CONCISE TEXTBOOK OF ORTHOPAEDICS: CBME CURRICULUM-2023 [1 ed.] 9789357829854

Table of contents :
Foreword
ACKNOWLEDGEMENTS
Contents
1. Introduction to Orthopaedics, Skeletal Trauma, Polytrauma
2. Fractures
3. Musculoskeletal Infection
4. Skeletal Tuberculosis
5. Rheumatoid Arthritis and Associated Inflammatory Disorders
6. Degenerative Disorders
7. Metabolic Bone Disorders
8. Poliomyelitis
9. Cerebral Palsy
10. Bone Tumors
11. Peripheral Nerve Injuries
12. Congenital lesions
MISCELLANEOUS
Gait
Osteoarthritis
Neuropathic Joint
Carpal Tunnel Syndrome
Tennis Elbow
Golfer's Elbow
De Quervain's Disease
Trigger Finger
Osteochondritis
Trendelenberg Gait
Bryants Triangle
Thomas Hip Flexion Test
13. Procedural Skills
14. Counselling Skills
15. Instruments & Implants
Rapid Review
References
Sample MCQ’s
Model Examination Question Paper

Citation preview

Dr Prasanna T Y M S Ortho (JIPMER), Ex SR (AIIMS, New Delhi) Fellowship in Arthroplasty and Arthroscopy   Vienna, Europe

DEDICATED TO MY LOVING MOTHER LATE MRS SUVARNA…

Credits: AthK

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Disclaimer: Science and technology are constantly changing fields. New research and experience broaden the scope of information and knowledge. The author has tried his best in giving information available to him while preparing the material for this book. Although all efforts have been made to ensure optimum accuracy of the material, yet it is quite possible some errors might have been left uncorrected. The author, the publisher & the printer will not be held responsible for any inadvertent errors or inaccuracies. ISBN: 978-93-5782-985-4 Copyright ©Author Illustrations and images © Dr Prasanna T Y First edition: 2023 All rights reserved. No part of this book may be reproduced or transmitted in any form or by any means, electronic or mechanical including photocopying, recording or any information and retrieval system without permission, in writing from the author, publisher and printer. It is punishable under law and will be dealt legally against the person/firm. In case of any dispute, all legal matters to be settled under Bengaluru Jurisdiction only. Printed by, Amaze Creations, Number 230-235, Shop no 1, Stomachs Building, Chickpet, Bengaluru- 560053.

Credits: AthK

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Foreword It gives me great pleasure to write a foreword for the book “Concise textbook of Orthopaedics” authored by Dr. Prasanna T Y. He was my Orthopaedic fellow at EKW Hospital, Vienna, Europe during 2019. He was a dedicated, hardworking, good fellow and I am happy to see my student presenting such a comprehensive academic book. This book has been written keeping in mind the fast pace of changes in medical technology, treatment and the protocols that have evolved in the current era. Lots of color diagrams, clinical photographs and X-rays have been used to simplify the understanding of the subject. This textbook is highly informative and well presented to guide with a better understanding of Orthopedics for undergraduates. I wish the best to him for his future endeavors.

Dr. Thomas Muellner. PhD Head, Dept of Orthopaedics and Traumatology             Evangelisches Krankenhaus Hospital         Vienna, Europe

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ACKNOWLEDGEMENTS I offer my utmost reverence to God for guiding me to complete this task. I am grateful to my mother late Mrs. Suvarna for encouraging and supporting me throughout my life. I thank my father Mr. Totiger Yallappa, my sisters Mrs. Sheela T Y and Mrs. Leela T Y and their families, grandmother Mrs. Renuka, my uncle Mr. Suresh M K, and aunty Mrs. Pushpa for building me in my formative years. I would also thank everyone who has supported me over the course of my life. I thank my wife Dr. Sujala S Aradhya for her unconditional support in all my ventures, my in-laws Dr. S Sacchidanand, Dr. B Jalajakshi, Dr. Prajwala S Aradhya and Dr. Kiran Konda R for their moral support. I thank all my teachers – from BMCRI, Bengaluru Dr. Ramesh Krishna and Dr. Vanamali B S, from JIPMER, Pondicherry Dr. Jagadish Menon, Dr. Gopishankar Balaji, Dr. Deep Sharma, Dr. Suresh Gandhi, Dr. Sandeep Kumar Nema, from AIIMS Dr. Rajesh Malhotra, Dr. H L Nag, Dr. C S Yadav, Dr. Vijay Kumar, Dr. Shah Alam Khan, Dr. Kamaran Farooque, Dr. Vivek Trikha, Dr. Samarth Mittal, Dr. Venkatesan Sampath Kumar, Dr. Vijay Kumar D all my seniors and colleagues. I sincerely thank my staff and colleagues of my department Dr. Roshan Kumar B N, Dr. Suresh I, Dr. Hashim S M, Dr. Mahesh Kumar, Dr. Gopinath K M, Dr. Raghavendra S, Dr. Sivaprasad K, Dr. Pramod Kumar M, Dr. Sandeep K M, Dr. Suhas D, Dr. Monesh K B, Dr. Khalid Fiyaz, Dr. Balasubramanian S, Dr. Venkatesh K, Dr. Lohith N, Dr. Akshay M, Dr. Varun Kumar N R, all my postgraduates and students of RRMCH, Bengaluru. I thank Dr. Naveen S, Principal and Dr. Shruthi B N, Anatomy HOD, RRMCH for their constant support and encouragement. I also thank Mr. Suresh for helping me with the editing of the images for this textbook, Mr Chittranjan from Amaze Creations for making this book a reality. In the end, I wish to thank in advance all the readers, who would support me and provide their valuable feedback to help me further improve this book.   Dr Prasanna T Y

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I would like to dedicate my entire achievements including this book to my parents Mrs. Nagarathna N and Mr. Rangashamaiah, They have instituted the right values in me and guided me in all aspects of my career and life. I thank my wife Dr. Jyothi Naik, my kids Hamsini and Daivik for their unconditional love, care, encouragement and support. They are also a source of inspiration for me to achieve my goals. My special thanks to my brother Dr. Prasanna Kumar A R who is currently working as a faculty in the department of Pediatric surgery, St John’s Hospital. He has been a role model and guide to me in my career and continues to do so till date. I am very grateful to all my teachers from primary school to postgraduation in orthopedics, as they have helped to shape my career and personality. I am also thankful to all my colleagues, students and staff of JIPMER and ESIC Medical College for their cooperation and support. Last but not least I would like to thank all the patients I have come across in my career who had helped me to acquire knowledge and skill during their treatment. I take this opportunity to thank and congratulate my colleague Dr. Prasanna T Y for bringing out this all-inclusive undergraduate textbook.                                                                                                           Dr Nataraj A R

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CHAPTER REVIEWERS: Dr. D K Patro                                                 Dr. Jagdish Menon M S Ortho, DNB,MRCS(Edin), FACS Professor & HOD

        M S Ortho, DNB, MNAMS,

        Professor

PIMS, Pondicherry, India                                  JIPMER, Pondicherry, India           

Dr. Vijay Sharma                                          Dr. Venkatesan Sampath Kumar                            M S Ortho, MRCSEd, FRCS                                  M S Ortho, DNB, MRCS, FRCS (Glas) Professor                                                                 Associate Professor JPNATC AIIMS, New Delhi, India                      AIIMS, New Delhi, India           

Dr. Suresh I       

        Dr. Roshan Kumar B N

D. Ortho, M S Ortho

         M S Ortho, FASM

Professor & HOD                                                  Professor RRMCH, Bengaluru, India                                 RRMCH, Bengaluru , India           

Dr. Ramesh Krishna K Seetharam

       Dr. Vanamali B

M S Ortho, MCh (Orth), FRCS (Glasg)         M S Ortho, DNB, MNAMS, MRCSEd (UK) Professor & HOD                                                 Professor & Fellowship Co-ordinator BMCRI, Bengaluru, India                                   BMCRI, Bengaluru, India

Dr. Hemanth Bansal                                    Dr. Kalyan Kumar Varma Kalidindi M S Ortho, DNB, FAA (Vienna, Europe)               M S Ortho, DNB, FNB (Spine), MNAMS, FMISS Assistant Professor                                                   Consultant Spine Surgeon AIIMS, New Delhi, India                                            AIG hospital, Hyderabad, India           

Dr. Puneeth K                                                      Dr. Shankar K M S Ortho, FAA

   M D Psychiatry

Orthopaedic Surgeon, Punya hospital                Assist. Professor, Dept. of Psychiatry Channapatna, Karnataka, India                             BMCRI, Bengaluru, India.           

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Contents Preface Sl. No 1

Chapters Introduction to Orthopaedics, Skeletal Trauma, Polytrauma Fractures Musculoskeletal Infection Skeletal Tuberculosis Rheumatoid Arthritis and associated inflammatory disorders Degenerative disorders Metabolic bone disorders Poliomyelitis Cerebral Palsy Bone Tumors Peripheral nerve injuries Congenital lesions Procedural Skills Counselling Skills Orthopaedic Instruments and Implants

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CBME CURRICULUM Competency# OR1.1

OR1.2

OR1.3

OR1.4 OR1.5

OR1.6

Competency title Skeletal Trauma, Polytrauma Describe and discuss the Principles of prehospital care and casualty management of a trauma victim including principles of Triage. Describe and discuss the aetiopathogenesis, clinical features, investigations, and principles of management of shock. Describe and discuss the aetiopathogenesis, clinical features, investigations, and principles of management of soft tissue injuries Describe and discuss the Principles management of soft tissue injuries.

of

Describe and discuss the aetiopathogenesis, clinical features, investigations, and principles of management of dislocation of major joints shoulder, knee, and hip. Participate as a member in the team for closed reduction of shoulder dislocation / hip dislocation / knee dislocation. 7

OR2.1

Fractures Describe and discuss the mechanism of injury, clinical features, investigations and plan management of fracture of clavicle

OR2.2

OR2.3 OR2.4

OR2.5

OR2.6

Describe and discuss the mechanism of Injury, clinical features, investigations and plan management of fractures of proximal humerus. Select, prescribe and communicate appropriate medications for relief of joint pain Describe and discuss the mechanism of injury, clinical features, investigations and principles of management of fracture of shaft of humerus and intercondylar fracture humerus with emphasis on neurovascular deficit. Describe and discuss the aetiopathogenesis, clinical features,mechanism of injury, investigation & principles of management of fractures of both bones forearm, Galeazzi and Monteggia injury

OR2.7

Describe and discuss the aetiopathogenesis, mechanism of injury, clinical features, investigations and principles of management of fractures of distal radius.

OR2.8

Describe and discuss the aetiopathogenesis, mechanism of injury, clinical features, investigations and principles of management of pelvic injuries with emphasis on hemodynamic instability.

OR2.9

OR2.10

OR2.11

OR2.12

Describe and discuss the aetiopathogenesis, mechanism of injury, clinical features, investigations and principles of management of spine injuries with emphasis on mobilisation of the patient. Describe and discuss the mechanism of injury, clinical features, investigations and principle of management of acetabular fracture. Describe and discuss the aetiopathogenesis, mechanism of injury, clinical features, investigations and principles of management of fractures of proximal femur

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OR2.13

OR2.14

OR2.15

OR2.16

Describe and discuss the aetiopathogenesis, mechanism of injury, clinical features, investigations and principles of management of (a) Fracture patella (b) Fracture distal femur (c) Fracture proximal tibia with special focus on neurovascular injury and compartment syndrome Describe and discuss the aetiopathogenesis, clinical features, investigations and principles of management of fracture shaft of femur in all age groups and the recognition and management of fat embolism as a complication Describe and discuss the aetiopathogenesis, clinical features, Investigation and principles of management of: (a) Fracture of both bones leg (b) Calcaneus (c) Small bones of foot. Describe and discuss the aetiopathogenesis, clinical features, Investigation and principles of management of ankle fractures Plan and interpret the investigations to diagnose complications of fractures like malunion, nonunion, infection, compartmental syndrome

OR3. 1

OR3. 2

Participate as a member in team for aspiration of joints under supervision OR3.

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Describe and discuss the mechanism of injury, clinical features, investigations and principles of management of open fractures with a focus on secondary infection prevention and management Musculoskeletal Infection Describe and discuss the aetiopathogenesis, clinical features, investigations and principles of management of Bone and Joint infections a) Acute Osteomyelitis b) Subacute osteomyelitis c) Acute Suppurative arthritis d) Septic arthritis & HIV infection e) Spirochaetal infection f) Skeletal Tuberculosis

Participate as a member in team for procedures like drainage of abscess, sequestrectomy/ saucerisation and arthrotomy

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OR4.1

OR5.1

OR6.1

OR7.1

OR8.1

OR9.1

OR10.1

OR11.1

OR12.1

Skeletal Tuberculosis Describe and discuss the clinical features, Investigation and principles of management of Tuberculosis affecting major joints(Hip, Knee) including cold abscess and caries spine Rheumatoid Arthritis and associated inflammatory disorders Describe and discuss the aetiopathogenesis, clinical features, investigations and principles of management of various inflammatory disorder of joints Degenerative disorders Describe and discuss the clinical features, investigations and principles of management of the degenerative condition of spine (Cervical Spondylosis, Lumbar Spondylosis, PID) Metabolic bone disorders Describe and discuss the aetiopathogenesis, clinical features, investigation and principles of management of metabolic bone disorders in particular osteoporosis, osteomalacia, rickets, Paget's disease Poliomyelitis Describe and discuss the aetiopathogenesis, clinical features, assessment and principles of management of a patient with Post Polio Residual Paralysis Cerebral Palsy Describe and discuss the aetiopathogenesis, clinical features, assessment and principles of management of Cerebral palsy patient Bone Tumors Describe and discuss the aetiopathogenesis, clinical features, investigations and principles of management of benign and malignant bone tumors and pathological fractures Peripheral nerve injuries Describe and discuss the aetiopathogenesis, clinical features, investigations and principles of management of peripheral nerve injuries in diseases like foot drop, wrist drop, claw hand, palsies of Radial, Ulnar, Median, Lateral Popliteal and Sciatic Nerves Congenital lesions 10

Describe and discuss the clinical features, investigations and principles of management of Congenital and acquired malformations and deformities of: a. limbs and spine - Scoliosis and spinal bifida b. Congenital dislocation of Hip, Torticollis. c. Congenital talipes equino varus

OR13.1

OR13.2

OR14.1

OR14.2

OR14.3

Miscellaneous Topics Procedural Skills Participate in a team for procedures in patients and demonstrating the ability to perform on mannequins / simulated patients in the following: i. Above elbow plaster ii. Below-knee plaster iii. Above-knee plaster iv. Thomas splint v. splinting for long bone fractures vi. Strapping for shoulder and clavicle trauma Participate as a member in team for Resuscitation of Polytrauma victim by doing all of the following : (a) I.V. access central - peripheral (b) Bladder catheterization (c) Endotracheal intubation (d) Splintage Counselling Skills Demonstrate the ability to counsel patients regarding prognosis in patients with various orthopedic illnesses like a. fractures with disabilities b. fractures that require prolonged bed stay c. bone tumors d. congenital disabilities Demonstrate the ability to counsel patients to obtain consent for various orthopedic procedures like limb amputation, permanent fixations etc. Demonstrate the ability to convince the patient for referral to a higher centre in various orthopedic illnesses, based on the detection of warning signals and need for sophisticated Management Orthopedic instruments and implants

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Medical Council of India, Competency based Undergraduate Curriculum for the Indian Medical Graduate, 2018. Vol III; pg 130-144. #

Credits: AthK

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Chapter 1

INTRODUCTION TO ORTHOPAEDICS The term Orthopaedics was coined in 1741 by Nicholas Andre. The term Orthopedia is a composite of two Greek words Orthos- Straight Paidios-Child Orthopaedics literally means straight child. It was the art of correcting and preventing deformities in children by using splints in bowed leg conditions like rickets. Andre’s book also depicted a crooked young tree attached to a straight and strong stake which has become the universal symbol of Orthopaedic surgery.

Fig 1.01: Emblem of Orthopaedics.

Early era: Hippocrates: He is considered as the Father of Medicine. He described various reduction maneuvers, principles of traction and counter-traction and correction of clubfoot deformity. The Hippocratic method of shoulder reduction is still used for reducing anterior shoulder dislocations. Middle ages: Discovery of microorganisms and antibiotics occurred in the middle era. Introduction of antisepsis principles appeared to revolutionize the surgical management of Orthopaedic injuries. Joseph Lister, Louis Pasteur, Robert Koch, Ignaz Semmelweis greatly contributed in the middle era. The modern era: The invention of X-ray in 1895 by Conrad Rontgen helped to identify fractures of bones. Sir John Charnley in 1960 popularized Total hip replacement.

INTRODUCTION TO ORTHOPAEDIC CONDITIONS: Orthopaedics is a branch of surgery concerned with conditions involving Congenital- Congenital talipes equino varus (CTEV), Congenital dislocation of hip(CDH),  congenital disorders and deformities. Traumatic-Musculoskeletal trauma, sports injuries Inflammatory- Inflammatory arthritis like Rheumatoid arthritis, Ankylosing spondylitis and degenerative diseases. Neoplastic- Bone tumors Infections- Osteomyelitis and Tuberculosis. Miscellaneous conditions like Torticollis, Slipped capital femoral epiphysis.

ANATOMY OF BONE Bone is a dense mineralized connective tissue. It is impregnated with 2/3rd inorganic calcium salts like calcium phosphate, calcium carbonate and traces of salts. The 1/3rd of organic matrix is made up of collagen type 1, glycosaminoglycans, osteonectin, osteocalcin etc. Parts of bone:

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A) Epiphysis: It is the end part of a long bone. It arises from the secondary center. B) Metaphysis: It is the epiphyseal end of the diaphysis. It has a maximum blood supply. C) Diaphysis: It is the strongest part of the bone. It arises from the primary center. D) Physeal plate: It separates epiphysis from metaphysis. It contributes to maximum growth. 

Fig1.02: Parts of a long bone: A) Epiphysis; B) Metaphysis; C) Diaphysis; D) Growth plate. Blood supply of long bones: 1) Nutrient artery: It enters the nutrient foramina and divides into ascending and descending branches in the medullary cavity. It terminates in the adult metaphysis by anastomosing with epiphyseal, metaphyseal and periosteal arteries. It supplies the inner 2/3rd of cortex and metaphysis. 2) Periosteal arteries: It arises from overlying vessels of the periosteum, enters the Volkmann’s canal and supplies the outer 1/3rd of cortex.

Fig 1.03: Blood supply to long bone: A) Epiphyseal vessels; B) Metaphyseal vessels; C) Nutrient artery. Microscopic structure of bone: Osteon (Haversian system): It is the structural and functional unit of bone. Types of bone cells: 1) Osteoblasts: These are bone-forming cells. They synthesize and secrete collagen fibers and organic components of the bone matrix. They contain alkaline phosphatase and pyrophosphatase. 2) Osteocytes: These are mature, non-dividing osteoblast surrounded by matrix and lying within the lacunae. 3) Osteoclasts: These are giant multinucleate cells. They are responsible for active erosion of bone by secreting acid phosphatase. These arise from circulating monocytes in the blood. 4) Osteoprogeniter cells: They differentiate into osteoblasts. Compact vs cancellous bone: Location Lamellae Bone marrow Nature

Compact bone In the shaft of long bone Arranged to form Haversian system Yellow, which stores fat after puberty. It is red before puberty Hard and ivory like

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Cancellous bone In the epiphysis of long bone Arranged in a meshwork, so Haversian system is not present It is red marrow Spongy

Fig 1.04: A) Cortical bone; B) Cancellous bone. Anatomical terms: 1) Anterior - Frontal aspect –Ventral aspect 2) Posterior - Rear aspect- Dorsal aspect 3) Medial - Facing towards the median plane 4) Lateral - Away from the median plane. Anatomical planes: 1) Saggital plane- Anterior-posterior axis (eg: sagittal suture of skull) 2) Coronal plane–It is a vertical plane that divides the body into ventral and dorsal section (eg: coronal suture of skull). 3) Transverse plane- It is a horizontal plane that divides the body into superior and inferior parts. It is also called the horizontal plane.  The above planes are used in CT and MRI scans. A combination of these helps in the assessment of overall 3D anatomy. 

Fig 1.05: Anatomical planes: S) Saggital plane; C) Coronal plane; T) Transverse plane. Movements at joints: 1) Flexion: It is defined as decreasing the angle of the joint. 2) Extension: It is defined as increasing the angle of the joint. 3) Adduction: When the limb is brought close to the midline of the body. 4) Abduction: When the limb is taken away from the midline of the body. 5) Medial rotation: Inward rotation of the limb. 6) Lateral rotation: Outward rotation of the limb. 7) Supination: When the palm is facing forwards or upwards. 8) Pronation: When the palm is facing downwards or backwards. 9) Subluxation- Partial disruption in continuity of the joint 10) Dislocation- Complete disruption in continuity of the joint.

Fig 1.06: A) Normal; B) Subluxation; C) Dislocation.

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Special terms: 1) Fracture dislocation- Dislocation that occurs in conjunction with a fracture of the bone. If incomplete, it is called fracture-subluxation. They are usually periarticular in location.

Fig 1.07: Fracture dislocation. 2) Strain- Injury to the muscle is called strain 3) Sprain- Injury to the ligament is called sprain

Fig 1.08: A) Strain; B) Sprain 4) Ankylosis: Restriction of joint motion.

Fig 1.09: A) Normal joint; B) Fibrous ankylosis; C) Bony ankylosis. 5) Arthrodesis: Surgical fusion of joints. 6) Arthroplasty- It is replacement of joint by prosthesis to restore motion and function of the joint. 7) Arthroscopy- It is examination of joint through an arthroscope. It is also called “keyhole surgery” 8) Bursa - Small fluid-filled sac between a tendon and bone. 9) Bursitis - Inflammation of a bursa.

SKELETAL TRAUMA, POLYTRAUMA Competency OR 1.1: Describe and discuss the Principles of pre-hospital care and causality management of a trauma victim including principles of Triage.

Traumatic injuries are one of the leading cause of death in young adults. Traumatic injuries may vary from small injuries to life threatening multi-organ injuries. To achieve the best possible outcomes while decreasing the risk of undetected injuries, the management of trauma patients requires a highly systematic approach.

TRIMODAL DEATH DISTRIBUTION Mortality from trauma can be grouped into 1)    Immediate( within seconds to minutes after injury) 2)    Early( within minutes to several hours after injury)

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3)    Late ( several days to weeks after injury) The first peak of death occurs within seconds to minutes of injury because of fatal disruption to great vessels, heart and lungs, laceration of the brain, brain stem or high spinal cord injury. The second peak of death occurs within minutes to several hours following injury. Subdural hematoma or epidural hematoma, hemothorax, laceration of spleen, liver, pelvic fractures and/or other multiple injuries associated with significant blood loss leading to fatal outcome. The third peak of death which occurs several days to weeks after the initial injury is most often due to sepsis and multiple organ system failure. Care provided during each of the preceding events has an impact on patient outcome. Thus the first and every subsequent person to care for the injured patient have a direct effect on long-term outcome.

Fig 1.10: Trimodal death distribution graph. Golden hour concept: In World War I which took place in 1918, there was a real appreciation of the time factor between wounding and adequate shock treatment. The first hour of care after injury is called the “golden hour”. If the patient was treated within one hour, the mortality was 10%. This increased markedly with time, so that after eight hours, the mortality rate was nearly 75%. Early trauma deaths: 1)    Failed oxygenation of the vital organs. 2)    Massive central nervous system injury. 3)    Both The mechanism of failed tissue oxygenation includes inadequate ventilation, impaired oxygenation, circulatory collapse and impaired end organ perfusion. Injuries that cause trauma mortality occur in predictable patterns based on the mechanism of injury, patient’s age, sex, body habitus and environmental conditions. Recognition of these patterns led to the development of advanced trauma life support (ATLS) by the American College of Surgeons. The ATLS is the standard of care for these patients and is built around a standard protocol for patient evaluation. This protocol ensures that the most immediate life-threatening conditions are actively identified and addressed in the order of their risk potential. The objectives for initial evaluation of the trauma patient are: 1) To stabilize the trauma patient. 2) To identify life-threatening injuries and to initiate adequate supportive therapy. 3) To efficiently and rapidly organize either definitive therapy or transfer to a facility that provides definitive therapy. Trauma victim management: Prehospital care by emergency medical personnel Transport to hospital ATLS: Primary survey Secondary survey Tertiary survey

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Fig 1.11: Management of a trauma victim. Pre-hospital trauma care: The importance of pre-hospital trauma care is gaining a lot of importance in recent years. Pre-hospital trauma care involves first aid and Basic Trauma Life Support (BTLS) administered by emergency medical personnel. Pre-hospital care of trauma patients is situation dependent and focused on airway maintenance, control of external bleeding and immediate transport to nearby emergency trauma hospital. Emergency trauma personnel typically perform an abbreviated version of ABCDE approach. Low threshold life saving interventions can be performed by emergency personnel before transport to a hospital, these may include Placement of cervical collar( if cervical spine trauma is suspected based on mechanism of injury) Oxygen delivery through cannula or intubation( if respiratory distress or altered mental status is suspected) Administration of intravenous fluid( if hypotension or hemorrhage is suspected) Placement of pressure bandages or tourniquets for control of bleeding.

Transport to hospital: Hospital care: In the hospital setting, the treatment of patients is guided by ATLS (Advanced trauma life support). It is divided into primary, secondary and tertiary survey. Each survey consists of an algorithm designed to diagnose and manage injuries in order of decreasing severity. 

ADVANCED TRAUMA LIFE SUPPORT Organization of care: Regardless of the clinical setting, organize the care team prior to patient’s arrival. Leadership and unity of command are essential for directing a rapid and efficient workup. Ideally a resuscitation area should be available for trauma patients. Proper airway equipment (laryngoscope, endotracheal tubes) should be organized, tested and placed where it is immediately accessible. The warmed intravenous crystalloid solution should be available and should be ready as soon as the patient arrives. Trauma team: The core trauma team is the group of professionals that receives and treats the patient. This includes: Team leader Anaesthesiologist Emergency physician Nurse anesthetist General Surgeon Two nurses Orthopaedic surgeon Radiographer Initial assessment: The initial evaluation follows the protocol: 1)    Primary survey 2)    Resuscitation 3)    Secondary survey 4)    Definitive treatment or transfer to an appropriate center for definitive care. This approach is the heart of ATLS system which is designed to identify life threatening injuries and to initiate stabilizing treatment in a rapidly efficient manner.

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Primary survey with simultaneous resuscitation: The steps of the primary survey are encapsulated in a mnemonic “ABCDE” A: Airway maintenance with restriction of cervical spine motion. B: Breathing and ventilation C: Circulation with hemorrhage control D: Disability (Neurological evaluation) E: Exposure and environmental control.

Airway maintenance with restriction of cervical spine motion: The airway is the first priority. It should be assessed to ascertain patency. The rapid assessment for signs of airway obstruction should include inspection for foreign bodies and facial, mandibular, tracheal or laryngeal fractures that might result in airway obstruction. Measures to establish a patent airway should be instituted while protecting the cervical spine. Initially, chin lift or jaw thrust maneuvers are recommended to achieve this task. If the patient can communicate verbally, the airway is not likely to be in immediate jeopardy. Severe head injury patients with altered loss of consciousness or a GCS score of < 8 usually require the placement of a definitive airway. The findings of non-purposeful motor response strongly suggest the need for definitive airway management. While assessing and managing the patient’s airway great care should be taken to prevent excessive movement of cervical spine. The patient’s head and neck should not be hyperextended, hyperflexed or rotated to establish and maintain the airway. It is based on the history of trauma incident, the loss of stability of cervical spine should be suspected. Protection of the spinal cord with appropriate immobilization devices (Philadelphia collar) should be accomplished and maintained. If immobilization devices must be removed temporarily, the head and neck should be stabilized with manual in-line immobilization by one member of the trauma team. Stabilization equipment used to protect the patient’s spinal cord should be left in place until cervical spine injury is excluded. Protection of spine and spinal cord is an important management principle. Breathing and ventilation: Adequate gas exchange is required to maximize oxygenation and carbon dioxide elimination. Ventilation requires adequate function of lungs, chest wall and diaphragm. Each component must be examined and evaluated rapidly. The patient’s chest should be exposed to adequately assess chest wall excursion. Auscultation should be performed to assure gas flow to the lungs. Percussion may demonstrate the presence of air or blood in the chest. Visual inspection and palpation may detect injuries to the chest wall that may compromise ventilation. Injuries that may acutely impair breathing are: 1)    Tension pneumothorax 2)    Flail chest with pulmonary contusion 3)    Massive haemothorax 4)    Open pneumothorax. These injuries should be identified in the primary survey. Circulation with Haemorrhage control: Hemorrhage is the predominant cause of post-injury deaths that are preventable by rapid treatment in the hospital setting. Hypotension following traumatic injury should be considered to be hemorrhagic in origin in predominant cases. Rapid and accurate assessment of the injured patient’s hemodynamic status is therefore essential. The elements of clinical observation that yield important information within seconds are: 1. Level of consciousness 2. Skin perfusion 3. Pulse External hemorrhage is identified and controlled in the primary survey. Rapid, external blood loss is managed by direct manual pressure on the wound. Pneumatic splinting devices may also help control hemorrhage. Tourniquets should not be used because they crush tissues and cause distal ischemia. Hemorrhage into the thoracic or abdominal cavities, soft tissue bleeding around major long bone fracture, bleeding into the retroperitoneal space from pelvic fracture or penetrating injuries are major source of occult blood loss.

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Disability (Neurologic evaluation): A brief neurologic evaluation is performed at the end of the primary survey. This establishes the patient’s level of consciousness as well as pupillary size and reaction. A simple mnemonic to describe the level of consciousness is the AVPU method.

A Alert V Responds to vocal stimuli P Responds only to painful stimuli U Unresponsive to all stimuli. The Glasgow coma scale (GCS) is a more detailed neurologic evaluation that is quick, simple and predictive of patient outcome. This should be performed as a part of more detailed secondary survey. If hypoxia and hypovolemia are excluded, then changes in level of consciousness should be considered to be of traumatic central nervous system until proven otherwise. Exposure/Environmental control: The final step in the primary survey includes patient exposure and control of immediate environment. The patient should be completely undressed usually by cutting the clothes to facilitate thorough examination and assessment. After the patient’s clothing is removed, it is imperative to cover the patient with warm blankets or an external warming device to prevent hypothermia. Intravenous fluids should be warmed before infusion and warm environment should be maintained.

Resuscitation: Aggressive simultaneous resuscitation and management of life-threatening injuries as they are identified are essential to maximize patient survival. A)   The airway should be protected in all patients and secured when the potential for airway compromise exists. A nasopharyngeal airway may initially establish and maintain airway patency in the conscious patient. If the patient is unconscious and has no gag reflex, an oropharyngeal airway may be helpful temporarily. A definitive airway should be established if there is any doubt about the patient’s ability to maintain airway integrity. Definitive control of the airway should be accomplished with continuous protection of the cervical spine. A surgical airway should be performed if oral or nasal intubation is contraindicated or cannot be accomplished. B)    A tension pneumothorax compromises ventilation and circulation dramatically and acutely, if suspected chest decompression should be accomplished immediately. Every injured patient should receive supplemental oxygen. If not intubated the patient should have oxygen delivered by mask/reservoir device to achieve optimal oxygenation. C)   Control bleeding by direct pressure or operative intervention. A minimum of two large caliber intra-venous catheters should be established. The maximum rate of fluid administration is determined by the internal diameter of catheter. When establishing the intravenous line, blood should be drawn for type, crossmatch and baseline hematological conditions. Intravenous fluid therapy should be initiated with a balanced salt solution. Ringer lactate solution is preferred as initial crystalloid solution and should be administered rapidly. Such bolus intravenous therapy may require the administration of two to three liters of solution to achieve an appropriate response in adult patient. All intravenous solution should be warmed. The shock state associated with trauma is most often hypovolemic in origin. If the patient remains unresponsive to bolus intravenous therapy, type specific blood may be administered. Hypovolemic shock should not be treated by vasopressors, steroids or sodium bicarbonate by continued fluid infusions. If blood loss continues it should be controlled by operative intervention. The endpoints of resuscitation are: 1. 2. 3. 4.

Normalization of vital signs Absence of blood loss Adequate urine output(0.5-1 ml/kg/hr) No evidence of end-organ dysfunction.

Adjuncts of Primary survey: 1)    ECG monitoring: Unexplained tachycardia, PVC’s, AF and ST segment changes indicate blunt cardiac injury. Pulseless electrical activity or electromechanical dissociation indicates cardiac

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tamponade, tension pneumothorax, and/or severe hypovolemia. Bradycardia, aberrant conduction and premature beats indicate hypoxia, hypoperfusion or hypothermia. 2)    X-rays and diagnostic studies: X-ray should be used judiciously and should not delay patient’s resuscitation. AP chest film and AP pelvis may provide information that can guide resuscitation efforts of the patient with blunt trauma. A lateral cervical spine X-ray that demonstrates injury is an important finding whereas a negative film does not exclude a cervical spine injury. 3)   Focussed Abdominal Sonogram for Trauma (FAST) and Diagnostic Peritoneal Lavage (DPL): These are useful tools for the quick detection of occult intra-abdominal bleeding. 4)    Urinary output: It is a sensitive indicator of the volume status of the patient and reflects renal perfusion. Monitoring of urinary output is best accomplished by insertion of indwelling bladder catheter. Transurethral bladder catheterization is contraindicated in patients in whom urethral transaction is suspected. Urethral injury should be suspected if there is: a)    Blood at penile meatus b)    Perianal ecchymosis c)     Blood in the scrotum d)    A high-riding prostate or non-palpable prostate e)    A pelvic fracture

Fig 1.12: Adjuncts of primary survey Monitoring:

Ventilatory rate and arterial blood gas should be used to monitor the adequacy of respirations. Pulse oximetry to measure the oxygen saturation Blood pressure monitoring.

Secondary survey: The secondary survey does not begin until the primary survey (ABCDE) is completed, resuscitative efforts are well established and the patient is demonstrating normalization of vital functions. The secondary survey is head to toe evaluation of trauma patient with complete history and a physical examination of all major systems is done. During this evaluation, the indicated X-rays are obtained. Specific radiological evaluation and laboratory studies are also obtained at this time. Patient transfer: During the primary survey and resuscitation phase, the evaluating doctor frequently has enough information to indicate the need for transfer of the patient to another facility. Once the decision to transfer is made, referring doctor to receiving doctor communication is essential before the transfer.

Tertiary survey: Once the patient reaches definitive care, the tertiary survey is performed to ensure all the injuries are identified and none have been overlooked.

TRIAGE Triage is the sorting of patients based on the need for treatment and the available resources to provide the treatment. Treatment is rendered based on ABC priorities. The objective of triage is to prioritize patients with a high likelihood of early clinical deterioration and transport patients to trauma center.

The triage of trauma patients considers: 1. 2. 3. 4.

Vital signs Mechanism of injury Patient’s age Comorbid conditions.

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Fig 1.13: Triage categories. Multiple causalities: The number of patients and the severity of their injuries does not exceed the ability of the facility to render care. In this situation, patients with life-threatening problems and those sustaining multiple system injuries are treated first. Mass causalities: The number of patients and the severity of their injuries exceed the capability of the facility and staff. In this situation, those patients with a greater chance of survival with least expenditure of time, equipment, supplies and personnel are managed first.

Questions: Long Essay: 1)     Advance trauma life support (ATLS) concept.

Short Essay: 1) Define triage and its management in polytrauma.

Competency OR 1.2:  Describe and discuss the aetiopathogenesis, clinical features, investigations and principles of management of shock.

Shock is defined as failure of the circulatory system to maintain adequate tissue perfusion, which initially leads to reversible cellular injury and if prolonged, to irreversible cellular injury. The first step in managing shock in trauma patients is to recognize its presence. Diagnosing shock in trauma patients relies on clinical evaluation and laboratory tests. The second step in the management of shock is to identify the probable cause of shock and initiate the treatment accordingly. Normal circulatory homeostasis: It is important to understand the mechanism by which arterial blood pressure is maintained in the body. The blood pressure depends on a)    Cardiac output b)    Peripheral resistance The cardiac output is defined as the volume of blood pumped by the heart per minute. It is the product of heart rate and stroke volume. The peripheral resistance is the systemic vascular resistance which is directly proportional to vessel length, viscosity and inversely proportional to the fourth power of radius of the vessel.

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Blood loss pathophysiology: A normal individual can compensate for loss of about 10% of total blood volume. However if blood loss is more, compensatory mechanisms are initiated. Depleting blood volume results in baroreceptor activation resulting in sympathetic nervous system activation and peripheral vasoconstriction. Due to sympathetic nervous activation, blood is diverted away from noncritical organs and tissues to preserve blood supply to vital organs like heart, brain and liver. The release of endogenous catecholamines also increases peripheral vascular resistance which in turn increases the diastolic blood pressure and reduces pulse pressure. At the cellular level, inadequately perfused and poorly oxygenated cells are deprived of essential substrates for normal aerobic metabolism and shift to anaerobic metabolism. This results in the formation of lactic acid and development of metabolic acidosis. If shock is prolonged it leads to subsequent end-organ damage and may result in multiple organ dysfunction.

Classification: A)   Hemorrhagic shock B) Non- hemorrhagic shock: 1) Cardiogenic shock 2) Cardiac tamponade 3) Tension pneumothorax 4) Neurogenic shock 5) Septic shock

HEMORRHAGIC SHOCK Hemorrhagic shock is defined as acute loss of circulating blood volume resulting in reduction of tissue perfusion below that is necessary to meet metabolic needs. A healthy normal 70 kg adult male has a circulating blood volume of approximately 5 liters. Physiological classification of hemorrhage: The physiological effects of hemorrhage are divided into four classes based on clinical signs, which help in estimating the percentage of acute blood loss.  Evaluation: The first step in managing hemorrhagic shock is recognition. The patient presents with cold and moist skin, collapse of superficial veins, thirst, air hunger and altered mental status. Rapid and weak pulse, blood pressure, heart rate, respiratory rate and delayed capillary refill are the signs. These signs are dependent on the amount of blood loss. In setting of trauma, an algorithmic approach via primary and secondary survey should be done. Physical examination, radiological evaluation and focussed assessment with sonography for trauma (FAST) are done to rule out intra-abdominal pathology.

Class I hemorrhage Class II hemorrhage Class III hemorrhage

Volume loss upto 15% of total blood volume, approximately 750 ml. Heart rate is Typically there is no change in blood pressure, pulse pressure or respiratory rate Volume loss from 15% to 30% of total blood volume from 750 ml to 1500 ml. Hea elevated. Pulse pressure begins to narrow, but systemic blood pressure may be Volume loss from 30-40% of total blood volume from 1500 to 2000 ml. A significa changes in mental status occurs. Heart rate and respiratory rate are significantly elevated refill time is delayed.

Class IV hemorrhage

Volume loss of over 40% of total blood volume. Hypotension with narrow pulse p pronounced and mental status becomes increasingly altered. Urine output is min delayed

Investigations: Chest X-ray, pelvis X-ray, ECG, measurement of central venous pressure, FAST scan, Diagnostic Peritoneal Lavage (DPL).  Blood investigations: Haematocrit, blood grouping and cross matching, coagulation profile, arterial blood gas analysis, serum lactate levels.

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Principles of management: The steps of management are 1. Vascular access and resuscitation of the patient with correct fluid replacement 2. Search for causative factors and treat them if possible. The guidelines for treatment of this condition are: Two large-bore IV cannulas are inserted and IV fluid infusion is initiated. The rate of fluid infusion depends on the severity of shock. The initial fluid of choice is crystalloids. Usually, upto one to two liters of fluid infusion will resuscitate most patients in whom hemorrhage has been arrested. Incomplete resuscitation indicates continued bleeding and probably need for operative control of hemorrhage. Based on patterns of fluid response, the patients are classified into rapid response, transient response and minimal or no response patients. a)    Rapid response: The patients in this group have typically minimal (40% of blood volume. Surgical and ICU care, massive transfusions are essential for patient care. Blood replacement: Blood is drawn for grouping and cross-matching as mentioned above. Blood should be ready for transfusion when required. The decision to initiate blood transfusion is based on the patient’s response. Patients who are transient responders or non-responders require packed RBC transfusion, plasma and platelets during the process of resuscitation. The main purpose of transfusion is to restore oxygen carrying capacity by RBC’s to periphery. Blood banks usually take about an hour to issue fully cross matched packed RBC’s. In severe exsanguinating hemorrhage, uncrossed matched O-negative blood transfusion can be done. The final goal of resuscitation is to restore organ perfusion and tissue oxygenation. This state is identified by appropriate urinary output, CNS status, skin color, return of pulse and blood pressure towards normal.  The volume of urinary output is a reasonably sensitive indicator for renal perfusion. The target goal for resuscitation is to maintain a urinary output of 0.5 ml/kg/hr in adults and 1 ml/kg/hr in pediatric patients. Massive transfusion: Massive transfusion is defined as a transfusion of >10 units of pRBCs within the first 24 hours of admission or more than 4 units in 1 hour. Simultaneous control of hemorrhage with early administration of pRBCs, plasma and platelets in massive bleeding patients helps to improve patient survival and minimize excessive crystalloid administration. This approach has been termed as “balanced”, “hemostatic” or “damage control” resuscitation.

NON- HEMORRHAGIC SHOCK 1)   Cardiogenic shock This is a condition in which heart is unable to maintain an adequate cardiac output for optimal tissue perfusion. The intravascular volume is normal but the patient becomes hypotensive due to myocardial infarction. Treatment for this condition includes oxygen support, use of inotropes like dobutamine, dopamine and may need mechanical support in severe conditions.

2) Cardiac tamponade Haemopericardium prevents diastolic filling of the heart. This results in hypotension, venous distension and muffled heart sounds classically called Beck’s triad. Chest X-ray shows globular heart. In stable patients, diagnosis can be confirmed by ECG and pericardiocentesis. Unstable patients are treated by urgent thoracotomy. 

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3) Tension pneumothorax In tension pneumothorax, the air continues to leak from an underlying pulmonary parenchymal injury resulting in increase in pressure within the affected hemithorax. The patient presents with respiratory distress, absent breath sounds and hyper resonant note in the hemithorax. The trachea is deviated away from the side of injury. Immediate therapy for this life threatening condition includes decompression of affected hemithorax by needle thoracostomy. A large bore needle (14-16 gauge) is inserted through the second intercostal space in the midclavicular line. A tube thoracostomy is then performed. 4) Neurogenic shock: This shock is characterized by loss of vasomotor control due to conditions like spinal cord injury and high spinal anesthesia. The clinical picture is of low blood pressure with a slow pulse rate. The blood volume is normal but due to loss of vasomotor tone, there is increased capacity of the arterioles and the venules. This results in a reduction of venous return to the heart leading to reduced cardiac output. Treatment is initially by giving IV fluids and if no response, then a vasopressor agent is administered. 

5) Septic shock It results from acute invasion of the bloodstream by microorganisms or their toxic products. The release of various toxins stimulates neutrophils, monocytes, macrophages and endothelial cells resulting in the release of cytokines, platelet-activating factors, complements resulting in myocardial depression and hypotension. In severe cases, it can lead to sepsis and multiorgan failure. Questions: Long Essay: 1)     Define shock and classify different types of hemorrhagic shock.

Short Essay: 1)    Non-hemorrhagic shock.

Competency OR 1.3: Describe and discuss the aetiopathogenesis, clinical features, investigations, and principles of management of soft tissue injuries. Soft tissue injuries refer to injury to any part of the body like skin, subcutaneous tissue, muscles, nerves, vessels other than bone and joints. Soft tissue injuries commonly present to emergency department and the injuries range from simple sprains to substantial ligamentous or musculotendinous ruptures leading to joint instability. To manage musculoskeletal injuries good knowledge of soft tissue anatomy and mechanism leading to the injury is essential. Early diagnosis and treatment are essential to prevent long-term implications of soft tissue injuries. Anatomy: A) The Skin is the largest organ of the body and is composed of two primary layers: 1)    Epidermis 2)    Dermis B) The hypodermis consists of fat, blood vessels and connective tissue. C) The muscle lies beneath the deep fascia. It has high metabolic demand and is relatively intolerant to ischemia. Classification: Closed wounds The overlying skin is intact with underlying soft tissue damage like contusion, hematoma, compartment syndrome etc.

Open wounds There is a breach in skin surface like laceration, avulsion, crush injury etc.

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Mechanism of injury: Direct injury: Road traffic accidents, domestic and work site accidents, assualt lead to direct soft tissue injury. Indirect injury: Avulsion injuries, ligament sprains and muscle injuries are commonly seen in sports injuries.

Fig 1.14: Injury management.

Closed injury: A)   Contusion: It is a closed injury to the subcutaneous tissue and small blood vessels caused by a blunt force such as a kick or fall resulting in pain, swelling, bleeding and discoloration. B)   Hematoma: It is the blood collection within the damaged tissue. Open injury: A)   Abrasion: Abrasion is a superficial breach in epithelial tissue with minor capillary bleeding. B)   Laceration: Laceration is an irregular tear in the skin and soft tissue structures. It may result in profuse bleeding and is often associated with a high risk of infection because of soft tissue contamination.

Fig 1.15: Lacerated wound C)   Incision: It is clean cut from sharp edges like broken glass. It may be associated with profuse bleeding. D)   Avulsion: Forceful tearing and partial detachment of full thickness of skin.

Fig 1.16: Avulsion injury E)   Crush injury: The injury caused by direct physical crushing of the muscles due to heavy force. They are usually caused due to run over by vehicle or industrial accidents.

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Fig 1.17: Crush injury of the forearm. Factors affecting soft tissue healing: Systemic factors •       Age •       Obesity •       Malnutrition •       Stress, smoking •       Drugs- Corticosteroids, cytotoxic drugs. •       Inflammatory arthritis like rheumatoid arthritis, SLE •       Metabolic diseases like gout and uremia.

Local factors •       Poor blood supply •       Extent of injury •       Edema •       Hematoma •       Local infection

Clinical features: Symptoms: Documentation of the patient’s symptoms is important and may provide clues to specific Injuries. The patient may complain of severe pain when he has an underlying fracture, foreign body or evolving compartment syndrome. Any loss of sensation, paraesthesia and bleeding may represent neurovascular injury. Signs: The patient should be examined for wound location, size and depth, adjacent swelling, neurovascular status and any bony deformity. Investigations: 1)    X-ray is done to rule out any foreign body or underlying fractures 2)    Local USG, CT and MRI are indicated on suspicion of neurovascular injuries.

STRAIN An injury to a muscle or tendon is called strain. Skeletal muscle fibers and fasciculi are freely perfused by a well-organized capillary system. Depending on torn muscle fibers, it can lead to bleeding varying from mild capillary ooze to formation of blood swelling called the hematoma. Mechanism of injury: a)    Direct trauma b)    Indirect trauma due to overstretching of muscles in sports persons. The muscles commonly ruptured are biceps brachii, supraspinatus, quadriceps etc. c)     Sudden or abrupt movements leading to muscle tear. Types: 1) First degree- Low-grade inflammatory response with no appreciable muscle tear. 2) Second degree- Partial tear of the muscle. 3) Third degree- Complete tear of the muscle.

Fig 1.18: Muscle strain. Clinical features: Symptoms: 1) Localised pain and muscle spasm 2) Diffuse bleed leading to swelling 3) A snapping sound may be heard by the patient in a complete tear. Signs: 1) Tenderness over affected muscles 2) A palpable gap between the muscles is felt. 3) Severe loss of function.

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Investigations: 1) X rays- X ray is done to rule out any bony injury. 2) Ultrasound and MRI scan to identify tear dimensions and to classify partial or complete muscular tear.  Treatment: A)   Immediate: RICE regimen a)    Rest by splint immobilization b)    Ice pack application c)     Compression bandage d)    Limb elevation B) Follow up: a) Incomplete muscle tears: Gentle Muscle stretching exercises Partial weight-bearing crutch walking can be started and slowly shifted to full weight-bearing. b) Complete muscle tear: Surgical muscle repair

SPRAIN A tear or injury of capsular ligament is called a sprain. Capsular ligaments are external covering of the joint and are made up of thick fibrous tissue binding the adjacent bones. The capsule may get thickened at specific locations to form ligaments and are attached to specific bony points or surfaces. These ligaments help in joint movements and maintain the limb in anatomical position. Ligament injuries are associated with bleeding as well as profuse effusion into joints. Sometimes the ligament can get detached from the place of bony attachment or the bony place of attachment may get fractured. This is called an avulsion fracture. The fibers of ligaments can give way leading to partial or total rupture of the ligament. It is graded into Grade 1: Few ligament fibers get affected or damaged. Grade 2: Partial tear of the ligament Grade 3: Complete tear of the ligament.

