NMS Surgery [7 ed.] 2021027576, 9781975112882, 9781975112912, 2015010501

Table of contents :
Half Title
Title Page
Copyright Page
Dedication
Foreword
Preface
Contributors
Contents
Part I: Foundations
1 Principles of Surgical Physiology
Fluid and Electrolytes
Acid–Base Disturbances
Coagulation
Packed Red Blood Cell Transfusion Therapy
Nutrition and the Surgical Patient
The Intensive Care Unit
Shock
2 Preoperative Considerations
General Principles for Evaluation and Management of the Surgical Patient
Prevention of Cardiac Complications
Prevention of Perioperative Infection
Prevention of Bleeding Complications
Prevention of Thromboembolic Disease
Prevention of Pulmonary Complications
Prevention of Renal Complications
Prevention of Hepatic Complications
3 Postoperative Considerations
Drains and Tubes
Postoperative Complications
Review Questions for Part I
Answers and Explanations
Part II: Thoracic Disorders
4 Principles of Thoracic Surgery
General Principles of Thoracic Surgery
Chest Wall Disorders
Pleural and Pleural Space Disorders
Pulmonary Infections
Solitary Pulmonary Nodules (Coin Lesions)
Bronchogenic Carcinoma
Bronchial Adenomas
Metastatic Tumor
Tracheal Disorders
Mediastinal Lesions
5 Cardiac Disorders
Anatomy and General Principles
Aortic Valve Stenosis
Aortic Insufficiency
Mitral Stenosis
Mitral Insufficiency
Tricuspid Stenosis and Insufficiency
Pulmonic Valve Disease
Coronary Artery Disease
Cardiac Tumors
Pericardial Disorders
Patent Ductus Arteriosus
Atrial Septal Defects
Ventricular Septal Defects
Tetralogy of Fallot
Transposition of the Great Arteries
Review Questions for Part II
Answers and Explanations
Part III: Vascular Disorders
6 Arterial Disease
Limb Ischemia
Extracranial Cerebrovascular Disease
Aortic Dissection
Aneurysms
Mesenteric Ischemia
Renal Artery Stenosis
7 Venous and Lymphatic Disease
Anatomy and General Principles
Acute Deep Venous Thrombosis
Pulmonary Embolism
Chronic Venous Disorders: Varicose Veins and Chronic Venous Insufficiency
Superficial Venous Thrombophlebitis
Lymphedema
Review Questions for Part III
Answers and Explanations
Part IV: Gastrointestinal Disorders
8 Esophageal Disorders
Anatomy and Physiology
Esophageal Motility Disorders
Esophageal Strictures
Esophageal Tumors
Esophageal Perforation
Mallory–Weiss Syndrome
9 Stomach and Duodenal Disorders
Stomach
Benign Stomach Disease
Gastric Cancer
Postgastrectomy Syndromes
10 Liver, Gallbladder, and Biliary Tree Disorders
General Principles
Hemangioma
Hepatic Adenoma
Focal Nodular Hyperplasia
Hepatocellular Carcinoma
Cholangiocarcinoma
Metastatic Malignant Tumors
Pyogenic Liver Abscess
Amebic Liver Abscess
Hydatid Cysts
Portal Hypertension
Cholelithiasis (Gallstones)
Gallbladder Carcinoma
Choledocholithiasis
Cholangitis
Biliary Dyskinesia
Primary Sclerosing Cholangitis
Primary Biliary Cholangitis
Choledochal Cysts
11 Pancreatic Disease
Anatomy and Physiology
Acute Pancreatitis
Relapsing Pancreatitis
Chronic Pancreatitis
Pseudocyst
Pancreatic Malignancies
12 Spleen Disorders
General Principles
Pathology
Splenectomy
13 Small Intestine Disorders
Anatomy and Physiology
Small Bowel Obstruction
Tumors
Crohn Disease
Diverticular Disease
Short Gut Syndrome
14 Colon, Rectal, and Anal Disorders
Anatomy and Physiology
Patient Evaluation
Bowel Preparation
Benign and Malignant Colorectal Tumors
Diverticular Disease
Angiodysplasia
Inflammatory Bowel Disease
Anorectal Dysfunction
Obstructed Defecation (Pelvic Floor–Outlet Obstruction)
Benign Anorectal Disease
Perianal and Anal Canal Neoplasms
15 Hernia Disorders
General Principles
Inguinal Hernia
Ventral Hernia
Femoral Hernia
Obturator Hernia
Lumbar Hernia
Parastomal Hernia
Spigelian Hernia
Review Questions for Part IV
Answers and Explanations
Part V: Breast and Endocrine Disorders
16 Breast Disorders
General Principles
Breast Evaluation
Benign Breast Disease
Malignant Diseases
17 Thyroid, Parathyroid, and Adrenal Gland Disorders
Thyroid Gland
Thyroid Dysfunction Requiring Surgery
Parathyroid Glands
Adrenal Gland
Tumors of the Endocrine Pancreas
Multiple Endocrine Neoplasia
Review Questions for Part V
Answers and Explanations
Part VI: Special Subjects
18 Acute Abdominal Surgical Emergencies
Acute Abdomen
Obstruction
Hemorrhage
19 Trauma and Burns
Trauma
Specific Injuries
Burn Injury
20 Pediatric Surgery
General Principles
Congenital Pulmonary Malformations (CPAM)
Esophageal Atresia (EA) and Tracheoesophageal Fistula (TEF)
Congenital Diaphragmatic Hernia (CDH)
Congenital Abdominal Wall Defects
Infantile Hypertrophic Pyloric Stenosis
Biliary Atresia
Necrotizing Enterocolitis (NEC)
Intestinal Malrotation With or Without Midgut Volvulus
Intestinal Atresia
Hirschsprung Disease
Anorectal Malformation
Solid Tumors
21 Surgical Oncology
Cancer
Cancer Etiology and Epidemiology
Screening and Diagnosis
Diagnostic Procedures
Staging
Surgical Treatment
Multidisciplinary Treatment
Research and Training
22 Organ Transplantation
General Principles
Heart Transplantation
Pulmonary Transplantation
Hepatic Transplantation
Kidney Transplantation
Pancreatic Transplantation
Small Bowel and Multivisceral Transplantation
Composite Tissue Allograft and Vascularized Composite Allograft Transplants
23 Minimally Invasive Surgery and Robotics
General Principles
Selected Laparoscopic Procedures
Robotic Technology
24 Bariatric Surgery
General Principles
Surgical Treatment of Obesity
25 Head and Neck Surgery
Anatomy
Disease Processes
Head and Neck Cancer
Benign Parotid Neoplasms
Review Questions for Part VI
Answers and Explanations
Part VII: Surgical Subspecialties
26 Neurosurgery
General Principles
Evaluating the Neurosurgical Patient
Head Injury
Spinal Cord Injury
Neurovascular Disease
Central Nervous System Tumors
Functional Neurosurgery
Degenerative Spine Disease
Tumors of the Spine
Spinal Deformity
Peripheral Nerves
27 Plastic and Reconstructive Surgery
Chapter Cuts
General Principles
Reconstructive Plastic Surgery
Skin and Soft Tissue Reconstruction
Craniofacial Surgery
Hand Surgery
Aesthetic Plastic Surgery
Innovation in Plastic Surgery
28 Urologic Surgery
Urologic Emergencies
Urinary Tract Stones
Benign Prostatic Disorders
Genitourinary Malignancies
Erectile Dysfunction
Voiding Dysfunction
29 Orthopedic Surgery
Orthopedic General Principles
Orthopedic Emergencies
Orthopedic Urgencies
Arthritis
Infections
Tumors
Adult Orthopedics
Review Questions for Part VII
Answers and Explanations
Index

Citation preview

Surgery ' * SEVENTH EDITION

Bruce E. Jarrell Eric D. Strauch Stephen M _ Kavic

O.Wolters Kluwer

NMS

Surgery SEVENTH EDITION

NMS

Surgery SEVENTH EDITION Bruce E. Jarrell, MD President University of Maryland, Baltimore Baltimore, Maryland Eric D. Strauch, MD Associate Professor of Surgery Clerkship Director, Medical Student Rotation in Surgery University of Maryland School of Medicine Baltimore, Maryland Stephen M. Kavic, MD Professor of Surgery Program Director, Residency in Surgery University of Maryland School of Medicine Baltimore, Maryland

Acquisitions Editor: Matt Hauber Senior Development Editor: Stacey Sebring Marketing Manager: Michael McMahon Production Project Manager: Barton Dudlick Design Coordinator: Stephen Druding Editorial Coordinator: Michael Jeffrey Cohen Manufacturing Coordinator: Margie Orzech Prepress Vendor: Lumina Datamatics Seventh Edition Copyright ©2022 Wolters Kluwer Library of Congress Cataloging-in-Publication Data Names: Jarrell, Bruce E, editor. | Strauch, Eric D., editor. | Kavic, Stephen M. (Stephen Michael) editor. Title: NMS surgery / [edited by] Bruce E Jarrell, l, MD, President, University of Maryland, Baltimore, Baltimore, Maryland, Eric Strauch, M.D., Associate Professor of Surgery, Clerkship Director, Medical Student Rotation in Surgery, University of Maryland School of Medicine, Baltimore, Maryland, Stephen Kavic, MD, Professor of Surgery, Program Director, Residency in Surgery, University of Maryland School of Medicine, Baltimore, Maryland. Description: Seventh edition. | Philadelphia : Wolters Kluwer, [2021] | Series: National medical series for independent study | Includes bibliographical references and index. Identifiers: LCCN 2021027576 | ISBN 9781975112882 (hardback) | ISBN 9781975112912 (ebook) Subjects: LCSH: Surgery--Examinations, questions, etc. | Surgery--Outlines, syllabi, etc. | BISAC: MEDICAL / Education & Training Classification: LCC RD37.2 .N58 2021 | DDC 617.0076--dc23 LC record available at https://lccn.loc.gov/2021027576 I. Jarrell, Bruce E., editor. II. Strauch, Eric D., editor. III. Kavic, Stephen M. (Stephen Michael), editor. IV. Title: National medical series surgery. V. Series: National medical series for independent study. [DNLM: 1. Surgical Procedures, Operative—Examination Questions. 2. Surgical Procedures, Operative—Outlines. 3. General Surgery—methods—Examination Questions. 4. General Surgery—methods—Outlines. WO 18.2] RD37.2 617.0076—dc23 2015010501 This work is provided “as is,” and the publisher disclaims any and all warranties, express or implied, including any warranties as to accuracy, comprehensiveness, or currency of the content of this work. This work is no substitute for individual patient assessment based on healthcare professionals’ examination of each patient and consideration of, among other things, age, weight, gender, current or prior medical conditions, medication history, laboratory data, and other factors unique to the patient. The publisher does not provide medical advice or guidance, and this work is merely a reference tool. Healthcare professionals, and not the publisher, are solely responsible for the use of this work including all medical judgments and for any resulting diagnosis and treatments. Given continuous, rapid advances in medical science and health information, independent professional verification of medical diagnoses, indications, appropriate pharmaceutical selections and dosages, and treatment options should be made and healthcare professionals should consult a variety of sources. When prescribing medication, healthcare professionals are advised to consult the product information sheet (the manufacturer’s package insert) accompanying each drug to verify, among other things, conditions of use, warnings, and side effects and identify any changes in dosage schedule or contraindications, particularly if the medication to be administered is new, infrequently used, or has a narrow therapeutic range. To the maximum extent permitted under applicable law, no responsibility is assumed by the publisher for any injury and/or damage to persons or property, as a matter of products liability, negligence law or otherwise, or from any reference to or use by any person of this work. shop.LWW.com

We thank the many mentors who have advised us each throughout our careers. We are forever indebted to them. I wish to thank my wife, Leslie, and my wonderful children for all of their support during my career, and for their understanding during the writing of the many editions of NMS Surgery—BEJ. I wish to thank my wife, Cecilia, my fantastic children, Jacob, Julia, Jessica, and Jenna, and my parents for all of their love and support—ES. Dedicated to my loving wife, Jennifer, and to my lovely daughter, Emily—SMK.

