therapy The goal of drug therapy for shock is to correct decreased tissue perfusion. Decisions on which drug to use should be based on the physiologic goal. Drugs used to improve perfusion in shock are given IV via an infusion pump and central venous line. Many of these drugs have vasoconstrictor properties that are harmful if the drug leaks into the tissues while being infused peripherally (Table 66.8).

TABLE 66.7 Fluid Therapy in Shock

Sympathomimetic Drugs Many of the drugs used in the treatment of shock influence the SNS. Drugs that mimic the action of the SNS are called sympathomimetic. The effects of these drugs are mediated through their binding to α- or β-adrenergic receptors. The various drugs differ in their relative αand β-adrenergic effects.10 Many of these drugs cause peripheral vasoconstriction and are called vasopressor drugs (e.g., norepinephrine, dopamine, phenylephrine). These drugs can cause severe peripheral vasoconstriction and an increase in SVR, further risking tissue perfusion. The increased SVR increases the workload of the heart and myocardial O2 demand. It can harm a patient in cardiogenic shock by causing further myocardial damage and increasing the risk for

dysrhythmias.1 Use of vasopressor drugs is limited to patients who do not respond to fluid resuscitation. Adequate fluid resuscitation must be achieved before starting vasopressors because the vasoconstrictor effects in patients with low blood volume will cause further reduction in tissue perfusion. Typically, if the patient has persistent hypotension after adequate fluid resuscitation, a vasopressor (e.g., norepinephrine, dopamine) and/or an inotrope (e.g., dobutamine) is given. The goal of vasopressor therapy is to achieve and maintain a MAP of greater than 65 mm Hg.10 Continuously monitor end-organ perfusion (e.g., urine output, level of consciousness) and serum lactate levels (e.g., every 3 hours for the first 6 hours) to ensure that tissue perfusion is adequate.

Vasodilator Drugs Patients in cardiogenic shock have decreased myocardial contractility, and vasodilators may be needed to decrease afterload. This reduces myocardial workload and O2 requirements. Although generalized sympathetic vasoconstriction is a useful compensatory mechanism for maintaining BP, excessive constriction can reduce tissue blood flow and increase the workload of the heart. The reason for using vasodilator therapy for a patient in shock is to break the harmful cycle of widespread vasoconstriction causing a decrease in CO and BP, resulting in further sympathetic-induced vasoconstriction. The goal of vasodilator therapy, as in vasopressor therapy, is to maintain the MAP greater than 65 mm Hg. Monitor hemodynamic parameters (e.g., CVP, CO, ScvO2/SvO2, SV, PA pressures) and assessment findings so that fluids can be increased or vasodilator therapy decreased if a serious fall in CO or BP occurs. The vasodilator agent most often used for the patient in cardiogenic shock is nitroglycerin. Vasodilation may be enhanced with nitroprusside or nitroglycerin in noncardiogenic shock.

Nutritional Therapy Protein-calorie malnutrition is common because of hypermetabolism.

Nutrition is vital to reducing mortality. Enteral nutrition (EN) should be started within the first 24 hours. However, full calorie replacement is not recommended for previously well-nourished adults early in a critical illness.11 Start the patient on a trophic feeding. This is a small amount of EN (e.g., 10 mL/hr). Early EN enhances the perfusion of the GI tract and helps maintain the integrity of the gut mucosa. Advance feedings as tolerated and as prescribed. Parenteral nutrition (PN) is used only if EN is contraindicated. Chapter 39 discusses enteral and parenteral nutrition.

TABLE 66.8 Drug TherapyShock

CVP, Central venous pressure; MVO2, myocardial O2 consumption; PAWP, pulmonary artery wedge pressure; PT, prothrombin time; PTT, partial thromboplastin time; SVR, systemic vascular resistance. ∗

Consult agency guidelines, pharmacist, pharmacology references, and drug manufacturer’s materials for more information and dosing recommendations.

Weigh the patient daily on the same scale (usually the bed scale) at the same time of day. If the patient has a significant weight loss, rule out dehydration before adding more calories. Large weight gains are common because of third spacing of fluids. Therefore daily weights serve as a better indicator of fluid status than caloric needs. Serum protein, total albumin, prealbumin, BUN, serum glucose, and serum electrolytes are all used to assess nutritional status.

Measures Specific to Type of Shock Cardiogenic Shock For a patient in cardiogenic shock, the overall goal is to restore heart function and the balance between O2 supply and demand in the myocardium. Cardiac catheterization is done as soon as possible after the initial insult.1 Specific measures to restore blood flow include angioplasty with stenting, emergency revascularization, and valve replacement (see Chapter 33). Until these interventions are done, we must support the heart to optimize SV and CO to achieve optimal perfusion (Tables 66.8 and 66.9). Hemodynamic management of a patient in cardiogenic shock aims to reduce the workload of the heart through drug therapy and/or mechanical interventions. Drug choice is based on the clinical goal and a thorough understanding of each drug’s mechanism of action. Drugs can be used to decrease the workload of the heart by dilating coronary arteries (e.g., nitrates), reducing preload (e.g., diuretics), afterload (e.g., vasodilators), and heart rate and contractility (e.g., βadrenergic blockers). The patient may benefit from a circulatory assist device (e.g., intraaortic balloon pump, ventricular assist device [VAD]) (see

Chapter 65). The goals of this intervention are to decrease SVR and left ventricular workload so that the heart can heal.12 A VAD may be used as a temporary measure for the patient in cardiogenic shock who is awaiting heart transplantation. Heart transplantation is an option for a small, select group of patients with cardiogenic shock.

Hypovolemic Shock The underlying principles of managing patients with hypovolemic shock focus on stopping the loss of fluid and restoring the circulating volume. We often calculate the initial fluid resuscitation using a 3:1 rule (3 mL of isotonic crystalloid for every 1 mL of estimated blood loss). Table 66.7 describes types of fluid used for volume resuscitation, the mechanisms of action, and specific nursing implications for each fluid type.

Septic Shock Patients in septic shock need large amounts of fluid replacement. The overall goal of fluid resuscitation is to restore the intravascular volume and organ perfusion. Initial volume resuscitation is achieved by giving 30 mL/kg of an isotonic crystalloid solution. Albumin 4% to 5% may be added when patients need substantial volumes. A fluid challenge technique (e.g., a minimum of 30 mL/kg of crystalloids) may be used and repeated until hemodynamic improvement (e.g., increase in MAP and/or CVP, change in SVV) is seen. Table 66.9 shows predetermined end points of fluid resuscitation along with methods to reassess volume status. One of these methods is a passive leg raise (PLR) challenge along with hemodynamic measures to monitor response.13 A PLR challenge provides a transient increase in fluid volume of 150 to 500 mL by placing the patient supine and raising the legs to 45 degrees (Fig. 66.7). Response is monitored within 1 to 2 minutes by measuring CO, CI, SV, SVV, or other parameters for improvement. If the response is positive, the patient is fluid responsive and should receive more fluids. To optimize and evaluate large-volume fluid resuscitation, hemodynamic monitoring with various noninvasive or invasive

monitors is needed. If the patient is hypotensive after initial volume resuscitation and no longer fluid responsive, vasopressors may be added. The first drug of choice is norepinephrine.14 Vasodilation and low CO, or vasodilation alone, can cause low BP despite adequate fluid resuscitation. Vasopressin may be added for those who are refractory to initial vasopressor therapy.14 Exogenous vasopressin can replace the stores of physiologic vasopressin that are often depleted in septic shock.

Drug Alert Vasopressin • Given along with norepinephrine. • Infuse at low doses (e.g., 0.03 units/min) using an IV pump. • Do not titrate infusion. • Use cautiously in patients with coronary artery disease. Vasopressor drugs may increase BP but can decrease SV. An inotropic agent (e.g., dobutamine) may be added to offset the decrease in SV and increase tissue perfusion (Table 66.8). IV corticosteroids may be considered for patients in septic shock who cannot maintain an adequate BP despite vasopressor therapy and fluid resuscitation. To try to meet the increasing tissue demands coupled with a low SVR, the patient initially has a normal or high CO. If the patient is unable to achieve and maintain an adequate CO and has unmet tissue O2 demands, CO may have to be increased using drug therapy (e.g., dopamine). ScvO2 or SvO2 monitoring is used to assess the balance between O2 delivery and consumption, and the adequacy of the CO (see Chapter 65). If balance is maintained, the tissue demands will be met.

Broad-spectrum antibiotics are an important and early part of therapy. They should be started within the first hour of sepsis or septic shock.15 Obtain cultures (e.g., blood, wound, urine, stool, sputum) before antibiotics are started. However, this should not delay the start of antibiotics within the first hour. Specific antibiotics may be ordered once the organism has been identified. Glucose levels should be maintained below 180 mg/dL (10.0 mmol/L) for patients in shock.16 Monitor glucose levels in all patients in septic shock according to agency policy. Stress ulcer prophylaxis with proton pump inhibitors (e.g., pantoprazole) and VTE prophylaxis (e.g., heparin, enoxaparin [Lovenox]) are recommended.17

Neurogenic Shock The specific treatment of neurogenic shock is based on the cause. If the cause is spinal cord injury, general measures to promote spinal stability (e.g., spinal precautions, cervical stabilization with a collar) are initially used. Once the spine is stabilized, treatment of the hypotension and bradycardia is essential to prevent further spinal cord damage. Treatment involves the use of vasopressors (e.g., phenylephrine) to maintain BP and organ perfusion (Table 66.8). Bradycardia may be treated with atropine. Infuse fluids cautiously as the cause of the hypotension is not related to fluid loss. The patient with a spinal cord injury is monitored for hypothermia caused by hypothalamic dysfunction (Table 66.9).

Anaphylactic Shock The first strategy in managing patients at risk for anaphylactic shock is prevention. A thorough history is key to avoiding risk factors for anaphylaxis (Table 66.1). The clinical presentation of anaphylactic shock is dramatic, and immediate intervention is required. Epinephrine is the first drug of choice to treat anaphylactic shock.5 It causes peripheral vasoconstriction and bronchodilation and opposes the effect of histamine. Diphenhydramine and histamine receptor blockers (e.g., famotidine) are given as adjunctive therapies to block

the ongoing release of histamine from the allergic reaction.

TABLE 66.9 Interprofessional CareShock

CVP, central venous pressure; PAWP, pulmonary artery wedge pressure.

FIG. 66.7 Passive leg raise challenge in a patient with septic shock. From Lough, M.E. Hemodynamic monitoring: Evolving technologies and clinical practice, Philadelphia, 2016, Elsevier.

Maintaining a patent airway is important because the patient can quickly develop airway compromise from laryngeal edema or bronchoconstriction. Nebulized bronchodilators are highly effective. Aerosolized epinephrine can reduce treat laryngeal edema. Endotracheal intubation may be needed to secure and maintain a patent airway. Hypotension results from leakage of fluid out of the intravascular space into the interstitial space because of increased vascular permeability and vasodilation. Aggressive fluid resuscitation, usually with crystalloids, is needed. IV corticosteroids may be helpful in

anaphylactic shock if significant hypotension persists after 1 to 2 hours of aggressive therapy (Tables 66.8 and 66.9).

Obstructive Shock The main strategy in treating obstructive shock is early recognition and treatment to relieve or manage the obstruction (Table 66.1). Mechanical decompression for pericardial tamponade, tension pneumothorax, and hemopneumothorax may be done by needle or tube insertion. Obstructive shock from a pulmonary embolism requires immediate anticoagulation therapy or pulmonary embolectomy. Superior vena cava syndrome, a compression or obstruction of the outflow tract of the mediastinum, may be treated by radiation, debulking, or removal of the mass or cause. A decompressive laparotomy may be done for abdominal compartment syndrome for patients with high intraabdominal pressures and hemodynamic instability.