Fig 1.19: Ligament injury: A) Grade 1; B) Grade 2; C) Grade 3. Most common ligament injury at the knee and ankle: Knee joint 1)    Injuries to collateral ligaments: a)    Medial collateral ligament injury b)    Lateral collateral ligament injury 2)    Injury to cruciate ligament: a)    Anterior cruciate ligament b)    Posterior cruciate ligament

Ankle joint 1)Lateral ligament injuries: a) Anterior talofibular ligament b) Middle calcaneofibular     ligament c) Posterior talofibular ligament 2)Medial ligament injury: a) Deltoid ligament

Investigations: 1) X-ray AP/lateral view of the joint to exclude hairline or avulsion fracture. A stress radiograph can be taken to visualize joint surface widening. 2) Local USG and MRI evaluation to assess ligamentous tear. Grade 1 sprain: The patient presents with slight pain and loss of function. On examination, there may be mild swelling, tenderness at local site and ligament stretch test will be positive. Treatment: Immediate treatment:

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•            RICE regimen: (Rest, Ice pack application, Compression with pressure bandage, Elevation to prevent swelling). Follow up: •       Begin isometric exercises of the affected muscles •       Weight bearing may be permitted Grade 2 sprain: Partial tear of the ligament. This occurs following a moderate injury. The patient presents with pain, acute swelling, bruising, limp and restriction of movements. On examination localized acute tenderness is present and stretch test is positive. Treatment: Immediate: RICE regimen Follow up: Isometric strengthening exercises. Partial weight bearing with walker and later on followed by weight bearing as permitted. Grade 3: Complete tear of the ligament. This injury occurs following severe violence. The patient presents with severe pain, gross swelling, inability to bear weight and complete loss of function. On examination localized acute tenderness is present and joint is unstable on stretch test. Treatment: Immediate: A)   Conservative management: •       RICE regimen: (Rest, Ice pack application, Compression with pressure bandage, Elevation to prevent swelling). •       POP cast for 6 to 8 weeks if there is an undisplaced complete ligament tear. B) Operative management: If the ligament is torn and displaced, surgical repair is done and protected with POP cast for 6 to 8 weeks. Strict non-weight bearing is followed for 6 to 8 weeks. Follow up: Isometric strengthening exercises. Partial weight bearing with a walker and later on followed by weight bearing as permitted.

TENDON INJURIES Tendons are tough elastic structure that attaches muscle to bone. Mechanism of injury: 1)    Trauma- sharp cutting injuries, crush injuries 2)    Repeated undue stress may lead to sudden snapping. These injuries may lead to partial or complete rupture of a tendon. Clinical features: The patient presents with severe loss of function in affected fingers and toes. On examination there may be a neglected or missed tendon tear overlying healed scar, a palpable gap may be present representing a complete tear. Investigations: X-ray is done to rule out any bony injury. Ultrasound and MRI scan to identify tear dimensions and to classify partial or complete muscular tears.  Treatment: Partial or complete tendon tear is repaired using non-absorbable monofilament sutures by modified Kessler’s technique.

TENOSYNOVITIS It is the inflammation of the tendon and its respective synovial sheath. Causes:

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1) Irritative: This is due to excessive friction or overuse. These include trigger finger, trigger thumb, de quervain tenosynovitis. 2) Infective: Pyogenic infection, chronic infection like tuberculosis. Treatment: 1)    Irritative A)Early stage: a) Rest with an appropriate splint b) Anti-inflammatory and analgesics

2)    Infective: A) Appropriate antibiotics B) Anti-inflammatory and analgesics.

B)Intermediate stage: a)    Local intra-lesional steroid injection C)Late stages: a)    Surgical excision

SYNOVIAL INJURIES The synovial membrane is a specialized connective soft tissue membrane that lines the capsule of the joint and tendon sheath. It secretes synovial fluid which lubricates articular cartilage and provides nourishment through diffusion. Inflammation of the synovial membrane is called synovitis. It is of two types A)   Acute synovitis: Trauma B)   Chronic synovitis: Inflammatory diseases like rheumatoid arthritis, gout, hemophilic synovitis and infective condition like tuberculosis. Pathophysiology: In chronic synovitis, the hypertrophied synovium (pannus) extends over the articular cartilage, bone and ligaments leading to joint destruction. Clinical features: The patient presents with joint pain, swelling and difficulty in the terminal range of movements. On examination, there is joint effusion and synovial membrane is tender on palpation. Fluid in the joint can be elicited clinically. The joint will assume the flexion attitude to accommodate the excess fluid. The progression of synovitis with ongoing inflammation leads to chronic synovitis. Chronic synovitis is associated with significant joint swelling, muscle atrophy and joint deformities. Investigations: 1)X-ray 2)MRI evaluation 3)Blood investigations-CBC with ESR, CRP, Serum uric acid, RA factor, Anti CCP 4)Synovial fluid aspiration and examination, synovial biopsy. Treatment: Acute synovitis: Early: A)   RICE regimen Rest Ice pack application Compression Elevation of limb B)   Isometric contraction of affected muscles. C)   Analgesics and Splinting

If swelling persists. Follow up(>48 hours) A)   Synovial fluid aspiration and analysis. B)   Isometric exercises C)   Partial weight bearing D)   Thermotherapy: ultrasound, TENS, Short wave diathermy (SWD).

Chronic synovitis: A)   Treatment of underlying disease condition. B)   Isometric exercises of the affected muscles. C)   Passive and assisted active range of motion exercises. D)   Synovial fluid aspiration and surgical/arthroscopic synovectomy.

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OVERUSE SOFT TISSUE INJURIES 1)   a) Tendinitis: Inflammation of tendon or its sheath because of repetitive microtrauma. b)    Tendinosis: It is defined as chronic degeneration of the tendon in response to overuse. It is more serious condition and difficult to treat. 2)   Bursitis: Inflammation of a bursa. Joint Tendinitis and Tendinosis Shoulder Rotator cuff tendinopathy Biceps tendinosis Elbow

Knee

Ankle

Bursitis Subacromial bursitis

Medial epicondylitis(Golfer’s elbow) Lateral epicondylitis(Tennis elbow)

Olecranon bursitis

Patellar tendinitis Iliotibial band syndrome

Prepatellar bursitis Infrapatellar bursitis

Achilles tendinopathy

Retrocalcaneal bursitis

Common overuse soft tissue injuries.

1) Tendinitis: It is inflammation of tendon or its sheath because of repetitive microtrauma. Types: A)Achilles tendinitis B)Supraspinatus tendinitis C)Tennis elbow D)Wrist tendinitis Causes: a) Repetitive exercises in sports like basketball players, swimmers, tennis players and golfers. b) Prior injury c) Lack of conditioning Symptoms: Pain, swelling over the affected tendon which worsens with activity, occasionally catching and grating sensation. Diagnosis: X-ray Local USG and MRI Treatment: a)RICE regimen b)Anti-inflammatory medication to decrease pain and swelling c)Splinting d)Shockwave therapy stimulates the release of growth factors. Platelet-rich plasma injections for tissue regrowth and healing. e)Surgery is indicated rarely.

2) Bursitis: Bursae are the thin membranous sac lined by a synovial membrane containing lubricating fluid. They are positioned between bone and soft tissues acting as cushions to help reduce friction. Due to repeated irritation or infection, there is inflammation of the sac leading to bursitis. Causes: a)Trauma b) Irritative bursitis is excessive pressure or friction eg: student’s elbow. c) Inflammatory causes: Rheumatoid arthritis, gout

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d)Infective causes: acute or chronic infection Common Sites: Upper limb a)    Subacromial bursitis b)    Olecranon bursitis- student’s elbow

Lower limb a)    Trochanteric bursitis b)    Prepatellar bursitis- House maid’s knee c)     Infrapatellar bursitis- Clergyman’s knee

Clinical features: The patient presents with swelling over the affected area sometimes associated with pain if infected or ruptured. On examination, there is fluid filled fluctuant sac. If infected, it is tender on palpation and associated with restriction of movements. Investigations: X-ray Local ultrasound and MRI evaluation. Treatment: A)   Acute bursitis 1)    Acute irritative bursitis: a)    Rest b)    Cryotherapy c)     Analgesics d)    Isometric muscle strengthening exercises. 2)    Acute infective bursitis: a)    Rest b)    Analgesics and antibiotics. B)   Chronic bursitis a)    Surgical excision of the bursa b)    Appropriate splints and padding. Common soft tissue injuries: Upper limb: Shoulder: a)    Rotator cuff injuries b)    Supraspinatus tendinitis c)     Labrum tear d)    Tendinitis of the long head of biceps

Lower limb: Hip: a)    Piriformis syndrome b)    Gluteal bursitis c)     Trochanteric bursitis

Elbow: a)    Tennis elbow b)    Golfers elbow c)     Student’s elbow

Knee: a)    Medial and lateral collateral ligament injury b)    ACL injury c)     PCL injury d)    Meniscal injury e)    Patellar tendinitis f)      Hamstring strain

Wrist: a)    Carpal tunnel syndrome b)    De Quervain’s tenosynovitis c)     Ganglion

Ankle and foot: a)    Ankle sprain b)    Achilles tendinitis c)     Plantar fascitis

PRINCIPLES OF MANAGEMENT OF SOFT TISSUE INJURIES Early management: 1)    Effective control of bleeding 2)    Relieve pain 3)    Minimizing tissue reaction to injury, especially the inflammatory swelling 4)    Positional facilitation 5)    Care of associated damage, if any other structures. Later management: 1)    Promoting the drainage of inflammation

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2)    Preservation of strength in non-injured segments and promotion of strength in the injured area 3)    Early joint mobilization 4)    Protective padding support or use of specific safety aids Complications: 1)    Infection 2) Delayed wound healing 3) Abnormal scar formation Questions: Short Essays: 1)    Sprain 2)    Strain 3)    Overuse soft tissue injuries.

ALGORITHMIC APPROACH TO VASCULAR INJURY:

Competency OR 1.4: Describe and discuss the Principles of management of soft tissue injuries.

PRINCIPLES IN MANAGEMENT OF SOFT TISSUE INJURIES The physician assisted by a physiotherapist plays a vital role in the curative treatment and rehabilitation process of soft tissue injuries. Most soft tissue injuries heal in one to six weeks. The length of time depends on age, general health and severity of soft tissue injury. Early and efficient treatment is essential for the reduction of disability in soft tissue injuries. The general principle for management of soft tissue injuries has been discussed below: Early management: 1)      Effective control of bleeding- This is successfully achieved by ice pack application in closed injuries. In open injuries, this is achieved by hemostasis, compression and limb elevation.

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2)    Relieving pain- Cold compression numbs the overlying painful nerve endings. Limb elevation, rest and analgesics help to relieve the pain early. 3)      Minimising the reaction to injury, especially the inflammatory edema- Cold compression causes vasoconstriction of the capillary bed and reduces the inflammatory exudate. Rest, limb elevation and anti-inflammatory medications also aid in the effective control of inflammatory edema. 4)      Positional facilitation- Resting the affected region with splint avoids movements resulting in reduction of circulatory demands which prevents swelling. 5)    Care of associated damage, if any other structures- Proper evaluation should be done to evaluate if there is any associated nerve, artery or soft tissue damage. Later management: Once the acute pain subsides and swelling is reduced, the second stage of hastening the repair by bringing the injured part to normal function is achieved by following principles: 1)    Promoting the drainage of inflammatory mediators: Application of thermotherapeutic measures like hot packs, short wave diathermy, infrared ray therapy, local ultrasound are used to drain away the inflammatory mediators away from the injured area. 2)      Promotion of strength in injured area and preservation of strength in non-injured segments: Early specific exercises are designed to strengthen the muscles depending on the grade of soft tissue injury. This helps muscles to regain adequate strength and maintain muscle balance. Muscle exercises are also encouraged into non-injured segments to preserve their strength. 3)      Early joint mobilization and progressive improvement in range of motion: Gentle manipulation for range of motion and promoting progressive passive to assisted active and then active range of motion will help regain full range of motion. 4)      Protective padding support or use of specific safety aids: Soft tissue injury heals rapidly with splinting but use of protective padding or support is essential in games and sports to prevent the recurrence of injury.

“RICE” and “no HARM” protocol for acute soft tissue Injuries: The initial treatment for acute soft tissue injuries is based on the principle of RICE and No HARM protocol. These are most important in first 48-72 hours of injury as it speeds up the recovery. “RICE” protocol: A)    Rest: Rest for 24-48 hours of injury is essential. Depending on the injury, use of a splint with crutches or sling help in decreasing pain and swelling B)   Ice: Wrap the ice pack in a towel and apply gently over the affected area for 15-20 minutes every 2-3 hours. Do not apply ice directly over the skin as it can lead to frostbite. C)   Compression: This involves wrapping the affected area with a compression bandage. The bandage should be wrapped firmly so that it does not restrict circulation or cause additional pain. If any fingers or toes turn blue (cyanotic) after application, the bandage should be removed immediately. D)    Elevation: This involves getting the injured extremity higher than heart level so it aids in drainage through gravity. The upper limb is elevated with the use of sling support and if there is lower limb injury, it is elevated with pillows while sleeping and stool while sitting. “No HARM” Protocol: A)   Heat: Avoid heat as it increases blood flow and circulation. B)    Alcohol: Alcohol increases blood flow and swelling. It can also make a person less aware of aggravating injury. C)   Running: Running or activities should be avoided as it leads to delayed healing. D)   Massage: Massage has to be avoided as it promotes blood flow and swelling. Management during later stages of soft tissue healing: Once the acute stage weans off, the patient is encouraged for no/partial weight bearing depending on the grade of injury. The patient should slowly resume his activities without compromising on the soft tissue healing process. The patient is encouraged to bear weight optimally without exacerbating pain which promotes repair, remodeling and builds tissue tolerance. Early specific exercises help surrounding muscles to restore strength, proprioception and mobility.

MANAGEMENT OF CHRONIC OVERUSE SOFT TISSUE INJURIES (TENDINITIS AND BURSITIS) The diagnosis and management of overuse injuries require a multidisciplinary approach as it results from repetitive microtrauma that leads to inflammation and local soft tissue damage in the form of cellular and extracellular degeneration. This includes a team of physician, physiotherapist, athletic trainers and coaches to correct the pathoanatomy and rehabilitation. These include

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1)    Inflammatory control:  RICE regimen, anti-inflammatory medications. 2)    Control abuse: Resting from repetitive activities and treating the underlying dysfunction. The treating team should identify, reinforce and remind the patient of necessary changes and if necessary splinting for support should be given. 3)      Promote soft tissue healing: Intralesional corticosteroid injections to decrease inflammation and autologous PRP injections for soft tissue healing are also used. Sometimes surgery is necessary to repair the damaged area. 4)      Increasing fitness: The patient should consult the treating team for musculoskeletal rehabilitation. Sports-specific rehabilitative exercises in athletes and general body conditioning help to restore strength and endurance. These generally help athletes to restore their previous level of function.

PREVENTION OF SOFT TISSUE INJURIES Injuries in the sports field are increasing with popularization of sports like running, volleyball, football, basketball, kabaddi etc. These injuries necessarily occur in otherwise healthy young adults. Prevention of sports injuries is an important aspect of sports and fitness training.

Few steps to prevent soft tissue injuries include: 1)    Balanced fitness 2)    Perform proper warm-up and cool-down routines before and after sports activities. 3)    Consistently incorporate strength training for muscles and stretching for flexibility. 4)    Healthy well-balanced diet to keep muscles strong 5)    Ensuring proper fitting shoes and wear gear that protects, fits well and is ideal for sport. 6)    Avoiding repetitive activities whenever possible that cause pain. Question: Short Essay: 1)    Principles of management in soft tissue injuries.

Competency OR 1.5: Describe and discuss the aetiopathogenesis, clinical features, investigations, and principles of management of dislocation of major joints shoulder, knee, hip.

DISLOCATION OF SHOULDER The shoulder joint is a ball and socket joint. Shoulder function is a compromise between excessive mobility and little stability hence commonly known as “mobility at the cost of stability”. When the head of humerus loses its articulation with the glenoid cavity of the scapula, a dislocation of the shoulder occurs. It is the most common joint to dislocate. Types: 1)    Anterior dislocation a)    Subcoracoid b)    Subgleniod c)     Subclavicular 2)    Posterior dislocation 3)    Inferior dislocation

Anterior dislocation: Anterior dislocation (98%) is more common than posterior dislocation (2%). It is common in sports like javelin & short put players, road traffic accidents. Shoulder abduction and external rotation movement beyond normal physiological limits cause an acute tear of the anteroinferior aspect of glenoid labrum called the Bankart lesion and thus the head of humerus comes to lie in front of scapular neck in the pouch thereby created. This may also result in depression of the humeral head in the posterolateral

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quadrant called the Hill- Sach’s lesion caused by impingement of the anterior edge of gleniod as it dislocates.

Fig 1.20: (A) Normal shoulder: a) Anterior capsule, b) Anterior glenoid labrum, c) Humeral head, d) Posterior glenoid labrum, e) Posterior capsule. (B) Bankart lesion: head of humerus dislocated anteriorly, causing avulsion of the labrum and capsule. i) Labrum avulsion; g) Anterior capsular tear; h) Hill Sachs lesion.

Fig 1.21: A) Normal shoulder; Anterior dislocation Types: a) Subgleniod; b) Subcoracoid; c) Subclavicular.

Clinical features: The patient presents with severe shoulder pain and dislocated upper limb attitude in flexion, abduction and external rotation. There is a loss of all movements in the shoulder. On examination: There is loss of normal round counter of shoulder. The anterior aspect of shoulder shows fullness below the clavicle due to a displaced head and can be felt by rotating the arm. The following clinical tests are performed for confirmation of diagnosis a. Hamilton ruler test- When the head of the humerus is in the glenoid cavity, the bulging contour of the deltoid muscle prevents from placing the ruler from touching acromian and lateral epicondyle of the humerus. If the tip of the acromian may be joined to the lateral epicondyle of humerus in a straight line by a ruler, it indicates dislocated shoulder with resulting loss of prominence of humeral head.  b. Callaway’s test: Increase in vertical axillary circumference due to shoulder dislocation. c. Dugas test: Normally the patient is asked to touch the opposite shoulder. The inability to touch the opposite shoulder signifies dislocation.  d. Regiment badge anesthesia: Loss of skin sensation over the lower half of deltoid muscle may be present due to axillary nerve injury.

Fig 1.22: Clinical features of anterior shoulder dislocation X-ray: Shoulder AP view is done for diagnosis of shoulder dislocation and to ascertain if there is any fracture of glenoid, greater tuberosity or surgical neck of humerus.

Fig 1.23: Radiograph of anterior shoulder dislocation Treatment: a)    Conservative management: Treatment consists of closed reduction under sedation/general anesthesia followed by immobilization of the shoulder in the chest arm bandage for three weeks. Reduction under sedation a)    Kocher’s maneuver- This is the most commonly performed maneuver. Closed reduction is attempted under general anesthesia. The patient lies supine on the examination table. With the elbow flexed in the right angle, steady traction is given along the dislocated upper limb and counter traction is given in the axilla with the help of folded towel by an assistant. Gradually and steadily externally rotate the shoulder with the arm by the side of body. After full external rotation, the elbow is lifted in saggital plane and arm is adducted across the chest wall. The arm is then

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internally(medially) rotated initiating the reduction. The shoulder reduces with a click sound and once reduced it is immobilized with a shoulder immobilizer or chest arm bandage. Thus this method consists of four important steps mainly traction with external rotation followed by adduction and medial rotation. (mnemonic: TEAM).

Fig 1.24: Kocher’s maneuver: Traction-countertraction, arm is externally rotated and adducted followed by medial (Internal) rotation of the arm. (TEAM) b)    Hippocrates maneuver- This procedure is performed with the patient lying in supine position. The practitioner holds the affected upper limb by forearm and hand. He places his heel in the axilla of the patient in semiabuducted arm. On applying firm and steady pull with foot as fulcrum, the arm of the patient is slowly adducted. This lever backs the head of humerus into position.  

Fig 1.25: Hippocrates maneuver. c)   Stimson’s gravity method: With the patient in a prone position, the weights are applied to the wrist and thus pull of gravity helps in reduction. 2) Operative management: Rarely open reduction is indicated under general anesthesia if there is a failure of closed reduction, soft tissue interposition or associated greater tuberosity or glenoid rim fracture.   Complication: a)    The most common nerve to be injured in shoulder dislocation is axillary nerve leading to regimental badge anesthesia. b)    Recurrent shoulder dislocation. Recurrent anterior dislocation of the shoulder: If a recurrent episode of dislocation occurs following the first episode, it is called recurrent dislocation. Pathology: A) Bankart lesion is a tear in anteroinferior aspect of gleniod labrum. B) Hill Sach’s lesion is a defect in the posterolateral part of the head of humerus. Types: A)    Traumatic Unilateral Shoulder dislocation with Bankart’s needs Surgery (TUBS): It is a traumatic injury leading to recurrent shoulder dislocation because of Bankart’s lesion. Surgery is the treatment of choice. B)   Atraumatic Multidirectional Bilateral shoulder dislocation and responds well to Rehabilitation and if necessary needs inferior capsular shift (AMBRI): It is seen in generalized ligamentous laxity patients leading to bilateral recurrent shoulder dislocations and it responds well to physiotherapy exercises.  Clinical features: Recurrent shoulder dislocation is more common in young patients. These patients present with repeated episodes of dislocation following lifting heavy weights, sports activities and even sometimes in sleep. Investigations: X-ray: Stryker notch view is used to identify lesion in glenoid region of the scapula. CT scan (bony lesion): Hill-Sach’s lesion is a depression in the humeral head on the posterolateral quadrant. MRI shoulder (soft tissue lesion): Bankart’s lesion is stripping of the glenoid labrum.

Treatment: a)    Putti-Platt’s procedure: In this procedure, double breasting of the subscapularis muscle is done with tightening of shoulder capsule. 

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b)    Shoulder arthroscopy and Bankart’s repair: Arthroscopic reattachment of anteriorly detached glenoid labrum is done using suture anchors. c)     Latarjet-Bristow’s procedure: If Bankart lesion is associated with bony glenoid fracture, then coracoid osteotomy is done and the osteotomised coracoid process is fixed to neck of scapula with a screw. This acts as bony block for the head of humerus during abduction, external rotation and prevents dislocation. Posterior dislocation of shoulder:  A posterior dislocation occurs when shoulder is forcefully adducted and internally rotated following an electric shock, epileptic fit or road traffic accident. The patient presents with pain and inability to move the affected arm. The front of the shoulder looks flat with a prominent coracoid process and the limb is fixed in a position of adduction and internal rotation. X-ray of shoulder AP view normally shows overlap of atleast one-third of the humeral head over posterior glenoid. This overlap is absent in posterior dislocation and humeral head looks like a light bulb, hence it is called light-bulb sign. Treatment is closed reduction under general anesthesia. Luxatio erecta: It is the downward dislocation of the shoulder. It happens when the patient holds his hand from a falling tree. The patient presents with the arm in full abduction. Treatment is by closed reduction under general anesthesia.

DISLOCATION OF HIP The hip joint is a ball and socket joint with stability conferred by bony and ligamentous restraints. The bony spherical head of femur articulates with the acetabular cup providing inherent bony stability. The surrounding hip joint capsule is formed by thick ligamentous restraints of the iliofemoral (ligament of Bigelow), ischiofemoral and pubofemoral ligaments. The hip function is a compromise between stability and mobility, hence commonly termed as “stability at the cost of mobility”. The blood supply to femoral head originates from medial and lateral circumflex arteries which form an extracapsular vascular ring at the base of femoral neck and these branches ascend along the femoral neck to supply the cartilage of femoral head. About 10% of the femoral head is supplied by artery of ligamentum teres. Depending on the relationship of the femoral head in relation to acetabulum, they are classified into: A)   Posterior B)   Anterior C)   Central

Posterior hip dislocation: Posterior dislocation is more common than anterior dislocation. Posterior dislocation is more common during road traffic accidents when an unrestrained passenger knee hits the dashboard (dashboard injury) of a vehicle. The forceful impact on a flexed knee results in posterior hip dislocation. Other commonly associated fractures during dashboard injury are stellate fracture of the patella, femur shaft and posterior acetabular rim fracture.

Fig 1.26: Dashboard injury. Clinical features: The patient presents with severe hip pain, deformity, unable to bear weight and complete loss of hip function. On examination, the lower limb is shortened with dislocated hip attitude in flexion, adduction and internal rotation. The head of the femur is felt as a hard mass in the gluteal region and it moves along with the femur. The patient should also be examined for signs of sciatic nerve injury.

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Fig 1.27: The classic attitudes in A) Posterior B) Anterior hip dislocation. Diagnosis: X-ray of AP pelvis with both hip joint shows that the femoral head is out of the acetabulum, broken Shenton's line (imaginary semicircular line joining the medial cortex of femoral neck and the lower border of superior pubic rami) and to rule out any associated acetabular fractures.

Fig 1.21: Radiograph of posterior hip dislocation on the left side. Treatment: 1)   Conservative management: Closed reduction and manipulation under general anesthesia: Hip dislocation is an emergency and should be reduced within 6-8 hours. a)    Allis maneuver: This is the most commonly performed method. The patient is anesthetized and placed supine on the floor. The pelvis is firmly grasped by an assistant. The hip and knee is flexed to 90° by the Surgeon and he exerts the axial pull with gentle rotation. Usually hip reduces by click and once reduced it is possible to move the hip in all range of motion. The leg is kept in traction and hip abduction for 3-6 weeks followed by hip mobilization exercises.

Fig 1.28: Closed reduction of posterior hip dislocation by Allis maneuver. b)    Stimson’s gravity method: With the patient in prone position, the affected leg is hung freely off the side of the stretcher. In this position, the assistant immobilizes the pelvis and the surgeon applies inferiorly directed force on the proximal calf region aided by the pull of gravity. Gentle rotation of limb may assist in hip reduction.

Fig1.29: Stimson’s method of reduction for posterior hip dislocation. c)     Bigelow’s method 2)   Operative management:

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Rarely open reduction is indicated under general anesthesia if there is a failure of closed reduction due to intra-articular bony fragments hindering the reduction, buttonholing of femoral head through capsule or associated femoral neck fracture.   Complication: A)    Early

1)    Sciatic nerve injury (upto 10%) occurs usually in posterior hip dislocation due to its close relation to the posterior acetabular wall. The common peroneal component of the sciatic nerve is more susceptible to injury. B)   Late: 1)      Avascular necrosis of femoral head occurs due to disruption of vascular supply during the dislocation. Usually it is evident after 1-2 years after the dislocation. 2)    Post-traumatic osteoarthritis is a late complication following hip dislocation. This may occur due to a deformed femoral head following avascular necrosis or acetabular fracture leading to incongruent articular surfaces resulting in post-traumatic osteoarthritis. 3)    Unreduced dislocation patients presenting late are treated by trial of closed reduction if it fails open reduction of hip is performed. Patients presenting very late are treated with hip replacement. 4)    Myositis ossificans

Anterior hip dislocation: These comprise about 10-15% of traumatic hip dislocations. This results from forceful abduction and external rotation force at hip resulting in anterior hip dislocation. Clinical features: The patient presents with severe hip pain, deformity, unable to bear weight and complete loss of hip function. The limb is in an attitude of flexion, abduction and external rotation. The vascular sign of Narath is positive. Injury to femoral vessels or nerves should also be examined. Treatment: Conservative: 1)    Classical Watson-Jones method 2)    Stimson’s gravity method 3)    Allis method. Complications: Early complications include neurovascular injury and irreducibility. Late complications are recurrent dislocation, avascular necrosis and secondary osteoarthritis of the hip.

Central hip dislocation: This is a very rare injury that results from a direct blow over the trochanter of the femur. This results in acetabular fracture with central hip dislocation.

DISLOCATION OF KNEE Knee dislocation occurs as the result of direct high-energy traumatic force resulting in displacement of tibia in relation to femur. The high energy force disrupts cruciate ligaments and one or both collateral ligaments. It is a limb-threatening condition with a high rate of neurovascular injuries.

Fig 1.30: AP and Lateral radiograph showing anterior knee dislocation. Types: Based on the displacement of tibia in relation to femur, it is classified into  1) Anterior 2) Posterior 3) Lateral 4) Medial Clinical features: The patient presents with severe knee pain, deformity and inability to bear weight. On examination, there is bruising and contusion around the knee. Knee deformity and instability is present. The distal

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neurovascular status has to be examined.   Diagnosis: X-ray knee- AP/lateral helps to give clear diagnosis. MRI is done to assess ligamentous injuries and capsular tears. Treatment: Non-operative management: Knee dislocation is an emergency. It is treated with emergent closed reduction and immobilization for 6 weeks in 20° knee flexion. Assessment of neurovascular status is mandatory after reduction. Operative management: Irreducible dislocation is managed by open reduction and external fixator application for knee stability. Ligament repair is done in indicated cases. Complications: Early: Early complications include popliteal vessel injury and common peroneal nerve injury. Late: Knee stiffness, instability. Questions: Long Essays: 1)    Describe the classification, clinical features, management and complications of shoulder dislocation. 2)    Classify dislocations of hip joint. Describe the mode of injury, clinical features and management of posterior dislocation of hip joint in a 30 year old young man. Enumerate the complications of posterior dislocation of hip joint. Short Essay: 1)    Knee dislocation.

Competency OR 1.6: Describe and discuss the aetiopathogenesis, clinical features, investigations, and principles of management of dislocation of major joints shoulder, knee, hip. Dislocation of joint is a true orthopedic emergency caused due to high velocity injuries like RTA, sports injuries. Patients with joint dislocations present with severe pain and it will not decrease unless dislocation is reduced. Dislocations have to be managed by an Orthopedic doctor after clinical examination and X-ray confirmation in the emergency department. Early and prompt reduction of dislocation is of paramount importance as the prognosis is proportional to the time interval between the dislocation and reduction. Delay in reduction threatens the viability of articular cartilage with a potential for serious long-term disability. General treatment principles for the management of dislocation: 1)    Efficient first aid care: This is done by splinting to prevent further complications 2)    Safe transport to the hospital 3)    Assessment of the general condition of the patient for shock and other injuries. 4)    Assessment of local condition of the injured limb regarding vascular injury, nerve involvement and other soft tissue injuries 5)    Resuscitation 6)    Radiography of the affected joint 7)    Reduction of the dislocation is done by the following steps: a) Gentle manipulation by Orthopedic surgeon for reduction, do not use too much force. b) Assistant help is necessary to provide a counterforce c) Support the injured limb after reduction gently with a splint/sling.

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8)    Immobilization of joint 9)    Early physiotherapy and rehabilitation to restore the full function of the joint. Most dislocations are reduced in the emergency department by using simple methods. The ideal method of closed reduction should be simple, easy, reliable, quick, effective, requires little assistance and should not cause additional injury to affected joint, musculoskeletal or neurovascular structures. However standard procedures for managing joint reduction are still lacking. Many methods have been advocated for shoulder, hip joint reduction with varying success rates and complications. If closed reduction fails, then an open reduction of joint is performed. The joint reduction techniques usually involve one or more maneuvers, these include a)    Traction- Counter traction b)    Adduction- Abduction c)     External rotation- Internal rotation. d)    Direct pressure for reduction. The combination of the above movements helps in the effective reduction of dislocated joint. These movements can be performed on a patient in a supine, sitting or prone position depending on the maneuvers.

SHOULDER DISLOCATION Closed methods of shoulder dislocation: 1)    Kocher’s method 2)    Hippocratic method 3)    Stimson gravity method 1)   Kocher’s method: Steps of reduction: a)    The patient is given general anesthesia and is in supine position. b)    The surgeon applies steady traction by gripping the flexed elbow in one hand and the wrist in other hand. c)     The assistant grips the shoulder around the axilla with a folded towel to apply counter-traction. d)    Gradually and steadily externally rotate the shoulder with the arm by the side of the body. After full external rotation, the elbow is lifted in the saggital plane and the arm is adducted across chest wall. The arm is then internally(medially) rotated, initiating the reduction. The shoulder reduces with a click sound and once reduced it is immobilized with a shoulder immobilizer or chest arm bandage. ( Refer Fig 1.24) Mnemonic: TEAM 2)   Hippocratic method: a)    The patient is given general anesthesia and he lies in a supine position on the floor. b)      The surgeon holds the dislocated limb at the wrist in a semi-abducted position and applies traction. c)     With the foot in axilla acting as counterforce, the limb is slowly adducted and the head of humerus is gently maneuvered into the glenoid cavity. ( Refer Fig 1.25) Post-reduction care: Following reduction, neurovascular evaluation and radiographs should be repeated. The shoulder is immobilized for 3 to 6 weeks following reduction. Early mobilization is particularly desirable in patients over forty years to prevent stiffness and strengthen shoulder muscles.  Complications of closed reduction: 1)    Humerus neck fracture especially in osteoporotic patients. 2)    Neurovascular injury

POSTERIOR HIP DISLOCATION Common closed methods for reduction of posterior hip dislocation: 1)    Allis maneuver 2)    Stimson’s gravity method 3)    Bigelow maneuver 1)   Allis maneuver: a)    Under general anesthesia, with the patient lying on the floor in a supine position b)    the assistant fixes the pelvis, while the surgeon flexes the hip and knee to 90° c)     The surgeon applies longitudinal traction along the axis of the femur.

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d)      With continued traction force acting on the limb, it is gently abducted, externally rotated and extended. The femoral head gets reduced with a click sound into the acetabular cavity.  ( Refer Fig 1.28) 2)   Stimson’s gravity method: a)      Under general anesthesia, with the patient in prone position and the lower limb hanging out of the table with hip and knee flexed to 90°. b)    A traction force is applied over the upper third of the leg by the Surgeon. c)        The assistant gives counter traction by stabilizing the pelvis using one hand. Then with the other hand, the head of the femur is gently maneuvered into the acetabulum with the help of rotary movements of the limb. ( Refer Fig 1.29) Aftercare: Following reduction, neurovascular evaluation and radiographs should be repeated. The hip joint is immobilized for 3 weeks with Thomas splint/traction followed by hip range of movements and weight bearing as tolerated. Complications of closed reduction: 1)    Femoral fracture 2)    Neurovascular injury

KNEE DISLOCATION Immediate closed reduction should be done to prevent injury to neurovascular structures. This classification is based on the displacement of proximal tibia (distal fragment) in relation to distal femur (proximal fragment). The reduction maneuvers are described below: 1)    Anterior: Axial limb traction is given, followed by lifting of the distal femur. 2)    Posterior: Axial limb traction is given, followed by lifting of the proximal tibia. 3)    Medial/lateral: Axial limb traction combined with medial or lateral translation of tibia. 4)    Rotatory: Axial limb traction combined with derotation of the tibia. After closed reduction, evaluation of neurovascular status and radiograph should be done. The function of common peroneal nerve should be evaluated. The pulse of the popliteal, dorsalis pedis and posterior tibial arteries should be palpated.  The recognition of popliteal vessel injury, if any is of paramount importance. Post-reduction care: The knee should be splinted in 20° of knee flexion with POP slab. Closed reduction requires 4 to 6 weeks of immobilization. External fixator application is done for the grossly unstable knee. Complications of closed reduction: 1)    Popliteal vessel injury 2)    Common peroneal nerve injury.

FRACTURES A fracture is a break or disruption in the continuity of a bone. Fractures occur when the bone is subjected to stress greater than it can absorb. Etiology: 1)Traumatic injuries like direct blows, crushing forces, sudden twisting movements and even extreme muscle contractions. 2)Metabolic bone diseases like osteoporosis, paget’s disease. Mechanism of injury: 1)    Direct force: The bone breaks at the point of impact and soft tissues are also damaged. 2)    Indirect force: The bone breaks at a distance away from where the force is applied. Based on breach of Skin: 1)    Closed (simple) fracture: Fracture that does not cause a break in the skin. 2)    Open (compound) fracture: Fracture that causes a break in the skin and is communicating with the environment. It can be internal compounding or external compounding. a)    Internal compounding: It is also called “in-to-out” injury whereby the sharp bone ends, penetrate the skin from beneath. b)    External compounding: It is also called “out-to-in” injury whereby high energy (eg: gunshot wounds, direct blow) penetrates the skin and injures soft tissues and bone.

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  Fig 2.01: Types of fractures: A) Closed fracture; B) Open fracture- internal compounding; C) Open fracture- External compounding. Types of fracture: 1) Incomplete fracture: A break occurs only through a part of the cross-section of the bone. 2) Complete Fracture: A break along the entire cross-section of the bone. The bone splits into two or more fragments. It is classified into: A) Transverse fracture- Fracture which breaks across the bone at a right angle to the long axis of the bone. B) Oblique fracture - Fractures that occur in a plane oblique to the long axis of the bone. C) Spiral fracture:  Fracture in which the bone has been twisted apart. D) Segmental fracture: Fracture happens at two separate regions in a single bone. E) Comminuted fracture:  Fracture in which bone is broken or splintered into multiple pieces.

Fig 2.02: Types of fracture:  A) Transverse; B) Oblique; C) Spiral fracture; D) Segmental fractures; E) Comminuted fracture. Force applied vs Fracture patterns: 1) Twisting injury: Spiral fracture 2) Compression: Oblique fracture 3) Tension: Transverse fracture 4) Bending force: Triangular fracture

Types of displacement: 1)Translation-fracture fragments may shift sideways or in anteroposterior direction 2)Angulation- tilting of fracture fragments 3)Rotation- twisting of fracture.

Fig 2.03: Types of fracture displacement: 1) Translation; 2) Angulation; 3) Rotation.    Factors affecting fracture healing:

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1) Local factors: a) Type of bone: Faster union in flat and cancellous bone. b) Degree of trauma: High-velocity trauma causing comminuted fractures and extensive soft tissue injury vs low energy trauma causing mild contusions and simple fractures. c) Disturbed pathoanatomy: Soft tissue interposition and ischemic fracture ends prevent faster healing. d) Vascular injury: Inadequate blood supply impairs healing, especially in vulnerable areas like the femoral head, talus and scaphoid bone. e) Immobilization: Immobilization stimulates fracture healing. f) Type of fracture: Intraarticular fractures communicate with synovial fluid which contains collagenases that retard fracture healing. g) Pattern of fracture: Comminuted fracture>spiral fracture>oblique fracture>transverse fracture. h) Open fractures may result in infections leading to delayed union or non union. 2) Chemical factors: a) Local cytokines, prostaglandins and leukotrienes. b) Growth factors like TGF, FGF, PDGF, IGF and BMPs. c) Vascular factors like metalloproteinases and angiogenic factors. 3) Systemic factors: a) Age: Fractures unite faster in children b) Nutrition c) Systemic disease: Patients on NSAIDs, steroids, immunocompromised states will delay healing. 4) Hormones: a) Estrogen: It stimulates fracture healing through receptor-mediated mechanism. b) Thyroid hormones: Thyroxine stimulates osteoclastic bone resorption. c) Glucocorticoids: It Inhibits calcium absorption from the gut causing increased PTH. d) Growth hormone: It is mediated through IGF-1(somatomedian-C). It increases callus formation and fracture strength.  Fracture healing: Fractures heal by direct or indirect bone healing. 1) Direct (primary) bone healing: Fracture healing where there is very less bone gap and minimal interfragmentary movement at fracture site. Bone is formed directly across fracture ends without forming a fracture callus. 2) Indirect (secondary) bone healing: It is the mechanism of healing in fractures that are not rigidly fixed. Fracture healing occurs by callus formation which subsequently undergoes endochondral ossification. Indirect(secondary) bone healing stages A) Hematoma formation

B)Stage of Granulation phase/soft callus

C)   Stage of hard callus formation

Lasts for 7 days. Blood leaks out of torn vessels and forms hematoma between and around the fracture. The coagulation cascade is stimulated. Inflammation leads to increased blood flow & vascular permeability. The periosteum and local soft tissues are stripped off.  Ischemic necrosis occurs leading to death of some osteocytes with sensitization of remaining precursor cells. Lasts for 2-3 weeks. Precursor cells form cells that differentiate and organize to provide fibroblasts, chondroblasts, osteoblasts and new vessels. New blood vessels invade the hematoma. Fibroblasts from the periosteum colonize the hematoma & produce collagen fibers. Collagen fibers loosely link the bone fragments. Granulation tissue gradually differentiates into fibrous tissue & subsequently fibrocartilage. Once fracture ends are linked by soft callus, hard

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D)   Remodelling

callus stage starts. Osteoblasts lay down woven bone at the periphery. The fibrocartilagenous callus begins to undergo endochondral ossification. New blood vessels continue to proliferate allowing further migration of mesenchymal stem cells. Progressive stiffening of callus. Once all interfragmentary motion has ceased, remodeling happens where woven bone is converted to lamellar bone.

Fig 2.04: Fracture healing: A) Stage of hematoma formation; B) Stage of granulation tissue/soft callus formation; C) Stage of hard callus formation; D) Bone remodeling.

Fig 2.05: Serial fracture X-rays of hip showing stages of fracture healing with implant in situ (A to D). Laws of bone remodelling: 1)    Wolff’s law: Bone remodelling occurs along the line of stress. 2)    Heuter Volkmann law: Remodelling occurs under the influence of distractive strain (traction) & compressive strain (compression). Clinical features: Pain, swelling, loss of function, deformity, shortening and crepitus. Investigations: 1)      X-ray: It localises the fracture & number of fracture fragments. It also indicates the degree of displacement and helps to identify any evidence of pre-existing disease in the bone. Rule of two: a) Two views: AP/lateral b) Two joints: Joint above and below

Fig 2.06: X-ray of forearm AP and lateral view showing midshaft fracture of radius and ulna. Note X-ray includes one joint above (elbow joint) and one joint below (wrist joint).

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2) CT: It is used to assess 3D orientation of fractures. 3) Ultrasound: it is used to reveal superficial soft tissue damage 4) MRI: It helps to evaluate soft tissue structures including blood vessels, nerves. Treatment: Reduction of fracture refers to the restoration of the fracture fragments to anatomical alignment and rotation. The limb is held in reduction with splints, tractions and fixation devices. It is classified into closed reduction and open reduction. 1) Closed reduction and immobilization: Closed reduction is accomplished by bridging the bone fragments into apposition through manipulation and manual traction. The extremity is held in the desired position and the surgeon applies splint, cast or any other device. Post-reduction X-rays are obtained to verify that the bone fragments are correctly aligned. Traction (skin or skeletal) may be used to maintain fracture reduction and immobilization.  2) Open reduction and fixation: It is the surgical approach, the fracture fragments are reduced. External or internal fixation devices may be used to hold the bone fragments in position until solid bone healing occurs. External fixation devices like external fixators or Ilizarovs are used. Internal fixation devices like metallic pins, screws, plates and rods are used.

Fig 2.07: Algorithmic approach to treatment of fracture. Complications: Complications Immediate Early Late

a)Injury to neurovascular structures a)Compartment syndrome b)infection a)Problem with Union 1)Delayed union 2)Malunion 3)Nonunion 4)Cross union b)Sudecks osteodystrophy c)Myositis ossificans d)Avascular necrosis e)Joint stiffness f)Osteomyelitis g)Osteoarthritis

Deformity: 1) Varum - Whenever the distal part is more medial. 2) Valgus- Whenever the distal part is more lateral. Genu- Pertains to knee 1) Genu varum- eg: Rickets, medial condyle fracture of distal femur with growth arrest. 2) Genu Valgum- eg: Rickets, lateral condyle fracture of distal femur with growth arrest.

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Fig 2.08: A) B/L genu varum; B) B/L genu valgum. Cubitus-Pertains to the elbow 1) Cubitus varus- medial condyle fracture of elbow with growth arrest. 2) Cubitus valgus- lateral condyle fracture of elbow with growth arrest, neglected supracondylar humerus fracture.

Fig 2.09: M- refers to midline along the shaft of humerus; A) Cubitus varus; B) Cubitus valgus. Coxa- Pertains to hip. 1)    Coxa vara- Decrease in femoral neck-shaft angle. Eg: Neck of femur fracture, intertrochantric fracture. 2)    Coxa valga- Increase in femoral neck shaft angle. Eg: Congenital, post fracture reduction.

Fig 2.10: A) Coxa vara; B) Normal neck shaft angle; C) Coxa valga. Fracture eponyms: Upper limb fracture Bankart fracture Hill Sachs lesion(H for humerus) Holstein lewis fracture Monteggia fracture Galeazzi fracture Essex Lopresti lesion

Nightstick fracture Barton fracture

Description Fracture of anteroinferior glenoid cavity of scapula. It is cortical depression on posterolateral head of humerus. Fracture of distal 1/3 humerus associated with entrapment of radial nerve resulting in wrist drop. Fracture of proximal 1/3 of ulna with dislocation of head of radius. Fracture of distal 1/3 radius with dislocation of radioulnar joint Fracture of radial head with disruption of interosseous membrane with dislocation of distal radio-ulnar joint. Minimally displaced oblique fracture of ulna without associated fracture of radius. Intraarticular fracture of distal radius with subluxation or

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Mechanism of injury Abduction and external rotation of shoulder. Abduction and external rotation of shoulder (shoulder dislocation). Blow to arm Blow to forearm Blow to forearm Fall from height

Direct blow to medial forearm. (injuries obtained from patient when struck by police) Fall on outstretched hand(FOOSH)

Colle fracture Smith fracture Chauffeur fracture Bennet fracture Rolando  fracture Boxer fracture Lower limb fracture Straddle fracture Bumper fracture Cotton fracture Jones fracture Choupart fracture dislocation

Segond fracture Stieda fracture: Runner fracture March fracture Toddler fracture Lisfranc fracture Spine fracture Jefferson fracture Clay shoveler’s fracture Chance fracture

dislocation of radiocarpal joint. Fracture of distal radius at corticocancellous junction 2 cm proximal to distal articular surface Reverse Colle fracture Fracture of radial styloid process Fracture base of 1st metacarpal which extends into carpometacarpal joint. Comminuted intraarticular fracture through base of 1st metacarpal bone. Fracture neck of 5th metacarpal. Description Bilateral fractures of superior and inferior pubic rami. Fracture of lateral tibial plateau caused by forced valgus of knee. Trimalleolar fracture Fracture of base of 5th metatarsal by avulsion of peroneus brevis. Midtarsal dislocation of foot associated with fractures of calcaneum, cuboid and navicular bone. Avulsion fracture of lateral tibial condyle of knee. Avulsion fracture of medial femoral condyle at the origin of MCL. Stress fracture of distal fibula 3-8 cm above lateral malleolus. Stress fracture occurring at the 2nd and 3rd bones of the foot. Undisplaced spiral fracture of distal tibia in children Fracture dislocation of midfoot Description Fracture of anterior and posterior arches of C1 vertebrae. Fracture of spinous process of C7 verebrae. Flexion injury of spine which consists of compression injury to anterior portion of vertebral body and transverse fracture through posterior elements of vertebrae.

Questions: Short Essays: 1)    How do you classify the fractures? 2)    Stages of fracture healing Short Answers: 1)    Fracture healing 2)    Callus

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Fall on outstretched hand FOOSH Forced ulnar deviation causing avulsion of radial styloid. Axial load along the metacarpal in a partially flexed thumb. Axial load along the metacarpal causes splitting of proximal articular surface. Boxing, punching a solid object. Mechanism of injury Fall from height, Road traffic accidents. Forced valgus of knee when struck from the side by a car bumper. Rotational ankle injury Inversion of ankle Fall from height, forced twisting injuries of foot. Internal rotation of knee Valgus injury to knee. Repeated axial stress on fibula Heavy or unaccustomed exercise. Low energy trauma, often rotational. Forced plantar flexion of foot. Mechanism of injury Vertical compression of neck Forced hyperflexion of neck. Hyperflexion of spine seen in car accidents when lap belts are used.

                  COMPLICATIONS OF FRACTURE Complications Systemic

Immediate a) Hemorrhagic shock

Early a) Hemorrhagic shock b)ARDS c)Fat embolism syndrome d)DVT and pulmonary embolism e)Crush syndrome

Local

a)Injury to neurovascular structures

a)Compartment syndrome b)Infection

Immediate complications: a)    Hemorrhagic shock Hemorrhagic shock is defined as a reduction in tissue perfusion below the necessary to meet metabolic needs. Trauma is the most common cause of hemorrhagic shock.

b)    Injury to neurovascular structures: Neural injuries: Nerves lie in close proximity to bones, hence are liable to be injured during fracture. As a consequence, it can lead to neuropraxia, axonotemisis and neurotemisis. Upper limb Penetrating neck injury, traction injury at birth Shoulder dislocation, intramuscular injuries Distal 1/3rd humerus fracture Supracondylar fracture

Brachial plexus injury Axillary nerve Radial nerve Anterior interosseous nerve (AIN), median nerve.