Foreword It is a tremendous honor for me to introduce the seventh edition of NMS Surgery. I accepted the Chair of Surgery at the University of Maryland School of Medicine only recently, and I have been impressed with the depth and breadth of clinical and academic work in this Department. This book, written almost entirely by the Department’s residents and faculty, continues to play an essential and unique role in educating medical students and refreshing resident knowledge of surgical disease processes. The outline format of the chapters allows for easy access to gain understanding of the basic principles of surgery. This edition has special significance to me, as it is the first time I have been asked to write a foreword. During the past year, I have been fortunate to get to know the faculty and residents who have contributed chapters to this edition. We are fortunate to have our prior Chair of Surgery, Dr. Bruce E. Jarrell, assume the role of President of the University of Maryland, Baltimore. He has continued to lend his guidance and support to the Surgery Department and to this important work. Dr. Eric D. Strauch is our Surgery Clerkship Director for the University of Maryland medical students, and he has remained a fixture here at our institution. Dr. Stephen M. Kavic, as the Program Director at the University of Maryland, continues to spearhead the writing and editing of the chapters in this educational book. As you will see, the contributors of this edition offer unique insight into surgical diseases and practice guidelines. The chapters are presented in a concise way and supplemented with pearls and key takeaways. This easy-to-read-and-understand book can fit in your lab coat pocket, making it accessible during rounding. I am very thankful for the opportunity to lead such a talented group of surgeons at the University of Maryland. I am quite proud to be a part of NMS Surgery and am sure you will find the team has done an excellent job once again with this edition. —Christine Lau, MD, MBA Dr. Robert W. Buxton Professor and Chair Department of Surgery, University of Maryland School of Medicine Surgeon-in-Chief, University of Maryland Medical Center

Preface Welcome to the seventh edition of NMS Surgery. This book is written primarily for students and residents in general surgery. It is meant to serve as an introduction to the field of surgery, rather than a comprehensive review. In this edition, we have reorganized the overall structure. First and foremost, we reduced the size to fit in a lab coat pocket, so you can carry it with you for quick reference. Accordingly, we pared down some of the text to focus on the essential information. New features to this edition include “Trusted Sources,” which are links to noncommercial websites and other sources of up-to-date details and practice guidelines on relevant topics. We have also aimed to create more alignment with the NMS Surgery Casebook. This involved changing the order of the chapters from the previous edition and adding “Cut to Casebook” cross-references to make it easier to find the appropriate cases to complement the textbook. We have also revised the outline of each chapter to open with highlights, called “Chapter Cuts.” The key points are immediately followed by “Critical Surgical Associations,” which provide triggers for medical students to remember important connections in the surgical thought process. For the tremendous work put into this edition, we thank the individual contributors. Their high-quality and frequently punctual contributions have made our jobs as editors pleasant. We are also grateful to the editorial team at Wolters Kluwer for their guidance and support throughout the process. —Bruce E. Jarrell, MD —Eric D. Strauch, MD —Stephen M. Kavic, MD

Contributors Hossam Abdou, MD Resident in Surgery University of Maryland Medical Center Baltimore, Maryland Brittany Aicher, MD Resident in Surgery University of Maryland Medical Center Baltimore, Maryland H. Richard Alexander, MD Chief Surgical Officer Robert Wood Johnson Medical School Rutgers University New Brunswick, New Jersey Andrea Bafford, MD Assistant Professor of Surgery University of Maryland School of Medicine Baltimore, Maryland Emily Bellavance, MD Surgical Oncologist Virginia Cancer Institute Richmond, Virginia Megan Birkhold, MD Resident in Surgery University of Maryland Medical Center Baltimore, Maryland Hugo Bonatti, MD Surgeon Meritus Surgical Specialists Hagerstown, Maryland Cherif Boutros, MB, ChB

Associate Professor of Surgery University of Maryland School of Medicine Baltimore, Maryland Jonathan Bromberg, MD, PhD Professor of Surgery University of Maryland School of Medicine Baltimore, MD Brandon Bruns, MD Associate Professor of Surgery University of Maryland School of Medicine Baltimore, Maryland Laura S. Buchanan, MD Assistant Professor of Surgery University of Maryland School of Medicine Baltimore, Maryland Whitney Burrows, MD Assistant Professor of Surgery University of Maryland School of Medicine Baltimore, Maryland Clint D. Cappiello, MD Assistant Professor of Surgery Johns Hopkins University School of Medicine Baltimore, Maryland Ilaria Caturegli, MD Resident in Surgery Brigham and Women’s Hospital Boston, Massachusetts Ifeanyi Chinedozi, MD Resident in Surgery University of Maryland Medical Center Baltimore, Maryland Amanda M. Chipman, MD Resident in Surgery University of Maryland Medical Center Baltimore, Maryland Arielle Cimeno, MD Chief Resident in Surgery

University of Maryland Medical Center Baltimore, Maryland R. Gregory Conway, MD Resident in Surgery University of Maryland Medical Center Baltimore, Maryland Kenneth M. Crandall, MD Clinical Assistant Professor of Neurosurgery University of Maryland School of Medicine Baltimore, Maryland Helena Crowley, MD Assistant Professor of Surgery University of Maryland School of Medicine Baltimore, Maryland Peter Darwin, MD Professor of Medicine University of Maryland School of Medicine Baltimore, Maryland Jose J. Diaz, MD Chief, Division of Acute Care Surgery University of Maryland School of Medicine Baltimore, Maryland Laura DiChiacchio, MD, PhD Resident in Surgery University of Maryland Medical Center Baltimore, Maryland Meagan Dunne, MD Resident in Urology University of Maryland Medical Center Baltimore, Maryland Steven Feigenberg, MD Professor of Radiation Oncology University of Pennsylvania Philadelphia, Pennsylvania Jessica Felton, MD, MS Resident in Surgery University of Maryland Medical Center

Baltimore, Maryland Alison O. Flentje, MD Resident in Surgery University of Maryland Medical Center Baltimore, Maryland James S. Gammie, MD Chief, Division of Cardiac Surgery University of Maryland School of Medicine Baltimore, Maryland Bryce Haac, MD Resident in Surgery University of Maryland Medical Center Baltimore, Maryland R. Frank Henn III, MD Program Director, Residency in Orthopaedics University of Maryland School of Medicine Baltimore, Maryland Ajay Jain, MD Chief, Division of Surgical Oncology Oklahoma University College of Medicine Oklahoma City, Oklahoma Stephen M. Kavic, MD Program Director, Residency in Surgery Professor of Surgery University of Maryland School of Medicine Baltimore, Maryland Alexander J. Kish, MD Resident in Orthopaedic Surgery University of Maryland Medical Center Baltimore, Maryland Mark D. Kligman, MD Associate Professor of Surgery University of Maryland School of Medicine Baltimore, Maryland Andrew Kramer, MD, MBA Urologist Chesapeake Urology

Baltimore, Maryland Natalia S. Kubicki, MD Assistant Professor of Surgery University of Maryland School of Medicine Baltimore, Maryland Chris T. Laird, MD Chief Resident in Surgery University of Maryland Medical Center Baltimore, Maryland John C. LaMattina, MD Associate Professor of Surgery University of Maryland School of Medicine Baltimore, Maryland Shannon M. Larabee, MD Resident in Surgery University of Maryland Medical Center Baltimore, Maryland Megan Lerner, MD Resident in Urology Tulane University School of Medicine New Orleans, Louisiana Matthew Lissauer, MD Associate Professor of Surgery Robert Wood Johnson Medical School Rutgers University New Brunswick, New Jersey Kerri Lopez, MD Resident in Surgery University of Maryland Medical Center Baltimore, Maryland Kimberly Lumpkins, MD Assistant Professor of Surgery University of Maryland School of Medicine Baltimore, Maryland Olivia A. Martin, MD Resident in Surgery University of Maryland Medical Center

Baltimore, Maryland Marco Dal Molin, MD Resident in Surgery University of Maryland Medical Center Baltimore, Maryland Khanjan H. Nagarsheth, MD Assistant Professor of Surgery University of Maryland School of Medicine Baltimore, Maryland Ledibabari M. Ngaage, MB, BCh Postdoctoral Fellow in Plastic Surgery University of Maryland School of Medicine Baltimore, Maryland Silke V. Niederhaus, MD Clinical Assistant Professor of Surgery University of Maryland School of Medicine Baltimore, Maryland Suliat Nurudeen, MD Assistant Professor of Surgery University of Maryland School of Medicine Baltimore, Maryland John A. Olson, Jr., MD, PhD Chief, Division of General and Oncologic Surgery University of Maryland School of Medicine Baltimore, Maryland Natalie A. O’Neill, MD Chief Resident in Surgery University of Maryland Medical Center Baltimore, Maryland Christina Paluskievicz, MD Resident in Surgery University of Maryland Medical Center Baltimore, Maryland Jonathan P. Pearl, MD Associate Professor of Surgery University of Maryland School of Medicine Baltimore, Maryland

Yvonne M. Rasko, MD Associate Professor of Surgery University of Maryland School of Medicine Baltimore, Maryland Ace St. John, MD Resident in Surgery University of Maryland Medical Center Baltimore, Maryland Charles A. Sansur, MD Assistant Professor of Neurosurgery University of Maryland School of Medicine Baltimore, Maryland Rajabrata Sarkar, MD, PhD Chief, Division of Vascular Surgery University of Maryland School of Medicine Baltimore, Maryland Joseph R. Scalea, MD Assistant Professor of Surgery University of Maryland School of Medicine Baltimore, Maryland Thomas Scalea, MD Physician-in-Chief R. Adams Cowley Shock Trauma Center University of Maryland School of Medicine Baltimore, Maryland Christine Schad, MD Fellow in Colorectal Surgery Washington University in St. Louis St. Louis, Missouri Max Seaton, MD Fellow in Surgical Oncology University of Miami Miami, Florida Nicole Shockcor, MD Resident in Surgery University of Maryland Medical Center Baltimore, Maryland

Eric D. Strauch, MD Professor of Surgery University of Maryland School of Medicine Baltimore, Maryland Tara Talaie, MD Resident in Surgery University of Maryland Medical Center Baltimore, Maryland Julia Terhune, MD Assistant Professor of Surgery University of Maryland School of Medicine Baltimore, Maryland Douglas Turner, MD Associate Professor of Surgery University of Maryland School of Medicine Baltimore, Maryland A. Claire Watkins, MD Clinical Assistant Professor, Cardiothoracic Surgery Stanford University School of Medicine Stanford, California Richelle Williams, MD Assistant Professor of Surgery University of Maryland School of Medicine Baltimore, Maryland Jeffrey S. Wolf, MD Professor of Otolaryngology—Head and Neck Surgery University of Maryland School of Medicine Baltimore, Maryland

Contents Foreword Preface Contributors

Part I: Foundations 1 Principles of Surgical Physiology Ace St. John, Matthew Lissauer and Helena Crowley Fluid and Electrolytes Acid–Base Disturbances Coagulation Packed Red Blood Cell Transfusion Therapy Nutrition and the Surgical Patient The Intensive Care Unit Shock 2 Preoperative Considerations Silke V. Niederhaus General Principles for Evaluation and Management of the Surgical Patient Prevention of Cardiac Complications Prevention of Perioperative Infection Prevention of Bleeding Complications Prevention of Thromboembolic Disease Prevention of Pulmonary Complications Prevention of Renal Complications Prevention of Hepatic Complications 3 Postoperative Considerations Kerri Lopez and Kimberly Lumpkins Drains and Tubes Postoperative Complications Review Questions for Part I Answers and Explanations