Nursing Management: Shock Nursing Assessment Your role is vital in caring for patients who are at risk for developing shock or are in a state of shock. Focus your assessment on the ABCs: airway, breathing, and circulation. Next, assess for tissue perfusion. This includes evaluating vital signs, level of consciousness, peripheral pulses, capillary refill, skin (e.g., temperature, color, moisture), and urine output. As shock progresses, the patient’s neurologic status declines, urine output decreases, skin becomes cooler and mottled, and peripheral pulses decrease. To understand the complexity of the patient’s clinical status, integrate all the assessment data. It is essential to obtain a brief history from the patient or caregiver, including a description of the events leading to the shock state, time of onset and duration of symptoms, and health history (e.g., medications, allergies). In addition, obtain details about any care the patient received before hospitalization.

Nursing Diagnoses Nursing diagnoses for the patient in shock may include: • Impaired cardiac output • Ineffective tissue perfusion • Anxiety Additional information on nursing diagnoses and interventions for the patient with shock is presented in eNursing Care Plan 66.1 (available on the website for this chapter).

Planning The overall goals for a patient in shock include (1) evidence of adequate tissue perfusion, (2) restoration of normal or baseline BP, (3) recovery of organ function, (4) avoiding complications from prolonged states of hypoperfusion, and (5) preventing health care– associated complications of disease management and care.

Nursing Implementation Health Promotion You have a vital role in the prevention of shock, beginning with the identification of patients at risk. In general, patients who are older, are immunocompromised, or have chronic illnesses are at an increased risk. Any person who has surgery or trauma is at risk for shock resulting from hemorrhage, spinal cord injury, sepsis, and other problems (Table 66.1). Planning is essential to help prevent shock after you identify an atrisk person. For example, a person with an acute anterior wall MI is at high risk for cardiogenic shock.1 The main goal for this patient is to limit the infarct size. This is done by restoring coronary blood flow through percutaneous coronary intervention, thrombolytic therapy, or surgical revascularization. Rest, analgesics, and sedation can reduce

the myocardial demand for O2. Modify the ICU environment to provide care at intervals that will not increase the patient’s O2 demand. For example, if the patient becomes tired with bathing, perform this care at a time that does not interfere with tests or other activities that may also increase O2 demand. A person with certain severe allergies, such as to drugs, shellfish, insect bites, and latex, is at increased risk for anaphylactic shock. This risk can be decreased if the patient is carefully assessed for allergies.

Safety Alert Preventing Allergic Reactions • Always confirm the patient’s allergies before giving drugs or starting diagnostic procedures (e.g., CT scan with contrast media). • Premedicate (e.g., diphenhydramine, methylprednisolone) patients who need a drug to which they are at high risk for an allergic reaction (e.g., contrast media). • Encourage patients with allergies to obtain and wear a medical alert device and report their allergies to their HCPs. • Tell patients about the availability of kits that contain equipment and drugs (e.g., epinephrine [EpiPen]) for the treatment of acute allergic reactions. Careful monitoring of fluid balance can help prevent hypovolemic shock. Ongoing monitoring of intake and output and daily weights is important. Identifying trends in the patient’s condition is more meaningful than any single piece of clinical information. Carefully monitor all patients for infection. Progression from an infection to sepsis and septic shock depends on the patient’s defense mechanisms. Patients who are immunocompromised are at high risk for opportunistic infections. Strategies to decrease the risk for health

care–associated infections (HAIs) include decreasing the number of invasive catheters (e.g., central lines, bladder catheters), using aseptic technique during invasive procedures, and paying strict attention to hand washing. Change equipment per agency policy. Thoroughly sanitize or discard (if disposable) equipment between patient use. Evidence-based guidelines are available to reduce the risk for HAIs (e.g., ventilator-associated pneumonia, central line infections, catheterassociated urinary tract infections). These guidelines, called care bundles, outline key interventions aimed at reducing infections.18

Acute Care Your role in shock involves (1) monitoring the patient’s ongoing physical and emotional status, (2) identifying trends to detect changes in the patient’s condition, (3) planning and implementing nursing interventions and therapy, (4) evaluating the patient’s response to therapy, (5) providing emotional support to the patient and caregiver, and (6) collaborating with other members of the interprofessional team to coordinate care.

Neurologic Status Assess the patient’s neurologic status, including orientation and level of consciousness using a valid tool, at least every 1 to 2 hours. The patient’s neurologic status is the best indicator of cerebral blood flow. Be aware of the clinical manifestations of neurologic involvement (e.g., changes in behavior, restlessness, blurred vision, confusion, paresthesias). Note any subtle changes in the patient’s mental status (e.g., mild agitation) and report them to the HCP. Orient the patient to person, place, time, and events on a regular basis. Orientation to the ICU environment is especially important. Reduce noise and light levels to control sensory input. Keep a daynight cycle of activity and rest as much as possible. Sensory overload and disruption of the patient’s diurnal cycle may contribute to delirium (see Chapter 59).

Cardiovascular Status

Most of the therapy for shock is based on information about the patient’s cardiovascular status. If the patient is unstable, continuously assess heart rate and rhythm, BP, CVP, and PA pressures, including CO, SVR, SV, and SVV (if available). Monitoring trends in hemodynamic parameters provides more important information than single values. Integration of hemodynamic data with physical assessment data is essential in planning strategies to manage the patient with shock. Chapter 65 discusses hemodynamic monitoring. Continuously monitor the patient’s ECG to detect dysrhythmias that may result from the cardiovascular and metabolic abnormalities associated with shock. Assess heart sounds for an S3 or S4 sound or new murmurs. An S3 sound usually indicates HF. Monitor the patient’s skin (e.g., upper and lower extremities) for signs of adequate perfusion. Changes in temperature, pallor, flushing, cyanosis, diaphoresis, and piloerection may indicate hypoperfusion. Give the prescribed therapy to correct cardiovascular system problems. Assess the patient’s response to fluid and drug administration as often as every 5 to 10 minutes. Make appropriate adjustments (e.g., drug titration) as needed. Once tissue perfusion is restored and the patient is stabilized, you can decrease the frequency of monitoring and slowly wean the patient off drugs to support BP and tissue perfusion.

Check Your Practice A 69-yr-old male patient has just been admitted to the ICU with a diagnosis of sepsis. Your assessment shows that he is confused, with weak peripheral pulses and a BP of 84/50. • What fluids would you expect to be ordered? • How much fluid would you expect to infuse to improve his BP? • Despite aggressive fluid resuscitation, the patient is still hypotensive. What drug would you expect to be given to improve tissue perfusion?

Respiratory Status Frequently assess the respiratory status of the patient in shock to ensure adequate oxygenation, detect complications early, and provide data about the patient’s acid-base status. At first, monitor the rate, depth, and rhythm of respirations as often as every 15 to 30 minutes. Increased rate and depth provide information about the patient’s attempts to correct metabolic acidosis. Assess breath sounds every 1 to 2 hours and as needed for any changes that may indicate fluid overload or accumulation of secretions. Use pulse oximetry to continuously monitor O2 saturation. Pulse oximetry using a patient’s finger may not be accurate in a shock state because of poor peripheral circulation. Instead, attach the probe to the ear, nose, or forehead (according to the manufacturer’s guidelines). Arterial blood gases (ABGs) give definitive information on ventilation and oxygenation status and acid-base balance. Initial interpretation of ABGs is often your responsibility. A PaO2 below 60 mm Hg (in the absence of chronic lung disease) indicates hypoxemia and the need for higher O2 concentrations or for a different mode of O2 administration. Low PaCO2 with a low pH and low bicarbonate level may mean that the patient is trying to compensate for metabolic acidosis from increasing lactate levels. A rising PaCO2 with a persistently low pH and PaO2 indicates the need for advanced pulmonary management. Many patients in shock are intubated and on mechanical ventilation. Maintaining a patent airway and monitoring for ventilator-related complications are critical. Chapter 65 discusses artificial airways and mechanical ventilation.

Renal Status At first, measure urine output every 1 to 2 hours to assess the adequacy of renal perfusion. Inserting an indwelling urinary catheter helps measure during resuscitation. Urine output below 0.5 mL/kg/hr may indicate inadequate perfusion of the kidneys. Use trends in serum creatinine values to assess renal function. Serum creatinine is a

better indicator of renal function than BUN levels, since BUN is affected by the patient’s catabolic state.

Body Temperature Monitor temperature every 4 hours if normal. In the presence of a high or subnormal temperature, obtain hourly core temperatures (e.g., urinary, esophageal, PA catheter). Use light covers and control the room temperature to keep the patient comfortably warm. If the patient’s temperature rises above 101.5°F (38.6°C) and the patient becomes uncomfortable or shows cardiovascular compromise, treat the fever with antipyretic drugs (e.g., ibuprofen, acetaminophen) and remove some of the patient’s covers. Consider a cooling device if fever persists despite treatment.

Gastrointestinal Status Auscultate bowel sounds at least every 4 hours. Monitor for abdominal distention. If a nasogastric tube is present, measure drainage and check for occult blood. Check all stools for occult blood.

Skin Integrity Hygiene is especially important for the patient in shock because impaired tissue perfusion predisposes the patient to skin breakdown and infection. Perform bathing and other nursing measures carefully because a patient in shock has problems with O2 delivery to tissues. Use clinical judgment in determining priorities of care to limit the demands for increased O2. Monitor trends in O2 consumption (e.g., SpO2, ScvO2/SvO2) during all nursing interventions to assess the patient’s tolerance of activity. The increased O2 demand that occurs during bathing and repositioning of patients with limited O2 reserves makes the prevention of pressure injuries challenging. Turn the patient at least every 1 to 2 hours. Maintain good body alignment. Use a pressurerelieving or pressure-reducing mattress or a specialty bed as needed. Perform passive range of motion 3 or 4 times a day to maintain joint

mobility and help prevent breakdown. Oral care is essential because mucous membranes may become dry and fragile in the volume-depleted patient. The intubated patient usually has difficulty swallowing, resulting in pooled secretions in the mouth. Apply a water-soluble lubricant to the lips to prevent drying and cracking. Brush the patient’s teeth or gums with a soft toothbrush every 12 hours. Swab the lips and oral mucosa with a moisturizing solution every 2 to 4 hours.

Emotional Support and Comfort Do not underestimate the effects of fear and anxiety when the patient and caregiver are faced with a critical, life-threatening situation (see Chapter 65). Fear, anxiety, and pain may worsen respiratory distress and increase the release of catecholamines. When implementing care, monitor the patient’s mental state and level of pain using valid assessment tools. Give drugs to decrease anxiety and pain as needed. Continuous infusions of a benzodiazepine (e.g., lorazepam) and an opioid or sedative (e.g., morphine, propofol [Diprivan]) are extremely helpful in decreasing anxiety and pain.19 Do not overlook the patient’s spiritual needs. Patients may want a visit from a chaplain, priest, rabbi, or minister. One way to provide support is to offer to call a member of the clergy rather than wait for the patient or caregiver to express a wish for spiritual counseling.

Check Your Practice Your patient is a 74-yr-old man recovering from septic shock after a perforated diverticulum. He has been in the ICU for 7 days, and his condition has finally stabilized. His wife has been at his bedside for the duration of his ICU stay. While caring for him, you suggest that she could take a brief walk and get some coffee. She bursts out with tears, “I can’t leave him. You know that he almost died.” • How can you support this caregiver?