Lower limb Hip dislocation Knee dislocation and neck of fibula fracture

Sciatic nerve Peroneal nerve

Blood vessels lie in close proximity to bones and hence are liable to be injured during fracture. It can lead to the following Signs (5 P’s): Pain, absent Pulse, Pallor, Paraesthesia, Paralysis. Vascular injuries: Supracondylar humerus fracture Supracondylar femur fracture and knee dislocation Thoracic and lumbar spine fracture

Brachial vessel injury Popliteal vessel injury Descending aorta

Early complications: Acute respiratory distress syndrome (ARDS): ARDS is a sudden, progressive form of respiratory failure characterized by severe dyspnea, refractory hypoxemia and diffuse bilateral infiltrates following polytrauma and long bone fractures. It is often referred to as shock lung, post-traumatic lung or capillary leak syndrome. Pathophysiology: In ARDS, there is acute endothelial damage, causing the release of proinflammatory cytokines which causes acute edema. Causes: Chest trauma, multiple fractures, multiple blood transfusions, infection, thromboembolism, multisystem organ failure.

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Clinical manifestations: The patient presents with acute onset of dyspnea, fever, and cyanosis. On examination: tachypnea, resistant hypoxia, intercostals retractions and ronchi. Investigations: 1) Chest X-ray shows diffuse bilateral patchy pulmonary edema. In ARDS, there is hypoxemia which is refractory to O2 supplementation and  PaO2/FIO2 ratio 120/min Fever Jaundice Anaemia Elevated ESR Renal signs: Anuria or oliguria. Fat macroglobinemia

Two major criteria or one major and four minor criteria suggest a diagnosis of FES. Investigations: ABG shows hypoxia i.e. PaO2 < 80 mmHg. X-ray finding shows snow-storm appearance. Sizzling test is done to detect the presence of fat in the urine. Treatment: Symptomatic treatment is given and it is a self-limiting condition but if marked hypoxia is present, then Intermittent Positive Pressure Ventillation(IPPV) and assisted ventilation will be required. Compartment syndrome: Compartment syndrome is defined as an increase in the intracompartmental pressure leading to loss of microvascular circulation of the distal limb. The normal compartment pressure is 0 – 8 mmHg. Pressure above 30 mmHg is abnormal. The causes of increased compartmental pressure are fractures, soft tissue injuries, tight plaster, crush injuries etc. Compartment syndrome can occur in both upper and lower extremity. In upper extremity, the forearm is the most common site. The muscles of the deep volar compartment of forearm (flexor digitorum profundus, flexor pollicis longus) generally gets involved first.

Fig 2.12: Compartment syndrome: (A) Skin; (B) Subcutaneous tissue; (C)Deep fascia; (D)Intermuscular septa; (E)Vessels and nerves; (F) inflamed and edematous muscle; (G) Fracture.

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Fig 2.13: Vicious cycle of compartment syndrome. Clinically there will be passive stretch pain. 5 P`s of compartment syndrome are pain, paresthesia, absent pulse, pallor and paralysis.

Fig  2.14: Fracture of proximal tibia leading to compartment syndrome with blister formation. It is confirmed by measuring the intracompartmental pressure by the Stryker method. Once the diagnosis is made, it is treated by fasciotomy. If not treated in time it leads to Volkmann’s ischemic contracture. Crush syndrome (Rhabdomyolysis): It is characterized by muscle necrosis and release of intracellular muscle constituents in the circulation. Pathophysiology: Myoglobin from the damaged muscle goes to circulation leading to myoglobinuria followed by acute renal failure. It usually takes 2 to 3 days to develop. Causes: 1)Multiple trauma 2)Crush injury 3)Surgery 4)Removal of forgotten tourniquet Clinical features: The patient will have scanty dark-colored urine with restlessness, apathy and delirium Investigations: 1)    Serum CPK- It indicates muscle injury 2)    Renal function tests 3)    Serum electrolytes- It shows raised serum potassium concentration. 4)    Urine analysis Treatment is removal of all necrotic material and supportive management for acute renal failure with or without dialysis.

Late complications: Problems with Union Delayed union Nonunion

Malunion Cross union

Union is delayed when healing has not advanced at an average rate for location and type of fracture FDA defines nonunion to be “established when a minimum of  9 months has elapsed since the fracture with no visible clinic-radiological progressive signs of healing for 3 months” Malunion is defined as fractured bone that has united in non anatomical position. When one bone cross unites with another bone. Eg: Radius and ulna, Tibia and fibula.

Malunion: Malunion is defined as fractured bone that has united in non-anatomical position.

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Causes:

a) Ineffective immobilization b) Inaccurate reduction Types of malunion: a) Translatory malunion b) Angulatory malunion c) Rotary malunion Among all the types, rotary malunion is most difficult to correct.

Fig 2.15: Types of malunion: A) Translatory malunion; B) Angulatory malunion; C) Rotary malunion. Clinical features: Deformity, shortening, muscle wasting, loss of function. Investigations: a) Plain radiographs b) CT scan

Fig 2.16: X-ray shows malunited shaft of femur fracture. Treatment: a) Observation b) Corrective osteotomy c) Ilizarov technique for bone shortening and deformity correction. Common fracture malunions and their deformities: a) Distal radius fracture- dinner fork deformity b) Supracondylar humerus fracture- gunstock deformity c) Intertrochantric fracture -coxa vara.

  Nonunion: FDA defines nonunion to be “established when a minimum of 9 months has elapsed since the fracture with no visible clinico-radiological progressive signs of healing for 3 months” Factors contributing to nonunion: Local factors a)Open fracture b)Infected fracture c)Segmental fracture d)Comminuted fracture e)Insecure fixation

Systemic factors a)Malnutrition b)Metabolic c)Nutritional status d)General health e)Tobacco and alcohol abuse

Classification: Nonunited fractures are of two types based on the viability of bone ends: 1) Hypervascular nonunion: It is caused by inadequate stability with adequate blood supply and biology. 2) Avascular nonunion: It is caused by inadequate blood supply and inadequate bone healing. 1) Hypervascular nonunion: A) Elephant foot B) Horse foot C) Oligotrophic

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Fig 2.17: Types of hypertrophic non-union (A) Elephant foot (B) Horse hoof (C) Oligotrophic 2) Avascular nonunion: A) Torsion wedge B) Comminuted nonunion. C) Gap nonunion D) Atrophic nonunion

Fig 2.18: Types of avascular non-union (A) Torsion wedge; (B) Comminuted nonunion; (C) Gap nonunion; (D) Atrophic nonunion. Clinical features: Symptoms: minimal or no pain, swelling, deformity Signs: painless abnormal mobility, shortening, scars, sinuses, deformity, wasting of limb muscles. Investigations: X-Ray AP/Lateral view to see gap between fracture fragments, fragments ends may be round and sclerotic with obliteration of medullary cavity.

Fig 2.19: Non-union shaft of humerus fracture Treatment: a)Low intensity ultrasound. b) Electrical and electromagnetic stimulation- It converts fibrous tissue to fibrocartilage and then to bone. Surgical: a) Hypertrophic nonunion: Stable fixation of fragments b) Atrophic nonunion: Decortication and bone grafting with stable fixation. Bone grafting: Bone graft provides stability and promotes osteogenesis. Types: a)    Cancellous bone graft: It provides less structural support but great osteoinduction. Eg- iliac crest graft.

Fig 2.20: Cancellous bone graft from iliac crest region. b) Cortical bone graft: It provides structural support but less osteoinduction, mainly used for nonunion of long bones. Eg: fibula strut graft

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Fig 2.21: Types of bone graft. Ilizarov technique: It is best for infected non union. It corrects both deformity and bone loss simultaneously. Myositis ossificans: It is a reactive process characterized by well circumscribed proliferation of fibroblasts, cartilage and bone within the muscle. It is also called post-traumatic ossification. Pathophysiology: There is ossification in the fracture hematoma due to invasion by the osteoblast cells from striped periosteum. It is a type of heterotrophic ossification. Sites: The most common site is around elbow and in the thigh. It is common in children due to loose periosteum, more common in patients with head injury and patients with paraplegia due to spinal injury. Clinical features: Symptoms: Pain, swelling and decreased range of motion. Signs: Palpable soft tissue mass, restricted range of motion. Investigations: 1)X-ray: It shows peripheral bone formation with central lucent area. 2)CT and MRI scan 3)Blood tests: It shows raised ESR and increased ALP levels.

  Fig 2.22: X-ray of elbow- lateral view showing myositis ossificans. Treatment: In active stage it should be plaster immobilized for a few weeks followed by active mobilization. In mature stage, if bone is hindering the joint motion then surgical excision of fragment is done. Avascular necrosis: Blood supply to some bones is such that vascularity of a part is seriously jeopardized following fracture resulting in necrosis. Avascular necrosis causes deformation of the bone. This leads to secondary osteoarthritis and painful limitation of joint movement. Common sites: a) Femoral head b) Scaphoid c) Talus

  Clinical features: Insidious onset of pain, localized tenderness Investigations: a) X-ray: It shows sclerosis of necrotic area, deformity of bone b) MRI c) Bone scan Treatment: Avascular necrosis can be prevented by early and energetic reduction of susceptible fractures. Late options include excision of avascular part, total joint replacement. Volkmann ischemic contracture: Volkmann contracture is the permanent shortening of muscles usually after compartment syndrome resulting in claw-like deformity of hand fingers and wrist. Volkmann contracture results from acute ischemia and necrosis of muscle fibres of flexor group of muscles of forearm especially flexor digitorum profundus and flexor pollicis longus.

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Fixed length phenomenon:

Fig 2.23: A) Volkmann’s hand B) Wrist extension leading to flexion of fingers C) Wrist flexion leading to extension of fingers Treatment: Physiotherapy and stretching of shortened muscles Surgery:  Maxpage muscle sliding surgery. Sudecks osteodystrophy/reflex sympathetic dystrophy/algodystrophy: It is a condition characterized by pain and extreme stiffness with loss of hair. It is clinically characterized by swollen, shiny and edematous limb. X-ray findings show characteristic “patchy osteoporosis”. Treatment is with exercises and analgesics initially, if conservative treatment fails, then later treated by sympathetic ganglion block or sympathectomy.

Questions: Long Essays: 1)    Define nonunion? Enumerate the causes of non-union. Describe various methods of treatments for nonunion. 2)    What is fat embolism syndrome? Discuss the clinical features, investigations, diagnosis and management of fat embolism syndrome.

Short Essays: 1)    Complications of fracture 2)    Types of bone union 3)    Nonunion 4)    Malunion 5)    Sudeck’s Osteodystrophy 6)    Myositis ossificans

TREATMENT OF FRACTURES Treatment of fractures can be divided into 1) Conservative management 2) Operative management 1)   Conservative management: A)   POP immobilisation: Plaster of Paris(POP) is used commonly for the preparation of slabs or cast for immobilization of fractures to aid healing in undisplaced or mildly displaced fractures. B)   Functional cast bracing: Functional cast bracing was popularized by Sarmiento. It is the secondary form of fracture treatment that stimulates osteogenesis, promotes soft tissue healing and permits early function of joints thus preventing stiffness and helps in early rehabilitation.

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Time of application: Usually 3 weeks after injury. Mode of action: On axial pressure of the limb without cast, the fracture fragments tend to shorten producing soft tissue bulging effect. After bracing, the muscles cannot stretch beyond the confines of the cast and the hydraulic action of muscle forces are driven towards the fracture site thus helping the fracture to be held firmly. These hydraulic forces control the fragments and resist fracture overlap, angulation and promote early callus formation.

Fig 2.24: Sarmiento brace: A) Relaxed muscle; B) Contracted muscle without cast displacing the fracture; C) Contracted muscle with cast. Indications: Simple fractures treated by closed reduction for tibia, humerus fractures. Contraindications: Compound fractures.

Fig 2.25: Approach to a fracture. 2)   Operative methods: The Association of Osteosynthesis (AO) group from Switzerland has advocated the principles of internal fixation of fractures based on anatomical location, fracture pattern, bone quality and status of soft tissue injuries.  AO principles of surgical treatment of fractures: (1) Anatomical reduction of the fracture fragments. (2) Stable internal fixation. (3) Preservation of blood supply. (4) Active, pain-free mobilization of adjacent muscles and joints. Stages of fracture fixation: a) Exposure of the fracture: In open reduction, the fracture site is adequately exposed through surgical dissection to develop three dimensional perspective of the fracture configuration. b) Reduction of the fracture: In open reduction technique, fracture realignment is done with traction by bone holding forceps which often result in anatomical reduction of fracture fragments. Closed reduction is achieved by bridging the bone fragments into apposition through manual traction and manipulation. The fracture reduction is usually confirmed under C-arm image intensifier.

Fig 2.26: Mobile C-arm image intensifier for X-ray imaging in operation theatre to confirm fracture reduction and implant fixation. b)    Stabilization of the fracture: c)     Mechanical stability across the fracture site can be achieved by plate and screws, nail or external fixator depending on the anatomical site, pattern of fracture and articular involvement. Simple

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fracture patterns and articular injuries are treated by open reduction and absolute stability.  Comminuted fracture patterns are treated by closed reduction and relative stability. Absolute stability It involves direct visualization of fracture, anatomic reduction and stable fixation with implants like lag screws, dynamic compression plating and tension band wiring.

Relative stability It involves indirect reduction and fracture fixation with implants like intramedullary nail, external fixator.

AO lag screw and plating: 1)   AO lag screw: A lag screw placed perpendicular to the oblique fracture line results in maximum inter-fragmentary compression. A gliding hole is drilled proximally and a thread hole distally, to achieve effective compression. It resists fracture shear force during axial loading. 2)   AO plate: Dynamic compression plates are the treatment modality of fracture fixation, where a plate is used on the surface of bone to achieve axial compression between the two fragments at the fracture site by tightening of screws. Principle: The inclined contour of screw holes and slope of the undersurface of screw head help in achieving spherical gliding principle. This causes the bone fragment to slide along the same direction on either side of the fracture to provide rigid compression. Plates can be used in neutralization, compression, bridging and locked modes depending on fracture configuration. Dynamic compression plate- Fracture site compression is achieved by the spherical gliding principle. Low contact-dynamic compression plate- In addition to fracture site compression by the plate, this also attains less contact with bone, so periosteal vascularity is preserved.  This allows better vascularisation of fracture. Locked plate- The screws and plate hold the fracture reduction and also the screw head locks to the plate. These plates are specially indicated in osteoporotic fractures.

Fig 2.27: AO Technique: Inter-fragmentary fracture compression with lag screw (A); Plate (B); Screws (C). Tension band wiring: Tension band wiring is used to achieve dynamic fracture site compression in patella and olecronon fractures. Principle of TBW: The distractive forces are converted into compression forces after tension band wiring.

Fig 2.28: Tension band wiring of patella. Intramedullary Nailing- Femur, Tibia Intramedullary nail is usually inserted after indirect fracture reduction which acts as internal splint to achieve relative stability. It is used commonly in fixation of long bone fractures like femur and tibia. These implant act as load sharing devices. Newer generation intramedullary nails have proximal locking and distal locking mechanism which also ensures fracture rotational stability.  The goal is restoration of length, alignment and rotation while preserving the biological environment for fracture healing.

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Fig 2.29: Intramedullary interlocking nail for fracture shaft of the femur.

External fixator External fixator is a device placed outside the skin that stabilizes the fractured bone held by multiple pins or tensioned wires that are connected to external frame. It acts as an external splint to stabilize the fracture. External fixation is of two types: 1)    Pin fixator 2)    Ring fixator. 1)   External pin fixator: The external pin fixator is a device placed outside the skin that stabilizes the fractured bone held by multiple pins that are connected to external rod. It is usually indicated in open long bone fractures, pelvic fractures. It helps to prevent infection, aids in regular wound dressings and if necessary, flap cover can be done. 2)   Ring fixator: The external ring fixator is a device placed outside the skin that stabilizes the fractured bone, held by tensioned wires that are connected to external metal ring. Ilizarov technique: Russian scientist G A Ilizarov in 1952 first described the first use of ring fixator in nonunions and limb lengthening procedures. In this technique, the external metallic ring is connected to the bone through a number of tensioned wires in multiple planes to provide bony stability. Depending on the ring fixator assembly, the fracture can be distracted or compressed and deformities can be corrected. Principle: The bone is lengthened under slow distraction of 1 mm/day through controlled and mechanically applied tension stress. It induces new bone formation. This is called distraction osteogenesis which is based on the law of tension force principle. Stages of application: 1. Ring fixator application followed by low-energy corticotomy to preserve the blood supply. 2. A short latency period of 7-10 days followed by initiation of distraction at corticotomy site. 3. Slow gradual distraction at the rate of 1 mm/day to stimulate ossification during elongation. 4. Newly formed bone extends from each end of the osteotomy in full cross-section parallel to the distraction force. Depending on the length of bony defect to be corrected, corticotomy site can be distracted upto two to three months. The osteogenic area rapidly remodels to form new bone that is indistinguishable from the host bone. Rate of distraction: the bone is distracted at the rate of 1 mm/day (0.25 mm/6 hours) using ring fixators.

Fig 2.30: Ilizarov technique A) Tibia with diaphyseal dead bone B) Excision of dead bone C) Corticotomy at tibial metaphysis D) Slow lengthening of corticotomy E) Closure of bony defect in the diaphysis.

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Indications: 1)      Limb lengthening- It is indicated in congenital bony shortening, polio etc.  The ring fixator is assembled and distracted at the metaphyseal region for new bone formation. 2)    Non union- Tibial non-unions are usually corrected by Ilizarov ring application and compression. 3)      Osteomyelitis- Excision of dead bone followed by correcting the bone gap by corticotomy and lengthening at metaphysis using Ilizarov technique. (Fig- 1.24). 4)      Deformity correction- Multiplanar deformities either congenital or acquired can be corrected by Ilizarov technique. 5)    Arthrodesis- Compression and joint fusion can be achieved by using Ilizarov ring compression. Advantages: 1) Stabilization of bone without fracture exposure reduces the chance of infection and also preserves vascularity. 2) Compression/distraction can be done at fracture site. Disadvantages: 1)    Since the ring is external and cumbersome, it hampers daily activities. 2)    Usually patients need a long duration of follow up. Complications: 1. Pin tract infection 2. Neurovascular injury. Questions: Short Essay: 1)    Internal fixation Short Answers: 1)    Interlocking nail. 2)    Ilizarov technique

FRACTURES IN CHILDREN Fracture is a break or disruption in the continuity of bone. Pediatric fractures are of special reference in Orthopedics because they differ from adult fractures and also these fractures vary in different pediatric age groups. Unique features of Paediatric skeleton: 1) Bone is relatively elastic and rubbery 2) Periosteum is quite thick and membranous 3) Ligaments are strong relative to bone 4) Presence of physis is a “weak link”

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5) Fractures heal quickly and have the capacity to remodel. Anatomy of pediatric bone: 1) Growth plate: The growth plate contributes to longitudinal growth of bone. Injury to the growth plate causes deformity. 2) Bone: Pediatric bone has increased collagen: bone ratio, so it has a lower modulus of elasticity so it bends before breaking. 3) Periosteum: It is thick, strong, and loosely adherent to the bone. It has an increased blood supply with high metabolic activity leading to more callus formation and rapid union.

Pediatric bone Long bone of a child is divided into epiphysis, physeal plate, metaphysis and diaphysis. Juvenile bone is more porous than adult bone because Haversian canal occupies much greater space. So fracture bends before breaking. The most common fractures include greenstick fractures, torus (buckle) fracture. Less osteoid density The physeal plate is “weak link” between epiphysis and metaphysis. So most commonly fractures occur along that plane.

Adult bone Long bone of an adult is divided into epiphysis, metaphysis and diaphysis Adult bone is stiff with fewer Haversian canals. More osteoid density Absent physis in adults.

Child presents with pain, swelling and deformity. On examination swelling & tenderness at local site, angular or gross deformity may be present. Distal neurovascular examination is necessary. X-ray AP/ Lateral view of bone with proximal and distal joints should be done.

Fig 2.31: X-ray lateral view shows disruption of distal femur physis. Types: 1) Greenstick fracture: A greenstick fracture occurs when there is sufficient energy to start the fracture but insufficient energy to complete it. The cortex fails on tension side and the cortex on compression side bends but remains intact. So it usually results in the break of one cortex.

Fig 2.32: Greenstick fracture of radius: A) Tension side; B) Compression side. 2) Buckle or torus fracture: Fracture of bone in compression results in buckle injury also known as “torus” fracture. It most commonly occurs in distal metaphysis where the porosity is greatest. 3) Physeal injuries: Physis is relatively weaker than bone and fails first. Important factors for prognosis include the age, severity of physeal injury, displacement and radiographic type.

Salter and Harris classification: a) Type 1: Fracture runs through the growth plate without injury to epiphysis or metaphysis.

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b) Type II: Fracture line first runs through the growth plate and then goes through metaphysis. It splits off a triangular metaphyseal fragment and is called Thurston Holland sign. c) Type III: Fracture line runs through a portion of physis and obliquely through epiphysis. d) Type IV: Fracture line traverses through epiphysis, physis and metaphysis. e) Type V: Crush injury of the physis. Mnemonic: SALTR: Type I: S-Sole injury to physis, Type II: A-Above (physis+ metaphyseal injury) Type III: L-Lower (physis+ epiphyseal injury) Type IV: T-Through and through (epiphysis, physis and metaphysis) Type V: R-(cRush of physis) Thurston Holland sign- It is a triangular metaphyseal fragment seen in type II Salter and Harris injury.

Fig 2.33: Salter and Harris classification: A) Normal B) Type I; C) Type II; D) Type III; E) Type IV; F) Type V. Treatment: Conservative: Closed reduction and cast immobilization in Salter and Harris type I & II injuries. Surgery: Open reduction and internal fixation with K wire, screws and intramedullary wires in Salter Harris type III & IV injuries. Complications: 1) Malunion 2) Physeal arrest 3) Limb length discrepancy 4) Infection Question: Short Essay: 1)    Greenstick fracture

Credits: AthK

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CHAPTER 2

FRACTURES Competency OR 2.1: Describe and discuss the mechanism of Injury, clinical features, investigations and plan management of fracture of clavicle.

FRACTURE CLAVICLE Clavicle is the only long bone placed horizontally in the body. It acts as a strut that connects the axial skeleton to the shoulder girdle through sternoclavicular joint and acromioclavicular joint respectively. The clavicle is S-shaped and the junction between the middle and outer one-third is the most common site of fracture. Mechanism of injury: The fracture occurs most commonly by fall on out-stretched hand, fall on the shoulder and direct trauma. The inner fragment is pulled upward by sternocledomastiod & the outer fragment is displaced downward and medial by the weight of upper limb.

Classification: Allman classification: It is based on the site of fracture location. Group I Group II Group III rd rd Middle 1/3 Lateral 1/3 clavicle Medial 1/3rd clavicle fracture fracture ( Incidence clavicle fracture (Most common upto 15%) (less common upto upto 80%) Subtypes: 5%) Type I: Nondisplaced with intact supporting ligaments Type II: Displaced because of coracoclavicular ligament rupture Type III: Articular fracture involving the acromioclavicular joint

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Fig 2.34: Allman classification for clavicle fracture. Clinical features: The patient presents with pain, swelling, deformity and inability to raise the shoulder and on palpation, abnormal mobility and crepitus can be elicited.

Fig 2.35:  Fracture of clavicle with (A) medial fragment pulled upwards by sternocleidomastoid; (B) lateral fragment pulled downwards by weight of upper limb leading to fracture displacement. Investigations: X-ray evaluation is done by AP view of the clavicle.

Fig 2.36: X-ray shows midshaft clavicle fracture. Management: Conservative: Treatment of closed undisplaced, mildly displaced fracture: Figure of ‘8’ Bandage with triangular sling.

Fig 2.37: Fig of 8 bandage with cuff and collar sling. Surgery is rarely indicated and consists of open reduction and rigid internal fixation with dynamic compression plate. The indications being open fractures, injury to neurovascular structures and soft tissue interposition.

  Fig 2.38: Open reduction and internal fixation with plate for fracture clavicle.

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Complications: Acute neurovascular injuries to brachial plexus and subclavian vessels, Malunion, Non-union. FRACTURE OF SCAPULA: The scapula is a flat bone placed on the posterolateral aspect of thoracic cage. Fracture is caused by direct high-velocity trauma. It has a thick muscular cover, so fractures heal early due to good blood supply. Treatment is by rest with a triangular sling & early mobilization. Question: Short Answer: 1)    Clavicle fractures Competency OR 2.2: Describe and discuss the mechanism of Injury, clinical features, investigations and plan management of fractures of proximal humerus.

FRACTURE PROXIMAL HUMERUS Fracture of proximal humerus is defined as fractures occurring at or proximal to surgical neck of humerus. Epidemiology: It is more common in older population related to osteoporosis with the incidence of male to female ratio of 1:2. Anatomy: The proximal humerus is divided into four parts the anatomical neck, greater tuberosity, lesser tuberosity and surgical neck based on epiphyseal lines. The blood supply to proximal humerus is by anterior and posterior circumflex axillary arteries which run from distal to proximal direction.

Fig 2.39:  Anatomy of proximal humerus; (A) Greater tubercle; (B) Lesser tubercle; (C) Anatomical neck of humerus; (D) Surgical neck of humerus.

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Mechanism of injury: 1) High-energy road traffic accidents 2) Indirect injury like fall on an outstretched hand especially in osteoporotic patients. Classification: The system of Neer’s fracture classification includes four segments: 1)    Head of humerus 2)    Greater tuberosity 3)    Lesser tuberosity 4)    Shaft of humerus. According to Neer, a fracture is displaced when there is more than 1 cm of displacement or >45° angulation of any of one fragment with respect to others. Hence they are classified into two-part fractures, three-part fractures and four-part fractures. Deforming muscular forces: 1)    Supraspinatus: It pulls the greater tuberosity superiorly 2)    Subscapularis: It pulls the lesser tuberosity medially 3)    Pectoralis major: It adducts the shaft medially. Clinical features: Symptoms: The patient presents with pain, swelling, restricted movements with fracture extremity held closely to the chest. Signs: On examination, there is proximal humerus tenderness, crepitus and painful range of motion. A neurovascular examination should be performed especially of axillary nerve. Investigations: Radiographic examination: 1)    X-ray shoulder AP/lateral view, 2)    CT scan for articular evaluation, fracture displacement.

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Fig 2.40: Open reduction and internal fixation (ORIF) of proximal humerus fracture with plate and screws. Treatment: 1)    Undisplaced/minimally displaced fracture: Shoulder immobilizer, sling immobilization 2)    Displaced fracture: Young patients: a) Closed reduction and percutaneous fixation with K wire. b) Open reduction and internal fixation (ORIF) with plate and screws. Old patients: a) ORIF with plate and screws. b) Comminuted fracture, 3 or 4 part fracturesShoulder replacement prosthesis. Complications: 1) Malunion 2) Non union 3) Shoulder stiffness. 4) Avascular necrosis of humeral head. Question: Short Note: 1)    Proximal humerus fractures Competency OR 2.3: Select, prescribe and communicate appropriate medications for relief of joint pain. Joint pain can be caused by varied conditions like 1)Primary and secondary osteoarthritis 2)Trauma 3)Obesity and heavy exercises 4)Gout 5)Inflammatory conditions: Rheumatoid arthritis, Psoriatic arthritis, Ankylosing Spondylitis Medications for joint pain relief: The medications should be prescribed based on the severity and underlying cause of joint pain. 1)    Topical agents: Over-the-counter topical skin creams made from capsaicin, diclofenac help to numb the joint area and provide pain relief in patients with arthritis. It is usually used in mild joint pain. 2)    Anti inflammatory pain killers(NSAID’s): 68

NSAID’s are designated to reduce joint inflammation and used to relieve mild to moderate pain. Few NSAID’s are available as overthe-counter medications and others by prescription. Most NSAIDs act either by blocking COX-1 or COX-2 enzymes. Non-selective COX inhibitors Aspirin Indomethacin Ibuprofen Diclofenac Ketorolac

Selective COX-2 inhibitors Celecoxib Rofecoxib Valdecoxib

Patients should be warned about side effects like stomach discomfort, heartburn and constipation. 3)    Other pain relieving arthritic drugs: Acetaminophen: Acetaminophin is non-opioid analgesic that does not address inflammation but works by interfering with the brain’s ability to process signals. Patients should be warned about side effects like liver damage when consumed exceeding the recommended dose or in pre-existing liver disease patients. Sometimes antidepressants like duloxetine are prescribed as offlabel indication for chronic osteoarthritis. Patients should be warned about side effects like dry mouth, blurred vision and drowsiness. 4)      Opiods: Narcotic drugs like codeine, tramadol relieve pain by acting on opioid receptors in the brain. They are used in moderate to severe pain and are available on prescription only. Since opiod drugs have a risk of tolerance, more dosage is required to produce the same effect in long term, often they are combined with acetaminophen or NSAID’s to enhance their effects.  Patients should be informed about side effects like constipation, drowsiness, dry mouth, difficulty in urination and risk of dependence or addiction. 5)      Steriods: Corticosteroid medications like prednisolone have a strong anti-inflammatory action that reduces pain and delays joint damage. They can be given via oral route or as an injection to joint. Patients should be warned about long-term oral intake of steroids as they lead to systemic side effects like hypertension, diabetes, weight gain etc. Commonly used steroids in Orthopaedics Cortisone Prednisolone Methylprednisolone Dexamethasone

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6)    DMRDs: DMRDs are the drugs that prevent joint damage and deformity in conditions like rheumatoid arthritis and other inflammatory arthritis. They act by suppressing the immune system. Commonly used DMRD’s include methotrexate, hydroxychloroquine and sulfasalazine. 7)    Gout drugs: In addition to anti-inflammatory and analgesic drugs for joint pain, gout is treated with colchicine during acute attacks to prevent supersaturation of uric acid crystals in the joint. For long-term uric acid suppression drugs like allopurinol and febuxostat are used. Question: Short Answer: 1)    Medications for joint pain relief.

Competency OR 2.4: Describe and discuss the mechanism of injury, clinical features, investigations and principles of management of fracture of shaft of humerus and intercondylar fracture humerus with emphasis on neurovasular deficit.

FRACTURE OF SHAFT HUMERUS Humerus shaft fracture constitutes 3 to 5% of all fractures. The shaft of humerus is mostly cylindrical proximally but changes to triangular shape in the distal 1/3rd region.

Fig 2.41: Parts of humerus A) Proximal humerus; B) Shaft; C) Distal humerus. Mechanism of injury: a)    Direct trauma to the arm like high-velocity injury or assault by a stick. b)    Indirect twisting injury like torsional or bending force leading to fracture. . Clinical features: 70

Symptoms are pain, swelling and extremity weakness. On examination abnormal mobility, crepitus, fracture angulation of the shaft of humerus may be present.  X-ray: Arm AP and lateral views.  It may show a fracture gap and lateral angulation.

Fig 2.42: AP and Lateral view showing fracture shaft of humerus Treatment: Conservative treatment For children: Arm-chest bandage.  Adults are treated by closed reduction and U-slab/ cast. In fracture lower 1/3 humerus hanging cast is applied.

Fig 2.43: Non operative treatment for fracture shaft of humerus A) ‘U’ slab B) Hanging cast. Operative treatment: ORIF with plating.

Fig 2.44: ORIF (Open reduction with internal fixation) with dynamic compression plate and screws for fracture shaft of humerus. Complication: 1) Injury to radial nerve 2) Delayed union/ non union

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Holstein-Lewis fracture- It is the fracture of distal 1/3 of the humerus resulting in entrapment of radial nerve. The patient presents with distal 1/3 humerus fracture with wrist drop.

Fig 2.45: Course of radial nerve in relation to humerus. Approach to radial nerve injury: The radial nerve winds around the shaft of humerus and is at risk of injury during humeral shaft fracture. This type of nerve injury results in neuropraxia or axonotemesis. The patient develops wrist drop associated with radial shaft fracture. It is treated with medications, cock up splint and physiotherapy. It generally recovers from weeks to months following injury. Surgical exploration is rarely needed. a) In case of closed fracture- Wait and watch for the nerve to recover. b) In case of open injury/post-reduction: Radial Nerve exploration is necessary. c) Delayed or Neglected nerve injury: Tendon transfer procedures are done.

INJURIES AROUND ELBOW Elbow joint is a hinge joint formed by articulation of distal humerus with proximal radius and ulna. Before skeletal maturity, trauma to epiphyseal region can lead to a variety of fractures. The common fractures around the elbow joint are: A)   Supracondylar fracture B)   Medial condyle fracture C)   Lateral condyle fracture D)   Radial head fracture E)   Olecranon fracture F)   Intercondylar fracture G)   Elbow dislocation

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Fig 2.46: Fractures around the elbow (A) Supracondylar humerus fracture (B) Medial condyle fracture (C) Lateral condyle fracture (D) Radial head fracture (E) Olecranon fracture. Clinical points: Three bony point relationship: In the elbow, three point bony relationship is formed by olecranon tip, medial and lateral epicondyle. In a flexed elbow these three points form an isosceles triangle and in an extended elbow these three points lie on a straight horizontal line.

Fig 2.47: Three-point bony relationship in elbow in flexion(A) and extension(B). Carrying angle: The carrying angle is defined as the angle made by the median axis of the arm and median axis of forearm in full supination and extension. It is usually 10 -11° in males and 14 -16° in females. SUPRACONDYLAR FRACTURE: A fracture that occurs above the condyles is called a supracondylar fracture. It is a common injury in age group of 5-10 years. The fracture occurs through a weak metaphyseal bone. Two types are commonly described: a)    Extension type 73

b)    Flexion type The extension type is more common than flexion type Mechanism of injury: a)    Extension type: Fracture occurs by fall on outstretched hand with axial force exiting at the supracondylar region of the humerus. b)    Flexion type: Fall on point of fully flexed elbow. Clinical examination: The child presents with pain, swelling and gross deformity of elbow. On examination, three-point bony relationship is maintained as fracture happens at the level of metaphyseal region of humerus. The child should be evaluated for associated nerve injuries like median and anterior interosseous nerve. Vascular assessment of radial & ulnar artery should be done to rule out vascular injuries.

Fig 2.48: Risk of neurovascular injury by proximal spike of supracondylar humerus fracture. A) Proximal fracture spike B) Brachial vessels. Investigations: X-ray of the elbow: AP/lateral view shows distal fragment displacement (extension type > flexion type- 95%: 5%). Supracondylar extension-type fracture displacement on X-ray shows posterior shift, posterior tilt and internal rotation. Gartland classification Extension type: A) Undisplaced fracture(fat pad sign) B) Displaced fracture with intact posterior periosteal hinge  C) Displaced fracture with periosteal disruption (a)posteromedial (b)posterolateral Flexion type

 

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Fig 2.49: Gartland classification for supracondylar humerus fracture. Treatment of supracondylar fracture: 1) Undisplaced fracture: Above elbow plaster in 90° flexion at elbow with full supination. 2) Displaced fracture: Closed reduction with plaster application. If not acceptable, closed reduction/open reduction with percutaneous K-wire fixation under C-arm guidance is done.

Fig 2.50: Reduction of supracondylar fracture with K wires.

Fig 2.51: Algorithmic approach to supracondylar humerus fracture. Complication: A) Immediate: 1) Brachial artery injury: It is injured due to sharp edge of proximal fragment. Treatment: Immediate closed reduction of the fracture. If pulse returns then treat like any other supracondylar fracture. If there is no return of pulse, further investigation should be done & if necessary, vascular exploration is done.  Pink pulseless hand: It is absent circulation from brachial artery with feeding collateral anastomosis around elbow leading to pink but pulseless hand.   2) Nerve injury: Most common is anterior interosseous nerve, median nerve followed by radial nerve.

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B) Early: 1) Compartment syndrome of forearm and hand. C) Late: 1)    Malunion is the most common complication of supracondylar fracture leading to cubitus varus (Gun-stock deformity). It is caused by medial fracture communition finally healing into varus.

Fig 2.52: Gun stock deformity of left upper limb following malunited supracondylar humerus fracture. 2)    Volkmann’s ischemic contracture: It is a rare but dreaded complication Finger flexion attitude of proximal interphalangeal joint is more than distal interphalangeal joint. Volkmann’s sign will be positive (fixed length phenomenon). Treatment is passive stretching initially followed by muscle sliding operation. 3)    Myositis ossificans: It is calcification occurring within the muscle following injury. The brachialis muscle is most commonly affected. FRACTURE OF LATERAL CONDYLE: Fall on the outstretched hand with valgus stress leads to fracture of lateral condyle along the physis. It is called the fracture of necessity because the fracture line communicates intraarticularly so fracture bathes in synovial fluid leading to nonunion. On clinical examination, the three-point bony relationship is altered. X-ray: elbow joint AP/lateral view. Treatment is ORIF with screw fixation. Complications: a. The most common complication is nonunion with cubitus valgus deformity(due to unopposed growth of medial condyle & lateral condyle physeal growth arrest). b. Tardy ulnar nerve palsy due to unopposed growth of medial condyle stretching the ulnar nerve. Treatment is by anterior transposition of ulnar nerve. 76

FRACTURE OF MEDIAL CONDYLE: Fall on the outstretched hand with varus stress leads to fracture of medial condyle along the physis.  If the fracture is intraarticular, it bathes in the synovial fluid leading to nonunion. On clinical examination, the three-point bony relationship is altered. X-ray: elbow joint AP/lateral view. Treatment: If undisplaced or extraarticular, it is managed conservatively. Surgical treatment is done by ORIF with screw fixation. Complications: 1) The most common complication is nonunion with cubitus varus deformity (due to unopposed growth of lateral condyle & medial condyle physeal growth arrest). 2) Tardy ulnar nerve palsy due to fracture callus engulfing the ulnar nerve. Treatment is by anterior transposition of ulnar nerve.  INTER CONDYLAR FRACTURE: High energy trauma in adults leads to ‘T’ or ‘Y’ shaped fracture. Treatment is open reduction and internal fixation with plating. Complications are mal-union, stiffness and post-traumatic secondary osteoarthritis.

Fig 2.53: Types of intercondylar fractures (A) T shaped (B) Y shaped. DISLOCATION OF ELBOW: Posterior dislocation of elbow is common usually caused by fall on out-stretched hand. Dislocation causes olecranon to move proximally compared to medial and lateral epicondyle leading to loss of threepoint bony relationship (reversal of triangle). It is treated by closed reduction under sedation. FRACTURE OF OLECRANON: The fracture occurs following a fall on tip of elbow. If undisplaced it is treated by A/E slab with elbow in 30° flexion. For displaced fracture ORIF with tension band wiring is done. Tension band wiring converts the distractive force of triceps into compressive force, hence aids fracture healing. The most common complication is nonunion.

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Fig 2.54: Tension band wiring (TBW) for fracture olecranon. FRACTURE OF RADIAL HEAD: It is caused by fall on out-stretched hand with valgus force. Treatment: 1) Undisplaced fracture: Above elbow slab followed by mobilization 2) Comminuted fracture: Excision of fragments and if necessary whole radial head. PULLED ELBOW: It is common in children age group 2-5 years. The radial head is pulled out from the annular ligament. The elbow is in the attitude of pronation with limitation of motion. X-rays looks normal. Treatment is closed reduction to relocate the radial head into the annular ligament.

Questions: Long Essays: 1)      A 8 year old kid was brought to emergency department with pain, swelling and difficulty on moving the left elbow. Parents give history of fall from height directly on elbow while playing. 1. What is the most common pediatric elbow/distal humerus fracture?  2. Mechanism of injury and classification 3.Management 4. Complications. 2)      Discuss the classification, mechanism, clinical features, radiological features, complication and treatment of supracondylar fracture of elbow joint in a child. Short Essays: 1)    Complications and management of supracondylar fracture of humerus in children 2)    Cubitus varus deformity 3)    Volkmann’s ischemic contracture Short Answers: 1)    What is carrying angle? What are the causes of cubitus varus deformity? 2)    Mention the complications of fracture of elbow.

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OR 2.5: Describe and discuss the aetiopathogenesis, clinical features, mechanism of injury, investigation & principles of management of fractures of both bones forearm, Galeazzi and Monteggia injury.

FRACTURE FOREARM BONES Radius and ulna are two bones of the forearm. The ulna has a stabilizing role whereas the radius is articulated in such a way that it rolls over ulna while moving the hand from supination to pronation. When radius and ulna are fractured together, it is called fracture of both bones of forearm. Mode of injury: Forearm fractures result from a fall on the outstretched hand or direct impact. Classification: They can be classified as proximal, middle and distal involving one or both forearm bones. They can be open or closed fracture. Deforming forces: Proximal 1/3rd fractures Middle 1/3rd fractures Lower 1/3rd fractures

The proximal fragment is flexed and supinated because of the unopposed action of biceps and supinator muscle. The middle fragment is in midprone position because of the action of supinator and pronator teres muscle. The distal fragment is in pronation because of the action of pronator quadratus.

Fig 2.55: Classification of forearm fractures. Clinical features: The patient presents with pain, swelling, deformity of forearm. On examination, abnormal mobility & painful crepitus can be elicited.  Investigation: X-ray of forearm with elbow and wrist joint: AP/Lateral

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Fig 2.56: AP and lateral X ray of forearm fracture. Treatment: Undisplaced fracture in children & adults: closed reduction with splinting. Displaced fracture adults: ORIF with plate and screw. Anatomical fracture reduction is necessary to regain forearm movements. Complication: 1. Compartment syndrome 2. Mal-union (with limitation of pronation and supination) 3. Cross-union(radius unites with ulna and ulna unites with radius)

Fig 2.57: Algorithmic approach to a forearm fracture.

MONTEGGIA FRACTURE DISLOCATION Fracture of proximal 1/3rd of ulna with subluxation/dislocation of radial head is called Monteggia fracture-dislocation. Mechanism of injury: 1)    It is caused by fall on outstretched hand with forced pronation. 2)    Direct injury.

Fig 2.58: Fracture of proximal 1/3rd ulna with radial head dislocation Clinical features:

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The patient presents with acute severe pain and swelling of forearm and elbow. On examination tenderness, abnormal mobility and crepitus can be elicited. Bado’s classification: Type 1 Type II Type III Type IV

Fracture of upper or middle third of ulna with anterior displacement of head of radius Fracture of upper or middle third of ulna with posterior displacement of head of radius Fracture of ulnar metaphysis with lateral displacement of head of radius Fracture of upper or middle third of both radius and ulna with anterior displacement of head of radius.

Investigations: X-ray of the entire length of radius and ulna including elbow and wrist joint should be taken. Anterior angulation of ulna with anterior dislocation of radial head is more common.

Fig 2.59: AP and lateral X-ray of Monteggia fracture. Treatment: It is a fracture of necessity. Fracture is invariably treated by open reduction with internal fixation of ulna with anatomical reduction of radial head. Complication: 1)Malunion with limitation of motion  2)Nonunion 3)Redislocation (M for Monteggia, M for medial bone (ulna) fracture)

GALEAZZI FRACTURE-DISLOCATION Fracture distal 1/3rd of radius with subluxation or dislocation of distal radioulnar joint (DRUJ).

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Fig 2.60:  Galeazzi fracture-dislocation showing distal 1/3rd radius fracture with DRUJ disruption AP view (A); Lateral view (B). Mode of injury: It is commonly caused by fall on extended and pronated wrist. Clinical features: The patient presents with pain, swelling & deformity of the forearm and wrist. On examination tenderness, abnormal mobility and crepitus at distal 1/3rd radius can be elicited. The head of the ulna displaces dorsally. Investigation: X-ray of the entire length of forearm including wrist and elbow joint should be taken.

Fig 2.61: AP and lateral X-ray of Galeazzi fracture-dislocation. Treatment: It is a fracture of necessity. Open reduction and internal fixation with plate for the fracture radius should be done. If DRUJ is unstable after radius fixation, it should be fixed with K-wire. Complication: 1)Malunion with limitation of motion. 2)Nonunion 3)DRUJ instability Questions: Short Essays: 1)    Monteggia fracture dislocation 2)    Galeazzi’s fracture dislocation.

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OR 2.6: Describe and discuss the aetiopathogenesis, mechanism of injury, clinical features, investigations and principles of management of fractures of distal radius

DISTAL RADIUS FRACTURE The lower end of radius articulates with carpus (radiocarpal joint) and also with head of ulna (radioulnar joint). The distal articular surface of the radius faces volarly and medially. The tip of distal radius is about 1 cm distal to tip of ulnar styloid process. Accurate anatomical reduction of distal radius is necessary to prevent secondary osteoarthritis.  Types: 1)    Colle’s fracture 2)    Smith’s fracture 3)    Barton’s fracture 1)   COLLE’S FRACTURE: It was first described by Abraham Colle in 1814. Colles fracture is defined as fracture of distal end of radius at its cortico-cancellous junction about 2cm from the distal articular surface. It is common in age group above 40 years, occurring most commonly in women with osteoporosis. Mechanism of injury: The injury results from a fall on an out-stretched hand.  Six fracture displacements: 1. Lateral tilt 2. Lateral displacement 3. Dorsal tilt 4. Dorsal displacement 5. Impaction 6. Supination

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Fig 2.62: Fracture displacements; AP view: Lateral tilt and lateral displacement of distal radius. Lateral view: Dorsal tilt and dorsal displacement of distal radius Clinical features: Pain, swelling, deformity-there is classic “dinner fork deformity” seen in Colles fracture

Fig 2.63: Dinner fork deformity after Colle’s fracture. X-ray: Wrist joint AP/lateral. AP view: lateral tilt (angulation) and displacement (translation) can be seen. Lateral view: dorsal tilt (angulation) and displacement (translation) can be seen. Treatment: Conservative method a)Undisplaced fracture: Closed reduction + below elbow cast (Colle’s cast) for 6 weeks. b) Displaced fracture-Manipulative reduction followed by immobilization in a Colle’s cast. Below elbow plaster is applied in Colles fracture: The dictum of fracture immobilization is to immobilize one joint above and one joint below, but in Colles fracture below elbow plaster is used because the fracture commonly occurs at old age, remains relatively stable with below elbow cast and it also helps to prevent elbow stiffness.

Fig 2.64: Colle’s fracture reduction 1) Traction; 2) Countertraction; 3) Correction of dorsal tilt and displacement; 4) Correction of radial tilt and displacement. Surgical method: Closed reduction and percutaneous pinning with K- wire. Open reduction and plate fixation. Complications: 1. Stiffness of joints due to plaster immobilisation. 2. Malunion. 3. Subluxation of the inferior radio-ulnar joint 84

4. Carpal tunnel syndrome- Fracture malunion leading to compression of median nerve in the carpal tunnel. 5. Sudecks osteodystrophy 6. Rupture of extensor pollicis longus tendon- friction tendinitis in the dorsal compartment over Lister’s tubercle.  2)   SMITH’S FRACTURE: It is also known as reverse Colles fracture. There is fracture of distal radius and the distal fragment is displaced anteriorly. The patient presents with a “Garden Spade” deformity.  X-ray of wrist AP/lateral is performed. Treatment is closed reduction and plaster application for 6 weeks. 3)   BARTON’S FRACTURE: It is intraarticular fracture of distal radius with subluxation or dislocation of carpal bones. Depending on the volar or dorsal fragment of distal radius, leading to carpus subluxation or dislocation. It is classified into 1) Volar Barton fracture: volar fragment 2) Dorsal Barton fracture: dorsal fragment

Fig 2.65: A) Volar Barton fracture; B) Dorsal Barton fracture. Clinical features: The patient presents with pain, swelling and deformity. Investigations: X-ray of wrist AP/lateral should be done.

Fig 2.66: Volar Barton fracture Treatment: Treatment is closed reduction and plaster application is attempted, if fails then ORIF and distal radius plating is done. Complications are malunion, carpal instability, post-traumatic osteoarthritis. SCAPHOID FRACTURE: The scaphoid is the most common fractured carpal bone. Scaphoid has a proximal pole, waist and distal pole. The blood supply to 85

scaphoid is primarily through radial artery. They enter through the distal pole, pass through the waist and supply the proximal pole. The most common site of fracture is waist of scaphiod caused by fall on an out-stretched hand. The patient presents with pain along the radial side of wrist and inability to move the wrist. On examination swelling is present and tenderness is elicited in the anatomical snuff –box. X-ray wrist AP/lateral and scaphoid view of wrist is essential for diagnosis. Treatment for undisplaced fracture is by closed reduction and plaster application in a glass holding position. If displaced, open reduction and internal fixation with Herbert screw is done. 

