Tachdjian’s Pediatric Orthopaedics [1, 5 ed.] 9781437715491, 9781455737406

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Tachdjian’s Pediatric Orthopaedics From the Texas Scottish Rite Hospital for Children

Tachdjian’s Pediatric Orthopaedics From the Texas Scottish Rite Hospital for Children FIFTH EDITION Volume 1

John A. Herring,

MD

Chief of Staff Emeritus Texas Scottish Rite Hospital for Children Professor of Orthopaedic Surgery The University of Texas Southwestern Medical Center Dallas, Texas

1600 John F. Kennedy Blvd. Ste. 1800 Philadelphia, PA 19103-2899

TACHDJIAN’S PEDIATRIC ORTHOPAEDICS FROM THE TEXAS SCOTTISH RITE HOSPITAL FOR CHILDREN

ISBN: 978-1-4377-1549-1 Volume 1 PN: 9996074501 Volume 2 PN: 9996074560 Volume 3 PN: 9996074625

Copyright © 2014, 2008, 2002, 1990, 1972 by Saunders, an imprint of Elsevier Inc. All rights reserved. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system, without permission in writing from the publisher. Details on how to seek permission, further information about the Publisher’s permissions policies, and our arrangements with organizations such as the Copyright Clearance Center and the Copyright Licensing Agency, can be found at our website: www.elsevier.com/permissions. This book and the individual contributions contained in it are protected under copyright by the Publisher (other than as may be noted herein).

Notices Knowledge and best practice in this ield are constantly changing. As new research and experience broaden our understanding, changes in research methods, professional practices, or medical treatment may become necessary. Practitioners and researchers must always rely on their own experience and knowledge in evaluating and using any information, methods, compounds, or experiments described herein. In using such information or methods, they should be mindful of their own safety and the safety of others, including parties for whom they have a professional responsibility. With respect to any drug or pharmaceutical products identiied, readers are advised to check the most current information provided (i) on procedures featured or (ii) by the manufacturer of each product to be administered, to verify the recommended dose or formula, the method and duration of administration, and contraindications. It is the responsibility of practitioners, relying on their own experience and knowledge of their patients, to make diagnoses, to determine dosages and the best treatment for each individual patient, and to take all appropriate safety precautions. To the fullest extent of the law, neither the Publisher nor the authors, contributors, or editors assume any liability for any injury and/or damage to persons or property as a matter of products liability, negligence or otherwise, or from any use or operation of any methods, products, instructions, or ideas contained in the material herein. Library of Congress Cataloging-in-Publication Data Tachdjian’s pediatric orthopaedics : from the Texas Scottish Rite Hospital for Children / [edited by] John A. Herring.—Fifth edition. p. ; cm. Pediatric orthopaedics Includes bibliographical references and index. ISBN 978-1-4377-1549-1 (3 vol. set, 2 vol. hardcover : alk. paper) I. Herring, John A., editor of compilation. II. Texas Scottish Rite Hospital for Children, issuing body. III. Title: Pediatric orthopaedics. [DNLM: 1. Child. 2. Orthopedic Procedures. 3. Infant. 4. Musculoskeletal Diseases—surgery. WS 270] RD732.3.C48 618.92′7—dc23 2013030018 Senior Content Stategist: Don Scholz Senior Content Development Specialist: Jennifer Shreiner Publishing Services Manager: Anne Altepeter Senior Project Manager: Doug Turner Project Manager: Louise King Design Manager: Louis Forgione Printed in the United States of America Last digit is the print number: 9

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CONTRIBUTORS

Richard C. Adams, MD Medical Director of Developmental Disabilities Texas Scottish Rite Hospital for Children Associate Professor of Pediatrics The University of Texas Southwestern Medical Center Neurodevelopmental Pediatrician Parkland Medical Center Dallas, Texas

Mark C. Gebhardt, MD Frederick W. and Jane Ilfed Professor of Orthopaedic Surgery Harvard Medical School Chief of Orthoapedic Surgery Beth Israel Deaconess Medical Center Associate in Orthopaedic Surgery Children’s Hospital Boston Boston, Massachusetts

Megan E. Anderson, MD Instructor in Orthopaedic Surgery Harvard Medical School Department of Orthopaedic Surgery Beth Israel Deaconess Medical Center Children’s Hospital Boston Boston, Massachusetts

John A. Herring, MD Chief of Staff Emeritus Texas Scottish Rite Hospital for Children Professor of Orthopaedic Surgery The University of Texas Southwestern Medical Center Dallas, Texas

John G. Birch, MD Assistant Chief of Staff Texas Scottish Rite Hospital for Children Professor of Orthopaedic Surgery The University of Texas Southwestern Medical Center Dallas, Texas

Christine Ho, MD Staff Orthopaedist Texas Scottish Rite Hospital for Children Assistant Professor of Orthopaedic Surgery The University of Texas Southwestern Medical Center Dallas, Texas

Alexander Cherkashin, MD Director, Division of Clinic Implementation and Data Management Texas Scottish Rite Hospital for Children Assistant Professor Department of Orthopaedic Surgery The University of Texas Southwestern Medical Center Dallas, Texas

Charles E. Johnston, MD Assistant Chief of Staff Texas Scottish Rite Hospital for Children Professor of Orthopaedic Surgery The University of Texas Southwestern Medical Center Dallas, Texas

Lawson A.B. Copley, MD Staff Orthopaedist Texas Scottish Rite Hospital for Children Associate Professor of Orthopaedic Surgery The University of Texas Southwestern Medical Center Dallas, Texas Molly E. Dempsey, MD Medical Director of Radiology Texas Scottish Rite Hospital for Children Dallas, Texas Henry Ellis, MD Staff Orthopaedist Children’s Medical Center Dallas, Texas

Lori A. Karol, MD Staff Orthopaedist Texas Scottish Rite Hospital for Children Professor of Orthopaedic Surgery The University of Texas Southwestern Medical Center Dallas, Texas Harry K.W. Kim, MD, MSc, FRCSC Director, Sarah M. and Charles E. Seay Center for Musculoskeletal Research Director, Center for Excellence in Hip Disorders Texas Scottish Rite Hospital for Children Associate Professor of Orthopaedic Surgery The University of Texas Southwestern Medical Center Dallas, Texas Veronica M. Meneses, MD, FAAP Director, Rainbow Clinics, Developmental-Behavioral Pediatrics Texas Scottish Rite Hospital for Children Clinical Instructor The University of Texas Southwestern Medical Center Dallas, Texas v

vi

Contributors

Pamela Nurenberg, MD Staff Pediatric Radiologist Texas Scottish Rite Hospital for Children Clinical Associate Professor of Radiology The University of Texas Southwestern Medical Center Dallas, Texas David A. Podeszwa, MD Staff Orthopaedist Texas Scottish Right Hospital for Children Associate Professor Department of Orthopaedic Surgery The University of Texas Southwestern Medical Center Dallas, Texas Brandon A. Ramo, MD Staff Orthopaedist Texas Scottish Rite Hospital for Children Children’s Medical Center Dallas Assistant Professor Department of Orthopaedic Surgery The University of Texas Southwestern Medical Center Dallas, Texas Karl E. Rathjen, MD Staff Orthopaedist Texas Scottish Rite Hospital for Children Professor Department of Orthopaedic Surgery The University of Texas Southwestern Medical Center Chief of Clinical Service Department of Orthopaedic Surgery Children’s Medical Center Dallas, Texas Anthony I. Riccio, MD Staff Orthopaedist Texas Scottish Rite Hospital for Children Assistant Professor Department of Orthopaedic Surgery The University of Texas Southwestern Medical Center Staff Orthopaedist Children’s Medical Center Dallas, Texas B. Stephens Richards, MD Chief Medical Oficer Texas Scottish Rite Hospital for Children Professor of Orthopaedic Surgery The University of Texas Southwestern Medical Center Dallas, Texas

Fay Z. Safavi, MBBS, FFARCS Director, Department of Anesthesiology and Pain Management Texas Scottish Rite Hospital for Children Professor of Anesthesiology and Pain Management The University of Texas Southwestern Medical Center Dallas, Texas Mikhail Samchukov, MD Co-Director, Center of Excellence for Limb Lengthening and Reconstruction Texas Scottish Rite Hospital for Children Associate Professor Department of Orthopaedic Surgery The University of Texas Southwestern Medical Center Dallas, Texas Daniel J. Sucato, MD Chief of Staff Texas Scottish Rite Hospital for Children Professor of Orthopaedic Surgery The University of Texas Southwestern Medical Center Staff Orthopaedist Children’s Medical Center Dallas, Texas David C. Wilkes, MD Staff Radiologist Texas Scottish Rite Hospital for Children Dallas, Texas Philip L. Wilson, MD Staff Orthopaedist Texas Scottish Rite Hospital for Children Associate Professor Department of Orthopaedic Surgery The University of Texas Southwestern Medical Center Staff Orthopaedist Children’s Medical Center Dallas, Texas Robert Lane Wimberly, MD Staff Orthopaedist Texas Scottish Rite Hospital for Children Assistant Professor Department of Orthopaedic Surgery The University of Texas Southwestern Medical Center Staff Orthopaedist Children’s Medical Center Dallas, Texas Megan Young, MD Instructor of Pediatric Orthopaedic Surgery George Washington University Children’s National Medical Center Washington, District of Columbia

PREFACE

This edition of Tachdjian’s Pediatric Orthopaedics is the third to be written and edited by the staff of Texas Scot­ tish Rite Hospital for Children. We are committed to the concept that this text should be the most comprehensive source for pediatric orthopaedic knowledge. We also con­ tinue to believe that what is written should be based on the best available evidence whenever possible. With each edition, all relevant literature is reviewed as the text is updated. Because Level I and Level II evidence are infre­ quently available, content must also be augmented by expert opinion. Our authors, who are leaders in many ields, base their opinions and recommendations on a very broad clinical experience in an academic environ­ ment. As academic leaders, they regularly present their research nationally and internationally, teach at virtually all major conferences, and are broadly aware of the advances in pediatric orthopaedics. What is a book, or a newspaper for that matter? As I began reading The New York Times on my iPad, I realized that this newspaper, which formerly was black and white and silent, now is augmented with colorful slides, nar­ rated commentary, and extensive links to all sorts of other information. The same is true for this textbook. The two print volumes contain the most frequently sought infor­ mation. Our digital, or online, version contains all three volumes and presents comprehensive information in a variety of forms. There are 58 surgical videos, each a live procedure narrated by one of the true surgical experts in the ield. Many readers of the previous edition have shared with me that these are of great value to their surgi­ cal care of patients.

This year we have added something new to ortho­ paedic texts: a collection of narrated videos of patient examinations, demonstrating usual and unusual physical indings. We hope that these will enhance the reader’s ability to recognize various orthopaedic conditions. These may also be used to educate ofice staff, students, and co­workers about the pediatric orthopaedic physical examination. During the lifetime of this edition we may add other enhancements as well. After all, it is truly a new era in information technology, and we are putting this technology to its best educational use. I would like to thank everyone who has made this edition possible. First, a large thank you goes to our medical and surgical staff for contributing time and effort in the preparation of the chapters. Our ofice per­ sonnel, especially Phyllis Cuesta, Louise Hamilton, and Cindy Daniel, have handled all of the organizational work, compiled the bibliographies, and typed text to meet many deadlines, and we are very grateful. The people in our administration, especially Robert Walker and J.C. Montgomery, Jr., and our board of directors, led by the honorable Ambassador Lyndon Olson, have under­ stood the importance of this work and supported it wholeheartedly. I would also like to thank our patients for all they have taught us and for helping us educate others about their conditions. Finally, I especially would like to thank our families, who have allowed us the time to complete the project and have been of great help along the way. John Anthony Herring March 2013

vii

A CKNOWL E DG ME NTS

Orthopaedic staff at Texas Scottish Rite Hospital for Children: Front row (left to right): Anthony I. Riccio, Lori A. Karol, John A. Herring, Daniel J. Sucato, B. Stephens Richards, Christine Ho, Brandon Ramo. Back row (left to right): Harry K.W. Kim, John G. Birch, Robert Lane Wimberly, Alexander Cherkashin, Mikhail Samchukov, David A. Podeszwa, Lawson A.B. Copley, Karl E. Rathjen, Philip L. Wilson, Charles E. Johnston, Henry Ellis.

Editor: John A. Herring, MD Managing Editors: Cindy Godwin Daniel Louise Nunes Hamilton

Video Production: Alexander Carduff Paul Jolly Operating Room Video: Margaret Taylor Sarah Tune

Project Manager: Phyllis Cuesta Media Production Services: Stuart Almond Lilla Tune Sarah Tune ix

ILLUSTRATED PROCEDURES

Plate 12-1 Exposure of the Spine for Posterior Instrumentation and Fusion Plate 12-2 Posterior Spinal Instrumentation and Fusion Using Hooks Plate 12-3 Posterior Spinal Instrumentation and Fusion Using Pedicle Screws Plate 12-4 Anterior Instrumentation of the Spine for Thoracolumbar or Lumbar Scoliosis Plate 15-1 Lateral Rotation Osteotomy of the Humerus Plate 15-2 Rerouting of the Biceps Brachii Tendon to Convert Its Motion From Supinator to Pronator of the Forearm (Zancolli Procedure) ePlate 15-1 Modiied Green Scapuloplasty for Congenital High Scapula (Sprengel Deformity) ePlate 15-2 Woodward Operation for Congenital High Scapula Plate 16-1 Closed Reduction and Casting for Developmental Dislocation of the Hip Plate 16-2 Medial Approach for Open Reduction of the Developmentally Dislocated Hip Plate 16-3 Open Reduction of Developmental Hip Dislocation Through the Anterolateral Approach Plate 16-4 Femoral Shortening and Derotation Osteotomy Combined With Open Reduction of the Hip Plate 16-5 Intertrochanteric Varus Osteotomy and Internal Fixation With a Blade Plate Plate 16-6 Greater Trochanteric Epiphysiodesis Plate 16-7 Distal and Lateral Transfer of the Greater Trochanter Plate 16-8 Lateral Advancement of the Greater Trochanter Plate 16-9 Wagner Intertrochanteric Double Osteotomy Plate 16-10 Lateral Closing Wedge Valgization Osteotomy of the Proximal Femur With Distal and Lateral Advancement of the Greater Trochanter Plate 16-11 Pemberton Osteotomy Plate 16-12 Salter Innominate Osteotomy Plate 18-1 Percutaneous Cannulated Screw Fixation (“Pinning”) of Slipped Capital Femoral Epiphysis Plate 18-2 Open Bone Graft Epiphysiodesis for Slipped Capital Femoral Epiphysis Plate 18-3 Scheme and Principles of the Dunn Procedure (Open Reduction of the Capital Epiphysis With Shortening of the Femoral Neck)

indicates plate is web only

292 294 297 302 479 481

539 540 544 549 550 554 558 565 566 568

570 575 656 659

Plate 18-4 Kramer/Barmada Osteotomy of 662 the Base of the Femoral Neck for Slipped Capital Femoral Epiphysis 664 Plate 18-5 Intraarticular Hip Fusion for Avascular Necrosis 676 Plate 19-1 Pauwels’ Intertrochanteric Y-Osteotomy ePlate 21-1 Dewar-Galeazzi Procedure for Recurrent Dislocation of the Patellofemoral Joint ePlate 21-2 Quadricepsplasty for Recurrent Dislocation of the Patella (Green Procedure) Plate 23-1 Open Reduction of Dorsolateral 865 Dislocation of the Talocalcaneonavicular Joint (Congenital Vertical Talus) 870 Plate 23-2 Plantar Fasciotomy Plate 23-3 Transfer of the Long Toe Extensors 872 to the Heads of the Metatarsals (Jones Transfer) 874 Plate 23-4 Dwyer Lateral Wedge Resection of the Calcaneus for Pes Cavus 876 Plate 23-5 Dorsal Wedge Resection for Pes Cavus 878 Plate 23-6 Japas V-Osteotomy of the Tarsus Plate 23-7 Correction of Hammer Toe by 882 Resection and Arthrodesis of the Proximal Interphalangeal Joint 940 Plate 24-1 Moseley Straight-Line Graph Plate 24-2 Epiphysiodesis of the Distal Femur 942 (the Green Modiication of the Phemister Technique) 946 Plate 24-3 Epiphysiodesis of the Proximal Tibia and Fibula (the Green Modiication of the Phemister Technique) 1005 Plate 25-1 Knee Fusion for Prosthetic Conversion in Proximal Focal Femoral Deiciency 1158 Plate 30-1 Hemipelvectomy (Banks and Coleman Technique) 1164 Plate 30-2 Hip Disarticulation Plate 30-3 Ischial-Bearing Above-Knee 1170 Amputation (Midthigh Amputation) 1176 Plate 30-4 Disarticulation of the Knee Joint Plate 30-5 Below-Knee Amputation 1180 Plate 30-6 Posterior Approach for Forequarter 1183 Amputation (Littlewood Technique) 1189 Plate 30-7 Disarticulation of the Shoulder Plate 30-8 Amputation Through the Arm 1191 Plate 30-9 Disarticulation of the Elbow 1193

661

The following sections are web only Plate 35-1 Percutaneous Achilles Tendon Lengthening Plate 35-2 Split Anterior Tibialis Tendon Transfer Plate 35-3 Extraarticular Arthrodesis of the Subtalar Joint (Grice Procedure) xxxix

xl

Illustrated Procedures

Plate 35-4 Lateral Column Lengthening Plate 35-5 Hamstring Lengthening Plate 35-6 Rectus Femoris Transfer Plate 35-7 Adductor Contracture Release Plate 35-8 Proximal Hamstring Release Plate 35-9 Shelf Acetabular Augmentation Plate 35-10 Dega Osteotomy Plate 35-11 Extensor Carpi Ulnaris–Extensor Carpi Radialis Brevis Transfer Plate 35-12 Fractional Lengthening of the Finger and Wrist Flexors in the Forearm Operative Technique Plate 36-1 Tibialis Tendon Transfer to the Calcaneus to Prevent or Correct Calcaneal Deformity Plate 36-2 Achilles Tendon–Distal Fibular Tenodesis for Mild Ankle Valgus in Skeletally Immature Patients Plate 36-3 Lumbar Kyphectomy in Myelomeningocele Patients With Fixation to the Pelvis Using the Dunn-McCarthy Technique Plate 37-1 Fractional Lengthening of the Hamstrings Plate 37-2 Iliopsoas Muscle Transfer for Paralysis of the Hip Abductors Plate 37-3 Lloyd Roberts Technique of Intertrochanteric Oblique Osteotomy of the Proximal End of the Femur

and Internal Fixation With Coventry Apparatus (Lag Screw and Plate) Plate 37-4 Anterior Transfer of the Peroneus Longus Tendon to the Base of the Second Metatarsal Plate 37-5 Anterior Transfer of the Posterior Tibial Tendon Through the Interosseous Membrane Plate 37-6 Posterior Tendon Transfer to the Os Calcis for Correction of Calcaneus Deformity (Green and Grice Procedure) Plate 37-7 Triple Arthrodesis Plate 37-8 Extraarticular Arthrodesis of the Subtalar Joint (Grice Procedure) Plate 37-9 Arthrodesis of the Ankle Joint via the Anterior Approach Without Disturbing the Distal Tibial Growth Plate Plate 37-10 Flexorplasty of the Elbow (the Mayer and Green Modiication of the Steindler Technique) Plate 37-11 Pectoralis Major Transfer for Paralysis of the Elbow Flexors Plate 39-1 Anterior Transfer of the Posterior Tibial Tendon Through the Interosseous Membrane Plate 39-2 Scapulocostal Stabilization for Scapular Winging (Ketenjian Technique) Plate 41-1 Posterior Release of Elbow Extension Contracture

VIDEO CONTENTS

Asymmetric Abdominal Relexes Sternocleidomastoid Release (Torticollis) Anterior Thoracoscopic Spinal Fusion and Release Video 12-2 T11 Posterior Hemivertebra Resection/ T10 to T12 Instrumentation and Fusion Video 12-3 Early Treatment of Infantile Scoliosis by EDF Casting Video 12-4 Risser Cast Application Video 12-5 Spine Growing Rod Concept T2 to L2 Video 14-1 Spinal Fusion L4 to S1 Spondylolisthesis: Kyphosis Correction Video 15-1 Woodward Procedure for Sprengel Deformity Video 15-2 Open Reduction of Congenital Pseudarthrosis of the Clavicle Video 15-3 Radial Polydactyly Reconstruction Video 16-1 Demonstration of Bilateral Dislocated Hips Video 16-2 Hip Examination: Bilateral Hip Dislocation Video 16-3 Developmental Dysplasia of the Hip Examination: Walking Age Video 16-4 Pavlik Harness With Femoral Nerve Palsy Video 16-5 Closed Reduction Left Hip/Arthrogram Video 16-6 Anterior Open Reduction of the Left Hip Video 16-7 Open Reduction Capsulorrhaphy Femoral Shortening Pemberton Osteotomy Video 16-8 Knee Reduction and Femoral Shortening: Infant Video 16-9 Salter Osteotomy Video 16-10 Pemberton Osteotomy Video 16-11 Periacetabular Osteotomy Video 16-12 Periacetabular Osteotomy Left Hip Video 17-1 Proximal Femur Varus Osteotomy: Legg-Perthes Video 17-2 Surgical Hip Dislocation With Femoral Neck Lengthening Video 18-1 Percutaneous Pinning: Slipped Capital Femoral Epiphysis Video 18-2 Surgical Dislocation of the Left Hip With Shortening of Neck and Reduction of Femoral Head: Slipped Capital Femoral Epiphysis Video 18-3 Surgical Hip Dislocation: Slipped Capital Femoral Epiphysis Video 21-1 Medial Patellofemoral Ligament Reconstruction Video 7-1 Video 11-1 Video 12-1

Video 22-1

Video 22-2 Video 23-1 Video 23-2 Video 23-3

Video 23-4 Video 23-5 Video 23-6 Video 23-7 Video 23-8 Video 23-9 Video 23-10 Video 23-11 Video 23-12 Video 23-13 Video 24-1 Video 24-2 Video 24-3 Video Video Video Video

25-1 25-2 25-3 25-4

Video 28-1 Video 33-1 Video 34-1

Video 34-2 Video 35-1 Video 35-2 Video 37-1

Varus Osteotomy Distal Right Femur and Valgus Osteotomy Distal Left Femur and Proximal Left Tibia Williams Intramedullary Concept: Right Tibia Excision of Os Trigonum Excision of the Accessory Navicular Z-Foot Correction: Calcaneus Lengthening First Metatarsal Osteotomy Bunion Correction Clubfoot Cast Removal and Application Clubfoot Correction: Posterior Medial Release Lateral Column Shortening Flexor Hallucis Longus Tendon Transfer to Metatarsal Head: Right Foot Anterior Tibialis Tendon Transfer to Cuneiform Lateral Column Shortening External Rotation Osteotomy: Left Tibia Triple Arthrodesis Severe Planovalgus: Left Foot Calcaneo-Navicular Coalition Dwyer (Closing Wedge) Calcaneal Osteotomy Osteotomy of Fourth Metatarsal With External Fixation The 8 Plate Bilateral Osteotomies: Femur and Tibia Varus Closing Wedge Medial Osteotomy With Blade Plate Syme Amputation, Fibular Hemimelia Type II Hemimelia Above-Knee Amputation: Left Leg Right Knee Disarticulation: Left Posterior Medial Release Excision of Anterior Vertebral Malformation Elbow Arthroscopy: Capitellar Osteochondritis Dissecans Débridement Anterior Cruciate Ligament Reconstruction With Posterior Medial Capsulorrhaphy Epiphyseal Anterior Cruciate Ligament Reconstruction Medial Distal Tibial Screw Hemiepiphyseodesis Adductor Tenotomy Hamstring Lengthening Rectus Femoris Transfer Peroneus Longus Transfer to Dorsum: Right Foot xli

CHAPTER 1

Growth and Development

John A. Herring

not to be doing so. Similarly, a 12-month-old child is likely to have some degree of genu varum, whereas the presence of genu varum in a 3-year-old child should be cause for concern and a focus of further investigation.

Chapter Outline Normal Growth and Development Disorders of Normal Growth and Development 3 Evolution of Proportionate Body Size Physical Growth 5 Developmental Milestones 6

3 5

This chapter on growth and development is presented irst for several important reasons. One of the unique aspects of pediatric care is the dynamic evolution of each individual from neonate to adolescent. During this period, a remarkable process of growth and development takes place in gross and ine motor skills; intellectual, social, and verbal skills; body size; gait; and sexual characteristics. Growth refers to an increase in an individual’s total body size or to an increase in the physical size of a particular organ or organ system.9,17 References to normal human growth parameters from the third trimester to adulthood are provided in Proceedings of the Greenwood Genetic Center: Growth References.10 This publication also provides parameters for growth patterns seen in speciic diseases, such as achondroplasia, diastrophic dysplasia, Down syndrome, Marfan syndrome, and skeletal dysplasias (comparative curves). Growth standards are also available in Hensinger’s Standards in Pediatric Orthopedics.7 Development refers to the physical changes of maturation that occur as a child ages. The developmental process encompasses other aspects of differentiation of form, but it primarily involves changes in function that transform humans into increasingly more complex beings.9 Development is inluenced by many interrelated factors, including genetics, physical trauma, nutrition, and socioeconomic status.17 The age at which children reach speciic milestones of development depends on the maturation rate of their central nervous system (CNS), which varies from child to child. Ranges for variations in normal have been developed to assist in the assessment of the pediatric patient, and the most commonly used assessment tool is the revised Denver Developmental Screening Test (DDST)5-7 (Fig. 1-1). It is important to know when a child should normally achieve expected milestones of growth and development so that potentially abnormal situations are evident to the physician who is taking a patient’s history and performing a physical examination. The signiicance of various indings must be related to the child’s particular stage of growth and development. Although no one should expect a 4-month-old infant to be walking, it is distinctly abnormal for an 18-month-old child

Normal Growth and Development Neonates are primarily relexive, but they do exhibit some cognitive traits.8 These traits include showing more curiosity about facelike igures than about other igures of comparable brightness, as well as a preference for black-and-white tones rather than gray. Neonates should turn their eyes toward sound and be able to distinguish their mothers from other people. The normal neonate is born with a predominant lexor tone, and physiologic lexion contractures are typical (Fig. 1-2). At birth the newborn’s limbs are maintained in lexion posture, and passive movement of the extremities and neck elicits strong lexor tone. A normal neonate’s limbs move in an alternating fashion when they are stimulated. Normal development progresses cephalocaudad; infants acquire the ability to control their head and hands before they are able to control their legs.8 During the irst few months, gaining head control predominates. Hand control, such as the ability to grasp objects, follows. As development continues, the infant gains more and more control of the legs. To determine whether an infant’s growth and development are progressing normally, the examiner needs to ind out from the parents what developmental milestones the child has attained and when and then compare them with the norms. If the child appears to have developmental delays, referral to a physician who specializes in growth and development problems is recommended. Because of the wide variations in the times at which developmental milestones are achieved and the numerous reasons for delays, the diagnosis of developmental delay can be dificult to make in the very young child. In addition, a child may exhibit delay in acquiring certain skills and unusual rapidity in acquiring others. When a delay is evident, the physician must determine the cause, which may be a neuromuscular condition. Factors suggesting a neurologic cause include failure of normal developmental responses to appear, prolonged retention of primitive infant relexes, or a delay in achieving gross motor milestones within normal limits.

Disorders of Normal Growth and Development Many pediatric orthopaedic problems result from disorders or conditions that adversely affect normal growth and 3

SECTION I Disciplines

4

Examiner: Date:

DENVER ll Months

2

4

6

Name: Birthdate: ID#: 9

12

15

18

24

Years 3

4

5

6

prepare c ereal b ru sh teeth, no hel p

P erc ent of c hil dren passing 25

50

7 5

pl ay b oard/ c ard g ames dress, no hel p pu t on t- shirt

90

test item

name f riend w ash and dry hands b ru sh teeth w ith hel p pu t on c l othes

G ross Motor

L ang u ag e

F ine Motor- A daptiv e

P ersonal –S oc ial

f eed dol l remov e g arment u se spoon/ f ork

86% c opy

draw person, 6 parts c opy , demonstrate pic k l ong er l ine c opy+ draw person, 3 parts c opy

88%

hel p in hou se

w ig g l e thu mb def ine 7 w ords tow er of 8 c u b es name 2 opposites initate ac tiv ites imit. v ert. l ine c ou nt 5 b l oc k s pl ay b al l w ith examiner tow er of 6 c u b es k now 3 adj ec tiv es w av e b y e- b y e tow er of 4 c u b es def ine 5 w ords indic ate w ants tow er of 2 c u b es name 4 c ol ors pl ay pat- a- c ak e du mp raisin, demonstrated u nderstand 4 prepostitions f eed sel f sc rib b l es speec h al l u nderstandab l e w ork f or toy pu t b l oc k in c u p k now 4 ac tions reg ard ow n hand b ang 2 c u b es hel d in hands u se of 3 ob j ec ts smil e spontaneou sl y thu mb - f ing er c ou nt 1 b l oc k g rasp smil e u se of 2 ob j ec ts responsiv el y tak e 2 c u b es name 1 c ol or pass c u b e reg ard f ac e k now 2 tak e raisin adj ec tiv es l ook f or y arn k now 2 ac tions b al anc e eac h f oot 6 sec reac hes name 4 pic tu res heel - to- toe w al k reg ard raisin speec h hal f u nderstandab l e b al anc e eac h f oot 5 sec f ol l ow 180 ° name 4 pic tu res b al anc e eac h f oot 4 sec hands name 6 b ody parts b al anc e eac h f oot 3 sec tog ether name 1 pic tu re g rasp hops c omb ine w ords rattl e b al anc e eac h f oot f ol l ow past point to pic tu res 2 sec midl ine 6 w ords b al anc e eac h f ol l ow f oot 1 sec 3 w ords to midl n. b road j u mp 2 w ords throw b al l ov erhand 1 w ord j u mp u p Dada/ Mama spec if ic k ic k b al l f orw ard j ab b ers w al k u p steps c omb ine sy l l ab l es ru ns Dada/ Mama w al k b ac k w ard nonspec if ic w al k w el l imitate speec h sou nds stoop and rec ov er sing l e sy l l ab l es stand al one tu rn to v oic e drink f rom c u p

stand 2 sec

tu rn to rattl ing sou nd

g et to sitting

sq u eal s

pu l l to stand stand hol ding on

l au g hs " O oo/ aah" v oc al iz es respond to b el l

sit–no su pport pu l l to stand no head l ag

rol l ov er c hest u p arm su pport w ear w t. on l eg s sit- head steady head u p 90 ° head u p 45° l if t head eq u al mov ements

Months

2

4

6

9

12

15

18

24

Years 3

4

5

6

FIGURE 1-1 The revised Denver Developmental Screening Test showing the range of age when a child should achieve milestones in the development of gross motor skills, ine motor-adaptive skills, language, and personal-social skills. (Modiied from Frankenburg WK, Dodds JB: The Denver Developmental Screening Test, J Pediatr 71:181, 1967; and Hensinger RN: Standards in pediatric orthopedics, New York, 1986, Raven Press.)

CHAPTER 1 Growth and Development

5

FIGURE 1-2 Typical position of the neonate with vertex presentation. The hips and knees are lexed, the lower legs are rotated internally, and the feet are rotated further inward on the lower leg. The lower limbs are contracted into this position for a variable period after birth.

development. The four major failures of normal growth and development are malformations, deformations, disruptions, and dysplasias.4,12

during organogenesis. A congenital constriction band in the limb is an example of a disruption.

Dysplasias Malformations Malformations are structural defects that result from interruption of normal organogenesis during the second month of gestation. Examples include myelomeningocele, syndactyly, preaxial polydactyly, Poland syndrome, and proximal focal femoral deiciency (congenital femoral deiciency).

Dysplasias are structural defects caused by abnormal tissue differentiation as cells organize into tissues. Examples include osteogenesis imperfecta, achondroplasia, and spondyloepiphyseal dysplasia.

Evolution of Proportionate Body Size Deformations Deformations are defects in the form, shape, or site of body parts caused by mechanical stress. The mechanical stress, which may be intrinsic or extrinsic, alters or distorts tissues. Because the fetus grows considerably faster than the infant, fetuses are more vulnerable to deformations. Examples include supple metatarsus adductus, calcaneovalgus feet, congenital knee hyperextension, and physiologic bowing of the tibia. Differentiating deformations from malformations is important. During a cursory examination, severe deformations may look like malformations.3 Careful assessment is essential if the child is to receive appropriate care for the condition. Malformations cannot be corrected directly, whereas deformations can often be reversed relatively easily either by eliminating the deforming force or by counteracting the force with stretching, casting, or bracing.

At birth, the neonate’s head is disproportionately large, comprising approximately one fourth of the body’s total length. During the irst year of infancy, the head continues to grow rapidly, and the head circumference usually is greater than the circumference of the infant’s chest. The evolution of body proportions is indicated by a change in the child’s upper to lower segment ratio (the relation of the center of gravity to body segments). This ratio is measured as the distance from the top of the head to the symphysis pubis, divided by the distance from the symphysis pubis to the bottom of the feet7 (Fig. 1-3). At birth, the ratio is approximately 1 : 7. At approximately 10 years of age, the upper and lower segments are almost equal in length (i.e., the ratio is ≈1.0). After 10 years of age, as individuals become adolescents and adults, the ratio normally becomes less than 1.0, as the upper segment becomes shorter than the lower segment.

Disruptions Disruptions are morphologic abnormalities that result from an extrinsic interference with or breakdown of the normal growth and development process. Disruptions can be caused by drugs or toxic materials. These structural defects may affect organs or systems that were normal

Physical Growth Head Circumference During infancy it is essential to obtain individual or serial measurements of the patient’s head circumference to

6

SECTION I Disciplines

6 mo fetus Newborn

2 yr

5 yr

13 yr

17 yr

Adult

FIGURE 1-3 Evolution of head-to-trunk proportion throughout growth. In the neonate the head is proportionately signiicantly larger relative to the trunk than it will be at skeletal maturity. (Reproduced from Hensinger RN: Standards in pediatric orthopedics, New York, 1986, Raven Press.)

determine whether head growth is slower or faster than normal. Head circumference should be measured at every physical examination during the irst 2 years and at least biennially thereafter. With the child supine, the examiner places a centimeter tape over the occipital, parietal, and frontal prominences of the head. The tape should be stretched and the reading noted at the point of greatest circumference. Possible conditions that can affect head circumference and growth include microcephaly, premature closure of the sutures, hydrocephalus, subdural hematoma, and brain tumor. Head circumference should be charted for age and percentile, as noted in Figure 1-4.