Caregivers need to be kept informed of the patient’s condition. Give the patient and caregiver simple explanations of all procedures before you carry them out and information about the plan of care. If they ask questions about progress and prognosis, give simple and honest answers. If possible, the same nurses should continually care for the patient. This decreases anxiety, limits conflicting information, and increases trust. If the prognosis becomes grave, support the patient’s caregiver when making tough decisions, such as withdrawing life support. The interprofessional care team must promote realistic expectations and outcomes. Remember, compassion is as essential as scientific and technical expertise in the total care of the patient and caregiver. Ensure that the caregiver can spend time with the patient, provided the patient perceives this time as comforting.20 Explain in simple terms the purpose of any tubes and equipment attached to or surrounding the patient. Tell them what they may and may not touch. If possible, place the patient’s hands and arms outside the sheets to encourage therapeutic touch. Encourage caregivers to perform simple comfort measures if desired. Provide privacy as much as possible while assuring the patient and caregiver that help is readily available should it be needed. Always position the call light in reach of the patient or caregiver.

Ambulatory Care Rehabilitation of the patient who had a critical illness requires (1) correction of the precipitating cause, (2) prevention or early treatment of complications, and (3) teaching focused on disease management or prevention of recurrence based on the initial cause of shock. Continue to monitor the patient for complications throughout the recovery period. These may include decreased range of motion, muscle weakness, decreased physical endurance, AKI (see Chapter 46), and fibrotic lung disease (from ARDS) (see Chapter 67). Patients recovering from shock often need diverse services after discharge. These can include admission to transitional care units (e.g., for mechanical ventilation weaning), rehabilitation centers (inpatient or

outpatient), or home health care agencies. Start planning for a safe transition from hospital to home as soon as the patient is admitted to the hospital.

Evaluation The expected outcomes are that the patient who has shock will have: • Adequate tissue perfusion with restoration of normal or baseline BP • Normal organ function with no complications from hypoperfusion • Decreased fear and anxiety and increased psychologic comfort

Systemic Inflammatory Response Syndrome and Multiple Organ Dysfunction Syndrome Etiology and Pathophysiology Systemic inflammatory response syndrome (SIRS) is a systemic inflammatory response to a variety of insults, including infection (referred to as sepsis), ischemia, infarction, and injury.21 Generalized inflammation in organs remote from the initial insult characterizes SIRS. Many different mechanisms can trigger SIRS. These include: • Mechanical tissue trauma: burns, crush injuries, surgical procedures • Abscess formation: intraabdominal, extremities • Ischemic or necrotic tissue: pancreatitis, vascular disease, MI • Microbial invasion: bacteria, viruses, fungi, parasites • Endotoxin release: gram-negative and gram-positive bacteria • Global perfusion deficits: postcardiac resuscitation, shock states

• Regional perfusion deficits: distal perfusion deficits Multiple organ dysfunction syndrome (MODS) is the failure of 2 or more organ systems in an acutely ill patient such that homeostasis cannot be maintained without intervention.22 MODS results from SIRS. These 2 syndromes represent the ends of a continuum. Transition from SIRS to MODS does not occur in a clear-cut manner (Fig. 66.1).

Organ and Metabolic Dysfunction When the inflammatory response is activated, consequences include the release of mediators, direct damage to the endothelium, and hypermetabolism. Vascular permeability increases. This allows mediators and protein to leak out of the endothelium and into the interstitial space. White blood cells begin to digest the foreign debris, and the coagulation cascade is activated (see Chapter 29). Hypotension, decreased perfusion, microemboli, and redistributed or shunted blood flow eventually compromise organ perfusion. The respiratory system is often the first system to show signs of dysfunction in SIRS and MODS.22 Inflammatory mediators have a direct effect on the pulmonary vasculature. The endothelial damage from the release of inflammatory mediators causes increased capillary permeability. This causes movement of fluid from the pulmonary vasculature into the pulmonary interstitial spaces. The fluid then moves to the alveoli, causing alveolar edema. Type I pneumocytes (alveolar cells) are destroyed. Type II pneumocytes are damaged, and surfactant production is decreased. The alveoli collapse. This creates an increase in shunt (blood flow to the lungs that does not take part in gas exchange) and worsening ventilation-perfusion mismatch. The result is ARDS. Patients with ARDS need aggressive pulmonary management with mechanical ventilation. See Chapter 67 for a complete discussion of ARDS. Cardiovascular changes include myocardial depression and massive vasodilation in response to increasing tissue demands. Vasodilation results in decreased SVR and BP. The baroreceptor reflex

causes release of inotropic (increasing force of contraction) and chronotropic (increasing heart rate) factors that enhance CO. To compensate for hypotension, CO increases by an increase in heart rate and SV. Increases in capillary permeability cause a shift of albumin and fluid out of the vascular space. This further reduces venous return and thus preload. The patient becomes warm and tachycardic with a high CO and a low SVR. Other signs include decreased capillary refill, skin mottling, increased CVP and PAWP, and dysrhythmias. ScvO2 or SvO2 may be abnormally high because the patient is perfusing areas not consuming much O2 (e.g., skin, nonworking muscle). Other areas may have blood shunted away from them. Eventually, either perfusion of vital organs becomes insufficient or the cells are unable to use O2 and their function is further compromised. Neurologic dysfunction in SIRS and MODS often presents as mental status changes. These acute changes can be an early sign of SIRS or MODS. The patient may be confused and agitated, combative, disoriented, lethargic, or comatose. These changes are due to hypoxemia, the effects of inflammatory mediators, and impaired perfusion. AKI is common in SIRS and MODS. Hypoperfusion and the effects of the mediators can cause AKI. Decreased perfusion to the kidneys activates the SNS and the renin-angiotensin system.22 Stimulation of the renin-angiotensin system causes systemic vasoconstriction and aldosterone-mediated sodium and water reabsorption. Another risk factor for the development of AKI is the use of nephrotoxic drugs. Many antibiotics used to treat gram-negative bacteria (e.g., aminoglycosides) can be nephrotoxic. Careful monitoring of drug levels is essential to avoid the nephrotoxic effects. The GI tract plays a key role in the development of MODS. GI motility is often decreased in critical illness, causing abdominal distention and paralytic ileus. In the early stages of SIRS and MODS, blood is shunted away from the GI mucosa, making it highly vulnerable to ischemic injury. Decreased perfusion leads to a breakdown of this normally protective mucosal barrier. This increases the risk for ulceration, GI bleeding, and bacterial movement from the

GI tract into circulation.21 Metabolic changes are pronounced in SIRS and MODS. Both syndromes trigger a hypermetabolic response. Glycogen stores are rapidly converted to glucose (glycogenolysis). Once glycogen is depleted, amino acids are converted to glucose (gluconeogenesis), reducing protein stores. Fatty acids are mobilized for fuel. Catecholamines and glucocorticoids are released and cause hyperglycemia and insulin resistance. The net result is a catabolic state with a loss of lean body mass (muscle). The hypermetabolism associated with SIRS and MODS may last for several days and cause liver dysfunction. Liver dysfunction in MODS may begin long before clinical evidence of it is present. Protein synthesis is impaired. The liver cannot make albumin, one of the key proteins in maintaining plasma oncotic pressure. This changes plasma oncotic pressure, causing fluid and protein to leak from the vascular spaces to the interstitial space. At this point, giving albumin does not normalize oncotic pressure in these patients. As the state of hypermetabolism persists, the patient cannot convert lactate to glucose and lactate accumulates (lactic acidosis). Despite increases in glycogenolysis and gluconeogenesis, eventually the liver cannot maintain an adequate glucose level and the patient becomes hypoglycemic. Hypoglycemia can also develop due to acute adrenal insufficiency. DIC may result from dysfunction of the coagulation system. DIC causes microvascular clotting and bleeding at the same time because of the depletion of clotting factors and excessive fibrinolysis. (Chapter 30 discusses DIC.) Electrolyte imbalances are common and result from the hormonal and metabolic changes and fluid shifts. These changes worsen mental status changes, neuromuscular dysfunction, and dysrhythmias. The release of ADH and aldosterone results in sodium and water retention. Aldosterone increases urinary potassium loss, and catecholamines cause potassium to move into the cell, resulting in hypokalemia. Hypokalemia is associated with dysrhythmias and muscle weakness. Metabolic acidosis results from impaired tissue

perfusion, hypoxia, and the shift to anaerobic metabolism. This increases lactate levels. Progressive renal dysfunction also contributes to metabolic acidosis. Hypocalcemia, hypomagnesemia, and hypophosphatemia are common.

Clinical Manifestations of SIRS and MODS The clinical manifestations of SIRS and MODS are described in Table 66.10.

Nursing and Interprofessional Management: Sirs and Mods The prognosis for the patient with MODS is poor, with mortality rates of 40% to 60%.22 Mortality increases as more organ systems fail. The most common cause of death continues to be sepsis. Survival improves with early, goal-directed therapy. So, the most important goal is to prevent SIRS from progressing to MODS. A critical part of your role is vigilant assessment and ongoing monitoring to detect early signs of deterioration or organ dysfunction. Interprofessional care for patients with SIRS and MODS focuses on (1) prevention and treatment of infection, (2) maintaining tissue oxygenation, (3) nutritional and metabolic support, and (4) appropriate support of individual failing organs. Table 66.10 outlines the management for patients with SIRS and MODS.

TABLE 66.10 Manifestations and Management of

SIRS and MODS

ALT, Alanine aminotransferase; AST, aspartate aminotransferase; GGT, γ-glutamyl transferase; PA, pulmonary artery; PAWP, pulmonary artery wedge pressure; PT, prothrombin time; PTT, partial thromboplastin time; ScvO2, O2 saturation in venous blood; SvO2, O2 saturation in mixed venous blood; SVR, systemic vascular resistance.

Prevention and Treatment of Infection Aggressive infection control strategies are essential to decrease the risk for HAIs. Early, aggressive surgery is recommended to remove

necrotic tissue (e.g., early debridement of burn tissue) that can provide a culture medium for microorganisms. Aggressive pulmonary management, including early mobilization, can reduce the risk for infection. Strict asepsis can decrease infections related to intraarterial lines, endotracheal tubes, indwelling urinary catheters, IV lines, and other invasive devices or procedures. Daily assessment of the ongoing need for invasive lines and other devices is an important strategy to prevent or limit HAIs. Despite aggressive strategies, infection may develop. Once an infection is suspected, begin interventions to treat the cause. Send appropriate cultures and start broad-spectrum antibiotic therapy, as ordered. Adjust therapy based on the culture results, if needed.

Maintenance of Tissue Oxygenation Hypoxemia often occurs because patients have greater O2 needs and decreased O2 supply to the tissues. Interventions that decrease O2 demand and increase O2 delivery are essential. Sedation, mechanical ventilation, analgesia, and rest may decrease O2 demand and should be considered. Treating fever, chills, and pain decrease O2 demand. O2 delivery may be optimized by using individualized tidal volumes with positive end-expiratory pressure, increasing preload (e.g., fluids) or myocardial contractility to enhance CO, or reducing afterload to increase CO.

Nutritional and Metabolic Needs Hypermetabolism can result in profound weight loss, cachexia, and further organ failure. Protein-calorie malnutrition is a key sign of hypermetabolism. Total energy expenditure is often increased 1.5 to 2.0 times the normal metabolic rate. Because of their short half-life, monitor plasma transferrin and prealbumin levels to assess hepatic protein synthesis. The goal of nutritional support is to preserve organ function. Providing early and optimal nutrition decreases morbidity and

mortality rates. EN is preferred. If it cannot be used, PN should be considered. (Chapter 39 discusses EN and PN.) Provide glycemic control with a goal of ≤180 mg/dL with insulin infusions in these patients.21

Support of Failing Organs Support of any failing organ is a goal of therapy. For example, the patient with ARDS requires aggressive O2 therapy and mechanical ventilation (see Chapter 67). DIC should be treated appropriately (e.g., blood products) (see Chapter 30). Renal failure may require dialysis. Continuous renal replacement therapy is better tolerated than hemodialysis, especially in a patient with hemodynamic instability (see Chapter 46). A final consideration may be that further interventions are futile. It is important to maintain communication between the health care team and the patient’s caregiver about realistic goals and likely outcomes for the patient with MODS. Withdrawal of life support and starting end-of-life care may be the best options for the patient.