Fig 2.67: Scaphoid fracture: A) Distal pole; B) Waist of scaphoid; C) Proximal pole fracture. Complications: a. Avascular necrosis: Proximal fragment will become sclerotic (blood supply is from distal to proximal in scaphoid) b. Delayed / nonunion HAND INJURY: Bennett’s Fracture dislocation: Oblique intraarticular fracture base of 1st metacarpal resulting from forced abduction. Treatment is by closed reduction with plaster application and if not acceptable ORIF. 

Fig 2.68: A) Bennet fracture B) Fracture displacement by abductor pollicis longus. ROLANDO’s fracture: Intraarticular comminuted “T” or “Y” shape fracture of base of I st metacarpal, which has a worse prognosis. Treatment is mostly ORIF. The most common complication is 1st carpo-metacarpal arthritis.

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Fig 2.69: A) Bennett fracture B) Rolando fracture. FRACTURE OF METACARPAL: Fall on outstretched hand, direct trauma and boxers sustain this fracture. Distracting forces will be interossei muscle attached to metacarpals. Boxer’s fracture is a fracture through the neck of 5th metacarpal. Treatment is by closed reduction with plaster or ball bandage can also be used. Jones position: Hand is immobilized by wrist extension, Metacarpophalangeal (MCP) joint flexion and Interphalangeal (IP) joint extension. This position keeps ligaments & tendons in a maximum stretched position. As fracture or soft tissue healing requires immobilization for upto six weeks. Jones position helps in regaining hand movements quickly.

Fig 2.70: Jones position for immobilization of metacarpal fractures. PHALANX FRACTURE:                        Phalanx fractures are common injuries. They can be extraarticular or intraarticular. Fracture can occur at head, neck, shaft or base of phalanx. These fractures can result from direct trauma to the finger. It can be closed or open fracture. The patient complains of pain, swelling, deformity of the finger. X-ray AP/oblique view of hand is essential for diagnosis. Non-operative management is the treatment of choice for non-displaced fractures, closed fractures with splints or buddy strapping. Operative management is indicated for comminuted and open fractures with K-wire fixation.

Fig 2.71: Buddy strapping MALLET FINGER: It is caused by sudden passive flexion at distal interphalangeal joint(DIP) resulting in the avulsion of extensor tendon from base of distal phalanx. Treatment is by immobilization in a splint for 6 weeks. Questions: Long Essays:

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1)    What are the fractures caused by fall on outstretched hand? Describe the clinical features, treatment and complications of Colle’s fracture. 2)    Describe the mechanism, clinical features and management of Colle’s fracture. Short Essays: 1)Colle’s fracture 2)Smith’s fracture Short Answers: 1)    Clinical features of Colle’s fracture 2)    Dinner fork deformity 3)    Smith fracture 4)    Fracture scaphoid 5)    Mallet finger.

Competency OR 2.7: Describe and discuss the aetiopathogenesis, mechanism of injury, clinical features, investigations and principles of management of pelvic injuries with emphasis on hemodynamic instability

FRACTURE PELVIS Anatomy: The pelvic ring is composed of a sacrum and two innominate bones joined anteriorly at the pubic symphysis and posteriorly by paired sacroiliac joints. The innominate bone is formed at maturity by the fusion of three ossification centers of the ilium, ischium and pubis through the 88

triradiate cartilage at the doom of acetabulum. The pelvic brim is formed by the arcuate lines that join the superior pubis anteriorly and sacral promontory posteriorly. Below this is the true pelvis which contains pelvic viscera. Above this is the false or greater pelvis which represents the inferior aspect of the abdominal cavity.

Fig 2.72: The Pelvic ring; A) Iliac bone; B) Sacrum; C) Acetabulum; D) Ilium; E) Ischium; F) Pubis. Stability of pelvis: A)Posterior attachments of Sacrum to ilium: 1) Sacroiliac ligamentous complex 2) Sacrotuberous ligament runs from the posterolateral aspect of the sacrum to ischial tuberosity. It helps to maintain vertical stability 3)Sacrospinous ligament runs from lateral margin of sacrum and inserts on to ischial spine. It helps to maintain rotational stability. B)Anteriorly symphyseal ligament connect the pubis. Mechanism of injury: Low energy injuries: These result from violent muscle contractions in young athletes that cause avulsion injury or straddle type injury. High energy injuries result from motor vehicle accidents, fall from height landing on one or both lower limbs or crush mechanism. Classification: Young and Burgess classification: The specific injury patterns vary by direction of force application. This can be 1)Lateral compression(LC) injuries 2) Anteroposterior compression(APC) injuries c) Vertical shear(VS) injuries 1) Lateral compression: Lateral compression is the most common mode of violence. A lateral force directed to the pelvis causes sacral compression fracture.

Fig 2.73: Lateral compression

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2) Anteroposterior compression: Direct anterior force is applied to the pelvis. So there is external rotation of both hemipelvis with posterior ligaments as a hinge. It results in a classical open-book injury.

Fig 2.74: Anteroposterior compression (open book injury). 3) Vertical shear: It results from longitudinal force applied to the extended lower limb following fall from height. Vertical shear results in injury to sacroiliac, sacrotuberous and sacrospinous ligaments.

Fig 2.75: Vertical shear injury. 4) Combined mechanism: A combination of the above mechanisms would lead to pelvic fracture. Tile’s classification: 1)Type A: Stable fractures 2)Type B: Partially stable – Rotationally unstable but vertically stable 3)Type C: Unstable- Both rotationally and vertically unstable Clinical evaluation: Perform primary survey according to ATLS protocol. ABCDE : Airway, breathing, circulation, disability, exposure. The goal of primary survey is to identify and begin treatment immediately for life-threatening injuries. Secondary survey: a) Identify all injuries to extremities and pelvis with careful assessment of distal neurovascular status. b) Look for other injuries of spine and chest. c) Apparent shortening of lower limb may be present. d) Bleeding can cause hemodynamic instability in pelvic fractures. e) Per rectal examination to assess for urethral rupture. Rarely femoral head may be palpable if there is central dislocation of hip.  High mortality is due to associated injuries like: a)    soft tissue injury b)    head injury c)     respiratory tract injury d)    abdominal injury 90

Investigations: X-rays: X-ray pelvis AP view, Pelvic inlet view and outlet views, oblique/Judet view is taken to understand fracture patterns. CT scan with 3D reconstruction: It is useful for posterior pelvic ring fractures and complex acetabular fractures. Treatment: Any polytrauma with suspected pelvis injury, ATLS protocol should be followed. Emergency management of hemorrhage and fracture should be done since the range of blood loss in pelvic fracture is about 1.5-2 liters. 2 large IV lines should be secured followed by infusion of colloids, crystalloids and blood as necessary. If a suspected pelvic fracture is unstable it is secured by wrapping firmly in bedsheet, penumatic antishock garments, Military Antishock Trousers (MAST). Conservative management: Uncomplicated stable injuries can be managed by analgesics, bedrest and skin traction for upto 4 weeks. Operative management: After the emergency management of patient, early reduction and stabilization of pelvic fracture is done by multidisciplinary approach by a team of Orthopaedician, Intensivist and General Surgeon. Indication for surgery: a)    Pubic symphysis diastasis >2.5 cm b)    Rotationally unstable injuries c)     Sacroilac joint disruption d)    Vertical shear fractures Fractures with disruption of pelvic ring are treated by following methods: 1)      Skeletal traction: The patient is treated by skeletal traction especially in vertical shear injuries to reduce the fracture anatomically. 2)      External fixator: This is performed as an emergency procedure. In this method, the pins are passed into iliac bones on each side and held together by clamps and rods. This helps to stabilize the pelvic ring, thus reducing the internal hemorrhage.

Fig 2.76: Pelvic external fixator. 3] Internal fixation: Open reduction and internal fixation with plates and screws is performed to stabilize the pelvis in grossly displaced fractures. This helps in early patient mobilization.

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Complications: a)    Haemodynamic instability: Displaced pelvic fractures significantly increase pelvic ring volume because of fractures or ligamentous injury. This results in blood accumulation from exposed fracture surfaces and injury to blood vessels. Cause: Pelvic hemorrhage is mainly venous from the shearing of presacral/preperitonial venous plexus and sometimes arterial because of injury to internal iliac vessels which leads to loss of blood volume from systemic circulation resulting in hemorrhagic shock. Clinical features: Sustained systemic blood pressure of 60 years is very high. Displaced or undisplaced femur neck fractures are treated by hemireplacement or total hip replacement prosthesis. Hemireplacement arthroplasty (only femoral side is replaced) Unipolar prosthesis a)Austin Moore prosthesis- if calcar femorale is present b)Thompson cemented prosthesis- If calcar femorale is absent

Total hip Replacement (Both femoral side and acetabulum are replaced) a)    Cemented total hip replacement b)    Uncemented total hip replacement

Bipolar prosthesis

Fig 2.98: Unipolar prosthesis- Austin Moore prosthesis

 

Fig 2.99: Unipolar prosthesis- Thompson cemented prosthesis.

Fig 2.100: Bipolar prosthesis.( Movements occur at 1,2) Children: 112

In Children, closed reduction and internal fixation is done with Moore's Pin / Knowles pin. Old Fractures: Sometimes patients can present late with nonunion neck of femur with or without AVN of femoral head. Surgeries for femoral neck fixation sometimes also lead to complications like varus collapse or AVN of femoral head leading to secondary hip arthritis. These patients can be treated as follows: In young adults without AVN of femoral head: a)      Meyer’s procedure: Open reduction and internal fixation of fracture neck of femur is done followed by quadratus femoris muscle pedicle bone graft is harvested and transferred to the posterior aspect of femoral neck nonunion. This increases vascularity and aids in fracture union.

Fig 2.101: Meyer’s procedure: A) Medial femoral circumflex vessels; B) Femoral neck nonunion; C) Quadratus femoris insertion. After surgery: D) Transfer of quadratus femoris graft to non-union site; E) Femoral neck fracture fixation with screws to achieve fracture site compression. b)      Mc Murray’s osteotomy: Intertrochanteric osteotomy is done where proximal part of shaft of femur is directly transferred under femoral head. This converts shearing stress at fracture site to compressive forces. This works on the principle of “arm-chair effect”.

Fig 2.102: Mc Murray’s osteotomy- osteotomy is done below the lesser trochanter and distal fragment is displaced medially. c) 

Valgus intertrochanteric osteotomy: An intertrochanteric osteotomy is done to reorient the fracture line with a high Pauwel’s angle which exhibits high vertical shear into a horizontal fracture line which induces compressive stress.       

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Fig 2.103: Valgus osteotomy for femoral neck fractures. In old patients: Femoral neck fractures with unsalvageable femoral head are treated by hemireplacement or total hip replacement prosthesis.

Fig 2.104: Algorithmic approach to fracture neck of femur. Complications: 1. Varus collapse: Decrease in femoral neck-shaft angle leading to coxa vara. 2. Non-union: If minimum of 3 months has elapsed after femoral neck fracture and the fracture shows no clinico-radiological signs of healing. It is called femoral neck nonunion. Unlike classic FDA definition of nonunion defined for 9 months, femoral neck nonunion is usually defined for 3 months because of its poor healing and thus there is a need for early intervention. The causes of nonunion in this fracture are: 1. Deprivation of the blood supply to the femoral head 2. Absence of a cambium layer of periosteum which could promote callus formation 3. Synovial fluid prevents the clotting of the fracture hematoma 4. Tamponade effect 5. Difficult to control proximal fracture fragment. Clinical features: Hip pain, positive Trendelenberg test and telescopy of hip joint. Investigations: X-ray of hip- AP/Lateral view, MRI of hip joint and bone scan to assess vascularity. Treatment:

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a)      If femoral head is viable- ORIF with muscle pedicle bone grafting/osteotomy. b)      If femoral head is nonviable- hemireplacement or total hip replacement can be done. 3. Avascular necrosis: As femoral head is supplied by endarteries. Any shearing of these blood vessels during fracture leads to AVN hip. X-ray changes can be seen at 3-6 months. Bone Scan is useful in diagnosis. 4. Thromboembolism. Fracture of necessity: It requires surgical intervention by closed/open reduction and internal fixation to achieve satisfactory fracture healing. 1) Galeazzi’s fracture 2) Monteggia fracture 3) Fracture neck of femur 4) Scaphoid fracture 5) Talus fracture.

INTERTROCHANTERIC FRACTURE Intertrochantric fractures are defined as extracapsular fractures of the proximal femur between greater and lesser trochanters. It is made up of dense trabecular bone. Calcar femorale is the vertical wall of dense bone that extends from posteromedial aspect of femoral shaft to posterior portion of femoral neck. This determines the stability of intertrochantric fractures. The intertrochantric region has a good blood supply due to vascular anastomosis.

Fig 2.105: AP view of pelvis showing left Intertrochantric fracture. Mechanism of injury: Intertrochantric fracture is caused by low-energy falls in elderly osteoporotic patients or by high-energy trauma in young patients. Clinical features: The patient presents with hip pain, unable to bear weight. On examination marked shortening of lower limb is present and complete external rotation of lower limb is present. 115

Investigations: X-ray: AP pelvis shows fracture in intertrochantric region. It may be associated with communition of lesser trochanter. Treatment: Trochantric fractures unite readily as fracture occurs along the cancellous region but usually malunites. Conservative management: Reduction and maintenance with upper tibial pin traction using Bohler Braun splint or Russell’s traction. It requires a prolonged period of immobilization for upto 6 weeks. It is indicated in patients not fit for surgery. Operative management: In adults closed reduction and internal fixation with dynamic hip screw (DHS)/intramedullary nail is done.

Fig 2.106: Radiograph showing Dynamic hip screw fixation for intertrochantric frature.

Fig 2.107: Radiograph showing proximal femoral nail fixation for intertrochantric frature. Complications: 1)    Malunion: The normal neck-shaft angle is 125° -135°. If it reduces then this, it is called coxa vara. This is because of medial wall collapse. 2)    Secondary osteoarthritis.

Difference between Neck of femur fracture and intertrochanteric fracture:

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Neck of femur fracture (Intracapsular) >50 years

Intertrochantric fracture (Extracapsular) >60 years

Incidence Age: Mechanism of injury Trivial Significant Clinical features: Inspection: Less More 1)    Shortening Upto 45° external >45° external 2)    External rotation rotation rotation Palpation: Over Scarpa’s Over greater 1)    Tenderness triangle trochanter Treatment Difficult, ORIF Can be managed always with traction or surgery. Complications: Common Absent 1)Avascular necrosis Nonunion Malunion 2) Union

SUBTROCHANTERIC FRACTURE Subtrochantric region is defined as fracture occurring from lesser trochanter to 5 cm distal to it. Mechanism of injury: It is caused by direct high-velocity trauma in young individuals. Clinical features: The patient presents with hip and thigh pain, swelling and unable to bear weight. On examination marked shortening of lower limb and deformity (varus alignment) is present.  Investigations: X-ray of hip- AP and lateral view. Treatment: Conservative management: Undisplaced fractures in young adults. Operative management: If severely comminuted fracture, CRIF/ORIF with inter locking nail or fixed angle plate. Questions: Long Essays: 1)    Classify fracture neck of femur. Discuss the clinical features, diagnosis and management of fracture neck of femur.

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2)    A 75 year old man slips and falls in the bathroom. He is not able to stand and walk with pain in his right hip. On clinical examination, limb is shortened with incomplete external rotation. What is the possible clinical diagnosis? What investigations and treatment will you do? 3)    Describe the history, clinical features, investigations and treatment of proximal femur fracture. Short Essays: 1)    Complications of fracture neck of femur. 2)    Causes of nonunion in fracture neck of femur. 3)    Intertrochanteric fracture of hip. Short Answer: 1)    Coxa vara Competency OR 2.12: Describe and discuss the aetiopathogenesis, clinical features, investigations and principles of management of fracture shaft of femur in all age groups and the recognition and management of fat embolism as a complication.

FRACTURE SHAFT OF FEMUR Femoral shaft fracture is defined as a fracture of diaphysis occurring from 5 cm distal to lesser trochanter to about 5 cm proximal to adductor tubercle. The femoral shaft is a tubular cortical long bone and the narrowest part of the femoral shaft is called the isthmus. The femoral shaft is highly vascular and is composed of thick strong muscle cover all around formed by anterior, medial and posterior compartments of thigh.

Fig 2.108: Femoral X-ray AP and lateral view showing femoral shaft fracture. Mechanism of injury: Direct injury: It is most common in young adults due to high speed motor vehicle accidents, fall from height and gunshot injuries. It can be associated with multiple systemic injuries and other bone fractures.

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Indirect injury: It is caused by twisting or bending forces. Classification: Based on site: 1)    Proximal1/3rd 2)    Middle 1/3rd 3)    Distal 1/3rd Distracting forces in proximal 1/3rd fracture is iliopsoas causing flexion of the proximal fragment. The strong adductors pull the attached fracture fragment medially.  In the distal 1 /3rd fracture, gastrocnemius flexes the distal end of fracture. Types of fracture femur: a)    Transverse fracture b)    Oblique fracture c)     Spiral fracture d)    Comminuted fracture e)    Segmental fracture Clinical features: The patient presents with pain, swelling, deformity of thigh. On clinical examination, tense swollen thigh is present in a closed fracture. The affected leg is often shortened and deformed. Distal neurovascular status has to be examined. Systemic examination of all other long bones and visceral organs should be carried out to rule out major injuries. Investigation: X-ray AP/ lateral view of entire femur including hip and knee joint should be done. Treatment 1) Immediate management: Fracture shaft of femur is usually associated with blood loss of about 1500 ml. Therefore immediate treatment includes IV fluids and blood products for adequate replacement of lost blood volume, emergency fracture splinting should be done by using a Thomas splint to decrease pain and realign the fracture. 2) Definitive management Adults: a) Conservative management: Undisplaced/mildly displaced fractures, head injury and unconscious patients are treated by skin traction, Thomas splint, skeletal traction using upper tibial pin and Bohler Braun splint. It is usually associated

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with prolonged period of bed rest with complications like bed sores, hypostatic pneumonia. b) Operative management: 1)    Closed reduction and Internal fixation with intramedullary nail: It is the insertion of intramedullary nail from the greater trochanter into the medullary canal of femur under C-arm guidance. Since fracture site is not exposed during the nailing procedure it helps to preserve fracture hematoma and facilitates early union.  Kuntschner nail: Kuntschner’s cloverleaf intramedullary nail was used previously for fracture shaft of femur. It was done either by closed anterograde technique with entry through femoral neck or by open retrograde technique through the fracture site. This nail has no locking option proximally and distally, hence fails to provide rotational stability.

Fig 2.109: A) Kuntschner nail. B) Fracture site. C) Intramedullary cavity. D) Hollow slot for nail removal. A) Kuntscher nail is a hollow slotted nail that is cloverleaf shaped in cross-section used for fixation of femoral shaft fractures. Interlocking nail: Interlocking nail is the treatment of choice after reaming by closed anterograde technique followed by interlocking the nail to bone using screws on either side of fracture site to provide rotational stability under C-arm guidance.  

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Fig 2.110: Intramedullary interlocking nail for fracture shaft of femur. 2)      Open reduction with dynamic compression plating(DCP): Open reduction and plating of shaft of femur fracture is indicated rarely as it needs large skin incision, extensive soft tissue stripping, loss of fracture hematoma during surgery and high risk of infection. Children: Age 0-2 years: The reduction is achieved using Gallows traction. The skin traction is applied to both lower limbs and the buttock is pulled up till they are lifted off the bed. This can be replaced by hip spica after 3 weeks.

Fig 2.111: Gallows traction- Note that the buttocks are lifted off the bed so that the body weight provides countertraction. Age 2-16 years: Undisplaced fractures: Hip spica, skeletal traction. Displaced fractures: Closed reduction and internal fixation (CRIF) with TENS nailing/ Open reduction and internal fixation (ORIF) with

plating.  Fig 2.112: TENS nailing for paediatric femoral shaft fracture.  Complications: 121

Immediate and early complications: 1)    Hemorrhagic shock: About 1-1.5 litres of blood will be lost even in closed fracture of femur and may manifest as hypovolemic shock. It should be treated with fluids, plasma expanders and blood components. 2)      Injury to neurovascular structures: It is uncommon but injury to femoral artery can occur by a sharp bony fracture spike and should be treated as a vascular emergency. Sciatic nerve injury may also vary from neuropraxia to complete severance of nerve. 3)      Fat embolism: Fat embolism is more common in young patients with multiple long bone fractures. Causes: a)      Shifting of the patient from the site of accident without proper splinting. b)      Intramedullary reaming of femoral shaft for insertion of intramedullary nail Pathogenesis: Femoral shaft fractures can cause the dissemination of fat globules from the marrow into the bloodstream. These fat globules embolise and block the capillaries of pulmonary and cerebral vessels leading to fat embolism syndrome. It usually manifests 2-3 days after fracture. Clinical features: The patient is usually asymptomatic for first 1248 hours. This can be followed by pulmonary, neurological and dematological features. Pulmonary: The patient can develop hypoxia, breathlessness and may cough out blood-tinged frothy secretion. ARDS can develop in severe cases. Neurological: Confusion, headache and in severe cases coma.  Dermatological: Petechie over chest, back, axillary and conjunctival region. Systemic signs like fever with tachycardia may be present. A high index of clinical suspicion is essential for the diagnosis of fat embolism syndrome. Investigations: a)Complete blood count for Hb, platelet counts and ESR levels. b)Chest X-ray: Chest X-ray shows diffuse bilateral chest infiltrates suggestive of “snowstorm” appearance. c)Urinary fat globules test d)Arterial blood gas analysis (ABG). Treatment: Mild to moderate cases:

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1)      Supportive measures like IV fluids and high-concentration oxygen supplementation. Low molecular weight dextran is started to maintain capillary perfusion. Severe cases: 1)    Intubation and mechanical ventilation. Late complications: 1)    Malunion 2)    Non-union 3)    Knee stiffness Question: Long Essay: 1)    Describe the classification, clinical features, radiological features and management of fracture shaft of femur.

Competency OR 2.11: Describe and discuss the aetiopathogenesis, mechanism of injury, clinical features, investigations and principles of management of (a) Fracture patella (b) Fracture distal femur (c) Fracture proximal tibia with special focus on neurovascular injury and compartment syndrome.

SUPRACONDYLAR FRACTURE OF FEMUR The supracondylar region extends from the distal femoral articular surface to 5 cm above it. It is composed of thick trabecular bone. Mechanism of injury: Direct injury like road traffic accidents, fall from height or indirect twisting injuries. Classification: a)    Extraarticular fractures: Fractures that occur just above the condyles. b)    Intra articular fractures: Fractures that involve either medial or lateral condyles or both. c)     Intercondylar fractures: “T” or “Y” shaped fractures. The distal fragment is angulated and displaced posteriorly due to pull of gastrocnemius muscle.

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Clinical features: The patient presents with knee pain, swelling and inability to bear weight. On examination, abnormal mobility and crepitus can be elicited. The distal neurovascular status should be assessed. Investigation: X-ray distal femur- AP/lateral

Fig 2.113: AP and lateral radiograph showing distal femur fracture. Treatment: Undisplaced fracture is treated by close reduction and above knee plaster for 6 weeks. Displaced Fracture is treated by open reduction and internal fixation with distal femur plating/Dynamic Condylar Screw (DCS). Complications: 1) Vascular injury to popliteal vessels 2) Knee stiffness 3) Delayed union 4) Malunion 5) Common peroneal nerve injury

FRACTURE PATELLA Patella is the largest sesamoid bone in the body. Its functions are to increase the mechanical advantage of the quadriceps. It protects the femoral condyle from injury and also aids in nutrition of articular cartilage. Mechanism of injury: A)   Direct injury causing comminuted fracture. It is classically known as “stellate fracture” of patella. B)    Indirect injury due to reflex quadriceps contraction can lead to transverse fracture. Avulsion of quadriceps or patellar tendon leads to fracture of proximal or distal pole of the patella. Clinical features: The patient presents with knee swelling, inability to walk. On examination knee hemarthrosis is present. The fractured patellar ends are usually palpable in displaced fracture. There is loss of active knee extension because of failure in the extensor quadriceps mechanism of knee.

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Investigation: X-ray Patella - AP/ Lateral and skyline view.

Fig 2.114: AP and lateral radiograph showing transverse fracture of patella.  Treatment Conservative management: Undisplaced fracture or displacement < 1-2 mm with intact quadriceps expansion is treated by cylindrical cast. Surgical management: Displaced fracture is treated by open reduction and internal fixation with tension band wiring for transverse fracture. A partial patellectomy is done for small proximal/distal pole fracture. Complete patellectomy with the reconstruction of extensor apparatus is performed for comminuted fracture.

Fig 2.115: Tension band wiring for patellar fracture.

FRACTURE OF PROXIMAL TIBIA The proximal tibia is composed of articular surface of medial and lateral tibial plateau. The medial and lateral articular surface of the tibia is separated by intercondylar eminence. The distal thick trabecular bone of proximal tibia continues with the tibial shaft. Mechanism of injury: It is caused by high-energy trauma. Axial loading causes fracture depression and varus or valgus force result in medial or lateral condyle fracture with associated ligamentous injuries. Bumper fracture is a high velocity bumper impact causing fracture of lateral tibial plateau. Clinical features: The patient presents with knee pain, swelling and inability to bear weight. On examination there is knee hemarthrosis, abnormal mobility and crepitus may be present. Any knee instability in varus and valgus, compartment syndrome and distal neurovascular status has to be assessed. 125

Investigations: a)X-ray proximal tibia with knee joint – AP and lateral view. b)CT scan with 3D reconstruction c)MRI of the knee to assess ligaments and other soft tissue injuries.

Fig 2.116: Radiograph of proximal tibia fracture. Treatment: Conservative management: A)   Undisplaced fracture is treated with above knee plaster for 6 weeks. B)   Lower tibial pin traction is applied in patients with poor general condition and associated head injury. Operative management: A)   Articular depression > 5-8mm, articular split fractures are treated by ORIF with anatomical articular reduction and plating B)   Knee spanning external fixator for open fractures Complications: Early a)      Neurovascular injury: The tibial condyles are closely related to popliteal vessels on the posterior aspect and any fracture in this region can cause popliteal vascular injury. The popliteal vessels extend proximally from the adductor hiatus and exit distally at the soleal hiatus. This segment of popliteal vessels is relatively fixed and prone to injuries. The spectrum of injury can vary from vascular spasm, thrombus formation to partial or complete laceration of popliteal vessels. Investigations like X-ray of proximal tibia, arterial doppler scan and CT angiography help to identify the vascular injury. Vascular injuries require external fixator application, vascular repair and if necessary fasciotomy is performed. Vascular injuries should be treated within 6-8 hours and any delay beyond that increases the risk of amputation Closed proximal tibia with fibular neck fractures commonly cause neuropraxia involving the common peroneal nerve. Open injuries involving fibular neck can cause partial or complete laceration of common peroneal nerve. Open injuries with nerve lacerations require nerve repair.

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b) 

Compartment syndrome: It is uncommon but devastating complication following proximal tibia fractures as it is a tight osteo-fascial compartment. High clinical suspicion, serial neurovascular assessment, aggressive evaluation by measuring the compartment pressure especially in unconscious and head injury patients is necessary. It is treated aggressively with ice packs, analgesics, limb elevation, fracture reduction by slab or pin traction and if needed emergency fasciotomy has to be performed.    

Fig 2.117: Impending compartment syndrome following proximal tibia fracture. Late: a)    Malunion b)    Knee stiffness c)     Secondary osteoarthritis of knee.

INJURIES OF KNEE LIGAMENT Knee joint is divided into three compartments called the medial, lateral and patellofemoral compartment .Tibio-femoral joint is a hinge type of synovial joint. Patello-femoral is saddle type of synovial joint. The knee joint is stabilized by anterior and posterior cruciate ligaments in the center. Medial and lateral collateral ligaments stabilize the medial and lateral joint side respectively. The Meniscus is a C-shaped fibrocartilagenous structure present in the medial (medial meniscus) and lateral (lateral meniscus) compartment respectively. Cruciate Ligament Injury: Anterior cruciate ligament prevents anterior translation of the tibia on femur. Posterior cruciate ligament prevents posterior translation. ACL tear is more common than PCL. ACL tear occurs during fall from height, contact and noncontact sports injuries causing sudden pivoting action of the knee. Mechanism of injury: The most common mechanism is valgus twisting injury on flexed knee during sports. PCL tear can be due to dashboard injury. Clinical features:

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The patient presents with pain, discomfort while walking and knee effusion. On examination: Acute injuries: 1)      Lachman's test: It is the translation test in 20° knee flexion. It is useful in acute ACL tear(acute hemarthrosis prevents further flexion for examination) Chronic injuries: 1)    Quadriceps wasting is present. 2)    Anterior & Posterior drawer's test: It is useful in chronic ACL and PCL tears. Clinical tests: Lachman test: Standing by the side of patient, grasp the lower thigh with one hand and with the opposite hand grasp the upper leg and flex the knee to 15°. Then applying force with both your hands try to move the leg first anteriorly and then posteriorly. Look for any subluxation anteriorly and compare it to the opposite knee. A positive anterior subluxation indicates ACL injury in an acutely injured knee. Anterior drawer test: The anterior drawer test is used to assess the integrity of ACL. The patient is supine with the hip flexed 45° and the knee flexed to 90°, the foot is stabilized by sitting on it. The proximal tibia is grasped firmly with both hands. Keeping the thumb anteriorly and fingers posteriorly a “push-pull” force is applied noting for any pain and laxity compared to opposite knee. When there is more anterior subluxation (positive anterior drawer sign), it indicates ACL insufficiency. Similarly, when there is comparatively more posterior subluxation (positive posterior drawer sign), it indicates PCL insufficiency. Investigations: X ray knee AP/Lateral, MRI knee Treatment: ACL reconstruction with patellar tendon/ hamstring graft. Complication: Cruciate ligament tears lead to increased knee translation which predisposes to knee instability and secondary osteoarthritis. Collateral ligament injuries: Medial collateral ligament is the most commonly injured ligament. It is associated with other ligament injuries. The patient presents with

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pain, localized swelling and discomfort while walking. On examination, valgus stress test is used to assess medial collateral ligament and varus stress test is for lateral collateral ligament.

Fig 2.118: (A) Varus stress test for Lateral collateral ligament; (B) Valgus stress test for Medial collateral ligament. Treatment: a) Incomplete tear is treated by cylindrical cast b) Complete tear is treated by surgical repair/reconstruction.                                                             Meniscus injuries: The meniscus is a C-shaped piece of tough, rubbery fibrocartilage that acts as a shock absorber between femur and tibia.

Function of meniscus: Makes joint stable Shock absorber Help in the knee locking mechanism Controls gliding and rolling motions of knee Weight transmission Increases contact area Mechanism of injury: The incidence of medial to lateral meniscus tear is about 20:1. Medial meniscus is less mobile and tears occurs on twisting injury when thigh (femur) is rotated internally with leg and foot anchored to the ground. 129

Classification: It is divided into 3 zones based on the blood supply 1) Red zone (peripheral) 2) Red-white zone (middle region) 3) White zone (inner region)

Fig 2.119: N) Normal Meniscus and its zones A) Radial tear B) Horizontal tear C) Bucket handle tear D) Parrot beak tear E) Vertical tear. Clinical features: The patient presents with symptoms like knee effusion, clicks and locking of knee. On examination signs like medial or lateral joint line tenderness, McMurray test and Apley's grinding test are positive suggestive of a meniscial tear. Investigations: MRI of knee to identify the site and length of tear. Treatment: White and red-white zone tears: Knee arthroscopy and partial menisectomy. Red zone tears: Resuturing the peripheral tear O' Donoghue’s unhappy triad: Injury to A)   Medial collateral ligament B)   Anterior cruciate ligament C)   Medial meniscus Special Points: Osteochondritis of tibial tubercle- Osgood Schlatter's disease Osteochondritis of lower patella pole - Sinding Larson Disease Injury to femoral attachment of medial collateral ligament with new bone formation- Pellegrini Stieda's disease Questions: Short Essay: 1)    Describe in brief the classification and management of fracture patella. Short Answers:

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1)    Fracture patella 2)    Anterior drawer test 3)    Cruciate ligament of knee

Competency OR 2.13: Describe and discuss the aetiopathogenesis, clinical features, investigation and principles of management of both bone leg.

FRACTURE BOTH BONES LEG Closed Fracture Tibia and Fibula: The tibia is weight-bearing long tubular bone with triangular in cross section. Fractures of tibia and fibula shaft are one of the most common long bone fractures. Mechanism of injury a)    Low energy trauma like fall. b)    High energy road traffic accidents leading to closed soft tissue injuries and bony comminution. Clinical examination: The patient presents with pain, swelling and deformity of leg. On examination, abnormal mobility and crepitus can be elicited and distal neurovascular status has to be assessed. Investigations: X-ray leg with knee joint and ankle joint – AP and lateral view.

Fig 2.120:  X-ray shows both bone leg fracture. Treatment: A) Conservative Treatment (95%): Close reduction and above knee(A/K) plaster for 3 weeks followed by PTB cast (Patellar tendon bearing cast). PTB is a functional cast bracing discovered by Sarmiento. It allows early knee movement, sitting, ambulation and fracture union.

Acceptable Reduction for closed fracture: 131

Ankle and knee joint surface should be parallel Acceptable varus / valgus in AP view is 5 ° Anterior/ posterior angulation in lateral view is 10 ° At least 50 ° apposition Shortening upto 1 cm is acceptable B) Surgery: If fracture reduction is unacceptable: a)    Closed reduction and internal fixation (CRIF)/Open reduction and internal fixation (ORIF) with Intramedullary nail. b)    Open reduction internal fixation with DCP.

Fig 2.121: Intramedullary interlocking nail for tibia fracture. Complications: a)    Malunion b)    Delayed union c)     Non union. Open tibia fracture: The anteromedial border of tibial bone is placed subcutaneously so it is more prone to open fractures. The nutrient artery originates from posterior tibial artery and enters the tibial shaft just distal to the insertion of soleus muscle. Fractures in distal 1/3rd tibial shaft causes disruption of nutrient vessels and lead to delayed union or nonunion. Mechanism of injury: Direct trauma caused by road traffic accidents, penetrating injuries, crush injuries lead to open tibial fractures and also associated soft 132

tissue injuries. Clinical features: The patient presents with pain, swelling, bleeding open wounds and fracture deformity. On examination circumferential evaluation of the soft tissue envelope should be done noting lacerations, ecchymosis, fracture deformity and distal neurovascular status should be examined. Investigations: X-ray of leg with knee joint and ankle joint – AP/lateral view. Treatment: Open tibial fracture splinting followed by prophylactic IV antibiotics with cephalosporin and aminoglycoside are started. Emergency soft tissue debridement in operation theatre is done and graded according to Gustillo Anderson classification. Skeletal stabilization of open tibia fracture is done either by ORIF with IM nail or external fixator based on the extent of soft tissue injuries or contamination. Open tibial fractures should be converted into closed fractures as early as possible. Complications: A)Compartment syndrome B)Osteomyelitis C)Infected nonunion D)Delayed union, nonunion and malunion. Predisposing Factors for tibia nonunion: Open fractures Significant initial displacement Comminution Soft tissue damage Infection especially in compound fracture Inadequate immobilization Intact fibula Infected nonunion Compartment syndrome. Questions: Long Essay: 1)    Write in detail on classification of fractures. Describe the types, diagnosis, complication and management of Compound fractures. Short Answer:

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1)    Compound fracture.

Competency OR 2.14: Describe and discuss the aetiopathogenesis, clinical features, investigation and principles of management of ankle fractures Ankle anatomy: Ankle joint is a complex hinge joint composed of tibia, fibula superiorly and talus inferiorly. It is stabilized by a complex ligamentous system. Ankle ligaments: The ankle joint is stabilized by following ligaments Medial collateral ligament a) Anterior tibiotalar ligament b)Deltoid ligament c)Posterior tibiotalar ligament

Lateral collateral ligament a) Anterior talofibular ligament b) Calcaneofibular ligament c) Posterior talofibular ligament

Syndesmotic ligaments a) Anterior inferior tibiofibular ligaments b) Interosseous ligament c) Posterior inferior tibiofibular ligaments

Fig 2.122: Ligaments of the lateral aspect of ankle: A) Anterior inferior tibiofibular ligament; B) Posterior inferior tibiofibular ligament; C) Anterior talofibular ligament; D) Calcaneofibular ligament; E) Posterior talofibular ligament. Movements of ankle: The ankle joint is a hinge joint with movements only in one axis. So only ankle dorsiflexion and plantar flexion is possible. Ankle mortise: The articular surfaces of medial and lateral malleoli, the distal articular surface of the tibia and the intervening tibiofibular ligament constitute the ankle mortise. Injuries around the ankle: Ankle fractures a)    Medial malleoli fracture b)    Lateral malleoli fracture

Ankle sprain a)    Medial ligament sprain b)    Lateral ligament sprain

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c)     Bimalleolar fracture- Medial and lateral malleoli fracture. d)    Trimalleolar fractureMedial, lateral and posterior malleoli fracture

ANKLE FRACTURE Ankle fractures are fractures involving the distal end of tibia and fibula. Ankle mortise is formed by the distal articular surfaces of the malleoli and tibia.

Fig 2.123: Radiograph of ankle showing bimalleolar fracture.  Mechanism of injuries: The pattern of ankle fracture depends on low-velocity or high-velocity injuries. 1) Low-velocity forces include a) Rotational stress: Rotational stress is caused by a twisting force to the ankle joint while walking or running. The positions of the foot, deforming force determine the series of fractures in the ankle. b) Axial stress: Axial stress on the ankle joint results in fracture involving the tibial plafond.  2) High-velocity forces such as road traffic accidents cause severe ankle injuries. Classification of ankle fractures: Lauge Hansen classification: This classification is based on the mechanism of injury. The first part of the classification specifies the position of foot during injury and the second part specifies the deforming force. Position of foot Supination Pronation

Deforming forces Adduction Abduction External rotation

Classification:

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1)   Supination –adduction injuries- With foot in supination, forceful adduction causes avulsion fracture of the fibula and oblique fracture of medial malleoli.

Fig 2.124: Supination (A)-adduction (B) injury: 1) Avulsion fracture of fibula. 2) Medial malleoli fracture. 2)   Supination- external rotation injuries- With foot in supination, forceful external rotation causes oblique fracture of the fibula, posterior malleolus followed by medial malleolus.

Fig 2.125: Supination(A)-external rotation(C) injury: 1) Fibula fracture; 2) posterior malleoli fracture; 3) Medial malleoli fracture. 3)   Pronation abduction injuries- With foot in pronation, forceful abduction causes avulsion fracture of medial malleoli and oblique fracture of fibula at or above the level of syndesmosis.

Fig 2.126: Pronation(A)-abduction(B) injury: 1) Avulsion fracture of medial malleoli; 2) Fibula fracture. 4)   Pronation-external rotation injuries- With foot in pronation, forceful external rotation causes, medial malleoli fracture followed by supra syndesmotic oblique fracture of the fibula and posterior malleoli fracture.

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Fig 2.127: Pronation(A)-external rotation(C) injury: 1) Medial malleoli fracture; 2) Supra syndesmotic oblique fracture of fibula; 3) posterior malleoli fracture. Weber’s classification: This is based on the level of fibula fracture. The higher the level of fibula fracture, more unstable is the ankle joint. 1)Type A: Fibula fracture below the tibiofibular syndesmosis( infrasyndesmotic injury) 2)Type B: Fibula fracture at the level of tibiofibular syndesmosis 3)Type C: Fibula fracture above the level of tibiofibular syndesmosis. (suprasyndesmotic injury). Clinical features: The patient typically presents with a twisting injury of the foot with pain, swelling and inability to bear weight. On examination ankle swelling, tenderness, abnormal mobility and crepitus can be elicited. If ankle deformity is present, immediate reduction should be done to prevent overlying skin complications. Investigations: 1)    X-ray of the ankle: AP, lateral and mortise view (ankle in 15° internal rotation) for fractures in medial or lateral malleoli, any disruption in tibiofibular syndesmosis and subluxation of talus should be assessed. 2)    CT scan of ankle with 3D reconstruction in complex ankle injuries. Treatment: The aim of treatment for ankle fracture is 1)    Smooth articular alignment of ankle mortise. 2)    Anatomical positioning of the talus. Conservative management: Stable fractures of ankle can be treated with analgesics and below knee(B/K) plaster cast for 6 weeks. Operative management: Displaced unstable fractures of the ankle can be treated by open reduction and internal fixation(ORIF).Internal fixation can be achieved by various options depending on the site of fracture, this includes 1)    Tension band wiring 2)    Compression/ malleolar screws

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3)    Plate and screw fixation for lateral malleolus. Open ankle fractures with crush injury to skin, muscles and bone are treated by external fixator. Complications: 1)    Fracture malunion 2)    Non-union 3)    Post-traumatic osteoarthritis 4)    Ankle stiffness.

ANKLE SPRAIN Injury to ankle ligament is called ankle sprain. Lateral ligament sprain: It is the most commonly injured ligament in the ankle. Mechanism of injury: This is due to supination-inversion injury in plantar flexed foot. It commonly occurs while running on uneven surfaces and athletes. The most common ligament injury is anterior talofibular ligament. Clinical features: The patient presents with pain, swelling of ankle and inability to walk. On examination ankle tenderness, swelling is present. Varus and valgus test helps to assess ankle stability. Investigations: a) X-ray ankle- AP/Lateral, b) MRI of the ankle to assess grade of ligament tear. Treatment: a)    RICE regimen- Rest, ice packs, compression and limb elevation. b)    Analgesics c)     Below knee plaster for 6 weeks Medial ligament sprain: Medial ligament sprain is due to eversion injury. The deltoid ligament is most commonly involved. It is treated by rest, analgesics and immobilization. Competency OR 2.13: Describe and discuss the aetiopathogenesis, clinical features, investigation and principles of management of: (b) Calcaneus (c) Small bones of foot

FRACTURE CALCANEUM

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The calcaneum is the commonest tarsal bone to fracture. It is involved in weight transmission.  Mechanism of injury: The most common mechanism of injury is falling from height and landing on the foot. Axial weight transmission leads to other associated injuries like lumbar spine fractures and lower limb injuries. Classification: Extraarticular fractures: The fractures donot involve the articular surface of calcaneum and include fractures in the posterior part of the body, avulsion fracture of tuberosity. Intraarticular fractures: The fracture lines extend into the subtalar joint. These are joint depression fractures with gross communition. Intraarticular fractures have poor prognosis with a high incidence of secondary osteoarthritis of subtalar joint.

Fig 2.128: Calcaneal fractures: A) Extra-articular fracture; B) Intraarticular fracture. Clinical features: Patient presents with pain, swelling of heel and unable to bear weight. On examination, there is marked tenderness and heel broadening may be present.  Investigations: 1)    X-ray Hindfoot AP/ lateral view: It is used to evaluate Bohler and Gissane angle. Axial calcaneal view is also done. 2)    CT scan with 3D configuration for fracture configuration. Treatment: Conservative treatment– Closed reduction with B/K Plaster with foot end elevation. Operative treatment– ORIF with K wire, plate and screws. Complications: 1)    Heel pain 2)    Subtalar arthritis

FRACTURE TALUS Talus is a tarsal bone with a precarious blood supply. 3/5th of bone is covered by articular cartilage with no muscles attached to it. Mechanism of injury:

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A fracture neck talus occurs due to sudden passive hyperextension of the foot (Aviators fracture).

Fig 2.129: Fracture of neck of talus. Parts of the talus: A) Head B) Neck C) Body. Classification: Talar fractures can happen in talar head, neck and body. The most common site of fracture is talar neck. Talar neck is called the fracture of necessity because of its precarious blood supply which passes from talar head (distal) to talar body (proximal). Hence early anatomical reduction and fixation should be done else it will lead to avascular necrosis of talar body. Clinical features: Pain, swelling and inability to bear weight on the foot. Investigation: X-ray ankle: AP/lateral and oblique views. Treatment: Conservative management: If the fracture is undisplaced a below knee plaster cast in planter flexion is applied for 6-8 weeks. Operative management: If the fracture is displaced, Open reduction with internal fixation with screws. Complications: 1) Non-union 2) Avascular necrosis (proximal part of talus) 3) Post-traumatic osteoarthritis.

INJURIES OF FOOT Tarsometatarsal (Lisfranc) injury: Lisfranc injury is a tarsometatarsal injury which can be either fracture, dislocation or a fracture-dislocation. Mechanism of injury: It is caused by a twisting injury of forefoot or heavy object falling on the foot. Clinical features: The patient presents with pain, swelling and variable deformity of the foot. On examination, plantar ecchymosis may be seen and tenderness over the tarsometatarsal region is present.

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Investigations: X-ray- AP/lateral and oblique views of foot. Surgery: Open reduction internal fixation with K wires. Complications: Compartment syndrome, chronic foot pain.

Metatarsal injuries: Jone's fracture: Avulsion fracture of base of 5th metatarsal due to forced inversion of the foot. Mechanism of injury: It is caused by the pull exerted by tendon of peroneus brevis. Clinical features: The patient presents with pain, swelling and discomfort while walking. On examination, tenderness over the base of 5th metatarsal can be elicited. Investigation: X-ray foot AP/oblique should be done.

Fig 2.130: Radiograph of Jone’s fracture. Treatment Below knee(B/K) plaster for 6 weeks. March (stress) fracture: Stress fracture usually affects the second metatarsal bone. The fracture is common over the metatarsal neck region. It is common in military and police recruits following marching. It also commonly occurs in tibia shaft, femur neck region. Clinical features: Foot pain is presenting feature Investigations: Initial X-ray may be normal but the radio-isotope scan shows increased uptake. No displacement occurs usually Treatment: Rest, analgesics and if severe below knee(B/K) plaster immobilization.

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Fractures of other Metatarsals and phalanges: Fractures of metatarsals and phalanges occur commonly following road traffic accidents or heavy objects falling on the foot. Treatment: Conservative: Undisplaced/partially displaced closed fractures are treated by below knee plaster for metatarsal fractures and buddy strapping for phalangeal fractures. Operative: Open and displaced fractures are treated by open reduction and internal fixation (ORIF) with K wire. Questions: Long Essay: 1)    Describe ankle injuries- classification, clinical features and management. Short Essays: 1)    Tibial fracture 2)    Injuries around the ankle.

Competency OR 2.15: Plan and interpret the investigations to diagnose complications of fractures like malunion, non-union, infection, compartmental syndrome. COMPARTMENT SYNDROME: The suspicion of compartment syndrome is mostly clinical based on type of injury, symptoms and clinical signs like pain on passive stretch, pallor, paraesthesia, pulselessness and paralysis. A needle can be attached to suspected compartment and a pressure monitor is used to record the pressure. It can also be confirmed by measuring the intracompartmental pressure by Stryker method. The normal compartment pressure is 0 – 8 mm of Hg. Pressures above 30 mm of Hg is abnormal. INFECTION: Infection of soft tissues and bone may occur due to microorganisms like streptococci, E coli, staphylococci and pseudomonas following compound fractures, postsurgical infections etc. Investigations: Lab investigations: Complete blood count shows normal or low HB and leucocytosis with neurophilic predominance and ESR, CRP is

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raised. Other investigations like bleeding time, clotting time, liver function, renal function tests, HIV and HBsAg is done. Culture: Gram stain and culture and sensitivity(C/S) of discharge X-ray of the affected part to see for any acute osteomyelitic changes, CT scan and MRI scan as necessary. MALUNION: Malunion is defined as fractured bone that has united in nonanatomical position. Investigations: A)X-ray AP/lateral view: To see for translation, angulation and rotation. It is also used to compare normal X-ray of the opposite limb for any limb length discrepancy.

Fig 2.131: Radiograph of both bone leg showing distal 1/3rd translatory and rotatory malunion of tibia. 2)CT scan with 3D reconstruction: To assess malunion in 3D plane and for preoperative planning for surgical correction. 3)MRI: MRI is performed to assess malunion in intraarticular pathology. NONUNION: FDA definition of nonunion as “established when a minimum of 9 months has elapsed since the fracture with no visible clinicoradiological progressive signs of healing for 3 months” Investigations: X-ray AP/Lateral view: 1) To assess the gap between fracture fragments 2) Nonunion fragment ends may be round and sclerotic with obliteration of the medullary cavity. 3) To determine whether it is atrophic or hypertrophic type of nonunion. 4)  if there is any radiological signs of infection.

Fig 2.132: AP and lateral radiograph showing proximal 1/3rd nonunion of tibia. Note the obliteration of medullary cavity and 143

sclerosis of fracture margins. CT scan with 3D reconstruction: To assess nonunion in 3D plane and for preoperative surgical planning. In infected nonunion to assess for any sequestrum and involucrum formation. Pus culture and sensitivity: It is sent in cases of infected nonunion with discharging sinus.

