Aorf textbook of orthopaedics by Prof. John E.O. Ating'a, Dr.Vincent M. Mutiso,Dr. Fred. M.T Otsyeno

AORF TEXTBOOK OF ORTHOPAEDICS

AORF TEXTBOOK OF ORTHOPAEDICS

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AORF Textbook of Orthopedic Copyright ŠAcrodile Publishing Limited, 2014 All rights reserved. No part of this book may be used or reproduced by any means, graphic, electronic, or mechanical, including photocopying, recording, taping or by any information storage retrieval system without the written permission of the publisher except in the case of brief quotations embodied in the case of brief quotations embodied in critical articles and reviews.

Acrodile Publishing Limited P.O.Box 15298-00509, Lang’ata-Nairobi, Kenya Email: info@acrodile.co.ke Website: www.acrodile.co.ke Print Edition ISBN 978-9966-007-30-8 Electronic Edition ISBN 978-9966-007-31-5 Typeset in Kenya by Andrew Anini Mweresah Printed in India

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Contents

Acknowledgements

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Foreword

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Chapter One: Orthopaedics: An Introduction

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Chapter Two: Biology of the Elements of the Musculoskeletal System

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Chapter Three: Evaluation of the Orthopaedic Patient

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Chapter Four: Congenital Malformations

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Chapter Five: The Limping Child

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Chapter Six: Infections

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Chapter Seven: Metabolic Disorders

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Chapter Eighta: Muscoloskeletal Tumours

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Chapter Nine: Trauma

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Chapter Ten: Emergency Management

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Chapter Eleven: The Spine

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Chapter Twelve: Casts and Splints

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Chapter Thirteen: Traction

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Chapter Fourteen: Specific Management of Injuries of the Upper Limb

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Chapter Fifteen: Treatment of Fractures and Dislocations in the Limb

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Chapter Sixteen: Specific Fracture in Children

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Chapter Seventeen: Management Option Applicable to Disorder of Joints

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Chapter Eighteen: Principles of Management of Non Osseous Musculoskeletal Structures

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Chapter Nineteen: Principles of Limb Ablation

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Chapter Twenty: Outcomes in Musculoskeletal Orthopaedic Care

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Appendix

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Index

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Acknowledgements

ARF Text book of Orthopaedics is a result of the collective effort of three practicing orthopaedic surgeons at Kenyatta National Hospital (Firm III), Nairobi Kenya, who are also teachers at the University of Nairobi and other institutions of higher learning; Prof. John E. O. Ating’a Dr. Vincent M. Mutiso Dr. Fred M. T. Otsyeno The three are the founder fellows of the African Orthopaedic Research Foundation.

The following is a list of contributors and reviewers who ably assisted in the compilation of this book: Dr. Johnson L. Murila Dr. Claude Masumbuko Dr. Asif A. Admani Dr. Stanley .T. Ng’ang’a Dr. Mark Murerwa Dr. Emelda A. Mang’uro Dr. Andrew K. Wainaina Dr. Angela Muoki Dr. Marylyn Kimeu Dr. Juma Wakhayanga Dr. Dorsi O. Jowi Dr. Pauline Nkirote Rintari

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Foreword

Orthopaedic Surgeons and Trainees, General Surgeons and General Practitioners will all find this new book interesting, valuable and helpful. It has been produced by three Orthopaedic Surgeons of the Kenyatta National Hospital in Nairobi, Kenya supported by a dozen contributors. It contains an incredible volume of data covering just about every orthopaedic and indeed many rheumatological conditions that occur in low and middle income countries (LMIC’s) as well as in richer parts of the world. Like all multi-authored books the contents vary in their presentation and the degree of emphasis given by each author to their own particular interests. In some ways this means that the most appropriate management in specific circumstances could be difficult to determine, but it is all there and of value.

The three principal authors are the founder fellows of the African Orthopaedic Research Foundation, a new and unique African organisation as far as I know and who obviously have carefully reviewed and summarised the available and relevant world literature. The book is well produced, relatively easy to read and I believe that a copy should be added to the medical/surgical libraries of all hospitals, clinics and private individuals who deal with musculo-skeletal problems.

Geoffrey Walker, FRCS, FCS(hon)ECSA.

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Table of Tables

Table 3.1: Prefered sites of reflex testing and response Table 4.1: Defects in club foot and their correction Table 5.1: Mile stones Table 5.2: Common causes of limping in children Table 6.1: Joint aspirate likely diagnosis and expected count Table 8.1: Shows the more likely tumour lesions at various age groups

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Table of Figures

Fig 2.1: The Structure of the cortical bone Fig 2.2: Diagram of compact bone Fig 2.3: Illustration of a typical long bone Fig 2.4: Osteoblasts Fig 2.5: Osteoclasts Fig 2.6: Diagrammatic representation of the blood supply to the long bones Fig 2.7: Stages in endochondral bone formation Fig 2.8: Growth and parts of an immature long bone Fig 2.9: Frontal bone Fig 2.10: Diagrammatic representation of a synovial joint Fig 2.11: The basic common structures for ligaments and tendons Fig 2.12: Muscle, tendon and bone Fig 2.13: Typical nerve cell Fig 3.1: Diabetic ulcer on the dorsum of the foot Fig 3.2: Epithelioma Fig 3.3: Inspection: The foot at risk in a diabetic Fig 4.1: Bilateral congenital Talipes Equinovarus Fig 4.2: Neglected congenital dislocation of the hip Fig 4.3: Syndactyly Fig 4.4: Post axial extra digit Fig 4.5: Radiograph of post axial bilateral extra digits Fig 4.6: Radial club hand Fig 5.1: Bifocal lengthening of the tibia Fig 5.2: Genu valgum Fig 5.3: Blount’s disease Fig 5.4: Arthrogryposis multiplex congenital Fig 5.5: Perthes disease Fig 5.6: Slipped capital femoral epiphysis Fig 6.1: Chronic Osteomyelitis the dead bone is coming out Fig 6.2: Chronic Osteomyelitis skin changes, sinuses and scars at different stages of healing.

Fig 6.3: Chronic Osteomyelitis sequestrum Fig 6.4: Chronic Osteomyelitis the sequestrum in the figure above has been removed Fig 6.5: Tuberculosis of the spine Fig 7.1: Formation of cholecalciferol Fig 7.2: Deformities in rickets Fig 7.3: Rickets before treatment and two years after treatment with calcium Fig 8.1: Site for predilection of different bone tumours in the long bone

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Fig 8.2: An image depicting an aneurysmal bone cyst Fig 8.3: Solitary osteochondroma Fig 8.4: Giant cell tumour, note the location Fig 8.5: Multiple lytic lesions in multiple myeloma Fig 8.6: Osteogenic sarcoma, sunrise appearance Fig 9.1: External fixation Fig 9.2: Circular external fixator applied to distal leg Fig 11.1: Spina bifida manifesta Fig 11.2: Right thoracic scoliosis Fig 11.3: Osteopathic, congenital malformations of the spine Fig 11.4: Determination of the Cobbs angle Fig 11.5: Tuberculosis of the spine note the kyphosis Fig 11.6: Spondylolisthesis L5 S1 Fig 12.1: Measuring the splinting material Fig 12.2: Ulnar gutter splint molded Fig 12.3: Elastic bandages applied to secure the splint Fig 12.4: Ulnar gutter cast (shown for comparison to ulnar gutter splint) Fig 13.1: A child with a fracture femur on skin traction Fig 13.2: Bucks traction Fig 13.3: Hamilton russels traction Fig 13.4: Perkins traction Fig 13.5: Buhler Braun frame Fig 13.6: Fisk’s traction Fig 13.7: 90-90 traction Fig 13.8: Pelvic Hammock Fig 13.9: Traction in the cervical spine Fig 17.1: the hand in rheumatoid arthritis Fig 17.2: Bilateral Osteonecrosis of the femoral head Fig 18.1: Tendon sheaths keep the tendons in place Fig 18.2: Examination of the fingers Fig 18.3: Splint is applied to limit movement after tendon surgery

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CHAPTER ONE

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ORTHOPAEDICS; An Introduction The Origin of Orthopaedic practice can be traced back to the 16th Century. NICHOLAS ANDRY (16581759), professor of Medicine at the University of Paris and Dean of the faculty of Physick, in 1741, at the age of 81, published a famous book entitled Orthopaedia or the Art of Correcting and Preventing Deformities in Children. In this book, the word Orthopaedic, which derives from the Greek words straight and child, is presented.

Long before the word orthopaedics was coined, the art of orthopaedics was practiced in line with other forms of medicine. In ancient Greece, the works of Hippocrates detail the treatment for dislocations of the shoulders, knees, and hips as well as treatments for infections resulting from compound fractures. In Egypt splints made of bamboo, reeds, wood or bark padded with linen have been found on mummies.

During the Greco-Roman period, there were also attempts to provide artificial prostheses. There are accounts of wooden legs, iron hands and artificial feet. There is a remarkable link between the origins of modern orthopaedics in the United Kingdom (and subsequently in North America) and the Anglesey bone setters of the 18th century.

Many developments in orthopedic surgery resulted from experiences during wartime. On the battlefields of the Middle Ages, the injured were treated with bandages soaked in horses’ blood which dried to form stiff, though unsanitary, splints. Traction and splinting developed during the 1st World War. Since the 2nd World War, orthopaedic treatment has evolved to include joint replacements, arthroscopy and a whole host of technologies.

Today the specialty is concerned with the following six broad areas; a) The bones of: • The extremities; the upper and lower limbs • The axial skeleton; the bones of the spine • The pelvic and shoulder girdles b) The joints formed by the articulation of the bones mentioned above c) The muscles and tendinous structures that move the joints d) The ligaments that stabilize the joints e) The spinal cord and the rest of the nervous tissue that control the movements and f) The skin and other soft tissues that provide coverage to the bones.

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An understanding of the entire body is essential in the diagnosis and management of orthopaedic diseases since all these systems are interrelated. Evaluation of any disease begins with general approach to the individual followed by review of the specific system involved and finally consideration of the other systems.

Musculoskeletal disorders arise from a variety of causes which can be congenital or acquired. These can be grouped as follows:

Traumatic disorders Trauma is derived from the Greek word ‘traumata’ meaning body wound or shock produced by sudden physical injury, as from violence or accident. Today trauma is the sixth leading cause of death worldwide [in sub-Saharan Africa, it is third only to diarrhoea and malaria (Murray, 1996)]. Satics show that trauma accounts for 10% of all mortality and is a serious public health problem with significant social and economic costs. Trauma may draw attention to an underlying orthopaedic condition or worsen a pre-existing one. Trauma may also predispose to conditions that may present much later in life for example; trauma to the ankle joint may lead to osteoarthritis of the same joint.