Case Study Shock

© Thinkstock.

Patient Profile K.L., a 25-yr-old Korean American, was not wearing his seat belt when he was driving a motor vehicle involved in a crash. The windshield was broken, and K.L. was found 10 ft from his car. He was face down, conscious, and moaning. His wife and daughter were in the car with their seat belts on. They sustained minor injuries and were very frightened and upset. All passengers were taken to the ED. This information pertains to K.L.

Subjective Data • States, “I can’t breathe” • Cries out when abdomen is palpated

Objective Data Physical Examination • Cardiovascular: BP 80/56 mm Hg; apical pulse 138 but no palpable radial or pedal pulses; carotid pulse 1+. ECG is below:

• Respiratory: respiratory rate 35 breaths/min; labored breathing with shallow respirations; asymmetric chest wall movement; absence of breath sounds on left side. Trachea deviated slightly to the right • Abdomen: slightly distended and left upper quadrant painful on

palpation • Musculoskeletal: open compound fracture of the lower left leg

Diagnostic Studies • Chest x-ray: hemothorax and 6 rib fractures on left side • Hematocrit: 28%

Interprofessional Care (in the ED) • Intraosseous access in right proximal tibia placed prehospital • Left chest tube placed, draining bright red blood • Fluid resuscitation started with crystalloids • High-flow O2 via nonrebreather mask

Emergency Surgical Procedures • Splenectomy • Repair of torn intercostal artery • Repair of compound fracture

Discussion Questions 1. What types of shock is K.L. experiencing? What clinical manifestations did he display that support your answer? 2. What were the causes of K.L.’s shock states? What are other causes of these types of shock? 3. Priority Decision: What are the priority nursing responsibilities for K.L.? 4. Priority Decision: What ongoing nursing assessment parameters are essential for this patient?

5. What are his potential complications? 6. Patient-Centered Care: K.L.’s parents arrive. English is their second language. They are very anxious and asking about their son. What can you do to provide culturally competent familycentered care? 7. Priority Decision: Based on the assessment data presented, what are the priority nursing diagnoses? 8. Collaboration: Identify the tasks that could be delegated to unlicensed assistive personnel (UAP). 9. Evidence-Based Practice: You are orienting a new graduate RN. He asks you why crystalloids are used for fluid resuscitation. What is your response? Answers available at http://evolve.elsevier.com/Lewis/medsurg.

Bridge to Nclex Examination The number of the question corresponds to the same-numbered outcome at the beginning of the chapter.

1. A patient has a spinal cord injury at T4. Vital signs include falling blood pressure with bradycardia. The nurse recognizes that the patient is experiencing a. a relative hypervolemia. b. an absolute hypovolemia. c. neurogenic shock from low blood flow. d. neurogenic shock from massive vasodilation. 2. A 78-yr-old man with a history of diabetes has confusion and temperature of 104°F (40°C). There is a wound on his right heel with purulent drainage. After an infusion of 3 L of normal saline solution, his assessment findings are BP 84/40 mm Hg; heart rate 110; respiratory rate 42 and

shallow; CO 8 L/min; and PAWP 4 mm Hg. This patient’s symptoms are most likely indicative of a. sepsis. b. septic shock. c. multiple organ dysfunction syndrome. d. systemic inflammatory response syndrome. 3. Treatment modalities for the management of cardiogenic shock include (select all that apply) a. dobutamine to increase myocardial contractility. b. vasopressors to increase systemic vascular resistance. c. circulatory assist devices such as an intraaortic balloon pump. d. corticosteroids to stabilize the cell wall in the infarcted myocardium. e. Trendelenburg positioning to facilitate venous return and increase preload. 4. The most accurate assessment parameters for the nurse to use to determine adequate tissue perfusion in the patient with MODS are a. blood pressure, pulse, and respirations. b. breath sounds, blood pressure, and body temperature. c. pulse pressure, level of consciousness, and pupillary response. d. level of consciousness, urine output, and skin color and temperature. 1. d, 2. b, 3. a, c, 4. d For rationales to these answers and even more NCLEX review questions, visit http://evolve.elsevier.com/Lewis/medsurg.

Evolve Website/Resources List http://evolve.elsevier.com/Lewis/medsurg

Review Questions (Online Only) Key Points Answer Keys to Questions • Rationales for Bridge to NCLEX Examination Questions • Answer Guidelines for Case Study on p. 1586 Student Case Studies • Patient With Acute Pancreatitis and Septic Shock • Patient With Cardiogenic Shock • Patient With Sepsis Nursing Care Plan • eNursing Care Plan 66.1: Patient in Shock Conceptual Care Map Creator Audio Glossary Content Updates

References 1. Tewelde SZ, Liu SS, Winters ME: Cardiogenic shock, Cardiol Clin 28:53, 2018. 2. Good VS, Kirkwood PL: Advanced critical care nursing, ed 2, St Louis, 2017, Elsevier. 3. Hamlin S, Strauss P, Chen H, et al: Microvascular fluid resuscitation in circulatory shock, Nurs Clin North Am 52:291, 2017.

4. Taylor MP, Wrenn P, O’Donnell AD: Presentation of neurogenic shock within the emergency department, Emerg Med J 34:157, 2016. Lee SE: Management of anaphylaxis, Otolaryngol Clin North Am 50: 1175, 2017.

6. Kleinpell R, Schorr C, Balk R: The new sepsis definitions: Implications for critical care practitioners, Amer J Crit Care 25:457, 2016. Singer M, Deutschman C, Seymour C, et al: The third international consensus definitions for sepsis and septic shock (Sepsis-3), JAMA 315:801, 2016.

8. O’Shaughnessy J, Grzelak M, Dontsova A, et al: Early sepsis identification, MEDSURG Nursing 26:248, 2017. Winters ME, Sherwin R, Vilke GM, et al: What is the preferred resuscitation fluid for patients with severe sepsis and septic shock? J Emerg Med 53:928, 2017. Stratton L, Verlin D, Arbo J: Vasopressors and inotropes in sepsis. Emerg Med Clin North Am 35:75, 2017.

11. McClave SA, Taylor BE, Martindale RG, et al: Guidelines for the provision and assessment of nutrition support therapy in the adult critically ill patient: Society of Critical Care Medicine (S.C.C.M.) and American Society for Parenteral and Enteral Nutrition (A.S.P.E.N.), J Parenter Enteral Nutr 40:159, 2016. 12. Jakovijevi D, Lip-Burn M, Scheueler S, et al: Left ventricular assist device as a bridge to recovery for patient with advanced heart failure, J Am Coll Cardiol 69:1924, 2017. Pickett J, Bridges E, Kritek P, et al: Passive leg-raising and prediction of fluid responsiveness: Systematic review, Crit Care Nurse 37:32,

2017.

14. Timmerman RA: Managing vasoactive infusions to restore hemodynamic stability, Nursing2019 Critical Care, 11:35, 2016. 15. Sherwin R, Winters ME, Vilke GM, et al: Does early and appropriate antibiotic administration improve mortality in patients with severe sepsis or septic shock? J Emerg Med 53:588, 2017. 16. Gunst J, Van den Berghe G: Blood glucose control in the ICU. How tight? Ann Transl Med 5:76, 2017. Rhodes A, Evans LE, Alhazzani W, et al: Surviving sepsis campaign. International guidelines for management of sepsis and septic shock, Intens Care Med 43:304, 2017.

18. Institute for Healthcare Improvement: Evidencebased care bundles. Retrieved from www.ihi.org/topics/Bundles/Pages/default.aspx. 19. Hariharan U, Garg R: Sedation and analgesia in critical care, J Anesth Crit Care Open Access 7:262, 2017. 20. Davidson JE, Aslakson RA, Long AC, et al: Guidelines for family-centered care in the neonatal, pediatric, and adult ICU, Crit Care Med 45:103, 2017. 21. Sauaia A, Moore FA, Moore EE: Postinjury inflammation and organ dysfunction, Crit Care Clin 33:167, 2017. 22. Gordy S: Multiple organ failure. In Moore L, Todd S, eds: Common problems in acute care surgery, New York, 2017, Springer. ∗Evidence-based information for clinical practice.

67

Acute Respiratory Failure and Acute Respiratory Distress Syndrome Eugene Mondor

LEARNING OUTCOMES 1. Discuss the etiology, pathophysiology, and clinical manifestations of hypoxemic and hypercapnic acute respiratory failure. 2. Describe the nursing and interprofessional management of hypoxemic or hypercapnic respiratory failure. 3. Discuss the pathophysiology and clinical manifestations of acute respiratory distress syndrome (ARDS). 4. Describe the nursing and interprofessional management of ARDS. 5. Select measures to prevent and manage complications of acute respiratory failure and ARDS.

KEY TERMS acute respiratory distress syndrome (ARDS), p. 1597 acute respiratory failure (ARF), p. 1588

alveolar hypoventilation, p. 1590 chronic respiratory failure, p. 1589 hypercapnic respiratory failure, p. 1588 hypoxia, p. 1591 hypoxemia, p. 1588 hypoxemic respiratory failure, p. 1588 PaO2/FIO2 (P/F) ratio, p. 1599 permissive hypercapnia, p 1601 refractory hypoxemia, p. 1598 shunt, p. 1590 V/Q mismatch, p. 1589 work of breathing (WOB), p. 1591 The closest thing to being cared for is to care for someone else. Carson McCullers http://evolve.elsevier.com/Lewis/medsurg

Conceptual Focus Acid-Base Balance Anxiety Gas Exchange This chapter discusses acute respiratory failure (ARF) and acute respiratory distress syndrome (ARDS). Nursing and interprofessional management of patients with ARF and ARDS focus on interventions to promote adequate oxygenation, ensure effective ventilation, identify and treat the underlying causes, and prevent complications. When respiratory function is insufficient, all body systems are affected

Acute Respiratory Failure The major function of the respiratory system is gas exchange. Acute respiratory failure (ARF) occurs when oxygenation, ventilation, or both are inadequate. ARF is not a disease. It is a symptom that reflects lung function. For example, not enough O2 is transferred to the blood or inadequate CO2 is removed from the lungs (Fig. 67.1). ARF occurs because of disorders involving the lungs or other body systems (Table 67.1). Conditions that interfere with adequate O2 transfer result in hypoxemia. This causes a decrease in arterial O2 (PaO2) and saturation (SaO2) to less than the normal values. Insufficient CO2 removal results in hypercapnia. It causes an increase in arterial CO2 (PaCO2). Arterial blood gases (ABGs) are used to assess changes in pH, PaO2, PaCO2, bicarbonate, and SaO2. We use pulse oximetry to assess arterial O2 saturation (SpO2). We classify ARF as hypoxemic or hypercapnic (Fig. 67.2). Hypoxemic respiratory failure is a PaO2 less than 60 mm Hg when the patient is receiving an inspired O2 concentration of 60% or more.1 In hypoxemic respiratory failure (also called oxygenation failure), the main problem is inadequate exchange of O2 between the alveoli and pulmonary capillaries. The PaO2 level shows inadequate O2 saturation. A less than optimal PaO2 level exists despite supplemental O2. Hypercapnic respiratory failure (or ventilatory failure) is a PaCO2 greater than 50 mm Hg with acidemia (arterial pH less than 7.35).2 The main problem is insufficient CO2 removal. This causes the PaCO2 to be higher than normal. For whatever reason, the body is unable to compensate for the increase. This allows acidemia to occur. Patients may have both types of respiratory failure at the same time. For example, a patient with chronic obstructive pulmonary disease (COPD) who has pneumonia could have “acute-on-chronic” respiratory failure. In other words, the patient has an underlying

chronic respiratory problem. The new infection, in addition to the chronic problem, results in the “acute-on-chronic” clinical picture.