Competency OR 2.16: Describe and discuss the mechanism of injury, clinical features, investigations and principles of management of open fractures with focus on secondary infection prevention and management of Open fractures. OPEN FRACTURES: It is break in skin and underlying soft tissue leading directly into or communicating with the fracture and its hematoma. It constitutes about 3% of all limb fractures. Types of injury: 1) Fall from height 2) Road traffic accidents 3) Fall of heavy object 4) Assault. Low-velocity injury

High-velocity injury:

Simple fracture with mild soft tissue injury and skin tear.

A)Segmental fracture B)Bone loss C)Compartment syndrome D)Crush syndrome E)Extensive degloving

Clinical examination: 1)Patient assessment involves ABCDE: Airway, Breathing, Circulation, Disability, Exposure. 2)Evaluate injuries to the head, chest, abdomen, pelvis and spine Look: Special attention to check for the wounds Feel: Sensory and motor deficits, pulse distal to injury Move: Check for abnormal mobility. 144

Open fracture classification: Gustilo-Anderson classification Type 1 Wound less than 1 cm. Clean wound Type II Wound size 1-10 cm. Moderate energy-Moderate soft tissue damage. Type III Wound size >10 cm in size High energy-Extensive muscle damage with significant contamination. IIIA: Adequate soft tissue cover IIIB: Bone exposed IIIC: Circulatory compromise It helps in treatment according to guidelines and gives an idea about the prognosis.

Fig 2.133: Gustilo and Anderson classification for open fractures. Infection rates in open fractures: Type 1 Type II Type III IIIA IIIB IIIC

0-2% 2-7% overall 10-25% about 7% 10-25% 25-50%

Fracture healing may be affected by 1) Escape of hematoma 2) Impaired vascularity of soft tissues 3) Loss of bone 4) Bone necrosis 5) Infection Poor tissue oxygenation and devitalisation of surrounding tissues including the bone provide a perfect culture medium for infection and bacterial multiplication.

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Fig 2.134: Open fracture of both bone leg. Principles of treatment: 1)    Antibiotic prophylaxis and tetanus injection 2)    Irrigation and urgent wound debridement 3)    Stabilization of fracture- initial and definitive management 4)    Early definitive wound cover 1)   IV antibiotics for open fractures: Bacterial contamination is always associated with open fractures. Bacterial count and infection can be significantly reduced by prompt administration of IV antibiotics in combination with surgical debridement. Since most infecting organisms are typical skin flora, Cephalosporins are used. For more severe open fractures wounds, add an aminoglycoside. If agricultural contamination is present, high dose IV penicillin with aminoglycoside and metronidazole injections are given. Antibiotic of choice: 1) Type 1- cefazolin 2) Type II- cefazolin + gentamycin 3) Type IIIb & IIIc- cefazolin+ gentamycin+ metrogyl 2)   Irrigation and debridement: Copious irrigation with a balanced salt solution like NS or RL helps to remove the bacteria bits of dead tissues, blood clots and improves the surgical ability to examine the wound. Debridement means surgical exposure of the whole pathological injury zone and removal of all necrotic contaminated and damaged tissue from soft tissues or bone. All dead and questionably viable tissue is excised systematically from each tissue layer: a) Skin b) Subcutaneous tissues and deep fascia c) Muscle d) Bone a) Skin margins: Excise skin margins if necessary and extend the wound.

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b) Fascia: Fasciotomy if there is any evidence of compartment syndrome c) Muscle debridement: Meticulous muscle debridement is essential since dead muscle is a major nidus for infection. Alive and healthy muscle is identified by 1)Colour- Normally red in colour 2)Consistency- Firm in consistency 3)Capacity to bleed 4)Contractility- Responsive to forceps pinch d) Bone debridement: Remove the small-size avascular segments. Retain large cortical and articular segments, debride if infection develops. Ischemic zone excision must be complete, meticulous and radical. Early wound debridement is the most important component of care in fractures. In case of significant amount of contaminated, dead or possibly ischemic tissue is present, additional wound excision is performed 48 hours later. 3) Open reduction and fixation: It is the surgical approach where the fracture fragments are reduced and held in position until solid bone healing occurs. External or Internal fixation devices may be used to hold the bone fragments in position. External fixation External fixator is a stabilizing frame used to hold fractured bones in alignment. The pins and screws holding the bone are attached to a bar outside the skin. Eg: External fixator, Ilizarov.

Internal fixation Internal fixation is a surgical procedure used internally (under the skin) to set and stabilize the fractured bone. Eg: plate and screw fixation, IMN.

Implants used:

Advantages

External fixator 1) Easy and quick procedure. 2) Relatively stable fixation. Eg: Type IIIB

Plate and screw fixation 1)Anatomic reduction 2)Rigid stabilisation 3)Early mobilisation

Intramedulary fixation 1)minimal soft tissue stripping

  2) good wound access for dressing 3)good stability

Eg: Closed & open type 1 147

Disadvantages

Type IIIC injuries, Open fractures with vascular injuries.

and type II fractures.

Eg: closed, open type I and type II fractures

1)Pin tract infections

1)More extensive exposure

1)Impairs endosteal circulation

2)Delayed union.

Fixation of open fractures: Open fractures need surgical stabilisation usually with an external fixator initially followed by delayed definitive closed/open reduction and Internal fixation with plate and screws or intramedullary nail. Surgical fixation either external or internal is the best way to stabilise open fracture.

Fig 2.135: External fixator application for open tibial shaft fracture: A) Open injury with loss of skin, subcutaneous tissue, muscle and bone loss. B) External fixator. 4) Wound coverage: Every attempt should be made to close the wound primarily, if there is skin and soft tissue loss during injury, wound closure has to be done in stages. 1)    Primary closure: If patient presents within 8 hours of injury to hospital, debridement and primary skin closure is done. 2)    Delayed primary closure: If patient presents late and is suspicious of infection, initial debridement is done and wound is inspected after 2-3 days, if clean delayed primary closure is done. 3)    Secondary closure: If wound is bad and infection is present, secondary closure is done after 8-10 days. 4)    Skin grafting or flap closure: If skin loss is present, skin grafting is done. If skin and soft tissue loss is there with exposed fracture, flap closure is necessary.  

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After initial debridement, it is generally advisable to reinspect the injury zone after eight hours under anaesthesia. This is called second look, to assess the viability of tissue and if needed to conduct any necessary further tissue excision. The most frequent causes of infection in patients with open fractures are: 1) Incomplete excision of poorly vascularised tissue 2) Inadequate hemostasis and hematoma evacuation. 3) Devascularisation of primary viable tissue 4) Metallic implants under poorly vascularised tissue. Primary amputation: It is rarely performed on a mangled extremity which is lifethreatening condition. Complications: 1)    Infection- It may result in cellulitis, osteomyelitis, sepsis despite aggressive and serial debridements. Late complications include chronic osteomyelitis, infected nonunion. 2) Compartment syndrome- It is a devastating complication from severe loss of function because of tight facial compartments of forearm and leg. It can be avoided by a high index of suspicion with serial neurovascular examinations accompanied by compartment pressure monitoring and facial release at the time of surgery. Questions: Long Essay: 1)    Write in detail on classification of fractures. Describe the types, diagnosis, complication and management of Compound fractures. Short Answer: 1)    Compound fracture.

Credits: AthK

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Chapter 3

MUSCULOSKELETAL INFECTION Competency OR 3.1: Describe and discuss the aetiopathogenesis, clinical features, investigations and principles of management of Bone and Joint infections a) Acute Osteomyelitis b) Subacute osteomyelitis c) Acute Suppurative arthritis d) Septic arthritis & HIV infection e) Spirochaetal infection f) Skeletal Tuberculosis OSTEOMYELITIS Is an acute or chronic inflammatory process of bone, bone marrow and its structures secondary to infection with microorganisms. Classification: Based on duration: 1) Acute (usually 6 weeks) Based on the mechanism: 1) Hematogenous route- It is mainly seen in children where the organisms reach the bone through bloodstream. It is most commonly after infection from tonsil, lungs, ears etc. 2) Exogenous route- It occurs following open fractures or surgery where organisms enter the wound from outside directly. Based on the host response: 1) Pyogenic 2) Granulomatous A)  ACUTE OSTEOMYELITIS:

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It is an acute progressive infection of bone and bone marrow resulting in destruction by pyogenic organisms. Etiology: ☐       Age: It is common in children and less common in adolescents and adults. ☐       Sex : Males to female ratio is about 4:1 ☐       Location: Metaphysis of long bone. ☐       Poor nutrition, unhygienic surroundings. Etiological Agents: Staphylococcus aureus is the most common organism responsible for infection in children. Infants < 1 year 1)Group B streptococci 2)Staphylococcous aureus 3)Escherichia coli

1- 16 years 1)Staphylococcus aureus 2) Streptococcus pyogenes 3)Hemophilius Influenza

> 16 years 1)Staphylococcus aureus 2)Staphylococcous epidermidis 3)Gram negative bacteria

Pathophysiology: Hematogenous osteomyelitis commonly starts at the metaphysis of long bones. It is most commonly seen over the distal end of femur or proximal end of tibia. The metaphysis is the most common site of infection because it is the growing end of bone and the vessels are arranged in the form of loop or hair pin arrangement. As a result, the blood flow becomes considerably slower and more turbulent resulting in endothelial leaks. There is also a defective phagocytosis at these hairpin loops. Repeated microtrauma in the metaphysis can lead to hemorrhage which acts as a culture media for bacterial growth. Pathogenesis: The infective embolus from the hematogenous route enters the nutrient artery of metaphysis. The organisms get trapped in the hairpin bend of vessels and starts multiplication. This causes neutrophilic infiltration resulting in inflammatory exudates and hyperemia. The release of proteolytic enzymes destroys medullary elements resulting in formation of pus and other debris. This results in acute increase in intramedullary pressure. The infection passes through Haversian and Volkman canals resulting in local cortical necrosis. It enters the subperiosteal space and strips the periosteum.

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The infection can enter into joint, if it bursts within the capsule(Fig 3.01 B) or into soft tissues and drains out(Fig 3.01 A).

Fig 3.01: A) (1) Acute osteomyelitis leading to metaphyseal abscess (2) subperiosteal abscess formation (3) avascular growth plate cartilage (4) knee joint capsule attached to epiphysis (5) Normal synovial fluid. B) (A) Metaphyseal abscess (B) Joint capsule attached to metaphysis (C) septic synovial fluid (D) metaphyseal vessels (E) Avascular growth plate cartilage.

Clinical features: Parents of the child bring with one or more following complaints: 1)    High-grade fever 2)    Inability to bear weight or move the limb (pseudoparalysis) 3)    Acute tenderness near the end of bone 4)    Local redness, swelling, warmth and edema, if pus escapes by perforating the periosteum. Newborns and infants are drowsy, irritable, lethargic and may have mild or no constitutional symptoms. Laboratory tests: 1)Hematological: It may show low hemoglobin levels, raised leucocyte count with neutrophilic predominance. Inflammatory markers like ESR, CRP are raised. 2)A blood sample should always be sent for culture and sensitivity before starting antibiotics. It is positive in upto 50% cases. 3)X-ray: It takes from 10 to 21 days for an osseous lesion to become visible on X-ray because a 30–50% reduction of bone density must occur before radiographic changes are apparent.

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4)MRI scan is sensitive in early stages of infection. 5)Bone scan: Tc-99 and WBC labelled gallium/indium bone scan shows increased uptake when bone inflammation is present. It is valuable in early localization (within 48 hrs) of bone infection. 6)Aspiration: The most definitive way to confirm the clinical diagnosis is by pus aspiration from metaphyseal subperiosteal abscess or in the adjacent joint. Treatment: High index of clinical suspicion, early diagnosis and treatment are essential in acute osteomyelitis. 1) 

Antibiotics: Emperical broad-spectrum IV antibiotics like amoxiclav or 3rd generation cephalosporins are started immediately after taking sample for blood culture. The IV antibiotics are changed later on according to culture and sensitivity report. Specific antibiotics should be continued for at least 4-6 weeks. 2)      Other drugs: Analgesics reduce pain and antipyretics reduce fever. IV fluid support to maintain fluid balance. 3)      Splintage: The limb should be immobilized and supported with plaster of paris slab or splint. This helps to reduce pain and prevent pathological fracture. 4)    Drainage of pus: If emperical antibiotics are started >48 hours of infection, there is risk of pus formation. If any localized swelling or abscess formation happens then immediate surgery should be done. The surgery consists of incision and drainage of pus followed by drilling multiple holes into the bone, hence the pus under tension is drained out. This is called bone decompression. The pus is sent for culture/sensitivity and specific antibiotic is started after the report.    

Complications of acute osteomyelitis: 1)    Bone abscess 2)    Septic Arthritis 3)    Septicemia 4)    Pathological fracture 5)    Physeal growth arrest 6)    Chronic osteomyelitis

SUBACUTE OSTEOMYELITIS Subacute osteomyelitis is a bone infection that is insidious in onset and is caused by organisms of low virulence or in an immunocompetent host. Hence patients present with mild local symptoms without constitutional symptoms.

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Brodie’s abscess: Brodie’s abscess is a type of subacute osteomyelitis usually occurring in the metaphyseal region of long bones in young adults. It is characterized by an abscess in metaphyseal region surrounded by zone of sclerosis. The most common sites are upper end of tibia or lower end of femur. Pathology: The most common organism is staphylococcus aureus which infects the metaphysis of long bones. Low-grade infection causes circumscribed round or oval cavity with pus formation in the metaphysis surrounded by zone of sclerosed bone. Clinical Features: The patient is a young adult who usually presents with deep seated dull pain with limping. Localised swelling, tenderness may be present. Investigations: 1)Hematological: Leucocyte count may be normal or raised. Inflammatory markers like ESR, CRP are raised. 2)X-ray shows a circumscribed or oval cavity surrounded by a zone of sclerosis.

Fig 3.02: Brodie’s abscess showing central lytic area surrounded by zone of sclerosis. 3)Fluid aspiration can be done and sent for culture and sensitivity.If surgery is done, biopsy is sent for histopathological examination. Treatment: 1)    Conservative treatment- If lesion is small it is treated with oral antibiotics for 6 weeks. 2)    Surgery- If the lesion is large, curettage of the cavity is done.

CHRONIC OSTEOMYELITIS

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Chronic osteomyelitis is severe, persistent and incapacitating infection of bone and bone marrow. Causes: 1) Inadequately treated acute osteomyelitis 2) Following open fractures 3) Following operation Etiological Agents: Staphylococcus aureus is the most common organism. Other organisms are streptococcus pyogenes, escherichia coli, staphylococcus epidermidis. Salmonella infection is most common in sickle cell patients and pseudomonas infection in IV drug abusers. Pathogenesis: The infection is caused by high virulence organisms or a weak host defense mechanism leading to a persistent inflammatory process that continues with time resulting in raised intramedullary pressure due to inflammatory exudate (pus). There is stripping of overlying periosteum due to pus and the underlying bone loses its blood supply leading to bone necrosis. This dead bone is called the sequestrum. The repair process gradually continues and new bone is laid subperiosteally. This is called involucrum. Pus discharge can happen through multiple sinus openings through the bony holes and through soft tissues which drain out into the skin. These bony holes are called cloacae. A cloaca is bony hole through which pus drains out into subcutaneous tissue and then to exterior through skin sinus. It usually communicates with sequestrum and occasionally may discharge bony spicules through sinus.   The involucrum is the sheath of reactive, new, immature, subperiosteal bone that forms around the sequestrum. The involucrum may gradually increase in density and thickness to form part of new bone. The sequestrum is a piece of dead bone surrounded by infected granulation tissue.

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Fig 3.03: Clinical picture, X-ray and diagrammatic representation of chronic osteomyelitis in the proximal humerus of a patient. (A) Epiphysis (B) Growth plate (C) Periosteal elevation (D) Sequestreum (E) Involucrum (F) Cloaca.  Types of sequestrum: Ivory Black Sandy or rice grain Diaphyseal Ring Feathery

Syphilitic osteomyelitis Fungal Osteomyelitis Tuberculosis Sickle cell anaemia patients secondary to salmonella typhi Infected pin tract Tuberculosis of ribs.

Clinical features: The most common complaint is the persistence of discharging sinus. The sinus may directly communicate to underlying sequestrum. There may be a history of occasional discharge of bony spicules from the sinus. On bony palpation, it is tender and irregularly thickened with soft tissue contractures. The surrounding skin appears to be inflamed and edematous. Constitutional symptoms like fever, weight loss, and loss of appetite may be present.

Fig 3.04: Chronic osteomyelitis leading to woody indurated leg and extruding sequestrum.

Fig 3.05: Type 3b Open both bone leg fracture treated by external fixator. 

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Laboratory tests: 1)Hematological: It may show low hemoglobin levels, raised leucocyte count with lymphocytic predominance. Inflammatory markers like ESR, CRP are raised. 2)X-ray: X-ray shows thickening and irregularity of cortex. There may be cavity in the bone. The presence of sequestra in the cavity is seen as dense shadow. The new bone formation (involucrum) can be seen around the sequestrum. Pathological fracture can be seen if any along the weakened bone.

Fig 3.06: Radiograph of chronic osteomyelitis of distal femur showing sequestrum in medullary cavity surrounded by involucrum. The patient has also developed distal femur deformity and is at a high risk of pathological fracture. 3)Sinogram: A radioopaque dye can be injected into the sinus tract and X-ray is taken. This helps to localize the direction of sinus tract into the bone and sequestrum if any. 4)CT and MRI scan is useful to identify bone destruction, abscess and sequestra. 5)Pus from discharging sinus is sent for culture and sensitivity. Treatment: 1. General treatment: Nutritional therapy by intake of enough calories, proteins, vitamins etc. 2. Antibiotic therapy: The antibiotics are started according to culture and sensitivity report before taking up for the surgery. 3. Splintage: Splints support helps to immobilize the limb. This helps to reduce pain and prevent pathological fracture. 4. Surgical treatment: a) Seqestrectomy: Removal of sequestrum is called sequestrectomy. Sequestrectomy is performed only after an adequate cortex in the form of involucrum is formed to decrease the risk of pathological fracture.

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b) Saucerisation: After the removal of sequestrum, the bony cavity is enlarged with chisel or osteotome to saucerise the cavity. This will eliminate all dead spaces and prevent accumulation of pus inside the cavity. c) Curettage: The infected granulation tissue is curetted from the cavity to remove the disease process. d) Obliteration of dead space: After the removal of disease process, the dead space can be filled up with either antibiotic-impregnated beads and later on cancellous bone grafting can be done to fill the bony void. e) Excision of sinus tract: The epithelialised sinus tract is excised and the wound is allowed to heal by secondary intention. f) Amputation: It is indicated in rare cases where patient has recalcitrant osteomyelitis.  Complications of chronic osteomyelitis: 1) Acute exacerbation of chronic osteomyelitis 2) Septicemia 3) Pathological fracture can occur in the bone weakened by chronic osteomyelitis. 4) Limb length discrepancy- Limb shortening can occur due to growth plate damage or limb lengthening can happen due to stimulation of growth plate because of increased hyperemia. 5) Joint stiffness due to adjacent soft tissue contractures. 6) Malignancy- A long-standing discharging sinus tract may rarely transform into squamous cell carcinoma (Marjolin’s ulcer). 7) Amyloidosis. Sclerosing osteomyelitis of Garre: It is a type of chronic osteomyelitis caused by low-grade pyogenic and anaerobic organisms primarily involving the diaphysis of bone characterized by periostitis. It is primarily a non-suppurative process with periosteal inflammation. This leads to subperiosteal new bone formation resulting in sclerosis. The patient presents with pain and swelling of the involved bone. It is treated with antibiotics.

ACUTE SUPPURATIVE ARTHRITIS It is an acute inflammation of synovial membrane with purulent effusion into joint capsule caused by pyogenic organisms.

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Etiological Agents: Staphylococcus aureus is the most common organism responsible for infection. The other organisms are streptococci, pneumococci, gonococci etc. Routes of infection 1)    Hematogenous route: Infection from distant foci can spread to the joint through bloodstream. 2)    Direct inoculation: It may result from penetrating trauma where the organisms can get directly inoculated into the joint. 3)    Direct spread from adjacent bone: Osteomyelitis usually begins in the metaphyseal region Pathogenesis: Once infected, the synovial membrane becomes hyperemic and there is exudative effusion into the joint. If untreated, the synovium becomes more inflamed and pus formation begins. Gradually the synovium and articular destruction starts by bacterial proteolytic enzymes. There is acute destruction of articular cartilage leading to exposure of subchondral raw bony surfaces. With resolution, the raw bony surfaces fuse ultimately leading to bony ankylosis. Clinical features: Symptoms: The disease is more common in children but also can happen in adults. Patients present with high grade fever and acute onset of joint swelling associated with throbbing pain.

Fig 3.07: Septic arthritis of left knee in a neonate. Signs: On inspection, the skin over the joint looks swollen and edematous. The joint is swollen and is held in a “position of ease” offering maximum joint space for the effusion. On palpation, there is local raise in temperature, tenderness present over the joint. Joint effusion can be elicited by fluctuation test. Range of motion is painful and restricted due to muscle spasm. Joint Shoulder Elbow Hip Knee Ankle

Position of Ease Adduction Flexion with pronation Flexion. abduction and external rotation Flexion Plantar flexion

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Fig 3.08:  Septic arthritis of knee.

Laboratory tests: 1)Hematological: Blood examination shows raised leucocyte count with neutrophilic predominance. Inflammatory markers like ESR, CRP are raised. 2)X-ray: X-ray in early stages show increase in joint space due to joint effusion. After few days to weeks, there is asymmetrical destruction of articular cartilage causing irregular and decreased joint space. There is patchy rarefaction of adjacent bone. Finally the joint space gets obliterated by bony trabaculae leading to bony ankylosis of the joint. 3)Ultrasound is helpful to evaluate effusion in deep joints like hip and shoulder. 4)Joint aspiration: Synovial fluid is aspirated, sent for gram stain, culture and sensitivity. If frank pus is aspirated then an emergency arthrotomy of joint is performed. Treatment: High index of clinical suspicion, early diagnosis and treatment is essential in septic arthritis. 1) 

Antibiotics: Emperical broad spectrum IV antibiotics like amoxiclav or 3rd generation cephalosporins are started immediately after knee aspiration. The IV antibiotics are changed later on according to culture and sensitivity report. Specific antibiotics should be continued for at least 4-6 weeks. 2)      Splintage: The limb should be immobilized and supported with plaster of paris or splint. 3)      Other drugs: Analgesics reduce pain and antipyretics reduce fever. IV fluid support is given to maintain fluid balance.    

Surgery: Arthrotomy and drainage: The joint is opened and all the pus is drained out. The joint is washed with plenty of saline and antibiotic solution. The capsule is sutured and the overlying muscle and skin is sutured with a suction drain in situ.

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Arthrodesis: If patients presents late, the articular cartilage and bone are damaged secondary to septic process then arthrodesis of joint in functional position is done. Complications of Septic arthritis: 1)    Cartilage and bone destruction 2)    Joint dislocation 3)    Acute osteomyelitis 4)    Secondary osteoarthritis 5)    Deformity and shortening of bone. Tom Smith Arthritis: It is septic arthritis of hip seen in infancy. Since femoral head and neck are intracapsular and physeal vessels supply the femoral head before the formation of growth plate (50% with bowel and bladder involvement. Paraplegia in TB spine: In 10-30 % of patients with TB spine, it results in paralysis of lower limbs. It is most common in the dorsal spine. Paraplegia in spinal tuberculosis is also called Pott’s paraplegia. It is classified to: 1)      Early onset paraplegia: Paraplegia that occurs during active stage of the disease usually within 2 years. It is caused by pressure on the spinal cord by inflammatory edema, caseous tissue, necrotic debris and sequestra.

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Fig 4.02: MRI in early onset paraplegia showing intervertebral disc destruction with abscess formation. 2)    Late-onset paraplegia: Paraplegia that occurs >2 years after the onset of disease. It usually has poor prognosis. The disease may be healed or sometimes occur due to reactivation. There is mechanical stretching of the spinal cord compromising the vascularity over kyphotic spine deformity.

Fig 4.03: MRI in late-onset paraplegia showing disc and vertebral body destruction resulting in kyphotic deformity and kinking of spinal cord. Diagnosis: Lab test: Complete hemogram, Montoux test Tuberculosis can be confirmed by taking the biopsy, testing for acid fast bacilli and culture on LJ media. HPE evaluation is done for tubercular granuloma. Radiology: X-rays: Early stages in tuberculosis show loss of intervertebral disc space. Vertebral bones look rarified and osteopenic after about 30% of calcium loss. In late stages, there is loss of disc space with collapse of vertebral body leading to anterior wedging. There can also be isolated central body collapse (concertina collapse). Paravertebral soft tissue swelling can also be seen due to cold abscess.

Fig 4.04: Dorso-lumbar spine X-ray shows intervertebral disc space destruction in early stages followed by bony ankylosis. CT Scan: This shows vertebral body destruction and spinal canal compromise. Paravertebral soft tissue calcification can also be seen. MRI:  This shows the extent of disc destruction, soft tissue involvement encroaching posteriorly into the spinal canal, cold abscess and destruction of vertebral bodies. Treatment: 176

Conservative Management: Antitubercular treatment: ATT remains the cornerstone of management for spinal tuberculosis especially when there is no neurological deficit. Osteoarticular tuberculosis is generally treated for longer periods. Multi-drug chemotherapy of 9-10 months is shown to have good results. First line chemotherapy drugs include: Drugs Dosage Isoniazid(H) 5 mg/kg Rifapicin(R) 10-15 mg/kg Streptomycin(S) 20 mg/kg Pyrazinamide(Z) 20-25 mg/kg Ethambutol(E) 25 mg/kg Policy of drug treatment: 1)Intensive phase for 2 months: HRZE 2)Continuation phase for 9-12 months: HR Newer drugs: 1)Amikacin, Kanamycin, Capriomycin 2Ciprofloxacin, Ofloxacin 3)Rifabutin, Clarithromycin Bed rest: Bed rest is advised for pain relief and to prevent further collapse of diseased vertebrae. Nutritional status: High protein diet to build patient’s immunity. Spine support: Minerva jacket and collar for cervical disease and Taylor’s or TLSO brace for dorsal and lumbar tuberculosis. Middle path regime: All TB spine patients do not require surgery & only those who donot respond to conservative measures should be operated. In this regime, initiation of chemotherapy is done and if conservative treatment fails like no progressive neurological recovery, new neurological deficits develops or worsening of neurological deficits occurs during the course of treatment, then spine surgery is indicated. Surgical management: Indication for surgery: 1) New onset of paraplegia when patient is on adequate line of ATT 2) Paraplegia not improving with conservative treatment. 3) Progression of paraplegia even after conservative management 4) Paraplegia associated with bowel and bladder symptoms

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Surgical Procedures: These are performed to drain the abscess, remove the inflammatory granulation tissue and achieve decompression of the spinal cord. A)Drainage of abscess: Cold abscess should be drained in a nondependent position using a wide bore needle undercover of ATT. B)Costotransversectomy: By posterior approach, 2 inches of rib and transverse process are removed to drain the paraspinal pus under tension.

Fig 4.05: Costotransversectomy: A) Vertebral body; B) Abscess; C) Rib; D) Transverse process. C)Anterolateral decompression: This is the treatment of choice. The initial procedure is same as costotransversectomy where the rib and transverse process is removed, after that the removal of anterior and lateral part of vertebral body is done to decompress the spinal cord.

Fig 4.06: Anterolateral decompression: A) Abscess; B,C) Vertebral body; D) Spinal cord; E) Transverse process; F)Rib. D)Hongkong Procedure: Radical debridement of almost whole of the vertebral body is done with spinal cord decompression and interbody fusion. E)Laminectomy: Posterior parts of spine that is the lamina and spinous process affected by tuberculosis are treated by laminectomy. It is also indicated in extradural granuloma of tuberculosis mimicking spinal tumor syndrome. Complications of T.B. Spine: 1) Paraplegia 2) Cold Abscess

COLD ABSCESS An abscess is a collection of liquefied tissue (pus) in the body. Tubercular abscess is usually called cold abscess because it is not accompanied by classical signs of inflammation like redness, pain, inflammation, fever which are usually found with pyogenic abscess.

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Fig 4.07: Cold abscess in the right lower lumbar region. Pathogenesis: Spinal tuberculosis is a localized destructive disease causing centrifugal destruction of bone with increasing amounts of tubercular granulation tissue, caseous material and necrotic bone which accumulate beneath the anterior longitudinal ligament. It gravitates along the fascial planes and presents externally at some distance from the site of original lesion. Sites: Paravertebral Abscess: 1. Cervical region – Neck, axillary and retropharyngeal abscess 2. Upper thoracic – Mediastinal and chest wall abscess. 3. Below D4 - Fusiform shaped abscess 4. Lumbar region: Unilateral or bilateral psoas abscess Clinical features: The patient presents with insidious onset of painless swelling and occasionally discharging sinus. In cervical spine tuberculosis, retropharyngeal abscess leads to dysphagia, hoarseness of voice and respiratory obstruction. The abscess may spread laterally into the sternomastoid muscle and forms an abscess in the neck.   In thoracic spine tuberculosis, the exudates can collect as a paravertebral abscess or they may penetrate the anterior longitudinal ligament to form mediastinal abscess. It may enter the spinal canal and compress the spinal cord leading to early onset paraplegia. In lumbar spine tuberculosis, the pus tracks along the psoas muscle towards the groin and presents as psoas abscess. It can also gravitate to lumbar triangle or medial aspect of the thigh. Investigations: Lab test: 1)Complete hemogram, Montoux test 2)Percutaneous or CT guided biopsy can be done for diagnosis and therapeutic drainage of large paraspinal abscess. It is sent for Ziehl Neelsen staining for acid fast bacilli and culture on LJ media. Histopathological evaluation is done for tubercular granuloma.

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3)X-rays: 1)    Cervical region – Soft tissue swelling of neck and retropharyngeal area can be seen because of cold abscess. 2)    Upper thoracic – V-shaped shadow due to mediastinal abscess 3)    Below D4 - Fusiform or bird nest shaped abscess 4)    Lumbar region: Unilateral or bilateral psoas shadow can be seen. 4)Ultrasound: Cold abscess can be seen as hypoechoic lesion and guided aspiration can be done. 5)CT scan: This shows vertebral body destruction and spinal canal compromise. Paravertebral soft tissue calcification in the abscess can also be seen. 5)MRI:  This shows anterior subligamentous extension and tracking of pus along the fascial planes. Treatment: 1)    ATT and aspiration: Palpable cold abscess should be aspirated in a non-dependent position using a wide bore needle undercover of ATT. 2)      USG guided aspiration: Paraspinal and deep abscess can be drained by USG-guided aspiration with antitubercular therapy (ATT). 3)      Open drainage: Open drainage of cold abscess is performed using non-dependent incisions for failed aspirations undercover of ATT.

TUBERCULOSIS OF THE HIP JOINT Tuberculosis hip is the second most commonly affected site followed by the spine. It accounts for about 10-15% of cases. It is commonly seen in the first three decades of life. Etiology: Tuberculosis of hip joint is secondary to a primary focus elsewhere like tuberculosis of lung, lymph nodes or ileocaecal region. The most common route of dissemination occurs through the bloodstream. The foci of infection are most often osseous or may rarely be synovial disease. Pathology: The osseous lesion is most commonly seen in 1) Acetabular roof 2) Subchondral portion of the femoral head 3) Babcock’s triangle (inferomedial portion of neck of femur) 4) Greater trochanter.

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Fig 4.08: Sites of TB hip: A) Acetabular roof; B) Subchondral region of the femoral head; C) Babcock’s triangle; D) Greater trochanter. Since most of the osseous lesions (acetabular roof, femoral neck and head) are intraarticular, the disease spreads to synovium initially leading to edema and congestion followed by hypertrophic synovium with thickened inflammatory granulation tissue leading to joint effusion. This is called the stage of synovitis. The hypertrophic synovitis (pannus) slowly extends over the articular surface of hip leading to joint destruction. This is called the stage of early arthritis. Further extension of pannus and inflammation of total articular surface leads to gross destruction of the joint. This is called the stage of late arthritis. Progressive complete articular destruction with bony erosion leads to stage of advanced arthritis associated with joint subluxation or dislocation. Occasionally cold abscess may form with or without discharging sinus. Clinical features: Symptoms: The most common early symptom is painful limp and constitutional symptoms like low-grade fever with evening raise of temperature, loss of weight and appetite. Signs: There is wasting of hip and thigh muscles with restriction of hip movements. History of night cries can be elicited. There can be soft tissue swelling around the hip due to cold abscess. Night cries in Tuberculosis: The joint is splinted by persistent muscle spasm during the day. Once the patient sleeps, the muscle spasm relaxes resulting in frictional movement of inflamed joint surfaces. So the patient gets up from sleep at night with severe excruciating pain. Once he is awake the pain gradually reduces. The disease progress through the following stages: Stages of T.B. Hip: 1)      Stage of synovitis (Stage of apparent lengthening): In the early stages of the disease, TB synovitis leads to joint effusion. To accommodate the increased volume of synovial fluid, the joint assumes the position of maximum capacity that is flexion, abduction and external rotation of hip joint. This also leads to apparent lengthening of limb. 2)    Stage of early arthritis (stage of apparent shortening):

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The hypertrophic synovial tissue (pannus) slowly spreads to the articular surface and leads to early joint destruction. The patient lies in lateral position (unaffected hip side) leading to flexion, adduction and internal rotation on the affected hip. There is an apparent shortening of the limb. Night cries are common in this stage. 3)    Stage of late arthritis (Stage of true shortening): Complete articular destruction of the femoral head and acetabulum leads to true shortening of limb. This leads to fibrous ankylosis of hip. The limb is in the position of exaggerated flexion, adduction and internal rotation. 4)      Stage of subluxation/ dislocation due to advanced arthritis: Complete joint with bony erosion leads to hip joint subluxation or dislocation, pestle and mortar appearance.

Fig 4.09: Flexion, adduction and internal rotation of right hip in late stage of arthritis. Investigations: Lab investigations: Complete hemogram, mantoux test, hip synovial biopsy for histopathology and LJ medium culture. X-ray hip AP/lateral: X-ray hip in early stages shows juxta-articular osteopenia, erosion of the articular surface, loss of joint space and in late stages, usually result in subluxated or dislocated hip, atrophic hip, pestle and mortar appearance, wandering acetabulum or protrusio acetabuli. MRI is done to evaluate joint effusion, hypertrophic synovitis and to plan tissue biopsy.

Fig 4.10: X-ray shows left side shallow and irregular acetabulum with destruction of femoral head and bony lysis. Treatment: 182

Medical management: The stage of synovitis and early arthritis can be treated by antitubercular treatment with traction to decrease muscle spasm, maintain joint space and correct deformity. Surgical management: If conservative management fails, synovectomy and joint debridement is performed to remove the disease process followed by gradual mobilization. In the stage of advanced arthritis based on age, stage of disease and radiology, surgery can be decided to be either a fixed or mobile hip joint. 1)Fixed joint- Surgery is performed to achieve ankylosis in functional position. A) Hip arthrodesis B) Osteotomy. 2)Mobile joint: A)    Girdlestone arthroplasty: It is also called excision arthroplasty where the femoral head is excised. This results in painless, mobile, unstable hip with limb shortening.

Fig 4.11: Girdlestone Arthroplasty procedure B) Total hip Arthroplasty: Total hip replacement is the preferred treatment these days once the patient is cured of TB hip. This gives the patient painfree, mobile, stable hip and is well accepted by the patient.

TUBERCULOSIS OF KNEE The knee joint is the largest synovial joint. It is the third most common site for skeletal tuberculosis accounting for nearly 10% of tuberculosis followed by spine and hip. Etiology: Tuberculosis of the knee joint is secondary to a primary focus elsewhere. The most common route of dissemination occurs through bloodstream. The foci of infection get lodged into the synovium or in the subchondral bone of the distal femur, proximal tibia and patella.   Pathogenesis: The synovial involvement is most often seen. In early stage of disease, the synovial membrane becomes edematous, congested and studded with tubercule, progressively the synovial lining becomes hypertrophic and thickened. The joint fluid increases, 183

initially looks serous and slowly turns to yellow opalescent fluid with fibrinous flakes. In advanced stages, the tubercular granulation tissue called the pannus erodes the articular surfaces and ligaments causing joint destruction resulting in pain, spasm and deformity. Sometimes osseous lesions may form directly in the epiphysis, metaphysis or in the subchondral bone. Clinical features: Symptoms: The onset and course of disease is insidious with progressive increase in pain, swelling of knee, painful progressive limp and generalized symptoms like evening low grade fever, loss of appetite and weight may be present. Signs: In early stages, the knee is warm with fullness over suprapatellar and parapatellar region. Synovium appears to be thickened and has doughy feel on palpation. As the disease course progresses, there is gross wasting of quadriceps and leg muscles. In delayed stages, there is flexion, posterior subluxation and lateral rotation of tibia due to spasm and contracture of biceps femoris and iliotibial band. This is called triple deformity of knee. Investigation: Lab investigations: Complete hemogram, mantoux test, knee synovial biopsy for histopathology and LJ medium culture. X-ray knee AP/lateral: X-ray knee shows juxta-articular osteopenia, erosion of the articular surface, loss of joint space and in late cases are associated with triple deformity and osteolytic lesions. MRI is done to evaluate joint effusion, hypertrophic synovitis and plan tissue biopsy.

Treatment: Medical management: Antitubercular treatment with adequate immobilization is indicated in the early stage of disease and synovial involvement. Surgical management: If conservative management fails, synovectomy and joint debridement is performed to remove the disease process. In late stages, knee arthrodesis is performed with Charnley compression arthrodesis.

TUBERCULOSIS OF SHOULDER Tuberculosis of the shoulder is a rare occurrence and is characterized by pain, limitation of movements and marked wasting of shoulder muscles. The disease is also called caries sicca (dry variety) because there is no effusion into the joint. Formation of cold abscess and draining sinus is rare. X-ray shows articular cartilage

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destruction and lytic lesions. It is treated by antitubercular therapy and immobilization. Once the infection heals, shoulder arthrodesis is done in the functional position.

TUBERCULAR DACTYLITIS Tuberculous dactylitis is also known as spina ventosa is a rare skeletal manifestation of tuberculosis where short tubular bones like phalanges, metacarpals, metatarsals are affected predominantly in children.  The disease follows a benign course without acute inflammatory changes. It is characterized by a cystic, ballooned-out appearance of the involved bone. X-ray shows lytic spindle-shaped expansile lesion in middle of the bone with subperiosteal new bone formation. Blood tests and biopsy confirms the diagnosis. It is treated by anti-tubercular therapy. Questions Long Essays: 1)    Discuss the types, etiopathology, clinical features , complications and management of tuberculosis of spine 2)    Discuss the etiopathogenesis, clinical features, and management of Potts paraplegia. 3)    Describe the etiopathology, clinical features, pathological features, radiological features, differential diagnosis and management of tuberculosis of Hip. Short Essays: 1)    Psoas abscess 2)    Gibbus 3)    Para vertebral abscess.

Credits: AthK

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Chapter 5

RHEUMATOID ARTHRITIS AND ASSOCIATED INFLAMMATORY DISORDERS Competency OR 5.1: Describe and discuss the aetiopathogenesis, clinical features, investigations and principles of management of various inflammatory disorders of joints

RHEUMATOID ARTHRITIS Rheumatoid arthritis is a chronic systemic inflammatory disease of unknown etiology affecting the synovium. It is characterized by progressive symmetrical inflammatory polyarthritis eventually resulting in joint damage causing severe disability. Etiology: Rheumatoid arthritis is a worldwide disease and affects all racial and ethnic groups. It affects 1-3% of the population. Female: male ratio is 3:1. The age range is 10-70 years. About 5-10% have a family history and 70% have HLA-DR4 positivity. It commonly affects joints like metacarpophalangeal, proximal interphalangeal, wrists, metatarsophalangeal and larger joints. Rheumatoid arthritis is an autoimmune disorder in which the immune system identifies the synovial membrane as a "foreign" antigen and begins attacking it. With long-term or intensive exposure to the antigen, normal antibodies become auto-antibodies that target selfantigens in the synovial membrane. The following factors are considered to be triggering factors: 1)Unknown etiology 2)Chronic infections: Viral, bacterial and fungal etiology 3)Genetic factors: Family history, HLA DR4 association 4)Smoking 5)Obesity Pathology:

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The disease process is characterised by synovitis, swelling and joint damage. Synovitis occurs as a consequence of leukocyte infiltration into the synovium and later followed by lymphocytes. The synovium becomes thickened because of infiltration and leads to hypoxia resulting in angiogenesis. This results in synovial hypertrophy. The inflammatory cytokines released IL-1, IL-6 and TNF-α result in joint effusion and joint destruction. The hypertrophic synovium erodes the articular cartilage from the periphery and is called the pannus. The pannus erodes cartilage, bone and ultimately arthritis develops. Clinical features 1. Early changes Pain, swelling and early morning stiffness of PIP and MCP joints of the hands is a common early finding. 2.  Intermediate changes Persistent tenosynovitis and synovitis lead to joint movements becoming restricted.

Fig 5.01: Rheumatoid hand. 3.  Later stages Acute pain of synovitis is replaced by more constant aches of joint destruction. The joint deformity becomes apparent. Rheumatoid deformities: Fingers: Swan neck deformity and Boutonniere’s deformity.

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Fig 5.02: A) Boutonniere’s deformity B) Swan neck deformity. Thumb: Z deformity of the thumb Wrist: Joint subluxation Knees: Triple deformity Extra-articular manifestations include rheumatoid nodules, Sjögren's syndrome, Caplan’s syndrome, episcleritis. Entrapment of nerves leads to carpal tunnel syndrome or ulnar nerve neuropathy.

Investigations: 1. Hematological a. Complete hemogram: Iron deficiency, megaloblastic or anaemia of chronic disease is common. The ESR and CRP is usually raised during active inflammation. b. Rheumatoid Factor (RF): RF is an autoantibody against Fc portion of IgG. It is positive in >80 % of patients. It can be false positive in patients with rheumatoid arthritis. c. Anti-citrullinated Protein Antibodies (ACPAS): It is more sensitive than Rheumatoid factor. It is the confirmatory test for rheumatoid arthritis and indicates a high risk of erosive disease. 2. Radiological investigations a)    X-rays b)    Ultrasound c)     MRI X-ray changes Early Stage: X-rays show only the features of synovitis, soft tissue swelling and periarticular osteoporosis Later Stage: Narrowing of joint space with subchondral osteopenia especially in proximal joints of hands and feet. In advanced disease, articular destruction and joint deformity are obvious.

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Fig 5.03: X-ray shows symmetrical destruction of joint space with juxta-articular osteopenia. MRI An MRI can detect proliferative pannus. It has the greatest sensitivity for detecting synovitis and joint effusions, as well as early bone and bone marrow changes.

ACR/EULAR classification for the diagnosis of RA: Joint involvement 1 large joint 1-10 large joints 1-3 small joints 4-10 small joints >10 joints

Score 0 1 2 3 5

Serology Negative RF and negative ACPA 0 Low positive RF and low positive 2 3 Anti-CCP High positive RF and high positive Anti-CCP Acute phase reactants 0 Normal ESR and CRP 1 Abnormal ESR and CRP Duration of symptoms 0 6 weeks *ACR- American College of Rheumatology/ EULAR- European league against Rheumatism Patients with score >6 are classified as having Rheumatoid arthritis. Management:

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Goals of management: To control inflammation, relieve pain and reduce disability associated with rheumatoid arthritis.

A) Conservative management: a) Physical Therapies: Splinting, rest, cold packs to reduce inflammation. Exercise helps to maintain muscle strength & joint mobility. b) Diet- Dietary intake of omega-3 fatty acids may reduce rheumatoid arthritis inflammation. c) Pharmacologic Therapies 1.  Non-steroidal anti inflammatory drugs(NSAIDS) 2. DMARDS 3. Glucocorticoids 4. Biologics 1.Non-steroidal anti inflammatory drugs:  They help to manage chronic pain, inflammation and swelling but they do not slow down the disease process. Eg: Aspirin, celecoxib, diclofenac, ibuprofen, ketoprofen, ketorolac. 2. DMARD’S: Disease modifying anti-rheumatic drugs These drugs alter the disease course. These are slow acting and take about 6 weeks to show the effects. Commonly used are methotrexate, hydroxychloroquine, sulfasalazine a)Methotrexate: It is a dihydrofolate reductase inhibitor that inhibits cytokine production, purine biosynthesis. It is started with an oral low dose of 7.5 – 15mg weekly. b)Hydroxychloroquine: It is used in mild RA or especially when one or few joints are involved. The need of periodic ophthalmologic examination is necessary for early detection of reversible retinal toxicity. Hydroxychloroquine is started with dose upto 400 mg /day for 4 -6 weeks followed by 200 mg for maintenance.

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c)Leflunomide: It is an immunomodulator that inhibits proliferation of stimulated lymphocytes. Arthritic symptoms are suppressed and radiological disease progression is retarded. Loading dose 100 mg daily for 3 days followed by 20 mg OD. 3) Immunosuppressive agents: Glucocorticoids: Low dose prednisolone is used as a second line agent. It has anti-inflammatory and immunosuppresent action, suppresses signs, symptoms and slows the appearance of new bone erosions. Route: Oral dose – prednisolone 7.5 mg/d. Intraarticular injection can be given for transient symptomatic therapy when systemic therapy fails. Less frequently used drugs include azathioprine, D- penicillamine, gold (auranofin), cyclophosphamide and cyclosporine. 4) Newer "second- line” drugs or "biologic" medications or TNFα inhibitors: 1. 2. 3. 4. 5.

Etanercept Infliximab Adalimumab Golimumab Certolizumab

Mechanism of action: It suppresses macrophage and T-cell function. It regresses the inflammatory changes in joint & new erosions are slowed. 5) JAK inhibitors •            JAK inhibitors are the newest class of drugs used to treat moderate to severe rheumatoid arthritis- Tofacitinib , Baricitinib B) Surgical Management a)Synovectomy b)Arthroscopy c)Arthroplasty d)Arthrodesis a)    Synovectomy:

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Synovectomy surgery is done to remove inflamed joint tissue (synovium) that is causing unacceptable pain or limiting the ability to function. b)    Arthroscopy: It is a type of keyhole joint surgery in which an arthroscope is inserted into the joint and hypertrophic synovial tissue debridement is done. c)     Joint replacement: The definitive treatment for advanced joint destruction in the late stages of rheumatoid arthritis can be successfully treated with total joint arthroplasty. Total knee arthroplasty and total hip replacement are well-proven modalities that can provide pain relief and restoration of joint mobility. d)    Arthrodesis: Joint fusion is a surgical procedure for the treatment of severe arthritis pain. It is now rarely performed. Seronegative spondyloarthropathy: They characteristically test negative for Rheumatoid factor(RA factor) and hence have been grouped as Seronegative spondyloarthropathy. 1)    Psoriatic arthritis 2)    Ankylosing spondylitis 3)    Inflammatory bowel disease 4)    Reiter syndrome( Mnemonic: PAIR)

ANKYLOSING SPONDYLITIS Definition: Ankylosing spondylitis is a chronic inflammatory autoimmune disease that mainly affects spine joints causing severe chronic pain and in advanced cases leading to spine fusion. Introduction: Ankylosing spondylitis is inflammatory arthritis belonging to the group of seronegative spondyloarthropathy.  It is also known by the eponym of “Marie-Strumpell” disease. It predominantly affects the axial skeleton starting from sacroiliac joints and ascends upwards to lumbar, thoracic and cervical spine. Etiology: The exact etiology is unknown. However, 90% are associated with HLA B27 positivity. The incidence of Male to female ratio is about 9:1 with the age group of presentation being about 20 to 40 years. Pathogenesis: It predominantly affects the axial skeleton. The proposed mechanism is lymphocyte activation and differentiation,

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innate cytokine response leading to inflammation of the fibroosseous junctions affecting the inter-vertebral disc, sacroiliac ligaments, symphysis pubis and bony insertions of large tendons (enthesitis). The inflammatory process leads to cell infiltration, granulation tissue formation and eventually ossification of fibrous tissue leading to bony ankylosis of the joint. Extra articular manifestations Ocular involvement- Uveitis Cardiovascular involvement- Aortitis, conduction disorders, dilatation of aorta Pulmonary involvement- Lung fibrosis and pleural thickening. Renal involvement- Secondary amyloidosis, Ig A nephropathy

Symptoms: Initial symptoms: The patient usually presents with insidious onset of low back pain and stiffness that occurs after periods of rest. It improves with movement and returns following period of inactivity. The pain tends to be worse at late night and early morning hours after sleep.  The pain usually becomes persistent and bilateral. There may be pain at spinous processes, iliac crests, greater trochanters, ischial tuberosities, tibial tubercles and heels. Neck pain and stiffness occur eventually from the involvement of the cervical spine. The patient may also have involvement of peripheral joints like hip, knee and shoulder joints. Late Presentation: Pain tends to be persistent early in the disease and then becomes intermittent with alternating exacerbations and quiescent periods. In a typical severe untreated case, the patient's posture undergoes characteristic changes with loss of lumbar lordosis, buttock atrophy and accentuated thoracic kyphosis. The cervical spine ossification leads to forward neck contracture. There may also be flexion contractures at the hips.