Part II: Thoracic Disorders 4 Principles of Thoracic Surgery Tara Talaie, Laura DiChiacchio and Whitney Burrows General Principles of Thoracic Surgery Chest Wall Disorders Pleural and Pleural Space Disorders Pulmonary Infections Solitary Pulmonary Nodules (Coin Lesions) Bronchogenic Carcinoma Bronchial Adenomas Metastatic Tumor Tracheal Disorders Mediastinal Lesions 5 Cardiac Disorders Laura DiChiacchio, A. Claire Watkins and James S. Gammie Anatomy and General Principles Aortic Valve Stenosis Aortic Insufficiency Mitral Stenosis Mitral Insufficiency Tricuspid Stenosis and Insufficiency Pulmonic Valve Disease Coronary Artery Disease Cardiac Tumors Pericardial Disorders Patent Ductus Arteriosus Atrial Septal Defects Ventricular Septal Defects Tetralogy of Fallot Transposition of the Great Arteries Review Questions for Part II Answers and Explanations

Part III: Vascular Disorders 6 Arterial Disease Alison O. Flentje and Khanjan H. Nagarsheth Limb Ischemia Extracranial Cerebrovascular Disease

Aortic Dissection Aneurysms Mesenteric Ischemia Renal Artery Stenosis 7 Venous and Lymphatic Disease Brittany Aicher, R. Gregory Conway and Rajabrata Sarkar Anatomy and General Principles Acute Deep Venous Thrombosis Pulmonary Embolism Chronic Venous Disorders: Varicose Veins and Chronic Venous Insufficiency Superficial Venous Thrombophlebitis Lymphedema Review Questions for Part III Answers and Explanations

Part IV: Gastrointestinal Disorders 8 Esophageal Disorders Jonathan P. Pearl Anatomy and Physiology Esophageal Motility Disorders Esophageal Strictures Esophageal Tumors Esophageal Perforation Mallory–Weiss Syndrome 9 Stomach and Duodenal Disorders Natalie A. O’Neill and Cherif Boutros Stomach Benign Stomach Disease Gastric Cancer Postgastrectomy Syndromes 10 Liver, Gallbladder, and Biliary Tree Disorders Arielle Cimeno and John C. LaMattina General Principles Hemangioma Hepatic Adenoma Focal Nodular Hyperplasia Hepatocellular Carcinoma

Cholangiocarcinoma Metastatic Malignant Tumors Pyogenic Liver Abscess Amebic Liver Abscess Hydatid Cysts Portal Hypertension Cholelithiasis (Gallstones) Gallbladder Carcinoma Choledocholithiasis Cholangitis Biliary Dyskinesia Primary Sclerosing Cholangitis Primary Biliary Cholangitis Choledochal Cysts 11 Pancreatic Disease Richelle Williams, Peter Darwin and H. Richard Alexander Anatomy and Physiology Acute Pancreatitis Relapsing Pancreatitis Chronic Pancreatitis Pseudocyst Pancreatic Malignancies 12 Spleen Disorders Shannon M. Larabee, Ajay Jain and Stephen M. Kavic General Principles Pathology Splenectomy 13 Small Intestine Disorders Olivia A. Martin and Douglas Turner Anatomy and Physiology Small Bowel Obstruction Tumors Crohn Disease Diverticular Disease Short Gut Syndrome 14 Colon, Rectal, and Anal Disorders Jessica Felton, Ilaria Caturegli, Bryce Haac, Christine Schad and Andrea Bafford

Anatomy and Physiology Patient Evaluation Bowel Preparation Benign and Malignant Colorectal Tumors Diverticular Disease Angiodysplasia Inflammatory Bowel Disease Anorectal Dysfunction Obstructed Defecation (Pelvic Floor–Outlet Obstruction) Benign Anorectal Disease Perianal and Anal Canal Neoplasms 15 Hernia Disorders Hossam Abdou, Ifeanyi Chinedozi and Stephen M. Kavic General Principles Inguinal Hernia Ventral Hernia Femoral Hernia Obturator Hernia Lumbar Hernia Parastomal Hernia Spigelian Hernia Review Questions for Part IV Answers and Explanations

Part V: Breast and Endocrine Disorders 16 Breast Disorders Christina Paluskievicz, Steven Feigenberg and Emily Bellavance General Principles Breast Evaluation Benign Breast Disease Malignant Diseases 17 Thyroid, Parathyroid, and Adrenal Gland Disorders Shannon M. Larabee and John A. Olson, Jr Thyroid Gland Thyroid Dysfunction Requiring Surgery Parathyroid Glands Adrenal Gland Tumors of the Endocrine Pancreas

Multiple Endocrine Neoplasia Review Questions for Part V Answers and Explanations

Part VI: Special Subjects 18 Acute Abdominal Surgical Emergencies Megan Birkhold, Laura S. Buchanan and Jose J. Diaz Acute Abdomen Obstruction Hemorrhage 19 Trauma and Burns Amanda M. Chipman, Brandon Bruns and Thomas Scalea Trauma Specific Injuries Burn Injury 20 Pediatric Surgery Chris T. Laird, Clint D. Cappiello and Eric D. Strauch General Principles Congenital Pulmonary Malformations (CPAM) Esophageal Atresia (EA) and Tracheoesophageal Fistula (TEF) Congenital Diaphragmatic Hernia (CDH) Congenital Abdominal Wall Defects Infantile Hypertrophic Pyloric Stenosis Biliary Atresia Necrotizing Enterocolitis (NEC) Intestinal Malrotation With or Without Midgut Volvulus Intestinal Atresia Hirschsprung Disease Anorectal Malformation Solid Tumors 21 Surgical Oncology Marco Dal Molin, Julia Terhune and Suliat Nurudeen Cancer Cancer Etiology and Epidemiology Screening and Diagnosis Diagnostic Procedures Staging

Surgical Treatment Multidisciplinary Treatment Research and Training 22 Organ Transplantation Tara Talaie, Joseph R. Scalea, Max Seaton, Silke Niederhaus and Jonathan Bromberg General Principles Heart Transplantation Pulmonary Transplantation Hepatic Transplantation Kidney Transplantation Pancreatic Transplantation Small Bowel and Multivisceral Transplantation Composite Tissue Allograft and Vascularized Composite Allograft Transplants 23 Minimally Invasive Surgery and Robotics Hossam Abdou, Natalia S. Kubicki, Hugo Bonatti and Stephen M. Kavic General Principles Selected Laparoscopic Procedures Robotic Technology 24 Bariatric Surgery Nicole Shockcor and Mark D. Kligman General Principles Surgical Treatment of Obesity 25 Head and Neck Surgery Jeffrey S. Wolf Anatomy Disease Processes Head and Neck Cancer Benign Parotid Neoplasms Review Questions for Part VI Answers and Explanations

Part VII: Surgical Subspecialties 26 Neurosurgery Kenneth M. Crandall and Charles A. Sansur General Principles Evaluating the Neurosurgical Patient

Head Injury Spinal Cord Injury Neurovascular Disease Central Nervous System Tumors Functional Neurosurgery Degenerative Spine Disease Tumors of the Spine Spinal Deformity Peripheral Nerves 27 Plastic and Reconstructive Surgery Ledibabari M. Ngaage and Yvonne M. Rasko General Principles Reconstructive Plastic Surgery Skin and Soft Tissue Reconstruction Craniofacial Surgery Hand Surgery Aesthetic Plastic Surgery Innovation in Plastic Surgery 28 Urologic Surgery Megan Lerner, Meagan Dunne, Jessica Felton and Andrew Kramer Urologic Emergencies Urinary Tract Stones Benign Prostatic Disorders Genitourinary Malignancies Erectile Dysfunction Voiding Dysfunction 29 Orthopedic Surgery Alexander J. Kish and R. Frank Henn III Orthopedic General Principles Orthopedic Emergencies Orthopedic Urgencies Arthritis Infections Tumors Adult Orthopedics Review Questions for Part VII Answers and Explanations Index

Part I: Foundations Chapter 1

Principles of Surgical Physiology Ace St. John • Matthew Lissauer • Helena Crowley

Chapter Cuts No one formula best determines fluid and electrolyte management. High insensible losses occur during and after surgical procedures. Hyperkalemia is a common, life-threatening electrolyte disorder that leads to cardiac dysrhythmia. It is treated by shifting potassium into cells (insulin/glucose), stabilizing cardiac cells (calcium), and increasing potassium excretion (potassium binders). New anemia in a surgical patient is surgical bleeding until proven otherwise. Enteral nutrition is preferred for most patients. Adequate oxygenation is reflected in blood pressure, pulse, urine output (end-organ function), pH, and overall appearance. Patients with inadequate oxygenation or increased work of breathing should be intubated for mechanical ventilation. Shock is the state of physiologic decompensation resulting in oxygen demand outstripping oxygen supply, and inadequate tissue perfusion.

Critical Surgical Associations If You Hear/See

Think

Adequate urine output

½ mL/kg/hr, or 250 mL per 8 hr

Maintenance fluid

½ Normal saline + 20 mEq KCl

Maintenance rate

60 mL/hr + 1 mL/hr per kg over 20 kg

Potassium replacement

10 mEq of IV KCL raises serum concentration by 0.1 mEq/L

Prothrombin time

Reflects extrinsic pathway

Partial thromboplastin time

Reflects intrinsic pathway

Spontaneous bleeding

Platelet dysfunction or thrombocytopenia

Nutritional supplements

Use the gut first

Increased work of breathing

Intubate early

Shock

Inadequate oxygen delivery relative to demand

Septic shock

Norepinephrine

Nitroprusside

Cyanide toxicity

FLUID AND ELECTROLYTES Normal Body Composition I. Body water: Water accounts for 50%–70% of total body weight (Fig. 1-1) and is higher in young people, thin people, and men. A. Two-thirds rule: Total body water comprises about two thirds of body weight. B. Plasma volume: ~5% of body weight is plasma volume (e.g., 3.5 L of plasma for a 70 kg male). Plasma is ~60% of the blood volume if the hematocrit is 40% (e.g., 5.8 L of blood for a 70 kg

male). II. Electrolyte composition: Electrolyte concentrations differ between intracellular and extracellular compartments due to ion pumps, principally Na+/K+ ATPase (Table 1-1). Osmotic pressure changes between compartments causes water to redistribute. A. Intracellular compartment: The principle osmotic cation is potassium. The concentration of osmotic and oncotic (protein) particles is higher than the extracellular compartment, thus allowing water to flow into the cell creating turgidity. B. Extracellular compartment: The principle osmotic cation is sodium. Interstitial and plasma composition is nearly equal.

Water and Electrolyte Maintenance I. Water: Required amount depends on the person’s weight, age, gender, and health. A. Water calculation methods 1. Amount of body water excreted a. Most water lost from the body is through urine production. Generally, 0.5 mL/kg/hr is the minimum needed to excrete the daily solute load. b. The next highest daily water loss is from insensible losses (i.e., sweat, respiration, stool). This is estimated at 600–900 mL/24 hr.