Congenital disorders Congenital causes are defined as conditions that have been present since birth. These may be as a result of: Genetic abnormalities Acquired abnormalities Combination of both.

These conditions are commonly referred to as malformations when the abnormality is at structural level such as congenital club foot or as defects when the aberration is at molecular level for example osteogenesis imperfecta.

In as much as these conditions are present at birth, their presentation to the health care provider may occur at any chronicle age of the individual: At birth, commonly, when a structural malformation is noticed, club foot is an example of one that is immediately evident at birth.

Later in life when the effect of the disorder may interfere with body functions; congenital Coxa vara is noted at about the age of one year when the child starts walking.

As a predisposing factor to a disorder of later life; evaluation of symptoms of osteoarthritis may reveal that a dysplastic hip had existed all along.

During screening; scoliosis may be evident during mass screening, it may also be apparent at the time when school age children undergo preschool medical examination.

As an incidental finding in the course of evaluation of other disorders, evaluation of back pain from other causes may reveal the presence of spina bifida occulta.

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Infections Infections may affect the musculoskeletal structures in a variety of ways: directly by eliciting an immunological response; by end functional tissue destruction and finally as an ever present real risk in every operative procedure. Various organisms cause infection directly depending on the virulence of the organism and the resistance of the host. The offending organisms can be categorized in the following ways:

Bacteria The term Osteomyelitis, when not otherwise specified, conventionally refers to pyogenic bacterial infection of the bones such as that due to Staphylococcus spp. Other bacteria such as Mycobacterium spp, Treponema pallidum (causes chronic granulomatous infections that will be qualified specifically by mentioning the disease); tuberculous arthritis of the hip and syphilitic tabes dorsalis, as examples, respectively.

Fungi Fungal infections are qualified specifically. For example, Madura foot is a fungal infection of the foot by madurella myecetoma. Fungi lead to an indolent response from the tissues of the affected person.

Parasites Parasitic infections are referred to as infestations; hydatid infestation of the femur is the infection of the femur with echinococcus granulosus. Infestations may predispose to fractures.

Viral infections Most viral infections in the body cause a limited illness then the body’s immune system destroys the virus, and the symptoms of the illness go away. Viruses are of interest in orthopaedics in a variety of ways. Polio is a contagious viral illness that in its most severe form causes paralysis, difficulty in breathing and sometimes death.

Several viruses are known to cause problems with joint inflammation and pain. Some of the most common are Parvovirus B-19, Hepatitis B infection, Rubella, and Human Immunodeficiency Virus. In viral arthritis, the immune system’s response to the virus causes inflammation in the joints. Even after the virus is eliminated from the body, the changes in the joint can continue to cause pain and swelling.

The joint may even become permanently damaged. Some kinds of arthritis with unexplained causes may be the result of a virus.

In some cases, viruses that cause arthritis type symptoms can be carried by insects. Alpha viruses, one such family of viruses, are carried by mosquitoes in Africa, Australia, Europe, and Latin America. All can cause arthritis symptoms. Dengue fever and Chikungunya belong to this group.

The cause of myasthenia gravis is unclear. However, researchers suspect viruses or bacteria might trigger the autoimmune disease (Cavalcante et al, 2010, Robinson et al, 2010). Transient synovitis of

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the hip joint is a condition that occurs in childhood causing hip pain. Transient synovitis may be related to a viral illness.

Transmission of HBV, HIV, and HCV has been well-documented in health care settings. Transmission of these viruses has been reported from patient to health care providers, from health care providers to patient, and from patient to patient. Although much attention has focused on preventing HIV transmission, it is important for health care providers to be mindful of all of these common blood borne pathogens. Measures for preventing transmission are common to all three of these viruses.

Infections may affect the musculoskeletal system by direct destruction of the end functional tissue structures. In other situations the end tissues are involved by secondary effects. These can occur as: Deformities secondary to motor neural damage such as those due to poliomyelitis.

Deformities secondary to sensory disturbances as in leprosy.

Kyphosis in tuberculosis as a consequence of destruction of bones due to the organism.

Whereas paraplegia may be caused by direct pressure on the spinal cord by inflammatory mass or compromise of the vascular supply by the inflammatory process.

Metabolic disorders Bone has organic and inorganic components. To keep bone in optimum health, there is continuous physiological turnover of its mineral content with the rest of the systems of the body; the extra cellular fluid and blood taking a leading role. This continuous turnover is under the influence of hormones secreted by endocrine glands such as the thyroid and the parathyroid. Physical activity and mineral uptake and therefore by extension dietary availability also contribute to this balance. Conditions that disrupt this system are referred to as metabolic disorders. Rickets in children, Osteomalacia in the adults and osteoporosis in the elderly all belong to this class of diseases.

Immunological disorders The body has an interacting combination of ways to recognize cells, tissues, objects and organisms that are not part of it and thus initiate the response to fight them. This immune response is often beneficial but at times it may malfunction and cause tissue damage leading to immunological diseases. The immune system may fail to recognize its own cells and tissues; it may over function or under function or even affect privileged compartments of the body. The joints of the body bear the brunt of these diseases. Rheumatoid arthritis and systemic lupus erythromatosis are examples of such immunological diseases. The trigger of this immune response may not be found. However, these diseases tend to run in families and different forms tend to affect the same individual. The presentations of these diseases are commonly medical chronic forms that show with deformities being the ones that present to the orthopaedic surgeon.

Neural disorders An intact neuromuscular system is essential for optimal skeletal function. Disorders of the brain (such as cerebral palsy), the spinal cord and the peripheral nerves ultimately present as orthopaedic diseases. Other diseases can act through this pathway to produce disorders. Examples of such include

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poliomyelitis, leprosy and spinal cord trauma. Muscle weakness can occur as a primary disorder or as a consequence of innervations and hence belongs to this group.

Degenerative conditions With the passage of time and continuous use of body structures, particularly joints, these structures undergo wear and tear. In this situation, degenerative musculoskeletal system disorders are said to be present. Osteoarthritis belongs to this group of disorders. This wear and tear may be accelerated in the presence of a predisposing condition.

Normal cell growth of the Tumours musculoskeletal system, just as with the rest of the body, is closely regulated. In some instances, this regulation fails, resulting in uncontrolled proliferation of these cells resulting in neoplasms. If this happens to the cells at the site and system of origin it is referred to as primary neoplasia. If the cells have their origin from elsewhere within the body but have seeded in the musculoskeletal system these are referred to as secondary neoplasms. These neoplasm’s, also referred to as tumours, may be benign or malignant. The long bones and the spine are common sites of Secondary neoplasms.

Systemic illness Systemic illnesses such as chronic renal failure, diabetes mellitus and sickle cell disease can result in orthopaedic problems. Definitive treatment and good control of those that are not totally curable will minimize the musculoskeletal effects of these diseases. Specific management of these complications depends on the individual presenting musculoskeletal complications.

Although we have classed the different possible types of afflictions separately, these conditions may present singly or in combinations thereof. An open traumatic injury can become infected; a child with developmental disorder of the hip may develop avascular necrosis of the femoral head requiring hip replacement.

In this manual, discussions of the musculoskeletal problems that may affect man are introduced, methods of diagnosis presented. The more common disorders are discussed in detail. Conservative, common, and relatively “easier� methods of management are presented whereas the more complicated usually operative methods are outlined. The reader is encouraged to refer to more specialized text books of orthopaedics for detailed information on a particular topic. Every effort is made to provide illustrations to enhance the application by the reader.

Bibliography and further reading 1. Cavalcante P., Serafini B., Mantegazza R. et al. Epstein-Barr virus persistence and reactivation 2.

in myasthenia gravis thymus. Ann Neurol; 2010; 67:726-738.

Fatal injuries in the slums of Nairobi and their risk factors of disease study. Results from a matched case-control study Injuries in Africa: a review. J Urban Health 2011

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3. Garrett, W. E, et al. American Board of Orthopaedic Surgery Practice of the Orthopaedic 4.

5.

6.

7.

8.

Surgeon: Part-II, Certification Examination. The Journal of Bone and Joint Surgery (American).

2006;88:660-667 Murray CJ, Lopez AD. Mortality by cause for eight regions of the world: Global burden of disease study. Lancet. 1997 May 3; 349(9061):1269-76 Murray, C.J.L. and Lopez, A.D. The global burden of disease. World Health Organization/ Harvard School of Public Health/World Bank. Harvard University Press, 1996.

Nordberg E; Review Injuries in Africa: A review. East Afr Med J. 1994 Jun; 71(6):339-45.

Robinson, Richard Active Epstein-Barr Virus Found in Myasthenia Gravis Thymus Neurology Today 5 August 2010; Volume 10(15); pp 20-21 Sir Robert Jones; Great Teachers of Surgery in the Past: Br J Surg. 1967 Feb: 54(2):85-90.

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CHAPTER TWO

Biology of the elements of the musculoskeletal system Bone Types of Bones Cortical bone This makes up 80% of the skeleton and is found in the outer shell of the bone. It is composed of tightlypacked osteons or Haversian canals made up of concentric lamellar (layers) of cylinders and surrounding systems up made up of a central co-vascular channel, connected by Haversian (Volkmann’s) canals.

Fig 2.1: The structure of cortical bone These Haversian canals contain capillaries, arterioles, venules, nerves and possibly lymphatic’s. Lying between these osteons are interstitial lamellae. Fibrils often connect lamellae but do not cross the cement lines that form the outer border of osteons. The intraosseous circulation provides for homeostasis of the bone including nutrition and hormonal balance. Cortical bone has a slow turnover rate and a high resistance to bending and torsion.

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Figure 2.2: Diagram of compact bone from transverse section of a long bone’s cortex demonstrating Osteon

Spongy or cancellous bone This is less dense and more elastic than cortical bone and has a higher turnover rate. It is organized in trabecular struts, with lamellae running parallel to the trabeculae. It is found in the epiphyseal and metaphyseal regions of long bones and throughout the interior of short bones.

Fig 2.3: Illustration of a typical long bone showing the location of cancellous bone, Osteon, lamellae, Haversian canal, canaliculi and Volkmann’s canal

Immature or developing bone This is woven and more random with more osteocytes than lamellar bone. It is the product of rapid bone formation resulting in an irregular, disorganized pattern of collagen orientation and osteocytes distribution. It is found in embryonic and foetal development and in healthy adults at ligament and tendon insertions. It also occurs in response to bone injury and dramatic changes in mechanical stimulation.

It provides a temporary mechanical adjunct to allow bone to maintain or return quickly to its role as a structural support.