FIG. 67.1 Normal gas exchange unit in the lung.

TABLE 67.1 Common Causes of Respiratory

Failure

Significant changes in PaO2 and PaCO2 occur with ARF. These may develop over several minutes to a few hours to 1 or 2 days. The patient may have hemodynamic instability (e.g. tachycardia, hypotension), increased respiratory effort, and decreased level of consciousness. Urgent intervention is required. Chronic respiratory failure develops more slowly, over days to weeks. The patient is usually more stable as the body had time to compensate for the small, but subtle, changes that have occurred.

FIG. 67.2 Classification of respiratory failure.

Etiology and Pathophysiology Hypoxemic Respiratory Failure Four physiologic mechanisms may cause hypoxemia and hypoxemic respiratory failure: (1) mismatch between ventilation (V) and perfusion (Q), often referred to as V/Q mismatch; (2) shunt; (3) diffusion limitation; and (4) alveolar hypoventilation. The most common causes are V/Q mismatch and shunt.

Ventilation-Perfusion Mismatch In normal lungs, the volume of blood perfusing the lungs and the amount of gas reaching the alveoli are almost identical. So, when you compare normal alveolar ventilation (4 to 6 L/min) to pulmonary

blood flow (4 to 6 L/min), you have a V/Q ratio of 0.8 to 1.2.3 In a perfect match, ventilation and perfusion would yield a V/Q ratio of 1:1, expressed as V/Q = 1. When the match is not 1:1, a V/Q mismatch occurs. This example implies that ventilation and perfusion are perfectly matched in all areas of the lung. This situation does not normally exist. In reality, some regional mismatch occurs. For example, at the apex of the lung, V/Q ratios are greater than 1 (more ventilation than perfusion). At the base of the lung, V/Q ratios are less than 1 (less ventilation than perfusion). Because changes at the lung apex balance changes at the base, the net effect is a close overall match (Fig. 67.3). Many diseases and conditions cause a V/Q mismatch (Fig. 67.4). The most common are those in which increased secretions are present in the airways (e.g., COPD) or alveoli (e.g., pneumonia) or bronchospasm is present (e.g., asthma). V/Q mismatch may result from pain, alveolar collapse (atelectasis), or pulmonary emboli. Pain interferes with chest and abdominal wall movement and increases muscle tension. This often compromises ventilation. The patient is often unwilling to take big, deep breaths. As a result, short, shallow respirations contribute to the development of atelectasis. This worsens V/Q mismatch. Pain activates the stress response, increasing baseline metabolic state. This increases O2 consumption and CO2 production (as a byproduct of cellular and tissue metabolism). The increased O2 demand, increased CO2, and decreased O2 supply increase ventilation demands. Since there is no effect on blood flow to the lungs, the result is V/Q mismatch. Pulmonary emboli affect the perfusion part of the V/Q relationship. When a pulmonary embolus occurs, it limits blood flow distal to the occlusion. Areas of normal lung ventilation remain, but there is decreased perfusion due to the vessel occlusion. This results in a V/Q mismatch. If the embolus is large, it can cause hemodynamic instability due to blockage of a large pulmonary artery.

FIG. 67.3 Regional V/Q differences in the normal lung. This difference causes the PaO2 to be higher at the apex of the lung and lower at the base. Values for PaCO2 are the opposite (i.e., lower at the apex and higher at the base). Blood that exits the lung is a mixture of these values.

FIG. 67.4 Range of ventilation to perfusion (V/Q) relationships. A, Absolute shunt, no ventilation because of fluid filling the alveoli. B, V/Q mismatch, ventilation partially compromised by secretions in the airway. C, Normal lung unit. D, V/Q mismatch, perfusion partially compromised by emboli obstructing blood flow. E, Dead space, no perfusion because of obstruction of the pulmonary capillary.

O2 therapy is an appropriate first step to reverse hypoxemia caused by V/Q mismatch. O2 therapy increases the PaO2 in the blood leaving normal gas exchange units, causing a higher-than-normal PaO2. This blood mixes with the poorly oxygenated blood from damaged areas, raising the overall PaO2 level in the blood leaving the lungs. The best way to treat hypoxemia caused by a V/Q mismatch is to treat the

cause.

Shunt A shunt occurs when blood exits the heart without having taken part in gas exchange. A shunt is an extreme V/Q mismatch. There are 2 types of shunt: anatomic and intrapulmonary. An anatomic shunt occurs when blood passes through an anatomic channel in the heart (e.g., a ventricular septal defect) and bypasses the lungs.4 An intrapulmonary shunt occurs when blood flows through the pulmonary capillaries without taking part in gas exchange.4 It is seen in conditions in which the alveoli fill with fluid (e.g., pneumonia) and gas exchange is severely impaired at the alveolar-capillary membrane.

FIG. 67.5 Diffusion limitation. Exchange of CO2 and O2 cannot occur because of the thickened alveolar-capillary membrane.

O2 therapy alone is not effective at increasing the PaO2 if

hypoxemia is due to shunt. Patients with a shunt are usually more hypoxemic than patients with V/Q mismatch. They often need mechanical ventilation with a high fraction of inspired O2 (FIO2) to improve gas exchange.

Diffusion Limitation Diffusion limitation occurs when gas exchange across the alveolarcapillary membrane is compromised by a process that damages or destroys the alveolar membrane or affects blood flow through the pulmonary capillaries (Fig. 67.5).5 Conditions that cause the alveolarcapillary membrane to become thicker (fibrotic) slow gas transport. These include pulmonary fibrosis, interstitial lung disease, and ARDS. The accumulation of fluid, white blood cells, or protein in the alveoli can decrease gas exchange between the alveolus and the capillary bed. A common example is pulmonary edema. The classic sign of diffusion limitation is hypoxemia that is present during exercise but not at rest. During exercise, blood moves more quickly through the lungs. This decreases the time for diffusion of O2 across the alveolar-capillary membrane. Diffusion limitation can occur in conditions in which CO is markedly increased (e.g., high-output heart failure [HF], severe traumatic brain injury [TBI]). As blood circulates rapidly through the pulmonary capillary bed, there is less time for gas exchange to occur.

Alveolar Hypoventilation Alveolar hypoventilation is a decrease in ventilation that results in an increase in the PaCO2. It may be caused by central nervous system (CNS) conditions, chest wall dysfunction, acute asthma, or restrictive lung diseases. Although alveolar hypoventilation is mainly a mechanism of hypercapnic respiratory failure, it contributes to hypoxemia.

Interrelationship of Mechanisms Rarely is acute hypoxemic respiratory failure caused by a single

factor. More often, it is a combination of 2 or more factors. For example, the patient with ARF from pneumonia may have a V/Q mismatch and shunt. Inflammation, edema, and exudate obstruct the airways (V/Q mismatch) and fill the alveoli with exudate (shunt). Other contributing factors include increases in O2 demand with anxiety and unrelieved pain.

Consequences of Hypoxemia Hypoxemia can lead to hypoxia if not corrected. occurs when the PaO2 falls enough to cause signs and symptoms of inadequate oxygenation. If hypoxia or hypoxemia is severe, the cells shift from aerobic to anaerobic metabolism. Anaerobic metabolism uses more fuel, produces less energy, and is less efficient than aerobic metabolism. The waste product of anaerobic metabolism is lactic acid. Lactic acid is harder to remove from the body than CO2, because it must be buffered with sodium bicarbonate. When the body does not have enough sodium bicarbonate to buffer the lactic acid, metabolic acidosis occurs. Left uncorrected, tissue and cell dysfunction, and ultimately cell death, occurs.

Hypercapnic Respiratory Failure In acute hypercapnic respiratory failure, sometimes referred to as ventilatory failure, the lungs are often normal. In this situation, the respiratory system cannot keep CO2 levels maintained within normal limits. This often occurs from an increase in CO2 production or a decrease in alveolar ventilation. Hypercapnic respiratory failure can be acute or chronic. It often reflects significant problems with the respiratory system. Many conditions can cause impaired ventilation. We group into 4 categories: (1) CNS problems, (2) neuromuscular conditions, (3) chest wall abnormalities, and (4) problems affecting the airways and/or alveoli. Acute hypercapnic respiratory failure can occur with CNS problems, neuromuscular conditions, and chest wall abnormalities in the presence of normal lungs.

Central Nervous System Problems A number of CNS problems can suppress the drive to breathe. A common example is an overdose of a respiratory depressant drug (e.g., opioids). In a dose-related manner, CNS depressants decrease CO2 reactivity in the brainstem. This allows arterial CO2 levels to rise. A brainstem infarction or TBI may interfere with normal function of the respiratory center in the medulla. Patients are then at risk for acute hypercapnic respiratory failure because the medulla does not change the respiratory rate in response to a change in PaCO2. High-level spinal cord injuries can affect nerve supply to the respiratory muscles of the chest wall and diaphragm. Brain injury with a decreased level of consciousness can hinder the patient’s ability to protect the airway, breathe, or manage secretions.

Neuromuscular Conditions Various neuromuscular problems place patients at risk for respiratory failure. For example, patients with Guillain-Barré syndrome and multiple sclerosis have respiratory muscle weakness or paralysis. As a result, they cannot eliminate CO2 and maintain normal PaCO2 levels. Exposure to toxins (e.g., carbamate/organophosphate pesticides, chemical nerve agents) can interfere with the nerve supply to muscles and lung ventilation. Respiratory muscle weakness can occur from muscle wasting during a critical illness or peripheral nerve damage.

Chest Wall Abnormalities Several conditions can prevent normal movement of the chest wall or diaphragm and limit lung expansion. In patients with flail chest, fractures prevent the rib cage from expanding normally. With kyphoscoliosis, the change in spinal configuration compresses the lungs and prevents normal expansion of the chest wall. In those with severe obesity, the weight of the chest and abdominal contents limit lung expansion.

Problems of the Airway and Alveoli

Patients with asthma, COPD, and cystic fibrosis have a high risk for hypercapnic respiratory failure because the underlying pathophysiology results in airflow obstruction and air trapping. Respiratory muscle fatigue and ventilatory failure occur from the added work of breathing needed to inspire air against increased airway resistance and air trapped within the alveoli.

Consequences of Hypercapnia The body can tolerate increased CO2 levels far better than low O2 levels. This is because with slow changes in PaCO2, the body may have time for compensation to occur. For example, consider the patient with COPD who has a slow increase in PaCO2 after an upper respiratory tract infection. Because the change occurred over several days, there is time for the kidneys to compensate (e.g., by retaining bicarbonate). This will initially minimize the change in arterial pH. Unless the primary cause is identified and corrected, the patient’s condition will likely get worse. (See Chapter 16 for a discussion of renal compensation for acid-base disorders.)