Tanner’s Stages of Development The physical maturation of a child can also be compared with his or her chronologic age by using the pubertal stages of development as described by Tanner15,16 (Figs. 1-12 and 1-13). The Tanner stages of maturation are based on breast size in girls, genital size in boys, and pubic hair stages for both girls and boys. The onset of menstruation is also an important milestone in the physical maturation of girls.

Developmental Milestones

Height and Weight

Gross Motor Skills

A child’s growth, as demonstrated by an increase in body height and weight within predetermined normal limits, is one of the best indicators of health during infancy and childhood. The child’s height and weight should be plotted on a standard growth chart to verify that normal progress is being made. Numerous tables, charts, and graphs depicting pediatric growth standards are available in Hensinger’s Standards in Pediatric Orthopedics7 and in Proceedings of the Greenwood Genetic Center: Growth References.10 The World Health Organization published an extensive study of child growth standards for length and height for age, weight for age, weight for length, weight for height, and body mass index for age.18 Height and weight should be charted for age and percentile, as noted in Figure 1-5. If growth measurements are lower than the 3rd percentile or higher than the 97th percentile, or if a recent deviation from previously stable percentile rankings is noted, further investigation is warranted.

The development of gross motor skills depends on maturation of the CNS, which proceeds in a cephalocaudal direction.8 The approximate ages at which children should normally attain various gross motor skills are given in Table 1-1. By 3 months of age, infants should be able to hold their heads above the plane of the body when they are supported in a prone position. By 6 months of age, the head should not lag when infants are pulled from a supine to a sitting position. Normally, infants will begin to roll over between 4 and 6 months of age and can sit with minimal external support at 6 to 7 months. They should be able to pull up to a standing position by holding onto furniture at 9 to 12 months and stand without support by 14 months. The average milestones of development of locomotion are as follows: the infant should be able to crawl by 7 to 9 months of age, cruise and walk with assistance at 12 months, walk forward without support by 12 to 16 months, and run at 18 months of age.1,2,11 Children should be able to ascend stairs with support by 18 months of age and without support by 2 years of age. They should be able to descend stairs with support at approximately 3 years of age and without support by 4 years. On gross inspection the independent gait of the infant has a wide base, the hips and knees are hyperlexed, the arms are held in lexion, and the movements are abrupt. With maturation of the neuromuscular system, the width of the base gradually diminishes, the movements become smoother, reciprocal swing of the upper limbs begins, and step length and walking velocity increase.13 The adult

Epiphyseal Growth and Closure During normal growth and development, the pattern in the appearance of centers of ossiication and fusion of epiphyses in the upper and lower limbs is orderly. This pattern varies among individuals and is different for boys and girls (Figs. 1-6 to 1-9). Thus the orthopaedist must understand the ranges of normal when treating the pediatric patient, particularly when interpreting radiographs. The percentage contribution of each epiphysis to longitudinal growth of the upper and lower extremity long bones is shown in Figures 1-10 and 1-11.

Text continued on page 20

CHAPTER 1 Growth and Development

Boys: birth to 36 months Physical growth NCHS percentiles B

3

Name

6

9

12

51 50 49

19

48 47

18

15

18

21

24

27

30

33

36 54 95 90

Head circumference

53 52

20

Record #

Age (months)

54 21

7

75 50 25 10 5

53

21

52 51

20

50 49 48

19

47 46

46

cm

in

43

21

46

42

20

44

41

19

42

40

18

40

17

38

45 44 17

16

38

95 90 75 50

37

25

15

36

10 5

14

39 15

14

13

16

8 6 4

lb

32 30

13

34

12

33

11

24

32

10

22

31

9

20

8

18

7

16

Weight

in cm

10

34

35

12

12

36

6

6

28 26

14 12

5

5

4

4

3

3

2

2

4

kg

lb

Length

kg cm

50

55

60

65

70

75

80

85

90

95

10 8 6

100

in 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 Date

Age

Length

Weight

Head circ.

Comment

A FIGURE 1-4 Normal head circumference parameters for boys and girls from birth to 36 months. A, Boys, birth to 36 months. NCHS, National Center for Health Statistics. (From the National Center for Health Statistics.) Continued

SECTION I Disciplines

Girls: birth to 36 months Physical growth NCHS percentiles B

3

Name

6

9

12

53 52

20

51 50 49

19

48 47

18

15

18

21

24

27

30

33

36

Age (months)

54 21

Record #

54 53

Head circumference

21

52 95 90

51

75

50

50

49

25 10 5

48

20

19

47 46

46

cm

in

43

21

46

42

20

44

41

19

42

40

18

40

17

38

45 44 17

16

39 15

95 90 75

38 37

14

15

50 25 10 5

36 35

13

16

14 13

8 6 4

lb

32 30 28

33

11

24

32

10

22

31

9

20

8

18

7

16

in cm

10

34

12

12

12

36

34

Weight

8

6

6

26

14 12

5

5

4

4

3

3

2

2

4

kg

lb

Length

kg cm

50

55

60

65

70

75

80

85

90

95

100

in 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 Date

Age

Length

Weight

Head circ.

Comment

B FIGURE 1-4, cont’d B, Girls, birth to 36 months. NCHS, National Center for Health Statistics.

10 8 6

CHAPTER 1 Growth and Development

Boys: birth to 36 months Physical growth NCHS percentiles B

42 41

3

6

Name

9

12

Record #

15

18

21

24

27

30

33

Age (months)

95 90

100

Length

90

25

95

cm

32

41 18

85 95

80

17

90

16

26

15

70

14

65

13

60

12

11

45

Weight

10

40

18 17 16

Age (months)

7

kg 12

15

18

21

24

27

30

33

lb

36

6

12

Mother's stature

Gestational

Father's stature

age

weeks

5 Date

10 9

20 19

8

14

11

22 21

9

in cm

13

24 23

15

15

26 25

50

17 16

29 27

5

55

19 18

31

28

10

21 20

33

30 25

23 22

35

32

50

25 24

37

34

75

27

38 36

75

29 28

40 39

31 30

in

10 5

34 33

39 38

50

95

41 40

100

75

36 35

42

105

38 37

36

105

40 39

9

Age

Length

Weight

Head circ.

Comment

Birth

4

8 7

3

6 5 4

lb

A

2

kg B

3

6

9

FIGURE 1-5 Normal length and weight parameters for boys and girls from birth to 18 years. A, Boys, birth to 36 months. NCHS, National Center for Health Statistics. (From the National Center for Health Statistics.) Continued

SECTION I Disciplines

Girls: birth to 36 months Physical growth NCHS percentiles B

42 41

3

6

Name

9

12

Record #

15

18

21

24

27

30

33

Age (months) 95

100

90

95

36 35

90

32

95

25

cm

41 18

85

17

80

16 90

15

75

50

60

13

12

10

11

45

Weight

10

40

20 19

8

18 17 16

Age (months)

7

kg 12

14

15

18

21

24

27

30

33

lb

36

6

12

Mother's stature

Gestational

Father's stature

age

weeks

5 Date

10 9

22 21

9

in cm

11

24 23

15

13

26 25

50

17

15

29 27

55

19

16

31

28

5

18

33

30

25

21 20

35

32 14

65

23 22

37

34 70

25 24

38 36

95

75

27 26

40 39

29 28

in

10 5

31 30

39 38

50

34 33

41 40

100

75

38 37

42

105

40 39

36

105

Length

10

Age

Length

Weight

Head circ.

Comment

Birth

4

8 7

3

6 5 4

lb

B

2

kg B

3

6

9

FIGURE 1-5, cont’d B, Girls, birth to 36 months. NCHS, National Center for Health Statistics.

CHAPTER 1 Growth and Development

Boys: 2 to 18 years Physical growth NCHS percentiles

Name

Mother's stature Date

Record #

Father's stature

Age

Stature

Weight

11

12

Comment

13

14

15

16

17

18

77 76

Age (years) 190

90 75

180

74 73 72 71

50

175

70 69

25

170 10 5

4

5

6

7

8

9

10

150 145

65 64

160

63 62

140 135

in

95

210

90

200

85

90

190 180

80

130

170 125

75

75

160 70

120

150

50

65

115 25

110

60

10

140 130

55

120

50

110

45

100

5

40 35

90 80 70

Weight

30 60 25 50

in cm

20

40

40 15

15

Age (years)

kg

lb kg

C

61

cm

95

42 41 105 40 39 100 38 95 37 36 90 35 34 85 33 32 80 31 30 75 29

30

68 67 66

165

155

155

Stature

62 61 60 59 58 57 56 55 54 53 52 51 50 49 48 47 46 45 44 43

3

75

185

95

2

11

2

3

4

5

6

7

8

9

10

11

12

13

14

15

16

17

30

lb

18

FIGURE 1-5, cont’d C, Boys, 2 to 18 years. Continued

SECTION I Disciplines

Girls: 2 to 18 years Physical growth NCHS percentiles

Name

Mother's stature Date

Record #

Father's stature

Age

Stature

Weight

11

12

Comment

13

14

15

16

17

18

77 76

Age (years) 190

180 175

70 69

95 90

170

75

62 61 60 59 58 57 56 55 54 53 52 51 50 49 48 47 46 45 44 43

3

4

5

6

7

8

9

10 25 10

155

65 64

160

63 62

155

in

95

210

140

90

200

135

85

150 145

95

190 180

130

80

125

75

170 160

90

70

120

150 65

115 75

60

110 50

25 10 5

140 130

55

120

50

110

45

100

40 35

90 80 70

Weight

30 60 25 50

in cm

20

40

40 15

15

Age (years)

kg

lb kg

D

61

cm

5

42 41 105 40 39 100 38 95 37 36 90 35 34 85 33 32 80 31 30 75 29

30

68 67 66

165 50

2

75 74 73 72 71

185

Stature

12

2

3

4

5

6

7

8

9

10

11

12

13

14

15

16

17

18

FIGURE 1-5, cont’d D, Girls, 2 to 18 years. NCHS, National Center for Health Statistics.

30

lb

CHAPTER 1 Growth and Development

Boys: prepubescent Physical growth NCHS percentiles Mother's stature Date

Name

Record #

Father's stature

Age

Stature

Weight

13

51 50

Comment

110

49 48

105

47 46

95

45

100

44 43

95

42

90

41

90

40 39

85

38

75

37 36

80

35

50

34

75

33 32

25

70

31 65

10

30

55

28

28

27

27

26

26

25

25

24 50

23 22

45

40

35

30

25

20

19

19

18

18

17

17

16

16

15

15

14

14

13

13 12

Stature kg in

90

95

100

105

110

115

120

125

130

135

140

55

50

22 21

lb kg

E

23

20

12

60

24

21

cm 85

65

29

Weight

60

30

5

29

45

40

35

30

25

lb

145

34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58

FIGURE 1-5, cont’d E, Boys, prepubescent. Continued

SECTION I Disciplines

Girls: prepubescent Physical growth NCHS percentiles Mother's stature Date

Name

Record #

Father's stature

Age

Stature

Weight

51 50

Comment

110

49 48

105

47 46 45

100

44 43

95

95

42 41

90

40 39 90

85

38 37 36

80

35

75

34

75

33 32 50

70

31 65

30

30 29

60

55

28

28 27

10

27

26

5

26 25

25 24

50

23 22

45

40

35

30

25

20

19

19

18

18

17

17

16

16

15

15

14

14

13

13 12

Stature kg in

90

95

100

105

110

115

120

125

130

135

140

145

34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58

FIGURE 1-5, cont’d F, Girls, prepubescent. NCHS, National Center for Health Statistics.

55

50

22 21

lb kg

F

23

20

12

60

24

21

cm 85

65

29

25

Weight

14

45

40

35

30

25

lb

CHAPTER 1 Growth and Development

Acromion appears 15-18 yr

15

Clavicle appears 17 yr

Humerus, head appears birth-3 mo

Coracoid process (main center) appears 1 yr

Greater tuberosity appears 6 mo-2 yr 3 mo-1.5 yr

Scapula appears 1 FW

Lesser tuberosity appears 3-5 yr

Subcoracoid element appears 10-12 yr Glenoid cavity appears 18 yr

Trochlea appears 9 yr 8 yr range 8-10 yr 7-9 yr Lateral epicondyle appears 12 yr 11 yr Capitulum appears 5 mo 4 mo range 6 wk-8 mo 1-6 mo Radius, head appears 5 yr 4 yr range 3-6 yr

Medial epicondyle appears 7 yr 5 yr range 5-7 yr 3-6 yr Olecranon appears 10 yr 8 yr Navicular appears 5.5 yr 4.5 yr range 2.5-9 yr Trapezium appears 5 yr 4 yr range 1.5-10 yr

Radial tuberosity appears 10-12 yr

Lunate appears 4 yr range 6 mo-9 yr

Ulna, distal epiphysis appears 6 yr 5 yr range 4-9 yr

Trapezoid appears 6 yr 4 yr range 2.5-9 yr

Radius, distal epiphysis range 1 yr 3 mo-1.5 yr

Pisiform appears 11 yr 9 yr range 6 mo-4 yr

Metacarpal I, epiphysis appears 2.5 yr 1.66 yr range 1.5-3.5 yr 1-2 yr Proximal phalanx I, epiphysis appears 5 mo-2.5 yr Distal phalanx I, epiphysis appears 1.5 yr 1 yr

Phalanges II-V, epiphysis appears 5 mo-2.5 yr

Triquetrum appears 2.25 yr 1.75 yr range 6 mo-4 yr Hamate appears 6 mo range birth-1.5 yr Capitate appears 6 mo range birth-1 yr

Metacarpals II-V, epiphysis appears 1-1.5 yr

FIGURE 1-6 Average age at appearance of secondary centers of ossiication in the epiphyses of the upper extremity, with ages for boys (blue) and girls (pink). FW, Fetal week. (Adapted from von Lanz T, Wachsmuth W: Praktische anatomie, Berlin, 1938, Julius Springer, p 28.)

16

SECTION I Disciplines

Acromion closure 18-19 yr

Clavicle (sternal epiphysis) closure 18-24 yr

Subcoracoid closure 18 yr

Coracoid closure 18-21 yr

Humerus, head and greater and lesser tuberosities fuse together 4-6 yr fuse to shaft 19-21 yr 18-20 yr

Scapula (vertical margin and inferior angle) closure 20-21 yr

Glenoid cavity closure 19 yr

Humerus, capitulum, lateral epicondyle, and trochlea fuse together at puberty fuse to shaft 17 yr 14 yr

Medial epicondyle closure 18 yr 15 yr

Radius, head closure 15-17 yr 14-15 yr

Olecranon closure 14-17 yr 14-15 yr

Radial tuberosity closure 14-18 yr

Radius, distal epiphysis closure 19 yr 17 yr Radius, styloid closure variable

Metacarpal I, epiphysis closure 14-21 yr Proximal phalanx I, epiphysis closure 14-21 yr Distal phalanx I, epiphysis closure 14-21 yr

Ulna, distal epiphysis closure 19 yr 17 yr Ulna, styloid closure 18-20 yr

Metacarpals II-V, epiphysis closure 14-21 yr

Phalanges II-V, epiphysis closure 14-21 yr

FIGURE 1-7 Average age at closure of growth plates (physes) in the epiphyses of the upper extremity, with ages for boys (blue) and girls (pink). (Adapted from von Lanz T, Wachsmuth W: Praktische anatomie, Berlin, 1938, Julius Springer, p 28.)

CHAPTER 1 Growth and Development

Ischial spine appears 13-15 yr Head of femur appears 4 mo

17

Iliac crest appears at puberty Iliac tubercle appears 13-15 yr Tubercle of pubis appears 18-20 yr

Greater trochanter appears 3 yr

Lesser trochanter appears 12 yr 11 yr

Acetabulum appears 10-13 yr Tubercle of ischium appears 13-15 yr

Femur, distal epiphysis appears 36 FW

Patella appears 4-5 yr 3 yr Fibula, proximal epiphysis appears 4 yr 3 yr

Tibia, proximal epiphysis appears 40 FW Tibial tuberosity appears 7-15 yr

Fibula, distal epiphysis appears 1 yr 9 mo Calcaneus appears 24-36 FW Cuboid appears 40 FW

Tibia, distal epiphysis appears 6 mo Talus appears 26-28 FW Navicular appears 3 yr 2 yr Cuneiforms appear 2 yr 1.5 yr 2.5 yr 2 yr 3-6 mo

FIGURE 1-8 Average age at appearance of secondary centers of ossiication in the epiphyses of the lower extremity, with ages for boys (blue) and girls (pink). FW, Fetal week. (Adapted from von Lanz T, Wachsmuth W: Praktische anatomie, Berlin, 1938, Julius Springer, p 28.)

18

SECTION I Disciplines

Head of femur closure 17-18 yr 16-17 yr

Iliac crest closure 20 yr

Greater trochanter closure 16-17 yr

Lesser trochanter closure 16-17 yr

Femur, distal epiphysis closure 18-19 yr 17 yr

Fibula, proximal epiphysis closure 18-20 yr 16-18 yr

Fibular malleolus closure 17-18 yr

Pelvic bones fuse at puberty

Tibia, proximal epiphysis closure 18-19 yr 16-17 yr

Tibial tuberosity closure 19 yr

Tibia, distal epiphysis closure 17-18 yr Malleolus, medial tip closure 18 yr 16 yr

Calcaneus, epiphysis closure 12-22 yr Closure variable Proximal phalanges I-V, epiphysis closure 18 yr Middle phalanges II-V, epiphysis closure 18 yr

Metatarsals I-V, epiphysis closure 14-21 yr Metatarsals, heads closure 14-21 yr

Distal phalanges closure 18 yr (begins proximally)

FIGURE 1-9 Average age at closure of growth plate (physis) in the epiphyses of the lower extremity, with ages for boys (blue) and girls (pink). (Adapted from von Lanz T, Wachsmuth W: Praktische anatomie, Berlin, 1938, Julius Springer, p 29.)

CHAPTER 1 Growth and Development

Femur Proximal 30% Humerus

Distal 70%

Proximal 80% Distal 20%

Fibula Radius

Ulna

Proximal 60%

Proximal 25%

Proximal 80%

Distal 40%

Distal 75%

Distal 20%

FIGURE 1-10 Average percentage contribution of the proximal and distal physes to the longitudinal growth of the upper extremity long bones.

Tibia Proximal 55% Distal 45%

FIGURE 1-11 Average percentage contribution of the proximal and distal physes to the longitudinal growth of the lower extremity long bones.

Table 1-1 Developmental Milestones for Gross Motor Skills Age

Gross Motor Skills

1 mo

Minimal progress from newborn; may lift head briely when supported in prone position

2 mo

Able to maintain head in plane of body when prone; partial head control when pulled from supine to sitting position

3 mo

Can hold head above plane of body when prone

4 mo

Able to lift head and chest off bed with weight on forearms when prone

6 mo

Able to lift head and chest off bed with weight on hands; head does not lag when pulled from supine to sitting position; sits with support; head held steady when sitting; turns head side to side; rolls over; almost full weight on legs when held in standing position

9 mo

Sits without support, legs extended; sits “tailor fashion”—external rotation; sits with legs in internal rotation; pulls self to stand; stands with two-hand support; crawls

12 mo

Leans and recovers balance when sitting; walks with one-hand support

14 mo

Stands without support; walks forward without support; stoops and recovers balance

18 mo

Ascends stairs with two-hand support

2 yr

Ascends stairs without support, one foot at a time; runs forward; jumps in place; kicks ball forward

3 yr

Ascends stairs without support, foot over foot; descends stairs with support, one foot at a time; able to stand briely on one foot; pedals tricycle

4 yr

Descends stairs without support, foot over foot; beginning to balance on one foot; hops on one foot; able to climb well

5 yr

Hops on one foot without support; skips one foot at a time; forward heel-toe walk

6 yr

Backward heel-toe walk; throws ball up and catches it with one hand

19

20

SECTION I Disciplines

pattern of gait develops between 3 and 5 years of age.14 A more complete description of normal pediatric gait patterns is provided in Chapter 5.

Fine Motor Skills The approximate ages at which children normally attain various ine motor skills are listed in Table 1-2. A child’s exploration of the environment by touch and the development of manual skills should emerge in an orderly and sequential manner. At 3 months of age, infants can apply

1

2

4

3

5

FIGURE 1-12 Tanner’s stages of development of secondary sexual characteristics: male.

lip pressure and coordinate sucking and swallowing during feeding (the sucking relex is present at birth in all normal full-term neonates but usually disappears at 3 to 4 months of age). By 6 months of age, children are able to feed themselves from hand to mouth. By 9 months, children can feed themselves food such as cookies. By 12 months of age, children can pick up a spoon from the table, chew cookies or toast, and drink milk from a cup if assisted. Between 12 and 18 months, they are able to feed themselves (messily) with a spoon and drink from a cup by using one or two hands. By 24 months, they can feed themselves semisolid food with a spoon and drink holding the cup in one hand or using a straw. Children should be able to purposefully grasp objects such as a bottle or toy rattle by 6 months of age. At 9 months of age, children use their ingers and thumb to grasp objects and are able to transfer objects from one hand to the other. By 12 months, children’s hand skills are such that they are able to hit two objects together, voluntarily release objects, manipulate and throw objects on the loor, and hold crayons and imitate scribbling. Between 18 and 24 months of age, their hand skills evolve to the point that they can build block towers, turn pages one at a time, and throw a ball (but inaccurately). Between 2 and 3 years of age, their writing skills evolve from imitating vertical, horizontal, and circular strokes to copying circles. Ambidexterity (i.e., lack of hand preference) is normal during the irst 18 to 24 months of age. If an infant

Anterior

A

1

2

3

4

5

1

2

3

4

5

1

2

3

4

5

Lateral

B

FIGURE 1-13 Tanner’s stages of development of secondary sexual characteristics: female. A, Breast development. B, Genital development.

CHAPTER 1 Growth and Development

Table 1-2 Developmental Milestones for Fine Motor Skills Age

Fine Motor Skills

3 mo

Symmetric head and arm posture in supine position; lip pressure on feeding; coordination of sucking and swallowing

6 mo

Purposefully reaches out and touches objects; palmar grasp of bottle or toy; involuntary release of bottle or toy; hand-to-mouth feeding

9 mo

Extended reach and grasp; uses ingers and thumb to grasp objects; releases object with lexed wrist; transfers object from hand to hand; can feed self cookies; can protrude tongue during feeding

12 mo

Attempts to stack one block on another (brings over and drops); hits two objects together; can voluntarily release object; rolls ball imitatively; puts round block into round hole; puts cube into container; can hold crayon and imitate scribbling; picks spoon up from table; chews cookies or toast; drooling controlled at all times; drinks milk from cup, if cup is held

18 mo

Builds three-block tower (1-in cube); turns pages (two or three at a time); puts pegs into hole (1-in diameter); pounds; hurls ball; points to nose, eyes, ears; drinks from cup (one- or two-handed); feeds self with spoon, but messily

2 yr

Builds six-block tower; turns pages one at a time; throws bean bags; strings beads (1 in); throws ball, but inaccurately; feeds self semisolid food with spoon; drinks from cup or glass with one hand or straw; imitates vertical, horizontal, and circular writing strokes (but cannot initiate them)

3 yr

Builds nine-block tower; creases paper neatly; rides tricycle; feeds self with fork; tries to use scissors, but cannot follow line

4 yr

Throws ball overhand; copies cross when drawing

5 yr

Bounces ball and catches it; performs three simple directions in sequence; draws recognizable person; colors within 1-inch area; uses scissors, follows line

6 yr

Able to cut food with knife and eat with fork; copies printing (A, B, C)

Table 1-3 Developmental Milestones for Personal, Social, and Verbal Skills Age

Personal, Social, and Verbal Skills

3 mo

Smiles when spoken to; vocalizes without crying

4 mo

Turns head toward sound; recognizes mother

6 mo

Laughs and smiles spontaneously

10 mo

Responds to “no”; waves bye-bye; plays pat-a-cake; vocalizes “da-da” and “ma-ma” (nonspeciic)

12 mo

Begins to show interest in picture books; recognizes familiar objects; starts cooperating with dressing (extends arm for sleeve); able to speak two or more words other than “da-da” or “ma-ma”

18 mo

Removes socks and shoes; vocabulary of 10 words, including names

2 yr

Uses three-word sentences; matches colors

3 yr

Unlaces and removes shoes; learns to lace shoes; takes off pants; dresses self with supervision; puts on shoes (not necessarily on correct foot); tries to wash and dry hands; knows age and sex

4 yr

Puts shoes on correct feet; laces shoes, but does not tie bow; dresses, knows back and front of clothes; manages buttons; washes and dries face; brushes and combs hair; brushes teeth; counts three objects correctly

5 yr

Dresses and undresses self completely (except for back fasteners); names four colors; names penny, nickel, dime; counts 10 objects correctly

6 yr

Buttons small buttons on shirt; ties bows on shoes; combs and brushes hair

21

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demonstrates evidence of hand preference during this time, it may be caused by some defect in the hand and arm not being used, and attention should be directed to that limb’s status. This may be the irst sign of spastic hemiplegia.

Personal, Social, and Verbal Skills The approximate ages at which children should normally acquire various personal, social, and verbal skills are provided in Table 1-3. At 2 to 3 months of age, infants smile when spoken to and vocalize without crying. By 4 months, children turn their head to sound and recognize their mother, and at 6 months, they are laughing and smiling. At 8 to 10 months, infants respond to “no.” By 10 months, they wave bye-bye, play pat-a-cake, and say “da-da” and

“ma-ma.” The sounds “a,” “ba,” “da-da,” and “ma-ma” represent the earliest phase of speech and communication development, but the sounds do not have any speciic meaning to the child at this stage. By 12 months of age, children should begin to show an interest in picture books and recognize familiar objects. At this age, they also start cooperating with dressing, such as extending their arms for sleeves. Between 12 and 15 months of age, children should be able to speak 4 or 5 words (other than “da-da” or “mama”), and they achieve a vocabulary of 10 words (including names) by 18 months. They should be able to speak 3-word sentences by 24 months of age.

References For References, see expertconsult.com.

CHAPTER 1 Growth and Development

References 1. Burnett CN, Johnson EW: Development of gait in childhood. I. Method, Dev Med Child Neurol 13:196, 1971. 2. Burnett CN, Johnson EW: Development of gait in childhood. II, Dev Med Child Neurol 13:207, 1971. 3. Chapple CC, Davidson DT: A study of the relationship between fetal position and certain congenital deformities, J Pediatr 18:483, 1941. 4. Dunne KB, Clarren SK: The origin of prenatal and postnatal deformities, Pediatr Clin North Am 33:1277, 1986. 5. Frankenburg WK, Dodds JB: The Denver developmental screening test, J Pediatr 71:181, 1967. 6. Frankenburg WK, Fandal AW, Sciarillo W, et al: The newly abbreviated and revised Denver Developmental Screening Test, J Pediatr 99:995, 1981. 7. Hensinger RN: Standards in pediatric orthopedics, ed 1, New York, 1986, Raven Press. 8. Illingworth RS: The development of the infant and young child: normal and abnormal, ed 9, New York, 1987, Churchill Livingstone. 9. Prechtl HFR, Connolly KJ: Maturation and development: an introduction. In Connolly KJ, Prechtl HFR, editors: Maturation and development: biologic and physiologic perspectives, Philadelphia, 1981, Lippincott.

22.e1

10. Proceedings of the Greenwood Genetic Center: growth references: third trimester to adulthood, Greenwood, SC, 1998, Keys Printing. 11. Sheridan MD: The developmental progress of infants and young children, Ministry of Health report. London, 1960, Her Majesty’s Stationery Ofice. 12. Spranger J, Benirschke K, Hall JG, et al: Errors of morphogenesis: concepts and terms. Recommendations of an international working group, J Pediatr 100:160, 1982. 13. Statham L, Murray MP: Early walking patterns of normal children, Clin Orthop Relat Res 79:8, 1971. 14. Sutherland DH, Olshen R, Cooper L, et al: The development of mature gait, J Bone Joint Surg Am 62:336, 1980. 15. Tanner J: Growth and endocrinology of the adolescent. In Gardner L, editor: Endocrine and genetic diseases of childhood, ed 2, Philadelphia, 1975, Saunders. 16. Tanner JM: Growth at adolescence, ed 2, New York, 1982, Blackwell Scientiic. 17. Vaughan VG, Litt I: Developmental pediatrics: growth and development. In Behrman RE, Vaughan VC, Nelson W, editors: Nelson textbook of pediatrics, ed 13, Philadelphia, 1987, Saunders, p 6. 18. World Health Organization: WHO child growth standards, Geneva, 2006, World Health Organization Press.

CHAPTER 2

The Orthopaedic History Chapter Outline Chief Complaint 23 History of Present Illness Family History 23 Birth History 23 Growth and Development: Key Questions 24

23

The comprehensive pediatric orthopaedic history includes questions that are not normally asked as part of routine history taking in adult patients. A history of the mother’s pregnancy, the neonatal period, the child’s neurologic development, and the family history often have a much greater impact on the subsequent physical examination and diagnosis in children than in adults. An outline of pertinent historical features included in the initial history and physical examination used at Texas Scottish Rite Hospital for Children in Dallas is presented in Chapter 3 (see Appendix 3-1).

Chief Complaint The orthopaedic history starts by recording the chief or presenting complaint or complaints. Common musculoskeletal complaints include deformities, limp, localized or generalized weakness, and joint swelling, pain, and stiffness. With pediatric patients, the orthopaedist needs to determine whether the chief complaint is the concern of the child, the parents, a schoolteacher, or some other person.

History of Present Illness Next the examiner should develop a clear, chronologic narrative of the present problem, including its onset, the setting in which it developed, its manifestations, and any previous treatments. The principal symptoms should be described according to their location, quality, quantity or severity, timing (onset, duration, frequency), setting, aggravating or relieving factors, and any associated manifestations. Because the musculoskeletal system is involved with support and locomotion, many related symptoms are caused by physical stress and motion. Thus it is important to determine whether the patient’s symptoms are related to physical activity. If the patient has any history of injury, details of the trauma should be investigated to determine its signiicance to the present complaint. All this information must be put into the proper context based on the patient’s age—that is, what the child’s status

John G. Birch

should be in normal growth and development. Finally, the examiner should determine how each family member responds to the child’s symptoms, why he or she is concerned, and the secondary gains the child (or other individuals) may acquire from the illness.

Family History The information sought in the family history should be relevant to the patient’s present illness and appropriate to the patient’s age. The age and health, or age and cause of death, of parents and siblings may be pertinent. Relevant health information about other relatives that may have an impact on the patient’s complaint should also be obtained. The presence of scoliosis, clubfeet, developmental dysplasia of the hip, skeletal dysplasias, repeated fractures, genetic conditions, and neuromuscular disorders in family members should be speciically obtained.

Birth History The child’s birth history, which includes the prenatal, natal, and neonatal periods, is particularly important when congenital disorders, neurologic impairments, or developmental problems are present. If necessary, the examiner should obtain the patient’s hospital records to conirm the parent’s historical information or to answer speciic questions that the parents are unable to answer.

Prenatal History During the irst trimester of pregnancy, embryogenesis (development of the embryo) and organogenesis (generation of the early organ systems during the end of the embryonic period of gestation) proceed at a rapid rate. By the end of the embryonic period, all the major body systems have been established and the principal body structure is complete. Any extrinsic interruption of normal organogenesis during the embryonic period can result in signiicant malformations (e.g., myelomeningocele, syndactyly, preaxial polydactyly). Thus any unusual incident during this period may be of clinical signiicance. • Was there any history of vaginal bleeding to indicate threatened abortion? • Did the mother have any infections during the irst trimester? • The deleterious effects of maternal rubella during the irst month of pregnancy, with consequent cataract, deafness, heart disease, mental retardation, and seizures in the child, are well established. 23

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SECTION I Disciplines

• Did the mother have a history of syphilis, toxemia, or diabetes mellitus during this period? • These conditions are also associated with a high incidence of abnormalities in the newborn. • Did the mother have genital herpes or herpes simplex? • Did the mother ingest any toxic substances or take any medications that could harm the fetus? Speciically, is there a history of illicit drug use or alcohol abuse during the pregnancy? • Did the mother suffer any accidents in which the abdominal wall was struck or in which there was excessive blood loss with critical lowering of her blood pressure? • Did the mother feel normal fetal movements between the fourth and ifth months of pregnancy? • A history of feebleness or absence of fetal movements during this period may be important in arthrogryposis multiplex congenita or Werdnig-Hoffmann disease.

Natal History Information should be obtained regarding the length of the pregnancy, the duration and nature of labor and delivery, and the condition of the newborn. • Was the onset of labor spontaneous or induced? • Did the mother receive an analgesic or other medications during labor, and if so, how long before delivery? • Was obstetric anesthesia (general, epidural, or other) used, or did the mother deliver without the use of anesthesia? • Were there any problems with the delivery of the infant? • Did the child present in a vertex or breech position? • Certain conditions, such as developmental dysplasia of the hip and congenital muscular torticollis, are more frequent in breech deliveries. • Occiput posterior or breech presentations may result in prolonged labor, resulting in a greater potential for anoxic episodes and other fetal distress. • Was the child premature? • What were the birth weight and length of the child?

Neonatal History The condition of the newborn during the neonatal period is particularly important in children with congenital disorders or neurologic impairments. • How long did it take for the infant’s irst breath and irst cry? What was the nature of the cry? • Were there any respiratory problems? Did the child require any time in an incubator? Was oxygen provided? Did the infant need to be intubated or otherwise resuscitated? • Were there any neonatal convulsions? • Was any exchange transfusion necessary? • What were the Apgar scores at 1 and 5 minutes? • What were the appearance and color of the newborn when irst seen by the parents?