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Fig 5.04: Late stage of ankylosing spondylitis. Clinical examination: A)   Test for sacroiliac joints: 1)      Pelvic compression test-The patient is in side lying and the examiner hands are placed over the upper part of iliac crest, pressing towards the floor. This movement causes forward pressure on the sacrum. An increased feeling of pressure in the sacroiliac joint indicates a possible sacroiliac lesion. 2)    Gaenslen test- The patient is being positioned supine with painful leg resting on the edge of treatment table. The examiner sagitally flexes the non-symptomatic hip while the knee is also flexed. The patient should hold the nontested leg with both arms and the examiner stabilizes the pelvis and applies passive pressure to the affected leg being tested. The downward force is applied to the affected lower leg putting it into hyperextension at the hip. This flexion-extension arc creates torque and incites pain in the sacroiliac joint. 3)    Patrik’s (FABER) test- It is used to evaluate pathology in the hip or sacroiliac joint. This test is performed by having the test leg flexed, thigh abducted and externally rotated. B)   Test for lumbar spine1) Modified Schober’s test With the patient standing upright, marks are made 5 cm below and 10 cm above the sacral dimples. The distance between these marks should increase from 15 cm to atleast 20 cm with lumbar flexion. A distance of less than 5 cm is abnormal and it indicates limited lumbar spine motion. C)   Tests for thoracic spine involvement: (Chest expansion test) It is measured as a difference between maximal inspiration and maximal forced expiration in the fourth intercostal space in males or just below the breasts in females. Normal chest expansion should be > 5 cm. D)   Tests for cervical spine involvement: (Occiput to wall distance test) The severity of cervical flexion deformity in ankylosing spondylitis can be assessed by measuring the occiput to wall distance. With the patient standing erect, the heel and buttocks are placed against a wall. The patient is instructed to extend his or her neck maximally in an attempt to touch the wall with the occiput. The distance between

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the occiput and the wall is a measure of the degree of flexion deformity of the spine. Normally the occiput to wall distance should be zero. Investigations: X-ray: a) Sacroiliac joints: It usually shows symmetrical and bilateral sacroilitis, subchondral erosions or sclerosis. b) Spine: Romanus lesion, diffuse syndesomophytic ankylosis leading to bamboo spine appearance. c) Hip: bony ankylosis of hip.

Fig 5.05: Bamboo spine appearance. Vertebral body (A); Narrow disc space (B). Modified New York criteria for diagnosis of Ankylosing Spondylitis Clinical 1) Low back pain and stiffness > 3 months which improves with exercise and not relieved by rest. 2) Limitation of lumbar spine in both sagittal and frontal planes 3) Limitation of chest expansion relative to normal for age and sex Radiological grading of sacroilitis 1) Grade 0: Normal 2) Grade 1:Suspicious 3) Grade 2:Sclerosis,some erosions 4) Grade 3: Severe erosions, widening of joint space, some ankylosis. 5) Grade 4:Complete ankylosis Ankylosing spondylitis is present if the radiological criteria are associated with at least one clinical criteria.

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Blood tests: •       HLA B27 is positive in 90% of patients. •       ESR and CRP are often elevated. •       Mild anemia. •       Elevated serum IgA levels. •       S ALP & CPK are often raised. Treatment: Physical therapy: It improves joint motion. These include •       swimming •       badminton •       jogging •       yoga •       deep breathing exercises Drug therapy 1)    NSAIDs like Aspirin, ibuprofen, phenylbutazone, indomethacin, naproxen and COX-2 inhibitors for spinal stiffness, pain, persistent synovitis or enthesopathy. 2)    DMARDs like methotrexate, sulfasalazine. 3)    Corticosteroids –It is used to reduce the immune system response through immunosuppression.

4)    Anti TNF agents: a)Etanercept b)Infliximab c)Golimumab d)Certolizumab e)Secukinumab

Contraindications for anti-TNF agents: a)Current or recurrent infections b)Tuberculosis c)Multiple sclerosis c)Lupus d)Malignancy e)Pregnant or lactating

Indication for Surgery: a)    Severe Deformity ( Kyphosis)- Corrective spinal osteotomy b)    Deformities Of The Hip And Knee- Joint replacement surgeries c)     Visual Difficulties- Corrective cervical osteotomy d)    Spinal nerve decompression surgeries.

GOUT      Gout is a metabolic disorder of purine metabolism characterised by hyperuricemia in which monosodium urate crystals are deposited in articular, periarticular and subcutaneous tissues. 196

Etiology: Predisposing causes 1)    Heredity 2)    Sex: Males are predominantly involved, females usually at menopause 3)    Age: It occurs usually at 40-60 years of age. 4)    Adrenal cortex malfunction. Pathophysiology: There is dysfunctional nucleic acid metabolism causing hyperuricemia. Sodium urate crystals deposit in the synovial membrane and periarticular soft tissues leading to inflammatory process activating proteases, prostaglandins and leukotrienes. A pannus is a hypertrophic synovial tissue that grows over the articular surface by destroying the cartilagenous surfaces ultimately leading to fibrous ankylosis. 1) Primary gout: Idiopathic disorder of nucleic acid metabolism that leads to hyperuricemia and deposition of monosodium urate crystals in joints. 2) Secondary gout: It is associated with diseases with high metabolic turnover like psoriasis, hemolytic anaemia, leukemia etc. Stages of gout: a) Asymptomatic b) Acute attack-Sudden onset of painful arthritic attack happens usually over the first metatarsophalangeal joint. c) Interval/intercritical periods- intermittent attacks of swelling, edema and joint pains. d) Chronic gout- Continous joint deposits of uric acid crystals lead to chronic joint pain. Articular cartilage is destroyed due to pannus and may result in joint deformities. Subcutaneous tophi occur over the pinna of external ear, eyelids. Clinical examination: Acute attacks are precipitated by pain, fever and sudden swelling usually at night times commonly over the first metatarsophalangeal joint. It can also happen over knee, ankle, wrist or finger joints. The patient may also have low grade fever. In chronic stage there may be persistent pain in multiple joints. Tophi formation results from the deposition of uric acid salts in the soft tissues.

Fig 5.06: Great toe involvement in Gout. A) Periarticular bony lysis B) Cartilage destruction C) Inflamed joint capsule D) Microscopic uric acid crystals deposition in the joint.

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Investigations: Radiographs: Imaging shows punched-out periarticular erosion with sclerotic overhanging borders. Soft tissue crystal deposition (tophi) may be seen. Labs a)Raised serum uric acid ( normal 4-6 mg%) b)Crystal analysis: Diagnosis is made by joint aspiration and crystal analysis. Monosodium urate (MSU) crystals are thin, tapered, needle-shaped intracellular crystals. These are strongly negatively birefringent. Differential diagnosis: a) Acute septic arthritis b) Psoriatic arthritis c) Other crystalline arthropathies Treatment: a) Acute gout:-Indomethacin (75-100 mg oral dose) and Colchicine. b) Chronic gout:-Allopurinol decreases uric acid production and Probenecid increases the excretion of uric acid. Oral, Intra articular or IV glucocorticoids are given if the patient is unable to take NSAIDs or Colchicine. Pseudogout: It is due to the deposition of calcium pyrophosphate dihydrate (CPPD) in synovium and menisci. It commonly affects the knee joint. X-ray shows calcification in the menisci or articular cartilage. Crystals are rhomboid in shape which are positively birefringent. It can be treated with indomethacin. Questions: Short Answers: 1. Swan neck deformity 2. Tests for sacroiliac joint 3. Gout.

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Chapter 6

DEGENERATIVE DISORDERS Competency OR 6.1: Describe and discuss the clinical features, investigations and principles of management of degenerative condition of spine (Cervical Spondylosis, Lumbar Spondylosis, PID) 1)Spondylosis: It is a degenerative condition of the spine. 2)Spondylolysis: Pars interatricularis defect without vertebral slippage. 3)Spondylolisthesis: Pars interarticularis defect with vertebral slippage. 4)Spondylitis: It is also called vertebral inflammation. The pain is due to swelling and inflammation of the spine due to infection. (Osteomyelitis, TB spine)

CERVICAL SPONDYLOSIS Cervical spondylosis is a degenerative disorder involving the cervical spine that may cause loss of normal spine structure and function. It most commonly affects people of age more than 50 years. Spondylosis affects the following spinal elements: Intervertebral disc: The degenerative effects of aging can weaken the annulus fibrosis causing wear and tear. The water content in the nucleus pulposus decreases with age. The structural alterations from degeneration may decrease disc height and increase the risk of disc herniation. Facet joints: The facet joints are also termed as zygapophyseal joints. These articulating joints of the spine enable flexion, extension and rotation. The cartilages in these joints have self-lubricating and low-friction gliding surfaces. Facet degeneration causes loss of cartilage and osteophyte formation. These changes lead to degenerative spine disease.  Bone and ligaments: Osteophytes form adjacent to end plates, which may compromise the blood supply to vertebrae. The vertebral end plates stiffen due to sclerosis. The degenerative changes in the ligaments lead to stiffness. The ligamentum flavum may thicken posteriorly and compress the dura mater.

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Pathogenesis: The degeneration causes a reduction in cervical disc space and osteophyte formation. The degeneration of facetal joints and osteophytes can cause nerve root compression resulting in radiculopathy. Clinical features: Symptoms: Neck pain and cervical stiffness are the most common complaints. Neck pain can be referred to occiput, between the shoulder blades or even the upper limb. The patient can have radiculopathy and neurological weakness of upper limb due to nerve root compression. Sometimes the patient can have giddiness or syncopal attacks due to vertebrobasilar insufficiency caused by osteophytes compressing the vertebral artery in the foramen. Signs: On examination, there is poorly localized neck tenderness with restricted range of neck movements. Neurological evaluation is performed for any sensory or motor deficits of the upper limb. Investigations: 1)X-ray: X-ray shows narrowing of disc spaces with osteophytic changes. 2)MRI: It is done when the patient is having severe radicular symptoms with or without neurological deficit. Differential diagnosis: Fibromyalgia and psychogenic neck pain Inflammatory disease—Rheumatoid arthritis, Ankylosing spondylitis, Metabolic diseases—Paget’s disease, osteoporosis Infections—Osteomyelitis or tuberculosis Malignancy—Primary tumors, secondary deposits or myeloma. Treatment: Although spondylosis can be painful, most patients respond favorably to non-surgical treatments. During the acute phase, analgesics along with short-wave diathermy of the neck are the usual treatment followed by isometric neck exercises for neck muscle strengthening. Surgery is indicated in cases of nerve root compression with radiculopathy, unresponsive to conservative treatment or those with neurological deficits.

LUMBAR SPONDYLOSIS Lumbar spondylosis is a degenerative spinal disorder affecting the discs, vertebral bodies and associated joints in lumbar vertebrae. It is common in more than 85% of the population over 60 years of age. The area of maximum mobility and stress such as L4-L5 and L5-S1 are commonly involved. Risk factors: 200

1)Genetics 2)Age 3)Repetitive strain of back 4)Occupations like heavy weight lifting and overhead workers 5)Spine injuries. Pathogenesis: There is disc degeneration with age and narrowing of disc space. The narrowing of disc space leads to approximation of facet joints. This results in slackening of posterior longitudinal ligament. This leads to detachment of periosteum and extruded disc material eventually calcifies to form a bony spur. Clinical features: The patient presents with low back pain which gets worse after activity, prolonged standing or sitting and is relieved by rest. Early morning low back stiffness can be present and is associated with difficulty in walking. Signs: There is vague low back tenderness with restricted range of lower back movements. In an acute attack, paraspinal muscle spasm can be present. Neurological evaluation is performed for any sensory or motor deficits of the lower limb. Investigations: X-ray: X-ray shows loss of disc height with osteophyte formation along the joint margins. MRI: MRI helps to give better soft tissue images of discs, nerves, spinal cord and muscles to rule out nerve root or cord compression. Treatment: Conservative management: 1)NSAIDs with muscle relaxants 2)Short wave diathermy/TENS 3)Work ergonomics and spinal strengthening exercises Surgery: In case of neurological deficits or instability of facet joints, spinal fusion is indicated.

PROLAPSED INTER VERTEBRAL DISC (PIVD) Anatomy of intervertebral disc: The intervertebral disc is a tough, fibrocartilaginous structure comprising one-quarter of whole vertebral column with the principal function of shock absorption and transmission of loads between the vertebral bodies. It is composed of three main structures: 1)    Central- Nucleus Pulposus (NP) 2)    Peripheral- Annulus fibrosus (AF) 201

3)    Vertebral end plates (EPs) Nucleus pulposus: The nucleus pulposus contains numerous proteoglycans that facilitate water retention, creating hydrostatic pressure that resists axial compression of the spine. It is a remnant of the notochord. Annulus fibrosis: It is composed of concentric type 1 collagen fibers connected to vertebral endplates enclosing the nucleus pulposus. Vertebral endplates: The intervertebral disc is bound superiorly and inferiorly by cartilaginous end plates. The disc derives its nutrition from the body of vertebrae through end plates by diffusion. Pathophysiology of disc herniation: In a normal healthy disc, the nucleus distributes the load equally throughout the annulus. As the disc undergoes dehydration, the nucleus loses its cushioning ability and transmits loads unequally into annulus. With increased stress or due to injury, the annulus fibrosis bulges posteriorly into the spinal canal, this is called disc bulge or protrusion. If the displacement continues further, there is rent in annulus fibrosis and nucleus pulposus herniates into the spinal canal. This is called disc herniation. Gradually the nucleus pulposus undergoes fragmentation in the spinal canal which is called disc sequestration. The most common site of disc prolpase is posterolateral because annulus fibrosis is weak in this region. However central disc prolapse also can occur. The pathophysiology of sciatica is believed to be a combination of mechanical compression of the nerve by bulging disc and local increase in inflammatory chemokines. The most common lumbar levels of herniated disc are L4-L5 and L5S1. In cervical spine C5-C6 and C6-C7 are the most common sites of disc prolapse mostly of degenerative etiology. Classification of disc herniation: I. II. III. IV.

Dehydration- Dehydration of the nucleus pulposus. Protrusion - Disc dehydration leads to asymmetrical stress on annulus fibrosis hence annulus fibrosis bulges into the spinal canal causing mild neural compression. Extrusion or herniation- The nucleus pulposus herniates into the spinal canal through a rent in annulus fibrosis but remains continuous with disc space. Sequestration-The disc material herniates through the annulus and is no longer continuous with disc space.

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Fig 6.01: Normal anatomy of the spine: A) Vertebral body; B) Intervertebral disc; C) Posterior longitudinal ligament; D) Spinal cord. N) Normal disc; I) Disc dehydration; II) Disc protrusion; III) Disc extrusion IV) Sequestration. Based on the location of disc 1)Central disc- Central disc protrusion causing compression of the spinal cord or multiple nerve roots. 2)Posterolateral disc- Disc protrusion occurs posterolaterally into the vertebral column and compresses the spinal nerve root. Causes of disc prolapse: 1)Genetic predisposition 2)Repetitive back stress and weight lifting activities 3)Trauma 4)Smoking 5)Obesity Clinical features: Symptoms The patient presents with acute onset of low back pain usually following lifting of a heavyweight with restriction of lumbar motion. The pain may radiate to buttocks and lower limbs along the course of sciatic nerve (sciatica). The patient may also complain of numbness or tingling sensation in the lower limb along the dermatome. Sometimes the patient even develops sensory and motor deficits. Signs: There is diffuse tenderness of lumbar spine with paraspinal muscle spasm. Straight leg raising test (Lasegue test): With the patient lying in supine position. The examiner gently raises the patient’s leg by flexing the hip with knee in extension. Normally the leg can be raised upto 70-90°.  The test is considered positive if the patient 203

experiences pain in gluteal or hip region radiating down to the leg along the course of sciatic nerve beyond 30° of leg raise. During SLRT, there is stretching of nerve root over the protruded disc resulting in radiating pain along the course of sciatic nerve.

Fig 6.02: Bending of spine in axillary and shoulder disc. A)    The patient bends to the same side in axillary disc. B) Patient bends to opposite side in shoulder disc. Lumbar disc prolapse:

L 4 L 5

Compresse d nerve root L5

L S1 5 S 1

Symptom Motor deficits s

Sensory deficits

Low back 1)Weakness of big pain, toe Sciatica extension(extenso r hallucis longus) and toes(extensor digitorum longus and brevis)

Diminished sensation over the anterolater al aspect of leg, dorsum of foot and great toe Diminished sensation over the lateral border of foot.

Low back pain, buttock pain, Sciatica

1)Weakness of plantar flexors of the foot 2)Absent ankle jerk

Cervical disc prolapse:

C 5C 6

Compresse d nerve root C6

C C7 6-

Symptoms Neck pain, radiculopath y

Neck pain, radiculopath 204

Motor deficits

Sensory deficits Biceps Lateral brachii, forearm, Extensor carpi thumb and radialis longus index Absent biceps finger or brachioradialis reflex Triceps Diminishe d

C 7

y

Flexor carpi radualis, Flexor digitirum superficialis Absent triceps reflex

sensation over the middle finger

Investigations: X-ray spine AP/Lateral: It is done to rule out any bone pathology. In late stages, there is a narrowing of disc space. Traction osteophytes are seen. MRI is the investigation of choice for intervertebral disc protrusion and to identify compression of the nerve root.

Fig 6.03: X-ray shows decrease in L4-L5 disc space. The same patient MRI images are suggestive of L4-L5 disc extrusion.  Treatment: Conservative management: It is indicated in acute or early cases where there are no neurological symptoms and MRI shows only protrusion. It consists of 1)    Absolute bed rest (30%.

LUMBAR CANAL STENOSIS Lumbar canal stenosis is defined as a decrease in the anteroposterior or lateral diameter of lumbar spinal canal due to 207

bone or ligament hypertrophy. Causes: 1) Degenerative- Osteophytes encroach and cause spinal canal narrowing. 2)Achondroplasia 3) Paget’s disease 4)Fluorosis 5)Fracture spine Clinical features: The patient presents with low back pain and classical symptoms of neurogenic claudication where there is pain in buttocks and legs after walking which decreases on sitting and forward bending. Neurological deficits may be present. Peripheral pulses are usually normal. Investigations: 1) X-ray for degenerative changes in the spine. 2) CT and MRI scan: For assessment of stenosis. Treatment: Conservative: Analgesics and spinal flexion exercises. Surgery:Cord decompression by laminectomy/laminotomy/foraminotomy.

Fig 6.06: Algorithmic approach to low back pain.

Question: Long Essay: 1)    What is straight leg raising test? Explain its significance in lumbar disc prolapse.

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Chapter 7

METABOLIC BONE DISORDERS Competency OR 7.1: Describe and discuss the aetiopathogenesis, clinical features, investigation and principles of management of metabolic bone disorders in particular osteoporosis, osteomalacia, rickets, Paget's disease. Bone metabolism: The bone is composed of collagenous matrix interspaced with minerals and cells. Matrix composition: 1)      The organic matrix is mainly composed of type 1 collagen, proteoglycans. 2)      An inorganic matrix is made up of mainly calcium and phosphate in the form of calcium hydroxyapatite, calcium carbonate, calcium fluoride etc. Cell types: 1) Osteoblasts: These are bone-forming cells derived from mesenchymal precursors. These cells produce alkaline phosphatase, an enzyme that is often used to identify osteoblasts and its osteoblastic activity. 2) Osteocytes: Osteocytes are derived from osteoblasts and are responsible for maintaining the bony architecture. 3) Osteoclasts: Osteoclasts are derived from circulating monocytes.  Osteoclasts form a ruffled border that attaches to the osteoid and secretes proteins that degrade the bone matrix. Calcium and phosphate homeostasis: Calcium: The body of a young adult male consists of about 1100 gm of calcium. There are three major pools of calcium in the body. a)      Intracellular calcium-It is the calcium present within the cells and is responsible for intracellular signaling, enzyme activation and muscle contractions. b)      Calcium in blood and extracellular fluid- Roughly half of the calcium in the blood is bound to proteins. This is called nonionized calcium, rest of the ionized calcium plays a crucial role in nerve conduction, blood clotting etc. c)        Bone calcium – About 99% of calcium is stored in bones of which 1% is in pool that can exchange with extracellular 209

calcium rapidly. Phosphate: The majority of phosphate of about 85% is present in mineral phase of bone. The rest of the phosphate is distributed both intracellularly and extracellularly for various metabolic functions.  Maintaining homeostasis is achieved by constant fluxes of calcium and phosphate between blood and other body compartments. The three organs participating in calcium and phosphate homeostasis are: 1) Small intestine- Dietary calcium and phosphate are directly absorbed through the small intestine.  2) Bone- It serves as a large reservoir of calcium and phosphate. Stimulating bone resorption releases calcium and phosphate into blood and the suppressing effect allows calcium and phosphorous to be deposited in the bone. 3) Kidneys- The kidneys are critically important for calcium homeostasis. Under normal circumstances, the calcium which enters the glomerular filtrate is reabsorbed from tubular system back into blood, which preserves blood calcium levels. If tubular resorption of calcium decreases, the calcium gets excreted in urine. The three hormones regulating calcium and phosphate metabolism are: 1)    1,25 Dihydrocholecalciferol (calcitriol) 2)    Parathyroid hormone 3)    Calcitonin 1)    1, 25 dihyrocholecalciferol (Calcitrol): Vitamin D is fatsoluble vitamin. Two important forms of vitamin D are vitamin D2 also called ergocalciferol which is derived from plants and vitamin D3 also known as cholecalciferol derived from animals. Cholecalciferol is also synthesized from skin of animals from 7dehydrocholestrol by exposure to sunlight. Cholecalciferol (vitamin D3) is converted into biologically active form by a process of hydroxylation, first in the liver by 25 alphahydroxylase to 25 hydroxycholecalciferol followed in the kidney by 1 alpha-hydoxylase to 1,25 dihydroxycholecalciferol or calcitriol which is the active form.

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Fig 7.01: Active form of Vit D3 (calcitriol) production. 2)    Parathyroid hormone: Parathyroid hormone is secreted by four parathyroid glands which are usually located behind the thyroid gland. Parathyroid hormone regulates calcium levels in the blood largely by acting through bone, kidney and intestine. 3)    Calcitonin: It is produced by parafollicular cells of thyroid gland and it is secreted in response to hypercalcemia. It reduces blood calcium levels by inhibiting the activity of osteoclasts and decreasing the resorption of calcium in the kidneys. Effect of hormones on various organs: Calcitriol Intestine: It increases calcium absorption from intestine. Kidney: It increases tubular resorption of calcium and phosphate Bone: It increases bone mineralization. Parathyroid Intestine: PTH acts with 1,25-dihydroxyvitamin hormone D to facilitate cellular calcium transport in the gut. Kidney: PTH increases calcium absorption from tubules and decreases the tubular reabsorption of phosphate. Bone: PTH mobilizes calcium from bone by osteoclastic osteolysis.

OSTEOPOROSIS Osteoporosis is a progressive systemic disorder characterized by low bone mass per unit volume of normally mineralized bone due to loss of bone protein. It is secondary to uncoupling of osteoclastosteoblast activity. There is a marked reduction of bone mass leading to decrease in mechanical strength of bone, making it vulnerable for fractures. Risk factors for osteoporosis: Non-modifiable risk factors Modifiable risk factors 1)AgeWomen >45 1)Drugs : Heparin, Methotrexate, years(after menopause), Steroids Male >60 years. 2)Metabolic causes: 2)Sex Hyperparathyroidism, Cushing syndrome, thyrotoxicosis, 3)Estrogen deficiency Diabetes. Rheumatoid arthritis, scurvy. 4)Genetics

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3)Alcoholism, smoking 4)Prolonged bed rest. Pathophysiology: In normal adults, the activity of osteoclasts is balanced by osteoblasts. In osteoporosis, the resorption of bone exceeds that of deposition of bone caused by increased osteoclastic activity compared to osteoblasts resulting in bone thinning. The osteoclastic activity is regulated by RANK receptor. RANK ligand attaches to osteoclasts is essential for its formation, function and survival. The osteoprotegrin(OPG) binds to RANK ligand and inhibits maturation of osteoclasts. In osteoporosis, levels of OPG decreases.

Fig 7.02: A) Normal bone B) Osteoporotic bone. Types of osteoporosis: a)Postmenopausal osteoporosis: In females after menopause there is a lack of estrogen which leads to rapid loss of trabecular bone and results in generalized osteoporosis. This increases the risk of distal radius, vertebral and femoral neck fractures. b) Senile osteoporosis: It affects patients with age >60 years in both males and females. Clinical features: Symptoms: Backache is the most common symptom. Osteoporosis is called the silent disease because most of the time it results in fragility fracture. Fragility fractures occur following trivial trauma. The most common sites are distal radius, vertebral fracture and neck of femur fracture. Signs: On examination, there is diffuse tenderness over spine with radiculopathy.  Vertebral compression fractures result in progressive kyphotic deformity of spine resulting in hunchback.

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Fig 7.03: Osteoporosis with hunchback deformity of spine. Investigations: Serum Investigation: S Calcium, Phosphatase, S PTH levels, S Vit D3.

S

Phosphorous,

Alkaline

X-ray shows thinning of trabaculae and generalised rarefaction. Osteoporotic vertebral compression fracture results in codfish vertebrae (biconcave shape). These are more commonly seen in lower thoracic & upper lumbar vertebrae.

Fig 7.04: X-ray spine lateral view showing osteoporotic vertebral compression fracture. Bone mass measurement by DEXA (Dual energy X-ray Densitometry) is the gold standard and helps to detect early osteoporosis. WHO definition: Bone mineral density (BMD): It is absolute, patient-specific score determined from certain anatomic areas like spine, hip, distal radius.

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T score: BMD of patient is compared to relative BMD in normal young matched controls (25 year old individuals). Osteopenia: If bone density is -1 to -2.5 standard deviation (T score) below peak bone mass Osteoporosis: Bone density of less then -2.5 standard deviation (T score) below peak bone mass. Z score: BMD of patient is compared to relative BMD to similar age matched patients.              Bone biopsy: Histology shows disrupted microarchitecture, thin trabeculae, decreased osteon size and enlarged Haversian & marrow spaces. Treatment: 1)    Prevention of Osteoporosis: Diet: Dairy products like milk, salmon, broccoli, dried figs are a good source of calcium. Lifestyle modifications like cessation of smoking, decreased alcohol consumption and regular exercise are necessary to maintain bone mass. 2)    Supplements: a)      Calcium intake: Intake of regular calcium may reduce bone loss particularly in post menopausal women. The recommended dose is 1000-1500 mg/day. b) Vitamin D: Intake of Vitamin D is important because it enables calcium absorption from gut, kidney. The recommended dose of vitamin D is about 800 IU in adults. 3)    Medications: a)    Bisphosphonates: Bisphosphonates inhibit osteoclastic activity and promote osteoclast apoptosis by disrupting its cytoskeleton. Drugs like alendronate, Ibandronate and zoledronic acid are used in treatment of osteoporosis. b)      Hormone (estrogen) replacement therapy is most effective treatment when started soon after menopause, it helps to maintain bone density. However, it has increased risk of breast cancer, blood clots etc. Selective estrogen receptor modulation (SERM) like raloxifine are a new class of agents with similar action to low doses of estrogen to improve bone mass with negligible side effects. c)        Calcitonin: It is a peptide hormone secreted by C-cells of thyroid. It inhibits bone resorption. It can be used as subcutaneous injection or as nasal spray. 214

4)    Newer drugs: a)      Teriparatide: Teriparatide is recombinant PTH that acts as an anabolic agent in the treatment of osteoporosis. It is the only drug that induces bone formation and decreases bone resorption. It has to be given daily as subcutaneous injection. b)    Denosomab: Denosomab acts by blocking protein called RANK ligand. Blocking this protein limits the activity of osteoclasts and reduces bone resorption.

RICKETS Rickets is a defect in the mineralization of osteoid matrix of growing bones due to vitamin D deficiency or its impaired metabolism leading to softening and weakening of bones. Etiology: 1) Vitamin  D deficiency a)low intake b)Inadequate sunlight exposure . 2) Abnormal vitamin D metabolism a) liver disease( absence of 25 hydroxylase) b) renal disease (absence of 1 hydroxylase) c)drugs(anticonvulsants) d)malabsorption 3) Hypophosphatemia a) Hypophosphatemic Vitamin D resistant rickets Pathogenesis: Vitamin D deficiency causes decreased absorption of calcium and phosphorous from the gut. This leads to decreased serum calcium levels leading to parathyroid stimulation and secretion of patathyroid harmone (PTH). Patathyroid harmone mobilizes calcium and phosphorous from bones leading to normal serum calcium and phosphorous levels. This decreases the calcium available in bones and failure of calcification of osteoid tissue. Clinical features: Symptoms: Delayed developmental hypotonia, stunted growth. Signs:

215

milestones,

lethargy

and

Skull: Craniotabes, frontal and parietal bossing, delayed frontanelle closure. Chest: Richatic rosary, Harrison sulcus, pigeon chest Extremities: Widening of the wrist, bowing of legs (genu varum), knock knees( genu valgum), windswept knees.

Fig 7.05: A) B/l genu varum. B) Left genu valgum. Spine: kyphosis, scoliosis, lordosis. Others: Potbelly due to hypotonia of abdominal muscles. Investigations: Laboratory studies show normal or low serum calcium levels, low serum phosphorous levels, serum alkaline phosphatase levels are markedly raised during active stage of disease, serum parathyroid harmone may be high with low vitamin D3 levels. Radiographs: In suspected rickets, radiographs of both wrists and knees AP/Lateral views should be done. It shows physeal widening, metaphyseal cupping (concave), fraying (irregular calcification). Xray of long bone shows generalized rarefaction with thinning of cortices and there may be bending of long bones.  A looser’s zone may be seen.

Fig 7.06: Radiological signs of rickets. A) Cupping of metaphysis; B) Splaying of metaphysis; C) Widened growth plate D) Small epiphysis. 216

Treatment: Medical management: Adequate sunlight exposure, Vit D supplementation at therapeutic doses of 200-600 IU/day orally or as six lakh units of vitamin D intramuscular injection initially followed by repeated dose after 3-4 weeks. Sclerosis develops as a radiological sign of healing. Orthopaedic treatment: Mild bony deformities are corrected by use of splints. Marked boney deformities need surgical correction by osteotomy.   Types of rickets: Nutritional rickets: Rickets occur due to dietary deficiency of vitamin D3. This gets corrected with Vitamin D3 supplementation. Vitamin D resistant rickets: This type of rickets does not get corrected with routine Vitamin D3 supplementation. Here the pathology is the inability of renal tubules to reabsorb phosphate leading to hypophosphatemia. Hence this condition is also called familial hypophosphatemia. Renal rickets: Chronic kidney disease results in deficiency of enzyme 1 alpha- hydroxylase which decreases the production of 1, 25 hydroxy vitamin D (calcitriol), the active form. It is corrected by supplementation of calcitriol injections. Fanconi syndrome: This is due to a defect in proximal tubule that prevents the reabsorption of phosphate, glucose and amino acids.

OSTEOMALACIA Osteomalacia is softening of bones due to defective bony mineralization caused by vitamin D deficiency in adults. Osteomalacia in children is called rickets. The patient presents with bone pain, backache, muscle weakness and occasionally pathological fractures. The radiograph shows band of radiolucency called looser’s zone commonly over femoral necks, pubis and ribs. Treatment is by calcium and vitamin D supplementation.

PAGET’S DISEASE OF BONE Definition: Paget’s disease is condition of unknown etiology characterized by excessive and abnormal bone remodeling involving one or several skeletal segments resulting in bone weakening, deformities and pathological fractures. Hence it is also called osteitis deformans. This condition was first described by Sir James Paget in 1877. Etiology:

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1) Genetic 2) Viruses like paramyxovirus It most commonly affects individuals older then 40 years of age. It is most common in males. Pathology: Paget’s disease can be either monosteotic (single-bone involvement) or polyosteotic (multiple-bone involvement). The most common involved are vertebrae, pelvis, skull or long bones like femur or tibia. The disease goes through the following phases: 1) Lytic phase- The disease begins with increased osteoclastic activity. 2) Mixed lytic and blastic phase- There is a rapid turnover of bone due to increased osteoclastic/osteoblastic process 3) Sclerotic phase- There is increased bone formation due to osteoblastic activity resulting in bony sclerosis. The bone turnover rate increases to as much as twenty times of normal. The end stage disease can complicate sometimes to osteosarcoma. Clinical features: Symptoms: Paget’s disease is mostly asymptomatic in early phase, when symptomatic they present with 1) Long bones: Deep aching bone pain worse at night, diffuse joint stiffness, musculoskeletal deformities and pathological fractures. 2) Skull: Overgrowth of bone in the skull can cause hearing loss or headache. 3) Pelvis: Paget’s disease in the pelvis can cause hip pain. 4) Spine: if spine is affected, nerve root can be compressed causing pain, tingling and numbness. Signs: There may be bony deformity or angulation, localized pain on palpation and increased warmth. Incomplete fractures are common in Paget’s disease. Neurological evaluation for spinal nerve root compression and auditory evaluation for hearing loss if any, has to be performed. Investigations: X-ray shows honeycomb or spongy appearance. Bone scan shows increased uptake. Serum alkaline phosphatase is raised. Treatment:

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Inactive lesions don’t require any intervention. Calcitonin and bisphosphanates like alendronate, zoledronic acid are used to halt the progression of disease. Complications: Secondary osteoarthritis, pathological fractures, neurological compression, development of osteosarcoma, high output cardiac failure.

HYPERPARATHYROIDISM Parathyroid glands are essential for maintaining calcium homeostasis in the body.  Hyperparathyroidism is a condition leading to excessive production of parathyroid hormone. Increased production of PTH inhibits phosphate reabsorption from kidneys and increased mobilization of calcium from the bones. It is most commonly seen in 3rd to 5th decade. Classification: Hyperparathyroidism is classified into 1) Primary: This occurs due to inherent pathology in parathyroid like adenoma or hyperplasia. 2) Secondary: This occurs due to persistent hypocalcemia in the body stimulating parathyroids eg: Renal rickets. 3) Tertiary: Persistent hypocalcemia for a prolonged time leads to conversion of parathyroid hyperplasia to an autonomous structure leading to persistent secretion of PTH. Clinical features: Symptoms: The disease is insidious in onset with nonspecific symptoms like generalized weakness, loss of muscle tone, anorexia, vomiting. These symptoms are classically due to hypercalcemia and are usually remembered as bones, stones, abdominal groans and psychic moans. Signs: Generalized bone tenderness, pathological fractures. Investigations: Lab investigations: The serum calcium levels are high and phosphorous is low. The serum parathormone and serum alkaline phosphatase are elevated. X-ray: Hand: Decalcification of bone causes bony cysts simulating a tumor and therefore are called brown tumors. Long bones: Long bones show widening of medullary canal and thinning of cortex. There may be generalized rarefaction with bony cysts and may lead to pathological fractures.

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Treatment: Primary hyperparathyroidism: Initially nonoperative management can be tried, if persistent surgical excision of parathyroid is necessary. Secondary hyperparathyroidism: Treatment is directed towards correcting the underlying pathology like renal causes of hyperparathyroidism. Tertiary hyperparathyroidism: Correcting the underlying condition and if necessary, then surgical excision. Treatment of deformities: In early stages by splinting and later by corrective osteotomy. Treatment of pathological or stress fracture: Immobilisation of fracture and once the disease process gets corrected and recalcification happens, surgery can be done. Questions: Short Essays: 1)    Metabolic bone disease 2)    Bow legs Short Answers: 1)    Radiological features in rickets 2)    Osteomalacia 3)    Paget’s disease of bone.

Credits: AthK

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Chapter 8

POLIOMYELITIS Competency OR 8.1: Describe and discuss the aetiopathogenesis, clinical features, assessment and principles of management in a patient with Post Polio Residual Paralysis. Definition: It is an acute infectious disease caused by a virus that inflicts typical temporary or permanent destructive changes in the central nervous system that can result in paralysis and deformities. Aetiopathogenesis: Poliovirus belongs to a member of enterovirus. The route of transmission of infection is either through fecal-oral route or droplet infection. Pathogenesis: Poliovirus is of three serotypes PV1, PV2 and PV3. The most virulent serotype is type 2 but most outbreaks of paralytic polio is due to type 1 virus. Phases of polio infection: Alimentary phase –   Following ingestion, the virus multiplies in the epithelial cells of the alimentary canal, lymphatic tissues, tonsils, peyer’s patches. Lymphatic phase - It spreads from the alimentary canal to adjacent mesenteric lymph nodes. Viremic phase – When the virus enters the bloodstream from the lymph nodes for the first time it is called primary viremia, following which it can enter into the extraneural tissues like the reticuloendothelial system and multiplies here. When the multiplied virus enters the bloodstream for the second time from the reticuloendothelial system it is called secondary viremia. Neural phase – Following secondary viremia, the virus can enter the spinal cord or brain producing different types of poliomyelitis 1)      Spinal polio: It is the most common type accounting for 79% of paralytic cases. The anterior horn cells of the spinal cord are the target cells and are affected. It produces a lower motor neuron type of lesion. It is characterized by asymmetric paralysis most commonly affecting the legs. The most common affection is seen towards the cervical and lumbar spine.

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2)    Bulbar polio – It accounts for 2% of cases and affects the brainstem and the cranial nerve nuclei of the brainstem which are 9,10,11,12. This causes weakness of the muscles innervated by these cranial nerves. 3)  Spinobulbar polio – It accounts for 19% of cases. It is a combination of bulbar and spinal paralysis.

Course of the disease – The incubation period for poliomyelitis is commonly 6 to 20 days and can range from 3 to 35 days. The response to poliovirus infection is highly variable and has been categorized based on the severity of clinical presentation. 1) Acute phase Severity A)Inapparent infection b)Abortive poliomyelitis

c)Non-paralytic poliomyelitis d)Paralytic poliomyelitis

Symptoms & signs No manifestation Sore throat Abdominal pain Constipation or diarrhea Anorexia Stiffness of the neck, back and legs. Severe muscle aches and spasms in the limbs or back. On examination there is flaccid paralysis and reduced muscle tone.

2) Convalescent phase – This encompasses the period following acute phase. Most of the muscle recovery occurs within the first 6 months due to axonal sprouting and reinnervation of motor units. 3) Chronic phase or Residual phase – any residual muscle weakness persisting after 2 years is permanent and does not recover. This residual paralysis is called post-polio residual paralysis (PPRP) which is responsible for muscle weakness and deformities associated with paralytic limb. Post-polio residual paralysis (PPRP) results in weakness, wasting and deformities of the limbs. They develop due to 1)    Muscle imbalance 2)    Unrelieved muscle spasm 3)    Bone growth 4)    Gravity and posture. 1)      Muscle imbalance: Flaccid paralysis is the main cause of functional loss and muscle weakness. When a muscle or

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groups of muscles are paralysed the opponent strong muscles pull the joints to their side. 2)      Unrelieved muscle spasm: Contractures of the paralysed muscles have a tendency for deforming the joint in the direction of contracture. This can be prevented by passive stretching and splinting. 3)      Bone growth:  Bone growth depends upon the stimulus by active healthy muscle stretching around the growth plate, which is lacking in polio-affected children causing limb length inequality, attenuation of blood vessels leading to reduced bone growth. 4)    Gravity and posture: Gravity plays important role in maintaining posture. The paralysed muscles cannot maintain posture leading to deformities.

Fig 8.01: A) Flexion deformity of knee; B)   Hyperextension of knee.                                             Functional assessment: 1)      Individual Muscle grading – power evaluation of individual muscle/muscles is done in upper limb, lower limb and abdominal muscles. 2)    The extent of contractures and deformities 3)    Ambulatory status 4)    Limb length deficiencies Individual muscle grading: Grade of motor recovery M0 M1 M2 M3 M4 M5

Clinical examination results No contraction Return of perceptible contraction in proximal muscles Return of perceptible contraction in proximal  and distal muscles Return of perceptible contraction sufficiently powerful to act against gravity. Muscle power to act against strong resistance Full recovery in all muscles

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Muscles: Lower limb Iliopsoas(flexor and lateral rotates of thigh) Gluteus maximus(extension and abduction of hip) Gluteus medius(abducts thigh) Adductor magnus(adducts and extends the thigh) Knee quadriceps(extension of knee) Hamstrings(knee flexion)

Gastrosoleus(plantar flexion of foot) Tibialis anterior(dorsiflexion and inversion of foot) Tibilais posterior(plantar flexion and inversion of foot)

Upper limb Trapezius Deltoid Biceps, brachialis, brachioradialis (elbow flexors) Triceps(elbow extensor) Flexor carpi radialis,flexor carpi ulnaris,flexor digitorum superficialis (wrist palmar flexors) Extensor carpi radialis longus, extensor digitorum,extensor carpi radialis brevis (wrist dorsiflexors) Flexor digitorum superficialis, flexor digitorum profundus (long finger flexors) Extensor digitorum,extensor digiti minimi(Long finger extensors) Opponens pollicis(Opposition of thumb)

Fig 8.02: Polio patient. Special Tests: 1) Obers test (ITB contracture): 224

With the patient lying on the lateral side, stabilize the pelvis. The knee is supported and flexed to 90° then the hip is abducted and extended. Release the knee support. Failure of the knee to adduct is a positive test.  2) Trendelenburg test (Gluteus medius paralysis): A positive Trendelenburg test demonstrates that the hip abductors (gluteus medius) are not functioning owing to weakness. To perform this test the patient stands on the unaffected leg and flexes the other knee at right angle. The pelvis should remain at a level or tilt up slightly due to non-weight bearing. The patient then stands on the affected leg and flexes the knee of the other leg. If the pelvis drops on the non-weight bearing side this signifies a positive Trendelenburg test.(Refer Fig 12.30) 3)   Thomas test for fixed flexion deformity of hip (iliopsoas): Thomas test is used to rule out hip flexion contracture. The patient lies supine on the examination table and holds the uninvolved knee to his or her chest while allowing the involved extremity to lie flat. Holding the knee to the chest flattens out lumbar lordosis and stabilize the pelvis. If the iliopsoas is shortened or contracture is present, the lower extremity on the involved hip will be flexed and will be unable to fully extend it. This constitutes a positive Thomas test. (Refer Fig 12.32) Extent of contractures and deformities: Polio patients have a random asymmetric pattern of muscle weakness. Upper limb

Lower limb

Dislocated shoulder. elbow contracture, hyperextension of elbow, Finger deformities. A)Hip jointFlexion, abduction, external rotation (ITB contracture), dislocated hip. B)Knee jointFlexion, posterior subluxation and external rotation(triple deformity), knee dislocation, genu recurvatum

Spine

C)Ankle joint- Equinovarus, equniovalgus,                 calcaneovalgu s, equinocavus. Scoliosis, kyphosis.

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Ambulatory status: 1)    Abductor lurch (or) trendelenburg gait: It is seen in cases of hip abductor paralysis or weakness of the gluteus medius. Drop of the pelvis on the opposite side occurs while standing on the affected limb. 2)    Extensor lurch: it is seen in cases of gluteus maximus paralysis During the stance phase of the affected limb, the hip needs to lock in extension but in cases of gluteus maximus paralysis it is not possible and there is a forward shifting of centre of gravity 3) Hand to knee gait – It is seen in weakness of quadriceps femoris. Extension of knee is not possible in midstance phase because of paralysis of quadriceps muscle so the patient uses his hand to extend the knee and prevent the knee from buckling. 4) Foot drop gait: It occurs due to paralysis of foot and ankle dorsiflexors. It can be due to common peroneal nerve injury. In foot drop gait, due to weakness of foot and ankle dorsiflexors there is slap of the foot on the ground. During swing phase there is high steppage as hip and knee goes into flexion for clearing the feet off the ground. 5) Calcaneal gait: It occurs due to weakness of plantar flexors (triceps surae) of the foot. 6) Short limb gait: This is seen in patients with limb length discrepancies. If the limb is shorter then 2 cms, the short limb gait is apparent. The shoulder and pelvis dips down in stance phase on the shorter side. Limb length discrepancy: A)Apparent length measurement is due to an apparent decrease in limb length due to muscle contracture. B)True length measurement is due to true decrease in limb length due to bone shortening. Lab diagnosis: Specimen: blood, CSF, feces, throat swab for viral isolation in the blood during primary viremia. Serodiagnosis – Neutralizing antibody tests, complement fixation test  

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Management during acute and convalescent stages: Medical treatment: 1. Absolute bed rest in isolation 2. Adequate fluid intake 3. Analgesics and moist heat to relieve muscle pains and spasm. 4. Tracheostomy, endotracheal aspirations, oxygen support in bulbar polio. Orthopaedic treatment: Objective 1) Splinting and braces to relieve pain and spasm. 2) Regular range of motion exercises several times a day to prevent stiffness. 3) Warm salt water baths – given to relieve muscle and nerve pain.

Management in residual paralysis: Conservative management: 1) Strengthening of unaffected muscles and stretching of shortened muscles. 2) ROM exercises of joint 3) Appropriate use of orthosis and calipers to improve gait. Surgical management: A) Release of contractures by fasciotomies and capsulotomies B) Re-establishment of power by tendon transfers C) Stabilization of a relaxed joint or a flail joint by arthrodesis D) Correction of bony deformities by osteotomies, arthrodesis E) Limb lengthening by Ilizarov’s technique. Procedures: A) Soft tissue release for soft tissue contractures: 1) Ober Yount procedure for ITB contracture 2) Soutters release for structures arising from anterior superior iliac spine for hip contracture. 3) Wilson release for knee flexion deformity 4) Tendoachillis lengthening for equinus deformity of foot 5) Steindlers release for cavus deformity of foot.

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B) Tendon transfers: 1) It helps to replace the function of paralysed muscle. 2) To remove the deforming force 3) To provide stability by improving muscle balance Common tendon transfers performed: A) Hamstring transfer to quadriceps. B) Peroneus brevis and tertius transfer to dorsum of foot. C) Arthrodesis: 1)It helps to stabilize the flail joints permanently 2)It eliminates the need for brace 3)It improves the function of joints Common arthrodesis surgeries: A)Knee arthrodesis for flail knee B)Triple arthrodesis for ankle D) Corrective osteotomy: In case of severe bony deformities due to muscle imbalance, osteotomies are performed. Corrective osteotomies: 1)    Proximal hip osteotomy for varus, valgus hip correction. 2)    Supracondylar corrective osteotomy of the knee E)Ilizarov technique For limb length equalization and deformity correction.

Deformities of the lower limbs: Hip deformities: 1)ITB contracture 2)Paralysis of gluteus maximus and gluteus medius 3)Paralytic dislocation of hip 4)Flail hip 1)   Iliotibial band: Origin – Anterolateral iliac tubercle portion of the iliac crest. Insertion – Gerdy’s tubercle, lateral condyle of the tibia.

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Fig 8.03: ITB contracture. Note the small atrophic limb with flexion, valgus and external rotation deformity at knee. Contracture of Iliotibial band leads to: 1)    Pelvic obliquity 2)    Increased lumbar lordosis 3)    Flexion, abduction and external rotation of hip 4)    Genu valgum and flexion contracture of knee 5)    Limb length discrepancy 6)    External tibial torsion with or without subluxation of knee joint 7)    Secondary foot and ankle deformities – secondary pes planus.

Fig 8.04: Note the fixed flexion deformity of left knee due to ITB contracture.