Figure 1-1: Water compartments. Table 1-1: Electrolyte Composition by Water Compartment Electrolytes

Intracellular Compartment

Extracellular Compartment

Anions/Cations





Sodium (Na+)

10 mEq/L

142 mEq/L

Potassium (K+)

140 mEq/L

4 mEq/L

Chloride (Cl−)

4 mEq/L

103 mEq/L

Bicarbonate (HCO −) 3

10 mEq/L

28 mEq/L

Phosphate (PO 3−) 4

75 mEq/L

4 mEq/L

Sulfate (SO 2−) 4

2 mEq/L

1 mEq/L

Calcium (Ca++)

75%: low risk. 2. (b) VO2max 35%–75%: moderate risk. 3. (c) VO2max < 35%: high risk, consider sublobar resections or nonoperative treatments. c. PPO FELV1, DLCO < 30%: CPET to measure VO2max—Follow algorithm noted previously. II. Adjuvant therapy: Further treatment using radiotherapy and/or chemotherapy. A. Postoperative adjuvant chemotherapy: Now indicated in all resected non-small cell lung cancer patients stage Ib and higher. B. Preoperative chemotherapy and radiation: Can be given to select patients with IIIa (N2) disease to sterilize their mediastinal node disease.

Quick Cuts Lung cancer is the leading cause of cancer death and has a 5-year survival rate of 15%. A chronic, unrelenting cough is the most common symptom of lung cancer. Corona radiata sign, which is the spiculated appearance of a lesion from fine linear strands extending outward, is highly suspicious of a malignancy. The most common lung neoplasm is a metastatic deposit from another primary malignancy. Horner syndrome is ptosis, miosis, enophthalmos, and anhidrosis.

BRONCHIAL ADENOMAS Overview I. Characteristics: Carcinoid tumors comprise 85% of bronchial adenomas, occur mainly in the proximal bronchi (20% mainstem, 60% lobar or segmental, and 20% peripheral). A. Carcinoid tumors: Arise from basal bronchial stem cells, which, in the process of malignant transformation, differentiate in the direction of neuroendocrine tissue. B. Growth: Grow slowly and protrude, often causing some bronchial obstruction. C. Peptide production: Can produce many different types, most commonly serotonin, which can (rarely) lead to carcinoid syndrome if released into systemic circulation. II. Signs and symptoms: Cough, recurrent infection, hemoptysis, pain, and wheezing. Patient may report a long history of recurrent pneumonia or asthma. III. Diagnosis: Chest x-ray or CT may reveal a mass with or without associated atelectasis or pneumonia. A tissue sample via bronchoscopy or FNA can be performed. IV. Treatment: Surgical excision. A. Lobectomy: Most commonly performed procedure; pneumonectomy is rarely required.

B. Octreotide: Used in cases of carcinoid syndrome (unresectable disease). V. Prognosis: Should be > 85% 5-year survival for typical carcinoid tumors, decreasing to < 50%– 70% for the atypical variant. CUT TO CASEBOOK

See NMS Surgery Casebook, 3rd edition, Case 4.6: Hemoptysis and Atelectasis in a Young Patient.

Adenoid Cystic Carcinoma (Cylindroma) I. Characteristics: Comprises 5 years can be 25% of all patients with completely resected pulmonary metastases.

TRACHEAL DISORDERS

Anatomy I. Structure: Trachea is 50% is normal. 2. EF(%) = stroke volume (SV)/end diastolic volume (EDV) × 100 C. Cardiac catheterization: Gold standard for coronary anatomy. 1. Right heart catheterization is used to determine pulmonary artery pressure (PAP), CO, pulmonary capillary wedge pressure (PCWP), and the presence of left-to-right shunts. 2. Left heart catheterization includes coronary artery angiography and ventriculography. D. Pulmonary function studies: Patients with pulmonary disease. V. Cardiac arrest A. Causes: Include anoxia/hypoxemia, ischemia/coronary thrombosis/MI, and electrolyte disturbances. B. Immediate cardiopulmonary resuscitation (CPR):Remember the “ABCs”: 1. Airway: Endotracheal intubation; surgical airway. 2. Breathing: Ventilatory and oxygen support. 3. Circulation a. Cardiac massage: Closed cardiac compressions. b. Electrical defibrillation: If cardiac arrest is from ventricular fibrillation. c. Drug therapy: (1) Epinephrine: Inotrope, chronotrope, vasopressor. (2) Calcium: Optimizes inotropic effects. (3) Sodium bicarbonate: To treat associated acidosis. (4) Vasopressors as needed (5) Atropine: To reverse bradycardia. d. Blood volume VI. Extracorporeal circulation (cardiopulmonary bypass) (Fig. 5-1) A. Technique: Venous blood is passed through an oxygenator and a heat exchanger, and pumped back arterially. B. Myocardial protection: Hypothermia and cardioplegia are protective. 1. High potassium concentration: In cardioplegia allows arrest of heart, minimizes myocardial energy consumption.

2. Widespread total body inflammatory response. 3. Vasoactive substance release: Epinephrine, norepinephrine, histamine, and bradykinin 4. Sodium and free water retention: Causes diffuse edema VII. Prosthetic valves (Fig. 5-2): A. Tissue valves: Porcine or bovine tissues do not require long-term anticoagulation but have limited durability. Aortic tissue valves can be expected to last 15 years, and mitral valves last 10 years. B. Mechanical valves: Require lifetime anticoagulation therapy to prevent thrombosis/embolism but typically last for life. C. Risks: Stroke risk of 1%–2% per year; higher risk for mitral valve. Tissue and mechanical valves have a similar risk of endocarditis. D. Valve selection: Balance between the risk of long-term anticoagulation versus the risk of reoperation. E. Heart valve repair: Possible for most patients undergoing mitral valve surgery and is preferred for many patients (Table 5-1).

Figure 5-1: Extracorporeal membrane oxygenation (ECMO) setup.

Figure 5-2: Heart valves. (From Anatomical Chart Co.)

Table 5-1: Mitral Valve Repair versus Mitral Valve Replacement Factor

Repair

Replacement

Operative mortality

1%

6%

Anticoagulation

Not required

Mandatory for 3 months for tissue, life for mechanical

Reoperation

8–9 mmHg. E. Cardiac catheterization: Used to calculate the mitral valve cross-sectional area, the mitral valve end-diastolic pressure gradient, PAP, and any associated valvular or CAD. Medical treatment: Beta-blockers or calcium channel blockers, anticoagulation as needed for arrhythmias, and diuresis as needed for pulmonary edema. Surgical treatment A. Indications: Recommended for all patients with symptomatic stenosis. B. Operations 1. Commissurotomy: a. Opening of the fused commissures can be accomplished under direct vision during surgical mitral valve repair or percutaneously by balloon mitral valvuloplasty. b. Percutaneous mitral valve balloon valvotomy is acceptable when the degree of fibrosis/calcification is modest and mitral regurgitation (MR) is mild. 2. Mitral valve replacement: Required for severe disease of the chordae tendineae and papillary muscles. C. Complications

1. Valve thrombosis, endocarditis, paravalvular leaks 2. Valve degeneration VII. Prognosis: Greater than 80% 10-year durability. CUT TO CASEBOOK

See NMS Surgery Casebook, 3rd edition, Case 4.11: Mitral Valve Disease that Requires Surgery.

MITRAL INSUFFICIENCY I. Classification A. Acute MR: MI, endocarditis, chordal rupture. B. Chronic MR: Volume overload and left ventricle (LV) dilation. II. Etiology A. Degenerative (primary)mitral valve disease 1. Degenerative mitral valve disease: Characterized by leaflet thickening and chordal elongation or chordal rupture. 2. Mitral valve prolapse: Defined as leaflet excursion above the plane of the annulus. Present in 1%–2% of the population. 3. Insufficiency secondary to rheumatic fever: Pathogenesis is similar to that in mitral stenosis. B. Secondary (functional) mitral regurgitation: Ventricular dilation, alters valvular geometry; occurs with ischemic or idiopathic cardiomyopathy. Mitral leaflets normal but are tethered toward the apex there is insufficient leaflet apposition (coaptation). 1. Pathophysiologic changes: Increased left atrial pressure during systole, late-appearing pulmonary vascular changes and increased left ventricular SV. 2. Other changes: Infective endocarditis and rheumatic fever. III. History and clinical presentation A. History: May range from asymptomatic, to dyspnea, fatigue, and exercise intolerance. B. Clinical presentation: 1. Signs and symptoms: Dyspnea on exertion, fatigue, and palpitations. 2. Atrial fibrillation IV. Diagnosis A. Physical examination: Holosystolic blowing murmur at the apex that radiates to the axilla, with an accentuated apical impulse. B. Echocardiography: Quantitates the degree of mitral regurgitation and can demonstrate underlying anatomic abnormalities of the valve. C. Cardiac catheterization: Determines presence of CAD. V. Medical Treatment A. There is no effective medical treatment for MR. B. Treat arrhythmias and volume overload if present. VI. Surgical treatment A. Only severe regurgitation should be considered for surgery. B. Indications: Severe regurgitation with:

1. Signs and symptoms: New York Heart Association (NYHA) class II or above (Table 5-2). 2. Evidence of left ventricular dysfunction: EF less than 60%, ventricular dilation, atrial fibrillation, or pulmonary hypertension. C. Operations 1. Mitral valve repair: Quadrangular resection of the posterior leaflet or insertion artificial expanded PolyTetraFluoroEthylene (ePTFE) cords and annuloplasty ring (cloth-covered ring that stabilizes the size of the mitral valve annulus). 2. Mitral valve replacement VII. Prognosis: Mortality is 50% at 5 years for severe disease if untreated. Table 5-2: New York Heart Association Functional Classification of Heart Failure Class

Signs and Symptoms *

Class I

No symptoms

Class II

Mild symptoms during ordinary activity

Class III

Significant symptoms during any activity

Class IV

Symptoms even while at rest

*Symptoms are typically angina and dyspnea.

Quick Cuts There is no effective medical therapy for mitral regurgitation. The NYHA system is useful to classify signs and symptoms of heart failure.

TRICUSPID STENOSIS AND INSUFFICIENCY I. Classification A. AHA guidelines: Tricuspid valve area (TVA) 0.7 cm for severe tricuspid regurgitation (TR). II. Etiology A. Organic tricuspid stenosis: Always caused by rheumatic fever, most commonly associated with mitral valve disease. B. Functional tricuspid insufficiency: Result of right ventricular dilatation secondary to pulmonary hypertension and right ventricular failure, most commonly from mitral valve disease. C. Tricuspid insufficiency: Sometimes seen in carcinoid syndrome, lupus, or secondary to blunt trauma or to bacterial endocarditis. III. History and clinical presentation A. Pathology 1. Stenosis secondary to rheumatic fever. 2. Elevation of right atrial pressure: Leads to peripheral edema, jugular venous distention, hepatomegaly, and ascites. B. Clinical presentation

IV.

V. VI.

VII.

1. Isolated tricuspid insufficiency: Usually well tolerated. 2. Right-sided heart failure: When this occurs, symptoms (e.g., edema, hepatomegaly, and ascites) develop. Diagnosis A. Physical examination: Prominent jugular venous pulse may be observed. 1. Tricuspid insufficiency: Produces a systolic murmur at the lower end of the sternum; the liver may be pulsatile. 2. Tricuspid stenosis: Produces a diastolic murmur in the same region. B. Chest x-ray: Enlargement of the right side of the heart. C. Echocardiography: Estimates the amount of tricuspid valve pathology and should include an evaluation of any associated aortic or mitral valve lesions and right heart function. D. Cardiac catheterization: Most accurate for diagnosis of tricuspid disease. Medical treatment: In mild to moderate insufficiency associated with mitral valve disease, opinion varies concerning the need for surgery. Surgical treatment A. Indications 1. Extensive insufficiency associated with mitral valve disease: Valve repair or (rarely) valve replacement is appropriate. 2. Significant stenosis: Commissurotomy or valve replacement. B. Operations 1. Valve repair: Annuloplasty, ring, commissurotomy. 2. Valve replacement. C. Complications 1. Heart block, pacemaker dependence. 2. Thrombosis, infective endocarditis. Prognosis A. Traditionally high perioperative mortality for isolated tricuspid disease with arguable long-term benefit. B. Best prognosis in concomitant mitral and tricuspid repair.