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Cellularity of Biology Osteoblasts Osteoblasts form osteoid, the non mineralized component of bone matrix. They differentiate from mesenchymal progenitor cells and contain extensive endoplasmic reticulum with multiple cisternae, well-developed Golgi bodies, numerous ribosomes and mitochondria allowing for their abundant synthesis and secretion of matrix. They initiate mineralisation of osteoid material possibly by modulating electrolyte fluxes between the extracellular fluid volume and osseous fluid spaces.

Fig 2.4: Plenty of osteoblast - They are basophilic, more or less cuboidal shaped, arranged in rows along the pieces of bone and the inner surface of the marrow spaces. They are close to the bone they are making, which is usually less densely stained than the cells.

Bone-lining cells They are narrow, flattened cells which differentiate from Osteoblasts but have fewer active organelles.

They envelop quiescent bone surfaces including endosteal, periosteal and intra-cortical surfaces.

Their function is to encase the bone surface and moderate site-specific mineralisation or resorption on activation by parathrohormone (PTH).

Osteocytes Osteocytes maintain bone and comprise 90% of all cells in the mature skeleton. They originate as Osteoblasts which have been trapped within osteoid, formed by surrounding Osteoblasts, forming a lacuna. They have a single nucleus, and an increased nucleus to cytoplasm ratio. Osteocytes are smaller in size and have fewer numbers of organelles than Osteoblasts therefore are not as active in matrix production. Osteocytes play a role in controlling the extracellular concentration of calcium and phosphate; they are directly stimulated by calcitonin and inhibited by PTH. Osteoclasts Osteoclasts act in opposition to Osteoblasts and their role is to resorb bone providing for coupling of bone formation and resorption. They are multinucleated, irregularly-shaped giant cells which arise from haematopoietic cell lines through the fusion of monocyte progenitor cells.

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Fig 2.5 Three big Osteoclasts are sitting on a piece of bone in the center of the field Osteoclasts are multinucleated: one shown here has at least nine nuclei, which is not a very unusual situation. Some have fewer and some have more, depending on the requirements of the time and place where they’re formed.

Matrix Bone matrix is made up of organic components (40% dry weight of mature bone) and inorganic components (60% dry weight).

Organic Components Collagen Collagen, mainly of type I, forms 90% of the bone matrix and provides the bone’s tensile strength.

Proteoglycans Proteoglycans contribute to the compressive strength of bone. Their function is unclear, but they are thought to play a role in the reservation of space for bone development, the binding and availability of local growth factors, and the deposition and structuring of collagen fibrils. Proteoglycans inhibit mineralisation.

Osteocalcin Osteocalcin is produced by Osteoblasts and makes up 10-20% of the collagenous protein of bone. It attracts Osteoclasts; therefore its function is associated with bone remodeling. Synthesis is induced by 1, 25 Dihydrocholecalciferol (Vitamin D3) and inhibited by PTH. Serum and urine levels are elevated in Paget’s disease, renal osteodystrophy and hyperparathyroidism.

Osteonectin Osteonectin is secreted by platelets, Osteoblasts and Osteoclasts. It is thought to either play a role in the regulation of calcium or the organisation of material within the matrix, as it binds with collagen. It also has a high affinity for both calcium and Hydroxyapatite, and localises to crystal-producing matrix vesicles.

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Osteopontin Osteopontin mediates the attachment of cells to bone matrix, similar to integrins.

Growth factors and cytokines These occur in small amounts in bone matrix.

Bone Morphogenic Proteins (BMPs) BMPs are members of the TGF-b super family of growth factors. They act on progenitor cells to induce differentiation into Osteoblasts and chondroblasts. They are responsible for ectopic bone formation by certain tumour cells, epithelial cells and demineralised bone. BMPs appear to be stored within the bone matrix and released during the resorptive activity that often follows injury.

Inorganic components Calcium Hydroxyapatite (Ca10 (PO4)6(OH) 2) Calcium Hydroxyapatite provides the compressive strength of bone. It makes up most of the inorganic matrix, and is responsible for mineralisation of the matrix (the transformation of Hydroxyapatite from a soluble to a solid form).

Osteocalcium Phosphate (Brushite) Osteocalcium phosphate comprises the remainder of inorganic matrix.

Fluid is also an important component of bone and its distribution in the various compartments of bone is as follows: Extra vascular 65% Lacuna 6% Haversian 6% Red blood cells 3%

Bone Remodeling Wolff’s Law states that bone grows and remodels in response to the forces that are placed upon it (Wolff 1896); the architecture and the mass of the skeleton are adjusted to withstand the prevailing forces imposed by functional need or deformity. Bone remodeling is affected by mechanical function, according to Wolff’s Law, which attempts to predict bone adaptation in the face of an altered loading environment.

Generally, remodeling occurs in response to stress and responds to piezoelectric charges. Crystals which acquire a charge when compressed, twisted or distorted are said to be piezoelectric. This provides a convenient transducer effect between electrical and mechanical oscillations. (Compression causes negative potential, which stimulates Osteoblastic activity & bone formation while tension causes positive potential, leading to Osteoclasts stimulation). Bone is dynamic hence coordinated Osteoblast and Osteoclast activity results in continuous remodeling of both cortical and cancellous bone throughout life.

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Cortical bone remodeling occurs by Osteoclasts which tunnel through to the bone forming “cutting cones�, followed by sheets of Osteoblasts which deposit osteoid in lamellae. Cancellous bone remodeling involves Osteoclasts resorption of bone, followed by the deposition of osteoid by Osteoblasts.

Bone Circulation Bones are well-supplied with arteries, receiving 5% of cardiac output under basal conditions. Long bones receive blood from: Periosteal arteries Nutrient arteries, Metaphyseal and Epiphyseal arteries.

Periosteal arteries enter the bone at various points and supply the outer third of the cortex of the diaphysis. This is a low pressure system. Nutrient arteries are branches of major systemic arteries and pass obliquely through the diaphyseal cortex to reach the medullary canal. Here they divide into longitudinally directed branches which supply at least the inner two-thirds of mature diaphyseal cortex. This endosteal supply is a high pressure system.

Metaphyseal and epiphyseal arteries supply the ends of bone and arise mainly from the periarticular vascular plexus. In growing bones they supply growth plates, so significant disruptions of blood flow disturb Fig 2.6: Diagrammatic representation of the Blood supply to the long bones bony growth.

Direction of flow In mature bone, arterial blood flows centrifugally from the high pressure nutrient arteries to the low pressure periosteal arteries. If a displaced fracture causes interruption of the nutrient artery system, the flow reverses as the periosteal system now predominates, so blood flow becomes centripetal.

In developing bone, arterial flow is centripetal because the periosteum is highly vascularised and is the major component of blood flow in bone. In mature bone, venous flow is centripetal; cortical capillaries drain to venous sinusoids, which then drain to emissary veins. As with other tissues and organs, hypoxia, such as at a high altitude, causes an increase in blood flow to bone, as does hypercapnia and sympathectomy.

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After an injury to a bone, blood flow to the site initially decreases due to disruption of vascular structures.

Blood flow then gradually increases over the following hours and days, peaking at around 2 weeks. By 3-5 months, flow has returned to normal. Fracture healing is largely reliant on bone blood flow - reaming of bone devascularises the central 50-80% of cortex, and thus is associated with delayed vascularisation with all types of fixation.

Regulation Blood flow to bone is regulated by humeral, metabolic and autonomic signals. The osseous vessels express various vasoactive receptors. These provide an avenue which has potential for exploitation by pharmacological agents for the treatment of bone diseases related to circulatory disturbances such as osteonecrosis, and fracture nonunions.

The tissue surrounding bone, Periosteum, is a dense connective tissue membrane which covers bone.

It is composed of an outer fibrous layer, which is contiguous with joint capsules, and an inner, or cambium, layer which is loose, more vascular, and contains cells; Osteoblasts (if bone formation is in progress on the surface) and Osteoblast precursors (If bone formation is not occurring). The outer layer is the main component of periosteum, and cells in this layer are sparse.

Fig 2.7: Stages in endochondral bone formation.

Bone marrow Red marrow is the tissue in which blood cells develop and is 40% water, 40% fat and 20% protein. In later stages of growth and in the adult, when the rate of blood cell formation has decreased, red marrow slowly changes to yellow marrow. Yellow marrow is made up mostly of fat cells (80% fat, 15% water, 5% protein). Under the appropriate stimulus, yellow marrow can revert to red marrow.

Endochondral bone formation/mineralisation Cartilage model Human bones are mostly preformed from hyaline cartilage. This originates as condensed mesenchyme beginning at 6 weeks gestational age. This model is gradually invaded by vascular buds which bring in osteoprogenitor cells that differentiate into Osteoblasts and form primary centers of ossification at around

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8 weeks. The cartilage model grows through appositional growth (new bone is applied to the surface of existing bone leading to an increase in width of bone) and interstitial growth (growth and replacement by bone of deeper layers of epiphyseal growth plate, pushing the epiphysis and its overlying articular cartilage away from the metaphysis and diaphysis leads to increased length of bone). Ossification thus spreads to replace the cartilage model. Marrow is formed by the resorption of the central cancellous bone and invasion by myeloid precursor cells, brought in by capillary buds.

Secondary centers of ossification develop at the ends of bone, to form epiphyseal centers of ossification which allow increase in bone length until the adult dimensions are attained. During the developmental stage, the epiphyses enjoys a rich arterial supply composed of an epiphyseal artery, metaphyseal arteries, nutrient arteries and perichondral arteries.

Regions of growing long bone Physis In immature long bones there are 2 growth plates: Horizontal (the physis) Spherical (allowing for the growth in the girth of the epiphysis; it has the same arrangement as the physis but is less organised).

Physeal cartilage is classified into zones according to growth and function. They include: Reserve zone - Here there is no evidence of cellular proliferation or active matrix production. There is decreased oxygen tension. Cells here store lipids, glycogen and proteoglycan aggregates for later growth. Therefore diseases such as lysosomal storage diseases (Gaucher’s) can affect this zone.

Proliferative zone - The cartilage cells undergo division and actively produce matrix, and longitudinal growth occurs with chondrocytes forming columns. The oxygen tension here is increased, and there is also increased proteoglycan in the surrounding matrix which inhibits calcification. Defects in this zone (affecting chondrocyte proliferation and column formation) occur in achondroplasia.

Hypertrophic zone - This may be subdivided into 3 zones: • Maturation • Degeneration and • Provisional calcification.

Here the cartilage cells are greatly enlarged (up to 5 times normal size), they have clear cytoplasm as a result of the glycogen accumulated, and the matrix is compressed into linear bands between the columns of hypertrophied cells. The cartilage cells accumulate calcium in mitochondria, then undergo aptosis (death), releasing calcium from matrix vesicles. Sinusoidal vessels bring Osteoblasts, which use the cartilage as a template for bone formation.