• Was there any cyanosis? • Was there any jaundice? If present, when was it irst noted? How was it treated (observation at home, observation in the hospital, phototherapy, or exchange transfusion)? When did it disappear? • Was there any asymmetry of the face or limbs? • Were there any obvious deformities of the limbs? • Were there any infections, injuries, or evidence of trauma? • Was the infant’s muscle tone laccid, tight, or normal? • What was the nature of bonding with the mother? • Was sucking or feeding normal, feeble, or absent? • Did the newborn have to be tube fed? • When was the infant discharged from the hospital? Did the infant go home with the mother?

Growth and Development: Key Questions Obtaining a growth and development history is particularly important in a child with delayed growth, psychomotor or intellectual retardation, or behavioral problems. The examiner should determine whether the child is reaching certain milestones of development within the expected time periods. To do so, the examiner looks for evidence of the functional adequacy of the neuromusculoskeletal system (posture, functional development of the lower and upper limbs) and the general responsiveness of the infant to parents and objects in the environment (activities of daily living, social development, and speech). • When did the child irst lift his or her head? • When did the child begin to roll over, sit, crawl, pull up to a standing position, walk unsupported, run, ascend or descend stairs, and hop on one foot without support? • When did the child hold a bottle, reach for and grasp a toy, and transfer objects from hand to hand? • When did the child offer his or her arm for a coat or foot for socks, feed self unaided with a spoon or fork, and pull off or put on clothes? • At what age did the child smile when spoken to, turn his or her head to sound, respond to “no,” wave bye-bye, play pat-a-cake, and say “da-da” and “ma-ma”? • When did the child begin to show an interest in picture books and recognize familiar objects? • At what age was the child able to speak a few words, and when did he or she achieve three-word sentences? • The examiner should also inquire about the following: • Day and night sleeping patterns • Age of toilet training (stool and urine) • When hand dominance was noted • Speech problems • Habitual behavior patterns • Discipline problems • Relationship with parents, siblings, and peers • Whether the child attends school (regular or special) and what characterizes his or her scholastic performance

CHAPTER 3

The Orthopaedic Examination: A Comprehensive Overview

Angular Deformity

Chapter Outline Recognizing Deformities Joint Range of Motion Muscle Strength 43 Neurologic Assessment

John G. Birch

25 27 44

This chapter covers virtually all aspects of the general musculoskeletal and neuromuscular examination of the neonate, infant, child, and adolescent. Because proper function of the musculoskeletal system depends on proper functioning of the neurologic system, the boundary between orthopaedics and neurology is often blurred at the diagnostic level. The orthopaedist is frequently the irst to be consulted for clumsiness or delayed walking in a child, conditions that may be due to static encephalopathy or muscular dystrophy. Malfunction of the neurologic system can also have a signiicant impact on the child’s developing skeletal system. For example, muscle imbalance resulting from cerebral palsy, myelomeningocele, or spinal cord injury may lead to scoliosis or dislocation of the hip joint. Thus the pediatric orthopaedist must not only be familiar with examination of the musculoskeletal system but also knowledgeable about the neurologic examination of the child at different developmental stages. The form used at Texas Scottish Rite Hospital for Children to record the principal indings of the initial orthopaedic examination is provided in Appendix 3-1.

Recognizing Deformities The examiner should look for signs of musculoskeletal deformity, determine what type of deformity exists, and ascertain its exact location. If deformities exist, speciic tests can help reveal them. Answers to the following questions will help accomplish this goal: • Is the deformity in the bones, the joints, or the soft tissues? • How severe is the deformity? • Is the deformity ixed, or can it be passively or actively corrected? • What factors are causing the deformity? • Is there associated muscle spasm, local tenderness, or pain with motion?

The description of angular deformities should specify the site of the deformity and the position of the distal segment of the deformity relative to the proximal portion. The speciic location of the deformity is denoted by its anatomic name, such as cubitus (elbow, forearm, ulna), coxa (hip), genu (knee), or pes (foot). The direction of the deformity is designated as either valgus or varus, terms that deine alignment in the coronal plane. Valgus denotes an angulation away from the midline of the body distal to the anatomic part named (i.e., the distal segment is deviated away from the midline). In cubitus valgus, the forearm is directed away from the midline, distal to the elbow. Approximately 10 to 15 degrees of cubitus valgus, or “carrying angle,” is normal. In coxa valga, the angle between the femoral neck and shaft is greater than normal and the distal segment is angled away from the midline. Varus describes an angulation toward the midline of the body distal to the anatomic part named (i.e., the distal segment is deviated toward the midline). In cubitus varus, the forearm is bent inward toward the midline of the body, distal to the elbow, whereas in coxa vara, the angle between the femoral neck and shaft is smaller than normal and the distal segment is angled toward the midline. Angular deformities are measured in degrees and are most accurately recorded using a hinged goniometer. With experience, the orthopaedist may be able to estimate angular measurements accurately, but more reliable measurements are usually obtained with a goniometer.10,68,80 However, when bony landmarks are not clear because of excess soft tissue coverage or other causes, the goniometer may give inaccurate results. If necessary, the examiner can gauge angles by visually dividing a 90-degree arc of motion into two 45-degree segments or three 30-degree segments and projecting the observed angle into these arcs. The affected limb should always be compared with the contralateral extremity. The degree of cubitus valgus, or carrying angle, of the elbow is measured with the elbow at the zero starting position (i.e., with the elbow fully extended and at 0 degrees of lexion).2,3 The goniometer is positioned on the volar surface of the arm and aligned with the midaxis of the humerus and the midaxis of the forearm30 (Fig. 3-1). Beals measured the mean carrying angle in a radiographic study conducted on 422 patients.7 Patients were divided into four age groups: newborn through 4 years of age, 5 through 11 years, 12 through 15 years, and adults, with approximately 25

26

SECTION I Disciplines

FIGURE 3-1 Measurement of the carrying angle of the elbow joint (cubitus valgus). (Reproduced from Greene WB, Heckman JD: The clinical measurement of joint motion. Rosemont, Ill, 1994, American Academy of Orthopaedic Surgeons.)

50 male and 50 female subjects in each group. The mean carrying angle was 15 degrees in the newborn to 4-year-old group and increased slightly with age to 17.8 degrees in adults, both men and women. Knee joint alignment is measured with the patient standing with the knee fully extended. The goniometer is aligned with the midaxis of the distal femur and proximal tibia (the anatomic axis of the knee; Fig. 3-2). For most clinical evaluations, this measurement is suficient; however, for hip surgery and lower extremity realignment, preoperative assessment of the axis of the hip, knee, and ankle (the mechanical axis) should be done using full-length, weightbearing radiographs. Normal knee alignment, as measured by the femoral-tibial angle, changes as a child grows older. Neonates usually have 10 to 15 degrees of varus angulation. The angulation evolves to a neutral femoral-tibial alignment between 14 and 22 months of age, with a maximum valgus of 10 to 15 degrees by 3 to 3½ years of age.23,69 This is followed by a gradual decrease in valgus, with normal mature alignment of 5 to 7 degrees of femoral-tibial angle realized by 6 to 8 years of age. Other objective methods of measurement can be used for speciic situations. The degree of genu valgum (knockknees) can be determined by measuring the distance between the medial malleoli when the knees are fully extended, the patellae are facing exactly forward, and the medial femoral condyles are brought together with moderately irm pressure to compress excessive subcutaneous fat. The degree of genu valgum can also be determined by measuring the angle between the lateral surface of the thigh and leg. The clinical appearance of knock-knees is exaggerated when there is excessive subcutaneous fat on the thigh or atrophy of the calf (especially of the medial head of the

FIGURE 3-2 Measurement of the standing femoral-tibial angle at the knee. (Reproduced from Greene WB, Heckman JD: The clinical measurement of joint motion. Rosemont, Ill, 1994, American Academy of Orthopaedic Surgeons.)

gastrocnemius). The degree of genu varum (bowlegs) can be similarly determined by bringing the medial malleoli together, irmly compressing them, and measuring the distance between the medial femoral condyles. The patellae must be facing exactly forward because medial rotation of the lower extremities at the hips will result in the appearance of bowlegs.

Contractures Contractures result from ibrosis of the tissues supporting the muscles or joints or from muscle iber disorders, either of which cause ixed resistance to passive stretch of a muscle. There is a shortening and loss of lexibility of muscles, joints, tendons, or fascia. Contractures can be either congenital or acquired. Examples of congenital contractures include congenital muscular torticollis, abduction contracture of the hip, and multiple pterygium syndrome. Children with spina biida often have capsular contracture of the posterior knee capsule. Acquired contractures of joints may be caused by muscle imbalance (as seen with cerebral palsy), inlammatory arthritis, muscle injury, periarticular trauma, or idiopathic conditions (e.g., morphea syndrome53). A tight iliopsoas muscle in a child with cerebral palsy or myelomeningocele may cause a hip lexion contracture. A displaced torn meniscus that impedes extension of the joint may cause lexion contracture of the knee. Synovial luid collection secondary to juvenile arthritis may block normal joint motion. Forearm ischemia from a compartment syndrome results in Volkmann’s contracture, which is characterized by pronation and

CHAPTER 3 The Orthopaedic Examination: A Comprehensive Overview

lexion of the hand, shrinkage and hardening of the forearm muscles, and loss of muscle power. Muscle or joint contractures can also occur after surgery if the patient does not perform appropriate strengthening and range-of-motion (ROM) exercises. Gastrocnemius contracture can occur if the ankle is immobilized with the foot in equinus. Evaluating contractures is an important part of the pediatric orthopaedic examination. Neonates have physiologic contractures of upper and lower limbs.15,25,63,65,81 In infants and younger children, contracture assessment primarily focuses on the lower extremities, whereas in older children, particularly those who participate in throwing sports, it is important also to inspect the upper extremity (i.e., the elbow and shoulder). When assessing two-joint muscles (e.g., hamstrings, gastrocnemius) for contracture, the examiner needs to restrict the movement of one joint before testing the second joint. For example, when examining for a hamstring contracture, irst the femur should be lexed and stabilized on the pelvis, and then the knee extended.

Joint Range of Motion Measuring joint ROM provides important information regarding orthopaedic diseases and disorders, and the results of treatment. The effect of acute illness or injury on joint motion can help in diagnosing the disease or disorder. For example, both transient synovitis and septic arthritis of the hip reduce joint mobility, but the loss of motion is much greater in the infected joint. Improvement in joint motion during treatment for septic arthritis indicates that the hip is responding to therapy. The extent and type of injury to a joint during athletic competition can be determined to some degree by how much joint mobility is lost. A return to normal joint motion is an important factor in deciding when an athlete is ready to return to competition. During the physical examination, joint motion can be measured actively, whereby the patient moves the limb, or it can be measured passively, whereby the examiner moves the patient’s limb. Active and passive ROM often differs when disease or injury to a joint renders the patient incapable of completing full ROM against gravity. When this occurs, both arcs of motion should be recorded. The examiner should also compare the motion of the affected extremity with that of the normal, contralateral one because joint mobility is normally the same on the right and the left sides.* Joint motion is most accurately measured with a goniometer,80 particularly at the elbow, wrist, inger, knee, and ankle joints. Because overlying soft tissue at the shoulder and hip obscures bony landmarks, it is more dificult to obtain consistent alignment of the goniometer at these joints. To measure an extended extremity, one arm of the goniometer is aligned with the axis of the proximal segment and the other arm is aligned with the axis of the distal extremity. The 0-degree mark is positioned on the distal segment. The proximal end of the goniometer is held in place while the joint is moved and the distal arm of the goniometer rotated. At completion of the movement, the degree of joint ROM is recorded from the goniometer.30 *References 9, 10, 34, 49, 57, 66, 76.

27

Box 3-1 Description of Joint Motions Flexion: Act of bending a joint; a motion away from the zero starting position. Extension: Act of straightening a joint; a return motion to the zero starting position. Hyperextension: When the motion opposite to lexion is an extreme or abnormal extension (as may be seen with the knee or elbow joint), and the joint extends beyond the zero starting position. Abduction: Lateral movement of the limbs away from the median plane of the body, or lateral bending of the head or trunk. Adduction: Movement of a limb toward the median plane of the body. Supination: Act of turning the forearm or hand so that the palm of the hand faces upward or toward the anterior surface of the body. Pronation: Turning of the palm of the hand so that it faces downward or toward the posterior surface of the body. Inversion: An inward turning motion (seen primarily in the subtalar joint of the foot). Eversion: An outward turning motion. Internal (inward) rotation: Process of turning on an axis toward the body. External (outward) rotation: Process of turning on an axis away from the body (opposite motion of internal rotation).

Motion is measured in degrees of a circle, with the joint as its center.12 The degrees of motion of a joint are added in the direction in which the joint moves from the anatomic zero starting position. To ensure conformity when measuring joint ROM, the extended anatomic position of a limb is designated as being 0 degrees (rather than 180 degrees).30 Thus when a fully extended extremity joint is bent from the anatomic zero position to a right angle, the range of motion is 90 degrees of lexion. The different joint motions are described in Box 3-1. Normal joint ROM varies among persons based on age and sex. Neonates typically have (1) decreased abduction of the shoulder, (2) greater external rotation and limited internal rotation of the hip, (3) greater dorsilexion and limited plantar lexion of the ankle, and (4) lexion contractures at the elbow, hip, and knee.25,35 By 3 months of age a child usually exhibits an adult arc of motion at all joints except the hip.35 The hip joint continues to show an increase in external rotation and a decrease in internal rotation until the child is 8 to 24 months of age.15,35,75 Joint ROM is greater in children than in adults because children have greater joint laxity.85 Children also have a greater inversion and dorsilexion of the foot and ankle than adults. As a person ages, connective tissue becomes progressively more rigid, particularly in and around muscles and tendons, resulting in decreased joint ROM.6 Because of greater ligamentous laxity, girls and women have greater ROM than boys and men in some joints,18,49 but not in all joints or in all planes of motion.49,57,67

Spasticity Spasticity refers to an abnormal increase in muscle tone (excessive muscle tension) that interferes with muscle

28

SECTION I Disciplines

180°

180° 180°

90°

90° 90°

A

0°

B

C 0°

0°

FIGURE 3-3 Total shoulder motion is a combination of scapulothoracic and glenohumeral movement. Stabilizing the scapula (A) allows the examiner to assess glenohumeral motion (B). Leaving the scapula free allows the examiner to assess total shoulder motion (C). Scapulothoracic motion is responsible for the difference between the motion measured in B and C. (Adapted from Committee for the Study of Joint Motion: Joint motion: method of measuring and recording. Chicago, 1965, American Academy of Orthopaedic Surgeons.)

relaxation, impedes normal joint ROM, and causes stiff and awkward movements. Spasticity can result from upper motoneuron injury, with cerebral palsy the most common cause of both. During the physical examination, the degree of actual spasticity in a particular muscle can change signiicantly depending on numerous factors, including patient anxiety, room temperature, and time of day. It is more dificult to put certain joints through passive ROM when a patient has spastic muscles (e.g., extension of the knee joint when the hamstrings are spastic). However, with gentle persuasion by the examiner, the spastic muscle usually will relax and greater joint motion can be attained. Changes in patient body position can also affect ROM. Because of this, measurements of the same parameter may vary during the examination. A review by Perry62 showed that ankle dorsilexion decreased as patients went from the supine position to sitting to standing. In 95% of patients with cerebral palsy, lexion of the knee permitted greater ankle dorsilexion. To accommodate this variability, the examiner should note at what degree initial resistance is encountered and the total ROM attained with persuasion. The reliability of goniometric measurements in determining joint motion in patients with spasticity is debatable.4,32 The examiner should also describe the general muscle tone of the patient, characteristics of the resistance (e.g., persistent initial resistance with ensuing relaxation, constant ixed resistance), and the position of adjacent joints (e.g., whether the hip or knee was lexed or extended, or the foot was neutral or supinated, when testing ankle dorsilexion). For example, one might record that the ankle has 10 degrees of dorsilexion with the knee extended.

Shoulder The shoulder has the greatest ROM of any joint in the body, allowing a myriad of positions and planes of motion.33 Shoulder motion is divided into true glenohumeral motion, pure scapulothoracic motion, and combined glenohumeral and scapulothoracic motion (Fig. 3-3). Maximum shoulder motion normally is a combined movement rather than motion in a single plane.30 For example, to achieve maximum elevation (lexion), there must be a combination of slight external rotation and abduction.11 Extension (backward motion) and lexion (forward motion) of the shoulder occur in the sagittal plane (Fig. 3-4). Abduction and adduction of the shoulder occur only in the horizontal plane from the midsagittal zero position of the body (Fig. 3-5). Abduction is motion of the arm away from the midsagittal axis of the body; adduction is movement of the arm toward the axis. During the physical examination, shoulder motion is assessed with the patient standing. However, if the examiner cannot control spine and pelvic motion, the patient should be supine when external rotation and elevation are measured. The term elevation (i.e., lexion) is used to deine all upward motions of the humerus in any plane; that is, motions entailing the vertical raising of the arms in any position of the horizontal plane of abduction or adduction33 (see Fig. 3-4, B). The zero starting position is with the arm at the side of the body. When assessing range of elevation of the glenohumeral joint, the examiner stands behind the patient and immobilizes the scapula by holding its inferior angle (see Fig. 3-3, A). Scapulothoracic joint motion

CHAPTER 3 The Orthopaedic Examination: A Comprehensive Overview

0°

29

0°

90°

40°

A

FIGURE 3-4 Extension (backward motion; A) and lexion (forward motion; B) of the shoulder in the sagittal plane.

B 0°

0°

180°

90°

90°

0° FIGURE 3-5 Abduction and adduction of the shoulder in the horizontal plane from the midsagittal zero position of the body.

can be further restricted by irmly placing a hand over the acromion of the upper limb being tested. In combined glenohumeral and scapulothoracic motion, the scapula rotates upward and forward over the chest wall, allowing the shoulder to elevate to 180 degrees (see Fig. 3-3, B and C). When the shoulder is elevated, the irst 20 degrees of motion represents pure glenohumeral joint motion, and the scapula does not move (Fig. 3-6, A). After this point, continued elevation of the arm results in combined movement of the glenohumeral and scapulothoracic articulations in a 2:1 ratio (i.e., for every 3 degrees of total shoulder elevation, 2 degrees of elevation represents motion of the glenohumeral joint and 1 degree of elevation comes from the scapulothoracic joint26; see Fig. 3-6, B). When the scapula

is immobilized, pure glenohumeral elevation is approximately 90 degrees (see Fig. 3-6, C). At approximately 120 degrees of combined shoulder elevation, the surgical neck of the humerus abuts the acromion process (see Fig. 3-6, D). Complete elevation of the shoulder (i.e., 180 degrees) is a combined glenohumeral and scapulothoracic movement. The elevation is made possible by external rotation of the shoulder, which turns the surgical neck of the humerus away from the tip of the acromion and increases the articular surface of the humeral head (see Fig. 3-6, E). Shoulder extension (posterior elevation) is motion of the extended arm in the opposite direction from that of forward elevation (see Fig. 3-4, A). For maximum extension, the shoulder must rotate internally.11 Normally, the shoulder is able to extend 45 to 55 degrees. Internal and external shoulder rotation are assessed with the patient’s arm in the neutral position and the examiner standing in front of the patient. The patient’s elbow must be at the side of the body and lexed 90 degrees to prevent substitution of adduction for external shoulder rotation and abduction for internal shoulder rotation. The forearm, which is parallel to the sagittal plane of the body, is rotated internally toward the sagittal axis of the body and externally away from the body. The shoulder is the axis and the forearm is the indicator of motion (Fig. 3-7, A). The normal range of internal shoulder rotation is 50 to 60 degrees (the chest wall blocks its motion), and the normal range of external shoulder rotation is 40 to 45 degrees. Shoulder rotation may also be assessed with the neutral zero position of the shoulder at 90 degrees of elevation and 90 degrees of abduction, and with the forearm parallel to the loor (see Fig. 3-7, B). In internal rotation, the arm is moved inferiorly toward the loor, with the average internal rotation approximately 70 degrees. Restricted internal rotation in this position may be due to shoulder instability.29 In external rotation, the shoulder is moved superiorly toward the ceiling, with the average external rotation approximately 100 degrees.

30

SECTION I Disciplines

90° 20°

2:1

A

B

FIGURE 3-6 A, When the shoulder is elevated, the irst 20 degrees of movement represents pure glenohumeral joint motion; the scapula does not move. B, From this point, continued elevation of the arm results in combined movement of the glenohumeral and scapulothoracic articulations in a 2:1 ratio. C, When the scapula is immobilized, pure glenohumeral elevation is approximately 90 degrees. D, At approximately 120 degrees of combined shoulder elevation, the surgical neck of the humerus abuts the acromion process. E, Complete elevation of the shoulder (i.e., 180 degrees) is a combined glenohumeral and scapulothoracic movement and is made possible by external rotation of the shoulder, which turns the surgical neck of the humerus away from the tip of the acromion and increases the articular surface of the humeral head.

C

180°

120°

D

E

90°

45°

0° 0° 45°

45°

45° 90°

A

90°

B 90°

FIGURE 3-7 A, Internal and external rotation of the shoulder measured with the arm at the side of the body. Normal range of internal rotation is 50 to 60 degrees; normal range of external rotation is 40 to 45 degrees. B, Internal and external rotation measured with the shoulder in neutral zero position at 90 degrees of elevation and 90 degrees of abduction (i.e., the forearm is parallel to the loor). Internal rotation moves the arm inferiorly toward the loor; external rotation moves the shoulder superiorly toward the ceiling.

CHAPTER 3 The Orthopaedic Examination: A Comprehensive Overview

A

D

B

31

C

E

F

FIGURE 3-8 Quick method of clinically assessing active shoulder range of motion. A, Elevation of both shoulders. B, Horizontal abduction and external rotation. C, Adduction and internal rotation. D, Extension, internal rotation, and adduction. E, Elevation, internal rotation, and adduction. F, Extension, adduction, and internal rotation.

There are a number of quick and easy methods of clinically estimating active shoulder ROM. To measure shoulder elevation, the patient should stand with elbows straight and forearms fully supinated, and then raise both arms vertically and touch the ingers over the head (Fig. 3-8, A). To measure horizontal abduction and external rotation, the patient should place both hands behind the neck and push the elbows posteriorly (see Fig. 3-8, B). Adduction and internal rotation are measured by having the patient reach across the chest and touch the opposite shoulder (see Fig. 3-8, C). Extension, internal rotation, and adduction are tested by having the patient reach behind the back and touch the lower angle of the opposite scapula (see Fig. 3-8, D). Elevation, internal rotation, and adduction are tested by having patient reach behind the head and neck and touch the upper angle of the opposite scapula (see Fig. 3-8, E). Finally, having the patient reach behind the back and touch the opposite buttock allows the examiner to measure extension, adduction, and internal rotation (see Fig. 3-8, F). (These measurements are best used comparing both sides.)

Elbow The elbow is a typical hinge joint in which there is only one freedom-of-motion plane. Although there are three sites of movement—the ulnohumeral, radiohumeral, and radioulnar articulations—elbow motion is centered at the ulnohumeral joint,3and the description of motion is typically limited to the lexion-extension plane.14 The zero starting position is with the elbow fully extended and straight (0 degrees) and the arm in supination. The normal elbow ROM is from 0 to 150 degrees of lexion and from 150 degrees (the angle of maximum lexion) to 0 degrees of extension (the zero starting position; Fig. 3-9, A). Hyperextension, measured as degrees by which the joint extends beyond the zero starting position, varies from 5 to 15 degrees.13,85 Hyperextension is not seen in all individuals. Restricted elbow ROM may be described, for example, as lexion from 30 to 90 degrees, or a joint that has a lexion deformity of 30 degrees with further lexion to 90 degrees (see Fig. 3-9, B).

32

SECTION I Disciplines

90°

90°

150°

150° 30°

0° Neutral 15° Hyperextension

180°

A

180°

0° Neutral

B

Normal

Limited motion

FIGURE 3-9 A, Normal arc of elbow lexion and extension. In the zero starting position the elbow is fully extended and straight (0 degrees), and the forearm is supinated. B, Examples of limited arcs of elbow motion.

Box 3-2 Cervical Range of Motion at Different Vertebral Levels Occiput to C1: Substantially greater extension than lexion C1-6: Flexion and extension approximately equal Lower cervical segments: Flexion/extension greater, with maximum movement at C5-6 C6-T1: Flexion greater than extension, particularly at C7-T1

90°

90° Supination

0°

Pronation

FIGURE 3-10 Supination is turning of the palm forward or anteriorly, such that the palm faces up. Pronation is turning of the palm backward or posteriorly, such that the palm faces down.

Forearm Rotation of the forearm is a combined motion of the proximal and distal radioulnar joints and the radiohumeral joint.2 The planes of motion are pronation (turning of the palm backward or posteriorly: the palm faces down) and supination (turning of the palm forward or anteriorly: the palm faces up; Fig. 3-10). To assess forearm rotation, the humerus is stabilized against the torso (to prevent any compensating adduction and abduction motion by the humerus to augment pronation and supination), and the elbow is lexed to 90 degrees.17 The zero starting position is with the extended thumb aligned with the humerus.30 To better evaluate the degree of pronation and supination, the examiner should palpate the radial and ulnar styloid as the forearm is being

rotated. Having the patient hold a pencil or similar object in the palm with lexed ingers can make it easier to discern forearm rotation. Normal range of pronation is 70 to 80 degrees, and normal range of supination is 80 to 90 degrees.9,71,79

Cervical Spine The cervical spine is the most lexible part of the vertebral column. There are goniometers speciic for measuring cervical spine motion; however, standard goniometers are just as accurate.86 Visual evaluation of cervical spine motion is not as reliable as goniometric measurement. The ROMs evaluated include lexion, extension, right and left lateral bending, and right and left rotation. Normally, opposite movements (e.g., lexion/extension, right/left bending, right/left rotation) are nearly equal.30,41 However, the ROM in particular planes varies at different vertebral levels1,20,41,60,61 (Box 3-2). Parameters for cervical spine mobility based on the age of the patient are provided in Table 3-1.34 Box 3-3 shows the movement of the vertebrae at the various levels of the cervical spine.30,54 A more extensive discussion of the various ROMs of the cervical spine can be found in The Cervical Spine, by the Cervical Spine Research Society.39

33

CHAPTER 3 The Orthopaedic Examination: A Comprehensive Overview

Table 3-1 Radiographic Cervical Spine Mobility in 160 Patients Aged 1 to 16 Years (10 Patients per Year of Age) Total (1-16 yr)

Age (yr)

Total (1-7 yr)

Displacement/Mobility

1

2

3

4

5

6

7

8

9

10

11

12

13

14

15

16

No.

(%)

No.

(%)

Anterior displacement C2-3 (marked)

4*

1

3

1

2

2

0

0

1

1

0

0

0

0

0

0

15

(9)

13

(19)

Anterior displacement C2-3 (moderate)

1

2

1

3

2

2

4

1

1

2

3

1

1

0

0

0

24

(15)

15

(21)

Anterior displacement C2-3 (total)

5

3

4

4

4

4

4

1

2

3

3

1

1

0

0

0

39

(24)

28

(40)

Measured AP movement ≥ 3 mm

5

4

5

2

5

6

5

2

4

5

4

6

7

4

4

3

71

(44)

32

(46)

Number of children with measured AP movement > 3 mm and observed anterior displacement at C2-3

4

3

3

1

3

4

3

0

1

3

1

1

1

0

0

0

28

(18)

21

(30)

Anterior displacement C3-4†

3

2

1

1

2

4

1

0

2

2

2

1

1

0

0

0

22

(14)

14

(20)

Overriding of anterior arch of atlas relative to odontoid (extension views)‡

2+

4++

3++

1

1+

3

0

1

0

0

0

0

0

0

0

0

14

(9)

14

(20)

Wide space between anterior arch of atlas and odontoid (lexion views)

2

2

3

2

2

2

1

0

0

0

0

0

0

0

0

0

14

(9)

14

(20)

Total (5-11 yr)

Presence of apical odontoid epiphysis

0

0

0

0

3

2

3

1

4

1

4

0

0

0

0

0

15

(9)

No.

(%)

18

(26)

Total (1-5 yr)

Presence of basilar odontoid cartilage plate

10

9

9

6

4

0

0

0

0

0

0

0

0

0

0

0

48

(30)

Angulation at single level

1

4

1

1

3

3

2

0

1

2

1

2

2

1

2

0

25

(16)

Absent lordosis in neutral position

3

0

0

0

0

0

0

1

2

1

3

2

2

5

1

2

22

(14)

Absent lexion curvature C2-7 in lexion view

1

2

1

6

4

1

0

0

2

3

1

1

1

1

2

0

26

(16)

No.

No.

38

(76)

From Cattell HS, Filtzer DL: Pseudosubluxation and other normal variations in the cervical spine in children: a study of one hundred and sixty children. J Bone Joint Surg Am 47:1295, 1965. AP, Anteroposterior. *Boldface numbers represent predominant age range for particular variable. † Twenty of 22 children with anterior displacement at C3-4 also had displacement at C2-3. ‡ Presence of wide atlanto-odontoid space in same child (each + represents one child).

Although goniometric measurement is more accurate, clinical evaluation is usually performed by visual assessment, with the patient’s nose and chin used as midline landmarks. Inclinometers may also be used during an examination. The tool is accurate in measuring lexion/ extension and lateral bending but is not as reliable for rotation.1

The zero starting position for measuring lexion/extension motion is with the neck aligned with the trunk (Fig. 3-11). The examiner should stabilize the trunk during the movements so that thoracic spine motion does not come into play. Flexion can be measured in degrees or, if motion is limited, by the distance remaining between the chin and sternum on maximum forward bending. With normal range

34

SECTION I Disciplines

0° Extension

0° Flexion

Left rotation

90°

Right rotation

90°

FIGURE 3-13 Measurement of rotation of the cervical spine.

FIGURE 3-11 Assessment of lexion and extension of the cervical spine.

0°

should be stabilized when testing lateral bending. The degree of bending is measured as the angle between the midaxis of the face and the beginning vertical line. Rotation is measured from the zero starting position (Fig. 3-13). If the neck is placed in maximum lexion, rotation is restricted to the upper cervical spine.18 Normally, a child’s cervical spine is mobile enough to permit touching of the ear to the adjacent shoulder when bending the neck, and touching of the chin to the shoulder when rotating the head. Cervical spine disorders result in a decreased ROM in the affected vertebral segments.19 However, because clinical demonstration of limited cervical motion indicates only that a disorder is present, radiographs are needed to determine the extent of the problem and its cause.

Thoracolumbar Spine

FIGURE 3-12 Assessment of lateral bending of the cervical spine.

Box 3-3 Movement of the Vertebrae at Various Levels of the Cervical Spine C1-2: 55%-60% of rotation occurs at this level. Occiput to C5: Flexion is coupled with rotation. C5-7: Extension is combined with rotation. Upper cervical spine: Lateral bending goes in opposite direction of rotation. Lower cervical spine: Bending goes in same direction as rotation.

of lexion, the patient should be able to touch the chin to the chest, and with normal range of extension, the patient should be able to look at the ceiling.36 The zero starting position for measuring lateral bending and rotation is with the nose vertical and perpendicular to the axis of the shoulders (Fig. 3-12). Again, the trunk

Like motion of the cervical spine, thoracolumbar spine motion represents a combination of movements of several joints to produce lexion/extension, right and left lateral bending, and right and left rotation.82,83 In the thoracic spine, lexion/extension is greatest in the lower thoracic spine, lateral bending is slightly increased in the lower thoracic region, and rotation is greatest in the upper thoracic segment. In the lumbar spine, lexion/extension is greatest in the lower lumbar vertebrae, lateral bending is most restricted at the lumbosacral junction, and rotational movements are relatively limited. Accurately measuring thoracolumbar joint motion can be dificult. Assessment can be made by visual estimation, goniometric measurements, skin distraction, or inclinometer techniques.30 The combination of extensive soft tissue coverage and obscured midline landmarks makes visual assessment extremely subjective and goniometric measurements dificult. The examiner usually is able to obtain more objective and accurate measurements of thoracolumbar motion using skin distraction21,24,29,48,78 or inclinometer techniques.42,64,70

Flexion The zero starting position for measuring lexion is with the patient standing with the hips and knees straight, the trunk aligned with the lower limbs, the feet slightly apart, and the

CHAPTER 3 The Orthopaedic Examination: A Comprehensive Overview

FIGURE 3-14 Zero starting position for testing thoracolumbar lexion.

arms hanging to the sides in a relaxed, extended position30 (Fig. 3-14). Measuring the distance between ingertips and loor when the patient is at maximum lexion (Fig. 3-15) is a simple technique, but this method of assessment has poor repeatability84 and is not considered reliable for patients with low back problems. The double inclinometer test can be used to measure lumbar lexion more accurately, but the test requires two inclinometers and a cooperative patient42,64,70 (Fig. 3-16). One inclinometer is placed over the sacrum and the other inclinometer is positioned over the spinous process of T12. With the patient in maximum lexion, the degree of lexion is obtained by subtracting the sacral inclinometer reading from the reading of the T12 inclinometer. When examining the lower back, it is important to remember that limited lexion of the lumbar spine may be caused by disorders that do not involve the spine, such as any restriction of hip lexion or contractures of the hamstrings.

Extension Back extension is evaluated by having the patient stand in the zero starting position with the palms on the buttocks and then bend backward as far as possible. Extension can be estimated visually or with a goniometer,8,21,24 or it can be more accurately measured with the double inclinometer test (Fig. 3-17). One inclinometer is placed over the sacrum and the other inclinometer is positioned over T12. With the patient in maximum extension, the degree of extension is obtained by subtracting the sacral inclinometer reading from the reading of the T12 inclinometer.

35

FIGURE 3-15 Visual inspection of thoracolumbar lexion. Normal lumbar lordosis disappears with lexion and a slight lumbar kyphosis is seen. When the patient is at maximum lexion, the examiner measures the distance between the patient’s ingertips and the loor.

Lateral Bending Lateral bending is measured by marking the spinous processes of T1, T2, and S1. The patient then starts in the zero starting position and inclines the trunk to the right and left while keeping the knees straight. The degree of bend can be estimated visually or with a goniometer21,24 (Fig. 3-18). Lateral bending also can be determined with a tape measure.52 The double inclinometer also can be used to measure lateral bending, with the inclinometers set the same as for measuring lexion and extension, and calculated by subtracting the sacral inclinometer reading from the T12 reading at maximum bending.