Fig 8.05: ITB contracture. Note the left small atrophic limb with valgus and external rotation deformity. Management for IT band contracture: Ober Yount procedure. 2) Paralysis of gluteus medius and gluteus maximus:

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Paralysis of gluteus medius leads to Trendelenburg gait. Paralysis of gluteus maximus leads to extensor lurch. Management: When both gluteus medius and maximus are paralysed, transfer of iliopsoas tendon with lesser trochanter to the greater trochanter is done. 3) Paralytic dislocation of hip: Muscle imbalance – The weak gluteus muscle and strong flexors and adductors cause hip dislocation. 4) Flail hip: When all the muscles around the hip are paralysed or weak it leads to flail hip. Management – 1) Hip knee ankle foot orthosis 2) Arthrodesis of hip Knee deformities The disabilities are caused by paralysis of the muscles acting across the knee joint. 1)Flexion contracture of the knee 2) Quadriceps paralysis. 3)Genu recurvatum 4)Flail knee 1) Flexion contracture of knee: Flexion contracture of the knee can be caused by a contracture of the iliotibial band. Triple deformity: Iliotibial band also causes genu valgum and an external rotation deformity of the tibia on the femur and posterior subluxation of tibia on femur Management: Posterior hamstring osteotomy of knee.

lengthening

and

capsulotomy,

corrective

2) Quadriceps Femoris Paralysis: It leads to hand to knee gait. During the stance phase of gait, quadriceps weakness is

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compensated for by tilting the trunk and center of gravity of the body forward. Management: Hamstring transfer to quadriceps. 3) Genu recurvatum: The knee is hyperextended. It is due to hamstrings and the gastrocnemius-soleus muscle weakness. Management: Closing wedge osteotomy for genu recurvatum. 4) Flail knee: The knee is unstable in all directions. Management: 1) Locking knee brace. 2) Knee arthrodesis. Foot and ankle deformities Foot and ankle are the most dependent parts of the body and are subjected to significant amount of deforming forces The most common deformities include: 1. Cavus deformity and claw toes 2. Talipes Equinus 3. Talipes EquinoVarus 4. Talipes Equino Valgus. 1)   Claw toe: It is hyperextension of metatarsophalangeal joint and flexion of interphalangeal joint. Procedure: Division of extensor tendon by Z-plasty. 2) Talipes equinus: Planter flexors are stronger than dorsiflexors and there is tight tendoachilles. Management: 1. Conservative management: exercises, serial casting, orthosis and molded shoe wear. 2. Surgical management: Lengthening of tendo-achilles by Z plasty.

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Fig 8.06: Z plasty for Tendo-achilles lengthening. 3) Talipes equino varus: Deformity: Equinus at ankle, inversion of heel at mid tarsal joint, adduction of fore foot. Cavus and clawing may develop in long standing cases. Surgical procedures: A) Steindler’s fasciotomy B) Tendon transfers C) Tendoachilles lengthening D) Triple arthrodesis (Surgical fusion of talocalcaneal, talonavicular and calcaneocuboid joint). Questions: Short Essay: 1)    What is triple deformity? Write briefly on its management. Short Answers: 1)    Stages of poliomyelitis 2)    Post polio residual paralysis 3)    Triple deformity of knee.

Credits: AthK

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Chapter 9

CEREBRAL PALSY Competency OR 9.1: Describe and discuss the aetiopathogenesis, clinical features, assessment and principles of management of Cerebral palsy patient. A group of permanent disorders of the development of movement and posture, causing activity limitation that is attributed to nonprogressive injury that occurred in the developing fetal or infant brain. Incidence: It is about 2.4 to 2.7 per 1000 live births. Improved health care in these high-risk groups has decreased mortality but increased morbidity in the form of brain injury. Etiology of cerebral palsy: Prenatal 1)TORCHES group of infection 2)Fetal exposure to drugs and alcohol 3)Maternal health problems like renal failure or infection 4)Rh incompatibility

Perinatal 1) Anoxia due to perinatal complications like prolapsed cord, placental abruption. 2)Premature delivery 3)Sepsis in the neonatal period

Postnatal 1)Meningitis in early childhood 2)Head injury 3) Hypoxia such as cardiopulmonary arrest.

Classification based on geographic distribution: A)Monoplegic type- One extremity is involved, usually the lower limb. B)Paraplegic type: Both lower extremities are involved equally. C)Quadriplegic type: All extremities involved equally D)Diplegic type: Lower extremities are involved more than upper limb. E)Hemiplegic type- Both extremities on the same side is involved. F)Total body: All extremities with neck involvement.

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Fig 9.01: Types of cerebral palsy: A) Monoplegia; B) Paraplegia; C) Quadriplegia; D) Diplegia; E) Hemiplegia; F) Total body involvement. Physiological classification: It describes the type of movement disorder

Fig 9.02: A) Spastic cerebral palsy due to cerebral cortex involvement; B) Dyskinetic cerebral palsy due to basal ganglia involvement ; C) Ataxic cerebral palsy in cerebellum. 1)Spastic - It is the most common type of cerebral palsy. It is associated with injury to pyramidal tract in immature skeleton. It is associated with tense contracted muscles. 2)Rigid: Most hypertonic form. It is associated with cogwheel or leadpipe rigidity. Athetoid- It is associated with injury to extrapyramidal tracts. It leads to constant dyskinetic purposeless movements of limbs, head and eyes. Choreiform: Continual purposeless movements of wrists, fingers and toes. Ataxic: It is associated with injury to the developing cerebellum. It is associated with disturbance of coordinated movements. 5)Hypotonia: It is associated with decreased muscle tone. Types: 1)Spastic diplegia: It is associated with bilateral spasticity of lower limbs predominantly when compared to upper limbs.  Spastic cerebral palsy patients can have toe walking due to gastrosoleus spasticity, flexed knee due to hamstring spasticity and scissoring due to bilateral adductor spasticity.

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2)Spastic hemiplegia: It is associated with spasticity of the ipsilateral upper and lower limb. In lower limb toe walking, flexed knee and adductor contracture can be seen. Delayed walking can be seen up to 18-24 months.  The affected upper limb has dystonic posture. 3)Athetoid cerebral palsy: Constant abnormal athetoid movements is seen. 4)Hypotonic cerebral palsy: It is associated with absent neck holding and decreased tone all over the body.

Fig 9.03: Cerebral palsy patient walking with assistance. Associated problems with cerebral palsy: Mental retardation

Vision disorders

Behavioral disorder Seizures

Hearing loss Drooling and dentition problems

Neurogenic bowel and bladder Dysphagia Autonomic dysfunction

Gross motor Function Classification System: GMFCS 1 Has nearly gross motor function. GMFCS 2 Walks independently but has limitations in running and jumping GMFCS 3 Uses assistive devices to walk and wheelchair for long distances GMFCS 4 Has the ability to stand for transfers, but minimal walking ability, depends on wheelchair for mobility GMFCS 5 Lacks head control. Can’t support his trunk and is dependent for all aspects of care. Assessment of child with cerebral palsy: 235

☐     Speech evaluation ☐     IQ Assessment ☐     Psychological evaluation ☐     Ophthalmological evaluation ☐     Occupational therapy evaluation ☐     Neurologist evaluation ☐     Orthopaedic assessment Orthopaedic assessment: Clinical examination: History Birth history.   Birth weight   Gestational age Any complications like if the child required Ventilator assistance or hospitalization in ICU. 

Delayed achievement of motor milestones. Preferential use of one hand or leg and early handedness, particularly left-handedness - clues of Spastic Hemi paresis

Signs: Increased tone Deep tendon reflexes are exaggerated Fine motor activities testing Retained infantile reflexes Balance, sitting and gait of the child

The child presents around the age of 2-3 years with parent’s complaining of inability to walk. The developmental milestones are delayed. On examination there is spasticity in the lower limbs, the degree of spasticity depends on the severity of disease. The main signs are spasm of adductors of hip and gastrosoleus muscle. When seen a few years later without treatment, the spasticity eventually gets converted to contracture.  The child may walk with a scissoring gait due to adductor contracture, flexion at knee due to hamstring contracture and equinus at ankle due to gastrosoleus contracture.

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Fig 9.04: Hamstring contracture resulting in flexion deformity of the knee in cerebral palsy. Upper limb in Cerebral Palsy: If affected, spasticity of the upper limb leads to flexion at elbow, wrist, fingers and also forearm pronation. Spine in Cerebral palsy: Spine involvement leads to scoliosis, spondylosis and spondylolisthesis. Gait in cerebral palsy: True equinus:  Gastrosoleus spasticity leading to ankle equinus Jump knee gait:   Hip and knee flexion due to psoas and hamstring spasticity. The gastrosoleus spasticity leads to ankle equinus. Apparent equinus: Hip and knee flexion leading to equinus. Crouch gait: Excessive dorsiflexion at ankle with hip and knee flexion. Investigations: a)X-ray- To determine joint subluxation or dislocation due to contractures. b)CT- To determine torsional bone deformities c)MRI- To determine soft tissue contractures. d)Cranial Ultrasound- For any injuries in the brain parenchyma. e)Gait analysis f)Test for hearing and vision. g)IQ test h)Histopathology in cerebral palsy: Periventricular leukomalacia, intraventricular and periventricular hemorrhage is seen. Differential diagnosis: 1)Tumors 2)Neurodegenerative disorders are to be considered if the child is born by normal delivery and has normal development of milestones for a few months and then deterioration. Treatment: Goals in treatment:

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A) Communication B) Education C) Mobility D) Ambulation The aim of treatment: For spasticity a) Physiotherapy b) Orthoses c) Oral medications d) Botulinum toxin e) Baclofen pump f) Neurosurgical intervention Conservative a)    Physiotherapy b)    Orthosis

c)     Drugs and injections

Surgery Problems in hip: a) Flexion contracture-Psoas tenotomy. b)Adduction contractureadductor release. Problem in knee: a)Flexion deformity of the Kneefractional lengthening of distal hamstrings

d)    Botulinum toxin Problem in ankle: e)    Baclofen pump f)      Selective dorsal rhizotomy a)Equinus Gastrosoleus recession techniques like Strayer,  Vulpius, Baker release.

Physiotherapy: It is the mainstay of treatment in all cases. It consists of passive movements of joints to stretch out the muscles and correct contractures.  A physical therapist will focus on helping the child with strength, balance, flexibility and coordination of motor skills for walking. The occupational therapist will help the child to improve skills for activities of daily living (ADL). Orthoses: Orthotics or splints are recommended for the child to correct muscle abnormalities. They improve posture and alignment, hence reducing energy expenditure for walking. Eg: ankle foot orthosis (AFO). Baclofen: Oral or Intrathecal baclofen which is GABA agonist is used to decrease the spasticity of muscle. It improves gait and posture in spasticity patients. 238

Botulinum toxin: Botox A is a polypeptide neurotoxin injected into muscles causing dynamic deformities. It irreversibly inhibits Ach receptors of muscles and has a temporary effect for upto 6 months after injection. It is indicated in children with spasticity causing dynamic adduction, knee flexion and equinus deformity. Neurosurgical intervention: A selective dorsal rhizotomy is performed in children with pure spastic diplegia. It limits sensory input from muscle spindles and reduces spasticity. Surgery: Release of contractures:  Tenotomy , fractional lengthening of tendons Neurectomy: Obturator neurectomy Arthrodesis and osteotomies. Problems in hip: a) Flexion contracture b) Adduction contracture Flexion contracture: Spastic iliopsoas can be corrected by psoas tenotomy over pelvic brim. Adduction deformity: Scissoring due to adductor contracture can be corrected by adductor tenotomy or obturator neurectomy. Problems in knee: Flexion deformity of the knee can be corrected by fractional lengthening of the hamstring tendons. Problem in ankle: Equinus- It is caused by gastrosoleus contracture. Procedures Gastrosoleus recession techniques A)Strayer B)Vulpius C)Baker release. Single-event multilevel surgery(SEMLS): Single-event multilevel surgery means when a number of orthopaedic procedures on cerebral palsy patient are performed at one time. This means the child needs only one anaesthesia for surgery for hip, knee and ankle deformities followed by one block rehabilitation therapy.

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Questions: Short Essay: 1.Define cerebral palsy. Write briefly about classification, clinical features and management in cerebral palsy. Short Answer: 1.SEMLS.

Credits: AthK

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Chapter 10

BONE TUMORS Competency OR 10.1: Describe and discuss the aetiopathogenesis, clinical features, investigations and principles of management of benign and malignant bone tumours and pathological fractures. Bone tumors develop when cells within the uncontrollably forming a mass of abnormal tissue Risk factors: 1) Genetic disorders

bone

divide

A)Li Fraumeni syndrome B)Rothmund Thomson syndrome 2) Paget’s disease 3) Radiation and chemotherapy 4) Bone marrow transplantation The most common primary malignant bone tumor is multiple myeloma and benign bone tumor is osteochondroma. Sites of origin: 1. Epiphyses a. Skeletally immature – Chondroblastoma b. Skeletally mature – Giant cell tumor (GCT). 2. Metaphysis a. Osteochondroma b. Osteosarcoma c. Chondrosarcoma d. Secondaries 3. Diaphysis a. Ewing’s sarcoma b. Osteoid osteoma c. Adamantinoma

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Fig 10.1: Diagram showing sites of tumor origin. Epiphysis: A) Chondroblastoma; B) Giant cell tumor Metaphysis: 1) Enchondroma; 2) Osteosarcoma; 3) Osteochondroma Diaphysis: a) Cortical fibrous dysplasia b) Osteoid osteoma c)Chondromyxoid fibroma d)Ewings sarcoma e) Myeloma f) Fibrous dysplasia g) Fibrosarcoma h) Fibrous cortical defect Tissue Bone Cartilage

Fibrous Marrow Blood vessel Unknown

Benign 1)Osteoid osteoma 2)Osteoblastoma 3)Osteoma 1)Enchondroma 2)Osteochondroma Chondroblastoma Chondromyxoid fibroma Fibrous cortical defect

Malignant Osteosarcoma

Hemangioma

Angiosarcoma

Aneurysmal bone cyst Giant cell tumor

Ewing’s sarcoma

Chondrosarcoma

Fibrosarcoma Lymphoma Myeloma

Difference between Benign bone tumor Slow growth Well defined margins

Malignant bone tumor Rapid growth Destructive, poorly defined margins No/less aggressive periosteal More aggressive periosteal reaction reaction Absence of soft tissue mass Soft tissue mass or extension Metastasis is rare Metastasis is common. Investigations: 1. X-ray

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X-ray is the gold standard investigation for arriving at the diagnosis of bone tumor. It shows the location, size and shape of the tumor.

2. CT scan CT is high-resolution X-ray taken from different angles merged with computer software. It provides a detailed 3D assessment of bone tumor. 3.MRI It is the most accurate method for assessing adjacent soft tissue involvement. It utilizes powerful magnet linked to a computer to create excellent soft tissue contrast, visualise bone marrow and soft tissue edema. 4.Radio Nuclide (bone) scanning Bone scanning employs 99m Tc radioisotope to detect skip lesions and silent secondary bone deposits. 5.PET scan: Fludeoxyglucose(F18) is injected into a vein and a scanner is used to make a detailed computerized analysis of areas inside the body. It detects metastasis of both bone and soft tissue structures. 6.Biopsy: It is the final diagnostic invasive procedure after all the above non-invasive investigations. It involves the removal of a piece of representative tumor sample using Jamshedi needle or biopsy gun for histopathological and immunohistochemistry studies. Types of biopsy Biopsy type Tissue obtained Examination Fine needle Cells Cytology of tumor. aspiration Core needle Small tissue core More tissue than fine needle aspiration Incisional Incision and Adequate tissue sample. biopsy adequate removal Excisional Tumor excision in Removes entire lesion biopsy toto 243

Staging: Enneking staging: IA: Low grade Intra-compartmental (lesion confined to single anatomical compartment). IB: - Low grade extra-compartmental (beyond single compartment). IIA: - High grade intra-compartmental. IIB: - High grade extra – compartmental. III: - Lesion high or low grade, intra or extra compartmental with regional or distant metastasis. TNM STAGING: T stages for bone cancer 1)Tx -Primary tumor cannot be measured 2)T0 -No evidence of tumor 3)T1- Tumor 8cm in size 5)T3 -Tumor is in more than in one place in same bone N stages for bone cancer 1)N0 No lymphnode spread near the tumor 2)N1 tumor has spread to nearby lymphnode M stages for bone cancer 1)M0 -No metastasis 2)M1 -Distant metastasis Principles of Surgery: The optimal treatment of the tumor often requires a combination of surgery, chemotherapy and radiation therapy.

Surgery: Malignant tumors: 1) Amputation: Amputation is the surgical removal of all or a part of the limb. It completely eradicates the tumor of the limb but it is associated with long term morbidity in gait pattern. 2) Limb Salvage: Limb salvage is a surgical procedure that replaces diseased bone with a metal implant or bone graft and thus to reconstruct into a functional limb. It has greater risks for infection, wound dehiscence, flap necrosis, and deep venous thrombosis.

Margins: In Orthopaedic oncology, the surgical margin is described by one of the four terms: A) Intra-lesional: An intra-lesional margin is one in which the plane of surgical dissection is within the tumor. This type of procedure is often described as “debulking” because it leaves behind a residual tumor.

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B)Marginal: It is achieved when the dissecting plane passes through the pseudo capsule. This type of margin usually is adequate to treat most benign lesions. C)Wide: The plane of dissection is in normal tissue. The entire tumor remains surrounded by a cuff of normal tissue. D)Radical: Radical margins are achieved when all the compartments that contain the tumor are removed en bloc.

Fig 10.02: Types of tumor excision: 1) Tumor; 2) Pseudocapsule (Reactive zone) A)Intra-lesional; B) Marginal; C) Wide; D) Radical. Benign bone tumors: Curettage:

Benign bone tumors are treated adequately by curettage. It is associated

with a higher rate of local recurrence.

Types: 1) Simple curettage: A large cortical window is made over the lesion. This window must be at least as large as the lesion itself. The bulk of the tumor is scooped out with a large curette. 2) Extended curettage: Extended curettage includes the use of adjuvants such as liquid nitrogen, phenol, polymethyl methacrylate or thermal cautery to extend the destruction of tumor cells. This greatly reduces recurrence rates of benign aggressive tumors. RADIATION THERAPY: Radiation causes cell death by inducing the formation of intracellular free radicals that subsequently cause DNA damage. The sensitivity of a cell to radiation depends on several factors including (1) The cell’s position in the cell cycle (actively mitotic cells are most sensitive) 245

(2) Tissue oxygenation- Local hypoxia provides a protective effect because oxygen-free radicals cannot be formed in hypoxic tissue. (3) The cell’s ability to repair DNA damage or its inability to undergo apoptosis in response to this damage.

CHEMOTHERAPY: Adjuvant chemotherapy refers to chemotherapy administered postoperatively to treat presumed micrometastases. Neoadjuvant chemotherapy refers to chemotherapy administered before surgical resection of the primary tumor. It causes regression of the primary tumor.

BENIGN TUMORS OSTEOCHONDROMA: Introduction: It is the most common benign lesion of the bone. It is a hamartomatous chondrogenic lesion arising from aberrant growth plate cartilage. It is also called exostosis. It is most common in adolescents and young adults. Mutation in EXT gene is seen. Site: The lesion is most common around the knee joint (Distal femur > Proximal tibia). Clinical features: It is a painless immobile mass near the joint. X-ray shows a sessile or pedunculated tumor with a cartilaginous cap. Clinically tumor appears to be larger compared to the X-ray because of radiolucent cartilaginous cap.

Fig 10.03: Solitary pedunculated osteochondroma in the distal femur. Treatment: 1) Observation 2)    Surgery- Extraperiosteal excision is done if there is pain due to trauma, compressive symptoms, rapid increase in the size of lesion and cosmetic abnormalities. 246

Complication: Bursitis, nerve impingement, risk of 1% malignant transformation to chondrosarcoma. Diaphysial achalasia: It is also called multiple exostosis. X-ray shows champagne glass appearance. It has higher chance (i.e. 5%) of malignant transformation into chondrosarcoma.

Fig 10.04: Multiple exostosis in distal femur, proximal tibia and fibula. ENCHONDROMA: Introduction: It is a benign  chondrogenic  tumor composed of  hyaline cartilage located in the  medullary cavity of diaphysis or metaphysis most commonly in hand. It is caused by an abnormality of  chondroblast function leading to incomplete endochondral ossification. Histology: Cells are in lacunae and have small dark nuclei. The cells appear bland with few chondrocytes and are similar in size and shape. Clinical features: Asymptomatic, discovered incidentally on radiographs. Pathologic fracture is often seen with enchondromas in the hand. Imaging:-Central well circumscribed lytic lesion that shows stippled calcification.

Fig 10.05: Enchondroma of left middle phalanx of the ring finger. Treatment:1)Intralesional curettage and bone grafting 2) Rarely amputation. Complications: Pathological fracture 1)Ollier's disease: Multiple enchondromas with deformity.

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2)Maffucci syndrome: Multiple enchondromas with cavernous hemangioma CHONDROBLASTOMA: Introduction: It is a cartilaginous tumor also called as Codman’s tumour. It occurs in patients aged less than 20 years (Before the closure of epiphysis). Site: The most common site is in the epiphysis around the knee joint. Investigation: Radiologically there will be a lytic area with speckled calcification (Chicken wire appearance). Treatment: Curettage with bone grafting FIBROUS DYSPLASIA: Introduction: It is the failure of production of the normal lamellar bone leading to areas replaced by fibrous tissue. The most common location is in the metaphysis. It is associated with GNAS mutation. It can be monostotic(80%) or polyostotic(20%). In case of monostotic lesion, it is most commonly seen in femur, tibia or ribs. In polyostotic lesion, multiple bones are involved. Histology: Fibroblast proliferation surrounded by islands of woven bone. Clinical features: It presents with pain, swelling or deformities. Diagnosis: Radiologically there is a lytic area with subperiosteal new bone formation (ground glass appearance). Shepherd crook deformity of the femur is seen. Blood tests show an increase in serum alkaline phosphatase. Treatment: Observation, bisphosphonate therapy, curettage with bone grafting Complications: Pathological fractures McCune Albright Syndrome: Precocious puberty in females with polyostotic fibrous dysplasia with café au liat spots. OSTEOMA: The most common site is skull and facial bone. It can be left alone but if cosmetically unacceptable then simple excision can be performed. OSTEOID OSTEOMA: Introduction: It occurs in persons aged 5-25 years with a 3:1 male to female ratio. Site: It is diaphysial in location. The most common site is tibia followed by posterior element of spine. Clinical features: It presents with dull aching pain which worsens at night and on drinking alcohol. The pain is characteristically relieved on taking aspirin (Aspirin tumor). Diagnosis: X-ray shows a zone of sclerosis surrounding a radiolucent nidus. Size of the tumor is < 2 cm. Treatment: Excision of the lesion. OSTEOBLASTOMA: 248

Introduction: It is an aggressive benign osteoblastic tumor of bone (nidus > 2cm). It is seen in persons aged 10-30 years with males to female ratio 2:1. It commonly arises in the posterior elements of spine and the sacrum. Clinical features: Slowly progressive dull aching type of pain not relieved by NSAIDS. Imaging: It is a lytic or mixed lytic-blastic lesion with radiolucent nidus > 2cm. Histology: Interlacing network of bone trabeculae in a loose fibrovascular stroma with prominent vessels and plump osteoblasts Treatment: Curettage and bone grafting. SIMPLE BONE CYSTS: Introduction: These are true cysts. The age of presentation is 10 20 years. Site: The most common site is the metaphysis of the upper end of humerus . Clinical features: It is usually asymptomatic unless there is a pathological fracture. The cyst is filled with fluid containing prostaglandins. The lesion present near the growth plate is called "active lesion" and if away from the growth plate it is called "static lesion". Diagnosis: Radiologically it is central in location. It is a lytic lesion with no or minimal expansion of the cortex. “Fallen fragment sign” is pathognomic. Treatment: 1. Aspiration of the cyst and injection of methylprednisolone. 2. Curettage with bone grafting is done in case of a large cyst. 3. If already fractured, then treatment is plaster application because healing of the lesion may occur spontaneously. Complication: Pathological fracture

Fig 10.06: X-ray of proximal humerus showing solitary bone cyst. Note the fallen fragment sign marked by an arrow. ANEURYSMAL BONE CYSTS: Introduction: It is a benign expansile bone lesion with blood-filled cavities. The age of presentation is between 10 - 20 years. Site: Metaphysis in young adults. Clinical feature: Pain Diagnosis: X-ray shows an eccentric radiolucent lesion with marked thinning of cortex. Air fluid levels may be seen on MRI. 249

Histology: Blood filled cystic spaces lined by fibrous septa. Cavity lining shows numerous benign gaint cells and spindle cells.

Fig 10.07: Aneurysmal bone cyst. Treatment: Extended curettage with bone grafting. Complication: Pathological fracture. HEMANGIOMA: Introduction: It is a benign vascular neoplasm. The most common site is vertebral body and skull. Clinical feature: Pain Diagnosis: Radiologically, there is a loss of the horizontal trabeculae with a prominence of the vertical trabeculae. (Corduroy appearance) Treatment: In case of pain – radiotherapy LOCALLY INVASIVE TUMORS ADAMANTINOMA: It is well circumscribed monostotic lesion occurring in the anterior cortex of the tibia. It is a diaphyseal radiolucent lesion radiologically. Treatment is by resection because local recurrence is very common after curettage. CHORDOMA: Chordoma is a locally malignant lesion arising from the remnant of notochord. The most common site is sacrum followed by the cervical area. The presenting symptom is pain with or without neurological abnormalities. Radio logically there will be destruction of bone with expansion. Treatment is by complete excision of tumor with or without radiotherapy. GIANT CELL TUMORS (OSTEOCLASTOMA): Introduction  : Giant cell tumor is a benign  but locally aggressive tumor arising from epiphysis. The most common age of presentation is 20 - 40 years. It typically involves epiphysiometaphyseal region. It often extends upto adjacent articular cartilage, which remains intact. The overlying cortex undergoes resorption and the contour of bone

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is expanded by the tumor which is covered by a thin shell of subperiosteal new bone. Pathology: Grossly the tumor is gray to reddish brown and is composed of soft, vascular and friable tissue. Microscopy: It is composed of osteoclast-like multinucleated giant cells in a moderately vascularised network of proliferating round, oval or spindle-shaped cells.  Site: The most common site is around the knee joint (Lower end femur> proximal tibia> distal end of radius).

Clinical features: 1)Insidious onset of pain in the involved extremity with activity. 2)Palpable mass •       Tenderness over the mass •       Soft tissue swelling Investigations: X-ray: Lytic lesion in the epiphysis but involves metaphysis and adjacent articular cartilage. It is usually eccentrically placed, expansile solitary lesion in the bone with a characteristic soap bubble appearance.

Fig 10.08: AP view of proximal tibia showing features of giant cell tumor. Note the tumor is osteolytic, eccentrically placed and showing a characteristic soap bubble appearance. MRI: It is useful to determine extraosseous soft tissue and joint involvement. A tumor biopsy is done for confirmation. Treatment:

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Medical: Medical management with denosumab, bisphosphonates for stable lesions. Surgery: Small lesion: a)Curettage with cryotherapy with or without bone grafting. b) Sandwich technique. Large lesion: a) Wide excision of the tumor with reconstruction by a large bone graft or prosthesis. b) Turn-o-plasty- In tumors affecting the lower end of femur, the affected part is excised and the defect created is made up by vertically splitting the tibia and turning it upside down and fixing it to the stump of femur. c) Amputation

Fig 10.09: GCT tumor of distal femur treated by turn-o-plasty. 5E’s of giant cell tumor: Epiphysial, Eccentric, Expansile, Egg shell cracking, Excision.

MALIGNANT BONE TUMORS OSTEOSARCOMA: Osteosarcoma is defined as a primary malignant tumor of bone in which the neoplastic cells produce osteoid matrix. Introduction: It affects the age group between 10-20 years. Males are affected more than females by a ratio of 3:2. The most common sites are distal femur, proximal tibia and proximal humerus. Types ➢            Primary: Most common age group of 10-20 years with no preexisting lesion. These tumor are usually aggressive. ➢            Secondary: It usually occurs in the age group of more than 45 years. Preexisting lesions being Paget's disease, fibrous dysplasia, bone irradiation. 252

Primary osteosarcoma: Li Fraumeni syndrome where germline mutation of P53 chromosome is seen. Other aberrant chromosomal mutations are also seen. Pathology Gross: It is a large destructive intramedullary tumor with poorly defined margins.It is predominantly metaphyseal extending upto epiphysis and also into soft tissues. Microscopy: Hypercellular, spindle cell tumor with extensive pleomorphism. Malignant osteoid is often laid down in a lace-like pattern in between the malignant cells. Classification: It is classified according to histopathology like osteoblastic, chondroid, fibroblastic, telangiectatic. Clinical features: 1)Bone pain 2)Loss of weight and appetite 3)Erythema, swelling and mass may be present. 4)Pathologic fracture – The bone weakens secondary to the tumor and results in fracture from minimal trauma. Investigations: 1)X-ray shows bone destruction with permeative erosion of the cortex with indistinct borders & pathological new bone formation. Codman triangle: It is a radiological triangle formed when an aggressive bone lesion grows faster than new periosteum can be ossified. Only the periosteum at very margin of the lesion has time to ossify creating a triangular lip of new bone.

Fig 10.10: X-ray of the proximal humerus AP view showing Osteosarcoma. Note the sunburst appearance (A) and subperiosteal bony elevation leading to codman triangle (B). Chest X-ray is essential for any evidence of secondaries in chest. Osteogenic sarcoma metastasizes very early to lungs. (Cannon ball metastasis). 2)CT scan /bone scan for local bony skip lesions and MRI for soft tissue extension. 3)Serum alkaline phosphatase is elevated and is of only prognostic value. 253

4)A biopsy is confirmatory. Treatment: Surgery: 1) Neoadjuvant chemotherapy and limb salvage resection in highgrade osteosarcoma: Preoperative chemotherapy is given for 8-12 weeks followed by surgery and later on maintenance chemotherapy for 6-12 months. Doxorubicin, cisplatin, etoposide and high dose methotrexate are commonly used chemotherapeutic agents. 2) Wide surgical resection: It is indicated in low-grade osteosarcoma  3) Amputation: It is done in case of pathologic fracture and tumors encasing neurovascular bundle. EWING SARCOMA: Introduction: It is a malignant tumor of bone arising from diaphysis. It is typically seen in patients  from 5-25 years of age. Ewings sarcoma is caused by translocation t(11,22) in most cases which produces EWS-FLI1 fusion transcription factor. Site: The most common site is diaphysis of long bone (two-third cases), flat bone (one-third cases) Clinical features: Pain is accompanied by mild fever It often mimics an infection Physical examination shows swelling and local tenderness. Diagnosis: The lesion may be purely lytic or have variable amounts of reactive new bone formation. It is a large destructive lesion having a permeative  moth-eaten appearance. The periosteal reaction may give "onion skin" appearance. CT scan /bone scan for local bony skip lesions and MRI for soft tissue extension. Lab findings may include anemia, leucocytosis and raised LDH levels. Biopsy shows uniform small cells arranged in a pseudo-rosette pattern. Treatment: It is a highly radiosensitive tumor (it melts like snow on radiation but recurrence rate with radiation is high). So Chemotherapy + limb salvage resection ± adjuvant radiation is the mode of treatment. The chemotherapeutic drugs used are Vincristine, doxorubicin, cyclophosphamide and dactinomycin. Preoperative chemotherapy (neoadjuvant) given for 8-12 weeks followed by surgical resection and maintenance chemotherapy/ radiotherapy is given for 6-12 months.

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Metastasis can occur through blood and bone-to-bone. These metastatic patients have a poor prognosis. MULTIPLE MYELOMA: Introduction: It is a malignant neoplasm of plasma cells. It affects the age group >50 years. Site: Multiple myeloma is a hematological neoplasm. It affects flat bones like skull, pelvis and vertebrae. Bone destruction is the clinical hallmark caused by the activation of osteoclasts by releasing IL-6, TNF and activation of RANK by myeloma cells. Solitary lesions are called plasmacytoma. Presenting complaints are severe back pain with or without pathological fractures, renal failure, bone marrow suppression, hypercalcemia, amyloidosis and neurological symptoms Diagnosis: 1)Radiologically multiple punched out, lytic lesions in the skull. 2)Blood: Significant increase in ESR (>100), Increase in serum protein level, reversal of A:G ratio, increase in serum calcium level with normal serum alkaline phosphatase. 3)M- Spike on electrophoresis is seen in 90% cases. IgG, IgA and IgM are released by malignant plasma cells. 4)Urine: Bence - Jones protein is present in 30% of cases 5)Biopsy: Percutaneous/open biopsy showing myeloma cells. Treatment: Chemotherapy with melphalan in combination with vincristine and prednisolone. Bortezomib is the novel monoclonal antibody used to treat multiple myeloma. In cases of neurological symptoms, local radiotherapy will help. CHONDROSARCOMA: Introduction: It is a malignant primary bone tumor composed of chondrocytes. Primary chondrosarcoma commonly involves the age group 40-60 years. Predisposing lesions like osteochondroma, multiple enchondromas leads to secondary chondrosarcoma. Clinical Features: Pain is the most common symptom. Sometimes it can present with a pathologic fracture. Investigations: X-ray will show bony destruction with intralesional mottled calcification (popcorn appearance).

Fig 10.11: Clinical picture and X-ray showing chondrosarcoma. Note the mottled calcification.

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Confirmation: Biopsy Histology: Chondrocytes are enlarged with plump multinucleated lacunae, hypercellularity and disorganization is seen. . Treatment: Chondrosarcomas are generally resistant to chemotherapy and radiation. So surgical procedures like wide resection, en-bloc excision is done.

METASTATIC BONE DISEASE  Tumors that originate at another site (eg- breast, lung, prostate, and thyroid) that spread to the bone are called metastatic bone disease. Lung cancer in men and breast cancer in women is the most common type. Bone cancers in the spine can compress the spinal cord and cause neurological deficits. Clinical features: Bone pain, hypercalcemia, pathological fractures    Radiology: X-ray- The predominant bone response to some tumors may be osteoblastic (bone forming), osteolytic (bone destruction) or mixed. Osteoblastic

Osteolyt ic 1)Prostate 1)Thyroi carcinoma d 2)Small cell carcino lung tumor ma 2)Renal cell cancer 3)Multipl e myelom a 4)Non small cell CA

Mixed 1)Breast carcinoma 2)Gastrointestin al cancers

CT and MRI scans are used to assess local bone and soft tissue tumor extension. The bone scan is an investigation of choice for distant bony metastasis. PET scan is used to identify both bone and soft tissue metastasis. Blood investigations show increase serum calcium level and high ESR in multiple myeloma, increased serum acid phosphatase levels in cases of prostatic cancer.

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Treatment is prophylactic fixation in cases of long bone lesion of size > 2cm or more than 50% involvement of bony width and in case of intractable pain.

PATHOLOGICAL FRACTURES A pathological fracture is a bone fracture caused by weakness of bone structure that leads to decreased mechanical resistance to normal mechanical loads. Causes of pathological fractures: Reduced bone mass Osteoporosis Neoplastic Primary bone tumors- eg: Osteosarcoma, chondrosarcoma Secondary/metastatic bone tumors- eg: breast Ca, lung Ca, prostate Ca. Tumor like lesions Solitary bone cyst Aneurysmal bone cyst Fibrous dysplasia Infections Osteomyelitis Metabolic causes Osteomalacia and rickets Scurvy Hormonal causes Cushing syndrome Hyperparathyroidism Developmental disorders Osteogenisis imperfecta, Achondroplasia Marrow cell disorders Histiocytosis, Gauchers disease. Fragility fractures: Low-energy osteoporotic fractures occurring in osteoporotic bone. The most common cause of pathological fracture is Osteoporosis. The common sites of fragility fractures are vertebral fracture, proximal femur fracture and distal radius fracture. Mechanism of injury: Pathological fractures may result from trivial trauma. Clinical examination: Symptoms: 1)Spontaneous fracture without trauma 2)Fractures after minor trauma There can be excessive pain at the site of fracture prior to injury History of malignancy Signs: Physical examination should be done to evaluate the fracture site or any evidence of primary disease such as lymphadenopathy, thyroid nodules, breast masses, prostate nodules.

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Laboratory evaluation: Blood tests 1)Complete blood count with red blood cell indices with differential count and peripheral smear. 2)Erythrocyte sedimentation rate, CRP 3)Liver function tests 4)Renal function tests with serum electrolytes 5)Thyroid profile

1)Metabolic profile: Serum calcium, serum phosphorous, alkaline phosphatase, PTH. 2)DEXA scan for osteoporosis 3)Serum and urine electrophoresis , urine examination for bence jones proteins for Multiple myeloma, 4)Ca-125 for Ovarian Carcinoma PSA, Acid phosphatase for prostatic carcinoma CEA for gastrointestinal tumors. C-telopeptide and N- telopeptide are markers for bone collagen breakdown.

Radiographic evaluation: 1) X-ray: The fracture line extends through the destructive lesion in the bone. It may be frequently associated with a soft tissue mass.

Fig 10.12: Osteolytic secondaries in the humerus shaft region leading to pathological fracture. 2)CT scan: It is most sensitive to determine a bony lesion. CT scan is used to search primary lesions in pelvis, abdomen and chest. 3)MRI scan: It can determine the extraosseous spread of tumor. It can be used to determine neurological involvement in spinal 258

metastasis. 4)Tc-99 Bone scan: It uses radionucleotide to detect occult lesions in the bone and response to therapy. 5)FDG PET scan: It is used to determine distant soft tissue metastasis. 6)Biopsy for lytic lesions: It should be obtained to confirm the diagnosis and plan for further management. Treatment: Non-operative management: 1)Bracing- It is indicated in patients with limited life expectancies and severe comorbidities. 2)Bisphosphonates: It inhibits bone resorption by reducing osteoclastic activity. 3)Analgesics: NSAIDs, opioid analgesics for pain relief. Operative management: Mirel developed a scoring system that is used to determine which lesions are at high risk of fracture and need prophylactic stabilization.

Site Pain Lesion Size

Score 1 2 upper lower limb limb mild moderate blastic mixed 2/3

Score < 7- No surgery Score >7- Prophylactic fixation surgery. 1)Treatment for local bone lesion: Resection and surgical stabilization/ radiation. 2)Treatment for skeletal metastasis: Radiation/ chemotherapy without or with prophylactic fixation by plate or nail. Questions: Long Essays: 1. A 11 year old boy was referred from a primary care centre with Osteosarcoma of femur. Discuss A. Clinical features B. Radiological and histological findings. C. Management. 2.Classify bone tumors. Discuss pathology, clinical features, diagnosis and management of Osteosarcoma.

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3.Discuss the benign tumors of bone including clinical features, radiological appearances and management. 4.Describe the clinical features, radiological appearance, pathological features and management of Gaint cell tumor on the distal end of radius. 5.Discuss the pathology, clinical features and management of osteosarcoma of lower end of femur. 6.Discuss the etiopathogenesis, mode of spread, clinical features and management of Ewing’s sarcoma right knee. Short Essays: 1.Osteoclastoma 2.Ewings sarcoma 3.Osteochondroma 4.Bone cyst 5.Pathological fracture Short Answers: 1.Osteoid Osteoma 2.Radiological features of Gaint cell tumor 3.Radiological picture in Osteosarcoma 4.Ewing’s tumor 5.Multiple myeloma.

Credits: AthK

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Chapter 11

PERIPHERAL NERVE INJURIES Competency OR 11.1: Describe and discuss the aetiopathogenesis, clinical features, investigations and principles of management of peripheral nerve injuries in diseases like foot drop, wrist drop, claw hand, palsies of Radial, Ulnar, Median, Lateral Popliteal and Sciatic Nerves.

PERIPHERAL NERVE INJURY ANATOMY Central nervous system Brain and spinal cord

Peripheral nervous system Cranial nerves: 12 pairs

Spinal nerves: 31 pairs: The mixed spinal nerve has three distinct components: 1) Motor 2) Sensory 3) Autonomic.

Peripheral nerves are bundles of axons conducting efferent impulses from cells in the anterior horn of spinal cord to the muscles and afferent impulses from peripheral receptors via cells in the posterior root ganglia to the cord. All motor axons and sensory axons are covered by a myelin sheath and interrupted by node of ranvier. Histology of peripheral nerve: A) Epineurium: The connective tissue that surrounds a group of fascicles to form the peripheral nerve. B) Perineurium: It is a fairly dense membranous tissue covering individual fascicles. C) Endoneurium: It is the loose fibrous tissue covering the axons.

Fig 11.01: Structure of nerve: A) Epineurium; B) Perineurium; C) Endoneurium; D) Vessels. 

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Etiology of peripheral nerve injury: Fractures and dislocations- Ischemia, compression, laceration. Direct cut injury by sharp objects like knife, glass piece. Traction injury eg: brachial plexus injury. Metabolic disease- hypothyroidism, liver failure, renal failure. Malignancy- Nerve infiltration, Compression. Heavy metal poisoning- lead and mercury Infection: leprosy Drugs-  Isoniazid, phenytoin Diabetic neuropathy Vitamin B12 deficiency- Demyelination Radiation, alcoholism Neuron: Neuron is the name given to a nerve cell and all its process. It is the structural and functional unit of the nervous system. Pathology: Nerve degeneration: When a peripheral nerve fiber is injured, degenerative changes occur in the nerve cell body and the nerve fibre of the same neuron and also adjoining neurons. The following changes can be seen: 1) Cell body: It is also called transneuronal degeneration. The nissel granules disintegrate into fragments by chromatolysis. There is disintegration of golgi apparatus. The nerve cell body swells due to accumulation of fluid and becomes round. 2) Proximal segment: The proximal part undergoes retrograde degeneration 3) Distal segment: The distal part undergoes Wallerian or orthograde degeneration. Wallerian degeneration: Wallerian degeneration is a pathological change that occurs in the distal cut end of axon nerve fibre. It is also called orthograde degeneration. It starts within 24 hours of nerve injury. The changes occur throughout the length of the distal part of nerve fiber and are destroyed by phagocytosis. Nerve regeneration: Regeneration begins within the first 24 hours of injury by axonal sprouting from the axonal stump. If the endoneurial tube is intact, the axonal sprouts readily cross the injured site. The rate of nerve regeneration is 1 mm/day.  If the endoneurial tube is disrupted, then the axonal sprouts grow and migrate aimlessly into epineurium and perineurium forming a neuroma. Tinel’s sign: The Tinel  sign is elicited on the patient on gentle percussion by a finger from the distal to proximal along the course of the injured nerve. A transient tingling sensation may be felt by the patient along the course of the injured nerve. A  positive  Tinel  sign is presumptive evidence that regenerating axonal sprouts are progressing along the endoneurial tube. Classification of nerve injuries: Sunderland classification:

Mild

Sunderland

Seddon

Injury

I

Neuropraxia

Physiological conduction

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Recovery period < 3 months

Moderate

II

Axonotemisis

III

IV

Most severe

V

Neurotemesis

block of the nerve Axon is not continuous, the nerve itself remains intact. Wallerian degeneration followed by axonal sprouting occurs. During healing, excessive scarring of endoneurium occurs that hinders axonal regeneration Nerve incontinuity, excessive scar blocks nerve regeneration

Nerve rupture

Upto 3 cm or 1 inch/month

50 % head involvement then surgical osteotomy is done to realign joint.

TRENDLENBERG GAIT

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Fig 12.29: Biomechanics of Hip. The stability of hip during walking is provided by hip joint which acts as a fulcrum. The effective contraction of the abductor muscle (gluteus medius) plays a very important role in stability during stance phase. It balances the body weight medially. Any disruption in the continuity of this system disrupts hip stability.

Fig 12.30: A-Normal (Note the normal spring contraction); B-Trendelenburg sign: Weight bearing on affected hip leads to drop of contralateral pelvis due to failure of hip abductor mechanism (Note the spring). In order to clear off the ground, the patient tilts the whole body towards affected side for walking. Trendlenberg gait: Any disruption in the stability of hip leads to Trendlenberg gait. Under normal circumstances, effective contraction of abductor muscles pulls up the opposite pelvis and helps to clear off the ground while walking. In conditions like a)     Failure of fulcrum: Dislocation of hip joint, fracture neck of femur etc. b)     Failure of abductor muscles. The hip abductor mechanism is unable to function effectively resulting in dropping of opposite pelvis. To restore stability during walking, the patient lurches to the affected side to clear off the ground for walking.

BRYANTS TRAIANGLE Bryant’s triangle is a hypothetical triangle that is drawn to determine the supratrochantric shortening of hip joint. With the patient lying supine, Line AB is drawn connecting ASIS to greater trochanter. The second vertical line (AC) is dropped from ASIS to bed. The third line 313

BC is perpendicular one drawn from top of greater trochanter to previous line AC. Measure and compare length of line BC drawn on both side of hips. Decrease in line BC indicates supratrochantric shortening. It may be caused due to fracture neck of femur, malunited trochantric fracture, posterior dislocation of hip, sequale of septic arthritis etc.

Fig 12.31: Bryant’s triangle.

THOMAS HIP FLEXION TEST The principle of Thomas test is to unmask the deformity of hip flexion which is masked by compensatory lordosis. With the patient in supine position, keeping his leg flat on the bed. If there is flexion deformity, the pelvis tilts forwards to maintain leg flat on the bed. Thus excessive lordosis develops to maintain body flat on bed. Now with the patient supine, flex the normal hip to the abdomen till the excessive lumbar lordosis is obliterated. This is accompanied by tilting back of pelvis which in turn lifts the affected hip to flexed position. This gives a true measure of hip flexion deformity on the affected side.

Fig 12.32: Thomas hip flexion test A: Note the exaggerated lumbar lardosis and right hip flexion deformity. B: On flexing the left hip (normal side), the exaggerated lumbar lardosis is obliterated and true estimation of right hip flexion deformity is obtained on hard couch.

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Questions Short Answers: 1)    Trendlenberg gait 2)    Thomas hip flexion test 3)    Golfer’s elbow 4)    Tennis elbow 5)    Trigger finger 6)    Carpal tunnel syndrome 7)    De Querivian tenosynovitis.

Credits: AthK

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Chapter 13

PROCEDURAL SKILLS Competency OR 13.2: Participate as a member in team for Resuscitation of Polytrauma victim by doing all of the following: (a) I.V. access central - peripheral (b) Bladder catheterization (c) Endotracheal intubation (d) Splintage

PERIPHERAL IV ACCESS Peripheral venous line involves placing a small flexible catheter into a patient's peripheral vein so that infusions can be inserted directly into the patient’s bloodstream. Cannulas are available in various colours, each of which corresponds to the size of the tube.

COLOUR CODING FOR IV CANNULAS Colour

Guage

Maximal flow rate(ml/min)

Yellow

24 G

13

Blue

22G

31

Pink

20G

67

Green

18G

103

Grey

16G

236

The required size depends on the rate the infusion is to run and solution to be infused like crystalloid, colloid, blood products or 316

medications. Procedure Steps: Step 01: Ensure that you have all of your equipment ready as follows. Gather equipment and place it around tray. A)   Alcohol cleanser. B)   Gloves. C)   An alcohol wipe. D)   A disposable tourniquet. E)   An IV cannula. F)   A suitable plaster. G)   A syringe. H)  Saline. Step 02: Sanitize your hands using alcohol cleanser. Step 03: Position the arm so that it is comfortable for the patient and identify a vein. Step 04: Apply the tourniquet and re-check the vein. Step 05: Put on your gloves, clean the patient’s skin with the alcohol wipe and let it dry. Step 06: Remove the cannula from its packaging and remove the needle cover ensuring not to touch the needle. Step 07: Stretch the skin distally and insert the needle, bevel upwards at about 30 degrees. Advance the needle until a flashback of blood is seen in the hub at the back of the cannula. Step 08: Once the flashback of blood is seen, progress the entire cannula a further, then fix the needle after advancing the rest of the cannula into the vein. Step 09: Release the tourniquet, apply pressure to the vein at the tip of the cannula and remove the needle fully. Remove the cap from the

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needle and put this on the end of the cannula. Step 10: Apply the dressing to the cannula to fix it in place and ensure that the date sticker has been completed and applied. Step 11: If there is any resistance, or if it causes any pain, or if you notice any localised tissue swelling, immediately stop flushing, remove the cannula and start again. Step 12: Carefully dispose of the needle in the sharps bin. Dispose of your gloves and equipment in the clinical waste bin once the procedure is over. Complications: Hemorrhage, extravasation, air embolism, phlebitis, infection.

CENTRAL VENOUS CATHETER INSERTION A central venous catheter is an indwelling intravenous device that is inserted to the vein of central vasculature like internal jugular, subclavian and femoral veins. The catheter can be inserted by routine technique using anatomical landmarks or real-time ultrasound guidance. The internal jugular vein is usually preferred to subclavian vein approach whenever possible as it is less likely to lead to pneumothorax and hemostasis can be effectively achieved by compression in jugular venous site rather than subclavian venous site. Indications for central venous catheter insertion: 1)Difficult peripheral venous access 2)Central venous pressure monitoring for optimal fluid balance 3)Hemodialysis Contraindications to central line (central venous catheter) insertion 1)Coagulopathy 2)Overlying skin and soft tissue infection Equipment required for central line (central venous catheter) insertion 1)Ultrasonography and sterile ultrasound 2)Sleeve 3)Sterile trolley 4)Sterile field, gloves, gown and mask 5)Central line kit 6)Saline flush 7)Chlorhexidine 8)Lignocaine 1 vial 318

9)Suture 10)Scalpel 11)Sterile dressing Pre-procedure and technique Set up sterile trolley. Having a nurse or assistant is helpful Position patient with head down and extension of neck at the shoulder level if they can tolerate it, with head facing away from side of insertion

Location Internal Jugular

Subclavian

Femoral

Advantage

Disadvantage

Most preferred vein Bleeding can be recognized and controlled Less risk of pneumothorax

Risk of carotid artery puncture

Most comfortable in a conscious patient

Highest risk of bleeding Vein is noncompressible Highest risk of pneumothorax

Easy to find the vein. The preferred site for emergencies

Highest risk of infection Risk of deep vein thrombosis.