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Metaphysis Here Osteoblasts from progenitor cells accumulate on cartilage bars formed by Physeal expansion.

Mineralization of primary spongiosa (calcified cartilage bars) occurs, forming woven bone which is remodeled to form secondary spongiosa and a “cutback zone” at the metaphysis. Cortical bone is formed when Physeal and intramembranous bones are remodeled in response to stress along the periphery of growing long bones.

Periphery of the Physis This has two main components: Groove of Ranvier - allow chondrocytes to travel to the periphery of the growth plate, resulting in lateral growth.

Perichondral Ring of LaCroix - dense fibrous tissue which anchors and supports the physis mineralization.

Collagen whole zones (between ends of molecules) are seeded with calcium Hydroxyapatite crystals, through branching and accretion.

Fig 2.8: Growth and parts of an immature long bone.

Fig 2.9: Frontal bone, the ossified areas are stained rather darkly compared to the rest.

Hormone and growth factor effects on the growth plate Hormones and growth factors affect the growth plate either directly or indirectly, through their effects on chondrocytes and matrix mineralisation. Some factors are produced and act within the growth plate, while others are produced at a distant site.

Intramembranous ossification The flat bones of the skull, the mandible and the clavicle ossify at least partly by intramembranous ossification. This occurs without a cartilage model by aggregation of layers of connective tissue cells at the site of future bone formation, and their differentiation into Osteoblasts. The Osteoblasts then form a centre of ossification which expands by appositional growth.

The irregular structures in the center of the image will form the spongy bone of the “sandwich” a typical flat bone displays in gross sections. The outer compact bone - the “tables” will be formed by ossification

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of the dense areas top and bottom in this field. Even though one region in this field will produce spongy bony and one compact bone, both arise via the intramembranous mode.

Bone injury and repair.

General principles Bone response to injury consists of overlapping phases of inflammation, repair (soft callus then hard callus formation) and remodeling. Fracture healing is affected by systemic factors such as age, hormones and nutrition and local factors such as degree of local trauma, type of bone affected and infection. a. Inflammation (Haemorrhage/Granulation Tissue-minutes/hours)

This begins immediately after the fracture, and is characterized by bleeding from the fracture site and surrounding tissues, causing haematoma formation, accompanied by edema and pain. b. Cellular Proliferation

Lysosomal enzymes are released and tissue necrosis occurs - Osteoclasts and macrophages remove necrotic bone and tissue debris from the fracture site. This is followed by the stimulation of proliferation of reparative cells such as Osteoblasts and endothelial cells. c. Repair (Immature Callus/Mature Callus-weeks/months)

Within 2 weeks, primary callus response occurs. If the bone ends are not in apposition to one another, soft (bridging) callus is formed around and between the fragments, reducing their mobility. This soft callus contains fibroblasts, proliferating Osteoblasts and often chondroblasts, embedded in a matrix rich in collagen and glycoprotein, into which new blood vessels grow. d. Consolidation

Hard (medullary) callus supplements the bridging callus – the soft callus is gradually converted into woven bone, mainly by endochondral ossification. This stage is reached about 3 or 4 weeks after injury and continues until firm bony union occurs (around 2 or 3 months later for most adult bones). The amount of callus formation is indirectly proportional to the degree of immobilization of the fracture. e. Remodeling (years)

This stage overlaps with hard callus formation and may continue for up to 7 years. It involves the gradual conversion of the woven bone of the hard callus to lamellar bone.

It is considered complete when the site of the fracture can no longer be identified either structurally or functionally. It allows the restoration of bone to its normal configuration and shape, according to the stresses placed on it (Wolff’s Law).

Joints Skeletal structures are connected to one another in many ways. These junctions are referred to as articulations, arthroses or joints. Joints are classified based on the extent of movements or the type of articular cartilage. a. The classification of articulations based on the extent of joint movements: Using this

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criteria, articulations can be classified as follows: Synarthroses: Fixed or rigid joints.

Amphiarthroses: Slightly movable joints.

Diarthroses: Freely movable joints. b. The classification of joints on the basis of histology emphasizes the type of tissue that characterizes the junctional area. These are categorized as follows:

Fibrous articulations Apposed bony surfaces are fastened together by fibrous connective tissue. These are further subdivided into three types: sutures, syndesmoses, and gomphoses. Sutures are limited to the skull and allow no active motion. They exist where broad osseous surfaces are separated only by a zone of connective tissue. This connective tissue, along with two layers of periosteum on the outer and inner surfaces of the articulating bone, is termed the sutural membrane or ligament. A syndesmosis may demonstrate minor degrees of motion related to stretching of the interosseous ligament or flexibility of the interosseous membrane. Gomphosis is a special type of fibrous joint located between the teeth and maxilla or mandible. At these sites, the articulation resembles a peg that fits into a fossa or socket.

Cartilaginous articulations Apposed bony surfaces initially or eventually are connected by cartilaginous tissue. There are two types of cartilaginous joints, symphysis and synchondrosis. In symphyses adjacent bony surfaces are connected by a cartilaginous disc, which is composed of fibro cartilaginous or fibrous connective tissue, although a thin layer of hyaline cartilage usually persists, covering the articular surface of the adjacent bone. Examples are the symphysis pubis and the intervertebral disc.

They allow a small amount of motion, which occurs through compression or deformation of the intervening connective tissue.

Synchondroses are temporary joints that exist during the growing phase of the skeleton and are composed of hyaline cartilage. Typical synchondroses are the cartilaginous growth plate between the epiphysis and metaphysis of a tubular bone, the neurocentral vertebral articulations and the unossified cartilage in the chondrocranium and the spheno-occipital synchondrosis. With skeletal maturation, synchondroses become thinner and eventually are obliterated by bony union or synostosis. Two synchondroses that persist into adult life are the first sternocostal and the petro basilar joints.

Synovial articulations Apposed bony surfaces are separated by an articular cavity that is lined by synovial membrane.

A synovial joint is a specialized type of joint that is located primarily in the appendicular skeleton. Synovial articulations generally allow unrestricted motion. The inner portion of the articulating surface of the apposing bones is separated by a space; the articular or joint cavity.

Articular cartilage covers the ends of both bones. Motion between these cartilaginous surfaces is

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characterized by a low coefficient of friction. The inner aspect of the joint capsule is formed by the synovial membrane which secretes synovial fluid into the articular cavity. This synovial fluid acts both as a lubricant encouraging motion and as a nutritive substance, providing nourishment to the adjacent articular cartilage.

Parts of a synovial joint The synovial joint is the commonest joint found in the body and may comprise of: Cartilage, Articular Capsule, Fibrous Capsule, Synovial Membrane, Intra-articular Disc (Meniscus), Labrum, Fat Pad, and Synovial Fluid.

Fig 2.10: Diagrammatic representation of a synovial joint; the hip joint.

Articular cartilage The articulating surfaces of the bone are covered by a layer of glistening connective tissue, the articular cartilage. Its unique properties include: Transmission and distribution of high loads Maintenance of contact stresses at acceptably low levels Enabling movement with little friction Shock absorption Articular cartilage is devoid of lymphatic vessels, blood vessels and nerves. A large portion of the cartilage derives its nutrition through the synovial fluid.

Articular capsule The articular capsule is connective tissue that envelops the joint cavity. It is composed of a thick, tough outer layer, the fibrous capsule, and a more delicate thin inner layer, the synovial membrane.

Fibrous capsule The fibrous capsule consists of parallel and interlacing bundles of dense white fibrous tissue. At each end of the articulation, the fibrous capsule is firmly adherent to the periosteum of the articulating bones.

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Synovial membrane The synovial membrane is the delicate, highly vascular inner membrane of the articular capsule. It lines the non-articular portion of the synovial joint and any intra-articular ligaments or tendons. The synovial membrane also covers the intracapsular osseous surfaces, which are clothed by periosteum or perichondrium but are without cartilaginous surfaces.

Intra-articular Disc (Meniscus), Labrum, and Fat Pad A fibro cartilaginous disc or meniscus may be found in some joints, such as the knee, wrist, temporomandibular, acromioclavicular, sternoclavicular, and cost vertebral joints. The disc may divide the joint cavity partially or completely. Complete discs are found in the sternoclavicular and wrist joints, whereas partial discs are noted in the knee and acromioclavicular articulations. In the temporomandibular joint, the disc may be partial or complete.

Fat pads represent additional structures that may be present within a joint. These structures possess a generous vascular and nerve supply, contain few lymphatic vessels, and are covered by a flattened layer of synovial cells. Fat pads may act as cushions, absorbing forces generated across a joint, thus protecting adjacent bony processes. They also may distribute lubricants in the joint cavity.

Synovial fluid Minute amounts of clear, colorless to pale yellow, highly viscous fluid of slightly alkaline pH are present in healthy joints. The exact composition, viscosity, volume, and color vary somewhat from joint to joint. This fluid represents a dialysate of blood plasma to which has been added a mucoid substance secreted by the synovial cells. A small number of cells are present within the synovial fluid, consisting of monocytes, lymphocytes, macrophages polymorphonuclear leukocytes and free synovial cells.

Functions of the synovial fluid are nutrition of the adjacent articular cartilage and disc and lubrication of joint surfaces, which decreases friction and increases joint efficiency. The cells within the synovial fluid are important in phagocytosis

Supporting structures A variety of supporting structures exist in periarticular locations or in a more general distribution.

Tendons Tendons represent a portion of a muscle and are of constant length consisting of collagen fibers that transmit muscle tension to a mobile part of the body. They are flexible cords, white in color and smooth in texture that can be angulated about bony protuberances, changing the direction of pull of the muscle.

Aponeuroses Aponeuroses consist of several flat layers or sheets of dense collagen fibers associated with the attachment of a muscle. The fasciculi within one layer of an aponeurosis are parallel and different in direction from fasciculi of an adjacent layer.

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Fasciae Fascia is a general term used to describe a focal collection of connective tissue. Superficial fascia consists of a layer of loose areolar tissue of variable thickness beneath the dermis. Deep fascia resembles an aponeurosis, consisting of regularly arranged, compact collagen fibers. Parallel fibers of one layer are angled with respect to the fibers of an adjacent layer. Deep fascia is particularly prominent in the extremities, and in these sites, muscle may arise from the inner aspect of the deep fascia. At sites where deep fascia contacts bone, the fascia fuses with the periosteum. It is well suited to transmit the pull of adjacent musculature. Intermuscular septa extend from deep fascia between groups of muscles, producing functional compartments. Retinacula are transverse thickenings in the deep fascia that are attached to bony protuberances, creating tunnels through which tendons can pass.