Clinical Manifestations Respiratory failure may develop suddenly (acute, minutes or hours) or gradually (chronic, several days or weeks). A sudden decrease in PaO2 and/or a rapid rise in PaCO2 implies a serious respiratory condition, which can rapidly become a life-threatening emergency. An example is the patient with asthma who develops severe bronchospasm and a marked decrease in airflow, resulting in respiratory muscle fatigue, acidemia, and ARF. Signs of respiratory failure are related to the extent of change in PaO2 or PaCO2, the speed of change (acute versus chronic), and the patient’s ability to compensate for this change. When the patient’s compensatory mechanisms fail, respiratory failure occurs. Because clinical signs vary, frequent patient assessment is a priority. A lack of O2 affects all body systems (Table 67.2). For example, a

decreased level of consciousness may occur without enough blood, O2, and glucose supplied to the brain. Permanent brain damage can result if hypoxia is severe and prolonged. Gastrointestinal (GI) system changes include tissue ischemia and increased intestinal wall permeability. Bacteria can migrate from the GI tract into systemic circulation. Renal function may be impaired. Sodium retention, peripheral edema, and acute kidney injury may occur. One of the first signs of acute hypoxemic respiratory failure is a change in mental status. Mental status changes occur early because the brain is extremely sensitive to changes in O2 (and to a lesser degree CO2) levels and acid-base balance. Restlessness, confusion, and agitation suggest inadequate O2 delivery to the brain. On the other hand, a morning headache and slow respiratory rate with decreased level of consciousness may indicate problems with CO2 removal. Tachycardia, tachypnea, slight diaphoresis, and mild hypertension are early signs of ARF.6 These changes indicate attempts by the heart and lungs to compensate for decreased O2 delivery and rising CO2 levels. It is important to understand that cyanosis is an unreliable indicator of hypoxemia. It is a late sign in ARF. It often does not occur until hypoxemia is severe (PaO2 45 mm Hg or less).7 The priority for the patient with ARF is immediate assessment of the patient’s ability to breathe and providing any assistive measures needed. Depending on the severity of the respiratory failure and hemodynamic status, this may involve intubation and starting mechanical ventilation. Observing the patient’s position helps assess the effort associated with the work of breathing (WOB). WOB is the effort needed by the respiratory muscles to inhale air into the lungs. Patients with mild distress may be able to lie down. In moderate distress, patients may be able to lie down but prefer to sit. With severe distress they may be unable to breathe unless sitting upright. The tripod position helps decrease the WOB in patients with moderate to severe COPD and ARF. The patients sit with the arms propped on the overbed table or on the knees. Propping the arms increases the anteroposterior

diameter of the chest and changes pressure in the thorax.

TABLE 67.2 Common Manifestations of

Hypoxemia and Hypercapnia

The patient in ARF may have a rapid, shallow breathing pattern (hypoxemia) or a slower respiratory rate (hypercapnia). Both changes predispose the patient to insufficient O2 delivery and CO2 removal. Increased respiratory rates require a substantial amount of work and can lead to respiratory muscle fatigue. A change from a rapid rate to a slower rate in a patient in respiratory distress, such as that seen with

acute asthma, suggests severe respiratory muscle fatigue. There is an increased chance for respiratory arrest. The patient’s ability to speak is related to the severity of dyspnea. The dyspneic patient may be able to speak only a few words at a time between breaths. For example, the patient may have “2-word” or “3word” dyspnea. This means the patient can say only 2 or 3 words before pausing to breathe. You may see dyspneic patients using pursed-lip breathing (see Table 28.12). This technique increases SaO2 by slowing respirations, increasing time for expiration, and preventing small bronchioles from collapsing. You may see retraction (inward movement) of the intercostal spaces or supraclavicular area and use of the accessory muscles (e.g., sternocleidomastoid) during inspiration or expiration. Use of the accessory muscles often signifies a moderate degree of respiratory distress. Paradoxical breathing occurs with severe respiratory distress. Normally, the thorax and abdomen move outward on inspiration and inward on exhalation. With paradoxical breathing, the abdomen and chest move in the opposite manner—outward during exhalation and inward during inspiration. Paradoxical breathing results from maximal use of the accessory muscles of respiration. The patient may be extremely diaphoretic from the increased WOB. Auscultate breath sounds. Note the presence and location of any abnormal breath sounds. Fine crackles may occur with pulmonary edema. Coarse crackles heard on expiration indicate fluid in the airways. This may be a sign of pneumonia or a degree of HF. Absent or decreased breath sounds occur with atelectasis, pleural effusion, or hypoventilation. Bronchial breath sounds over the lung periphery occur with lung consolidation from pneumonia. You may hear a pleural friction rub if pneumonia involves the pleura.

Diagnostic Studies The most common diagnostic studies used to evaluate ARF are chest x-ray and ABG analysis. A chest x-ray helps identify possible causes

of respiratory failure (e.g., atelectasis, pneumonia). ABGs evaluate oxygenation (PaO2) and ventilation (PaCO2) status and acid-base (pH, bicarbonate) balance. Pulse oximetry monitors oxygenation status indirectly. Other diagnostic studies that may be done include a complete blood cell count, serum electrolytes, urinalysis, and 12-lead ECG. Blood and sputum cultures (Gram stain, culture and sensitivity) may reveal infection. A CT scan or V/Q lung scan may be done if a pulmonary embolus is suspected. For the patient in severe ARF who needs intubation, end-tidal CO2 (EtCO2) may be used during ventilator management to assess trends in lung ventilation.8

Nursing and Interprofessional Management: Acute Respiratory Failure Because many different problems cause ARF, initial management and specific care varies. Factors taken into consideration include patient age, severity of onset of respiratory failure, underlying co-morbidities, and suspected or most likely cause of the respiratory failure. We then tailor management strategies to what best meets the patient’s unique needs. This section discusses general assessment and interventions most commonly used for patients with ARF. In acute care settings, collaboration between nursing and the interprofessional team (e.g., ICU physicians, respiratory therapists, pharmacists) is essential. In severe ARF, the patient will be cared for in an intensive care unit (ICU). ICU care will include central venous pressure (CVP) and arterial BP monitoring. Arterial BP will be monitored at least hourly. Central or mixed venous O2 saturation [ScvO2 or SvO2] data help determine the adequacy of tissue perfusion and the patient’s response to treatment. The patient may need advanced hemodynamic monitoring to evaluate parameters such as CO and pulmonary capillary wedge pressure (PCWP). Chapter 65 discusses hemodynamic monitoring.

Nursing Assessment Table 67.3 presents subjective and objective data that you should obtain from the patient with ARF. A thorough assessment may result in early detection of respiratory insufficiency. This allows us to intervene sooner and can prevent worsening respiratory failure. Monitor patients with preexisting cardiac and/or respiratory disease closely. A slight change in their overall condition can cause significant decompensation. It is important to observe trends in ABGs, pulse oximetry, and assessment findings. You must identify the changes that are occurring from hypoxemia or hypercarbia. Your ability to detect problems, notify the HCP, implement appropriate treatment, and evaluate response to therapy is essential.

Nursing Diagnoses Nursing diagnoses for the patient with ARF may include: • Impaired gas exchange • Impaired respiratory system function Additional information on nursing diagnoses and interventions for the patient with ARF is presented in eNursing Care Plan 67.1 (available on the website for this chapter).

Planning The overall goals for the patient with ARF include (1) independently maintain a patent airway, (2) absence of dyspnea or recovery to baseline breathing patterns, (3) effectively cough and able to clear secretions, (4) normal ABG values or values within the patient’s baseline, and (5) breath sounds within the patient’s baseline.

Nursing Implementation

Prevention For the patient at risk for ARF, prevention and early recognition of respiratory distress are important. This is especially important for patients with neuromuscular diseases, cardiac problems, or respiratory problems (e.g., COPD). Do a thorough history and physical assessment to identify risk factors, then start appropriate interventions. Early strategies may include teaching patients about deep breathing and coughing, use of incentive spirometry, and early ambulation. Preventing atelectasis, pneumonia, and complications of immobility, and optimizing hydration and nutrition, can decrease the risk for ARF. Those patients at high risk should be assessed more often with attention given to preventive measures.

Respiratory Therapy The goals of respiratory care include maintaining adequate oxygenation and ventilation and correcting acid-base imbalance. Interventions include O2 therapy, mobilization of secretions, and positive pressure ventilation (PPV) (Table 67.4).

TABLE 67.3 Nursing AssessmentAcute

Respiratory Failure

Subjective Data Important Health Information Past health history: Age, weight, altered level of consciousness, tobacco use (pack-years), alcohol or drug use, hospitalizations related to either acute or chronic lung disease, thoracic or spinal cord trauma, occupational exposures to lung toxins Medications: Use of home O2, inhalers (bronchodilators), home nebulization, over-the-counter drugs; immunosuppressant (e.g.,

corticosteroid) therapy, CNS depressants, illicit substances Surgery or other treatments: Intubation and mechanical ventilation, recent thoracic or abdominal surgery

Functional Health Patterns Health perception–health management: Exercise, self-care activities, immunizations (flu, pneumonia, hepatitis) Nutritional-metabolic: Eating habits, bloating, indigestion; recent weight gain or loss, change in appetite. Use of vitamins or herbal supplements Activity-exercise: Fatigue, dizziness, dyspnea at rest or with activity, wheezing, cough (productive or nonproductive), sputum (volume, color, viscosity), palpitations, swollen feet, change in exercise tolerance Sleep-rest: Changes in sleep pattern, use of CPAP Cognitive-perceptual: Headache, chest pain or tightness, chronic pain Coping–stress tolerance: Anxiety, depression, feelings of hopelessness. Risk for drug and/or alcohol use, nicotine withdrawal

Objective Data General Restlessness, agitation

Integumentary Pale, cool, clammy skin or warm, flushed skin. Peripheral and central cyanosis. Peripheral dependent edema

Respiratory Shallow, increased respiratory rate progressing to decreased rate. Use of accessory muscles with evidence of retractions, increased diaphragmatic excursion or asymmetric chest expansion, paradoxical chest and abdominal wall movement. Tactile fremitus, crepitus, or deviated trachea on palpation. Absent, decreased, or adventitious breath sounds. Pleural friction rub. Bronchial or bronchovesicular sounds heard in other than normal location, inspiratory stridor

Cardiovascular Tachycardia progressing to bradycardia, dysrhythmias, extra heart sounds (S3, S4). Bounding pulse. Hypertension progressing to hypotension. Pulsus paradoxus, jugular venous distention, pedal edema

Gastrointestinal Abdominal distention, ascites, epigastric tenderness, hepatojugular reflex

Neurologic Somnolence, confusion, slurred speech, restlessness, delirium, agitation, tremors, seizures, coma, asterixis, ↓ deep tendon reflexes, papilledema

Possible Diagnostic Findings ↓/↑ pH, ↑/↓ PaCO2, ↑/↓ bicarbonate, ↓ PaO2, ↓ SaO2, abnormal

hemoglobin, ↑ WBC count, changes in serum electrolytes. Abnormal findings on chest x-ray. Abnormal central venous or pulmonary artery pressures. Initially cardiac output may be ↑ due to the stress response. As hypoxemia, hypercapnia, and acidosis become more severe, cardiac output will ↓.

TABLE 67.4 Interprofessional CareAcute

Respiratory Failure

Diagnostic Assessment • Vital signs • History and physical examination • Arterial blood gases (ABGs) • Pulse oximetry • Chest x-ray • CBC and differential • Serum electrolytes • 12-Lead ECG • Blood, sputum, and/or urine cultures (if indicated) • Hemodynamic monitoring: CVP, SVV, PAWP (if indicated)

Management Respiratory Therapy • O2 therapy • Mobilization of secretions • Positioning • Effective coughing • Chest physiotherapy • Suctioning of the airway

• Oral and/or IV hydration • Humidification (of O2) • Ambulation (early mobility) • Positioning: head of bed elevated • Positive pressure ventilation (PPV) • Noninvasive positive pressure ventilation (e.g. CPAP, BiPAP) • Intubation with positive pressure ventilation

Drug Therapy • Reduce airway inflammation (e.g., corticosteroids) • Relief of bronchospasm (e.g., albuterol) • Reduce pulmonary congestion (e.g., furosemide [Lasix], morphine) • Treat pulmonary infections (e.g., antibiotics) • Reduce anxiety, pain, and restlessness (e.g., lorazepam, fentanyl, morphine)

Supportive Therapy • Management of the underlying cause of respiratory failure • Monitor hemodynamic status • Optimize balance between activity and rest • Monitor for deterioration in patient condition CVP, Central venous pressure; SVV, stroke volume variation; PAWP, pulmonary artery wedge pressure.