Rotation Spinal rotation can be visually estimated by having the patient rotate to the right and left while the examiner holds the pelvis irmly in place and maintains the scapula in a neutral position. The degree of thoracolumbar rotation is estimated based on an imaginary line transecting the plane of the patient’s shoulders (Fig. 3-19). Average spinal rotation is approximately 45 degrees.

Hip The hip is a complex ball-and-socket joint capable of threedimensional compound or rotatory motion. However, its ROM is signiicantly less than the shoulder’s (also a balland-socket joint), because the acetabulum is substantially deeper than the glenoid. The normal hip ROM for children at different ages has been published by a number of authors15,25,30,31,76 (Table 3-2).

36

SECTION I Disciplines

T12

Midsacrum

A

B

FIGURE 3-16 Double inclinometer test for lumbar lexion. A, One inclinometer is placed over the sacrum and the other is placed over T12. B, With the patient in maximum lexion, the degree of lexion is obtained by subtracting the sacral inclinometer reading from the reading of the T12 inclinometer.

FIGURE 3-17 In the double inclinometer test for lumbar extension, one inclinometer is placed over the midsacrum and the other is placed over T12. With the patient in maximum extension, the degree of extension is obtained by subtracting the sacral inclinometer reading from the reading of the T12 inclinometer.

A

B

FIGURE 3-18 Measuring lateral bending of the thoracolumbar spine. A, The patient stands in the zero starting position, with the arms hanging down by the sides. B, When the patient is in maximum lateral bend, the ingers usually touch the knee.

CHAPTER 3 The Orthopaedic Examination: A Comprehensive Overview

37

Table 3-2 Normal Range of Hip Motion in Children at Different Ages (in Degrees) Age Motion

Newborn

4 Years

8 Years

11 Years

Flexion

128 ± 4.8

150 ± 12.5

146 ± 11.3

138 ± 14.5

Extension

−30 ± 3.9

29 ± 6.3

27 ± 6.3

25 ± 4.0

Abduction

79 ± 4.3*

54 ± 9.0

49 ± 7.3

45 ± 10.8

Adduction

17 ± 3.5

30 ± 5.0

28 ± 6.0

29 ± 6.3

Internal rotation

76 ± 5.6

55 ± 17.8

54 ± 17.5

48 ± 6.0

External rotation

92 ± 3.0

46 ± 16.8

43 ± 17.5

42 ± 15.3

From Greene WB, Heckman JD: The clinical measurement of joint motion. Rosemont, Ill, 1994, American Academy of Orthopaedic Surgeons. *Measured in lexion. Measurements at other ages in abduction with hip extended (in neutral). Data are means ± 1 SD for newborns and ± 2 SD for other age groups.

45°

0°

0°

45°

FIGURE 3-19 Visual estimate of thoracolumbar rotation. The patient rotates to the right and left while the examiner holds the pelvis irmly in place and maintains the scapula in a neutral position. The degree of rotation is estimated based on an imaginary line transecting the plane of the shoulders.

All normal newborns have some degree of lexion contracture of the hip and knee because of the intrauterine lexed posture (Fig. 3-20). Neonatal hip lexion contracture is typically approximately 30 degrees, but various studies have reported ranges from 20 to 60 degrees.25,31,35,73,81 The neonatal hip also has more external rotation than internal rotation.25,31 By 4 to 6 months of age, the hip and knee usually can be extended to neutral positions, and by 1 year of age, the hip lexion contracture and excessive external rotation have gradually resolved.15,63 Newborns also have a greater range of hip rotation (average, 170 degrees25) than children 1 year of age or older (average range, 90 to 100 degrees). This increase in hip rotation may be due to the associated lexion contracture, insofar as rotation is greater when the hip is lexed. With increasing age, hip rotation decreases by 15 to 20 degrees each decade during the irst 20 years, and by approximately 5 degrees per decade thereafter. Hip abduction decreases on average by 10 to 15 degrees per decade for the irst 20 years.

FIGURE 3-20 Typical position of the neonate with vertex presentation. The hips and knees are lexed, the lower legs are rotated internally, and the feet are rotated further inward on the lower leg. The lower limbs are contracted into this position for a variable period after birth.

Flexion/Extension It is important to observe the pelvis carefully while examining passive motion of the hip joint. Signiicant lexion deformity may be hidden by forward tilt of the pelvis and excessive lumbar lordosis. During examination of hip motion, the examiner should ensure that the pelvis does not rotate or tilt. The examiner should place one hand on the iliac crest or anterior superior iliac spine to note the point at which the pelvis begins to move. The examination starts with the patient lying supine on a lat, irm surface. First one hip and then the other is held in full lexion. Normal range of hip lexion is from 0 to 110 or 120 degrees (Fig. 3-21).

38

SECTION I Disciplines

30° 0°

FIGURE 3-21 Normal range of hip lexion.

A

FIGURE 3-23 The amount of hip lexion deformity can also be determined with the patient prone. The pelvis is stabilized, the patient’s thigh is raised toward the ceiling, and the tested hip is extended. Normal extension is 30 degrees.

B

20°

C FIGURE 3-22 The Thomas test. A, In the supine position, normal lumbar lordosis is present in fully extended hips. B, If lexion contracture is present, the legs still lie on the examining surface, but there is increased lumbar lordosis. C, The Thomas test is performed by irst lexing both hips until the lumbar spine is lattened, then extending the affected hip. The amount of lexion contracture is represented by the angle between the thigh and the examining surface.

Hip extension (or lack of full extension [lexion contracture]) is tested with the patient in the supine position using the Thomas test (Fig. 3-22). Both of the patient’s hips are completely lexed until the lumbar spine (which serves as a reference point) is lattened. The hip to be tested is then extended while the opposite hip remains lexed until the pelvis rotates. At the point where further extension is not possible, the angle between the thigh and the examining table is the degree of lexion deformity. Hip lexion deformity can also be determined by having the patient lie prone with both hips lexed over the end of the table to latten the lumbar spine74 (Fig. 3-23). The pelvis is stabilized by the examiner placing a forearm over the

FIGURE 3-24 The degree by which the hip fails to reach neutral position is the degree of deformity.

ilium and lumbosacral spine. Then, with the opposite hand, the examiner raises the patient’s thigh toward the ceiling and extends the tested hip (motion of the lower spine should be prevented during this maneuver). Normally, a hip should extend 10 to 20 degrees. If the joint cannot be brought to the neutral position, there is lexion deformity. The degree by which the hip fails to reach the neutral position is the degree of deformity (Fig. 3-24). If lexion deformity of the hip is signiicant in the standing position or if the patient is unable to compensate exclusively by increased lumbar lordosis, the knee of the affected limb will be held in lexion and only the toes will touch the ground. This causes the extremity to look shorter than the opposite limb.

Abduction/Adduction When evaluating hip abduction, it is important that the anterior superior iliac spines be level. Abduction can be

CHAPTER 3 The Orthopaedic Examination: A Comprehensive Overview

39

0°

90°

FIGURE 3-25 Hip abduction assessed with the patient’s knees and hips in 90 degrees of lexion.

90°

90°

0°

30°

FIGURE 3-26 Abduction of the hip. The child is placed supine with the pelvis held in a ixed position by abducting the opposite hip and steadied by the examiner’s hand.

assessed with the patient’s legs straight or with the patient’s knees and hips in 90 degrees of lexion (Fig. 3-25). The latter position is commonly used when examining newborns and young infants. With the patient still supine, the pelvis is held in a ixed position by abducting the opposite hip; it is steadied by the examiner’s hand, which will detect any pelvic motion (Fig. 3-26). Abduction is measured in degrees of outward motion of the limb from the zero starting position. The normal amount of hip abduction with the hip in extension is 30 to 45 degrees. Hip abduction can also be rapidly and grossly assessed by having the patient spread the legs as far apart as possible while standing or lying supine. The degree of abduction is

FIGURE 3-27 Adduction of the hip. The opposite limb is raised so that the tested leg can pass under it.

determined by measuring the intermalleolar separation or the angle made by the legs when abduction is symmetric. When assessing adduction of the hip, the examiner should raise the opposite limb so that the tested leg can pass under it (Fig. 3-27). Adduction can also be assessed by passing the examined leg over the opposite leg, but the estimation of the amount of adduction will be slightly inaccurate because the hip will be lexed. The presence and degree of abduction contracture of the hip is determined by the Ober test58 (Fig. 3-28). With the patient lying on the side opposite the one being tested, the underneath hip and knee are maximally lexed to latten the lumbar spine and stabilize the pelvis. The hip to be tested is then lexed to 90 degrees (with the knee lexed to a right angle), fully abducted, and brought into full hyperextension and allowed to adduct maximally. During this maneuver, the knee of the tested extremity should always be kept at 90 degrees of lexion. The angle of the thigh and a horizontal line parallel to the examination table represents the degree of abduction contracture. A normal limb will drop well below this horizontal line. If there is abduction contracture, the hip cannot be adducted to neutral position. When examining infants for evidence of hip abduction contracture, the examiner should place them prone and stabilize their pelvises in a neutral position with the legs abducted, then gently adduct one leg at a time. With an abduction contracture, the pelvis will move under the examiner’s hand as the leg is adducted.

Rotation Rotation of the hip in lexion is assessed with the patient supine. The hip and knee of the limb are examined with both lexed 90 degrees (Fig. 3-29). Internal (inward) rotation of the hip is measured by rotating the lower leg externally away from the midline of the body, with the thigh as the axis of rotation. External (outward) rotation of the hip is measured by rotating the lower leg internally toward the

40

SECTION I Disciplines

Lumbar spine flattened by acute flexion of underneath hip

Flex hip 90°

B

A

Abduct hip fully

Extend hip

D

C

Adduct hip maximally Note 20° abduction contracture

E FIGURE 3-28 Ober test for determining the presence and degree of abduction contracture of the hip. A, The lumbar spine is lattened by acute lexion of the hip below. B, Flex the hip 90 degrees. C, Abduct the hip fully. D, Extend the hip. E, Adduct the hip maximally; note the 20-degree abduction contracture.

midline of the body, again with the thigh as the axis of rotation. Rotation of the hip in extension is best assessed with the patient prone and the knee lexed 90 degrees (Fig. 3-30). During the maneuver, the pelvis should be stabilized to ensure that the rotation is entirely femoral. Internal rotation of the hip is measured by rotating the leg outward, external rotation is measured by rotating the leg inward. The tibiae are used as markers to facilitate measurement as the hips are rotated internally and externally. The normal amount of internal and external rotation in extension is 45 degrees at skeletal maturity. Younger patients typically have more total rotation, and more internal than external rotation (see Table 3-2).

Trendelenburg Test Examination of the hip in ambulatory patients must include an assessment of the presence or absence of the Trendelenburg sign by performing the Trendelenburg test. During the test, the examiner is seated behind the patient. The patient

is suficiently undraped so that the examiner can see the pelvic area, including the iliac crests and the lower extremities. The test is performed with the patient irst standing evenly on both legs and then standing on one leg, holding the opposite leg up by lexing the hip and knee. The examiner rests his or her ingers on the iliac crests or the ingertips over the skin dimples overlying the posterior iliac spines. During a normal examination, the patient will elevate the unsupported pelvis by abducting the stance-leg hip, using the hip abductor musculature (primarily the gluteus medius) to bring the center of gravity over the stance leg. To conduct the examination properly, the patient should not be allowed to gain support by holding on to a table, wall, or other surface (unless ataxia prevents the patient from otherwise performing the test). The patient also should not be allowed to brace the unsupported leg against the stance leg. Absence of Trendelenburg sign (i.e., a normal examination) indicates that the patient has adequate hip joint range and arc of motion, normal morphology, no inlammation in or around

CHAPTER 3 The Orthopaedic Examination: A Comprehensive Overview

the joint, good to normal muscle strength, and normal central and peripheral neurologic functions. Any deviation from the aforementioned technique results in a positive test or may make it dificult for the examiner to properly assess the presence or absence of the Trendelenburg sign. Trendelenburg sign is present (i.e., the test result is positive) if the unsupported side drops when the patient attempts to stand on one leg, usually with exaggeration of lateral lexion of the lumbar spine in an attempt to place as much body mass as possible over the stance leg (Fig. 3-31).

90°

41

There are a number of variations of the Trendelenburg test. A “delayed” Trendelenburg sign is assessed by having the patient stand unsupported for a prescribed period of time (e.g., 10 seconds). An alternative is the stress Trendelenburg test: as the patient stands on one leg, the examiner pushes down on the shoulder on the unsupported side to test the abductor strength of the opposite (supporting) hip (Fig. 3-32).

90°

45°

45° 0°

A

Normal

B

Positive

FIGURE 3-31 Trendelenburg test. A, Normal; Trendelenburg sign is not elicited. B, Positive test; Trendelenburg sign is elicited.

FIGURE 3-29 Rotation of the hip in lexion is assessed with the patient supine and the hip and knee lexed 90 degrees.

External rotation

0°

Internal rotation

FIGURE 3-30 Rotation of the hip in extension is assessed with the patient prone and the knee lexed 90 degrees.

FIGURE 3-32 The “stress” Trendelenburg test. The patient is positioned the same as for the traditional Trendelenburg test. The examiner then pushes on the shoulder on the unsupported side to test the strength of hip abductors on the supporting side.

42

SECTION I Disciplines

Flexion

20°

FIGURE 3-33 Assessment of knee range of motion.

50° FIGURE 3-34 Measurement of dorsilexion and plantar lexion of the ankle.

The presence or absence of Trendelenburg sign in a patient in the standing position is different from the behavior of the hips, pelvis, and hip abductor muscles during normal gait. During normal gait, the pelvis on the unsupported side lowers because of adduction of the stance hip controlled by the eccentric contraction of the stance limb (see Chapter 5).

Knee Flexion and extension are the primary measured knee motions. Although rotation of the tibia on the femur occurs during knee movement, it cannot be accurately measured by physical examination alone.30 The zero starting position for assessing knee lexion is with the patient sitting or supine and the leg fully extended (Fig. 3-33). The degree of lexion is how far the knee can be bent from 0 degrees to its maximum lexion. Extension is measured in degrees opposite to lexion at the zero starting position. In the normal knee, lexion is restricted only by the calf abutting the thigh, and extension should be to 0 degrees. A few degrees of knee hyperextension may be seen in young children,13,85 but this usually decreases with age.

Ankle and Foot The primary motions of the ankle (tibiotalar joint) are lexion (i.e., dorsilexion) and extension (i.e., plantar lexion). The zero starting position for measuring ankle motion is with the knee lexed (to relax the gastrocnemius muscle) and the foot perpendicular (at a right angle) to the tibia (Fig. 3-34). The goniometer is aligned with the axis of the foot by placing it along the lateral border of the foot. Dorsilexion is measured by having the patient move the foot toward the anterior surface of the leg, whereas plantar lexion is measured when the foot is moved away from the anterior surface of the leg.22 During dorsilexion and plantar lexion, most of the motion takes place at the tibiotalar joint, but other joints are also involved.46,59,72

In the foot, consistency in choosing landmarks is important to ensure reproducibility. Active ROM measurements appear to provide more consistent measurements than passive ROM assessment and should be used whenever possible.30 With infants and young children, active ROM assessment may not be reliable, and passive ROM evaluation may be necessary to assess joint motion. Because there are many joints in the foot, it is dificult to accurately measure the motion of a speciic joint complex. In children, the degree of joint motion is normally the same in both feet. Thus, it is possible to compare the affected foot with the opposite foot to determine any limitation of motion.9 Foot motion occurs in the planes of inversion/eversion and supination/pronation. Inversion and eversion, tested passively, primarily demonstrate motion at the talocalcaneal joint. The motions are estimated in degrees, or percentages of motion compared with the opposite foot. The zero starting position is with the patient prone, the knee lexed, and the ankle in slight dorsilexion30,50 (Fig. 3-35). Having the foot in slight dorsilexion (i.e., just before the soft tissues become tight) restricts lateral motion of the tibiotalar joint and better denotes subtalar joint motion.30 Inversion is assessed by stabilizing the ankle with one hand, irmly grasping the hind part of the foot in the cup of the hand, and turning the heel inward with the ankle in a zero neutral starting position (Fig. 3-36, A). Eversion is assessed by turning the heel outward (Fig. 3-36, B). The degrees of motion can be recorded with a goniometer. Supination and pronation, which are tested actively, are more complex motions that involve all the joints of the foot.47 Active supination (which entails inversion, adduction, and plantar lexion of the midfoot) is assessed by having the patient direct the forepart of the foot so that the sole is turned medially (Fig. 3-37, A). Pronation (which is made up of eversion, abduction, and dorsilexion of the midfoot) is assessed by having the patient turn the foot so that the sole is turned laterally (Fig. 3-37, B).

CHAPTER 3 The Orthopaedic Examination: A Comprehensive Overview

FIGURE 3-35 Zero starting position for testing foot motion. The patient is prone, the knee is lexed, and the ankle is in gentle dorsilexion. (Reproduced from Greene WB, Heckman JD: The clinical measurement of joint motion. Rosemont, Ill, 1994, American Academy of Orthopaedic Surgeons.)

0°

0° Inversion

A

Eversion

B

FIGURE 3-36 Assessment of inversion (A) and eversion (B) of the ankle. (Reproduced from Greene WB, Heckman JD: The clinical measurement of joint motion. Rosemont, Ill, 1994, American Academy of Orthopaedic Surgeons.)

Muscle Strength The evaluation of muscle strength is often an important part of the orthopaedic physical examination. Detailed descriptions of the techniques for testing speciic muscles are available in a number of textbooks.16,36,43 In general, during the orthopaedic physical examination, proximal muscles are tested as functional groups (e.g., hip abductors, hamstrings) and distal muscles are tested separately (e.g., lexor pollicis longus, extensor digitorum communis). The examiner should look for a pattern in any detectable weakness. Speciic patterns may indicate a lower motoneuron lesion affecting a peripheral nerve or nerve root. Weakness that worsens with repeated effort and improves with rest suggests myasthenia gravis. Repetitive testing also may reveal lack of endurance, which is a more subtle form of weakness.

A

0° Supination (inversion, adduction, and plantar flexion)

B

43

0° Pronation (eversion, abduction, and dorsiflexion)

FIGURE 3-37 Assessment of supination (A) and pronation (B) of the ankle. (Reproduced from Greene WB, Heckman JD: The clinical measurement of joint motion. Rosemont, Ill, 1994, American Academy of Orthopaedic Surgeons.)

Examining infants and young children for muscle weakness can be dificult. Gross defects in movements can be detected by observing the spontaneous activity of the infant and watching the small child at play. The examiner should also watch the child walk, run, climb stairs, or get up from the loor. Stimulating relexes such as the Moro relex can also be a means of determining muscle strength in infants.40,87 For older patients, the strength of various muscle groups (e.g., hip lexors, hamstrings, quadriceps) can be quantiied by using dedicated muscle power testing machines, such as the Biodex System 3 (Biodex Medical Systems, New York), or similar devices. Muscle strength and power can be classiied as kinetic or static. Kinetic power is the force used when changing positions. It is tested by having the patient perform movements against gravity or against resistance provided by the examiner. Static power is the force used when resisting movement. It is tested by having the patient resist active effort by the examiner to move speciic parts of the patient’s body. Paresis or weakness denotes an impairment of muscle strength, whereas paralysis means complete loss of strength. In addition to a loss of kinetic and static power, patients with muscle weakness exhibit increased fatigue, decreased rate of motion, irregular and clumsy movements, tremors, lack of coordination, and diminished ability to perform skilled acts. If a patient has muscle weakness, the examiner needs to determine whether it is localized or diffuse. Localized (or focal) loss of muscle strength may be due to involvement of a speciic muscle, of a nerve that innervates various muscles, or of a certain segment of the spinal cord that innervates a group of muscles. Localized muscle weakness may also involve multiple muscles that affect a speciic movement or an entire limb. Monoplegia refers to paralysis of one limb, hemiplegia to paralysis of one half of the body, diplegia to relatively symmetric involvement of the right and left sides with greater involvement of the legs than the arms (double hemiplegia), paraplegia to paralysis of the

44

SECTION I Disciplines

lower limbs, and quadriplegia or tetraplegia to paralysis of all four limbs. Weakness of one side of the body suggests an upper motoneuron lesion. A polyneuropathy causes symmetric distal weakness, and a myopathy usually causes proximal weakness. Diffuse (or generalized) loss of muscle strength may be due to myopathies (e.g., the muscular dystrophies), various types of myositis and myasthenia gravis, electrolyte imbalance, and toxic and deiciency states. The extent, nature, and cause of the muscle weakness must also be determined. The examiner should ascertain whether there are associated sensory changes, whether the relexes have been affected, whether muscle atrophy is present, whether there is muscle ibrillation or fasciculation, and whether paralysis (if present) is laccid or spastic. If a muscle is kept in a shortened, contracted position for an extended time, a myostatic contracture may develop that prevents the muscle from being stretched back to its original length. Myostatic contractures may result from overaction of one group of muscles unopposed by weakened antagonists or from prolonged muscle spasms, as occur in acute poliomyelitis or in association with spastic paralysis. Contractures, and bone and joint deformities, may increase muscle weakness. If there is limitation to or absence of joint ROM, the examiner should determine if it is the result of swelling of the joint, ibrous or bony ankylosis, voluntary or involuntary muscle spasm, or paralysis. Finally, the orthopaedist must decide if the muscle weakness is a permanent condition or a reversible process, and if surgical intervention can improve function. The examiner should objectively grade and record the degree of muscle strength on a chart so that the patient’s progress can be followed by comparative tests. A sample of the comprehensive muscle test record for the upper and lower extremities as used at Texas Scottish Rite Hospital for Children is reproduced in Appendix 3-2. The original method of testing and grading muscle strength published by Lovett and Martin44,45 is still helpful in evaluating a patient’s neuromuscular status (Table 3-3). Another system that is commonly used for grading muscle strength is based on a scale of 0 to 5 (Table 3-4). At Texas Scottish Rite Hospital for Children, we have modiied these grading systems to record results on the manual muscle evaluation test. Grades of muscle strength range from 0 to 5, with grades 1 through 4 further deined as trace, poor minus, poor, poor plus, fair minus, fair, fair plus, good minus, good, and good plus (Table 3-5). Innervation of the muscles responsible for movements of the shoulder and upper limb is given in Table 3-6, and innervation of the muscles responsible for movements of the lower limbs is given in Table 3-7.

Developmental Relexes A number of primitive relexes (infantile automatisms) are present in neonates and infants and are associated with normal development. Primitive relexes are present at birth and disappear as the child matures. Other relexes appear during infancy and young childhood, and some continue throughout life. The two major divisions of the central nervous system (CNS) that control neuromuscular functions are the cerebral cortex and the subcortical nuclei. At birth, the behavior patterns characteristic of the neonate are mediated by the subcortical nuclei, with some functions essentially remaining under its control throughout life. As the cerebral cortex develops, it exercises a greater inluence over neuromuscular functions and also an inhibitory inluence on some of the activities of the subcortical nuclei. Cortical maturation is relected in behavior by the suppression or diminution of Table 3-3 Lovett and Martin’s Grading of Muscle Strength Grade

Description

Zero

No palpable contraction of muscle

Trace

Palpable contraction of muscle; no motion of part that muscle should move; no joint motion when gravity is eliminated

Poor

Muscle able to move part through its complete ROM when gravity is eliminated, but not against gravity

Fair

Muscle able to carry part through its complete ROM against gravity, but not against added resistance

Good

Muscle able to carry part through its complete ROM against gravity with some resistance (“good minus” and “good plus” used to indicate variations in resistance)

Normal

Muscle exhibits normal strength; is able to carry part through its complete ROM with full resistance

Modified Grades Used in Practice Poor minus Muscle able to move part, but not through complete ROM and not against gravity Fair minus

ROM, Range of motion.

Table 3-4 Grading of Muscle Strength Grade

Neurologic Assessment A detailed neurologic examination is important in the diagnosis of musculoskeletal disorders. This is particularly true when there is evidence of muscle weakness, incoordination, or other disturbances in neuromuscular function. The examiner should assess the patient’s developmental relexes, deep and supericial relexes, sensory function, cranial nerves, and mental and emotional state.

Muscle able to move part against gravity, but not through complete ROM

Description

0

No muscular contraction detected

1

Trace of contraction barely detectable

2

Active movement with gravity eliminated

3

Active movement against gravity

4

Active movement against gravity and some resistance

5

Active movement against full resistance

45

CHAPTER 3 The Orthopaedic Examination: A Comprehensive Overview

certain neuromuscular activities, and by the emergence and integration of other neuromuscular performances. Development tends to proceed cephalocaudad.51 The relexes and reactions discussed in this section are the most important ones, and the orthopaedist should be most familiar with them because there is an association between functional motor achievement and the underlying relex structure. The absence or presence of these relexes may be a negative or positive predictor of immediate or eventual cortical function. Their absence often indicates a delay in normal neurologic development, and their persistence beyond the expected time of disappearance suggests neurologic impairment or dysfunction.28 The normal timing of the appearance and disappearance of these relexes and reactions is summarized in Table 3-8 and illustrated in Figure 3-38.

Palmar (Hand) Grasp Relex The hand grasp relex is tested with the infant supine, the arms semilexed, and the head in the midline position (not rotated to one side or the other). If the head is not in the

Table 3-5 Grading of Muscle Strength (Texas Scottish Rite Hospital for Children) Grade

Description

0

Absent

1T

Trace, mere tension on palpation

1P−

Poor minus, beginning motion

2P

Poor, full range, gravity eliminated

2P+

Poor plus, begin motion antigravity

2F−

Fair minus, almost full range antigravity

3F

Fair, full range antigravity

3F+

Fair plus, full range, minimal resistance

3G−

Good minus

4G

Good, full range, moderate resistance

4G+

Good plus

5

Normal, maximum resistance

Table 3-6 Innervation of Muscles Responsible for Movements of the Shoulder Girdle and Upper Extremity Muscle Trapezius

Segmental Innervation Cranial XI; C(2)3-4

Peripheral Nerve Spinal accessory nerve

Levator anguli scapulae

C3-4 C4-5

Nerves to levator anguli scapulae Dorsal scapular nerve

Rhomboideus major

C4-5

Dorsal scapular nerve

Rhomboideus minor

C4-5

Dorsal scapular nerve

Serratus anterior

C5-7

Long thoracic nerve

Deltoid

C5-6

Axillary nerve

Teres minor

C5-6

Axillary nerve

Supraspinatus

C(4)5-6

Suprascapular nerve

Infraspinatus

C(4)5-6

Suprascapular nerve

Latissimus dorsi

C6-8

Thoracodorsal nerve (long subscapular)

Pectoralis major

C5-T1

Lateral and medial anterior thoracic

Pectoralis minor

C7-T1

Medial anterior thoracic

Subscapularis

C5-7

Subscapular nerves

Teres major

C5-7

Lower subscapular nerve

Subclavius

C5-6

Nerve to subclavius

Coracobrachialis

C6-7

Musculocutaneous nerve

Biceps brachii

C5-6

Musculocutaneous nerve

Brachialis

C5-6

Musculocutaneous nerve

Brachioradialis

C5-6

Radial nerve

Triceps brachii

C6-8(T1)

Radial nerve

Anconeus

C7-8

Radial nerve

Supinator brevis

C5-7

Radial nerve

Extensor carpi radialis longus

C(5)6-7(8)

Radial nerve

Extensor carpi radialis brevis

C(5)6-7(8)

Radial nerve Continued

46

SECTION I Disciplines

Table 3-6 Innervation of Muscles Responsible for Movements of the Shoulder Girdle and Upper Extremity, cont’d Muscle

Segmental Innervation

Peripheral Nerve

Extensor carpi ulnaris

C6-8

Radial nerve

Extensor digitorum communis

C6-8

Radial nerve

Extensor indicis proprius

C6-8

Radial nerve

Extensor digiti minimi proprius

C6-8

Radial nerve

Extensor pollicis longus

C6-8

Radial nerve

Extensor pollicis brevis

C6-8

Radial nerve

Abductor pollicis longus

C6-8

Radial nerve

Pronator teres

C6-7

Median nerve

Flexor carpi radialis

C6-7(8)

Median nerve

Pronator quadratus

C7-T1

Median nerve

Palmaris longus

C7-T1

Median nerve

Flexor digitorum sublimis

C7-T1

Median nerve

Flexor digitorum profundus (radial half)

C7-T1

Median nerve

Lumbricales 1 and 2

C7-T1

Median nerve

Flexor pollicis longus

C8-T1

Median nerve

Flexor pollicis brevis (lateral head)

C8-T1

Median nerve

Abductor pollicis brevis

C8-T1

Median nerve

Opponens pollicis

C8-T1

Median nerve

Flexor carpi ulnaris

C7-T1

Ulnar nerve

Flexor digitorum profundus (ulnar half)

C7-T1

Ulnar nerve

Interossei

C8-T1

Ulnar nerve

Lumbricales 3 and 4

C8-T1

Ulnar nerve

Flexor pollicis brevis (medial head)

C8-T1

Ulnar nerve

Flexor digiti minimi brevis

C8-T1

Ulnar nerve

Abductor digiti minimi

C8-T1

Ulnar nerve

Opponens digiti minimi

C8-T1

Ulnar nerve

Palmaris brevis

C8-T1

Ulnar nerve

Adductor pollicis

C8-T1

Ulnar nerve

From Dejong RN: The neurological examination. New York, 1967, Hoeber Medical Division, Harper & Row, p 456.

Table 3-7 Innervation of Muscles Responsible for Movements of the Lower Extremities Muscle

Segmental Innervation

Peripheral Nerve

Psoas major

L(1)2-4

Nerve to psoas major

Psoas minor

L1-2

Nerve to psoas minor

Iliacus

L2-4

Femoral nerve

Quadriceps femoris

L2-4

Femoral nerve

Sartorius

L2-4

Femoral nerve

Pectineus

L2-4

Femoral nerve

Gluteus maximus

L5-S2

Inferior gluteal nerve

Gluteus medius

L4-S1

Superior gluteal nerve

Gluteus minimus

L4-S1

Superior gluteal nerve

CHAPTER 3 The Orthopaedic Examination: A Comprehensive Overview

Table 3-7 Innervation of Muscles Responsible for Movements of the Lower Extremities, cont’d Muscle

Segmental Innervation

Peripheral Nerve

Tensor fasciae latae

L4-S1

Superior gluteal nerve

Piriformis

S1-2

Nerve to piriformis

Adductor longus

L2-4

Obturator nerve

Adductor brevis

L2-4

Obturator nerve

Adductor magnus

L2-4 L4-5

Obturator nerve Sciatic nerve

Gracilis

L2-4

Obturator nerve

Obturator externus

L2-4

Obturator nerve

Obturator internus

L5-S3

Nerve to obturator internus

Gemellus superior

L5-S3

Nerve to obturator internus

Gemellus inferior

L4-S1

Nerve to quadratus femoris

Quadratus femoris

L4-S1

Nerve to quadratus femoris

Biceps femoris (long head)

L5-S1

Tibial nerve

Semimembranosus

L4-S1

Tibial nerve

Semitendinosus

L5-S2

Tibial nerve

Popliteus

L5-S1

Tibial nerve

Gastrocnemius

L5-S2

Tibial nerve

Soleus

L5-S2

Tibial nerve

Plantaris

L5-S1

Tibial nerve

Tibialis posterior

L5-S1

Tibial nerve

Flexor digitorum longus

L5-S1

Tibial nerve

Flexor hallucis longus

L5-S1

Tibial nerve

Biceps femoris (short head)

L5-S2

Common peroneal nerve

Tibialis anterior

L4-S1

Deep peroneal nerve

Peroneus tertius

L4-S1

Deep peroneal nerve

Extensor digitorum longus

L4-S1

Deep peroneal nerve

Extensor hallucis longus

L4-S1

Deep peroneal nerve

Extensor digitorum brevis

L4-S1

Deep peroneal nerve

Extensor hallucis brevis

L4-S1

Deep peroneal nerve

Peroneus longus

L4-S1

Supericial peroneal nerve

Peroneus brevis

L4-S1

Supericial peroneal nerve

Flexor digitorum brevis

L4-S1

Medial plantar nerve

Flexor hallucis brevis

L5-S1

Medial plantar nerve

Abductor hallucis

L4-S1

Medial plantar nerve

Lumbricales (medial 1 or 2)

L4-S1

Medial plantar nerve

Quadratus plantae

S1-2

Lateral plantar nerve

Adductor hallucis

L5-S2

Lateral plantar nerve

Abductor digiti quinti

S1-2

Lateral plantar nerve

Flexor digiti quinti brevis

S1-2

Lateral plantar nerve

Lumbricales (lateral 2 or 3)

S1-2

Lateral plantar nerve

Interossei

S1-2

Lateral plantar nerve

From Dejong RN: The neurological examination. New York, 1967, Hoeber Medical Division, Harper & Row, p 483.