Ligaments Ligaments represent fibrous bands that unite bones. They do not transmit muscle action directly but are essential in the control of posture and the maintenance of joint stability.

Tendon and ligaments A tendon (or sinew) is a tough band of fibrous connective tissue that usually connects muscle to bone and is capable of withstanding tension. Tendons are similar to ligaments and fasciae as they are all made of collagen except that ligaments join one bone to another bone and fasciae connect muscles to other muscles. Tendons and their muscles work together as units. Tendons are viscoelastic structures and are more stretchable than ligaments. When stretched, tendons have a soft tissue mechanical behavior.

Normal healthy tendons are composed mostly of parallel arrays of collagen fibers closely packed together. The dry mass of normal tendons, which makes up about 30% of the total mass(the rest being water), is composed of about 86% collagen, 2% elastin, 1–5% proteoglycans, and 0.2% inorganic components such as copper, manganese, and calcium. The collagen portion is made up of 98% type I collagen with small amounts of other types of collagen. These include type II collagen in the cartilaginous zones, type III collagen in the reticulin fibres of the vascular walls, type IX collagen, type IV collagen in the basement membranes of the capillaries, type V collagen in the vascular walls, and type X collagen in the mineralized fibrocartilage near the interface with the bone. Collagen fibres coalesce into macroaggregates.

After secretion from the cell, the terminal peptides are cleaved by procollagen N- and C-proteinases and the tropocollagen molecules spontaneously assemble into insoluble fibrils. A collagen molecule is about 300 nm long and 1-2 nm wide and the diameter of the fibrils that are formed can range from 50500 nm. In tendons, the fibrils then assemble further to form fascicles which are about 10 mm in length with a diameter of 50-300 μm, and finally into a tendon fiber with a diameter of 100-500 μm. Groups of fascicles are bounded by the epitendon and peritendon to form the tendon organ.

The collagen in tendons is held together with proteoglycan components including decorin and in compressed regions of tendon, aggrecan, which are capable of binding to the collagen fibrils at specific locations. The proteoglycans are interwoven with the collagen fibrils - their glycosaminoglycan (GAG) AORF TEXTBOOK OF ORTHOPAEDICS

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side chains have multiple interactions with the surface of the fibrils - showing that the proteoglycans are important structurally in the interconnection of the fibrils. The major GAG components of the tendon are dermatan sulfate and chondroitin sulfate which associate with collagen and are involved in the fibril assembly process during tendon development.

Dermatan sulfate is thought to be responsible for forming associations between fibrils while chondroitin sulfate is thought to be more involved with occupying volume between the fibrils to keep them separated and help withstand deformation. The dermatan sulfate side chains of decorin aggregate in solution and this behavior can assist with the assembly of the collagen fibrils. When decorin molecules are bound to a collagen fibril, their dermatan sulfate chains may extend and associate with other dermatan sulfate chains on decorin that is bound to separate fibrils therefore creating interfibrillar bridges and eventually causing parallel alignment of the fibrils.

The tenocytes produce the collagen molecules which aggregate end-to-end and side-to-side to produce collagen fibrils. Fibril bundles are organized to form fibres with the elongated tenocytes closely packed between them. There is a three-dimensional network of cell processes associated with collagen in the tendon. The cells communicate with each other through gap junctions and this signaling gives them the ability to detect and respond to mechanical loading.

Blood vessels may be visualized within the endotendon running parallel to collagen fibres, with occasional branching transverse anastomoses.The internal tendon bulk is thought to contain no nerve fibres but the epi- and peritendon contain nerve endings. Golgi tendon are present at the junction between tendon and muscle.

Fig 2.11: The basic common structures for ligaments and tendons; schematic presentation. Â The largest structure in the above schematic presentation is the tendon or the ligament. The ligament or tendon then is split into smaller entities called fascicles. The fascicle contains the basic fibril of the ligament or tendon and the fibroblasts which are the biological cells that produce the ligament or tendon.

There is a structural characteristic at this level that plays a significant role in the mechanics of ligaments

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and tendons: the crimp of the fibril. The crimp is the waviness of the fibril. This contributes significantly to the nonlinear stress strain relationship for ligaments and tendons and indeed for basically all soft collagenous tissues.

Fig 2.12; Muscle, tendon and bon.

Specific attributes of tendons Anatomy Tendons contain collagen fibrils (Type I), a proteoglycan matrix and fibroblasts (biological cells) that are arranged in parallel rows. The type 1 collagen that makes 86% of the tendon’s dry weight and consists of:  Glycine (~33%) Proline (~15%) Hydroxyproline (~15%, almost unique to collagen, often used to identify them).

Basic functions Tendons carry tensile forces from muscle to bone They carry compressive forces when wrapped around bone like a pulley

Blood supply Vessels in perimysium (covering of tendon) Periosteal insertion Surrounding tissues Tendon length varies in all major groups and from person to person. Tendon length is practically the discerning factor where muscle size and potential muscle size is concerned. For example, should all other relevant biological factors be equal, a man with a shorter tendon and a longer biceps muscle will have greater potential for muscle mass than a man with a longer tendon and a shorter muscle. Successful bodybuilders will generally have shorter tendons. Conversely in sports requiring athletes to excel in AORF TEXTBOOK OF ORTHOPAEDICS

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actions such as running or jumping, it is beneficial to have longer than average Achilles tendon and a shorter calf muscle.

Tendon length is determined by genetic predisposition and has not been shown to either increase or decrease in response to environment unlike muscles which can be shortened by trauma, use imbalances and a lack of recovery and stretching. Tendons have been traditionally considered to simply be a mechanism by which muscles connect to bone functioning simply to transmit forces. However, today, tendons are known to posses elastic properties of tendons allowing them to function as springs. This allows tendons to passively modulate forces during locomotion providing additional stability with no active work. It also allows tendons to store and recover energy at high efficiency. For example, during a human stride, the Achilles tendon stretches as the ankle joint dorsiflexes. During the last portion of the stride as the foot plantar-flexes, the stored elastic energy is released. Furthermore because the tendon stretches, the muscle is able to function with less or even no change in length allowing the muscle to generate greater force.

The mechanical properties of the tendon are dependent on the collagen fiber diameter and orientation.

The collagen fibrils are parallel to each other and closely packed but show a wave-like appearance due to planar undulations, or crimps on a scale of several micrometers. In tendons, the collagen I fibres have some flexibility due to the absence of Hydroxyproline and proline residues at specific locations in the amino acid sequence which allows the formation of other conformations such as bends or internal loops in the triple helix and results in the development of crimps. The crimps in the collagen fibrils allow the tendons to have some flexibility as well as a low compressive stiffness. In addition, because the tendon is a multi-stranded structure made up of many partially independent fibrils and fascicles, it does not behave as a single rod. This property also contributes to its flexibility.

The proteoglycan components of tendons also are important to the mechanical properties. While the collagen fibrils allow tendons to resist tensile stress, the proteoglycans allow them to resist compressive stress. The elongation and the strain of the collagen fibrils alone have been shown to be much lower than the total elongation and strain of the entire tendon under the same amount of stress, demonstrating that the proteoglycan-rich matrix must also undergo deformation, and stiffening of the matrix occurs at high strain rates. These molecules are very hydrophilic, meaning that they can absorb a large amount of water and therefore have a high swelling ratio. Since they are noncovalently bound to the fibrils, they may reversibly associate and disassociate so that the bridges between fibrils can be broken and reformed.

This process may be involved in allowing the fibril to elongate and decrease in diameter under tension.

Specific attributes of ligaments Ligaments link bones to other bones and provide support to joints. They allow normal range of movement to occur within a joint but prevent unwanted movement that would render the joint unstable. In order to fulfill this function, ligaments must possess immense mechanical tensile strength. Ligaments are classified as dense connective tissue, consisting of collagen fibres. The organisation of collagen fibres gives the ligament its tensile strength. Another function of ligaments is to provide proprioceptive input

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to the central nervous system in that it allows a person to know what position the joints are. This helps to perform the complex coordinated activities needed for sport. A normal ligament consists of: 90% Type 1 collagen 9% Type 3 collagen 1% fibroblast cells (the cells that produce collagen).

Type 1 collagen is mature collagen tissue and has the greatest tensile strength. Type 3 collagen is immature collagen tissue and does not provide a great deal of tensile strength to the ligament. After being laid down by fibroblast cells it takes approximately three months for Type 3 collagen to mature into Type 1 collagen. As with other cells in the body, this process of renewal occurs continually.

Microscopically collagen fibres in a ligament are arranged in a longitudinal pattern to resist the stress that is placed upon the ligament. This is similar to tendon in hierarchical structure though the collagen fibrils are slightly less in volume fraction and organization than tendon and there is also a higher percentage of proteoglycan matrix than tendons.

Blood supply to the ligaments It is mainly derived from microvasculature at the insertion sites and provides nutrition, necessary for matrix synthesis and repair, for cell populations.

As with all biological tissues the hierarchal structure of ligaments and tendons has a significant influence on their mechanical behavior but unlike bone. However, not as much experimental, statistical, or analytical data is available on the structure, function and relationships for ligaments and tendons.

This is for two reasons: The hierarchical structure of ligaments and tendons is much more difficult to quantify than bone, and Ligaments and tendons exhibit both nonlinear and viscoelastic behavior even under physiologic loading, which is more difficult to analyze than the linear behavior of bone.

The Nervous System The nervous system consists of billions of nerve cells with processes that run throughout the body like strings making connections with the brain, other parts of the body and often with each other. The system is divided into the central nervous system of the brain and spinal cord and the peripheral nervous system. Peripheral nerves consist of bundles of nerve fibers. These fibers are wrapped with many layers of tissue composed of a lipid substance called myelin. These layers form the myelin sheath which speeds the conduction of nerve impulses along the nerve fiber. Nerves conduct impulses at different speeds depending on their diameter and on the amount of myelin around them.

The nervous system consists of: The somatic nervous system The autonomic nervous system.

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Somatic nervous system This system consists of nerves that connect the brain and spinal cord with muscles controlled by conscious effort (voluntary or skeletal muscles) and with sensory receptors in the skin. (Sensory receptors are specialized endings of nerve fibers that detect information in and around the body).

Autonomic nervous system This system connects the brain stem and spinal cord with internal organs and regulates internal body processes that require no conscious effort. Examples are the rate of heart contractions, blood pressure, the rate of breathing, the amount of stomach acid secreted and the speed at which food passes through the digestive tract. The autonomic nervous system has two divisions: Sympathetic division: Its main function is to prepare the body for stressful or emergency situations (fight or flight).

Parasympathetic division: Its main function is to prepare the body for ordinary situations.