PULMONIC VALVE DISEASE I. Classification: Grading of pulmonic stenosis: A. Peak velocity 4 m/s (severe). B. Peak gradient 64 mmHg (severe). II. Etiology A. The majority of pulmonic valve disorders are congenital. B. Carcinoid syndrome may produce pulmonic stenosis. III. History and clinical presentation A. Generally presents with shortness of breath, dyspnea on exertion. B. Can present with cyanosis, failure to thrive in infants. IV. Diagnosis A. Auscultation: Heart murmur. B. Echocardiography: Regurgitation or stenosis.

C. Cardiac catheterization V. Medical treatment: Medical management of pulmonary hypertension (pulmonary vasodilators, diuretics), especially with pulmonic regurgitation. VI. Surgical treatment A. Indications 1. Rare in the absence of congenital malformation. 2. Severe disease with tricuspid dysfunction or right heart failure. B. Operations 1. Balloon valvuloplasty. 2. Open valve replacement. C. Complications 1. Paravalvular leak. 2. Pulmonary artery rupture (during balloon valvuloplasty). 3. Valve thrombosis. VII. Prognosis A. Durability depends on indication and type of repair/replacement. B. With replacement in adults, durability of valve at 10 years is 90%

CORONARY ARTERY DISEASE I. Classification: Reduced blood flow to myocardium (heart muscle). TRUSTED SOURCE American Heart Association 2018 Prevention Guidelines Tool CV Risk Calculator. Available at: http://static.heart.org/riskcalc/app/index.html#!/baseline-risk II. Etiology A. Atherosclerosis: Predominant pathogenic mechanism. B. Risk factors: Hypertension, smoking, hypercholesterolemia, family history of heart disease, diabetes, and obesity. III. History and clinical presentation A. Clinical presentation: 1. Angina pectoris: Substernal chest pain lasting 5–10 minutes. Precipitated by stress or exertion, relieved by rest. a. Stable angina: Unchanged for a prolonged period. b. Unstable angina: Shows a change from a previous pattern. c. Other: Angina at rest and postinfarction angina. 2. MI: Ischemic ECG changes and troponin elevation. 3. Other: CHF or sudden death. 4. Hibernating myocardium: Dysfunctional muscle that improves with revascularization. 5. Stunned myocardium: Temporary dysfunction following revascularization. IV. Diagnosis: A. History: Diagnosis is most often made by patient history. B. Cardiac catheterization: Location and size of coronary lesions can be both diagnosed and

treated. Left ventricular function may be assessed. C. ECG: Normal in up to 75% of patients when they are at rest without pain. ST-segment changes and T-wave changes may be seen, and evidence of a previous infarction may be apparent. D. Exercise stress testing: Evaluates inducible ischemia, ventricular dysfunction, and associated ECG changes. E. Radio thallium scan: Delineates ischemic areas of myocardium. V. Medical treatment: Focuses on control of risk factors. A. Drugs: Aspirin, beta-blockers, statins, aldosterone blockade, and antihypertensives. B. Additional therapy: Low-fat diet, smoking cessation, and a graded exercise program. C. Interventions: 1. Balloon angioplasty: Relieves obstruction, but stenosis often recurs. 2. Coronary stenting: Stent may be “bare metal” or coated with a drug (e.g., sirolimus) that elutes to prevent restenosis. VI. Surgical treatment A. Indications: Left main disease >50% stenosis, proximal left anterior descending (LAD) or circumflex disease >70% stenosis, triple-vessel disease, angina refractory to medical management, or failed percutaneous coronary intervention. B. Operations: 1. Coronary artery bypass surgery (CABG): Construction of bypass grafts to downstream segments of the affected coronary arteries to re-establish normal blood flow to the myocardium (Fig. 5-3). 2. Common grafts: Left internal mammary artery to LAD coronary artery, reversed saphenous vein grafts from the ascending aorta to the target vessel, and radial artery or right internal mammary artery grafts. C. Complications: 1. Mechanical complications of MI are increasingly rare. 2. Ventricular aneurysms: Myocardium remodels following infarction and can thin or become aneurysmal. 3. Ruptured ventricle: Rare; the untreated mortality rate is 100%. 4. Rupture of the interventricular septum (VSD): Mortality rate of 50% without immediate operation.

Figure 5-3: Coronary artery bypass surgery. (Panel A from Nath JL. Using Medical Terminology, 2nd ed. Wolters Kluwer; 2012. Panel B from Porrett PM, Drebin JA, Pavan A, Karakousis GC, Roses RE. The Surgical Review, 4th ed. Wolters Kluwer; 2015).

5. Intra-aortic balloon pump can help with infarct-related VSD or papillary muscle rupture until surgery. 6. Papillary muscle dysfunction or rupture: Posterior papillary muscle is usually involved. VII. Prognosis A. CABG is highly successful at relieving angina pectoris. B. CABG 10-year patency rates: Internal mammary artery more than 90%, saphenous vein ~50%. C. Overall mortality is 2%–3%; risk is increased in patients with renal failure, urgency of operation, pulmonary disease, peripheral vascular disease, and history of stroke or diabetes.

Quick Cuts Coronary artery disease is common and diagnosed by history of angina. Coronary stenting is first line treatment for many lesions. Coronary artery bypass grafting is highly successful, and the most successful conduit is the internal mammary artery. CUT TO CASEBOOK

See NMS Surgery Casebook, 3rd edition, Case 4.10:

Progressively Increasing Substernal Chest Pain.

CARDIAC TUMORS I. Classification: A. Benign B. Malignant C. Metastatic (non-cardiac primary) II. Etiology A. Benign tumors: Myxomas are the most common benign cardiac tumors. Others include rhabdomyosarcomas, papillary elastofibromas, lipomas. B. Malignant tumors: Overall, account for 20%–25% of all primary cardiac tumors. Sarcomas and angiosarcomas are the most common. C. Metastatic tumors: Occur more frequently than primary cardiac tumors. 1. Autopsy studies: Show cardiac involvement by metastatic disease in ~10% of cancer deaths. 2. Types: Renal cell carcinoma, neuroblastoma, melanoma, lymphoma, and leukemia often metastasize to the heart. III. History and clinical presentation A. Myxomas typically result in embolization. B. Additional presentations include CHF, pericardial effusion and tamponade, and arrhythmia. IV. Diagnosis A. Primary by echocardiography B. Cross-sectional imaging and cardiac catheterization can provide additional details V. Medical treatment: Treatment is surgical excision VI. Surgical treatment A. Indications: All cardiac tumors, malignant or benign, should undergo resection. B. Operations: Most common approach is left atriotomy or trans-septal atrial incision through median sternotomy approach. C. Complications 1. Recurrence: Generally due to inadequate resection or seeding during excision. 2. Valvular dysfunction following resection VII. Prognosis: Malignant tumors originating from the heart carry a very poor prognosis.

PERICARDIAL DISORDERS I. Classification A. Pericardial effusion B. Acute or chronic pericardititis C. Chronic constrictive pericarditis II. Etiology A. Pericardial effusion: Pericardium responds to noxious stimuli by increasing fluid production; volume as small as 100 mL may produce symptomatic tamponade if the fluid accumulates rapidly. B. Acute pericarditis: Infection, uremia, traumatic hemopericardium, malignant disease, and

III.

IV.

V.

VI.

VII.

connective tissue disorders. C. Chronic pericarditis: Etiology is often impossible to establish. Often unnoticed until it results in the chronic constrictive form. History and clinical presentation A. Pericardial effusion may be asymptomatic. B. Dressler syndrome is pericarditis up to 2 weeks following an acute MI. C. Pericarditis classically presents with chest pain. Diagnosis A. ECG changes: Pericarditis associated with ST elevations in all leads. B. Pericardium may become calcified, which is evident on chest x-ray. C. Cardiac catheterization may be needed for confirmation. Medical treatment A. Treatment of Dressler syndrome is nonsteroidal anti-inflammatory drugs. B. Management of the underlying cause. Surgical treatment A. Pericardial effusions are typically drained via a subxyphoid approach. B. Chronic effusions may require pericardiectomy. C. Pericardiectomy is considered for constrictive pericarditis. Prognosis: Following treatment, there are generally no negative sequelae.

PATENT DUCTUS ARTERIOSUS I. Classification: Small, moderate, or large degree of left (systemic circulation) to right (pulmonary circulation) shunting. II. Etiology A. Pathophysiology: Hypoxia and prostaglandins E1 (PGE1) and E2 (PGE2) act to keep the ductus open in utero. B. Most preterm infants weighing less than 1.5 kg will have a PDA. III. History and clinical presentation A. Common complaints: Dyspnea, fatigue, and palpitations, signifying CHF and/or pulmonary hypertension. B. Associated with other defects: VSD and coarctation of the aorta. IV. Diagnosis A. Based primarily on the physical findings and echocardiogram. B. Physical examination: Classic continuous “machinery-like” murmur may be absent until age 1 year. C. Pulses: Widened pulse pressure and bounding peripheral pulses. D. Cyanosis: Right-to-left shunt from pulmonary vascular disease. V. Medical treatment: Prostaglandin inhibitors such as indomethacin or ibuprofen can achieve closure in premature infants with symptomatic simple PDA. VI. Surgical treatment A. Indications: Reserved for premature infants with severe pulmonary dysfunction or CHF within the first year of life, and asymptomatic children with a patent ductus that persists until age 2–3 years.

B. Operations: Open ligation, or percutaneous closure via catheterization. C. Complications: Rare, generally well tolerated. VII. Prognosis: Overall prognosis depends on concomitant malformations.

ATRIAL SEPTAL DEFECTS I. Classification A. Ostium secundum defect: Most common ASD, found in the midportion of the atrial septum. B. Patent foramen ovale is not considered an ASD. The septa primum and secundum fail to fuse, which occurs in 30% of normal hearts. C. Sinus venosus defect: Located high up on the atrial septum, often associated with anomalies of pulmonary venous drainage. D. Ostium primum defects: Components of atrioventricular septal defects, located on the atrial side of the mitral and tricuspid valves. E. Eisenmenger syndrome: Is a sequence of events consisting of the following: 1. Congenital left to right shunt (from ASD or PDA). 2. Subsequent pulmonary hypertension. 3. This increased pressure reverses the shunt. 4. Cyanotic symptoms develop. II. Etiology: Most are sporadic and isolated.

Figure 5-4: Atrial septal defect. Blood is shunted from the left atrium to the right atrium. This hole is usually the area of the foramen ovale, which normally closes at birth. (From Rosdahl CB, Kowalski MT. Textbook of Basic Nursing, 10th ed. Philadelphia: Lippincott Williams & Wilkins; 2011, Figure 72-9B).