47

48

SECTION I Disciplines

Table 3-8 Normal Times of Appearance and Disappearance of Infantile Relexes and Reactions Relex or Reaction

Timing

Palmar (hand) grasp relex

Present in neonates and very young infants; normally disappears between ages 2 and 4 mo

Plantar (foot) grasp relex

Present in neonates and infants; usually disappears between ages 9 and 12 mo

Moro relex

Present at birth; gradually disappears by ages 3-6 mo

Startle relex

Appears at birth; present throughout life

Vertical suspension positioning

Relex normally disappears after age 4 mo

Placing reaction

Normally present at birth in full-term neonates; upper limb placing usually disappears by ages 2-4 mo and lower limb placing by ages 1-2 mo; both responses may persist up to age 12 mo or older

Walking or stepping relex

Normally present at birth; usually disappears by ages 1-2 mo

Crossed extension relex

Present at birth; normally disappears by ages 1-2 mo

Withdrawal relex

Present at birth; disappears between ages 1 and 2 mo

Positive support response/legstraightening relex

Present at birth; normally disappears at approximately 4 mo

Extensor thrust relex

Present at birth; normally present up to 2 mo

Galant relex (trunk incurvation)

Present at birth; disappears at approximately 2-2½ mo

Rotation relex

Time of disappearance varies

Tonic neck relexes

Asymmetric relex present at birth, normally disappears by 4-6 mo; symmetric relex usually present by 5-8 mo, often diminished or absent by 12 mo

Landau relex

Normally present from 6 mo to 24-30 mo

Parachute reaction

Appears at approximately 6 mo; remains throughout life

Neck-righting relex

Normally present from birth to approximately 6 mo

Body-righting relex

Appears around 6 mo; can disappear any time after 5 yr or persist throughout life

Oral relexes

Usually disappears at 3-4 mo; may be present longer during sleep

midline, the grasp relex will be more pronounced on the side to which the occiput is directed. It is also important not to touch the dorsum of the infant’s hand during the test. Such tactile stimulation will cause the infant to open the hand instinctively, resulting in a conlict between relexes. To elicit the hand grasp relex, the examiner places a inger or an object (e.g., a pencil, rod, an empty thermometer case) into the infant’s palm from the ulnar side. This stimulates the palm and enhances lexor tonus. The ingers will then lex and grip the object (Fig. 3-39). The thumb will not oppose the ingers but will lex with them if it was in an extended position before the object was introduced. If the object is retracted after the infant grasps it, the lexor tone is increased synergistically in other lexor muscles of the upper limb and is facilitated by stretch. This causes the muscles of the arm and shoulder girdle to contract. If the response is marked, the grip is so strong that it is possible to suspend the infant for a moment by the object being held. The hand grasp relex is present in neonates and very young infants, and normally disappears between 2 and 4 months of age. The hand grasp relex is strongest at birth. The examiner should assess its intensity and symmetry. The relex may be asymmetric in patients with spastic hemiplegia. Absence on one side may indicate laccid paralysis, such as that seen in obstetric brachial plexus paralysis. The relex

should also be assessed for persistence after it should have normally disappeared. Persistence in infants older than 4 months may be an indication of lexor hypertonicity, as is seen in spastic cerebral palsy.

Plantar (Foot) Grasp Relex The plantar grasp relex in the foot is very similar to the hand grasp relex.27 The relex is tested with the infant supine. When light digital pressure is applied to the plantar surface of the foot (especially on its distal portion just proximal to the toes), tonic lexion and adduction of the toes should occur (Fig. 3-40). The plantar grasp relex is present in neonates and infants, and usually disappears between 9 and 12 months of age. Its absence may indicate laccid paralysis. Its persistence beyond 1 year of age may be due to spasticity of the leg and foot muscles. The relex may also persist in children with birth injuries and delayed development.

Moro Relex This important vestibular relex was irst described by Moro in 191856 and well reviewed by Mitchell in 1960.55 To test the Moro relex, the patient is placed supine with both upper and lower limbs in full, natural extension. A variety of stimuli can be used to elicit this relex. Common among the different methods is a sudden extension of the infant’s neck. The examiner can lift the infant in the supine position

CHAPTER 3 The Orthopaedic Examination: A Comprehensive Overview

49

Reflexes Crossed extension

Average age of appearance and disappearance

Walking Asymmetric tonic neck Palmar grasp Moro Placing reaction Plantar grasp Landau Parachute reaction Symmetric tonic neck

Righting reflexes Neck Optical Labyrinthine Body

Tilting reactions Prone Sitting All fours Standing 0 1 2 3 4 5 6 7 8 9 10 11 12 18 2 3 4 5 6 7 8 9 10 11 12 18 19

Months

Years

FIGURE 3-38 Relex maturation chart showing normal timing of appearance and disappearance of infantile relexes and reactions.

FIGURE 3-40 Plantar (foot) grasp relex. When light pressure is applied to the plantar surface of the foot, tonic lexion and adduction of the toes will occur. FIGURE 3-39 Palmar (hand) grasp relex. To elicit the relex, the examiner places a inger or object into the infant’s palm from the ulnar side. If the response is marked, the grip will be strong enough to suspend the infant for a moment.

several inches above the examining table with one hand placed under the infant’s thoracic spine and the other hand under the back of the head.5 The hand supporting the head is then suddenly removed, allowing neck extension (Fig. 3-41, A). The examiner can also hold the infant in the supine position, supporting the head, back, and legs, then suddenly lower the entire body approximately 2 feet and stop abruptly. Alternatively, the infant can be gently raised slightly off the table by holding the infant’s hands and then quickly releasing them, causing sudden extension of the

cervical spine (Fig. 3-41, B). The examining physician must handle the infant gently during any of these maneuvers to avoid excessive or disconcerting head and neck movement. The relex can also be evoked by producing a loud noise (e.g., sharply banging the examination table with the palms of the hand on both sides of the infant’s head) or with a sudden tap on the infant’s abdomen. The irst phase of the Moro relex consists of sudden abduction and extension of all four limbs and extension of the spine, with extension and fanning of the ingers, except for lexion of the distal phalanges of the index inger and thumb (Fig. 3-41, C). This is followed by the second phase, in which there is adduction and lexion of all four limbs, with the arms coming forward over the body in a clasping

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SECTION I Disciplines

A

B

C

D

FIGURE 3-41 The Moro relex. A, Sudden removal of hand supporting the infant’s head causes extension of the neck. B, Holding the infant by the hands and then quickly releasing them also causes extension of the neck. C, First phase of a positive response: sudden abduction and extension of all four limbs and extension of the spine. D, Second phase: adduction and lexion of all four limbs.

movement as if the infant were embracing (Fig. 3-41, D). The relex may also be accompanied by crying. The Moro relex is present at birth and gradually disappears by 3 to 6 months of age. Various conditions can cause abnormalities of this relex. It may be decreased when there is severe hypertonicity because the increased muscle tone prevents full motion of the limbs. Depending on the severity of the hypertonicity, the limbs may move only partially at the height of the relex, the hands may fail to open, or there may be no response because the limbs are so tightly lexed. The Moro relex may also be decreased or absent in patients with generalized muscle weakness, marked hypotonicity (e.g., amyotonia congenita), or laccid paralysis. In premature infants, the limbs tend to fall backward to the table during the adduction phase because of the weakness of their antigravity muscles. The response may be asymmetric if the infant has sustained a peripheral nerve injury (e.g., obstetric brachial plexus paralysis). The relex may persist after it should have disappeared if there is developmental delay of the CNS (as seen in cerebral palsy).

Startle Relex The startle relex is a mass myoclonic relex that is normal in infants and young children. It is not the same as the Moro relex and should not be confused with the latter. The infant

is placed supine with all four limbs in natural extension. The relex is elicited by making a sudden loud noise or by tapping the infant’s sternum. The normal response is for the elbows and knees to lex (not extend, as in the Moro response) and the hands to remain closed. The startle relex appears at birth and is present through life. Its absence indicates severe hypotonia. An asymmetric response may be due to obstetric brachial plexus paralysis.

Vertical Suspension Positioning The infant is held upright and facing away from the examiner, with the examiner’s hands under the axillae for support. Normally, the infant will maintain the head in the midline and lex the legs at the hips and knees. Fixed extension and crossed adduction of the legs (scissoring) indicate spastic paraplegia or diplegia. This relex normally disappears after 4 months of age.

Placing Reaction The placing reaction is tested separately for the lower and upper limbs. To elicit the placing reaction for the lower limbs, the examiner supports the patient upright by holding the infant under the axillae with the examiner’s thumbs supporting the back of the head and the infant facing away (vertical suspension position). The anterior aspect of the

CHAPTER 3 The Orthopaedic Examination: A Comprehensive Overview

A

A

B

B

distal tibia or dorsal surface of one foot is then brought against the edge of the examining table (Fig. 3-42, A). The infant will spontaneously lex the hip and knee, dorsilex the ankle, and place the foot on the table, extending the lower limb on active or passive contact of the sole with the table (Fig. 3-42, B). The process is then repeated with the other foot. To elicit the placing reaction for the upper limbs, the infant is held at the waist and facing away from the examiner, and the dorsum of the infant’s ulna is placed against the edge of the table (Fig. 3-43, A). The infant will respond by lexing the elbow and placing the hand on the table (Fig. 3-43, B). In older children, these responses must be differentiated from voluntary placing. The placing reaction is normally present at birth in fullterm neonates. Upper limb placing usually disappears by 2 to 4 months of age and lower limb placing by 1 to 2 months of age, but both responses may persist up to 12 months of age or older. If the relex is absent at birth, the infant may have neurologic dysfunction.

51

FIGURE 3-42 Placing reaction with lower limbs. A, The anterior aspect of the distal tibia or dorsal surface of one foot is brought against the edge of the examining table. B, The infant will spontaneously lex the hip and knee, dorsilex the ankle, and place the foot on the table, extending the lower limb on active or passive contact of the sole with the table.

FIGURE 3-43 Placing reaction with upper limbs. A, The dorsum of the infant’s ulna is placed against the edge of the table. B, The infant will respond by lexing the elbow and placing the hand on the table.

Walking or Stepping Relex The walking or stepping relex is elicited by supporting the trunk and holding the infant upright. The soles of the feet are pressed (touched) against the examining table or ground, and the infant is gently inclined and moved forward (Fig. 3-44, A). This automatically initiates alternating lexion and extension of the lower limbs, simulating walking (Fig. 3-44, B and C). The response is rhythmic and coordinated, needing only forward movement (no propulsion) for stimulus. This automatic walking relex should not be confused with mature, independent walking because there is neither balance nor associated movement of the upper limbs. Automatic relex walking can be elicited only in forward motion; it does not occur with backward movement. The walking relex is normally present at birth and disappears by 1 to 2 months of age. Its absence at birth may be a result of laccid paralysis. If the relex is present after 3 to 4 months of age, the infant may have neurologic impairment.

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SECTION I Disciplines

A

B

C

FIGURE 3-44 Walking or stepping relex. A, The soles of the infant’s feet are pressed (touched) against the examining table or ground, and the infant is gently inclined and moved forward. B and C, This automatically initiates alternating lexion and extension of the lower limbs, simulating walking.

A

B

C

FIGURE 3-45 Crossed extension relex. A, The relex is elicited by holding one lower limb in extension at the knee and applying irm pressure by rubbing or stroking its sole. B, The opposite, free hip will initially lex and abduct. C, This is followed by adduction and extension of the limb.

Crossed Extension Relex The infant is placed supine with the lower limbs in midline and the hips and knees extended. The relex is elicited by holding one lower limb in extension at the knee and applying irm pressure by rubbing or stroking the sole (Fig. 3-45, A). The opposite, free hip will initially lex and abduct (Fig. 3-45, B), then adduct and extend (Fig. 3-45, C), as if the infant were trying to push away from the stimulus. There may be associated fanning of the toes of the

stimulated leg. Stimulation of the sole of the foot causes lexion of the ipsilateral limb, moving it away from the stimulus, and extension of the contralateral limb, moving it toward the stimulus. In neonates, a similar response can be elicited by applying strong pressure in the inguinal region, which causes lexion of the ipsilateral limb and extension of the contralateral hip and knee. The crossed extension relex, also known as Philippson relex, is present at birth and normally disappears by 1 to 2

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months of age. If it is absent at birth, the neonate may have laccid paralysis. Its presence beyond 2 months of age is indicative of a partial or incomplete spinal lesion or neurologic dysfunction.

Withdrawal Relex The infant is placed supine with the lower limbs in midline and natural extension. The relex is elicited by applying a pinprick to the sole of the foot. The infant will withdraw the limb from this noxious stimulus by dorsilexing the ankle and lexing the hip and knee. The withdrawal relex is present at birth and disappears between 1 and 2 months of age. The relex is weak or absent in infants born with meningomyelocele, and in children with laccid paralysis due to other intraspinal lesions. Abnormal persistence may be due to spasticity of the lower limbs, as is seen in infants with cerebral palsy.

Positive Support Response/Leg-Straightening Relex The infant is held upright in a standing position, with the examiner providing support under the axillae and around the chest. The soles of the infant’s feet are pressed to the table or ground several times. When the support response is positive, the lower limbs and trunk will go into extension; the legs act as strong supporting pillars for weight bearing. This relex is present at birth and normally disappears at approximately 4 months of age so that further motor development can occur. If the relex persists, reciprocal leg movements cannot appear and the infant will be unable to stand or walk.

Extensor Thrust Relex When pressure is applied to the sole of the infant’s foot with the lower limb in a lexed position, the infant will suddenly extend the entire leg. This extension is sometimes followed by lexion. This relex can also be tested by holding the infant by the chest wall and axilla, and lowering the infant’s feet toward the top of the examining table. When the soles of the feet are pressed against the table, there is progressive extension of the legs from the feet proximally. The extensor thrust relex is present at birth and normally up to 2 months of age. Its absence may be due to laccid paralysis. Its presence beyond 2 months of age indicates neurologic dysfunction and developmental delay of the CNS.

Galant Relex (Trunk Incurvation) To elicit this relex, the infant is placed in the prone position and the examiner strikes one side of the lumbar region of the back (between the tenth rib and the iliac crest, approximately 1 cm from the midline along a paravertebral line extending from the shoulder to the buttocks) with the index inger (Fig. 3-46). When the relex is present, the infant’s trunk will curve (lex laterally) toward the stimulated side, with the shoulders and pelvis moving in the same direction. A similar response can be elicited by pricking the outer side of the gluteal area, whereby the trunk will lex to the side stimulated. Galant relex is present at birth and disappears at approximately 2 to 2½ months of age. If the response persists and is dominant unilaterally, the patient may develop scoliosis.

FIGURE 3-46 Galant relex (trunk incurvation). Stimulating one side of the lumbar region of the infant’s back causes the trunk to curve (lex laterally) toward the stimulated side.

Tonic Neck Relexes There are both asymmetric and symmetric tonic neck relexes. Of the two, the asymmetric form is tested more often. To test the asymmetric tonic neck relex, the infant is placed in the supine position with the head in midline. To elicit the relex, the infant’s head is turned to one side (without lexion), maintained in that position for 5 to 10 seconds by holding the chin over the shoulder, and then turned to the opposite side. With a positive response, the arm on the side to which the chin is rotated becomes rigid and the elbow goes into extension (the leg on that side may also extend; Fig. 3-47). On the opposite side (the “occiput” side), the arm (and sometimes the leg) goes into lexion. This is the classically described “fencer’s position.” The grasp relex may be more easily elicited on the lexion side. The asymmetric tonic neck relex is present at birth and normally disappears by 4 to 6 months of age. Its absence indicates laccid paralysis or severe hypotonia. The relex is considered abnormal when it occurs every time it is evoked. In pathologic conditions, such as severe cerebral palsy, the relex persists and may even increase. Increased extensor tone on the “chin” side and increased lexor tone on the “occiput” side may be the only indings when the positive response is weak. The symmetric tonic neck relex is tested with the infant resting in the prone position over the examiner’s knees (the quadriceps position; Fig. 3-48, A). When the head and neck are extended, the upper limbs extend (or extensor tone increases), whereas the lower limbs lex (or lexor tone increases; Fig. 3-48, B). When the head and neck are lexed, the upper limbs lex (or lexor tone increases) and the lower limbs extend (or extensor tone increases). The symmetric tonic neck relex usually is present by 5 to 8 months of age. If this relex is absent, the infant will be unable to assume a four-point kneeling position. There is no absolute time for its normal disappearance; however,

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SECTION I Disciplines

it is often diminished or absent by 12 months of age. Its persistence can interfere with alternating lower limb motion and prevent crawling or hinder ambulation. It can also cause adduction and medial rotation, resulting in lexion gait patterns.

Landau Relex To test the Landau relex, the infant is held in the air in the prone position, with the examiner’s hand supporting the

infant under the abdomen and lower thorax. The infant’s body should be parallel with the loor. The examiner should note whether the neck, spine, and hips assume a hyperextended position or whether the limbs hang lifelessly. The head and neck are irst passively lexed and then extended; the respective positions of the limbs and trunk are noted. The Landau relex is positive when, on passive lexion of the head and neck with the body in the extended position, the trunk and upper and lower limbs go into lexion, and when on passive extension of the head and neck, the trunk and limbs are brought into the extended position. This relex is normally present from 6 months of age to 24 to 30 months of age. Its absence indicates motor weakness. If it persists beyond 30 months of age, the child may have delayed relex development (which usually interferes with the predominant lexion patterns seen in infants).

Parachute Reaction/Protective Extension of Arms Relex

FIGURE 3-47 Asymmetric tonic neck relex. The arm on the side to which the infant’s chin is rotated becomes rigid and the elbow goes into extension (the leg on that side may also extend). On the opposite side, the arm (and sometimes the leg) goes into lexion.

A

The parachute reaction can be tested with the patient prone, sitting, or standing. In the irst position, the child is suspended prone in the air by the waist (Fig. 3-49, A) and the head is moved suddenly toward the loor by tipping or plunging it downward. With a positive response, the child will immediately extend the arms and wrists forward to protect the head, as if to break the force of the fall (Fig. 3-49, B). In the sitting or standing neutral position, the response is elicited by suddenly tipping or pushing the child backward with enough force to offset the child’s balance. The positive response will be a backward extension of both arms, with the ingers extended and abducted, and the weight borne on the hands. The parachute reaction can be obtained in blindfolded children, because it does not depend on vision. This relex appears at approximately 6 months of age and remains throughout life. Absence of this relex indicates delayed neurologic development (in infants) or severe neurologic dysfunction.37,38

Neck-Righting Relex To test this relex, the child is placed in the supine position with the head in midline and all four limbs fully extended.

B

FIGURE 3-48 Symmetric tonic neck relex. A, This relex can be tested with the child lying prone over the examiner’s knee. When the head and neck are extended, the upper limbs extend and the lower limbs lex. B, When the head and neck are lexed, the upper limbs lex and the lower limbs extend. Persistence of this relex after 12 months of age is abnormal.

CHAPTER 3 The Orthopaedic Examination: A Comprehensive Overview

A

55

B

FIGURE 3-49 Parachute reaction (protective extension of arms relex). A, In the prone testing position, the child is suspended prone in the air by the waist, and the head is moved suddenly to the loor. B, With a positive response, the child immediately extends the arms and wrists forward to protect the head, as if to break the force of the fall.

The relex is elicited by lexing and rotating the head to one side and maintaining it in this position for approximately 10 seconds. When the relex is present, the child’s entire body will rotate in the same direction as the head. When it is absent, the body will not rotate. The neck righting relex normally is present from birth to approximately 6 months. If it is absent after 1 month of age, the infant may have delayed neurologic development. Abnormal persistence after 6 months of age indicates neurologic impairment.

Body-Righting Relex This relex also is tested with the child supine, the head in midline position, and all four limbs in extension. The relex is elicited in the same manner as the neck-righting relex. The head is lexed and rotated to one side and maintained in this position for 10 seconds. A positive response in this case, however, is sequential or segmental cephalocaudal rotation of the trunk—irst the shoulder rotates, then the trunk, and inally the pelvis (in contrast to the body as a whole, with the neck-righting relex). This relex appears around 6 months of age (when the neck-righting relex should disappear) and can disappear any time after 5 years of age or persist throughout life.

Oral Relexes The sucking relex is elicited by introducing a inger or a nipple into the infant’s mouth. The rooting or search relex is a feeding relex that enables the infant to ind the mother’s nipple without having to be directed to it. The infant should be supine, with the head in the midline position and the hands resting on the anterior chest. When the corner of the mouth is lightly stroked with the foreinger, the lower lip on that side is lowered, the tongue moves toward it, and the head turns to the stimulated side. When the examiner’s inger is moved upward along the oronasal groove, the infant’s head extends; when the inger is moved laterally, the head turns to follow it. When the middle of

the lower lip is stroked, the lip is lowered, the tongue moves toward it, and the chin drops. If the examiner’s inger is moved toward the chin, the mandible is depressed and the neck lexes. When the middle of the upper lip is stroked, the mouth opens and the head extends. The oral relexes are best elicited when the infant is hungry, just before the normal feeding time. These oral relexes are present in all normal full-term neonates. Their absence is indicative of severe developmental impairment or marked prematurity. They usually disappear at 3 to 4 months of age but may be present longer during sleep.

Deep Tendon Relexes (Muscle Stretch Relexes) The corticospinal pathways are not fully developed at birth; thus the spinal relex mechanisms are variable during infancy. The deep tendon relexes (biceps, triceps, knee, ankle) are assessed by tapping the appropriate tendons. In the neonate, the examiner can test the biceps by placing the index inger of the examiner’s nondominant hand on the tendon and then tapping with a ingertip of the dominant hand. This technique allows for a tactile perception of the quality of the relex contraction (which can be dificult to observe directly). Triceps relexes usually are not present until after 6 months of age. The effects of the relex contraction of the quadriceps and gastroc-soleus can be directly observed by tapping the patellar and Achilles tendons with the ingertip. Hyperactive deep tendon relexes indicate an upper motoneuron lesion. To test for ankle clonus (alternating contraction and relaxation of the gastrocnemius and soleus muscles), the infant’s hip is abducted and lexed and the knee is lexed; the ankle is then quickly but gently dorsilexed. Although ankle clonus is an abnormal relex movement that indicates hypertonicity, its presence alone is not a deinitive sign of neurologic dysfunction. In general, unsustained ankle clonus of three to six beats is normal,77 whereas sustained ankle

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SECTION I Disciplines

clonus suggests severe CNS disease. Further tests would be required for a diagnosis.

Peripheral Relexes/Abdominal Relexes Babinski relex is elicited by applying irm, steady, slow strokes with an object, such as a tongue blade, along the lateral aspect of the sole of the foot in a posteroanterior direction. The stimulus should not be painful. A normal response is withdrawal of the foot with plantar lexion of the toes. An abnormal response is a slow, tonic hyperextension of the great toe. The other toes may also hyperextend or they may slowly spread apart (fanning). Babinski relex is present in some normal neonates (less than 10%) and may persist for as long as 2 years. A hyperactive or persistent Babinski response may indicate an upper motoneuron lesion. Hoffmann relex is elicited by licking the nail of the infant’s second or third inger with the examiner’s nail. A brisk lexion of the distal phalanx of the thumb may be seen in patients with impaired corticospinal tract function. There

is usually no response or minimal response in normal children. The cremasteric relex is elicited in male patients by stroking the inner portion of the thigh in a distal-proximal direction. This maneuver should result in symmetric contraction of the scrotum. Absence or asymmetric response also suggests corticospinal tract involvement. Abdominal relexes are stimulated by gently stroking the abdomen. The strokes should be lateral to medial and should be directed at the umbilicus. The examiner should start just above the umbilicus, then move laterally to the umbilicus, and inally stroke just below the umbilicus. The relexes should be present bilaterally. Unilateral absence usually is associated with acquired corticospinal impairment, such as syringomyelia of the spinal cord.

References For References, see expertconsult.com.

CHAPTER 3 The Orthopaedic Examination: A Comprehensive Overview

Appendix 3-1 Texas Scottish Rite Hospital for Children Initial History and Physical Examination Form Name of patient ________________________________________________________ Chart number ______________________ Date of visit ______________________ • Chief complaint • Present illness • Past history (significant findings appropriate to age of patient) Pregnancy, labor, delivery, neonatal history Immunizations Previous surgery Usual childhood illnesses • S oci al history Emotional status Behavioral/activities of daily living E duc ational status • Review of systems Physical therapy, occupational therapy, and equipment presently used by patient Allergies Present medications Grow ht and development • Family history • Physical ex amination Height B lood pr essure Weight Temperature Respiration Pulse H ENT E Thorax and chest Neck Abdomen Heart • Neurologic ex amination Mental status Cranial nerves Cerebellar M otorand DT R s Sensory • M uscl e ex amination Atrophy S ength tr Contractures • U pp er extremities ex amination • L ow er extremities ex amination Ambulatory status Leg lengths: Right and left Hips: Right and left A. E ternal x rotation B. Internal rotation C. Flexion D. E tension x E. Abduction F. Adduction Knees: Right and left A. Flexion B. E tension x Ank es: l Right and left A. Plantar flexion B. Dorsiflexion Feet: Right and left A. Eversion B. Inversion Long bones • S pin e /pelvis ex amination • Impression • Plan (Course of action to include family’s and/or guardian’s expectations for and involvement in the assessment, treatment, and continuous care of the patient. ) DTRs, Deep tendon relexes; HEENT, head, ears, eyes, nose, and throat. (Adapted by John G. Birch.)

57

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SECTION I Disciplines

Appendix 3-2 Manual Muscle Tests of the Lower and Upper Extremities Name ______________________________________________________________________________ Trunk and Legs

Dates

Left-Side Grades

Dates

Muscle

Peripheral Nerves

Sternocleidomastoid C1-4

—

Neck flexors C1- 8

—

Neck extensors C1-8; T1

—

Back extensors T1-12; L1-5; S1-3

—

Upper rectus abdominis T5-12

—

Lower rectus abdominis T5-12

—

External oblique T5-12

—

Internal oblique T7-12

—

Iliopsoas L(1), 2, 3, 4

Lumbar plexus, femoral

S a r t o r i u s L 2 , 3 , (4 )

Femoral

Right-Side Grades

Hip adductors L2, 3, 4 (Adductor magnus L2-5; S1)

Obturator

Gracilis L2, 3, 4 Q u ad r i c e p s L 2 , 3 , 4

Femoral

Tensor fasciae latae L4, 5; S1 Gluteus medius L4, 5; S1

Superior gluteal

Hip medial rotation L4, 5; S1 Extensor digitorum longus L4, 5; S1

Peroneal

Peroneus longus L4, 5; S1

Superficial peroneal

Peroneus brevis L4, 5; S1 Extensor digitorum brevis L4, 5; S1 Extensor hallucis longus L4, 5; S1

Deep peroneal

Anterior tibialis L4, 5; S1 Hip lateral rotation L4, 5; S1, 2

Sacral plexus obturator

Semitendinosus L4, 5; S1, 2

Sciatic

Semimembranosus L4, 5; S1, 2 Gluteus maximus L5; S1, 2

Inferior gluteal

Biceps femoris L5; S1, 2, 3

Sciatic

Gastrocnemius S1, 2 Soleus L5; S1, 2 Posterior tibialis L(4), 5; S1 Flexor digitorum longus L4, 5; S1 (2) Flexor digitorum brevis L4, 5; S1

Tibial

Lumbricals L4, 5; S1, 2 Flexor hallucis longus L4, 5; S1, 2 Flexor hallucis brevis L4, 5; S1, 2 Muscle strength graded using following scale: 0 = Absent 1 = T Trace: mere tension on palpation P− Poor minus: beginning motion 2 = P Poor: full range, gravity-eliminated P+ Poor plus: begin motion antigravity F− Fair minus: almost full range antigravity

3 =F F+ G− 4 =G G+ 5 =G Notes:

Fair: full range antigravity Fair plus: full range, minimal resistance Good minus Good: full range, moderate resistance Good plus N Normal, maximum resistance

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CHAPTER 3 The Orthopaedic Examination: A Comprehensive Overview

Appendix 3-2 Manual Muscle Tests of the Lower and Upper Extremities, cont’d Name ______________________________________________________________________________ Upper Extremities/Shoulders

Dates

Left-Side Grades

M u sc l e

Pe ri p h e ra l N e rve s

Dates

Right-Side Grades

Upper trapezius CN XI C2, 3, 4 Middle trapezius CN XI C2, 3, 4

Accessory, ventral ramus 2, 3, 4

L ow er trapezius CN XI C2, 3, 4 Rhomboids C3, 4, 5

Cervical, dorsal scapular

Anterior deltoid C5, 6 Middle deltoid C5, 6

Axillary

Posterior deltoid C5, 6 Shoulder external rotators C(4), 5, 6

Suprascapular, axillary

Shoulder internal rotators C5, 6, 7

Upper and lower subscapular

Pectoralis major:

L a te r a l p e c t o r a l

Clavicular head C5, 6, 7 Sternal C6, 7, 8; T1

Lateral and medial pectoral

Serratus anterior C5, 6, 7, 8

Long thoracic

Latissimus dorsi C6, 7, 8

Thoracodorsal

B i c e p s C 5, 6

Musculocutaneous

Brachioradialis C5, 6 Supinator C5, 6, (7)

Radial

Triceps C6, 7, 8; T1 Pronator teres C6, 7

Median

Pronator quadratus C7, 8; T1 Extensor carpi radialis longus C5, 6, 7, 8 Extensor carpi radialis brevis C5, 6, 7, 8 Extensor carpi ulnaris C6, 7, 8 Extensor digitorum 1 C6, 7, 8 2 C6, 7, 8 3 C6, 7, 8

Radial

4 C6, 7, 8 Extensor pollicis brevis C6, 7, 8 Extensor pollicis longus C6, 7, 8 Abductor pollicis longus C6, 7, 8 Flexor carpi radialis C6, 7, 8 Opponens pollicis C6, 7, 8; T1 Abductor pollicis brevis C6, 7, 8; T1 Flexor digitorum superficialis 1 C7, 8; T1

Median

2 C7, 8; T1 3 C7, 8; T1 4 C7, 8; T1 Flexor pollicis brevis C6, 7, 8; T1

Median, ulnar

Flexor pollicis longus C(6), 7, 8; T1 Flexor digitorum profundus 1 C8; T1

Median

2 C8; T1 Continued

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Appendix 3-2 Manual Muscle Tests of the Lower and Upper Extremities, cont’d Name ______________________________________________________________________________ Upper Extremities/Shoulders, cont’d

Dates

Left-Side Grades

Muscle

Peripheral Nerves

Dates

Right-Side Grades

3 C7, 8; T1 4 C7, 8; T1

Ulnar

Flexor carpi ulnaris C7, 8; T1 Palmaris longus C(6), 7, 8; T1 Lumbricals 1 and 2 C(6), 7, 8; T1

Median

Lumbricals 3 and 4 C(7), 8; T1 Dorsal interossei C8; T1 Palmar interossei C8; T1 Adductor pollicis C8; T1

Ulnar

Abductor digiti minimi C(7), 8; T1 Opponens digiti minimi C(7), 8; T1 Muscle strength graded using following scale: 0 = Absent 1 = T Trace: mere tension on palpation P− Poor minus: beginning motion 2 = P Poor: full range, gravity-eliminated P+ Poor plus: begin motion antigravity F− Fair minus: almost full range antigravity

3 = F Fair: full range antigravity F + Fair plus: full range, minimal resistance G− Good minus 4 = G Good: full range, moderate resistance G+ Good plus 5 = N Normal, maximum resistance Notes:

CHAPTER 3 The Orthopaedic Examination: A Comprehensive Overview

References 1. Alund M, Larsson SE: Three-dimensional analysis of neck motion. A clinical method, Spine 15:87, 1990. 2. An KN, Morrey BF: Biomechanics of the elbow. In Morrey BF, editor: The elbow and its disorders, Philadelphia, 1985, Saunders, p 43. 3. An KN, Morrey BF, Chao EY: Carrying angle of the human elbow joint, J Orthop Res 1:369, 1984. 4. Ashton BB, Pickles B, Roll JW: Reliability of goniometric measurements of hip motion in spastic cerebral palsy, Dev Med Child Neurol 20:87, 1978. 5. Baird HW, Gordon EC: Neurological evaluation of infants and children, Clin Dev Med 84:85, 1983. 6. Baxter MP: Assessment of normal pediatric knee ligament laxity using the genucom, J Pediatr Orthop 8:546, 1988. 7. Beals RK: The normal carrying angle of the elbow. A radiographic study of 422 patients, Clin Orthop Relat Res 119:194, 1976. 8. Beattie P, Rothstein JM, Lamb RL: Reliability of the attraction method for measuring lumbar spine backward bending, Phys Ther 67:364, 1987. 9. Boone DC, Azen SP: Normal range of motion of joints in male subjects, J Bone Joint Surg Am 61:756, 1979. 10. Boone DC, Azen SP, Lin CM, et al: Reliability of goniometric measurements, Phys Ther 58:1355, 1978. 11. Browne AO, Hoffmeyer P, Tanaka S, et al: Glenohumeral elevation studied in three dimensions, J Bone Joint Surg Br 72:843, 1990. 12. Cave EF, Roberts SMA: A method for measuring and recording joint function, J Bone Joint Surg Am 18:455, 1936. 13. Cheng JC, Chan PS, Hui PW: Joint laxity in children, J Pediatr Orthop 11:752, 1991. 14. Committee for the Study of Joint Motion: Joint motion: method of measuring and recording, Chicago, 1965, American Academy of Orthopaedic Surgeons. 15. Coon V, Donato G, Houser C, et al: Normal ranges of hip motion in infants six weeks, three months and six months of age, Clin Orthop Relat Res 110:256, 1975. 16. Daniels L, Williams M, Worthington C: Muscle testing: techniques of manual examination, Philadelphia, 1958, Saunders. 17. Darcus HD, Salter N: The amplitude of pronation and supination with the elbow lexed to a right angle, J Anat 87:169, 1953. 18. Dvorak J, Antinnes JA, Panjabi M, et al: Age and gender related normal motion of the cervical spine, Spine 17(Suppl 10):S393, 1992. 19. Dvorak J, Panjabi MM, Grob D, et al: Clinical validation of functional lexion/extension radiographs of the cervical spine, Spine 18:120, 1993. 20. Dvorak J, Panjabi MM, Novotny JE, et al: In vivo lexion/extension of the normal cervical spine, J Orthop Res 9:828, 1991. 21. Einkauf DK, Gohdes ML, Jensen GM, et al: Changes in spinal mobility with increasing age in women, Phys Ther 67:370, 1987. 22. Elveru RA, Rothstein JM, Lamb RL: Goniometric reliability in a clinical setting. Subtalar and ankle joint measurements, Phys Ther 68:672, 1988. 23. Engel GM, Staheli LT: The natural history of torsion and other factors inluencing gait in childhood. A study of the angle of gait, tibial torsion, knee angle, hip rotation, and development of the arch in normal children, Clin Orthop Relat Res Mar-Apr:12, 1974. 24. Fitzgerald GK, Wynveen KJ, Rheault W, et al: Objective assessment with establishment of normal values for lumbar spinal range of motion, Phys Ther 63:1776, 1983. 25. Forero N, Okamura LA, Larson MA: Normal ranges of hip motion in neonates, J Pediatr Orthop 9:391, 1989. 26. Freedman L, Munro RR: Abduction of the arm in the scapular plane: scapular and glenohumeral movements. A roentgenographic study, J Bone Joint Surg Am 48:1503, 1966. 27. Futagi Y, Otani K, Imai K: Asymmetry in plantar grasp response during infancy, Pediatr Neurol 12:54, 1995.