These divisions work together usually with one activating and the other inhibiting the actions of internal organs. For example, the sympathetic division increases pulse, blood pressure and breathing rates and the parasympathetic system decreases each of them.

Fig 2.13: Typical nerve cell

A nerve cell (neuron) consists of a large cell body and nerve fibers, one elongated extension (axon) for sending impulses and usually many branches (dendrites) for receiving impulses. Each large axon is surrounded by oligodendrocytes in the brain and spinal cord and by Schwann cells in the peripheral nervous system. The membranes of these cells consist of a fat (lipoprotein) called myelin. The membranes are wrapped tightly around the axon, forming a multilayered sheath. This myelin sheath resembles insulation, such as that around an electrical wire. Nerve impulses travel much faster in nerves with a myelin sheath than in those without one. If the myelin sheath of a nerve is damaged, nerve transmission slows or stops.

Cranial and spinal nerves Nerves that connect the brain with the eyes, ears, nose, and throat and with various parts of the head, neck, and trunk are called cranial nerves. There are 12 pairs of them. Nerves that connect the spinal cord with other parts of the body are called spinal nerves. The brain communicates with most of the body through the spinal nerves. There are 31 pairs of them, located at intervals along the length of the spinal

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cord. Several cranial nerves and most spinal nerves are involved in both the somatic and autonomic parts of the peripheral nervous system.

Spinal nerves emerge from the spinal cord through spaces between the vertebrae. Each nerve emerges as two short branches (called spinal nerve roots); one at the front of the spinal cord and one at the back.

Motor (anterior) nerve root The motor root emerges from the front of the spinal cord. Motor nerve fibers carry commands from the brain and spinal cord to other parts of the body particularly to skeletal muscles.

Sensory (posterior) nerve root The sensory root enters the back of the spinal cord. Sensory nerve fibers carry sensory information (about body position, light, touch, temperature, and pain) to the brain from other parts of the body. The sensory nerve fibers from a specific sensory nerve root carry information from a specific area of the body called a dermatome.

After leaving the spinal cord, the corresponding motor and sensory nerve roots join to form a single spinal nerve. Some of the spinal nerves form networks of interwoven nerves called nerve plexuses. In a plexus, nerve fibers from different spinal nerves are sorted and recombined so that all fibers going to or coming from one area of a specific body part are put together into one nerve. There are two major nerve plexuses: the brachial plexus, which sorts and recombines nerve fibers traveling to the arms and hands and the Lumbosacral plexus which sorts and recombines nerve fibers going to the legs and feet.

Bibliography and further reading 1. Baron R. E. Anatomy and ultra structure of bone in primer on Metabolic Bone Diseases and Disorders of Mineral Metabolism. 3rd ed. Philadelphia, Pa: Lippincott Raven; 1996.

2. Cooper, R. R.; Milgram, J. W.; and Robinson, R. A. “Morphology of the Osteon: An Electron Microscopic Study,” Journal of Bone and Joint Surgery; 1996; 48:1239-1271.

3. McCarthy I. The physiology of bone blood flow: A review. J. Bone Joint Surg. Am. 2006; 88:4–9.

4. McKibbin, B. The biology of fracture healing in long bones. Journal of bone and joint surgery.

British volume (London),1978; 60-B, 150-62.

5. Miller M. D. Miller’s Review of Orthopedics 2nd ed.W.B. Saunders;1996.

6. Mow V. C. Flatow E. L. and Ateshian G. A. Biomechanics. In: Orthopaedic Basic Science.

Rosemont, Ill: American Academy of Orthopaedic Surgeons: 2002; 148-158.

7. Pfeiffer, S., Crowder, C., Harrington, L. and Brown, M. “Secondary Osteon and Haversian Canal Dimensions as Behavioral Indicators,” American Journal of Physical Anthropology, 206; 131 (4): 460 - 468.

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8. Rhinelander FW: The normal microcirculation of diaphyseal cortex and its response to fracture.

J Bone Joint Surg 50A:784, 1968 9. Rosier R. N., Bukata S. V. Bone metabolism and metabolic bone diseases. In: Orthopaedic Knowledge Update 7. Rosemont, Ill: American Academy of Orthopaedic Surgeons: 2002; 141154.

10. Wolff, J. The Law of Bone Remodeling. Springer Verlag, Heidelberg; 1986.

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CHAPTER THREE

3

Evaluation of the orthopedic patient

Introduction In this chapter the various steps that are necessary in arriving at a diagnosis of an orthopedic condition are outlined. Though they are described as if they are independent, these steps are not exclusive and the order in which they appear here is a reflection of the traditional approach in reporting rather than the preference or importance of eliciting them. In this book they are presented in the manner one will present a patient’s details to a third party.

Signs and symptoms A symptom is defined as any feature which is noticed by the patient. A sign is a feature noticed by other people. A patient presents with a symptom of fever; the health worker confirms the temperature of 40 degrees as a sign. A skin rash may be noticed by either the patient as a symptom or the healthcare professional as a sign; since it is noticed by both, then the rash is both a symptom and a sign. Discussion on the management of each specific symptoms and signs is not included in this chapter.

Step one: History taking Over 80% of the clinical diagnosis of a patient’s illness can be made on the history and physical examination alone. As the initial step in the evaluation of a patient it is very important that an accurate history covering all the pertinent points of the patients’ condition is taken. The approach to the patient should be with an open mind. Patients will only impart the necessary information if they feel confident and in control. In as much as the history is about the patient’s illness in his own words, the medical notes are prepared after consideration of all the findings gathered during each step of evaluation.

I. Demographic data The evaluation begins with identity of the patient; the subject is a human being with a name and not a case with a disease. The geographical origin, the race and any other peculiar aspects which may have a bearing on the prevalence of the conditions being suspected are sought after.

The sex of the patient is also important: some conditions occur exclusively in certain sexes, some have

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a higher incidence in one gender and for others, sex may need to be taken into account when making a plan of management.

Age is especially important: Some diseases are more common at some age groups and others occur exclusively within certain age groups. Also, similar symptoms may point to different diagnoses based on the age of presentation. Age also influences management options.

II. Presenting complaints.

These are also referred to as the symptoms. They are written in the patient’s own words and not in medical terms, for example “Pain in the left forearm”, should not be described as “neuropathic pain located in the distal part of the left ulna”. The duration of complaint is also included.

Diseases may reveal themselves as incidental findings; without showing signs and symptoms, this is the situation when a condition that is not of concern to the individual becomes evident during screening or evaluation for other conditions.

III. History of presenting complaint This expands on the presenting complaint in terms of nature of onset, its progression, associated symptoms, relieving or exacerbating factors and any other peculiarities.The following are the possible ways in which patients with orthopedic diseases may present:

Trauma History of injury is the commonest complaint and is in fact the presentation in nearly all the problems caused by trauma. More evaluation of injury is guided by additional symptoms such as the site of pain, the presence of bruising and swelling, deformity and continued use of the part affected.

Pain

“There would be no hospitals without pain” Anonymous.

As a matter of fact, most patients will only seek medical attention when they are in pain.

“Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage”. (The International Association for the Study of Pain (I.A.S.P).

Pain signals actual or potential injury to the body and is conveyed to the brain by sensory neurons. The International Association for the Study of Pain (I.AS.P) classifies pain according to: Region of the body involved (abdomen, lower limbs ...)

System whose dysfunction may be causing the pain (nervous, gastrointestinal ...)

Duration and pattern of occurrence Intensity and time since onset Etiology Description of pain based on the origin (initiation) of the stimulus: Nociceptive, neuropathic, psychogenic, breakthrough pain, incident pain and abnormal pain.

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Nociceptive Pain-sensing neurons are called nociceptors. They are capable of transmitting a pain signal to the brain that indicates the location, nature, and intensity of the pain. For example, stepping on a nail sends an information-packed message to the brain: the foot has experienced a puncture wound that hurts a lot. Nociceptive pain is caused by stimulation of peripheral nerve fibers that respond only to stimuli approaching or exceeding harmful intensity (nociceptors). Virtually every surface and organ of the body is served with these neurons whose central part of these cells is located in the spine.

Nociceptors are classified according to the stimulus that prompts them to transmit a pain signal (mode of noxious stimulation): Thermoreceptive nociceptors are stimulated by temperatures (“thermal” -heat or cold).

Mechanoreceptive nociceptors respond to a pressure stimulus “- “mechanical” (crushing, tearing...)

Chemo-receptors “chemical” (iodine in a cut, chili powder in the eyes).

Polymodal nociceptors are the most sensitive and can respond to temperature and pressure.

They also respond to chemicals released by the cells in the area from which the pain originates.

Pain perception also varies depending on the location of the pain. The kinds of stimuli that cause a pain response on the skin include pricking, cutting, crushing, burning, and freezing. These same stimuli would not generate much of a response in other organs such as the intestine.

Pain may also be divided into “visceral,” “deep somatic” and “superficial somatic” pain. Visceral pain is diffuse, difficult to locate and often referred to a distant, usually superficial, structure. It may be accompanied by nausea and vomiting and may be described as sickening, deep, squeezing, and dull.

Deep somatic pain is initiated by stimulation of nociceptors in ligaments, tendons, bones, blood vessels, fasciae and muscles, and is dull, aching, poorly-localized pain. Examples include sprains and broken bones. Superficial pain is initiated by activation of nociceptors in the skin or other superficial tissue, and is sharp, well-defined and clearly located. Examples of injuries that produce superficial somatic pain include minor wounds and minor (first degree) burns.

Neuropathic Neuropathic pain is caused by damage or disease affecting any part of the nervous system involved in bodily feelings (the somatosensory system). Peripheral neuropathic pain is often described as “burning,” “tingling,” “electrical,” “stabbing,” or “pins and needles”. Bumping the “funny bone” elicits acute peripheral neuropathic pain.

Psychogenic Psychogenic pain, also called psychalgia or somatoform pain is pain caused, increased, or prolonged by mental, emotional, or behavioral factors. Headache, back pain, and stomach pain are sometimes diagnosed as psychogenic. Sufferers are often stigmatized because both medical professionals and the general public tend to think that pain from a psychological source is not “real”. However, it is no less actual or hurtful than pain from any other source.

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Breakthrough pain This is pain that comes on suddenly for short periods of time and is not alleviated by the patients’ normal pain suppression management. It is common in cancer patients who commonly have a background level of pain controlled by medications.

Incident pain Incident pain is pain that arises as a result of activity, such as movement of an arthritic joint or stretching a wound.

Abnormal pain Often arises from some damage to the nervous system. These include: Allodynia which refers to a feeling of pain in response to a normally harmless stimulus.