III. History and clinical presentation A. Infancy and early childhood: Mild dyspnea and easy fatigability. B. Children: Reduced exercise tolerance and recurrent respiratory infections. C. Adults: Atrial fibrillation and CHF. D. Other: Patients may present with neurologic symptoms (cerebrovascular accident or transient ischemic attack) or Eisenmenger syndrome. IV. Diagnosis A. Physical examination: Systolic murmur in the left second or third intercostal space and a fixed,

split, second heart sound. B. Chest x-ray: Moderate enlargement of the right ventricle and prominence of the pulmonary vasculature. C. ECG: Right ventricular hypertrophy. D. Echocardiography: Defines the ASD and notes the direction of shunting. E. Cardiac catheterization: Left-to-right shunt may be calculated. V. Medical Treatment: Based on the size of the left-to-right shunt; some close spontaneously. VI. Surgical treatment A. Indications for ASD closure: Pulmonary blood flow is more than 1.5 times greater than the systemic blood flow, neurologic events, heart failure, arrhythmia, or right ventricular volume overload. B. Approach: Closure may be attempted percutaneously. C. Complications: Surgery carries a mortality risk of less than 1%; ideal timing is age 4–5 years. VII. Prognosis: Good for isolated ASD repair. TRUSTED SOURCE Centers for Disease Control and Prevention. What are Congenital Heart Defects? Available at https://www.cdc.gov/ncbddd/heartdefects/facts.html

VENTRICULAR SEPTAL DEFECTS I. Classification: Figure 5-5. A. Membranous defect: Most common ventricular, 70%–80%. B. Muscular defects: May be single or multiple, 10%–15%. C. Inlet defect: Atrioventricular canal type, endocardial cushion defect, 5% of isolated defects. D. Outlet defects: 5%–10% (also called supracristal or conoseptal defects). II. Etiology: Single most common congenital lesion. III. History and clinical presentation A. Children with large defects usually have dyspnea on exertion, easy fatigability, and an increased incidence of pulmonary infections. B. Other adverse effects: Poor feeding, failure to thrive, frequent respiratory tract infections, and increased pulmonary vascular resistance. C. Fifty percent of VSDs are associated with PDA, aortic coarctation, or tetralogy of Fallot.

Figure 5-5: Ventricular septal defects. Some oxygen-rich blood from the left ventricle flows through the defect and recirculates through the lungs. (From Rosdahl CB, Kowalski MT. Textbook of Basic Nursing, 10th ed. Philadelphia: Lippincott Williams & Wilkins; 2011, Figure 72-9A).

IV. Diagnosis A. Physical examination: Harsh pansystolic murmur. B. Chest x-ray and ECG: May show evidence of biventricular hypertrophy.

C. Cardiac catheterization: Determines the severity of the left-to-right shunt, pulmonary vascular resistance, and the location. V. Medical treatment: Treatment is surgical closure. VI. Surgical treatment A. Indications: Symptomatic VSDs; asymptomatic children who have not had spontaneous closure by age 2 years, or pulmonary blood flow greater than 1.5 times systemic blood flow. B. A contraindication to repair of an ASD or VSD is fixed, irreversible pulmonary hypertension. C. Operations 1. Generally performed via open, median sternotomy approach. 2. If defect 5.5 cm in men and >5 cm in women, and there are good endovascular options.

Critical Surgical Associations If You Hear/See

Think

Aortic dissection, ascending aorta

Surgery

Aortic dissection, descending aorta

Blood pressure control

TIA and carotid lesion

Carotid endarterectomy

AAA > 5.5 cm

Repair

AAA and abdominal pain

Rupture, emergent repair

Aortic graft, fever

Graft infection

Aortic graft, GI bleed

Aortoenteric fistula

Extremity rest pain, tissue loss

Urgent revascularization

Popliteal aneurysm

Limb threatening (thrombosis)

Food fear, pain out of proportion

Mesenteric ischemia

Pain on passive range of motion

Compartment syndrome

AAA, abdominal aortic aneurysm; GI, gastrointestinal; TIA, transient ischemic attack.

LIMB ISCHEMIA Anatomy I. Anatomic extent and location: Occlusive disease is most frequently seen in the superficial femoral artery (SFA). II. The most common location for femoral occlusive disease is in the distal SFA at the level of Hunter canal (Fig. 6-1).

Acute Ischemia

I. Etiology A. Acute thrombosis: Most common cause of acute arterial insufficiency. B. Embolism 1. Cardiac origin: Mural thrombus in patients with atrial fibrillation, ventricular thrombus after myocardial infarction (MI), rheumatic valvular abnormalities, vegetations. 2. Noncardiac embolic sources: Atherosclerotic or aneurysmal, thoracic outlet syndrome, iatrogenic. C. Dissection D. Arterial trauma II. History and clinical presentation A. Signs and symptoms: Of acute arterial insufficiency includes the following: 1. The 6 P’s: Pain, pallor, paresthesia, paralysis, pulselessness, and poikilothermia. 2. If present with worsening pain at rest or wounds, ask about prior history of pain with ambulation. III. Diagnosis A. Physical exam: Comparison with the contralateral extremity motor and sensory deficits. As above, look for the “6 P’s”, including diminished pulse and cold extremity. B. Ankle-brachial index 1. Perform quickly at bedside with Doppler and blood pressure cuff. 2. Procedure: Measure blood pressure in both arms and ankle; take best pressure value for pedal signal and brachial signal.

Figure 6-1: The arterial tree of the lower extremity.

3. Calculation: Divide systolic ankle pressure by highest of the two brachial pressures (Table 61). 4. Significance a. An ankle-brachial index (ABI) of approximately 1 is normal. b. Values >1 indicate calcified vessels. c. Values 70% stenosis with CEA and best medical management compared with medical management alone. D. CEA: Involves removal of atherosclerotic plaque from within the distal common, and proximal internal, and external carotid arteries. 1. Indication: Symptomatic patients with >50% stenosis. 2. Complications: Stroke, TIA, bleeding, cranial nerve injury. E. Carotid angioplasty and stent 1. Indications: Surgically inaccessible lesion (skull base), previous carotid surgery (restenosis), irradiated neck, and severe comorbid cardiopulmonary conditions that preclude open carotid repair. 2. Complications: Stroke, TIA, carotid dissection, bleeding. VI. Prognosis: Surgical morbidity is low. Quick Cuts CT scans may be falsely negative in early stroke; MRI may be more sensitive. CEA reduces the risk of stroke over medical management alone.

AORTIC DISSECTION I. Pathophysiology/etiology A. Tear in the intima resulting in blood to flow in between the layers of aortic wall rather than inside the lumen. B. True and false lumens are created with formation of intimal flap; true indicates continuity with aortic root. C. Patient risk factors include hypertension, aneurysmal disease, and Marfan syndrome. II. Classification A. Timing 1. Acute: Within 2 weeks from the onset of symptoms. a. Complicated: Rupture, impending rupture, or evidence of end-organ ischemia and is a surgical emergency. b. Uncomplicated: No evidence of ischemia or rupture. Medical management and tight blood pressure control. 2. Subacute: Diagnosis more than 2 weeks after symptom onset.

3. Chronic: Diagnosis more than 2 months after symptom onset.

Figure 6-3: DeBakey and Stanford classification systems for aortic dissection.

B. Anatomy (Fig. 6-3). 1. DeBakey classification: Based on location of tear and extent of involvement of aorta with dissection. a. DeBakey type I: Involves the entire aorta from the root down and is a surgical emergency. b. DeBakey type II: Involves the ascending aorta and is a surgical emergency. c. DeBakey type III: Starts distal to the subclavian artery. Treatment is dictated by occurrence of complications. 2. Stanford: Based on location of entry tear only. a. Stanford type A: Entry tear located in ascending aorta and is a surgical emergency. b. Stanford type B: Entry tear located distal to origin of left subclavian artery; medical management.

III. History and clinical presentation A. Significant HTN is typical. B. Pain: Severe, “tearing” chest, back, or abdominal pain. 1. Patients usually describe “worst ever” pain. 2. Misdiagnosis is common, as other causes (MI, pulmonary embolism) are usually ruled out first. C. End-organ hypoperfusion: May cause symptoms when the dissection compromises blood flow through branch vessels. 1. Lactate level to assess for ischemia. 2. Basic metabolic profile (BMP) to assess for renal failure. IV. Diagnosis: CTA of chest abdomen and pelvis is gold-standard diagnostic modality of choice. V. Medical management A. Uncomplicated type B: Strict blood pressure control with IV medications (goal: mean blood pressure = 60–70 mmHg). 1. First-line IV beta-blockers (e.g., esmolol). 2. Add vasodilator IV sodium nitroprusside as needed. VI. Surgical management A. Type A dissection: Urgent open prosthetic graft replacement. B. Complicated type B aortic dissection: Thoracic endovascular aortic repair (TEVAR) or operative restoration of flow to malperfused organ or limb. C. Aneurysmal dilation: Is an important late complication of dissection. VII. Prognosis A. Type A: If left untreated, mortality is 1% per hour with a 90% 30-day mortality. Surgical mortality is 10%–20%. B. Type B: 25% 3-year mortality

Quick Cuts Thoracic aortic aneurysms tend to dissect; AAA do not. Ascending aortic dissections require emergent surgical repair; descending dissections are treated medically with blood pressure control.

ANEURYSMS Aortic Aneurysms I. Pathophysiology: Permanent localized dilation of an artery. Arterial dilation >1.5 times the normal vessel diameter. Associated with hypertension and atherosclerosis. II. Classification: Thoracic or abdominal (infrarenal vs. pararenal). III. History and clinical presentation A. Asymptomatic: Most aneurysms are diagnosed incidentally on physical examination. B. Symptomatic 1. May have symptoms from compression, such as early satiety, hydronephrosis, and/or venous

thrombosis. 2. May have pain on palpation. C. Impending rupture or ruptured aneurysms: Present with severe abdominal/back pain, tender pulsatile abdominal mass, and possible signs of shock. D. Risk factors for rupture: Advanced age, male gender, smoking, family history, and size (Table 6-2). E. Complications: Rupture, embolization to lower extremities (blue toe syndrome), dissection, and fistulization to adjacent structures. Table 6-2: Abdominal Aortic Aneurysm Rupture Risk AAA Diameter (cm)

Rupture Risk (%/year)

8

30–50

AAA, abdominal aortic aneurysm. IV. Diagnosis A. Screening: Family history of aneurysm or males aged 65–75 years who are cigarette smokers. B. Abdominal x-ray: “egg shell sign”, calcification of the aneurysm wall. C. Abdominal ultrasound: Valuable noninvasive tool for diagnosis, screening, and monitoring AAA. D. Abdominal CT scan with contrast: Gold-standard diagnostic test; it accurately identifies the presence, size, and extent of aneurysm. CUT TO CASEBOOK

See NMS Surgery Casebook, 3rd edition, Case 5.10: Pulsatile Mass in the Abdomen. V. Surgical treatment A. Indications for repair: Any symptomatic AAA, AAA with size ≥5.5 cm (in female patients and those with Marfan syndrome, the size cutoff is 5 cm), and rapidly expanding aneurysm. B. Types of surgical repair: 1. Endovascular repair: Performed via common femoral artery access. a. Specific anatomic criteria (1) Aortic neck: Length (>10–15 mm), diameter that provides appropriate proximal sealing zone, and angle 2 cm, and any size in women of childbearing age. 2. Endovascular treatment: Coil embolization or stenting. 3. Open surgical repair: Proximal and distal ligation of splenic artery with or without aneurysmectomy; for aneurysms located in distal splenic artery, splenectomy is performed. III. Popliteal artery aneurysms A. Risk factors: Male gender. B. Clinical presentation: 1. Asymptomatic: Palpable pulsatile mass behind knee. 2. Symptomatic: Can cause distal embolization, compress nearby structures, or acutely thrombose, resulting in acute lower leg ischemia. C. Surgical treatment 1. Indications for repair: Symptomatic aneurysm of any size; asymptomatic aneurysm >2.5 cm in diameter. 2. Anticoagulation: Patients with acute limb ischemia require therapeutic anticoagulation and emergent arteriography. 3. Open repair: Ligation of aneurysm and arterial bypass or excision of aneurysm and interposition graft. 4. Endovascular repair: For patients who are high operative risk. 5. Thrombolysis: Consider in stable patient with intact function but must be followed by staged, definitive repair.

Quick Cuts Endovascular repair has lower perioperative mortality compared with open AAA repair. Bloody diarrhea after AAA repair is ischemic colitis until proven otherwise. The rate of splenic artery aneurysm rupture is >90% with pregnancy.

MESENTERIC ISCHEMIA Acute Mesenteric Ischemia I. Pathophysiology

II. III.

IV.

V.