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28. Futagi Y, Tagawa T, Otani K: Primitive relex proiles in infants: differences based on categories of neurological abnormality, Brain Dev 14:294, 1992. 29. Gill K, Krag MH, Johnson GB, et al: Repeatability of four clinical methods for assessment of lumbar spinal motion, Spine 13:50, 1988. 30. Greene WB, Heckman JD: The clinical measurement of joint motion, Rosemont, Ill, 1994, American Academy of Orthopaedic Surgeons. 31. Haas SS, Epps CH Jr, Adams JP: Normal ranges of hip motion in the newborn, Clin Orthop Relat Res 91:114, 1973. 32. Harris SR, Smith LH, Krukowski L: Goniometric reliability for a child with spastic quadriplegia, J Pediatr Orthop 5:348, 1985. 33. Hawkins RJ, Bokor DJ: Clinical examination of shoulder problems. In Rockwood CA, Matsen FA, editors: The shoulder, Philadelphia, 1990, Saunders, p 149. 34. Hensinger RN: Standards in pediatric orthopaedics, New York, 1986, Raven Press. 35. Hoffer MM: Joint motion limitation in newborns, Clin Orthop Relat Res 148:94, 1980. 36. Hoppenield S: Physical examination of the spine and extremities, New York, 1976, Appleton-Century-Crofts. 37. Jaffe M, Kugelman A, Tirosh E, et al: Relationship between the parachute reactions and standing and walking in normal infants, Pediatr Neurol 11:38, 1994. 38. Jaffe M, Tirosh E, Kessel A, et al: The parachute reactions in normal and late walkers, Pediatr Neurol 14:46, 1996. 39. Jofe MH, White AA, Panjabi M: Kinematics. In Bailey RW, editor: The cervical spine, Philadelphia, 1983, JB Lippincott, p 23. 40. Johnson EW: Examination for muscle weakness in infants and small children, JAMA 168:1306, 1958. 41. Johnson RM, Hart DL, Simmons EF, et al: Cervical orthoses. A study comparing their effectiveness in restricting cervical motion in normal subjects, J Bone Joint Surg Am 59:332, 1977. 42. Keeley J, Mayer TG, Cox R, et al: Quantiication of lumbar function. Part 5: reliability of range-of-motion measures in the sagittal plane and an in vivo torso rotation measurement technique, Spine 11:31, 1986. 43. Kendall HW, Kendall FP: Muscles: testing and function, Baltimore, 1983, Williams & Wilkins. 44. Lovett RW: Fatigue and exercise in treatment of infantile paralysis: study of one thousand eight hundred and thirty-six cases, JAMA 69:168, 1917. 45. Lovett RW, Martin EG: Certain aspects of infantile paralysis, with a description of a method of muscle testing, JAMA 66:729, 1916. 46. Lundberg A, Goldie I, Kalin B, et al: Kinematics of the ankle/foot complex: plantarlexion and dorsilexion, Foot Ankle 9:194, 1989. 47. Lundberg A, Svensson OK, Bylund C, et al: Kinematics of the ankle/foot complex—part 2: pronation and supination, Foot Ankle 9:248, 1989. 48. Macrae IF, Wright V: Measurement of back movement, Ann Rheum Dis 28:584, 1969. 49. Mallon WJ, Brown HR, Nunley JA: Digital ranges of motion: normal values in young adults, J Hand Surg Am 16:882, 1991. 50. Mann RA: Principles of examination of the foot and ankle. In Mann RA, Coughlin MJ, editors: Surgery of the foot and ankle, St Louis, 1992, Mosby, p 45. 51. McGraw MB: The neuromuscular maturation of the human infant, New York, 1963, Haffner. 52. Mellin GP: Accuracy of measuring lateral lexion of the spine with a tape, Clin Biomech 1:85, 1986. 53. Miller JJ 3rd: The fasciitis-morphea complex in children, Am J Dis Child 146:733, 1992. 54. Mimura M, Moriya H, Watanabe T, et al: Three-dimensional motion analysis of the cervical spine with special reference to the axial rotation, Spine 14:1135, 1989. 55. Mitchell RG: The Moro relex, Cereb Palsy Bull 2:135, 1960.

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56. Moro E: Das erste Tremenon, Munchen Med Wochenschr 65:1147, 1918. 57. Murray MP, Gore DR, Gardner GM, et al: Shoulder motion and muscle strength of normal men and women in two age groups, Clin Orthop Relat Res 192:268, 1985. 58. Ober FR: The role of the iliotibial band and fascias: a factor in the causation of low back disabilities and sciatica, J Bone Joint Surg Am 18:105, 1936. 59. Ouzounian TJ, Shereff MJ: In vitro determination of midfoot motion, Foot Ankle 10:140, 1989. 60. Panjabi M, Dvorak J, Duranceau J, et al: Three-dimensional movements of the upper cervical spine, Spine 13:726, 1988. 61. Penning L, Wilmink JT: Rotation of the cervical spine. A CT study in normal subjects, Spine 12:732, 1987. 62. Perry J: Determinants of muscle function in the spastic lower extremity, Clin Orthop Relat Res 288:10, 1993. 63. Phelps E, Smith LJ, Hallum A: Normal ranges of hip motion of infants between nine and 24 months of age, Dev Med Child Neurol 27:785, 1985. 64. Portek I, Pearcy MJ, Reader GP, et al: Correlation between radiographic and clinical measurement of lumbar spine movement, Br J Rheumatol 22:197, 1983. 65. Reade E, Hom L, Hallum A, et al: Changes in popliteal angle measurement in infants up to one year of age, Dev Med Child Neurol 26:774, 1984. 66. Roaas A, Andersson GB: Normal range of motion of the hip, knee and ankle joints in male subjects, 30-40 years of age, Acta Orthop Scand 53:205, 1982. 67. Roach KE, Miles TP: Normal hip and knee active range of motion: the relationship to age, Phys Ther 71:656, 1991. 68. Rothstein JM, Miller PJ, Roettger RF: Goniometric reliability in a clinical setting. Elbow and knee measurements, Phys Ther 63:1611, 1983. 69. Salenius P, Vankka E: The development of the tibiofemoral angle in children, J Bone Joint Surg Am 57:259, 1975. 70. Salisbury PJ, Porter RW: Measurement of lumbar sagittal mobility. A comparison of methods, Spine 12:190, 1987. 71. Salter N, Darcus HD: The amplitude of forearm and of humeral rotation, J Anat 87:407, 1953. 72. Sammarco GJ, Burstein AH, Frankel VH: Biomechanics of the ankle: a kinematic study, Orthop Clin N Am 4:75, 1973.

73. Schwarze DJ, Denton JR: Normal values of neonatal lower limbs: an evaluation of 1,000 neonates, J Pediatr Orthop 13:758, 1993. 74. Staheli LT: The prone hip extension test: a method of measuring hip lexion deformity, Clin Orthop Relat Res 123:12, 1977. 75. Staheli LT, Corbett M, Wyss C, et al: Lower-extremity rotational problems in children. Normal values to guide management, J Bone Joint Surg Am 67:39, 1985. 76. Svenningsen S, Terjesen T, Aulem M, et al: Hip motion related to age and sex, Acta Orthop Scand 60:97, 1989. 77. Swaiman KF: Neurologic examination after the newborn period until 2 years of age. In Swaiman KF, editor: Pediatric neurology: principles and practice, St Louis, 1993, Mosby, p 43. 78. van Adrichem JA, van der Korst JK: Assessment of the lexibility of the lumbar spine. A pilot study in children and adolescents, Scand J Rheumatol 2:87, 1973. 79. Wagner C: Determination of the rotary lexibility of the elbow joint, Eur J Appl Physiol Occup Physiol 37:47, 1977. 80. Watkins MA, Riddle DL, Lamb RL, et al: Reliability of goniometric measurements and visual estimates of knee range of motion obtained in a clinical setting, Phys Ther 71:90; discussion 96, 1991. 81. Waugh KG, Minkel JL, Parker R, et al: Measurement of selected hip, knee, and ankle joint motions in newborns, Phys Ther 63:1616, 1983. 82. White AA: Analysis of the mechanics of thoracic surgery in man: an experimental study of autopsy specimens, Acta Orthop Scand 127:1, 1969. 83. White AA, Panjabi M: Kinematics of the spine. In White AA, Panjabi M, editors: Clinical biomechanics of the spine, Philadelphia, 1990, JB Lippincott. 84. Williams R, Binkley J, Bloch R, et al: Reliability of the modiiedmodiied Schober and double inclinometer methods for measuring lumbar lexion and extension, Phys Ther 73:33, 1993. 85. Wynne-Davies R: Familial joint laxity, Proc R Soc Med 64:689, 1971. 86. Youdas JW, Carey JR, Garrett TR: Reliability of measurements of cervical spine range of motion–comparison of three methods, Phys Ther 71:98; discussion 105, 1991. 87. Zausmer E: The evaluation of motor development in children, Phys Ther 44:247, 1964.

CHAPTER 4

The Orthopaedic Examination: Clinical Application

Screening Examinations

Chapter Outline Screening Examinations 61 The Focused Examination 63 The Art of Examining the Pediatric Patient

John G. Birch

68

It is important for orthopaedic surgeons to be familiar with the numerous musculoskeletal and neuromuscular examinations detailed in Chapter 3. Over time the orthopaedist will most likely perform many of these examinations on different patients presenting with a variety of complaints. If the nature of the patient’s medical condition is unclear, the physician may have to perform a comprehensive examination to arrive at a differential diagnosis. In most cases, however, the orthopaedic surgeon does not have the time or the need to perform an all-encompassing examination on every patient seen in the clinical setting. In the real world, the pediatric orthopaedic examination must be tailored to the child’s age, level of cooperation, and chief complaint. The two most common types of examinations performed are the screening examination and focused examination. Screening examinations are performed as part of a comprehensive or abbreviated examination to detect disorders that may be asymptomatic but could cause signiicant morbidity or mortality if undiagnosed and untreated. Focused examinations concentrate on speciic abnormalities for which the patient has been referred, or on the chief presenting complaint. With these factors in mind, the examiner should make the clinical assessment as orderly and organized as possible to avoid neglecting any essential parts of the examination. However, the examination also needs to be performed as expeditiously as possible, before the examiner loses the child’s initial cooperation because of patient apprehension, fatigue, or boredom. The inal section of this chapter addresses the art of examining the pediatric patient. Although it is not dificult to outline the recommended principles for conducting the pediatric examination, rarely does the physician have the luxury of the ideal environment when seeing patients in the clinic. An uncooperative child, the presence of multiple family members, and limited time provide an impetus to perform the examination as expeditiously as possible while still maintaining good rapport with the patient and parents. To assist physicians inexperienced in examining children, we offer a number of suggestions based on years of personal experience that should help the physician conduct an examination that is eficient and enjoyable.

Screening examinations are conducted to determine whether the patient has any undiagnosed disorders that may be potentially harmful or deleterious if left unmanaged. In pediatric orthopaedics, two primary disorders of this sort are undetected developmental dysplasia of the hip (DDH) and scoliosis.

Hip Examination All children are at risk for DDH, which, if not treated appropriately, can result in a limp and early degenerative arthritis. Because the condition is asymptomatic, all newborns and infants should be screened regularly for the condition until they have developed a mature normal gait. The most common clinical methods of detecting DDH are the tests for the Barlow sign2 and Ortolani sign.20 First, the test for the Barlow sign is performed to determine whether the hip is dislocatable (i.e., whether the femoral head can be pushed out of the acetabulum on examination; Fig. 4-1). The examiner attempts to subluxate or dislocate the femoral head from within the acetabulum by gently pushing the relaxed infant’s hips laterally and posteriorly, with the leg in 90 degrees of lexion and neutral abduction. If there is instability, the femoral head will dislocate from the acetabulum and then spontaneously reduce, with a distinct “clunk” when pressure on the leg is relaxed. This may be the only physical inding on examination. Next, the examiner should determine whether the femoral head is dislocated out of the acetabulum by testing for the Ortolani sign (Fig. 4-2). In neonates, it is usually possible to reduce the dislocated femoral head temporarily by gently abducting the hip and lifting the upper leg forward. A distinct clunk will be felt as the head is reduced. When pressure on the leg is released, the femoral head will dislocate again. If the hip is dislocated, physical indings may include limited abduction (normal abduction is approximately 90 degrees), asymmetric thigh folds (excess on the affected side), and shortening of the leg compared with the opposite side. One point to emphasize regarding these two maneuvers is that the examiner cannot elicit both the Barlow and Ortolani signs from the same hip. Either the femoral head is sitting in the acetabulum and can be temporarily dislocated on examination (Barlow sign), or the head is dislocated and can be temporarily reduced on examination (Ortolani sign). If the physical examination indings are equivocal and the patient is considered to be at high risk for DDH, ultrasound studies should be ordered. 61

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A

A

B

B

FIGURE 4-1 Test for the Barlow sign to determine whether the femoral head is dislocatable. A, With the infant relaxed and the hip and knee lexed, the examiner gently adducts the hip while attempting to displace the femoral head posteriorly. B, With a positive test, the femoral head will be felt to dislocate posteriorly.

Other Newborn Screening Examinations Newborns should also be screened for spinal deformities and malformations (e.g., torticollis, spinal dysraphism), digital anomalies (e.g., syndactyly, absence), long bone deformities, and foot deformities (e.g., intoeing, rigid metatarsus adductus, clubfoot, calcaneovalgus foot). All children should also be evaluated for normal lower extremity alignment, limb length inequality, kyphosis, and gross motor skills. In addition, the child’s height, weight, and head circumference should be measured and charted to determine if the following are present: 1. Weight or height is excessively high or low 2. Weight or height is disproportionate 3. Head circumference is disproportionate for height and weight 4. Weight, height, or head circumference deviates from the percentile line identiied for any particular child

Scoliosis Examination Scoliosis can result in severe cosmetic deformity and pulmonary compromise. The forward-bending test is a reliable means of screening for scoliosis. The examiner views the patient from the back during the test. The patient stands evenly on both legs, with the knees straight, and then bends forward at the waist, with the arms hanging free. The examiner evaluates the back for elevation of one hemithorax or lank relative to the other to determine the presence of a rotational deformity caused by scoliosis.

General Childhood Screening Examination An initial screening examination to help detect other potential deformities or disorders can be done simply by

FIGURE 4-2 Test for the Ortolani sign to determine whether the femoral head is dislocated but reducible. A, The examiner attempts to reduce the dislocated femoral head by gentle traction, abduction, and anterior translation of the thigh. B, With a positive test, the femoral head will be felt to reduce into the acetabulum.

observing the child during certain maneuvers. Observing the patient standing upright with feet together identiies any bowlegs or knock-knees, foot deformities, or limb length inequality. The child’s gross motor skills can be assessed in a number of ways. Having the patient heel-walk, toe-walk, and hop on each foot in turn allows the examiner to evaluate gross strength in the legs and balance. When the child walks and runs, the examiner should look for limping or other gait abnormalities that may be caused by muscle weakness or spasticity. Many neuromuscular disorders disrupt this normal motion and function. How easily the patient rises from a supine position on the loor is a general indication of neurologic integrity or may indicate the presence of proximal leg muscle weakness, as seen in muscular dystrophy. Having the child bend over to pick up an object tests eye-hand coordination and muscle balance and also helps determine the severity of back pain, if that is the chief complaint. Screening examinations should be cost-effective, reliable, and speciic in identifying the disorder in question. Ideally, there should also be a cost-effective treatment available that can signiicantly alter the natural history of the disorder if applied early. Such is the case with DDH, in which early use of the Pavlik harness usually corrects the condition and prevents the need for more costly treatment later. Scoliosis screening is more controversial, however. Although the forward-bending test is a reliable means of screening for scoliosis, it may be too sensitive because many false-positive results occur with this maneuver. Radiography is highly speciic for identifying scoliosis but is not a costeffective means of screening the population at risk. In addition, whether treatment can effectively change the natural history of the deformity has been under debate. The beneits of early detection of other commonly encountered orthopaedic conditions are detailed in the chapters dealing with the speciic entities.

CHAPTER 4 The Orthopaedic Examination: Clinical Application

Box 4-1 Quick Rule-Out Examination

63

Line of progression

Have the patient do the following in continuous succession: • Hop off the examination table. • Walk back and forth. • Hop on one foot. • Hop on the other foot. • Heel-walk. • Toe-walk. • Walk on the lateral border of the feet. • Squat down and stand up. If the patient does all these without noticeable abnormality, the examiner can rule out muscular dystrophies, cerebral palsy, ataxias, Charcot-Marie-Tooth disease, septic arthritis in the lower extremity, tarsal coalition, patellar dislocation, and drop foot. The patient with DDH may have such a subtle gait deviation that it is not noted on this brief examination. Angle of gait

The Focused Examination The focused clinical examination provides an expedient, organized approach to the assessment of commonly encountered pediatric orthopaedic complaints (Box 4-1). The topics discussed here are intoeing, latfoot, leg length discrepancy, and spinal deformity. These entities collectively account for a large proportion of presenting complaints of pediatric patients and referrals by their pediatricians when children are seen by orthopaedic surgeons in a nonemergent or ofice setting. Detailed differential diagnoses and the management of the disorders are discussed in the respective chapters on the various conditions.

Intoeing One of the most common parental concerns prompting an orthopaedic evaluation is intoeing, or walking with an excessively inward foot progression angle.5,8,11 Typically the parent is concerned that the child will have a permanent disability or that the condition will interfere with the child’s physical performance. In most cases, however, the problem is minor and self-limiting, and no treatment is necessary. The most common benign causes of intoeing are metatarsus adductus, increased or persistent internal tibial torsion, and increased or persistent femoral anteversion.8,11 Other benign causes include structural anomalies of the legs or feet. Most of these conditions do not need to be treated. Instead the parents simply need to be reassured that the condition usually resolves on its own and the patient should be observed on a regular basis to ensure that the foot progression angle gradually returns to normal. Occasionally, however, intoeing can be a manifestation of a more signiicant problem that necessitates further evaluation and may require treatment. Examples include static encephalopathy, other neurologic disorders, some mild tibial deiciencies, infantile Blount disease, metabolic bone diseases, and skeletal dysplasias. Patients with these conditions are sometimes referred or present with an initial complaint of intoeing. Thus, the focused examination of the child with intoeing is concerned with ruling out one of the aforementioned serious causes, making sure that the child has normal neurologic function, and conirming that the cause of the

FIGURE 4-3 Assessment of the patient with an intoed gait. The foot progression angle is estimated as the angle between the axis of the foot and line of direction of gait.

problem is benign. The physician should ascertain whether there is a family history of DDH, neuromuscular disease (especially muscular dystrophies), or other, relatively rare, hereditary neurologic conditions, such as Charcot-MarieTooth disease or familial spastic paraparesis. The examiner should be familiar with the child’s neonatal history and developmental history when assessing the patient’s neurologic status. In addition the age of the child can be of help in determining the cause of the intoeing. Typically metatarsus adductus becomes evident after birth and before walking, increased internal tibial torsion is seen in toddlers to preschoolers, and increased femoral anteversion is most commonly found in school-age children to adolescents. During the history taking, the younger child should be allowed to play or move about the room freely. From this free movement, the physician can gain some idea of the nature and severity of the problem, which can be especially helpful if the patient becomes resistive or uncooperative during the formal physical examination. If it is not possible to observe the child walking or running while taking the history, the examiner should do so afterward, but from a safe distance. The child should be undressed from at least the knees down during the physical examination. While the patient is ambulating, the examiner should irst look for evidence of impaired mobility, signiicant balance problems, lethargy, or weakness in movement. Barring any of these problems, the physician should then try to discern the source of the intoed gait and its approximate severity (Fig. 4-3). Important observations to make while the patient is walking or running include the following: 1. Noting whether the lateral border of the foot is turned in, as occurs with metatarsus adductus 2. Observing whether the feet are oriented medially relative to the knee, as occurs with increased tibial torsion 3. Noting whether the entire leg rotates inward, with “squinting” patellae, as seen with increased femoral anteversion (Fig. 4-4)

64

SECTION I Disciplines

Older children may try to mask an intoed gait during the physical examination. To counter this attempt, the examiner should have the patient heel-walk, toe-walk, and hop across the room on each leg. This will make the intoeing gait more evident to the examiner, as it is to the parent who sees it on a daily basis. Having the child perform these maneuvers will also provide the physician with valuable initial information regarding the neurologic status of the patient. Although neurologic conditions are not the most common cause of intoeing, it is important for the examiner to rule them out as the cause of the problem.

A

B

C

FIGURE 4-4 Evaluation of the cause of intoed gait in healthy children. A, When the cause of the intoed gait is increased internal tibial torsion, the foot progression angle will be negative and the patellae will point forward. B, Alternatively, the child may rotate the entire lower limb externally through the hip, resulting in a neutral foot progression angle, externally rotated patellae, and apparent tibia vara. C, When the cause is increased femoral anteversion, the foot progression angle is negative and the patellae are rotated medially.

External rotation

A

0°

The torsional proile can be expediently assessed with the patient prone on the examining table, as described by Staheli.25 With the patient in this position, the examiner can determine the amount of internal and external rotation of the hip as an indication of the amount of femoral anteversion, assess the thigh-foot axis to estimate tibial torsion, and examine the shape of the lateral border of the foot (Fig. 4-5). If, however, a younger child is uncomfortable or feels threatened in this position, the examination can be conducted with the child in the comfort and safety of the parent’s lap, making for a calmer patient. With the patient in this position, the lateral aspect of the foot can be assessed, bimalleolar axis of the ankle relative to the knee can be estimated, and amount of internal and external rotation of the hip in the lexed position can be assessed. The examiner should also feel the patient’s muscle tone to determine whether there is hypertonia (suggesting spasticity) or hypotonia (suggesting muscle weakness). Particular clinical manifestations are associated with the three most common causes of intoeing. Typically metatarsus adductus is characterized by an inward deviation of the lateral border of the foot from the base of the ifth metatarsal. This deviation may or may not be lexible. With increased internal tibial torsion, there is an excessive inward (or negative) thigh-foot angle or bimalleolar axis. Excessive femoral anteversion is typiied by increased internal rotation and decreased external rotation of the hip in lexion or extension.

Flatfoot When assessing children with latfoot deformity, the examiner should irst consider the patient’s age because certain underlying conditions tend to be age-speciic. An infant may have a simple positional deformity, medial arch fat pad obscuring visual evidence of the underlying arch, calcaneovalgus foot, or—least likely but most signiicant—congenital

Internal rotation

B

FIGURE 4-5 Torsional proile examination with the patient prone. The examiner can expediently assess the thigh-foot axis to estimate tibial torsion and examine the shape of the lateral border of the foot to assess the presence of metatarsus adductus (A) and to determine the amount of internal and external rotation of the hip as an indication of the amount of femoral anteversion (B). (Adapted from Staheli LT: Torsional deformity, Pediatr Clin North Am 24:799, 1977.)

CHAPTER 4 The Orthopaedic Examination: Clinical Application

rocker bottom foot (vertical talus).10 The young child most likely has a lexible latfoot deformity.17,27 An adolescent may have a tight heel cord with secondary midfoot breakdown or a peroneal spastic latfoot caused by tarsal coalition1,13 or another problem.15 While taking the history, the examiner should determine whether there is associated pain, where it is located, and when it occurs. Pain that is not related to exercise may be caused by inlammatory arthritis (the tarsal joints are a common location for juvenile arthritis), infection or, rarely, a bone lesion. Nonspeciic foot, ankle, or lower leg pain in the adolescent or preadolescent patient may be caused by tarsal coalition. Examination of the feet starts by having the patient walk and observing whether the gait pattern is normal, antalgic, or indicative of neuromuscular dysfunction (e.g., hemiparesis). The child should then be asked to heel-walk, toe-walk, and hop on each foot in turn, if possible. This allows further assessment of neurologic and musculoskeletal function, as well as a stress examination if pain is present. If the longitudinal arch is absent when the patient is standing still, the examiner should look for reconstitution of the arch when the patient is walking on the toes. With the patient standing facing forward, the examiner should look for evidence of muscle atrophy, swelling, erythema, or deformity of the lower leg. The lower extremity alignment should be checked to determine if there is femorotibial valgus. Next the patient’s foot should be examined from behind because it is easier to assess hindfoot valgus from this position. Reconstitution of the longitudinal arch can also be assessed at this point by having the patient stand on the toes. The examiner should also note whether the hindfoot swings from valgus to varus. If the hindfoot stays in valgus, tarsal coalition may be present. Next the examiner should have the patient sit with the feet hanging freely over the edge of the examination table (younger children can sit in the parent’s lap). Passive range of motion should be checked, speciically to rule out the presence of a tight heel cord. A tight heel cord, regardless of cause, can lead to latfoot because of compensatory midfoot breakdown. The examiner should then rock the subtalar joint into inversion and eversion. Any stiffness (with or without discomfort) or peroneal muscle spasm during this maneuver suggests the presence of tarsal coalition, or possibly inlammatory arthritis. If the physician has not yet checked for reconstitution of the longitudinal arch, it should be done at this point. The examination concludes with a neurologic assessment of the lower extremities. The extent of this evaluation is based on the indings from the history and preceding physical examination and the examiner’s degree of suspicion at this point regarding the cause of the deformity. The most common type of latfoot that the pediatric orthopaedist will see is the so-called lexible latfoot deformity of childhood. There is no pain associated with this condition. Typically the child is between 18 months and 6 years of age, when physiologic genu valgum is the norm and may not be noticed by the parents. The foot will have supple range of motion on examination and the longitudinal arch will readily reconstitute during toe-walking or when the foot is in a non–weight-bearing position (Fig. 4-6). Most lexible latfeet resolve spontaneously, with no residual

A

65

B

FIGURE 4-6 Clinical photographs of a child with a lexible latfoot deformity. A, When the child is bearing weight on the foot, the medial longitudinal arch is lattened. B, When the child is not weight bearing, the longitudinal arch is restored.

adverse effects as the child ages; surgery is rarely indicated to treat this condition.7,27 Congenital vertical talus is characterized by a ixed lattening of the longitudinal arch, tight heel cord, variable degree of pain, and usually a palpable dorsolateral dislocation of the navicular on the talus.10 Because of the severity of this deformity, the patient usually is referred during infancy or shortly after walking age, at the latest. Classic, symptomatic tarsal coalition is characterized by ixed lattening of the longitudinal arch, ixed hindfoot valgus, and nonspeciic or exercise-induced pain.14 During rapid passive inversion of the subtalar joint by the examiner the patient may experience peroneal muscle spasm. During gait the patient will have an externally rotated, inlexible foot, as if the patient were wearing or had just come out of a short-leg walking cast. Patients with tarsal coalition typically are between the ages of 8 years and adolescence. Patients with midfoot breakdown secondary to a tight heel cord may present at any age after walking. The longitudinal arch may or may not reconstitute when the foot is in the non–weight-bearing position. The cause of the tight heel cord itself should be sought (e.g., static encephalopathy, tethered cord or other intrathecal anomaly, idiopathic) by further examination, as dictated by the clinical setting.

Leg Length Discrepancy Actual or apparent leg length discrepancy is a commonly encountered pediatric orthopaedic disorder that may be congenital or acquired. Actual limb length discrepancy is caused by a true structural difference between the two lower limbs. In apparent limb length discrepancy joint position or contracture decreases the functional length of the affected limb; however, the structural components of the limb may actually not be shorter than those of the opposite extremity. In addition, unilateral weakness of the abductor muscle of the lower extremity may produce a Trendelenburg gait, giving the impression of a short-leg gait. When taking the patient’s history the examiner should determine how long the shortening has been present, whether the patient has any neuromuscular disorders, and whether the limb has sustained a preceding noxious event (e.g., fracture, infection, surgery). During the physical examination the patient should be undressed as much as possible, taking modesty into account, so that an adequate assessment can be conducted. The examination starts with the patient walking toward and away from the examiner. The examiner looks for asymmetric gait and compensatory toe-walking on the shorter limb

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or excessive knee lexion of the longer limb.12,24 Evidence of muscle wasting or weakness in the power of the gait should also be noted. With the patient standing erect and facing forward, the physician notes the position of the joints and looks for evidence of angular deformity of the lower extremities. Particular attention should be paid to the relative height of the knees and to whether the patient has a tendency to stand on the toes of the shorter leg. The examiner then assesses these same features from behind the patient. Viewing the patient from behind, the physician can evaluate the relationship of the dimples over the posterior iliac spine or place his or her hands on the iliac crests to gain an appreciation of the magnitude of the limb length inequality. An excellent method of assessing and quantifying limb length discrepancy while the patient is standing is to use graduated blocks. The patient should be standing evenly on both legs, with the feet lat on the loor and the knees straight. Then blocks are placed under the shorter limb until the pelvis is level. The height of the blocks represents the patient’s true limb length discrepancy if there is no joint deformity. If there is associated joint postural deformity, the height of the blocks provides the functional limb length discrepancy. With the patient supine, the examiner checks the range of motion of the hips, knees, and ankles, looking speciically for lexion adduction or abduction contracture of the hips

ASIS

and lexion contracture of the knees. Subtle angular or rotational deformities of the shorter limb should again be assessed. These deformities include mild valgus of the knee, with increased external rotation of the hip (as seen with congenital femoral deiciency or partial ibular deiciency) and tibial diaphyseal valgus deformity, which may be the result of posteromedial bowing of the tibia. The actual and apparent limb lengths can be determined using a tape measure, with the patient supine (Fig. 4-7). During the measurement it is important that the joints be in a neutral position with respect to lexion of the hips and knees and abduction and adduction at the hips. Otherwise the measurement will incorrectly create the impression that limb length discrepancy exists when in reality it is not present. The relative lengths of the femora are determined by measuring from the anterior iliac spine to the medial joint line; the relative lengths of the tibiae are measured from the medial joint line to the medial malleolus. Another useful assessment that can be performed at this time to assess apparent or functional limb length discrepancy is to measure the distance from the umbilicus to the medial malleolus for each limb. With the patient still supine, the examiner performs manual muscle testing, sensory examination, and relex assessment, as needed. Based on the physical indings from the clinical examination, imaging studies may be necessary to determine the

ASIS

Apparent leg length Actual leg length

Normal

Adduction contracture Note apparent shortening

Abduction contracture Note apparent lengthening

FIGURE 4-7 Measurement of actual and apparent limb length inequality. In these examples, apparent limb length inequality is produced by pelvic obliquity. Hip and knee lexion deformities also produce apparent limb length inequality. ASIS, Anterior superior iliac spine. (Adapted from von Lanz T, Wachsmuth W: Praktische anatomie, Berlin, 1938, Julius Springer, p 24.)

CHAPTER 4 The Orthopaedic Examination: Clinical Application

A

B

67

C

FIGURE 4-8 Assessing spinal deformity. A, A patient with limb length inequality exhibits prominence of the entire length of the long side of the trunk during forward bending because of pelvic obliquity. Dotted line, Iliac wings. B, A patient with true scoliosis has truncal prominence localized to the convexity of the curve(s)—in this example, a right thoracic deformity. C, When viewed from the side, a patient with a kyphotic deformity has an increased or sharply localized kyphosis when in the forward-bending position.

degree and nature of the patient’s limb length inequality more precisely so that appropriate management can be initiated.

Spinal Deformity Orthopaedists are often asked to evaluate patients who have apparent spinal deformity, usually because the parents or referring physician are concerned about the possibility of scoliosis (of any cause) or kyphosis.4 If the patient complains of pain, the examiner needs to determine its location, nature, and onset and whether there is a history of antecedent trauma. Other important information to be obtained from the history includes the following: 1. The patient’s normal activity level 2. Whether there has been any change in that normal level 3. How much the spinal deformity or pain is interfering with physical activities 4. Whether there are any neurologic symptoms, such as radiating pain or loss of bowel or bladder control The physician should also determine whether there is a family history of scoliosis, connective tissue disease (e.g., Marfan syndrome, neuroibromatosis),9,23 or neuromuscular disease (particularly muscular dystrophy).6,7,16,18 The physician starts the examination by checking the patient’s neck range of motion and, while doing so, looking for evidence of facial, neckline, or scapular asymmetry. The mouth is checked for a high-arched palate, which may be seen in patients with Marfan syndrome.22 A cranial nerve examination can be performed at this time, if deemed necessary. The upper extremities should be examined for evidence of restricted range of motion and muscle wasting. The latter may be an indication of peripheral neuropathy or atrophy caused by syringomyelia. The patient’s inger lengths should be checked for signs of arachnodactyly, another indication of Marfan syndrome. The clinician then examines the patient from behind, with the patient standing evenly on both feet and the knees straight. The examiner looks for waistline, scapular, or paraspinal asymmetry.21 The level of the posterior sacral dimples

is checked to ensure that leg length inequality is not creating an apparent scoliosis. The relative position of the scapulae on the posterior chest wall is determined to rule out an associated or isolated Sprengel deformity.3,19 The physician should also look for a shift of the trunk to the right or left of the pelvis (Fig. 4-8, A). A plumb line held over the base of the occiput or the C7 spinous process can aid in this clinical assessment. The skin over the spine is inspected for pigmented spots, hairy patches, and deep pits that might overlie external openings of sinus tracts extending to the spinal cord. The presence of café au lait spots and neuroibromata should be noted. Flattening of the buttocks with apparent loss of lumbar lordosis may indicate the presence of spondylolisthesis. Defects of the vertebral bodies may be palpated by running the ingers along the spine and palpating for stiff curvature or defects in the spinous process. If the patient complains of pain, the examiner should percuss the spine for areas of tenderness. The examiner next stands behind the child while the child bends forward, as if touching the toes, with the arms hanging freely, to evaluate spinal lexion and hamstring tightness. The examiner should observe how smoothly the patient bends forward. A child with full lexibility should be able to touch the toes with the knees straight. While the patient is in the forward-bending position, the spine is irst examined for evidence of rotational deformity secondary to scoliosis (see Fig. 4-8, B), which, if present, can be measured with a scoliometer, as described in Chapter 12. The examiner should then view the patient’s spine from the side to rule out excessive thoracic kyphosis (see Fig. 4-8, C). After the back has been thoroughly examined, the patient should be asked to walk on his or her heels and toes and to hop on each foot in turn. These maneuvers provide a good indication of the patient’s general strength, muscle tone, and coordination. Finally, formal testing of joint range of motion, muscle strength, and relexes is performed with the patient on the examination table. The straight-leg raising test is also

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performed at this time. If the patient has scoliosis and there also is a possibility of syringomyelia, the abdominal relexes should be checked for asymmetry and for hypesthesia to light touch in the concavity of the deformity.26 This examination allows an observant examiner to assess patients rapidly for scoliosis, kyphosis, and other possible causes of spinal deformity (e.g., neuromuscular disease, spinal dysraphism, Marfan syndrome, neuroibromatosis).9,22,23 Appropriate imaging studies can then be ordered based on indings from the clinical examination.