Hyperalgesia is somewhat related to Allodynia in that the response is to a painful stimulus but it is more extreme than would be expected.

Phantom limb pain occurs after a limb is amputated whereby the nervous system continues to perceive pain originating from the area.

The second way of describing pain is based on duration; acute or chronic pain. Acute pain is usually transitory, lasting only until the noxious stimulus is removed or the underlying damage or pathology has healed, but some painful conditions, such as rheumatoid arthritis, peripheral neuropathy, cancer and idiopathic pain, may persist for years. Pain that lasts a long time is called chronic. Traditionally, the distinction between acute and chronic pain is based on the interval of time from onset being 3 months and 6 months respectively. Some theorists and researchers have however placed the transition from acute to chronic pain at 12 months. Others apply acute, to pain that lasts less than 30 days, sub acute to pain that lasts from one to six months and chronic to pain of more than six months duration. A popular alternative distinction defines chronic pain as “pain that extends beyond the expected period of healing�.

Depression usually accompanies chronic pain.

A third way of describing pain is based on its characteristics; Severity of the Pain Grade I: Can be ignored (mild) Grade II: Cannot be ignored (moderate) Grade III: Cannot be ignored and is present most of the time (severe) Grade IV: Totally incapacitating (excruciating) A fourth category based on neurochemical mechanism has been proposed.

Lump A lump is a protuberance or localized area of swelling that can occur anywhere on the body. It can also be described as a bump, nodule, contusion, tumour and cyst. Lumps can be caused by any number of conditions, including infections, inflammation, tumours or trauma. They may be single or multiple, soft or firm, painful or painless and may grow rapidly, slowly or may not change in size. Establish the development, progression, mobility, color, temperature, pain, associated symptoms and recurrence or intermittency.

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Ulcer Skin ulcers are open sores that are often accompanied by the sloughing-off of inflamed tissue. They can be caused by a variety of events, such as trauma, exposure to heat or cold, problems with blood circulation, or irritation from exposure to corrosive material. Pressure ulcers, also known as decubitus ulcers or bedsores, are skin ulcers that develop on areas of the body where the blood supply has been reduced because of prolonged pressure. Other health conditions that can cause skin ulcers include chronic venous insufficiency, diabetes, infection, and peripheral vascular diseases. Skin ulcers may become infected, with serious health consequences.

It is important to determine the site, shape, size, margins, the floor and base of an ulcer.

Some characteristic shapes of the edges of ulcers include: Non-specific ulcer Tuberculous ulcer with an undermined edge Basal-cell carcinoma (rodent ulcer) with rolled up edge which may exhibit small blood vessels Epithelioma with heaped up, everted edge and irregular thickened base (fig 32).

Syphilis with punched out edge and thin base.

Fig 3.1: Diabetic ulcer on the dorsum of the foot.

Fig 3.2: Epithelioma; squamous cell carcinoma notice everted edges.

Stiffness Stiffness is a very general term for a common but abnormal condition in which a person feels a sensation of discomfort, inflammation, soreness, or pain. Stiffness is often occurs in the joints, but can also occur in muscles and other parts of the body. It is a symptom of a wide variety of mild to serious diseases, disorders and conditions. It can occur in any age group or population as a result of infection, trauma, malignancy, autoimmune diseases, and other abnormal processes. It can indicate a relatively benign condition or a serious condition that can even be life-threatening such as rheumatoid arthritis, spinal cord injury or meningitis. Depending on the cause, it can occur suddenly and severely or can be chronic and ongoing over a long period of time.

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Locking “In normal situations, the knee is a smoothly operating mechanism, like a door hinge swinging open and shut”. Locking is a symptom that occurs when a patient cannot bend or straighten their knee. The locking can either be due to something physically blocking motion of the knee, or pain preventing normal knee motion.

One way to determine if there is something physically blocking knee motion is to inject the knee with a numbing medication. True locking of the knee: something that physically prevents the knee from fully straightening out or bending and holds the knee rigidly in place. It’s often painful and can be quite frightening. Usually, the locking is caused by a torn piece of cartilage, or possibly a loose bone fragment resulting from a bone disorder called osteochondritis dissecans. Sometimes the obstruction is from a misalignment of the bones and muscles around the knee.

Many times, say following an injury, a person will experience an inability to move the knee that can feel like a locking of the knee, but in reality there’s nothing physically interfering with the movement of that knee. This is known as a pseudo-lock.

Deformities This may be physiological variations from the normal and some may disappear with growth. Descriptions such as knock knees, bow legs, hunch back and flat feet are easier for the patient to relay. When single bone or joint is involved they may simply be described as crooked. Progression of the deformity usually signifies seriousness of the condition.

Muscle weakness, change in sensibility, instability Muscle weakness, or myasthenia, is a decrease in strength in one or more muscles. It is a common symptom of: Muscular disorders such as muscular dystrophy and dermatomyositis Neurological disorders such as Guillain-Barre syndrome (an autoimmune nerve disorder), amyotrophic lateral sclerosis (also known as Lou Gehrig’s disease), stroke, a pinched nerve and rarely, Charcot-Marie-Tooth disease.

Autoimmune neuromuscular disorder such as myasthenia gravis.

Metabolic disorders such as Addison’s disease and hyperthyroidism Other possible causes include: paralytic shellfish poisoning, botulism, and low levels of potassium in the blood.

Depending on the cause, weakness may occur in one muscle, a group of muscles, or all the muscles, and it may be accompanied by pain, atrophy, cramping, or other types of muscular symptoms.

Paresthesia Paresthesia is an abnormal condition in which one feels a sensation of burning, numbness, tingling, itching or prickling. It can also be described as pins-and-needles or skin-crawling sensation and most often occurs in the extremities, such as the hands, feet, fingers, and toes. It may be accompanied by pain and other symptoms.

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Chronic paresthesia or intermittent paresthesia over a long period of time is generally a sign of a neurological disease or traumatic nerve damage. Paresthesia usually arises from nerve damage due to infection, inflammation, trauma, or other abnormal process such as stroke and tumours.

Causes of paresthesia include: Sitting or standing in the same position for a long time Injury to a nerve Pressure on the spinal nerves, such as from a herniated disk Pressure on peripheral nerves from enlarged blood vessels, tumours, scar tissue, or infection Shingles or herpes zoster infection Lack of blood supply to an area (for example, from atherosclerosis or frostbite) Other medical conditions, including: Carpal tunnel syndrome, Diabetes, Migraines, Multiple sclerosis, Seizures. Stroke, Transient ischemic attack, sometimes called a “ministroke”, hypothyroidism, and Raynaud’s phenomenon.

Paralysis Paralysis is the loss of muscle function in part of the body. It happens when something goes wrong with the way messages pass between the brain and muscles. It can be complete or partial, bilateral or unilateral, diffuse or focal. Paralysis can be accompanied by sensory loss in the affected area. Most paralysis is due to strokes or injuries such as spinal cord injury or a broken neck. Other causes of paralysis include: Nerve diseases such as amyotrophic lateral sclerosis Autoimmune diseases such as Guillain-Barre syndrome Bell’s palsy, which affects muscles in the face Polio used to be a cause of paralysis, but it no longer occurs Temporary paralysis occurs during REM sleep, and dysregulation of this system can lead to episodes of waking paralysis.

Some drugs that interfere with nerve function, such as curare, can also cause paralysis.

Pseudo paralysis is voluntary restriction or inhibition of motion because of pain, in coordination, or other cause, and is not due to actual muscular paralysis. In infants, it may be a symptom of congenital syphilis.

IV. Past medical history Enquire about past medical illnesses as the patients may not appreciate their role in causation of the current illness. These illnesses may also influence surgical decisions and choice of anesthesia. In particular, enquire about asthma, myocardial infarction, diabetes, hypertension, stroke and jaundice.

V. Drug history Regular medication that the patient has been taking prior to coming to hospital needs to be obtained as the patient may need to continue taking these drugs, up to and maybe even during surgery.

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VI. Family history This is not of much relevance to trauma cases, as in other causes such as the so called rheumatic diseases. It is very important to ask about any congenital bone or metabolic diseases as well as any bone or joint disorders.

VII. Social history This is often overlooked, despite being an essential part of the history. It gives an indication of the patient’s quality of life and previous level of functioning. Enquire about the patient’s job, living arrangements, children and hobbies. Also enquire about smoking, alcohol and any illicit drug use.

VIII. Systemic enquiry Make sure that all the systems are covered. Ask about all the obvious and not so obvious (for example pregnancy) symptoms associated with each system.

Step two: Examination General examination It seeks to find out the overall health of the individual.

Vital signs: temperature, respiratory rate, blood pressure and pulse.

The appearance and nutritional status of the individual as well as the presence of anaemia, jaundice, generalized lymphadenopathy and skin lesions are important.

Local examination of the limb or presenting system Most orthopedic conditions are localized to a particular area; the extremities or the axial skeleton. The site and side must be adequately described. When it is in the upper limb, information on handedness is also important. Evaluation proceeds in this manner: Inspection Palpation Movements Special tests

Inspection Watch the patient’s movements as he walks into the examination room confirming any suspicious gait later in the examination.Notice if there is any limb length discrepancy. Describe the position of the limb and joints when standing, moving and lying on the examination couch.

The site, size, shape, and visual appearance of a Fig 3.3: Inspection; the foot at risk in a diabetic, hammer toes signifying motor impairment, prominent lesion can be made out on inspection. vessels suggesting autonomic affection

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Palpation (feel) This includes superficial palpation for warmth, dryness as well as sensory testing.

Sensory testing: S0- Absence of all modalities of sensation in the area exclusively supplied by the affected nerve.

S1- Recovery of deep pain sensation.

S2- Recovery of protective sensation (skin touch, pain and thermal sensation) S3- Recovery of protective sensation with accurate localization. Sensitivity and hypersensitivity to cold are usual.

S4-Recovery of ability to recognize objects and texture; any residual cold sensitivity and hypersensitivity should now be minimal. In the case of the hand- recovery of two point discrimination to less than 8mm.

S5足-Normal sensation Deep palpation addresses tenderness, mobility of masses to determine attachment to underlying structures including bone and the skin, regional lymphadenopathy and peripheral pulses.

Test movements Test if the range of movements of joints is in question. If you notice any impairment, do motor assessment beginning with bulk, tone and muscle power.

Motor Assessment: M0-No active motion can be detected.

M1-A flicker of muscle contraction can be seen or felt on palpation, but the activity is insufficient to cause any joint movement.

M2-Contraction is very weak, but can produce movement so long as the weight of the part can be countered by careful positioning of the limb.

M3-Contraction is still weak but can produce movement against gravitational resistance.

M4-Strength is not full, but can produce movement against gravity and some added resistance.