Oxygen Therapy The primary goal of O2 therapy is to correct hypoxemia. This requires

O2 administration. Always administer O2 at the lowest possible FIO2 (O2 concentration) needed to keep SpO2 and PaO2 within patientspecific goals. Never withhold O2 from a patient. It is essential to observe the patient’s response to O2 therapy. Closely monitor patients for changes in mental status, respiratory rate, and ABGs, until their PaO2 level has reached their baseline normal value. Several methods are available to provide O2 to patients in ARF. Chapter 28 and Table 28.19 discuss O2 delivery devices. The device selected depends upon the patient’s overall condition, degree of respiratory failure, ability to maintain a patent airway, the amount of FIO2 that the device can deliver, and, most importantly, the patient’s ability to breathe spontaneously. Ideally, the selected O2 delivery device must maintain PaO2 at 60 mm Hg or higher and SaO2 at 90% or higher. The patient is often agitated, disoriented, and restless. A face mask, though appropriate, may cause anxiety from feelings of claustrophobia. Anxiety can cause dyspnea and increase O2 consumption and CO2 production. The patient may try to remove the mask. In this case, you need to explore other O2 therapy options. Breathing high O2 concentrations for prolonged periods is not without potential adverse effects. Exposure to higher FIO2 (greater than 60%) for longer than 48 hours poses a risk for O2 toxicity. In this situation, oxygen free radicals from the high O2 levels cause inflammation and cell death, by disrupting the alveolar-capillary membrane. Absorption atelectasis is another risk. O2 has the ability to replace nitrogen and other gases normally present in the alveoli. Without nitrogen to help maintain size and shape of the alveolus, structural support is lost and the alveolus collapses. Other effects of prolonged exposure to high levels of O2 include increased pulmonary capillary permeability, decreased surfactant production, surfactant inactivation, and fibrotic changes in the alveoli.9 Another risk of O2 therapy is specific to patients with chronic hypercapnia (e.g., patient with COPD). Chronic hypercapnia blunts

the response of chemoreceptors to high CO2 levels as a respiratory stimulant. Initial O2 therapy may be provided to patients with chronic hypercapnia through a low-flow device, such as a nasal cannula at 1 to 2 L/min or a Venturi mask at 24% to 28%. The patient with COPD who does not respond to O2 therapy or other interventions may need mechanical ventilation with higher FIO2.

Mobilization of Secretions Retained pulmonary secretions may cause or worsen ARF. This occurs because the movement of O2 into the alveoli and removal of CO2 is severely limited or blocked. Secretions can be mobilized by proper positioning, effective coughing, chest physiotherapy, suctioning, humidification, hydration, and, when possible, early ambulation.

Patient Positioning Position the patient upright, either by elevating the head of the bed at least 30 degrees or by using a reclining chair or chair bed. This helps maximize respiratory expansion, decrease dyspnea, and mobilize secretions. A sitting position improves pulmonary function by promoting downward movement of the lungs. When lungs are upright, ventilation and perfusion are best in the lung bases. If there is a chance for aspiration, position the patient side-lying. Patients with one-sided lung disorders may be placed in a lateral or side-lying position. This position, called good lung down, allows for improved V/Q matching in the affected lung. Pulmonary blood flow and ventilation are better in dependent lung areas. This position allows secretions to drain out of the affected lung so they can be removed with suctioning. For example, place a patient with rightsided pneumonia on the left side. This will maximize ventilation and perfusion in the “good” lung and aid in secretion removal from the affected lung (postural drainage). Patients with ARF often have problems with both lungs. They may need repositioning at regular intervals on both sides to optimize air movement and drainage of secretions.

Effective Coughing When secretions are present, encourage the patient to cough. Unfortunately, not all patients will have enough strength or force to produce a cough that will clear the airway of secretions. Augmented coughing (quad coughing) may benefit some patients. To aid with augmented coughing, place 1 or both hands at the anterolateral base of the patient’s lungs (Fig. 67.6). As you observe deep inspiration end and expiration begin, move your hands forcefully upward. This increases abdominal pressure and helps the patient cough. It increases expiratory flow and promotes secretion clearance.

FIG. 67.6 Augmented coughing is performed by placing 1 or both hands on the anterolateral base of the lungs. After the patient takes a deep inspiration and at the beginning of expiration, move the hand(s)

forcefully upward. This increases abdominal pressure and helps produce a forceful cough. From American Association of Critical Care Nurses: AACN advanced critical care nursing, St Louis, 2009, Mosby.

Huff coughing is a series of coughs performed while saying the word “huff” (see Table 28.21).10 This technique prevents the glottis from closing during the cough. The patient takes a deep breath, holds the breath for 2 or 3 seconds, and then exhales. The huff cough is effective in clearing central airways. It may help move secretions upward. COPD patients generate higher flow rates with a huff cough than with a normal cough, and it is less tiring. The staged cough also helps clear secretions. To perform a staged cough, the patient assumes a sitting position, breathes in and out 3 or 4 times through the mouth, then coughs while bending forward and pressing a pillow inward against the diaphragm.

Chest Physiotherapy Chest physiotherapy is indicated for all patients who are producing sputum or have evidence of severe atelectasis or pulmonary infiltrates on chest x-ray. Postural drainage, percussion, and vibration to the affected lung segments help move secretions to the larger airways. Then, they can be removed by coughing or suctioning. Chest physiotherapy is discussed in Chapter 28. Contraindications include TBI and increased intracranial pressure (ICP), unstable orthopedic injuries (e.g., spinal fractures, fractured ribs, fractured sternum), and recent hemoptysis.11

Suctioning Suctioning may be needed if the patient is unable to expectorate secretions. Suctioning through an artificial airway (e.g., endotracheal tube [ET], tracheostomy) is done only as needed (see Chapters 26 and 65). Perform suctioning beyond the posterior oropharynx with caution, while monitoring the patient for complications. These include hypoxia, increased ICP, dysrhythmias, hypotension (from sudden elevation in intrathoracic pressure), hypertension and tachycardia

(from noxious stimulation), and bradycardia (possible vasovagal response).

Humidification Humidification is an adjunct in secretion management. We can thin secretions with aerosols of sterile normal saline or mucolytic drugs (e.g., acetylcysteine mixed with a bronchodilator) given by nebulizer. O2 given by aerosol mask can thin secretions and promote their removal. Aerosol therapy may cause bronchospasm and severe coughing, causing a decrease in PaO2. Frequent assessment of the patient’s tolerance to therapy is critical. Closely monitor the patient’s respiratory status.

Hydration Thick, viscous secretions are hard to expel. Unless contraindicated, adequate fluid intake (2 to 3 L/day) keeps secretions thin and easier to remove. The patient who is unable to take enough fluids orally needs IV hydration. Assess cardiac and renal status to determine whether the patient can tolerate the IV fluid volume and avoid HF and pulmonary edema. Regularly assess for signs of fluid overload (e.g., crackles, dyspnea, increased CVP).

Check Your Practice You are caring for a 72-yr-old male patient admitted with acute hypoxemic respiratory failure. He has a history of atrial flutter and COPD. A chest x-ray shows left-sided pneumonia. Your patient is awake but mildly confused. He has a productive cough (thick, yellow-green purulent sputum). • What respiratory interventions would you expect to be ordered?

Positive Pressure Ventilation

If initial measures do not improve oxygenation and ventilation, enhanced ventilatory assistance may be needed. Noninvasive positive pressure ventilation (NIPPV) is one option for patients with acute or chronic respiratory failure. During NIPPV, a mask is placed tightly over the patient’s nose or nose and mouth (Fig. 67.7). When the patient breathes spontaneously, a mechanical ventilator or table-top unit delivers PPV to the patient. With NIPPV, it is possible to provide O2 and decrease WOB, avoiding the need for endotracheal intubation. NIPPV is most useful in managing chronic respiratory failure in those with chest wall or neuromuscular problems. It may be used with patients with a chronic respiratory problem that is worse due to cardiac problems or infection. It is an option for patients who refuse intubation, but still want some degree of ventilatory support (e.g., patients with end-stage COPD). NIPPV is not appropriate for patients who have a decreased level of consciousness, high O2 requirements, facial trauma, hemodynamic instability, or excessive secretions. NIPPV used after extubation can help avoid reintubation. There are 2 forms of NIPPV used for patients with ARF. Continuous positive airway pressure (CPAP) delivers 1 level of pressure—a constant pressure—to the patient’s airway during inspiration and expiration. Bilevel positive airway pressure (BiPAP) uses 2 different levels of positive pressure (one on inspiration, another on expiration) (Fig. 67.8). With both CPAP and BiPAP, the patient must be awake and alert, have stable vital signs, and be able to support spontaneous ventilation. The most often used NIPPV for ARF is BiPAP.12 BiPAP provides O2 therapy and humidification, decreases WOB, and reduces respiratory muscle fatigue. It helps open collapsed airways and decrease shunt. If respiratory status worsens with NIPPV, PPV via mechanical ventilation and higher O2 concentrations is needed. Chapter 65 discusses mechanical ventilation.

Drug Therapy Drug therapy depends on several factors. These include the cause of

ARF, the patient’s preexisting medical condition, and whether infection is present. Goals of drug therapy include to (1) reduce airway inflammation and bronchospasm, (2) relieve pulmonary congestion; (3) treat infection; and (4) reduce anxiety, pain, and restlessness.

FIG. 67.7 Noninvasive bilevel positive airway pressure ventilation. A mask is placed over the nose or nose and mouth. Positive pressure from a mechanical ventilator aids the patient’s breathing efforts,

decreasing the work of breathing. Courtesy Richard Arbour, RN, MSN, CCRN, CNRN, CCNS, FAAN and Anna Kirk, RN, MSN.

FIG. 67.8 Stages of edema formation in ARDS. A, Normal alveolus and pulmonary capillary. B, Interstitial edema occurs with increased flow of fluid into the interstitial space. C, Alveolar edema occurs when the fluid crosses the alveolar-capillary membrane.

Reduce Airway Inflammation and Bronchospasm Corticosteroids (e.g., IV methylprednisolone [Solu-Medrol]) are often used in combination with other drugs, such as bronchodilators, for relief of inflammation and bronchospasm. It may take several hours to see their effects. Inhaled corticosteroids require 4 to 5 days for optimum therapeutic effects, so they will not relieve ARF.

Drug Alert IV Corticosteroids • Monitor potassium levels. Corticosteroids worsen hypokalemia caused by diuretics. • Prolonged use causes adrenal insufficiency. Relief of bronchospasm increases alveolar ventilation. In acute bronchospasm, short-acting bronchodilators (e.g., albuterol), may be given at 15- to 30-minute intervals until a response occurs. Give these drugs using a hand-held nebulizer or a metered-dose inhaler with a spacer. Side effects include tachycardia and hypertension. Prolonged use can increase the risk for dysrhythmias and cardiac ischemia. It is important to monitor the patient’s vital signs and ECG for any changes.

Relieve Pulmonary Congestion Interstitial fluid can accumulate in the lungs because of direct or indirect injury to the alveolar capillary membrane from HF or fluid overload. Use of IV diuretics (e.g., furosemide [Lasix]), morphine, or

nitroglycerin can decrease pulmonary congestion caused by HF. Use extreme caution when giving these drugs. Changes in heart rate and rhythm and significant decreases in BP are common. (Chapter 34 discusses HF.)