The Art of Examining the Pediatric Patient This discussion is intended to provide guidance to those orthopaedists who are new to or inexperienced in the examination of the child. In the real world it is rarely possible to conduct the pediatric examination in the orderly comprehensive sequence in which it is taught. Reality more often involves a harried physician chasing an uncooperative child around the examining room, occasionally to the accompaniment of fundamentally undermining comments from the child’s parent or caretaker, such as the intolerable “Do you want the doctor to give you a needle?,” which only serves to guarantee a continued lack of cooperation from the child. The following are a number of suggestions that we have found to be helpful in the expedient acquisition of a good history and when performing a proper physical examination (Box 4-2). Over time, as the examiner becomes more comfortable examining children, the experience should be informative and enjoyable. • Never wear a white coat. The typical image of the physician is a person in a white laboratory coat, clothing that lends professional authority to its wearer and plays an introductory and role assumption role. This symbol may be appropriate when dealing with adults, but can be selfdefeating when treating pediatric patients. Based on past personal experience or on what they have heard from others, children often perceive a person in a white coat as a threatening igure, and its presence can thwart any opportunity of cooperation from the patient. Doing without a white coat avoids this visible reminder that you are the ominous doctor. The best way to identify yourself physically to the parents and patient as a physician is with an identiication badge. Minimizing your identity in this manner, however, should never be used to ambush a child. If an uncomfortable or painful examination must be performed, you should carefully explain, at an appropriate time, to the child and parents why, how, and when there will be discomfort. To do otherwise would only reinforce any negative attitudes the child might have regarding physicians. • Treat your patients and their parents with dignity. Introduce yourself to all who are present and inquire about their relationship to the child. When introducing yourself, shake the child’s hand. To show that you are interested in the child not only as a patient but as a person, ask about school, friends, and extracurricular activities that are of interest to the child. Be aware of and respect the child’s concerns, modesty, and apprehensions.

Box 4-2 Art of Examining the Pediatric Patient • • • • • • • • • • • • • • • • •

• •

•

•

Never wear a white coat. Treat your patients and their parents with dignity. Maintain your own professional dignity. Try to obtain the chief complaint and other information from the patient. Find out who is concerned about the patient’s presenting complaint, and why. Avoid threatening words. Respect the patient’s modesty as much as possible while still performing an adequate examination. Never miss an opportunity to examine children without touching them. Make the irst touch innocuous and nonthreatening in an area that does not hurt. Perform the examination without appearing to do so. Examine infants and young children while they are sitting in their parent’s lap. Examine the normal asymptomatic limb irst. Minimize the discomfort of the examination without compromising its purpose. If you are unable to perform an adequate examination, ask the parent to do it while you observe. Always have a parent witness the examination. When discussing your indings, agree as much as possible with the observations of the parent(s). Recognize and acknowledge when you have been unable to elicit a good history or perform an adequate examination. Always appear calm and unhurried. When faced with a complex problem that demands more time than you have at that particular moment, tell the family that you need to spend more time considering the child’s problem before a deinitive answer can be provided. When the family is unable to understand a complex orthopaedic problem, write them a letter, e-mail, or text message explaining your assessment and the treatment alternatives. Always communicate with the referring physician and, when appropriate, any previous treating physicians.

• Maintain your own professional dignity. This begins by dressing appropriately. Do not participate in or, worse, initiate pejorative commentary about another physician’s care. If you are confronted by an argumentative accusatory parent, maintain a calm demeanor and quietly but irmly outline your assessment and recommendations. When you treat the patient and parents with dignity, you can and should expect to be treated with the same dignity. • As much as possible, try to obtain the chief complaint and other information from the child or adolescent. Experienced physicians know that they must tolerate and assimilate interjections from the parents when talking to the pediatric patient. However, by talking directly with the child or adolescent and asking them about her or his problem, the clinician establishes a rapport that will help when performing the physical examination. However, be sure to check with the parent that the information provided by the patient is essentially correct as the parent perceives it.

CHAPTER 4 The Orthopaedic Examination: Clinical Application

• When taking the history, irst ind out who is concerned with the patient’s presenting complaint, and why. With conditions such as intoeing, the primary caretaker may not have been troubled initially by the deformity, but was prompted (or urged) by other family members, teachers, or even complete strangers to bring the child in for an evaluation. You should also ind out whether the child has been previously treated for the condition— if so, by whom, and what the qualiications of the individual were, how the condition was treated and the results of the treatment, whether older family members were treated for similar complaints and, if so, when and how they were managed. Answers to these questions may not establish the speciic diagnosis, but you will be in a better position to know who is most concerned about the condition and why. • Try to avoid threatening words such as “hurt.” Saying “This won’t hurt!” has two immediate negative effects. First, it introduces the subject of pain to the child, who promptly forgets the preface, “This won’t. . . .” Second, it suggests to the child that something else later in the examination will hurt. It is important, however, not to minimize or trivialize a procedure that will be traumatic. Doing so will cause the patient to distrust you once he or she has discovered the true nature of the procedure. • Respect the modesty of children and adolescents as much as possible while still performing an adequate examination. Be mindful of siblings or friends in the room who should be excused from the examining area if the patient, parent, or physician wishes it. • Never miss an opportunity to examine children without touching them. Observe the child wandering around the room while you are quietly soliciting the history from the parents. Have the child walk or, better yet, run in a corridor. Look for a luid coordinated gait. Also, check for normal arm swing to rule out upper extremity posturing that may indicate spasticity. Ask the older child to heel-walk, toe-walk, and hop on each foot in turn. The child’s ability to execute these tasks well strongly suggests normal neurologic and musculoskeletal function. These evaluations should be the irst part of the examination in case a subsequent direct, more formal examination results in loss of cooperation from the child. • Make your irst touch of the child an innocuous nonthreatening one in an area that you know doesn’t hurt. If you irst touch an area that doesn’t hurt, the child becomes aware that not everything you do will be painful, and you will quickly gain a sense of how cooperative the child will be. If it is clear from this initial maneuver that the child intends to ight off any examination, you may be able to modify your approach and the examining atmosphere to gain the child’s cooperation. This reaction should make an astute parent aware of the challenge to your ability to obtain a cooperative examination. Thus, if the child exhibits any negative reactions, the parent cannot wrongly ascribe it to a noxious event committed by the physician or medical staff. • Perform the examination without appearing to do so. One obvious way to accomplish this is to observe the child playing, walking, running, or climbing, as noted. When examining a child in the parent’s lap, do not

•

•

•

•

•

•

69

formally examine the legs. Instead check the toenail polish, look for other bruises or insect bites that are invariably present on the legs, and examine the soles of the feet for dust picked up in your examining room. By approaching the child in this manner, you will be able to gain an excellent impression of muscle tone, hip lexion, extension, and rotation, knee range of motion, and ankle lexibility without the child’s realizing that an examination has taken place. Occasionally, you may need to explain to the parent the purpose of your method. Examine infants and younger children in a parent’s lap. Infants and younger children are often frightened and uncomfortable when placed on an examination table. As a result, an examination can become a wrestling match between you and the uncooperative, combative child who is pinned prone to the table. The result is frustration on the part of the examiner and, in most cases, an inadequate examination. With the patient in the comfort and safety of the parent’s lap, you will have a more cooperative child and still be able to obtain valuable information. For example, being able to appreciate that the child’s hip range of motion is luid without guarding, with an approximation of the arc of motion as determined by examination of the hip while the child is in the parent’s lap, is more informative than a failed formal examination of the hips with the child on an examining table. When examining the extremities, examine the normal asymptomatic limb irst. Again, this will allow you to see how the child will react to your touch as you continue the examination and will provide the child with some idea of what to expect during the examination. Don’t be offended by the inevitable comment from the patient or parent, “Doctor, it’s the other one.” The simple response, “That’s why there are two, to compare,” should sufice. Minimize the discomfort of the examination as much as possible without compromising its purpose. Keep symptomatic limbs supported in some way. For example, when performing the Thomas test on an uncomfortable hip, lex the symptomatic hip to a comfortable degree and support it before lexing the asymptomatic hip maximally. Then extend the symptomatic hip gently while supporting the leg. This avoids lexing the symptomatic hip against its contracture with the whole weight of the leg levering against the tender area, which occurs when the Thomas test is performed as described (Fig. 4-9). If you are unable to perform an adequate examination, ask the parent to do the examination while you observe. This strategy works best in cases of ill or limping children who whimper and shy away every time you try to touch them. Quietly instruct the parent to palpate the child’s limbs gently and take them through a range of motion. Be sure that the parent starts with the normal asymptomatic extremity. If the child is being seen for possible diskitis, be sure to have the parent percuss the spine for tenderness. Always have a parent witness the examination. If the relationship is adversarial in any way, also have a neutral health care professional observe the examination. This is important for medical and legal reasons. When discussing your indings, agree as much as possible with the parents with respect to their observations. This is not meant to be a placating or condescending

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A

B

FIGURE 4-9 Examination of the patient with a painful hip. A, Flex both hips gently and then extend the symptomatic hip while supporting the limb. B, If only the asymptomatic hip is actively lexed, the unsupported symptomatic hip will begin to lex passively, resulting in avoidable discomfort to the patient.

comment. Parents are able to observe the child’s behavior in the child’s normal environment, which often provides a better picture of the child’s condition than that elicited in a strange examination room. In addition, complete offhanded dismissal of the parent’s concerns will only erode your relationship with the parent. For example, if the complaint is intoeing and it is present, agree with the parent that the child does have the condition. However, if the deformity is benign and does not require treatment, patiently explain to the parent why the condition is not medically signiicant. • Recognize and acknowledge when you have been unable to elicit a good history or perform an adequate examination. If you believe that the patient’s complaint or condition mandates a good examination, you should seek an opportunity to try again after an appropriate interval. For example, if you have tried to examine an infant’s hips for DDH but the infant would not relax and allow you to conduct a proper examination, try after or while the infant is being fed or have the patient return later that day or another day in the next week or two. Continue until you are able to perform a satisfactory examination. Don’t presume your indings or give up simply out of frustration. • Always appear calm and unhurried, even when that is not the case. A rushed manner tends to disorganize your thinking. Furthermore, the parents will feel as though inadequate attention has been paid to their concerns and they may not appreciate the amount of time and energy that you have put into the history taking and examination. If possible, sit down when you are speaking to the parents, so that you appear to have the time to listen to and respect their concerns. Also, provide explanations to the parents regarding their concerns as well as you can. • When faced with a complex problem that demands more time than you have at that particular moment, tell the family that you need to spend more time considering the child’s problem before a deinitive answer can be provided. Tell the family if you need to study your

indings from the history and examination, confer with physicians who have previously treated the child, or study previous imaging studies and other diagnostic tests. Set a speciic date and manner in which you will communicate further with them. Most families will appreciate that you are spending extra time and effort on behalf of the child’s problem in a concerned but unhurried manner, and will gladly agree to your request. • When faced with a complex orthopaedic problem that the family is having trouble comprehending, take the time to write them a letter or an e-mail explaining your assessment and treatment alternatives. You should outline the problem as you see it, describe the treatment alternatives and their respective advantages and disadvantages, and explain your personal recommendation and how you believe management of their child should proceed. • Always communicate with the referring physician and, when appropriate, any previous treating physicians, even when you will be assuming care of the patient. The referring physician will want to know what you think and should be guided by your advice regarding further follow-up or clinical manifestations that may require additional orthopaedic evaluation. Any previous physician should be contacted, even if there is an unsatisfactory relationship between the parents and that physician. Discussing the case with a previous surgeon implies respect for that surgeon’s care of the patient. Assume that prior treating physicians knew what they were doing and that they had made a genuine effort to treat the patient appropriately. Frequently, the prior surgeon will be able to provide insight into the history and previous care that the patient received, which the patient and/or parents may not be able to recount or may remember differently.

References For References, see expertconsult.com.

CHAPTER 4 The Orthopaedic Examination: Clinical Application

References 1. Agostinelli JR: Tarsal coalition and its relation to peroneal spastic latfoot, J Am Podiatr Med Assoc 76:76, 1986. 2. Barlow TG: Early diagnosis and treatment of congenital dislocation of the hip, Proc R Soc Med 56:804–806, 1963. 3. Bernard TN Jr, Burke SW, Johnston CE 3rd, et al: Congenital spine deformities. A review of 47 cases, Orthopedics 8:777, 1985. 4. Boachie-Adjei O, Lonner B: Spinal deformity, Pediatr Clin North Am 43:883, 1996. 5. Briggs RG, Carlson WO: The management of intoeing: a review, S D J Med 43:13, 1990. 6. Cambridge W, Drennan JC: Scoliosis associated with Duchenne muscular dystrophy, J Pediatr Orthop 7:436, 1987. 7. Daher YH, Lonstein JE, Winter RB, et al: Spinal deformities in patients with muscular dystrophy other than Duchenne. A review of 11 patients having surgical treatment, Spine 10:614, 1985. 8. Dietz FR: Intoeing—fact, iction and opinion, Am Fam Physician 50:1249, 1262, 1994. 9. Funasaki H, Winter RB, Lonstein, JB, et al: Pathophysiology of spinal deformities in neuroibromatosis. An analysis of seventy-one patients who had curves associated with dystrophic changes, J Bone Joint Surg Am 76:692, 1994. 10. Greenberg AJ: Congenital vertical talus and congenital calcaneovalgus deformity: a comparison, J Foot Surg 20:189, 1981. 11. Karol LA: Rotational deformities in the lower extremities, Curr Opin Pediatr 9:77, 1997. 12. Kaufman KR, Miller LS, Sutherland DH: Gait asymmetry in patients with limb-length inequality, J Pediatr Orthop 16:144, 1996. 13. Kelo MJ, Riddle DL: Examination and management of a patient with tarsal coalition, Phys Ther 78:518, 1998.

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14. Lahey MD, Zindrick MR, Harris EJ: A comparative study of the clinical presentation of tarsal coalitions, Clin Podiatr Med Surg 5:341, 1988. 15. Lowy LJ: Pediatric peroneal spastic latfoot in the absence of coalition. A suggested protocol, J Am Podiatr Med Assoc 88:181, 1998. 16. McDonald CM, Abresch RT, Carter GT, et al: Proiles of neuromuscular diseases. Duchenne muscular dystrophy, Am J Phys Med Rehabil 74(Suppl):S70, 1995. 17. Mosca VS: Flexible latfoot and skewfoot, Instr Course Lect 45:347, 1996. 18. Oda T, Shimizu N, Yonenobu K, et al: Longitudinal study of spinal deformity in Duchenne muscular dystrophy, J Pediatr Orthop 13:478, 1993. 19. Orrell KG, Bell DF: Structural abnormality of the clavicle associated with Sprengel’s deformity. A case report, Clin Orthop Relat Res 258:157, 1990. 20. Ortolani M: Congenital hip dysplasia in the light of early and very early diagnosis, Clin Orthop Relat Res 119:6, 1976. 21. Raso VJ, Lou E, Hill DL, et al: Trunk distortion in adolescent idiopathic scoliosis, J Pediatr Orthop 18: 222, 1998. 22. Robin H, Damsin JP, Filipe G, et al: [Spinal deformities in Marfan disease.] Rev Chir Orthop Reparatrice Appar Mot 78:464, 1992. 23. Sirois JL 3rd, Drennan JC: Dystrophic spinal deformity in neuroibromatosis, J Pediatr Orthop 10:522, 1990. 24. Song KM, Halliday SE, Little DG: The effect of limb-length discrepancy on gait, J Bone Joint Surg Am 79:1690, 1997. 25. Staheli LT: Torsional deformity, Pediatr Clin North Am 24:799, 1977. 26. Zadeh HG, Sakka SA, Powell MP, et al: Absent supericial abdominal relexes in children with scoliosis. An early indicator of syringomyelia, J Bone Joint Surg Br 77:762, 1995. 27. Zollinger H, Exner GU: [The lax juvenile lexible latfoot—disease or normal variant?] Ther Umsch 52:449, 1995.

CHAPTER 5

Gait Analysis Chapter Outline Phases of Gait 71 Temporal Parameters 71 Neurologic Control of Gait Function of Gait 72 Gait Energy 72 Kinematics 73 Muscle Activity 74

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Lori A. Karol the plantigrade foot. Finally, the heel rises at terminal stance. Stance phase can be divided into single-limb support and double-limb support phases. There are two periods of double-limb support, when both legs are in contact with the ground at the same time. The irst period occurs at initial contact. The second period of double-limb support occurs at the end of stance phase just before swing phase as the body weight is shifted onto the other limb and the heel rises from the loor in preparation for push-off.

Swing Phase Observing a child’s gait, whether in a sophisticated computerized laboratory or simply in the hallway of a clinic, is an integral part of the orthopaedic examination. A systematic approach to gait analysis—that is, looking at the trunk and each joint moving in all three planes (sagittal, coronal, and transverse)—can yield valuable information about the patient’s condition and help in establishing a treatment plan. For a child’s gait to be examined properly, the patient needs to be as unclothed as deemed appropriate. The examination should begin with an assessment of lower extremity passive range of motion and muscle strength. The physician should then observe the child walking from the level of the child—for example, sitting while examining the gait of small children. Whenever possible, the child should also be asked to run. There should be adequate space for the child to walk comfortably and naturally. A thorough evaluation of the head, trunk, upper extremities, hips, knees, and ankles, with the child viewed from the front and side, should be completed. Joint motion during gait can then be compared with passive range of motion and strength.

Phases of Gait The gait cycle is divided into two phases, stance and swing (Fig. 5-1). Stance phase is deined as the time during which the limb is in contact with the ground and supporting the weight of the body. Conversely, swing phase is the time when the limb is advancing forward off the ground. During swing phase, the advancing limb is not in contact with the ground and body weight is supported by the contralateral limb. Stance phase occupies 60% of the gait cycle and swing phase occupies 40%. Both phases can be subdivided further.

Stance Phase Stance phase begins when the foot contacts the ground, termed heel strike or initial contact. Next, loading response occurs as the foot plantar-lexes to the ground and weight is accepted. In midstance, the tibia moves forward over

Swing phase encompasses three separate periods—initial swing, midswing, and terminal swing. Initial swing begins with toe-off and continues as the foot is raised from the ground and the limb moves forward. Midswing starts as the swing limb advances past the contralateral stance limb, the knee extends, and the foot travels in a forward-swinging arc. Deceleration, or terminal swing, occurs at the end of swing phase as the musculature of the forward-moving swing limb smoothly stops the limb, preparing for initial contact with the ground, and the gait cycle is completed.

Time Spent in Each Phase The percentage of time spent in each phase of gait is consistent among normal individuals. As the speed at which a person walks increases, the amount of time that is spent in double-limb support decreases. During running, doublelimb support disappears and is replaced by double-limb loat, a period during which neither leg is in contact with the ground.40

Temporal Parameters Distance and time measurements calculated during gait analysis are referred to as cadence parameters (Box 5-1). Step length is deined as the distance between the two feet during double-limb support and is measured from the heel of one foot to the heel of the contralateral foot. Step length can differ between the right and left sides. Stride length is the distance one limb travels during the stance and swing phases. It is measured from the point of foot contact at the beginning of stance phase to the point of contact by the same foot at the end of swing phase. Step time is the amount of time used to complete one step length. Cadence is the number of steps taken per minute. Walking velocity is the distance traveled per time (usually measured in meters per second). Normal values matched for age are available for these cadence parameters.54 Small children walk with greater cadence but smaller step and stride lengths, resulting in many quick, small steps. As children grow, their step and stride lengths increase and 71

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SECTION I Disciplines

STANCE Weight acceptance Initial contact

Loading response

SWING Single-limb support

Midstance

Terminal stance

Limb advancement Preswing

Initial swing

60%

Midswing

Terminal swing

40%

FIGURE 5-1 The gait cycle for the right leg. In stance phase, the foot is in contact with the ground and the limb supports the weight of the body; in swing phase, the limb advances forward off the ground.

Box 5-1 Cadence Parameters

Function of Gait

Step length: Distance between two feet during double-limb support Stride length: Distance one limb travels during stance and swing phases Step time: Time needed to complete one step length Cadence: Number of steps per minute Walking velocity: Distance traveled per time (m/sec)

The simplest function of gait is to travel from one point to another. Normal ambulation is likened to a controlled forward fall. The swing limb comes forward to stop the fall and accept the weight of the body. The joint motions inherent in normal gait serve this purpose. Body weight is transferred from one limb to the other in a smooth fashion, and the forward momentum of the body is sustained.

cadence decreases.3,48,54 Step length increases linearly with increasing leg length.54 Nomograms have been constructed to determine normal cadence parameters for children based on their height.56

Neurologic Control of Gait The entire neurologic system plays a role in gait. Most of the muscular actions that occur during gait are programmed as involuntary relex arcs involving all areas of the brain and spinal cord. The extrapyramidal tracts are responsible for most complex, unconscious pathways. Miller and Scott proposed the concept of the “spinal locomotor generator,” designated neurons within the spinal cord that are responsible for relex stepping movements.36 Golgi tendon units, muscle spindles, and joint receptors produce neurologic feedback and serve as dampening devices for the coordination of gait. Voluntary modulation of gait (e.g., altering speed, stepping over an obstacle, changing direction) is made possible through interaction of the motor cortex.25 The cerebellum is important in controlling balance. A child’s gait changes as the neurologic system matures.31 Infants normally walk with greater hip and knee lexion, lexed arms, and a wider base of gait than older children. As the neurologic system continues to develop in a cephalocaudal direction, the eficiency and smoothness of gait increase.48 However, when the neurologic system is abnormal (e.g., in cerebral palsy), the delicate control of gait is disturbed, leading to pathologic relexes and abnormal movements.

Gait Energy Although gait is designed to be energy-eficient, bipedal gait is inherently unstable and ineficient. Quadrupeds (e.g., dogs) run faster than humans, regardless of size. Their center of gravity is suspended between the four limbs on the ground, and the vertebral and trunk muscles act to augment stride. In human gait, the center of gravity is not balanced between the limbs, nor do the trunk and spinal muscles play a signiicant role in walking. To conserve energy, coordinated movements of the joints of the lower extremities minimize the rise and fall of the center of gravity, located just anterior to the second sacral vertebra.24 Muscular activity during gait is precisely timed, and very few concentric contractions of the muscles are required during normal ambulation. Inertia is used to its fullest advantage to lessen the work of walking. Abnormal deviations in gait can have signiicant physiologic costs and substantially increase the energy required to walk. Deviations such as a weak muscle, contracted joint, or impediment of a cast may change gait enough to increase the metabolic requirements, thereby causing the individual to tire easily. The amount of energy required to walk can be measured by quantifying oxygen consumption and oxygen cost.9 Oxygen uptake and oxygen cost during walking are greater in children younger than 12 years than in teenagers.59 An indirect measure of energy expenditure is the heart rate, which rises as oxygen consumption increases.44 The physiologic cost index (PCI) is calculated using the child’s heart rate and walking speed.6 Repeatability in PCI data ranges in the literature from high to low.5,6,9

CHAPTER 5 Gait Analysis

73

Table 5-1 Six Determinants of Gait

Sagittal Plane

Determinant

Strategy

Pelvic rotation

Decreases angle between limbs and ground, lattens arc of pathway of center of gravity, allowing stride to lengthen without increasing drop of center of gravity at point of initial contact

Pelvic tilt

Decreases vertical displacement of center of gravity by approximately 50% and shortens pendulum of limb by knee lexion in swing phase

Knee lexion after initial contact in stance phase

Reduces vertical displacement of center of gravity as weight of body is carried forward over stance limb

Foot and ankle motion

Smooths out path of center of gravity when coupled with knee motion

Knee motion

Smooths out path of center of gravity when coupled with foot and ankle motion

Lateral displacement of pelvis

Reduces lateral movement of center of gravity toward stance foot during gait cycle

In the sagittal plane, the pelvis is tilted anteriorly approximately 15 degrees (see Fig. 5-2, A). There is minimal motion of the anterior tilt as each leg is advanced forward. Alterations in pelvic tilt can occur when there are contractures of muscles around the hip. For example, if the hamstrings are tight, the pelvis typically assumes a more posterior tilt. The hip is lexed at initial contact and then extends fully during stance phase as the body advances over the planted foot (see Fig. 5-2, B). At heel rise and push-off, the hip lexes rapidly to pull the stance phase limb off the ground. The hip continues to lex during swing phase. The knee exhibits a more complex pattern (see Fig. 5-2, C). At initial contact, the knee lexes approximately 15 degrees, buffering the acceptance of body weight through knee lexion. The knee then extends during stance phase to neutral position or minimal lexion. At heel rise, the knee begins to lex again, reaching maximal lexion in early swing phase to allow the foot to clear the ground as the limb advances. During the remainder of swing phase, the knee extends passively, using forward momentum. The normal kinematics of the knee is disturbed in gait secondary to spasticity from cerebral palsy. Deviations range from hyperextension of the knee in stance phase if the heel cord is tight, to crouch gait, resulting in lexion in stance phase caused by tight hamstrings, to inability to lex the knee in swing phase caused by inappropriate rectus femoris action.18 Ankle sagittal plane kinematics starts with a neutral ankle at initial contact, when the heel normally strikes the ground (see Fig. 5-2, D). The ankle then plantar-lexes 5 to 10 degrees as the forefoot comes to rest on the ground. This plantar lexion is known as irst rocker. The ankle dorsilexes throughout midstance as the tibia moves forward over the plantigrade foot (second rocker). During third rocker, the ankle plantar-lexes and the heel rises to prepare for pushoff (Fig. 5-3). Dorsilexion of the ankle back to a neutral position is seen during swing phase to allow for clearing of the foot. In patients with peroneal nerve palsy and foot drop, dorsilexion during swing phase is impaired. The individual compensates by hyperlexing the knee and hip in swing phase to avoid dragging the toes, a pattern termed steppage gait.

In 1953, Saunders and colleagues described the six determinants of gait whereby the body reduces the amount of energy required to ambulate (Table 5-1).45 These six strategies work in harmony to minimize the rise and fall of the center of gravity (vertical displacement) and the side to side motion of the pelvis (horizontal displacement). The end result is the establishment of a smooth pathway for the forward progression of the body’s center of gravity during gait. The center of gravity displaces an average of ⅛-inch during gait, with the lowest point at 50% of the gait cycle during double-limb support.45 An example of these determinants in action is lexion of the knee coupled to ankle joint motion in stance phase. If one imagines how much rise and fall is felt when walking with a cylinder cast with knee extension, the contribution of knee lexion in stance phase (the third determinant) to minimizing energy required for walking is easily appreciated.

Kinematics Kinematics is deined as the study of the angular rotations of each joint during movement. In simpler terms, kinematics denotes the motions observed and measured at the pelvis, hip, knee, and ankle during the stance and swing phases of gait (Fig. 5-2). Kinematics can be observed in three planes—the sagittal plane (lexion and extension), coronal plane (hip abduction and adduction), and transverse plane (rotation of the hips, tibiae, or feet). The data are collected by the three-dimensional tracking of markers placed over bony landmarks by infrared cameras positioned in the gait laboratory. Normal kinematics14 for each plane are briely described in the following sections.

Coronal Plane Pelvic obliquity is observed in the coronal plane (see Fig. 5-2, E). Each hemipelvis rises slightly during swing phase to augment the ability to advance the swing limb. Pelvic rise must be accompanied by a contralateral fall, so in the stance phase the hemipelvis drops slightly. Accentuated pelvic obliquity may be seen in patients with limb length discrepancy, and accentuated pelvic drop in swing phase is seen in patients with abductor lurches or Trendelenburg gait (e.g., patients with myelomeningocele). Minimal hip motion in the coronal plane occurs during normal gait (see Fig. 5-2, F). Each hip slightly adducts during stance phase and abducts during swing phase. If a patient has a scissoring gait, as is often seen in cerebral palsy, the adduction is more extreme and may occur throughout the gait cycle, leading to dificulty advancing the swing limb.

74

SECTION I Disciplines

PELVIC TILT

HIP FLEXION/EXTENSION

45

60

Flexion

Anterior

40 30

Degrees

Degrees

20

15

0

Extension

0

Posterior –10

0

25

50

75

A

–20

100

0

50

75

100

% Gait cycle ANKLE DORSIFLEXION/PLANTAR FLEXION

KNEE FLEXION/EXTENSION 75

45

Flexion

Dorsiflexion

60

30

45

15

30

Degrees

25

B

% Gait cycle

Degrees

15

0

–15

0

–30

Extension

Plantar flexion

–15

0

25

C

50

75

–45

100

% Gait cycle

0

25

50

75

100

% Gait cycle

D

PELVIC OBLIQUITY

HIP ABDUCTION/ADDUCTION

20

30

Adduction

Up

20 10 10

Degrees

Degrees

0

0

–10 –10 –20

Down

Abduction –20

0

E

25

50

75

–30

100

% Gait cycle

0

F

25

50

75

100

% Gait cycle

FIGURE 5-2 Kinematics (joint rotation angle) of the pelvis, hip, knee, and ankle during stance and swing phases of gait in the sagittal and coronal planes. Stance phase begins at 0% of the gait cycle. Swing phase begins at the dotted vertical line. A, Anterior tilt of the pelvis. B, Hip lexion and extension. C, Knee lexion and extension. D, Ankle plantar lexion and dorsilexion. E, Pelvic obliquity rise and fall. F, Hip adduction and abduction.

Transverse Plane

at the beach. The normal foot progression angle is approximately 10 to 15 degrees externally (Fig. 5-4).

In the transverse plane, kinematic data measure rotation. The pelvis and hips rotate minimally during gait. The tibiae should not exhibit a range of motion but, instead, have a mild ixed external rotation. The foot progression angle is the angle that the foot makes with the path the subject is walking, which can be likened to footprints in the sand

Muscle Activity Gait is initiated through muscle activity (Box 5-2). Once started, the transition of the body to a steady gait pattern

CHAPTER 5 Gait Analysis

75

Box 5-2 Muscle Activity During Gait •

• • Rocker 1

Rocker 2

Types of muscle contraction: ■ Concentric—generates power and accelerates body forward ■ Eccentric—slows down and stabilizes joint motions during gait Stance phase—muscles of leg and foot work to stabilize plantigrade foot Swing phase—momentum generated by gastrocsoleus and hip lexors at terminal stance carries leg forward

Rocker 3

FIGURE 5-3 Kinematics of the ankle in the sagittal plane. First rocker, Ankle plantar-lexes 5 to 10 degrees as the forefoot comes to rest on the ground; second rocker, ankle then dorsilexes throughout midstance as the tibia moves forward over the plantigrade foot; third rocker, ankle then plantar-lexes and the heel rises to prepare for push-off.

Raw cycle vs. % gait cycle 71 mV

R. rectus femoris

65 mV

R. vastus medialis

56 mV

R. med. hamstrings

227 mV

R. tibialis anterior

231 mV

R. gastrocnemius

221 mV

R. soleus

0 10 20 30 40 50 60 70 80 90 100 Left cycle: 3 Right cycle: 3 FIGURE 5-5 Normal electromyographic patterns of muscle activity during gait. Initial contact occurs at the left edge of the box, and the division between the stance and swing phases occurs at 60% of the gait cycle (vertical line).

Foot progression angle (approx. 10-15° external) FIGURE 5-4 Foot progression angle, the angle that the foot makes with the path on which the subject is walking (often likened to footprints in the sand). The normal foot progression angle is approximately 10 to 15 degrees externally.

is accomplished in approximately three steps.35 Gait is maintained by a combination of momentum and muscle contraction. The presence of electrical activity in the muscles of the lower extremity can be recorded by electromyography during walking. Surface electrodes, which are applied to the skin surface for supericial muscles, or needle electrodes, inserted into the muscle for deeper muscles such as the posterior tibialis, can document the timing of muscle activity while walking.27,64 There are set patterns to muscle activity observed by electromyography in normal children during gait63 (Fig. 5-5), and these patterns vary with walking velocity.42 Deviations from these normal

patterns are seen in pathologic gait, such as the gait exhibited by patients with cerebral palsy.

Types of Muscle Contraction Two types of muscle contractions occur during gait. A concentric contraction occurs when the muscle shortens, thereby generating power. An eccentric contraction occurs when the muscle lengthens, despite electrical contraction. Concentric contractions generate power and accelerate the body forward. Eccentric contractions slow and stabilize joint motions during gait, thereby minimizing energy requirements. Muscles undergoing eccentric contractions outnumber those with concentric contractions during gait.

Concentric Contractions Two large concentric contractions occur at terminal stance. The gastrocsoleus muscle contracts to lift the heel off the ground and push off. The iliopsoas muscle also contracts concentrically, lexing the hip and pulling the stance phase limb off the ground at terminal stance and early swing. The

76

SECTION I Disciplines

gastrocsoleus and iliopsoas muscles are believed to be the two primary accelerators of gait, although controversy exists as to which muscle contributes more toward forward propulsion of the body.42,52,61 During swing phase, the anterior tibialis muscle undergoes a concentric contraction. This dorsilexes the ankle and provides clearance for the swing foot.

Eccentric Contractions Eccentric contractions slow down and smooth joint motions. The anterior tibialis muscle contracts eccentrically at initial contact, iring despite plantar lexion of the ankle as the foot is lowered to the ground. In doing so, the foot is gently lowered to the loor and acceptance of body weight can occur gradually. If the anterior tibialis muscle does not ire, the foot “slaps” to the loor at initial contact. The gastrocsoleus contracts eccentrically throughout the second rocker of stance phase, controlling the rate of dorsilexion of the ankle as the tibia advances forward over the plantigrade foot.53 In the absence of normal gastrocsoleus strength, the ankle dorsilexes excessively, resulting in poor push-off and calcaneus gait.28,46 A powerful eccentric contraction occurring during weight acceptance in stance phase is that of the hip abductors. The abductors of the stance phase limb ire to limit contralateral pelvic drop as the swing limb comes off the ground. Meanwhile, the stance limb hip adducts slightly. If the gluteal muscles are weak, they cannot generate a suficient eccentric contraction and the hemipelvis of the swing limb drops, resulting in a Trendelenburg gait. The trunk can compensate for the pelvic drop by swaying over the stance limb. This brings the center of gravity over the affected hip and lessens the pelvic drop. Patients with Trendelenburg gait use more energy to walk.