M5-Normal power is present.

Reflex testing: Muscle stretch (also called tendon tap) reflex testing can be used to detect nerve root compression, peripheral neuropathy, or central nervous system (CNS) pathology.

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Myotatic Reflex Arc Components: Receptor (muscle spindle) Afferent axon Spinal cord synapse Efferent axon Effector (homonymous muscle)

Technique Quick stretch of tendon via hammer taps.

To evaluate, compare with normal side.

Hypoactive = root compression or peripheral neuropathy Hyperactive = CNS pathology.

Table 3.1: Preferred sites of reflex testing and response.

Muscle stretch (deep tendon) reflexes Reflex

Stimulus

Response

Biceps

Tap biceps tendon

Contraction of biceps

Brachioradialis (periosteradial)

Tap styloid process of radius (insertion of Brachioradialis)

Flexion of elbow and pronation of forearm

Jaw (maxillary)

Tap mandible in half-open position

Closure of jaw

Patellar

Tap patellar tendon

Extension of leg at knee

Tendocalcaneus

Tap Achilles tendon

Plantar flexion at ankle

Triceps

Tap triceps tendon

Extension of elbow

Wrist extension

Tap wrist extensor tendons

Extension of wrist

Wrist flexion

Tap wrist flexor tendon

Flexion of wrist

Useful reflexes and the nerve roots being tested: Biceps Brachii C5 Brachioradialis C6 Triceps Brachii C7 Quadriceps Femoris L2 Gastroc- Soleus S1

Grading of reflexes 0 - no response 1 - Low normal

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2 3 4

- normal - Brisk - Very brisk Clonus

Babinski sign When present, suspect CNS pathology.

Technique - non painful stroke on lateral border of plantar surface of foot; dorsiflexion of the great toe with fanning of remaining toes is a positive Babinski sign.

Special tests Special examination techniques relevant to a particular condition are carried out when the condition is suspected; Ortolani test in congenital dysplasia of the hip, straight leg raising test in low back pain.

Examination of the Hip Differences between the lengths of the upper and/or lower arms and the upper and/or lower legs are called limb length discrepancies (LLD). Except in extreme cases, arm length differences cause little or no problem in how the arms function. For the lower limb, assess: True verses apparent discrepancy Source of discrepancy Magnitude of discrepancy.

Real (or True length) This is the measure from anterior superior iliac spine to medial malleolus. To obtain accurate True Length measurements, the two limbs must be placed in comparable positions relative to pelvis. Metal end of tape is placed immediately distal to anterior superior iliac spine and pushed up against it. Tip of index is placed immediately distal to medial malleolus and pushed up against it. Thumb nail is then brought down against tip of index with tape in between. Point of measure is indicated by thumb nail.

Apparent or False Discrepancy It is only necessary when there is incorrectable pelvic tilt and this is taken from the xiphisternum to the medial malleolus. The legs must be placed parallel to one another and in line with trunk; square pelvis and hips neutral. You should beware of fixed flexion deformity; put the legs in equivalent positions for both leg length measurements to medial malleolus for apparent amount of apparent shortening is the sum of the true shortening plus the shortening due to fixed deformity. It is the apparent shortening that matters to the patient.

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Assess if Discrepancy is above or below the knee Galleazi Test Knees should be positioned at 90° with hips and ankles at 45°.

Put malleoli at same level and look at the level of knees and parallelism of femora & tibia. If the knees are at different levels and the tibias are parallel, the discrepancy is not above knee (it is in the tibia). If the femora parallel to the discrepancy is not below the knee (it is in the femur).

Assessment of Shortening above Greater Trochanter Bryant’s triangle This is constructed with the patient supine as a rough means of detecting disturbance of the normal anatomy of the femoral head and neck. It is a right-angled triangle, with the following sides: a. A straight line connecting the greater trochanter of the femur with the anterior superior iliac spine; b. A vertical line down from the anterior superior iliac spine towards the bed; c. A horizontal line starting at the greater trochanter, and meeting side B. The length of C is gauged on each side, and the sides compared. Pathology of the femoral head or neck which displaces the greater trochanter will tend to shorten this side of the triangle.

Nelaton’s line A line drawn from the anterior superior iliac spine to the tuberosity of the ischium; normally the great trochanter lies in this line, but in cases of iliac dislocation of the hip or fracture of the neck of the femur the trochanter is felt above the line 2.

Procedure Patient lying on sound side ASIS to ischial tuberosity by the shortest route (normally crosses the top of the greater trochanter). Compare one side with the other.

Schoemaker’s line Patient lies supine Draw a line from greater trochanter through Anterior Superior Iliac Spine Projection from each side should cross proximal to umbilicus If there is shortening above greater trochanter then lines will cross below umbilicus.

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Muscle power assessment Different muscle group impairment will suggest the nerves affected; Abductors (gluteal nerves) Adductors (obturator nerve) Flexors (femoral nerve).

Impingement test It is carried out by passively moving the hip joint in flexion (to 90°), internal rotation, and adduction.

The test is regarded as being positive on reproduction of groin pain.

FABER (Flexion, Abduction, External Rotation) test The hip joint is passively flexed, abducted, & externally rotated with the knee flexed (figure-of-fourposition). The ankle is brought to rest just above the contra lateral knee & slight pressure is applied to the medial side of the knee, approximating it to the examination table. The test is regarded as being positive on production of groin pain.

Sacroiliac joint Lateral pelvic compression for Sacroiliac Joint - Tenderness in assessment of pelvic fracture suggests posterior elements disruption.

Gaenslin’s test - The patient is supine, with the buttock of the involved side projecting off the bed. The hips are maximally flexed, and then the same leg is allowed to drop over the side of the table into full extension (with the other leg still in full flexion). Pain in the SIJ is positive.

On the side Ober’s test (for iliotibial tract) is a test for abduction contracture.

Abduct the hip & flex the knee to relax the Iliotibial tract allow hips to come together if they do then there is no abduction contracture.

Perform Abductor power test for active abduction as you palpate contraction over the grade the power.

Hip extension; femoral stretch test.

Prone position Check for Gluteal bulk and rotation in extension.

Other areas to be evaluated in hip disease include spine (a spinal cause for the patient’s pain must be considered, and if present, its proportional cause of the symptoms curtailed), the Abdomen (for abdominal aortic aneurysm AAA), Per Rectal examination (for prostate) and the knee as well as other large joints.

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Examine related systems Examine other systems Make an impression and the differential diagnosis.

Step three: Investigations Laboratory a) Routine laboratory investigations include: Hemoglobin White blood cell count (Total/Differential) C Reactive Protein Erythrocyte Sedimentation Rate Urinalysis Stool Ova/Cysts b) Special Tests are useful in determination of the extent of the illness as well as for management options.

Urea/Electrolytes Liver Function Tests Markers Some disease conditions, mainly tumours, present elaborate biochemical substances in the body systems that can be assayed. This may raise suspicion of or outrightly confirm the condition. They are also useful for follow up. Exclusion investigations are those that are done to rule out a certain condition, for example, a child suspected to have Osteomyelitis may also have a fever thus blood slide for malaria may need to be taken. c) Baseline investigations - These are the initial mandatory tests done prior to starting treatment. They are also useful in follow up. d) Definitive investigations These are confirmatory tests including histological diagnosis.

Radiological Tests Plain x-rays Remember the rule of twos: For the limbs, include the joint below and above At least two views - postero-anterior and lateral For children, compare with the normal limb.

Films may need to be taken on more than one occasion.

Tomograms where there are no CT scans.

Ultrasound for joints, soft tissues and the abdomen.

Computed tomography for metastasis. This gives a good assessment of bone pathology.

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Magnetic Resonance Imaging is superior to the other modes of imaging in evaluation of soft tissue pathology.

Radioisotope scanning.

Functional studies of nerve conduction include nerve conduction tests and Electromyography (EMG).

At the end of the evaluation, the diagnosis or impression is stated followed by the differential diagnosis.

The existence of more than one condition should be appreciated and noted.

Prognosis: an attempt is made to stage the disease and hence the expectation.

Step four: Management and Prevention Having completed the above sequence, a clear outline of both supportive and definitive management as well as preventive measures completes the evaluation of the orthopedic patient.

Bibliography and references 1. Chinnery P. F. Muscle diseases. In: Goldman L, Ausiello D, eds. Cecil Medicine. 24th ed.

Philadelphia, Pa: Saunders Elsevier: 2011; chap 429.

2. Griggs R. C., Jozefowicz R. F., Aminoff M. J. Approach to the patient with neurologic disease.

In: Goldman L, Ausiello D, eds. Cecil Medicine. 24th ed. Philadelphia: Saunders Elsevier: 2011; chap 403.

3. Howard F. M. Electromyography and conduction studies in peripheral nerve injuries. Surg Clin North Am; 1972; 52: 1343.

4. Bonica J. J.(Ed.), Advances in neurology. Vol. 4. Pain. New York: Raven Press, 1974. Pp.563572. Orne, M. T. Hypnosis. In G. Lindzey, C. Hall, & R 5. Kimura J. Electro diagnosis in Diseases of Nerve and Muscle: Principles and practice A Davis, Philadelphia; 1983.

6. Merskey H. & Bogduk N. Classification of Chronic Pain. 2 ed. Seattle: International Association for the Study of Pain; 1994.

7. NivD, KreitlerS, DiegoB, Lamberto A. The Handbook of Chronic Pain. Nova Biomedical Books; 2007. ... Classification of ChronicPain. 2 ... taxonomy of chronicpain 8. Reider B., Ed. The Orthopaedic Physical Examination. Philadelphia, Saunders: 1999; 2–17.

9. Resnick D. & Niwayama G. Diagnosis of bone and joint disorders, vol 1, Diagnostic Techniques, 2nd edn. W. B. Saunders, Philadelphia; 1988.

10. Rothstein, J.M., S.H. Roy, and S.L. Wolf . The Rehabilitation Specialist’s Handbook, 2nd ed.

Philadelphia: F.A. Davis Co; 1998.

11. Rowland L. P. Diagnosis of pain and paresthesia. In: Rowland LP, ed.Merritt’s Neurology. 11th ed. Baltimore, Md: Lippincott Williams & Wilkins: 2005; chap 5.

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12. Schwartz, M. A., & William S. Textbook of Physical Diagnosis: History and Examination, 3rd ed. Philadelphia, PA: Saunders; 1998.

13. Watt L.. Musculoskeletal system in nuclear medicine: Applications to surgery (Eds ER Davies, WEG Thomas). Castle house Pub, Tunbridge Wells; 1988; 219-253.

14. Woolf C. J. et al. Towards a mechanism-based classification of pain: 1998; 77(3):227–9.

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