Treat Infection Lung infections (e.g., pneumonia, acute bronchitis) can result in excessive mucus production, fever, increased O2 consumption, and inflamed, fluid-filled, and/or collapsed alveoli. Alveoli that are fluid filled or collapsed cannot take part in gas exchange. Consequently, pulmonary infections can either cause or worsen ARF. IV antibiotics are often given to treat infection. Chest x-rays can show the location and extent of an infection. Sputum cultures help identify the organisms causing the infection and their sensitivity to antimicrobial drugs.

Reduce Anxiety, Pain, and Restlessness Anxiety, pain, and restlessness may result from hypoxia. They increase O2 consumption and CO2 production (from an increased metabolic rate) and increase WOB. For the nonintubated patient, this may cause tachypnea and ineffective ventilation. For the intubated patient, this may cause ventilator dyssynchrony and increase the risk for unplanned extubation. We promote patient comfort in several ways. Benzodiazepines (e.g., lorazepam, midazolam), and opioids (e.g., morphine, fentanyl) may decrease anxiety, restlessness, and pain. They are often given IV. For the nonintubated patient, they should be started at the lowest dose possible. Address treatable causes of restlessness (e.g., hypoxemia, pain, delirium). Often, restlessness and mental status changes are the first signs of hypoxemia or ventilator dyssynchrony. You should address the causes and not depend solely on the use of analgesics and sedatives.

Safety Alert Managing Restlessness and Sedation • Pain, hypoxemia, electrolyte imbalance, TBI, and drug reactions can cause restlessness. • Assess and aggressively treat all reversible causes of restlessness. • Monitor patients closely for CNS, cardiac, and respiratory depression when giving sedative and analgesic drugs, especially in the nonintubated patient. • Sedative and analgesic drugs may have a prolonged effect in critically ill patients. This can delay weaning from mechanical ventilation and increase length of stay.

Medical Supportive Therapy Goals and interventions targeted to improving the patient’s oxygenation and ventilation status are essential to improve O2 delivery. The primary goal is to treat the underlying cause of the ARF. Patients with V/Q mismatch, shunting, or diffusion limitation are managed differently, depending on the underlying cause. Patients are continuously monitored for their response to therapy, including changes in respiratory status, trends in ABGs, and signs of clinical improvement.

Nutritional Therapy Maintaining protein and energy stores is especially important in patients with ARF. The hypermetabolic state in critical illness increases the caloric requirements needed to maintain a stable body weight and muscle mass. Nutritional depletion causes a loss of muscle mass, including the respiratory muscles, which may delay recovery. The dietitian often determines the best method of feeding and optimal caloric and fluid requirements. Ideally, enteral or parenteral nutrition should be started within 24 to 48 hours (see Chapter 39).

Evaluation The expected outcomes are that the patient with ARF will • Independently maintain a patent airway • Achieve normal or baseline respiratory system function • Maintain adequate oxygenation as shown by normal or baseline ABGs • Have normal hemodynamic status

Gerontologic Considerations: Acute Respiratory Failure Many factors contribute to an increased risk for respiratory failure in older adults. The reduced ventilatory capacity that accompanies aging places the older adult at risk for ARF. Physiologic changes in the lungs include alveolar dilation, larger air spaces, and loss of surface area for gas exchange. Decreased elastic recoil within the airways, decreased chest wall compliance, and decreased respiratory muscle strength occur.13 In older adults, the PaO2 falls further and the PaCO2 rises to a higher level before the respiratory system is stimulated to change the rate and depth of breathing. This delayed response contributes to the development of respiratory insufficiency. A history of tobacco use is a major risk factor that can accelerate age-related respiratory changes. Poor nutritional status and less physiologic reserve in the cardiopulmonary system increases the risk for further compromising respiratory function and leading to ARF.

Acute Respiratory Distress Syndrome Acute respiratory distress syndrome (ARDS) is a sudden and progressive form of ARF in which the alveolar-capillary membrane becomes damaged and more permeable to intravascular fluid (Fig. 67.8). Next to septic shock, ARDS is one of the most common

conditions seen in the adult ICU. ARDS accounts for about 10% of all adult ICU admissions.14 The incidence of ARDS in the United States is estimated at more than 200,000 cases each year.14 Despite supportive therapy, the mortality rate from ARDS is around 50%.

Etiology Table 67.5 lists conditions that predispose patients to developing ARDS. The most common cause is sepsis. ARDS may also develop because of multiple organ dysfunction syndrome (MODS). Patients with multiple risk factors are 3 or 4 times more likely to develop ARDS. Either a direct or indirect lung injury causes ARDS. In direct lung injury, the pathogen comes into contact with the tissue of the lung. For example, aspiration of gastric contents into the lung will immediately initiate the inflammatory response. In an indirect injury, ARDS develops due to a problem somewhere else in the body. For example, necrotizing pancreatitis or bowel obstruction with perforation cause widespread inflammation and infection. As a result, septic mediators gain entrance to the bloodstream and often move toward the lungs, which provide a favorable, dark, moist environment for their proliferation. This is the beginning of acute lung injury.

TABLE 67.5 Predisposing Conditions to ARDS

Pathophysiology The pathophysiologic changes in ARDS are divided into 3 phases: (1) injury or exudative phase, (2) reparative or proliferative phase, and (3) fibrotic or fibroproliferative phase. The pathophysiology of ARDS is shown in Fig. 67.9.

Injury or Exudative Phase The injury or exudative phase usually occurs 24 to 72 hours after the initial insult (direct or indirect).15 It generally lasts up to 7 days. Engorgement of the peribronchial and perivascular interstitial space causes interstitial edema. Fluid in the parenchyma of the lung surrounding the alveoli crosses the alveolar membrane and enters the alveolar space. V/Q mismatch and intrapulmonary shunt develop because the alveoli fill with fluid. Blood in the capillary network cannot be oxygenated. The exact cause for the damage to the alveolar-capillary membrane is not known. Some think it is caused by stimulation of the inflammatory and immune systems. This stimulation attracts neutrophils to the pulmonary interstitium. The neutrophils release biochemical, humoral, and cellular mediators that produce changes in the lung. These changes include increased pulmonary capillary membrane permeability, destruction of collagen, formation of pulmonary microemboli, and pulmonary artery vasoconstriction. Hypoxemia and the stimulation of juxtacapillary receptors in the stiff lung parenchyma (J reflex) initially cause an increase in respiratory rate and a decrease in tidal volume (VT). This breathing pattern increases CO2 removal, producing respiratory alkalosis. CO increases in response to hypoxemia, a compensatory effort to increase pulmonary blood flow. However, as atelectasis, pulmonary edema, and pulmonary shunt increase, compensation fails and hypoventilation, decreased CO, and decreased tissue O2 perfusion occur.

FIG. 67.9 Pathophysiology of ARDS.

The changes caused by ARDS damage both alveolar type I cells and alveolar type II cells (which make surfactant). This damage, in addition to fluid and protein accumulation, results in surfactant dysfunction. The function of surfactant is to maintain alveolar stability and prevent alveolar collapse. When surfactant synthesis is decreased or surfactant becomes inactivated, alveoli become unstable and collapse (atelectasis). Widespread atelectasis further decreases lung compliance, compromises gas exchange, and contributes to hypoxemia. Necrotic cells, protein, and fibrin form hyaline membranes that line the inside of each alveolus. These thick hyaline membranes contribute to the development of fibrosis and atelectasis, leading to a further decrease in gas exchange capability and reduced lung compliance. Severe V/Q mismatch and shunting of pulmonary capillary blood result in hypoxemia unresponsive to increasing concentrations of O2.

This is the classic signs of ARDS, called refractory hypoxemia. In other words, despite receiving higher concentrations of O2, the patient’s condition does not improve but continues to get worse. Diffusion limitation, caused by hyaline membrane formation, contributes to and worsens hypoxemia. As the lungs become less compliant because of decreased surfactant, pulmonary edema, and atelectasis, the patient must generate higher airway pressures to inflate “stiff” lungs. Reduced lung compliance increases the patient’s WOB. At this point, the patient needs mechanical ventilation.

Reparative or Proliferative Phase The reparative or proliferative phase of ARDS begins 1 to 2 weeks after the initial lung injury.16 During this phase, there continues to be an influx of neutrophils, monocytes, lymphocytes, and fibroblasts as part of the inflammatory response. Increased pulmonary vascular resistance and pulmonary hypertension may occur because fibroblasts and inflammatory cells destroy the pulmonary vasculature. Lung compliance continues to decrease due to interstitial fibrosis. Hypoxemia worsens because of the thickened alveolar membrane. This causes V/Q mismatch, diffusion limitation, and shunting. Airway resistance is severely increased from fluid in the lungs and secretions in the airways. The proliferative phase is complete when the diseased lung is replaced by dense, fibrous tissue. If the reparative phase persists, widespread fibrosis results. If the reparative phase stops, the lesions will often resolve.

Fibrotic or Fibroproliferative Phase The fibrotic phase (chronic or late phase) of ARDS occurs 2 to 3 weeks after the initial lung injury. Not all patients who develop ARDS enter the fibrotic stage. For those who never fully recover from ARDS, the lung is completely remodeled by collagenous and fibrous tissues. Diffuse scarring of the lungs, interstitial fibrosis, and alveolar duct fibrosis result in decreased lung compliance.17 This reduces the surface area for gas exchange because the interstitium is fibrotic, and

hypoxemia continues. Varying degrees of pulmonary hypertension may result from pulmonary vascular destruction and fibrosis.

Clinical Progression Progression of ARDS varies among patients. Some survive the acute phase of lung injury. Pulmonary edema resolves, and complete recovery occurs within a week or so. The chance for survival is poorer in those who enter the fibrotic stage. Patients may need several weeks of long-term mechanical ventilation. It is not known why injured lungs repair and recover in some patients and in others ARDS progresses. Several factors are important in determining the course of ARDS. These include the nature of the initial injury, extent and severity of comorbidities, and pulmonary complications (e.g., pneumothorax). Genetics may account for a person’s predisposition to developing ARDS.18

Clinical Manifestations and Diagnostic Studies The initial presentation of ARDS is often subtle. At the time of the initial injury, and for 24 to 72 hours, the patient may not have respiratory symptoms or may have only mild dyspnea, tachypnea, cough, and restlessness. Lung auscultation may be normal or reveal fine, scattered crackles. ABGs may show mild hypoxemia and respiratory alkalosis caused by hyperventilation. The chest x-ray may be normal or reveal diffusely scattered, but minimal, interstitial infiltrates. As ARDS progresses, symptoms worsen because of fluid in the lung parenchyma and alveoli and increased secretion accumulation in the airways. Respiratory distress becomes evident as WOB increases. Tachypnea and intercostal and suprasternal retractions may be present. Tachycardia, diaphoresis, changes in mental status, cyanosis, and pallor may occur. Lung auscultation usually reveals scattered to diffuse crackles and coarse crackles on expiration. After 72 hours, the chest x-ray often shows diffuse and extensive bilateral interstitial and alveolar infiltrates (Fig. 67.10).

As ARDS progresses, ABGs reflect changes in oxygenation and ventilation. Refractory hypoxemia is the hallmark characteristic of ARDS. Hypercapnia often signifies that respiratory muscle fatigue and hypoventilation have severely affected gas exchange, and respiratory failure is imminent. To help evaluate the severity of hypoxemia in ARDS, we can calculate the PaO2/FIO2 (P/F) ratio . This measure reflects the ratio of the patient’s PaO2 to the FIO2 that the patient is receiving. Under normal circumstances (e.g., PaO2 80 to 100 mm Hg; FIO2 0.21 [room air]), the P/F ratio is greater than 400 (e.g., 95/0.21 = 452). With the onset and progression of lung injury and impairment in O2 delivery through the alveolar-capillary membrane, the PaO2 may remain lower than expected despite increased FIO2. The P/F ratio distinguishes among mild (