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1)    Routine technique: a)    Internal jugular vein: ➢              Right side is preferred because thoracic duct is situated on left side. ➢       Trendelenbuerg position(10-15 degrees) ➢       Head rotated to approximately 15°left ➢            At the level of the cricoid while palpating carotid pulse, introduce needle into apex of strenocleidomastoid-clavicular triangle at 30-40° angle to the skin. Aim the needle caudally towards patient’s ipsilateral nipple. b)    Subclavian vein: ➢       Right side is preferred ➢       Supine position, head neutral, arm abducted ➢       Trendelenburg position(10-15°) ➢       Shoulder neural with mild retraction. ➢       Junction of medial and middle thirds of clavicle. ➢            The site of insertion lies about 1 cm inferior to clavicle allowing for the needle to pass under the clavicle. ➢       Needle should be parallel to skin ➢       Aim towards supraclavicular notch. c)     Femoral vein: ➢       Supine or flat position ➢              Palpate the femoral artery pulse just distal to the inguinal ligament ➢       The femoral vein lies just medial to this. 2) Real-time ultrasound to define the anatomy. Procedure for central line (central venous catheter) insertion 1)Wash hands and don sterile gown and gloves 2)Clean the area and apply sterile field. 3)Make sure to have some spare gauze swabs ready. 4)Confirm the anatomy 5)Apply sterile sleeve to the ultrasound probe 6)Inject lignocaine subcutaneously and around the vessel after checking by aspiration. 7)Whilst lignocaine has time to work, flush all lumens of the line and then clamp all lumens except the port for the guide wire 8)Ensure caps are available for the lumens 9)By routine technique/ultrasound guidance take the Seldinger needle attached to syringe and insert into the central vein 10)When blood is freely aspirated remove syringe and immediately insert the J-tipped guide wire straightened by the introducer. This should pass easily. Keeping hold of the inserted wire, remove the needle. Ensure the wire stays in the vein as you do this

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11)Use scalpel to make a small incision in the skin (approx 3mm). This should be done with sharp margin away from the wire so as not to damage it. 12)Pass the dilator over the wire and gently but firmly dilate a tract through into the vein. 13)At this stage there may be some bleeding so ensure to have some swabs ready 14)Remove the dilator and pass the central line over the wire. Do not advance the line until you have hold of the proximal end of the wire Once the central line is in place, remove the wire 15)Aspirate and flush all lumens, re clamp and apply lumen caps. Suture the catheter to allow 4 points of fixation. Dress with a clear dressing so the insertion point can be clearly seen Post-procedure a) Attach central line to pressure bag to allow CVP monitoring b)Chest X-ray to confirm placement and to check for pneumothorax c)Run a blood gas to ensure a venous sample d)Clear documentation of date of insertion and monitor for infection In the event of failure Stop procedure Seek senior help.

BLADDER CATHETERIZATION Bladder catheterization is sterile procedure where a flexible catheter is placed through the urethra into the bladder to empty the patient’s bladder urine. Catheter size refers to circumference of catheter.  It is measured in “French” ( “Fr”). 1 Fr is equivalent to 0.33 mm. The average size of catheter size used by adult men ranges from 14 Fr to 16 Fr. The average catheter size used by adult women ranges from 10 Fr to 12 Fr. Catheters are color-coded based on their French sizes. Indications for bladder catheterization 1) Drain bladder: Unconscious patient, Intubated patient. 2) Monitor output: Polytrauma patient Contraindications for bladder catheterization 1)Blood at the meatus 2)Frank hematuria 3)High riding prostate on rectal examination 4)Penile, scrotal, perineal hematoma Equipment required for bladder catheterization 321

1)Catheter 2)Sterile gloves 3)10 cc syringe 4)Sterile water 5)Cotton gauze with betadine 6)Lignocaine jelly 7)Anchoring tape 8)Urine collection bag 9)Disposal bag Procedure: Step 1: Clean Hands with alcohol hand rub or soap & water Step 2: Clean the trolley and gather equipment, position them in bottom shelf Step 3: Apply a disposable apron Step 4: Open catheter pack and arrange contents using non-touch technique Step 5: Open Equipment onto critical aseptic field using No-Touch Technique(NTT) Step 6: Clean hands with alcohol, hand rub or soap and water. Apply sterilised gloves Step 7:  Prepare equipment using NTT Step 8:  Clean the urethral orifice with normal saline and betadine gauze              Step 9: Apply aseptic field drapes over genitals & between legs Step 10: Insert lubricating gel Step 11: Dispose of gloves, clean hands and apply sterilized gloves Step 12: Insert catheter using NTT by touching only the plastic wrapping Step 13: Inflate the balloon using NTT Step 14: Attach collection bag using NTT Step 15: Dispose off waste and gloves Step 16: Clean hands with alcohol hand rub or soap and water Step 17: Clean the trolley Complications: 1)Hematuria 2)Urethral injury 3)Urinary tract infection

ENDOTRACHEAL INTUBATION Endotracheal intubation is the placement of a flexible plastic tube either orally or nasally into the trachea for airway management. Indications for Endotracheal intubation: 1)To secure airway 2)Upper airway obstruction eg: bleeding, maxillary fracture 3)Cardiopulmonary resuscitation 4)Ventilatory therapy in ICU.

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Equipments: 1)    Sterile gloves 2)    Bag valve mask ventilation 3)    Laryngoscope with blade 4)    Endotracheal tube of proper size The average size of tube: Adult female: 7-8 mm id Adlt male: 7-8.5 mm id Pediatric size: (age in years/4) + 4. 5)    Lubricant and malleable stylet 6)    Stethescope 7)    Syringe 8)    Source for ventilation 9)    Suction. SKILL LAB: Note: Initially the student ventilates the patient with bag valve mask ventilation attached to a reservoir and oxygen with the initiation of ventilation immediately. The Examiner watches following steps The student takes or verbalizes about body substance isolation precautions Open airway manually Elevate the patient’s tongue and insert a simple airway adjunct (oropharangeal/nasopharangeal airway) Note: Examiner checks for gag reflex and “If no gag reflex is present and patient accepts airway adjunct” The student ventilates the patient immediately using a BVM device unattached to oxygen Hyperventilates the patient with room air Note: Examiner checks if ventilation is being performed without difficulty Attaches the oxygen reservoir to the BVM Attaches the BVM to high-flow oxygen(15 liter per min) Ventilates the patient with at a proper volume and rate(800-1200 ml/breath and 10-20 breaths/min) Note: After 30 seconds, the examiner must auscultate the patient’s chest and inform the candidate that the breath sounds are present and equally bilaterally, medical direction has ordered endotracheal intubation. The examiner must now take over the ventilation of the patient. The student directs to hyperoxygenate the patient.

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Identifies/selects the proper equipment for endotracheal intubation Checks equipment Checks for cuff leaks Checks laryngoscope operation and bulb tightness Note: The examiner must remove the oropharangeal airway(OPA) and move out of the way when the candidate is prepared to intubate the patient. The student should position the head properly Insert the laryngoscope blade into the patient’s mouth while displacing the patient’s tongue laterally Elevate the patient’s mandible with a laryngoscope Introduce the endotracheal tube and advance the tube to proper depth Inflates the cuff to the proper pressure Disconnects the syringe from the cuff inlet port Directs assistant to ventilate the patient Confirms proper placement of the endotracheal tube by auscultation bilaterally and over the epigastrium. Note: The examiner asks “if u had a proper placement, what would u expect to hear” Secures the endotracheal tube

Fig 13.01: Endotracheal intubation procedure. Following bag and mask ventilation (A) Visualisation through laryngoscope; (B) Visualisation of larynx and vocal cords; (C) Introduction of proper size endotracheal tube; (D) Confirmation of endotracheal tube placement by ventilation and auscultation of lungs.

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Complications: 1)Tube in esophagus 2)Endobronchial intubation 3)Trauma to lips 4)Bleeding 5)Air leak 6)Barotrauma to lungs.

SPLINTAGE Determine if the patient is stable. Pain, swelling, deformity and loss of function in the patient limb are suggestive of a fracture. Indications: Suspected or obvious extremity fracture Procedure: Step 1: Remove or cut away clothing from the injured area. Step 2: Cover all open wounds using a sterile dressing. Have a helper to manually stabilise the fracture. Step 3: Assess distal motor, sensory and circulatory function before splinting. Step 4: Fracture need to be splinted with whatever material is available at the site of accident. The splint should be positioned while maintaining stabilization of the fracture. Immobilize the bone above and below the joint. Step 5: Elevate the extremity after splinting, if possible. The pulses, motor and sensory function must be re-evaluated after the splint is secured. SPLINTAGE AT SITE OF TRAUMA: Humerus Radius/ulna

Sling and swathe. Wooden plank, padded board with sling and swathe, Air or vacuum splint, Appropriate commercially made splint.

Pelvis

Long backboard immobilization. Unstable pelvic fracture with low blood pressure, MAST should be used.

Femur Tibia/fibula

Traction splint Cardboard splint,

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Full leg air splint or vacuum splint, Appropriate commercially made Splint.

Fig 13.02: Splinting at the trauma site. Newspaper splint (A); Pillow splint (B); Wooden board splint(C); Cramer wire splint (D).

SPLINTS A splint is a device used for support or immobilization of limb. Functions: 1)Temporary immobilisation of sprains, fractures and reduced dislocations. 2)Control of pain 3)Facilitates patient transportation 4)Prevention of further soft tissue or neurovascular injuries SPLINTS Thomas splint Bohler Braun splint Cock up splint Knuckle bender splint Foot drop splint Taylor (TLSO) brace

Fracture femur Fracture femur, tibia Radial nerve palsy Ulnar nerve palsy Common Peroneal Nerve palsy Spine fractures.

Plaster of Paris (POP): It is a commercially available customisable splint for fractures.  The POP bandage consists of a roll of muslin cloth stiffened by dextrose or starch and impregnated with

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hemihydrate of calcium sulfate. When water is added, calcium sulfate takes up its water for crystallisation. CaSO4.1/2 H20+ 1 1/2 H2O—>CaSO4.2H20+△

Setting time: Time taken to change from powder to crystalline form. It is about 3-9 minutes. Drying time: Time taken to change from crystalline form to anhydrous form. It is about 24-72 hours. Padding: Cotton padding is placed from distal to proximal with 50% overlap with a minimum of two layers and extra padding at fibular head, malleoli, patella and olecranon is done. POP forms: Slab: Only a part of the circumference of limb is incorporated. 8 inch width for thigh 6 inch width for leg 4 inch width for arm & forearm. Cast: It encircles the whole circumference of limb. Advantages:

Disadvantages:

1)Cost-effective 2)Non-allergic

Radio-opaque so may occlude fracture lines. Heavy Easily breaks when comes in contact with water.

Complications of POP: Due to tight cast 1)Pain 2)Pressure sores 3)Compartment syndrome 4)Peripheral nerve injuries.

Due to improper application 1)Plaster blisters 2)Breakage 3)Loose cast

Synthetic fiberglass: Current bandages of synthetic materials are often used. Knitted  fiberglass  or thermoplastic bandages are impregnated with polyurethane. Advantages 1)Lightweight 2)Radiolucent, so better imaging on X-ray 3)Low risk of thermal injury

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Disadvantages 1)Expensive 2) Difficult to mould.

Traction: 1)Traction: It is the effective pulling force exerted on skin or skeletal structure by means of special devices or apparatus. 2)Counter traction: It is a force acting in opposite direction to achieve effective traction. Counter traction can be achieved by (a) Fixed traction: when the counter traction acts through an appliance that fixes to a point on the body it is called fixed traction. Eg: Thomas splint fixed to ischial tuberosity (countertraction). (b)Sliding traction: when the weight of all or part of the body acting under the influence of gravity is utilised to provide counter traction. The arrangement is called sliding traction. Thus this method helps in restoring alignment to a fracture through gradual neutralisation of muscular forces. Uses: 1)Reduction of fractures and dislocations 2)Immobilising painful and inflammed joint 3)Preventing deformities 4)Correction of soft tissue contractures Types of traction: 1)Skin traction 2)Skeletal traction 1)Skin traction: a)Adhesive/non adhesive strap is applied on skin and traction is applied. b)Acts over a large area c)Maximum weight permissible 6.7 kg

Fig 13.03: Skin traction.

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2) Skeletal traction: Traction applied through pin/wire driven through bone.

Pins used: Steinmann pin and Bohler stirrup: a)Steinman pin: One sharp trocar pointed end, round oval shaft and blunt opposite end with quadrangular cross-section. b)Denham pin: It is a centrally threaded Steinman pin used for giving skeletal traction in the lower limb. The threads in the centre of pin hold the cortex of osteoporotic bone. c)Bohler stirrup: It is exclusively used in skeletal traction where the rounded loop end is used for tying nylon traction cord and the two limbs of U-shaped part is used to fix the stirrup with a Steinman pin. This enables to line/alter the traction. Sites of skeletal traction: 1)Proximal tibia skeletal traction 2)Distal femur pin traction 3)Calcaneal traction

Fig 13.04: Upper tibial skeletal traction with Steinman pin and Bohler stirrup. Complications of upper tibial skeletal traction: 1)Pin tract infection 2)Damage to neurovascular structures- common peroneal nerve(CPN) palsy causing foot drop. Difference between:

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Age Applied with Applied to Site

Skin traction Children Adhesive plaster Skin Below knee

Weight permitted Duration

Upto 3-4 kg Short

Skeletal traction Adults Pins Bone Upper tibial pin traction Upto 20 kg Long

Complications of traction: 1)Injury to nerves/vessels 2)Pin track infection 3)Over distraction 4)Loss of position BRYANT’S TRACTION: It is useful for treatment of femoral shaft fractures in infants and small children. Both the patient’s limbs are suspended in the air vertically at a 90⁰ angle from the hips and knee slightly flexed. The patient body provides the counter traction. The status of limb circulation should be frequently checked as there is danger of vascular complications.

Competency OR 13.1: Participate in a team for procedures in patients and demonstrating the ability to perform on mannequins / simulated patients in the following: i. Above elbow plaster ii. Below knee plaster iii. Above knee plaster iv. Thomas splint v. Splinting for long bone fractures vi. Strapping for shoulder and clavicle trauma

PLASTER OF PARIS APPLICATION PROCEDURE Materials required: 1)Plaster of Paris (3 or 4 inch depending on size of limb.) 2)Stockinette 3)Soft padding 4)Bandage

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5)Gloves, Scissors Procedure: STEP 1: Define the position of the limb before application Step 2: Choose the appropriate width of stokinette and measure the length Step 3: Roll up the stockinette before applying to overcome sliding and remove all wrinkles and creases. Step 4: Apply padding to the limb by wrapping. Use extra padding for any bony prominences. It is recommended to wear gloves before preparing POP. Step 5: Plaster slabs consist of layers of plaster bandage. Plaster slabs of 8-10 layers of thickness in adults and 6 layers in children are described. For plaster cast application, plaster bandages should be dipped in tepid water and gently rolled over fully circumferentially. Step 6: Measure the length of slab required and cut to length. The slab should be trimmed with plaster scissors so that it will fit the limb without being folded over. Step 7: Wetting the slab by carefully holding both ends and immerse completely in tepid water, lift out and momentarily bunch up at an angle to expel excess water. Consolidate the layers by holding the plaster at one end and pulling between two adducted fingers. Repeat the procedure from other edge. Step 8: Carefully position the slab on limb and smoothen it down with the hands so that the slab fits closely to the contours of limb. Step 9: Bandages used to secure plaster slabs should be thoroughly wetted. Apply the bandage to the limb firmly without too much pressure. Step 10: Splints sets in about 5-8 minutes and completely sets over 24-48 hours.

i. Above elbow plaster- The above elbow plaster slab or cast is applied from knuckles of the hand and extends upto the lower twothirds of arm. ii. Below knee plaster- This is done ideally in prone position. The

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heel, head of the fibula should be adequately padded. The ankle should be placed in neutral position and knee should be in flexion. Distally the POP should support the metatarsal heads, freedom of toes should be ensured and proximal extend ends below knee. Plaster should be thick at heels for walking casts. iii. Above knee plaster- An A/K plaster cast or slab is done in supine position. Cotton padding is applied from distal to proximal ensuring adequate thickness over heel, head of fibula region and anterior to patella. The knee should be maintained at 5-20° of flexion. The distal extent is upto metatarsophalangeal joints and proximally it covers the lower two-thirds of thigh.

Fig 13.05: Above elbow slab.

Fig 13.06: Below knee slab applied for patient lying in prone position.

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Fig 13.07: Above knee slab. Care: 1.Counsel patients on signs of neurovascular compromise like excessive pain, swelling and bluish discolouration of digits. 2.Keep the plaster slab or cast dry 3.Limb elevation 4.Mobilise all the joints which are not incorporated in the plaster to their full range of motion. IV. Thomas splintIt was designed by H O Thomas as a device for treatment of tuberculosis of knee. Parts: a) Well-padded oval or circular ring b) Medial bar: The length is shorter than outer bar and it is straight. The ring is set at an angle of 120° to inner side bar. c) Lateral bar is angled about 5 cm below the ring to accommodate trochanteric prominence. Its length is more than medial bar. W-shaped joining 2 bars: It connects medial and lateral bar. The W is useful for giving fixed traction. Application of Thomas splint: 1)Girth should be taken at the uppermost part of thigh near ischial tuberosity and add 5 cm to it. 2)Measure from crotch to heel and it should be 15-23 cm beyond the heel. 3)The ring should be angled at 120° to inner side bar 4)Countertraction is provided by ischial tuberosity. 5)Skin traction can be used to provide traction along the Thomas splint.

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Fig 13.08: Thomas splint: A) oblique metal ring; B) Ischial tuberosity; C) Outer bar; D) fracture shaft femur; E) Inner bar; F) Skin traction; G) W shaped bar. Bohler Braun splint: It is Bohler’s modification of Braun’s splint. It is a traction unit with pulleys. The pulleys help to change the angle of traction without changing traction arrangements. Pulley A: Calcaneal /distal tibia traction. Pulley B: Proximal tibia traction. Pulley C: Distal femur traction. Pulley D: To prevent equinus deformity in foot drop. Indications: Sliding traction with Bohler Braun frame can be used for management of shaft and supracondylar region of femur. It is also used in fracture of tibia.

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Fig 13.09: Bohler Braun splint. v. Splinting for long bone fractures: Step 1: Determine scene and situation is safe. Verbalise with the patient and follow universal precautions Step 2: Direct patient regarding the application of manual stablisation and application of splint for injury Step 3: Assess distal circulatory, motor and sensory(CMS) function before splinting Step 4: Measure and select the appropriate padded board splint Step 5: Apply the splint Step 6: Immobilise the joint above and below the injury site Step 7: Secure the entire injury extremity Step 8: Immobilise the hand/foot in the position of function Step 9: Reassess distal circulatory, motor and sensory (CMS) function.

vi. Strapping for shoulder and clavicle trauma 1)Methods of conservative treatment for clavicle trauma: (A) Strapping and sling suspension (B) Cuff  and collar sling (C) Figure of ‘8’ bandaging A) Strapping and sling suspension: Strips of bandage is used to strap the fracture and broad arm sling provide support for weight of arm. B) Cuff and collar sling: It is used to give first aid or to treat undisplaced fractures at shoulder or clavicle. The purpose of the sling is to rest the arm. C)Figure of 8 bandage: The patient should be sitting on stool and asked to brace back the shoulders. Pads of gamgee or cotton wool is positioned round both shoulders. A wool roll bandage is applied in figure of 8 fashion.

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2)Methods of conservative treatment for shoulder trauma: A)Velpeau or chest arm bandage: The Velpeau or chest arm bandage is used for holding the arm and forearm in fixed position in treatment of fractures and dislocations of shoulders. The injured arm is placed across the chest and turns of bandage are made from beneath the sound axilla over the injured shoulder infront of injured arm and beneath the elbow to pass again to sound axilla. It is completed by transverse turns. B) Shoulder immobilizer: These are customized commercially available splints. It has soft, comfortable armrest bag fixed by loop fastener to adjustable shoulder strap. The chest strap helps to strengthen fixation.

Fig 13.10: Fig of “8” bandage with arm pouch. SKILLS: 1)   Application of basic splints and slings(I) 2)   Basic fracture and dislocation management(O) 3)   Compression bandage(I)

SKILLS 2) Basic fracture and dislocation management: Step 1: Determine scene and situation is safe. Assure the patient’s airway is open and that breathing and circulation are adequate. Step 2: Expose the injured area to locate and identify fracture/ dislocations. Control bleeding as appropriate. Step 3: Assess distal circulatory, motor and sensory(CMS) function before splinting Step 4: Following fracture/dislocation

guidelines

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are

used

to

splint

the

a) An open fracture should be covered with dry sterile dressing and any bleeding should be controlled. b) The injured joint should be immobilized in the position in which it was found. c) A severely angulated extremity fracture should be straightened by applying gentle traction to it. d) The femur fracture should be immobilized with traction splint. Step 5: Reassess distal circulatory, motor and sensory (CMS) function. Transport the patient in position of comfort to the nearest hospital for further evaluation. 3) Compression bandage: A compression bandage is a type of stretchy bandage that is wrapped around the body to exert pressure on it. It is commonly used to treat sprains and strains as a part of therapy known as RICE regimen (Rest, ice, compression and elevation) A compression bandage helps to reduce swelling and pain by restricting the blood flow. The bandage shouldnot be too tight to restrict blood circulation or too loose which may not provide adequate compression. The bandage should be wrapped firmly and should have a snug fit. The correct size of a compression bandage is necessary depending on the sites like adult or paediatric upper and lower limb injury. Depending on the site of injury, various sizes are available like 6inch, 4-inch, 3-inch or 2-inch for effective compression. Application: Step 1: Hold the rolled compression bandage in one hand and the loose end in the opposite hand. Start from the distal region. Step 2: Place the loose end at the edge of the foot or hand Step 3: Hold the loose end in place. Apply some tension and wrap the rolled bandage from the ball of foot or base of the fingers over the loose end Step 3: Continue to wrap around overlapping about half the width of bandage as we go proximally Step 4: When we reach the heel in lower limb, leave the heel exposed and wrap around the ankle. After that cross over the foot and wrap the heel in figure of eight pattern. Step 5: Extend and wrap the bandage around the leg or forearm. Secure with tape or clips that are provided with the compression bandage.

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Questions: Short Essay: 1)    Classify traction and write briefly on indications, site of applications and complications of skeletal tractions. Short Essay: 1) Thomas splint 2) Plaster of Paris Short Answers: 1)    Thomas splint 2)    Skeletal traction 3)    Cast syndrome

Credits: AthK

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Chapter 14

COUNSELING SKILLS Competency OR 14.1: Demonstrate the ability to counsel patients regarding prognosis in patients with various orthopedic illnesses like a. fractures with disabilities b. fractures that require prolonged bed stay c. bone tumours d. congenital disabilities. OR14.2. Demonstrate the ability to counsel patients to obtain consent for various orthopedic procedures like limb amputation, permanent fixations etc. OR14.3. Demonstrate the ability to convince the patient for referral to a higher centre in various orthopedic illnesses, based on the detection of warning signals and need for sophisticated management Counseling: Counseling is a process that helps the patient to feel and behave more satisfyingly through interaction with a counselor who provides services that stimulates the patient to develop behaviours which enable him to deal effectively with himself and the environment. Counseling addresses the present problem and its future path hence it helps to bring about behavioral change, positive mental health, problem resolution and decision making. Counseling therefore helps families to effectively cope with patient’s demands through special educational needs. a. Fractures with disabilities: Most of the fractures cause temporary disability and get corrected over a few months. However fracture with complications like soft tissue and bone loss, restricted range of motion, neurovascular damage can dramatically and severely compromise patient’s function and performance. The patient’s characteristics including age, socio-economic status, preinjury health and social support have to be considered for counseling process. The counsellor should understand the approximate fracture healing time, possible complications that may arise, any risk factors for long term disability and design an appropriate rehabilitation program. 339

b. Fractures that require prolonged bed stay: Orthopaedic patients sometimes need prolonged bed rest in conditions like vertebral fractures, spinal cord injury or in polytrauma patients admitted in ICU care. These patients should be counselled regarding the risks of pressure sores, deep vein thrombosis, hypostatic pneumonia, weak muscles and bones, stiff joints. The importance of airbed mattress, regular physiotherapy of upper and lower limbs, incentive spirometry, chest physiotherapy, frequent position changes should be emphasized.  c. Bone tumors: Counseling regarding the prognosis of bone tumor depends on the type of tumor, various treatment options available, any preoperative need of chemotherapy. Surgery for tumor removal depending on the site and extent of tumor, implants for fixation or prosthesis, the need of bone graft and further risk of post-operative infection. Consent for possible limb amputation should always be explained and taken before all tumor surgeries. Following surgery, the need for regular follow should be explained for any chance of tumor recurrence. d. Congenital disabilities: Various disorders like spina bifida, genetic abnormalities, joint deformities, limb deficiency like femoral focal deficiency, tibial hemimelia may pose various physical challenges.  They should be explained the need for serial follow up for the disease condition, long term use of orthosis, need for multiple surgeries with age, prolonged rehabilitation protocols. Congenital disabilities causing permanent limb length discrepancy may need lifelong prosthesis. Counseling and psychosocial support play a major part for patients with congenital disorders and their families.    2Demonstrate the ability to counsel patients to obtain consent for various orthopedic procedures like limb amputation, permanent fixations etc. Consent for Limb amputation: An amputation procedure is removal of part of limb that has been irreparably damaged by major trauma, tumor, infection or poor blood supply. The patient should be counselled regarding the course and outcome of the procedure. The surgical risks include blood loss during surgery, possible need for blood transfusions, post-operative abnormal feeling of limb presence and pain(phantom limb), delayed

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wound healing and infection, scar, need for physiotherapy and lifelong need of prosthesis for walking. Consent for permanent fixations: The patient should be counselled regarding the associated fracture and its possible treatment options. The type of implant used, its cost, possible postoperative implant infection, abnormal scar and pain at implant site, the risk of implant failure and breakage, fracture malalignment and shortening and the need for redo surgery if necessary, should be discussed. 3. Demonstrate the ability to convince the patient for referral to a higher centre in various orthopedic illnesses, based on the detection of warning signals and need for sophisticated management Few Orthopaedic conditions needing referral: 1)    Polytrauma patient after hemodynamic stabilization and splinting 2)    fractures with vascular injuries 3)    Unstable spine fractures with or without neurological deficits 4)    Pelvic fractures. 5)    Fractures with head injuries Warning signals: 1)Bleeding in open fractures with hemodynamic compromise 2)Inappropriate drowsiness or difficulty in awakening after polytrauma 3)Weakness of one or both leg or arm with spine injury 4)Vascular injuries with fractures 5)Convulsions or fits The patient attenders should be counselled for immediate tertiary care referral as they can be severe and life-threatening conditions that warrants a multidisciplinary team approach by Orthopaedic surgeon, General surgeon, Intensivist, CTVS surgeons for extremely specialized hospital care for short or extended period. The need for possible blood transfusions, ICU care with advanced equipments and emergency operation theatre for management should be explained. High-risk consent should be taken by writing the diagnosis, treatment given, patient vitals and general condition before referring to higher centre for further management.

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Credits: AthK

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INSTRUMENTS & IMPLANTS This section intends to introduce the most commonly used instruments in Orthopaedic surgery and is by no means an exhaustive list.

Langenbeck Retractors: Used to retract soft tissue while operating on a particular site.

Bone lever: It is used for retraction of soft tissues.

Bone awl: Used to enter the medullary cavity

Periosteum elevator: Used for stripping the periosteum over bone.

Bone cutter: Used for cutting bone

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Bone nibbler: Smoothing the cut bone end of amputation

Mallet: Used to hammer chisel, osteotome etc.

Bone chisel: It has a sharp edge on one side and a beveled edge on the other. It is used for chiseling out a bony growth.

➢       Osteotome: Both edges are sharp. It is used to cut bone.

A)   Chisel; B) Osteotome.

➢       Bone gouge: It is a concave bladed chisel. It is used to extract the bone graft from iliac crest.

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Bone curette: Used to remove or curette infected granulation tissue /hematoma.

Reduction clamps: Sharp serrated pointed jaws used for holding long bones during manipulation and reduction of fractures.

Plate-holding forceps: It is used to hold a plate over fractured bone for fixation.

T handle: It is used to hold shanz pin while introducing into bone

  Screw driver: Different types of tips are available – Hexagonal, square etc.

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Spanner: Used to tighten the nuts in external fixators

Amputation saw

Bone file: Used to blunt the sharp edges of bone after amputation IMPLANT It is defined as a material inserted or grafted into intact tissues or body cavity with some specific purpose.

Types: Metallic alloys: 1)Iron 2)Cobalt 3)Titanium NonmetallicBiodegradable implants are new implants which are made of material which gets absorbed in the body over a period of time. 1) External fixation: It is the method of fixing the fracture outside the body with the cluster of pins connected with bars.

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A)Provides stable fixation B)Force can be applied along any axis C)Helps in wound care & reconstructive surgery

Tubular rods: long rod connecting Schanz pins through clamps.

Shanz pin: Cortical or cancellous threads at the tip with smooth shaft pin.

Pin clamps: clamps used to hold the smooth part of Schanz pin and rod.

External fixator application in a patient with leg fracture.

Steinman pin: used for applying skeletal traction through lower femoral, upper tibial or lower tibial sites.

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Denham pin: It is a modified Steinmann pin which has central cancellous threads for the application of skeletal traction in osteoporotic patients.

Bohler stirrup: U-shaped steel road twisted at the base to form a loop for traction.  It is used for the application of skeletal traction.

2)Internal fixation: A) Extramedullary implants: Plates and screws. B) Intramedullary implants: Intramedullary nails eg: K nail, V nail. A) Extramedullary fixation: Bone plates hold the fracture ends, maintain alignment and transmit forces from one end of the bone to another bypassing the fracture site. Dynamic Compression plate: Screw holes are designed in a sloping way to utilize the spherical gliding principle. The plate is applied over the bone. Screws are passed through the hole of plate onto the bone via predrilled holes over the bone. When screws are tightened on either side of plate, it leads to fracture site compression. Hence it is called a dynamic compression plate.

Indications: Fracture shaft humerus, fracture of radius & ulna and sometimes fracture shaft femur.

Low-contact dynamic compression plate: It attains less contact with bone so periosteal vascularity is preserved.

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Reconstruction plate: Can be molded or bent in all planes. It is used in distal humerus and clavicle fractures.

Cortical screws: It is used for plate fixation in diaphyseal fractures (cortical bone) of radius, ulna, femur, tibia and humerus fractures.

Cancellous screws: It is used for fixation of epiphyseal and metaphyseal fractures where the cancellous bone is present. It is used in proximal/distal tibia, distal femur, proximal humerus and calcaneum fractures. Dynamic hip screw: It has a side plate and cannulated barrel. The side plate is fixed to the femoral shaft with cortical screws. Richard screw goes through the neck of femur and it slides inside cannulated barrel allowing the controlled collapse of fracture site.

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Indications: 1) Fracture neck femur 2) Trochanteric fracture INTRA MEDULLARY FIXATION Standard Intramedullary nail act as an internal splint and aid in fracture healing. Indications: 1)    Fracture shaft femur 2)    Fracture tibia 3)    Fracture shaft humerus 4)    Fracture radius and ulna Kuntschers nail: German Surgeon Gerhard Kuntscher designed clover leaf shaped nail based on the femur cross-section for fixing fracture femur. It works by the principle of three-point fixation but does not provide sufficient rotational stability.

There are two methods of insertion: Antegrade nailing: The entry point is the piriformis fossa on the superior surface of femoral neck. Initial hole is made with bone awl and the nail is inserted from the proximal fragment to fracture site and then hammered gently into the distal fragment. Retrograde nailing: The fracture site is opened. The nail is first introduced from fracture surface into proximal fragment and then through piriforms fossa on the superior surface of femoral neck and finally brought outside

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through skin incision. The fracture is then reduced and the nail is hammered back into distal fragment. Complications of surgery: splintering of fracture, fat embolism during reaming. Femoral interlocking nail: These are advanced generation nails. These are also called intramedullary interlocking nails. Unlike the K nail, after intramedullary nailing, locking at proximal and distal end of fracture is done to provide rotational stability to the fracture site. 

V-nail: Tibia in cross section is V shaped. V-nail is used in intramedullary fixation of tibia. Tibial interlocking nail: Used in fracture shaft tibia. It is called tibial intramedullary interlocking nail. The tibial nail has a smooth 11⁰ bend in anteroposterior direction at the proximal region called the Herzog bend.

Square nail: It is square shaped in cross-section. Indications: Fracture of both ulna & radius Rush nail It is used for intramedullary nailing. It is used in fracture fixation of radius and ulna.

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K wire: Also known as Kirschner wire. A thin wire is pointed at both ends. It is used for small bone fracture fixation like metacarpal/metatarsal fracture, phalanx fracture, supracondylar humerus fracture.

PROSTHESIS: Austin Moore prosthesis: It is an uncemented unipolar(movement at prosthesis and acetabulum only) prosthesis. In elderly patients, it is used for the replacement of head and neck of femur in which femoral neck fracture has an intact calcar. Parts: Head is spherical fits into acetabulum. Neck: constriction below head. Collar: It rests on calcar femorale of femoral neck. The body weight gets transmitted from acetabulum, through head and neck of collar finally onto strong calcar femorale when the patient is standing.

Thompson’s prosthesis: It is cemented unipolar prosthesis. It is used in femoral neck fracture with absent calar. Parts: Head articulates with acetabulum providing range of movements. It has a collarless, non-fenestratated stem. Bone cement is necessary for fixation.

Bipolar Prosthesis: It is indicated in neck of femur patients who are >60 years old. It is bipolar, that means movement occurs at:

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1) Acetabular component & head component. 2) Acetabulum & acetabular component of prosthesis. Components are metallic acetabular cup with inner polyethylene core and the metallic stem with a small head fits into the cup.

Total hip replacement: It is indicated in end stage hip arthritis. An artificial prosthesis used to replace both acetabulum and head of femur. The acetabulum is replaced by acetabular cup and femoral head is replaced by metallic head with stem. Both the components are fixed to respective bones by bone cement. Recently cementless fixation options are also available.

A) Acetabular cup; B) Femoral head; C) Femoral stem. Total knee replacement: It is indicated in severe knee arthritis. Total knee prosthesis has femoral component, polyethylene insert and tibial component.

A) Femoral component; B) polyethylene insert; C) tibial component. Arthroscopy: Arthroscopy is a surgical technique used for visualization and sometimes for operation of a joint through a thin instrument called the arthroscope. It is

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also commonly known as “keyhole surgery”. Advantages: The advantages of arthroscopic procedures compared with arthrotomy are the following: 1. Reduced postoperative morbidity. 2. Smaller incisions. 3. Less intense inflammatory response leading to less postoperative pain, faster rehabilitation and faster return to work. Disadvantages: 1. Equipment is expensive 2. Long learning curve to perform the surgeries. Indications: Knee joint:

Shoulder joint:

Elbow and wrist joint:

Loose body removal

Loose body removal

Synovial biopsy

Subacromial decompression

Removal of loose body

Partial or complete meniscectomy Ligament reconstruction.

Synovial biopsy

Arthroscopic Bankart repair

Procedure: The procedure can be done under spinal or general anesthesia. The joint is cleaned and draped. The arthroscope and surgical instruments are introduced through portals which are visualized on a TV moniter and diagnostic or surgical procedures are performed.

Arthroscopy tower. Complications: 1)    Infection 2)    Hemarthrosis

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3)    Injury to vessels and nerves 4)    Instrument breakage.

Questions: Short Essays: 1) Arthroscopy 2) Arthroplasty Short Answers: 1)    K wire 2)    K nail

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RAPID REVIEW Types of Gait: Antalgic gait: Seen in a painful condition of lower limb Trendelenburg gait:  Unstable hip due to femoral neck fracture, gluteus medius weakness. Stiff hip gait: Seen in hip ankylosis. Duck waddling gait: Seen in B/L Congenital dislocation of hip Scissoring gait: Seen in Cerebral palsy High stepping gait: Seen in foot drop Circumduction gait: Seen in hemiplegia Charlie-Chaplin gait: Seen in external tibial torsion. Classification: Salter and Harris classification: For physeal injuries Neer classification: For proximal humerus fractures Gartland classification: For supracondylar humerus fracture of the elbow Denis Weber classification: For spinal column injury classification Tile’s classification: For Pelvic fracture Pauwel’s classification: For fracture neck of femur Garden’s classification: For fracture neck of femur Lauge Hansen’s classification:  Ankle injuries Gustillo Anderson classification: For open fractures Kumar’s classification: Clinical classification for TB spine. Enneking classification: Tumor classification Angles: Carrying angle: Elbow Neck shaft angle: Femoral neck fracture Pauwel’s angle: Fracture neck of femur Bohler’s angle: Fracture of calcaneum Kite’s angle: Angle in CTEV Special views: 356

Judet view: for acetabular fracture Shenton’s line: Hip X-ray Skyline view: Patella fracture Mortise view: For ankle injuries Von Rosen view: For CDH. Classical features: Sunray appearance: Osteosarcoma Soap bubble appearance: Osteoclastoma Onion-peel appearance: Ewing’s sarcoma Shepherd crook deformity: Fibrous dysplasia Rissers’s sign: Epiphysis of iliac bone Trethowan sign: Slipped capital femoral epiphysis Fabella: Sesamoid bone in the lateral head of gastronemius Wormian bones: Osteogenesis imperfecta Spondylosis: Degenerative spine disease Spondylolysis: Break in posterior elements( pars interarticularis) Spondylolisthesis:  Adjacent vertebral slip Named surgeries: Bankart’s procedure: For recurrent dislocation of shoulder Putti-plat procedure: For recurrent dislocation of shoulder Bristow’s procedure: For recurrent dislocation of shoulder Tension band wiring: For Fracture patella, olecronon Meyer’s operation: For fracture neck of femur Girdlestone arthroplasty: For TB hip Soutter’s release: For flexion deformity of hip in polio Yount’s release: For flexion deformity of knee in polio Dwyer’s osteotomy: For varus of heel in CTEV Dilwyn Evan’s procedure: Correction of CTEV Turco’s procedure: For CTEV Named signs and tests:

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Adson’s test: For thoracic outlet syndrome Allen’s test: Testing patency of radial and ulnar artery Alli’s test: For congenital dislocation of hip (CDH). Apley’s grinding test: Meniscus injury Apprehension test: For recurrent dislocation of shoulder. Barlow test: For congenital dislocation of hip (CDH). Blue sclera: Osteogenesis imperfecta Partial claw hand: For ulnar nerve palsy Cozen’s test: For tennis elbow Anterior drawer test: For ACL injury Posterior drawer test: For PCL injury Finkelstein’s test: For de Quervain's tenosynovitis Foot drop: For common peroneal nerve injury Froment’s sign: for ulnar nerve injury Gaenslen’s test: For sacroiliac joint involvement Galleazzi sign: For CDH Gower’s sign: For muscular dystrophy Hamilton-ruler test: For anterior dislocation of shoulder Lasegue’s test: For disc prolapse Lachmann test: For ACL injury Mcmurray’s test: For meniscal injury Ober’s test: For tight iliotibial band(e.g. in polio) O’Donoghe triad: Triad of ACL, MCL and medial meniscus injury Ortholani’s test: For CDH Pivot shift test: For ACL injury Policeman tip: For Erb’s palsy Thomas test: For flexion deformity of hip Trendlenberg test:  For unstable hip Tinel’s sign: For detecting improvement in nerve injury Volkman sign: For ischemic contracture of forearm muscles. Wrist drop: For radial nerve injury.

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Credits: AthK

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REFERENCES: 1) Advanced Trauma Life Support Manual- 10th edition

  2) Handbook of Fractures by Kenneth Egol, Kenneth J Koval, Joseph D Zukerman

  3) Campbell’s Operative Orthopaedics-14th edition

  4) Tuberculosis of Skeletal System- S M Tuli 5) Harrison’s Principles of Internal Medicine 6) Congenital Clubfoot- I V Ponseti 7) Journal Articles.

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SAMPLE MCQ’S 1.    The neurovascular structure most commonly injured as a result of anterior dislocation of the shoulder is: A. Musculocutaneous nerve B.                 Axillary nerve C.                 Axillary artery D.                 Median nerve. 2.    An early sign of compartment syndrome in the hand includes: A. Pain with passive stretch of the digits B.                 Absent radial pulse C.                 Motor paralysis D.                 Swelling of the digits. 3.    A Greenstick fracture: A. It occurs chiefly in the elderly B. Does not occur in children C. Is a spiral fracture of tubular bone D. Is a fracture where part of the cortex is intact and part is cracked.              

4.    Which of the following is the fracture of atlas vertebrae? A. Jefferson’s fracture C.  Bennet’s fracture B. Essex-Lopresti fracture D. Greenstick fracture 5.    A Lisfranc fracture is a fracture-dislocation involving: A. Calaneocuboid joint B.                 Tarsometarsal joint C.                 Metatarsophalangeal joint D.                 Talocalcaneal dislocation.

6.    What tract is the main descending motor pathway in the cervical spinal cord? A. Posterior column C. Anterolateral corticospinal tract B. Lateral spinothalamic tract                       D. Anterior 361

spinothalamic tract 7.    Acute osteomyelitis is commonly caused by: A. Staphlococcous aureus                C. Streptococcous pyogenes B. Haemphilus Influenzae                D. Salmonella. 8.    What is not true of Brodie’s abscess: A. Form of chronic osteomyelitis  B.  Intermittent pain and swelling C. Common to diaphysis D. Excision is very often required. 9.    Tuberculosis of the spine most likely originates from: A. Intervertebral disc B. Cancellous vertebral body C. Ligamentous structures D. Paravertebral soft tissue. 10.            Melon seed bodies in the joint fluid are characteristic of: A. Rheumatoid arthritis           B. Tuberculous arthritis C. Septic arthritis           D. None of the above. 11.                 The type of crystals found in pseudogout are: A. Monosodium urate C. Calcium pyrophosphate B. Calciumthiosulfate D. Sodium tartarate.

12.     All of the following can cause osteoporosis except A. Hyperparathyroidism C. Steroid use B. Fluorosis D. Thyrotoxicosis. 13.            Regarding osteomalacia, all are false except; A. Is due to vitamin A deficiency B. May present with pseudo-fractures C. Serum calcium is increased D. A bone biopsy would show an increase in mineralized 362

osteoid. 14.                                                                                                             Which bone tumor occurs in the epiphysis? A. Osteoclastoma Ewing’s sarcoma

     C.

B. Chondromyxoid fibroma                   D. Osteosarcoma. 15.            Regarding osteosarcomas, all are true except; A. Affects the metaphysis of long bones B. Are most commonly seen around the knee and in the proximal humerus C. Haematogenous spread can result in pulmonary metastases D. X-ray shows a ‘sunburst’ appearance due to soft tissue involvement. 16.            Multiple myeloma tumor cells resemble: A. Granulocytes C.  Plasma cells B. Lymphocytes D. Chondrocytes. 17.                  The most common osteolytic metastases in bones are derived from the: A. Lung C. Breast B. Stomach                      D. Kidney. 18.                 Positive pivot shift test in knee is due to injury of: A. Posterior cruciate ligament     C. ACL B. MCL                                                 D. Posterolateral complex tear. 19.             Osgood-Schlatter disease affects? A. Upper tibia C. Lower tibia B. Distal femur D. Proximal femur.

20.              Von Rosen splint is used in? A. Congenital dislocation of hip

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B. Congenital talipes equinovarus       C. Shaft of femur D. Scoliosis. Answer keys: 1. B 2.A 3.D 4.A 5.B 6.C 7.A 8.D 9.A 10.B 11.C 12.B 13.B 14.D 15.D 16.C 17.A 18.C 19.A 20.A

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III MBBS Phase II

MODEL EXAMINATION QUESTION PAPER Time: 3 hours                                                                  Total Marks: 100               PART A (GENERAL SURGERY) - 50 MARKS Long essay, Short essay, Short answers and MCQ’s will be asked related to General Surgery. PART B (ALLIED SPECIALITIES) (ORTHOPAEDICS+ ANAESTHESIA+RADIODIAGNOSIS+DENTISTRY)

Long Essays- 10 Marks Each (1X10=10 Marks) 1. A 6 year old kid was brought to emergency department with pain swelling and in left elbow with difficulty on moving the elbow. Parents give a history of fall from height directly on elbow while playing. 1. What is the most common pediatric elbow/distal humerus fracture? 2. Mechanism of injury and classification 3. Management 4. Complications- acute and chronic (1+3+3+3= 10Marks) Short Essay- 5 marks each (4X5=20 Marks) 1. Osteosarcoma - definition, histology, management 2. MRI scan 3.Osteomyelitis– Pathogenesis, Classification and Management 4. Epidural anaesthesia Short Answers- 2 marks each (5X2=10 Marks) 1. Describe a Thomas Splint 2. List the clinical features of Saturday Night Palsy 3. Enumerate the chemical formula and uses of POP 4. Enumerate the clinical features of Bennett’s Fracture 5. Describe the Stages of Fracture Healing

MCQ's (10X 1 = 10 marks) 1.Spina ventosa is seen in? a-tuberculosis dactylitis c-malignant melanoma

b-meningomyelocele d-all of the above

2. Which of the following is the fracture of atlas vertebrae?

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a-Jefferson’s fracture c-Essexloprestti frx

b- Bennet’s fracture d-Greenstick fracture

3. Bankart’s lesion involves the of the glenoid labrum? a-anteriorlip

b- superiorlip

c-anterosuperiorlip

d- anteroinferior lip.

4. Monteggia fracture is a. Distal radius fracture with DRUJ injury            b. Treated by conservative management c. Ulna fracture with proximal radioulnar dislocation d. Occurs in children only. 5. Treatment for displaced neck of femur fracture in 40 year old man a. Heals with good callus b. Conservative management with traction c. Accurate reduction and internal fixation d. Hemiarthroplasty 6. Commonest type of hip dislocation is a.Anterior                                   c. Central b.Posterior                                 d. Dislocation with femoral shaft fracture 7.    Finkelstein’s test is done in: a. Tennis elbow c. Golfer’s elbow b. De Quervain tenosynovitis d. Carpal tunnel syndrome. 8.    ”Unhappy triad” of O’ Donoghue includes all except: a. Medial meniscus tear c. ACL rupture b. PCL rupture d. Medial collateral ligament injury. 9. HLA B27 is associated with a.Rheumatoid arthritis  b.Ankylosing spondylitis

c. SLE d.Gouty arthritis

10.                                                                                                                                                  A 10 year old boy presented with pain and massive swelling of left thigh. On radiological evaluation it reveals diaphyseal lesion with soft tissue swelling. The most likely diagnosis is

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a.Osteosarcoma                                                           c.Ewing’s sarcoma b.Osteoclastoma        d.Chondrosarcoma

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Table of Contents Foreword ACKNOWLEDGEMENTS Contents 1. Introduction to Orthopaedics, Skeletal Trauma, Polytrauma 2. Fractures 3. Musculoskeletal Infection 4. Skeletal Tuberculosis 5. Rheumatoid Arthritis and Associated Inflammatory Disorders 6. Degenerative Disorders 7. Metabolic Bone Disorders 8. Poliomyelitis 9. Cerebral Palsy 10. Bone Tumors 11. Peripheral Nerve Injuries 12. Congenital lesions MISCELLANEOUS Gait Osteoarthritis Neuropathic Joint Carpal Tunnel Syndrome Tennis Elbow Golfer's Elbow De Quervain's Disease Trigger Finger Osteochondritis Trendelenberg Gait Bryants Triangle Thomas Hip Flexion Test

3 4 7 13 64 150 171 186 199 209 221 233 241 261 275 306 306 307 308 308 309 310 310 311 311 312 313 314

13. Procedural Skills 14. Counselling Skills 15. Instruments & Implants Rapid Review References 368

316 339 343 356 360

Sample MCQ’s Model Examination Question Paper

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