A. Interruption of main blood supply: Occlusion of celiac axis, superior mesenteric artery (SMA), or IMA from thrombus, embolus, atherosclerosis, hyperplasia, or external constriction. B. Interruption of collateral circulation: Pancreaticoduodenal between celiac and SMA or marginal artery between IMA and SMA. C. Impaired flow through collateral arcades: The marginal artery of Drummond and the arc of Riolan are the collateral arcades between the SMA and the IMA; may be compromised by low flow states. Epidemiology: Patients tend to be older adults with significant comorbidities. Classification: Based on etiology. A. Cardiac source (atrial fibrillation): Most common cause of embolic occlusion of mesenteric vessels. 1. The emboli usually lodge distal to the origin of proximal jejunal branches and middle colic artery, which spares the proximal jejunum and ascending colon. 2. The SMA is the most common abdominal artery affected from embolus due to its oblique origin from the aorta. B. Acute thrombosis: In 20% of cases, preexisting severe atherosclerotic stenotic lesion thrombosis is seen. The entire small and large bowel supplied by SMA is affected. C. Nonocclusive mesenteric ischemia: Due to vasospasm. Most commonly seen in patients with shock. D. Mesenteric venous thrombosis: Involves thrombosis of superior mesenteric vein with or without extension into portal or splenic vein. It can be spontaneous or secondary to abdominal injury, hypercoaguable states, inflammation, or infection. History and clinical presentation A. Pain: Out of proportion on physical exam. B. Peritonitis: Is seen late, once infarction of bowel occurs. Diagnosis A. Plain abdominal x-rays: May show ileus in early cases or pneumatosis in advanced cases. B. Duplex ultrasound of mesenteric vessels: Identifies stenoses of celiac and SMA. C. CTA: Good to assess the patency of mesenteric vessels. D. Mesenteric angiogram: Diagnosis and potential treatment. CUT TO CASEBOOK

See NMS Surgery Casebook, 3rd edition, Case 5.13: Chronic Postprandial Abdominal Pain and Weight Loss. VI. Surgical treatment A. Bowel infarction 1. Exploratory laparotomy and resection of nonviable bowel. 2. Second look laparotomy typically is performed within 24 hours to ensure viability of residual bowel. B. Embolism: Embolectomy is performed with therapeutic anticoagulation (can be open or endovascular). C. Acute arterial thrombosis: Aortomesenteric or iliomesenteric bypass. D. Nonocclusive mesenteric ischemia: Usually treated with supportive care including bowel rest, antibiotics, and fluid resuscitation.

E. Mesenteric venous thrombosis: Systemic anticoagulation. VII. Prognosis:Is related to timing of intervention. Early restoration of blood flow leads to good outcomes.

Chronic Mesenteric Ischemia I. Pathophysiology: In normal individuals, blood flow to intestine increases 30–90 minutes after food ingestion. II. Etiology A. Atherosclerosis: Is the most common etiology. B. Seen in patients with slowly progressive stenosis/occlusion of origin of mesenteric vessels. III. History and clinical presentation A. Most commonly seen in middle-aged women with a long history of smoking. B. Patients are usually cachectic with typical symptoms of postprandial epigastric pain, fear of food, and weight loss. IV. Diagnosis A. Mesenteric duplex ultrasound: Screening tool with > 80% sensitivity and specificity. B. CTA: Diagnostic modality of choice. C. Mesenteric angiogram: Gold-standard tool for diagnosis and treatment. V. Surgical treatment A. Endovascular revascularization: Balloon angioplasty and stent placement. B. Open revascularization: Performed either by transaortic mesenteric endarterectomy or by aortomesenteric/iliomesenteric bypass. VI. Prognosis: Can be well managed with revascularization when recognized.

Quick Cuts “Food fear” may represent poor blood flow to the gut or mesenteric ischemia. Pain out of proportion to physical exam is classic for acute mesenteric ischemia. Duplex ultrasound is the initial diagnostic test of choice for mesenteric ischemia.

RENAL ARTERY STENOSIS I. Pathophysiology A. Renal Artery Stenosis (RAS) can cause refractory HTN and can also lead to kidney failure. B. Renovascular HTN 1. Stenosis at the level of the renal artery is sensed by receptors in kidney, which secretes renin. 2. Renin increases angiotensin, which causes vasoconstriction and stimulates the adrenal cortex to secrete aldosterone. 3. Aldosterone increases blood volume and blood pressure (Fig. 6-4). II. Etiology A. Atherosclerosis causes 90% of RAS. 1. Involves the ostium or proximal one third of renal artery; bilateral involvement. 2. Males greater than females.

B. Fibromuscular dysplasia 1. Younger women. 2. Involves middle or distal portion of renal artery. 3. Right side greater than left side; 30% of cases bilateral. 4. These lesions respond very well to endovascular intervention. C. Other causes: Traumatic or spontaneous dissection or disruption, vasculitis, thromboembolic disease, renal artery aneurysm, extrinsic compression, radiation injury. III. History and clinical presentation A. Asymptomatic RAS: Diagnosed incidentally. B. Symptomatic: Sudden worsening of renal failure or sudden-onset HTN.

Figure 6-4: Pathophysiology of renovascular hypertension. Renal artery stenosis activates the renin–angiotensin system, which produces aldosterone. Elevated blood volume and vasoconstriction translate into elevated blood pressures.

IV. Diagnosis A. Functional tests: Captopril scintigraphy and renal vein renin assay. B. Imaging: Duplex ultrasound of the renal arteries, CTA, magnetic resonance angiography (MRA), and conventional renal angiography. V. Surgical treatment: Percutaneous angioplasty and stent placement. VI. Prognosis: Good initial success rates. Disease may recur in 25% of cases.

The authors wish to acknowledge the contribution of Dr. Thomas S. Monahan III to the content of this chapter.

Chapter 7

Venous and Lymphatic Disease Brittany Aicher• R. Gregory Conway•Rajabrata Sarkar

Chapter Cuts Surgery is a proinflammatory state, and all surgical patients are at increased risk for deep venous thrombosis (DVT). Many have no symptoms or physical findings. Initial treatment of venous thrombosis is anticoagulation. Proven prophylaxis is provided by pneumatic compression devices and low-dose anticoagulation. Inferior vena cava (IVC) filters prevent pulmonary emboli in some patients with venous thrombosis. Pulmonary embolism is life threatening, diagnosed with computed tomography (CT) angiogram, and treated with systemic anticoagulation.

Critical Surgical Associations If You Hear/See

Think

Iliac veins

No valves

Unilateral calf swelling post-op

Deep venous thrombosis (DVT)

Hypoxia and DVT

Pulmonary embolism

Virchow triad

Stasis, intimal injury, hypercoagulability

Warfarin-induced skin necrosis

Protein C deficiency

ANATOMY AND GENERAL PRINCIPLES I. Three venous compartments: Superficial, perforating, and deep veins. II. Deep veins: Are named according to paired arteries: Internal jugular, brachial, axillary, subclavian, common femoral, femoral, deep femoral, popliteal, peroneal, anterior and posterior tibial veins.

Figure 7-1:Varicose veins. A. In a healthy vein, the valves help blood to flow back toward the heart and prevent it from pooling. B. In varicose veins, the valves no longer function properly, allowing the blood to pool. (From Carter PJ. Lippincott Textbook for Nursing Assistants, 3rd ed. Lippincott Williams & Wilkins; 2011.)

III. Blood flow: From superficial to deep veins through perforating veins. In the lower extremity, compression of the deep veins by calf muscles contributes to venous return (frequently called the calf muscle pump or musculovenous pump).

IV. Valves: Prevent reflux of blood (Fig. 7-1).

ACUTE DEEP VENOUS THROMBOSIS I. Classification A. More than 900,000 cases of deep venous thrombosis (DVT) diagnosed in the United States annually. B. Thirty percent of patients with a DVT experience a recurrence within 10 years. C. Untreated proximal DVT carries a 40% risk for pulmonary embolism (PE) and 12% mortality. II. Etiology—Virchow Triad A. Stasis: Immobility, venous compression, presence of indwelling catheter. B. Hypercoagulable state: Obesity, oral contraceptives, tobacco, malignancy, Factor V Leiden. C. Endothelial injury: Surgery, trauma, presence of indwelling catheter. III. History and clinical Presentation A. Signs and symptoms: Lower extremity pain, edema, pain on passive dorsiflexion (Homan sign), erythema, local warmth, prominent superficial veins, and peripheral cyanosis. B. Acute complicated DVT 1. Phlegmasia alba dolens: Nonischemic limb with pitting edema and blanching. 2. Phlegmasia cerulean dolens: Reversible phase of ischemic venous occlusion (painful blue leg), with risk of limb loss. 3. Venous gangrene: Irreversible phase of ischemic venous occlusion. IV. Diagnosis A. Duplex ultrasonography 1. Ninety percent sensitive in detecting iliofemoral DVTs. 2. Limited in assessment of veins in the pelvis or below the knee. B. D-Dimer 1. Detects degradation products of fibrinolysis and is highly sensitive. 2. Useful for exclusion of DVT, but elevated D-dimer is nonspecific. C. Magnetic resonance venography: Highest sensitivity and specificity for pelvic and central vein thrombosis. CUT TO CASEBOOK

See NMS Surgery Casebook, 3rd edition, Case 5.15: Postoperative Leg Swelling. V. Medical treatment A. Prevention of DVT 1. Stasis prevention: Compression stockings, sequential compression devices (which also activate fibrinolysis), early mobility, calf exercises. 2. Anticoagulation a. Prophylactic dose of subcutaneous low-molecular-weight heparin (LMWH; e.g., enoxaparin) or unfractionated heparin (UFH). b. Without prophylaxis, there is a 10%–40% risk of DVT in general surgery patients, and nearly 60% risk in orthopedic surgery patients.

TRUSTED SOURCE American Society of Hematology 2019 guidelines for management of venous thromboembolism: prevention of venous thromboembolism in surgical hospitalized patients. Available at https://ashpublications.org/bloodadvances/article/3/23/3898/429211? _ga=2.172483371.962202370.1595939154-1948724850.1595939154 B. Treatment of established DVT—Anticoagulation 1. Therapeutic dose of LMWH, fondaparinux, UFH, warfarin, direct oral anticoagulants (DOACs; dabigatran, rivaroxaban, etc.). 2. Patients should be transitioned to warfarin or DOAC for prolonged treatment; patients must be “bridged” to warfarin with therapeutic heparin. 3. Treatment duration a. Isolated DVT or reversible provoking factor: 3 months. b. Cancer, second venous thromboembolic events (VTE) and low bleeding risk: Indefinite. 4. All therapies increase bleeding risk. C. Complications of anticoagulation therapy 1. Bleeding. a. Risks with LWMH: Postoperative bleeding (6%), major hemorrhage (3%). b. Treatment: Cessation of anticoagulation, consider IVC filter. c. Reversal (1) Warfarin: Prothrombin complex concentrates (PCC), fresh frozen plasma (FFP), vitamin K. (2) Heparin: Protamine (rarely needed clinically; heparin half-life is ~90 minutes). (3) DOACs: Specific reversal agents vary by DOAC mechanism. 2. Heparin-induced thrombocytopenia (HIT): Antibody response against neoantigens expressed on platelet factor 4 (PF4) upon binding to heparin. a. Findings: Thrombocytopenia or thrombosis following heparin use. b. Diagnosis: Heparin-induced platelet aggregation assays, heparin antibody test, serotonin release assay (SRA). c. Treatment: Discontinue all heparin, initiate direct thrombin inhibitor (e.g., argatroban, lepirudin, bivalirudin). 3. Warfarin-induced skin necrosis a. Occurs with administration of warfarin without anticoagulant “bridge”. b. Secondary to decreased levels of proteins C and S before pro-coagulant factor inhibition takes effect, resulting in a pro-thrombotic state. VI. Surgical treatment A. IVC filters: Prevent PE but do not treat existing DVT (Fig. 7-2). 1. Indications: Proximal DVT with contraindication, complication, or failure of anticoagulation. 2. Complications: Occur in 4%–11% of patients; recurrent DVT, insertion site or IVC thrombosis, IVC injury, filter migration. B. Catheter-directed thrombolysis 1. Tissue plasminogen activator is infused near the DVT. Some devices have a high-velocity jet to promote disintegration. 2. Decreases severity of post-thrombotic syndrome (PTS) symptoms for patients with iliofemoral

DVT compared to anticoagulation alone.

Figure 7-2:Retrievable IVC filter. A. Note the retrieval hook at the upper end of the filter. The filter has four “petals” for centering in the IVC. B. Optimally placed permanent IVC filter (Vena Tech LP, Braun) with apex (white arrow) at the level of the lowest (left in this case) renal vein (black arrow). The “dead space” where clot may form above the filter if IVC thrombosis occurs is minimized. Figure part B from Casserly IP, Sachar R, Yadav JS. Practical Peripheral Vascular Intervention, 2nd ed. Wolters Kluwer; 2011, Fig. 29-13).

3. Indications: Select patients with acute iliofemoral DVT, limb-threatening venous occlusion, rapid thrombus extension, or IVC thrombosis. 4. Contraindications: Active bleeding, intracranial tumor, vascular malformation, aneurysm, cerebral infarction, or head trauma, ophthalmic or neurologic procedures within 3 months are absolute contraindications. 5. Complications: Bleeding (5%–11%), immediate rethrombosis. C. Venous thrombectomy 1. Indications: Infra-inguinal balloon catheter thrombectomy is used in patients with worsening venous edema or venous gangrene in which thrombolysis is not possible. 2. Complications: Rethrombosis; risks of general anesthesia and invasive procedure. VII. Prognosis

A. Prompt treatment with anticoagulation carries a good prognosis. B. Chronic complicated DVT: PTS. 1. Characterized by venous hypertension, proximal obstruction and valvular dysfunction: Limb swelling, limb fatigue, pain, venous claudication, hyperpigmentation, eczema, erythema, skin ulceration. 2. Occurs in ~40% of patients with iliofemoral DVT; 4% of patients with DVT will develop severe manifestations including ulceration. 3. Severe PTS may be treated with iliac vein stenting if proximal stenosis or obstruction is present, thereby reducing venous pressure in the affected limb.

Quick Cuts Up to 50% of DVT are asymptomatic. All anticoagulants increase bleeding risk (hemorrhage and hematoma). Post-thrombotic syndrome can be a significant complication following DVT.

PULMONARY EMBOLISM I. Classification: Temporal, physiologic, anatomic, and symptomatic factors. A. Temporal 1. Acute: Symptoms immediately following embolic event. 2. Subacute: Symptoms days to weeks following embolic event. 3. Chronic: Over a prolonged period. May present with pulmonary hypertension. B. Physiologic 1. Submassive: No evidence of hemodynamic instability. 2. Massive: Characterized by hemodynamic instability. a. Systolic blood pressure (SBP) 60 g or in whom other pathology exists. 3. Minimally invasive prostatic surgical options: Microwave therapy, laser ablation, and transurethral needle ablation. V. Prognosis: Generally good. TRUSTED SOURCE Urology Care Foundation: What is Benign Prostatic Hyperplasia (BPH)? Available at https://www.urologyhealth.org/urologic-conditions/benign-prostatic-hyperplasia-(bph)

Nonbacterial Prostatitis I. Definition: Benign inflammation; typically seen in young patients. II. Clinical Presentation (Table 28-1) A. “Male pelvic pain syndrome”: Urinary frequency, urgency, perineal pain, and dysuria. B. Pain: Hallmark symptom. C. Character: Symptoms tend to be more irritative and painful rather than obstructive. III. Diagnosis: History and physical exam. IV. Treatment: Combination of antibiotics, alpha blockers, muscle relaxants, and biofeedback. V. Prognosis: Good; symptoms are life altering, but not life threatening.

Table28-1: Diagnostic Features of Prostatitis Type of Prostatitis

Symptoms

Systemic Signs

Increased WBCs in EPS

Positive Culture

Acute bacterial prostatitis

Yes

Yes

Yes

Yes

Chronic bacterial prostatitis

Yes

No

Yes

Yes

Nonbacterial prostatitis

Yes

No

Yes

No

Prostadynia

Yes

No

No

No

EPS, expressed prostatic secretions; WBC, white blood cell count. Quick Cuts BPH is extremely common with aging. BPH is first treated medically, but there are surgical options.

GENITOURINARY MALIGNANCIES Prostate Tumors I. Epidemiology A. Prostate cancer is the most common noncutaneous cancer among men. B. Lifetime risk in the United States is one in six men. II. Clinical Presentation: Often asymptomatic, but it can present with urinary symptoms (e.g., dysuria, frequency, incontinence or hematuria). III. Diagnosis A. DRE: Traditional cancer detection method, assessing for induration or a nodule. B. Prostate-specific antigen (PSA) level: PSA is a serine protease that serves to liquefy semen after ejaculation. 1. Roles: Diagnostic and in following response to cancer treatment. 2. When combined with DRE, determination of the PSA level improves the ability to detect cancers. 3. PSA test has a high specificity, but low sensitivity. C. Prostate biopsy 1. Office-based procedure performed with transrectal ultrasound guidance in men who have a suspicious DRE and/or an elevated PSA. 2. Risks: Bleeding (urinary tract or rectal) and infection. IV. Treatment A. Expectant management 1. Watchful waiting: Noncurative treatment; goal is to limit morbidity. a. Treatment is delayed until symptoms become evident, at which time androgen deprivation therapy (ADT) is initiated. b. For those expected to live 3 years).

Renal Pelvis and Ureter Transitional Cell Carcinoma I. Pathogenesis A. Epidemiology: Uncommon, usually unilateral tumor. B. Risk factors: Similar to bladder lesions and Balkan nephropathy. C. Disease Progression: 3% of people with bladder transitional tumors develop upper tract lesions; one-half of those with upper tract tumors develop a bladder lesion. II. Clinical Presentation: Gross hematuria, microscopic hematuria, and flank pain. III. Diagnosis: CT scan, retrograde pyelography, and ureteroscopy (Figs. 28-5 and 28-6). IV. Treatment A. Nephroureterectomy 1. Traditional radical treatment: Removal of the kidney, entire ureter, and a cuff of bladder at the ureteral orifice. 2. Conservative excision: a. May be appropriate for low-grade, low-stage ureteral tumors. b. Involves tumor excision with primary ureteroureterostomy or ureteral reimplantation (into the bladder) for distal ureteral lesions.

Figure 28-5: A 71-year-old male presented with gross hematuria. CT scan without contrast demonstrates left-sided hydroureteronephrosis. In the distal left ureter, a dense mass appears to be causing the hydronephrosis. Final pathology demonstrated urothelial carcinoma.

Figure 28-6: This retrograde ureterogram was made by injecting contrast up the ureter with a ureteroscope. Contrast does not fill up the entire ureter because it contains a mass. The U-shaped defect is also referred to as a goblet sign. In an obstructing stone, the ureter would spasm around the filling defect. Here, the ureter is dilated in the area of the mass.

B. Endoscopic treatment: Reserved for patients with low-grade papillary tumors in solitary renal units or for patients whose health precludes major surgical intervention. V. Prognosis: Depends largely on stage; when completely resected, prognosis is good.

Renal Cell Carcinoma I. Epidemiology A. Incidence 1. ~65,000 new cases per year in the United States. 2. More common in men than in women. 3. Peak incidence in the fifth to seventh decades of life. B. von Hippel–Lindau disease: Associated with renal cell carcinoma. II. Clinical presentation A. Commonly discovered incidentally. B. Paraneoplastic syndromes: Occur in ~20% and include Stauffer syndrome (nonmetastatic hepatic dysfunction), hypercalcemia (unclear etiology), hypertension, erythrocytosis, and endogenous pyrogen production. III. Diagnosis

A. Ultrasonography: Differentiates a simple cyst from a complex or solid lesion. B. CT scan with intravenous (IV) and oral contrast: Most cost-effective diagnostic and staging modality; noncontrast CT scans often miss large renal lesions (Fig. 28-7).

Figure 28-7: Renal carcinoma. A. CT scan without contrast demonstrates a normal-appearing right kidney. B. Portal venous phase (with contrast) demonstrates a large posterior lesion with solid and cystic components, consistent with renal cell carcinoma.

C. Magnetic resonance imaging: Can benefit patients who cannot have contrast and may help define involvement of the renal vein. D. Percutaneous aspiration and biopsy: A reasonable method of diagnosis for patients with metastatic disease. IV. Treatment A. Radical nephrectomy (open or laparoscopic): Surgical removal of the ipsilateral adrenal gland, kidney, and investing adipose tissue and fascia; regional lymphadenectomy may also be performed. B. Cardiopulmonary bypass: May be required when renal cell carcinoma invades the renal vein and inferior vena cava and extends to the right atrium. V. Prognosis: Stage dependent. A. Stage I: 5-year cancer-specific survival rate is >90%. B. Stage IV: Median survival is 16–20 months, and the 5-year survival rate is 60 years. II. Clinical presentation and diagnosis A. Painless testicular swelling or enlargement: Classic presenting sign, often diagnosed by selfexam. B. Pain (15%–50%): Suggests hemorrhage or infarction. C. Physical examination: Firm, mildly tender mass or diffuse testicular swelling. D. Reactive hydrocele occurs in 5%–10% of cases. III. Diagnosis A. Ultrasonography: Gold standard. B. Alpha-fetoprotein (AFP), beta-human chorionic gonadotropin (HCG), and lactate dehydrogenase: Serum marker levels are useful for diagnosis, following response to treatment, and identifying recurrent disease.

1. AFP can be elevated in patients with yolk sac tumors and embryonal carcinoma. 2. Beta-HCG: Elevation may accompany choriocarcinoma, embryonal carcinoma, and seminomas. IV. Treatment: A. Initial treatment: Surgical exploration via an inguinal approach to avoid potential contamination of scrotal lymphatic draining during tumor manipulation. B. Varies with cell type and disease stage 1. Seminoma: Uniquely radiosensitive and chemosensitive. a. Low stage: Options include close observation, single-agent carboplatin therapy, or radiation therapy; survival approaches 100%. b. Highstage: Up to four courses of chemotherapy with cisplatin, etoposide, and bleomycin. (1) Postchemotherapy radiation: Considered for residual retroperitoneal mass. (2) Prognosis: 67% complete response rate to chemotherapy and an overall survival rate of 72%. 2. NSGCTs a. Lowstage: Inguinal orchiectomy and either modified retroperitoneal lymphadenectomy (RPLND), primary chemotherapy, or intense surveillance. (1) Surveillance: Generally reserved for compliant patients at low risk of micrometastatic disease. (2) RPLND (~30% of stage I patients): Surgical removal of specific high-risk lymphatic tissue; most patients with micrometastases receive adjuvant platinum-based chemotherapy. (3) Survival approaches 92% for both groups. b. High-stage NSGCT (1) Patients with minimal nodal involvement radiographically or failure to normalize markers postorchiectomy should undergo either RPLND or chemotherapy alone. (2) Intermediate prognosis tumors have 5-year survival of 80%; poor prognosis tumors have a 5-year survival of 50%.

Quick Cuts The only two curative therapies for prostate cancer are radiation and surgery. The renal cell carcinoma classic triad of pain, hematuria, and flank mass is now very uncommon with the advent of frequent CT scans. >50% are now found incidentally. Testicular cancer is most common malignancy in men age