Muscle Activity During Stance and Swing Phases More muscle activity occurs during stance phase than during swing phase. During stance phase, the muscles of the leg

and foot work to stabilize the plantigrade foot. In swing phase, momentum generated by the gastrocsoleus and hip lexors at terminal stance carries the leg forward. Knee lexion in early swing, and then extension at terminal swing, occur passively. The main concentric contraction that occurs during swing phase is that of the anterior tibialis, which dorsilexes the foot for easier clearance during swing and prepositions the foot for initial contact.

Kinetics Kinetics are the forces generated by the muscles and joints during gait. Kinetic data are reported as moments (forces acting about a center of rotation) and powers. These forces can be measured from force plates in a gait analysis laboratory. If one knows the motion occurring kinematically at a joint and which muscles are active during that period, the kinetic forces can be better understood. For example, the anterior tibialis ires at initial contact while the ankle is plantar-lexing to lower the foot to the ground. The result of this eccentric contraction is power absorption, the magnitude of which can be measured in the laboratory (Fig. 5-6). The gastrocsoleus ires at terminal stance as the ankle plantar-lexes at push-off. This concentric contraction leads to power generation. There are characteristic patterns of power generation and absorption at each joint (Fig. 5-7).26,41 Kinetics depend on walking velocity.13,47,58,61 Kinetics in younger children differ from adult kinetics. Differences include diminished ankle plantar lexion moment and power generation and decreased hip abductor movement.10 An adult pattern of kinetics is probably reached by 5 years of age.40

Pedobarography Pedobarography is the measurement of plantar pressures during gait. Using specialized force plates with a high number of sensors per area, the contact area of the foot and pressure and timing of the pressure can be documented. The foot is divided into different segments, termed masks, and the pressure in each mask can be studied (Fig. 5-8).

ANKLE FLEXION MOMENT

TOTAL ANKLE POWER

1

3

Gen

Nm/kg

Watts/kg

Pla

Dor –1 0

A

Abs 25

50

Gait cycle (%)

75

–1 0

100

B

25

50

75

100

Gait cycle (%)

FIGURE 5-6 Ankle kinetics graphs showing joint net moments and powers. A, Ankle lexion moment during stance (measured in newton-meters per kilogram [Nm/kg]). B, Total ankle power (measured in W/kg). Note the burst of power at terminal stance caused by the concentric contraction of the gastrocsoleus (and the short period of power absorption at initial contact). Abs, Absorption (−); Gen, generation (+).

CHAPTER 5 Gait Analysis

Pressure data for the feet of younger children demonstrate a number of differences compared with those of adults.32 For example, younger children typically have higher medial midfoot pressure, which correlates clinically with lack of the longitudinal arch of the foot.4

Pathologic Gait Deviations from normal gait occur in a variety of orthopaedic conditions. Disorders that result in muscle weakness (e.g., spina biida, muscular dystrophy), spasticity (e.g., cerebral palsy), or contractures (e.g., arthrogryposis) lead

TOTAL HIP POWER 2

Watts/kg

Gen

Abs –2 0

25

50

75

100

77

to abnormalities in gait.11,12,43 Pathologic gaits are described in greater detail in their respective neuromuscular chapters.

Gait Analysis Laboratories The study of gait in a laboratory dates back to 1957, when Inman began evaluating joint motion.24 From that start, gait analysis was used primarily to document neuromuscular gait, irst in patients with poliomyelitis and then in those with cerebral palsy and myelomeningocele. Over time, computer software has been developed that allows threedimensional analysis. Although most software measures motion at the pelvis, hip, knee, and ankle, models have been developed to assess motion in smaller joints (i.e., segments of the foot), the upper extremity, and the trunk.34,57 Gait analysis is most often used for preoperative planning and documentation of postoperative outcome in patients with cerebral palsy (Fig. 5-9).* Despite standard methodology, variation is present in data measured in different laboratories on different days. This can result in differing surgical or nonsurgical recommendations in children with cerebral palsy.39 Repeat testing in children with spasticity on either the same day or on different days shows less reproducibility than in normal children.50 Motion analysis now is also being applied to spinal deformity,29 and it has been used as an outcome measurement for evaluating surgical treatment of nonneurologic orthopae-

% Gait cycle FIGURE 5-7 Kinetics graph of hip power (measured in W/kg). Note the burst of power generation at terminal stance as the iliopsoas pulls the leg off the ground. Abs, Absorption (−); Gen, generation (+).

A

B

*References 7, 8, 11, 15-17, 31, 38, 55, 62. † References 2, 14, 22, 28, 30, 37, 49, 51, 60.

C

D

FIGURE 5-8 Pedobarograph of right foot with equinocavovarus deformity. A, Pressure mapping shows excessive weight bearing underneath the ifth metatarsal base and head. B, Improved pressure distribution after plantar fascia release, posterior tibialis lengthening, Achilles tendon lengthening, irst metatarsal osteotomy, and split anterior tibialis tendon transfer. C, Before surgery, initial contact (green dot) occurs in the lateral forefoot. D, After surgery, initial contact occurs at the heel (red square) and the center of pressure progresses normally to the second toe.

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SECTION I Disciplines

FIGURE 5-9 Six-year-old boy with spastic diplegia undergoing gait analysis. Markers are used to collect kinematic data; electromyographic data are being simultaneously gathered.

dic conditions, such as clubfeet, fractures, and degenerative joint arthritis.† Research in motion analysis continues in the ields of arthroplasty, prosthetics,1 and orthotics,23 stimulating the development of newer products and lending a scientiic basis to new and innovative designs. Although gait analysis can provide data regarding joint movement and gait dysfunction, it is time-consuming and not readily available in many orthopaedic centers. Other

nontechnical means of quantifying gait deviations, such as the functional mobility scale and observational gait scale, and the use of video gait analysis have been proposed for use in the clinical setting.19-21,33

References For References, see expertconsult.com.

CHAPTER 5 Gait Analysis

References 1. Ashley RK, Vallier GT, Skinner SR: Gait analysis in pediatric lower extremity amputees, Orthop Rev 21:745, 1992. 2. Asperheim MS, Moore C, Carroll NC, et al: Evaluation of residual clubfoot deformities using gait analysis, J Pediatr Orthop B 4:49, 1995. 3. Beck RJ, Andriacchi TP, Kuo KN, et al: Changes in the gait patterns of growing children, J Bone Joint Surg Am 63:1452, 1981. 4. Bertsch C, Unger H, Winkelmann W, et al: Evaluation of early walking patterns from plantar pressure distribution measurements. First-year results of 42 children, Gait Posture 19:235, 2004. 5. Boyd R, Fatone S, Rodda J, et al: High- or low-technology measurements of energy expenditure in clinical gait analysis? Dev Med Child Neurol 41:676, 1999. 6. Butler P, Engelbrecht M, Major RE, et al: Physiological cost index of walking for normal children and its use as an indicator of physical handicap, Dev Med Child Neurol 26:607, 1984. 7. Chang FM, Rhodes JT, Flynn KM, et al: The role of gait analysis in treating gait abnormalities in cerebral palsy, Orthop Clin North Am 41:489, 2010. 8. Chang FM, Seidl AJ, Muthusamy K, et al: Effectiveness of instrumented gait analysis in children with cerebral palsy—comparison of outcomes, J Pediatr Orthop 26:612, 2006. 9. Corry IS, Duffy CM, Cosgrave AP, et al: Measurement of oxygen consumption in disabled children by the Cosmed K2 portable telemetry system, Dev Med Child Neurol 38:585, 1996. 10. Cupp T, Oefinger D, Tylkowski C, et al: Age-related kinetic changes in normal pediatrics, J Pediatr Orthop 19:475, 1999. 11. De Luca PA: Gait analysis in the treatment of the ambulatory child with cerebral palsy, Clin Orthop Relat Res 264:65, 1991. 12. Duffy CM, Hill AE, Cosgrove AP, et al: Three-dimensional gait analysis in spina biida, J Pediatr Orthop 16:786, 1996. 13. Eng JJ, Winter DA: Kinetic analysis of the lower limbs during walking: what information can be gained from a three-dimensional model? J Biomech 28:753, 1995. 14. Fowler E, Zernicke R, Setoguchi Y, et al: Energy expenditure during walking by children who have proximal femoral focal deiciency, J Bone Joint Surg Am 78:1857, 1996. 15. Gage JR: Gait analysis. An essential tool in the treatment of cerebral palsy, Clin Orthop Relat Res 288:126, 1993. 16. Gage JR: The clinical use of kinetics for evaluation of pathologic gait in cerebral palsy, Instr Course Lect 44:507, 1995. 17. Gage JR, De Luca PA, Renshaw TS: Gait analysis: principle and applications with emphasis on its use in cerebral palsy, Instr Course Lect 45:491, 1996. 18. Gage JR, Perry J, Hicks RR, et al: Rectus femoris transfer to improve knee function of children with cerebral palsy, Dev Med Child Neurol 29:159, 1987. 19. Graham HK, Harvey A, Rodda J, et al: The Functional Mobility Scale (FMS), J Pediatr Orthop 24:514, 2004. 20. Grunt S, van Kampen PJ, van der Krogt MM, et al: Reproducibility and validity of video screen measurements of gait in children with spastic cerebral palsy, Gait Posture 31:489, 2010. 21. Harvey A, Gorter JW: Video gait analysis for ambulatory children with cerebral palsy: why, when, where and how! Gait Posture 33:501, 2011. 22. Hilding MB, Lanshammar H, Ryd L: A relationship between dynamic and static assessments of knee joint load. Gait analysis and radiography before and after knee replacement in 45 patients, Acta Orthop Scand 66:317, 1995. 23. Hirsch G, McBride ME, Murray DD, et al: Chopart prosthesis and semirigid foot orthosis in traumatic forefoot amputation. Comparative gait analysis, Am J Phys Med Rehabil 75:283, 1996. 24. Inman VT: Conservation of energy in ambulation, Bull Prosthet Res 26:9, 1968. 25. Joseph J: Neurological control of locomotion, Dev Med Child Neurol 27:822, 1985.

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26. Kadaba MP, Ramakrishnan HK, Wootten ME: Measurement of lower extremity kinematics during level walking, J Orthop Res 8:383, 1990. 27. Kadaba MP, Wootten ME, Gainey J, et al: Repeatability of phasic muscle activity: performance of surface and intramuscular wire electrodes in gait analysis, J Orthop Res 3:350, 1985. 28. Karol LA, Concha MC, Johnston CE 2nd: Gait analysis and muscle strength in children with surgically treated clubfeet, J Pediatr Orthop 17:790, 1997. 29. Khodadadeh S, Eisenstein SM: Gait analysis of patients with low back pain before and after surgery, Spine 18:1451, 1993. 30. Kitaoka HB, Wikenheiser MA, Shaughnessy WJ, et al: Gait abnormalities following resection of talocalcaneal coalition, J Bone Joint Surg Am 79:369, 1997. 31. Lee EH, Goh JC, Bose K: Value of gait analysis in the assessment of surgery in cerebral palsy, Arch Phys Med Rehabil 73:642, 1992. 32. Liu XC, Thometz JG, Tassone C, et al: Dynamic plantar pressure measurement for the normal subject: free-mapping model for the analysis of pediatric foot deformities, J Pediatr Orthop 25:103, 2005. 33. Mackey AH, Lobb GL, Walt SE, et al: Reliability and validity of the Observational Gait Scale in children with spastic diplegia, Dev Med Child Neurol 45:4, 2003. 34. MacWilliams BA, Cowley M, Nicholson DE: Foot kinematics and kinetics during adolescent gait, Gait Posture 17:214, 2003. 35. Mann RA, Hagy JL, White V, et al: The initiation of gait, J Bone Joint Surg Am 61:232, 1979. 36. Miller S, Scott PD: The spinal locomotor generator, Exp Brain Res 30:387, 1977. 37. Mittlmeier T, Morlock MM, Hertlein H, et al: Analysis of morphology and gait function after intraarticular calcaneal fracture, J Orthop Trauma 7:303, 1993. 38. Narayanan UG: Management of children with ambulatory cerebral palsy: an evidence-based review, J Pediatr Orthop 32(Suppl 2):S172, 2012. 39. Noonan KJ, Halliday S, Browne R, et al: Interobserver variability of gait analysis in patients with cerebral palsy, J Pediatr Orthop 23:279, 2003. 40. Ounpuu S: The biomechanics of running: a kinematic and kinetic analysis, Instr Course Lect 39:305, 1990. 41. Ounpuu S, Gage JR, Davis RB: Three-dimensional lower extremity joint kinetics in normal pediatric gait, J Pediatr Orthop 11:341, 1991. 42. Perry J: Kinesiology of lower extremity bracing, Clin Orthop Relat Res 102:18, 1974. 43. Rao S, Dietz F, Yack HJ: Kinematics and kinetics during gait in symptomatic and asymptomatic limbs of children with myelomeningocele, J Pediatr Orthop 32:106, 2012. 44. Rose J, Gamble JG, Medeiros J, et al: Energy cost of walking in normal children and in those with cerebral palsy: comparison of heart rate and oxygen uptake, J Pediatr Orthop 9:276, 1989. 45. Saunders JB, Inman VT, Eberhart HD: The major determinants of normal and pathological gait, J Bone Joint Surg Am 35:543, 1953. 46. Segal LS, Thomas SE, Mazur JM, et al: Calcaneal gait in spastic diplegia after heel cord lengthening: a study with gait analysis, J Pediatr Orthop 9:697, 1989. 47. Stansield BW, Hillman SJ, Hazlewood ME, et al: Sagittal joint kinematics, moments, and powers are predominantly characterized by speed of progression, not age, in normal children, J Pediatr Orthop 21:403, 2001. 48. Statham L, Murray MP: Early walking patterns of normal children, Clin Orthop Relat Res 79:8, 1971. 49. Steenhoff JR, Daanen HA, Taminiau AH: Functional analysis of patients who have had a modiied Van Nes rotationplasty, J Bone Joint Surg Am 75:1451, 1993. 50. Steinwender G, Saraph V, Scheiber S, et al: Intrasubject repeatability of gait analysis data in normal and spastic children, Clin Biomech 15:134, 2000.

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51. Sucato DJ, Tulchin K, Shrader MW, et al: Gait, hip strength and functional outcomes after a Ganz periacetabular osteotomy for adolescent hip dysplasia, J Pediatr Orthop 30:344, 2010. 52. Sutherland D: An electromyographic study of the plantar lexors of the ankle in normal walking on the level, J Bone Joint Surg Am 48:66, 1966. 53. Sutherland DH, Cooper L, Daniel D: The role of the ankle plantar lexors in normal walking, J Bone Joint Surg Am 62:354, 1980. 54. Sutherland DH, Olshen R, Cooper L, et al: The development of mature gait, J Bone Joint Surg Am 62:336, 1980. 55. Thomason P, Selber P, Graham HK: Single Event Multilevel Surgery in children with bilateral spastic cerebral palsy: a 5-year prospective cohort study, Gait Posture 37:23, 2013. 56. Todd FN, Lamoreux LW, Skinner SR, et al: Variations in the gait of normal children. A graph applicable to the documentation of abnormalities, J Bone Joint Surg Am 71:196, 1989. 57. Tulchin K, Orendurff M, Karol L: A comparison of multi-segment foot kinematics during level overground and treadmill walking, Gait Posture 31:104, 2010.

58. van der Linden ML, Kerr AM, Hazlewood ME, et al: Kinematic and kinetic gait characteristics of normal children walking at a range of clinically relevant speeds, J Pediatr Orthop 22:800, 2002. 59. Waters RL, Hislop HJ, Thomas L, et al: Energy cost of walking in normal children and teenagers, Dev Med Child Neurol 25:184, 1983. 60. Westhoff B, Martiny F, Reith A, et al: Computerized gait analysis in Legg-Calve-Perthes disease—analysis of the sagittal plane, Gait Posture 35:541, 2012. 61. Winter DA: Energy generation and absorption at the ankle and knee during fast, natural, and slow cadences, Clin Orthop Relat Res 175:147, 1983. 62. Winters TF Jr, Gage JR, Hicks R: Gait patterns in spastic hemiplegia in children and young adults, J Bone Joint Surg Am 69:437, 1987. 63. Wootten ME, Kadaba MP, Cochran GV: Dynamic electromyography. II. Normal patterns during gait, J Orthop Res 8:259, 1990. 64. Young CC, Rose SE, Biden EN, et al: The effect of surface and internal electrodes on the gait of children with cerebral palsy, spastic diplegic type, J Orthop Res 7:732, 1989.

CHAPTER 6

The Limping Child Chapter Outline Abnormal Gait Patterns in Children Special Considerations Based on Age Group 81 Differential Diagnosis of Limping in Children 82

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Limping is common in children, and it may represent a diagnostic challenge for the orthopaedist.24,26,48-50 A painful or painless limp may be caused by myriad conditions, with the differential diagnosis ranging from the benign (e.g., an unrecognized splinter in the foot) to the serious (e.g., a septic hip or a malignant neoplasm).* It is important that the clinician approach each patient in a systematic and orderly manner to avoid missing or delaying the correct diagnosis. A thorough history and physical examination are the irst steps toward achieving this goal,† and they may lead to early identiication of the underlying problem causing the limp. The joints are inspected for irritability, swelling, effusion, erythema, and warmth; the presence of muscle atrophy is noted and measured; and both active and passive ranges of motion are assessed. Particular attention is paid to the child’s gait. Because various pathologic conditions often produce a characteristic limp, careful observation of the child’s gait can be extremely helpful in diagnosing the cause. The need for ancillary diagnostic tests is based on the history and clinical examination indings.‡ These tests may include laboratory studies, radiography, and, in some cases, ultrasonography, bone scintigraphy, computed tomography (CT), or magnetic resonance imaging (MRI). In general, for the younger child who presents with a limp but is otherwise normal on physical examination and appears well, the gait disturbance is likely to be self-limiting, and radiographs are unlikely to assist in making a diagnosis. Persistent symptoms, however, warrant further investigation. This chapter describes the different abnormal gait patterns associated with childhood limps (normal gait is described in detail in Chapter 5) and presents a general overview of many of the possible conditions that may be responsible for a limp. More thorough explanations of these disorders are provided in their respective chapters. Limps resulting from an obvious injury are not addressed. Disorders most commonly responsible for an abnormal gait generally vary based on the age of the patient. Thus to enable the clinician more effectively to address the diagnostic challenge of a limp, the special considerations of three different *References 3, 14, 19, 25, 31, 53, 56, 62-65, 72, 77. † References 4, 5, 7, 8, 11, 13, 31, 55, 63, 64, 68, 69, 83. ‡ References 2, 4, 6, 8, 11, 13, 68, 69, 83.

John A. Herring John G. Birch age groups—toddlers (1 to 3 years), children (4 to 10 years), and adolescents (11 to 15 years)—also are presented63,65 (Box 6-1).

Abnormal Gait Patterns in Children A child’s gait pattern can be affected by numerous factors, including pain or inlammation, weakened muscles, abnormal muscle activity, joint abnormalities, and limb length discrepancy.31,63-65,92 Each of these pathologic conditions produces a characteristic limp, which can be recognized by observing the movements of the pelvis and trunk and the position of the joints of the lower extremities as the child walks and runs. Familiarity with these abnormal patterns helps signiicantly in correctly diagnosing the underlying cause of a limp. Additional gait disturbance patterns exist; however, the abnormal patterns described here relect the majority of conditions that may cause limping in a child.

Antalgic Gait An antalgic gait, which is caused by pain in a lower extremity or occasionally in the back, is generally the most common type of gait disturbance in the limping child. In an attempt to avoid the pain, the child takes quick, soft steps on the affected leg (“short stepping”) that reduce the amount of time the extremity is in the stance phase of gait. If the source of pain is in the hip, the patient also leans toward the affected side during stance phase to decrease the abductor force across the joint. Because the unaffected limb is brought forward more quickly than normal in swing phase, it remains longer in stance phase. An antalgic gait can be caused by any condition that causes pain during weight bearing in a lower extremity, and the pain can originate from any part of the extremity, from the foot to the hip. Another form of antalgic gait may be observed in children whose pain results from spinal disorders such as diskitis or vertebral osteomyelitis. In such cases the child walks very slowly or refrains from walking altogether to avoid jarring the back and aggravating the pain.

Trendelenburg Gait A Trendelenburg gait is observed in patients with functionally weakened hip abductor muscles, a condition that makes it dificult to support the body’s weight on the affected side. This gait disturbance is commonly observed in children with developmental dysplasia of the hip (DDH), congenital coxa vara, or coxa vara secondary to another disorder (i.e., Legg-Calvé-Perthes disease or slipped capital femoral epiphysis [SCFE]).31 In all these conditions the abductor muscles themselves are normal but are at a mechanical disadvantage. As a result, during the stance phase of gait, the hip abductors function ineffectively, and the pelvis tilts 79

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Box 6-1 Differential Diagnosis of Limping in Various Age Groups TODDLER (1-3 YR) Transient synovitis Septic arthritis Diskitis Toddler’s fracture Cerebral palsy Muscular dystrophy Developmental dysplasia of the hip Coxa vara Pauciarticular juvenile arthritis Rarities Leukemia Osteoid osteoma

CHILD (4-10 YR) Transient synovitis Septic arthritis Legg-Calvé-Perthes disease Discoid meniscus Limb length discrepancy

ADOLESCENT (11-15 YR) Slipped capital femoral epiphysis Hip dysplasia Chondrolysis Overuse syndromes Osteochondritis dissecans

toddler or young child. The lack of hip extensor strength forces the child to walk with increased lordosis of the lumbar spine to remain upright. Gowers sign is often present as the child arises from a sitting position. The child must “climb up” himself by pushing off with the hands against the shins, knees, thighs, and inally the hips (Fig. 6-2). As the proximal musculature, in particular the gluteus medius and maximus, weakens further, the child “lurches” back and forth over the hips to maintain balance.

Spastic Gait

FIGURE 6-1 Trendelenburg gait. In this example the hip abductor muscles on the involved right side cannot effectively support the weight of the body. The pelvis tilts down and away from the right hip. In an effort to compensate, the patient leans toward the affected side.

away from the affected side. In an attempt to lessen this effect, the child compensates by leaning over the affected hip. This brings the center of gravity over the hip and reduces the degree of pelvic drop (Fig. 6-1). The characteristic pattern of the Trendelenburg gait usually is obvious after the child has repeated the gait cycle a couple of times. Because the child has no pain, the amount of time spent in stance phase on the affected side may be normal (this is distinctly different from an antalgic gait).

Proximal Muscle Weakness Gait Weakness of the proximal musculature, as seen in children with muscular dystrophy, may cause limping in the older

A spastic gait, as is seen in children with cerebral palsy, is caused by hypertonicity and imbalanced activity among muscle groups.§ Spastic hamstring muscles restrict extension of the knee and thus may cause the child to crouch at the knee and walk with a shortened stride length. Spastic quadriceps muscles may result in a stiff, extendedknee gait. Children with cerebral palsy often exhibit a scissoring gait secondary to excessive hip adduction throughout the gait cycle that results in dificulty moving the swing leg forward. Sustained activity of the gastrocsoleus may cause ankle equinus and toe-walking. A patient with hemiplegia may appear to be dragging the affected extremity. Usually the spastic gait is a combination of several of these indings. Lower extremity spasticity becomes even more apparent when the child runs, and subtle upper extremity posturing may be noted (i.e., elbow lexion, forearm pronation, wrist lexion, and clenched ist). In some cases, however, these gait patterns and the clinical presentation may be very subtle, thereby making the diagnosis dificult. For example, in patients with very mild hemiplegia in whom increased tone in the gastrocsoleus leads to slight ankle equinus, the only gait abnormality may be excessive hyperextension of the knee during the stance phase (needed to place the foot lat on the ground).

§

References 9, 18, 35, 37, 59, 73, 81, 91.

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FIGURE 6-2 Gowers sign. Weakness of the proximal hip muscles can severely limit the child’s ability to rise from a sitting position. To stand, the patient uses his or her hands and arms to “climb up” the body by pushing off from the shins, knees, thighs, and inally the hips.

Short-Limb Gait Gait asymmetry is usually seen in children when limb length discrepancies are in excess of 3.7% to 5.5%.38,74 In an effort to keep the pelvis level throughout the gait cycle, the child walks on the toes of the foot of the shorter limb. The child may be forced to maintain lexion of the hip and knee of the longer extremity when it is in stance phase. Children with discrepancies of less than 3.7% to 5.5% usually are able to use a combination of compensatory strategies to normalize the mechanical work performed by the lower extremities.

Special Considerations Based on Age Group Toddler (Ages 1 to 3 Years) Determining the cause of a limp is most dificult in toddlers. It often is dificult to obtain a reliable history directly from them because they are unable or unwilling to talk or because they cannot accurately describe the problem. In addition, their parents may not recall minor incidents that can result in a limp, such as a splinter in the foot or a toddler’s fracture of the tibia. Because toddlers often are apprehensive or frightened at the physician’s ofice, the least intimidating part of the examination should be conducted irst. The examiner should observe toddlers’ gait while they are walking uninhibitedly with their parents and look for limited range of motion of the joints of the lower extremity to help localize an abnormality responsible for the limp. Other important indings include localized tenderness on palpation and evidence of inlammation, speciically erythema, heat, swelling, and pain. Because the neuromuscular development in toddlers is immature, their normal gait pattern is distinctly different

from that of older children and adults. To achieve better balance, toddlers walk with a wide-based gait, increased lexion of the hips and knees, and arms held out to the sides with the elbows extended. To maintain their balance during the gait cycle, they spend more time in double-limb stance. Because toddlers cannot increase their speed by extending their step length, they compensate by increasing their cadence, which may make their gait appear uncoordinated and quick. Increasing maturity is accompanied by smoother movements, reciprocal arm swing, and an increase in step length and walking velocity. Although the most common reason that children limp is to lessen pain from an extremity, toddlers in particular often limp for other reasons. Painless disorders that can cause limping in toddlers include DDH, limb length discrepancies, and mild static encephalopathies, to name just a few. Painless toe-walking in toddlers is a common indication for pediatric orthopaedic referral (Fig. 6-3). The differential diagnosis of toe-walking in these young children primarily includes idiopathic, mild spastic diplegia, and hereditary spastic paraparesis.20,23,34,58 A thorough evaluation of the perinatal and family histories and close examination of the gait for underlying spasticity usually identify a neurologic or inherited cause. Some idiopathic toe-walkers have full range of motion, whereas others have limited dorsilexion because of a shortened tendo Achilles. On occasion, further helpful information can be gained from a gait analysis study.41 Other, less obvious causes of toe-walking should always be considered, particularly if the toe-walking is asymmetric.42 If the toe-walking is idiopathic, conservative management with casting or bracing is used on occasion but has not proved effective.80 Surgical intervention is rarely needed.

Child (Ages 4 to 10 Years) Evaluating a limp in this age group is easier than in toddlers because older children communicate better and are more cooperative. In addition, their gait is more mature.

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FIGURE 6-3 A 4-year-old idiopathic toe-walker. Despite frequent heel cord stretching exercises and encouragement to stand with his heels down, he constantly walks on his toes. Other diagnoses, such as mild spastic diplegia or hereditary spastic paraparesis, must be excluded.

Normally, by 5 years of age the child has developed a stable velocity pattern, and an adult gait pattern is usually attained by 7 years of age. Because children in this age group usually are more interested in play than in ancillary gains, limping and complaints of pain should always be taken seriously. Parents may report that the child complains of leg discomfort, typically in the evening before bedtime, that is alleviated only after massage and, on occasion, medication. Before dismissing such discomfort as “growing pains,” the clinician should perform a thorough evaluation to rule out an underlying disorder.

Adolescent (Ages 11 to 15 Years) The limping adolescent usually can provide the clinician with an accurate history. However, symptoms may be understated if the individual wishes to return quickly to enjoyable activities or exaggerated if the individual hopes to avoid unpleasant physical activity requirements. During a thorough evaluation the examiner usually can determine the true nature and extent of the condition.

Differential Diagnosis of Limping in Children Inlammatory and Infectious Disorders Transient Synovitis Transient (toxic) synovitis of the joint is probably the most common cause of lower extremity pain and likely

responsible for the majority of cases of limping secondary to an irritable joint.29,64,82,83,87,89 The condition is seen most often in children between 3 and 8 years of age and manifests with the rapid onset of hip pain, limited joint range of motion, and limping (or an inability to walk, if the condition is severe). Often, the child has a history of an antecedent viral illness. Although the clinical presentation may mimic that of septic arthritis, patients rarely have a temperature higher than 38° C or indications of systemic illness. The white blood cell (WBC) count, C-reactive protein level, and erythrocyte sedimentation rate (ESR) usually are within normal limits. Radiographs are normally unremarkable. Ultrasound examination of the affected hip shows the effusion associated with transient synovitis3,57,83 (Fig. 6-4). Aspiration of the joint may be necessary to rule out the diagnosis of septic arthritis. Analysis of the joint aspirate usually reveals a WBC count between 5000 and 15,000 cells/mL, with more than 25% polymorphonuclear leukocytes. The primary aim of treatment is to expedite spontaneous resolution of the underlying inlammatory synovitis. This objective is best met with a brief period of bed rest and non–weight bearing in combination with the use of oral nonsteroidal antiinlammatory drugs. Light traction during bed rest may be beneicial. Routine aspiration of the joint has not been shown to be of therapeutic beneit. When the pain has subsided, the patient should be instructed to use crutches until the limp is no longer present. Clinical symptoms usually resolve gradually and completely over several days to weeks (average duration, 10 days), and the longterm outcome is generally favorable.

Septic Arthritis Septic arthritis requires urgent medical management because of the potential for signiicant joint destruction29,53,72,89 (Fig. 6-5). It must be differentiated from transient synovitis because both conditions produce a limp secondary to joint pain.29 During the acute phase, it is crucial that the clinician accurately distinguish between the two disorders. As a result, hospitalization of the child for clinical evaluation, laboratory investigations, and medical management is common. Like patients with transient synovitis, patients with septic arthritis usually present with the acute onset of joint pain. The child may walk with a limp or refuse to walk because of pain. He or she may have a history of antecedent mild trauma to the extremity or concurrent infection or illness. Unlike transient synovitis, septic arthritis usually progresses to a febrile systemic illness, and the child has fever, chills, and malaise. On clinical examination, the child holds the affected extremity immobile. Swelling of the joint, erythema, warmth, and tenderness on palpation may be noted. Passive movement of the affected joint through its range of motion causes the child obvious pain, as does weight bearing on the affected extremity. Some patients present with less dramatic indings, especially those who have been partially treated. Unless the patient is immunocompromised, laboratory values (WBC count, C-reactive protein, and ESR) usually are elevated.26 Blood culture results may be positive in approximately 30% of patients with septic arthritis.

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C

C

E E

M

M

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FIGURE 6-4 Ultrasound examination in a 4-year-old boy with a painful left hip associated with limited range of motion demonstrates an effusion (arrows) anterior to the metaphysis (M) of the femoral neck in the left hip (A) and a normal right hip (B). C, Capsule, E, epiphysis.

A

B

C FIGURE 6-5 An 18-month-old girl presented with a 14-day history of fevers and pain in the right hip. Incision and drainage conirmed the diagnosis of septic hip. A, Radiograph shows widening of the joint space and increased density of the ossiic nucleus before incision and drainage. B, Five months later, the ossiic nucleus had resorbed. C, At age 11 years 7 months, the right hip exhibits the residual changes associated with the septic process. The right lower extremity is 3.5 cm shorter than the left side.

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Kocher and associates introduced an evidence-based clinical prediction algorithm in 1999 that differentiated between septic arthritis and transient synovitis of the hip.45 Four independent clinical predictors were used: history of fever, non–weight bearing, ESR of at least 40 mL/hr, and serum WBC count of more than 12,000 cells/mL. The predicted probability of septic arthritis was less than 0.2% for zero predictors, 3.0% for one predictor, 40.0% for two predictors, 93.1% for three predictors, and 99.6% for four predictors. Although this prediction algorithm was found useful in improving the eficiency of care at the institution at which the algorithm originated,43,44 other investigators reported less success with this algorithm in differentiating septic arthritis from transient synovitis.52 Except for signs of tissue swelling, radiographic indings may be negative when radiographs are obtained at the onset of symptoms. Radiographic changes secondary to bone infection typically do not become apparent until 7 to 10 days after the infection has started. Radiographic changes indicate a protracted active infectious process. In more advanced infection, erosion and joint space narrowing may be noted as the articular cartilage is destroyed. Bone scans are not required if the lesion can be localized to a joint or periarticular region or if the diagnosis of septic arthritis can be made based on indings from the history, physical examination, laboratory studies, and radiographs. If not, acute triphase scintigraphy is very accurate in localizing the abnormality.16 However, a bone scan may fail to identify infection if the scan is performed within 24 to 48 hours of the onset of symptoms. Under such circumstances, consideration should be given to 24-hour delayed imaging with the bone scan or supplemental MRI, especially if clinical suspicion remains high. Joint aspiration is important to corroborate the diagnosis and identify the causative bacterial organism. The aspirate WBC count is generally between 80,000 and 200,000 cells/ mL, with greater than 75% polymorphonuclear leukocytes. However, lower cell counts may occasionally be present if infection is identiied in its earliest stages or as the cell count is on the rise. Gram stain is helpful in selecting the appropriate initial antimicrobial agent. Newer bacterial DNA tests can be performed on synovial luid to conirm the presence of infection.54 These tests require a minimum of time and may have greater sensitivity than standard diagnostic tests, such as Gram stain. Commonly, the synovial luid is culture positive unless the patient has recently taken antibiotics. Staphylococcus aureus is the most common organism associated with septic arthritis. Haemophilus inluenzae, previously found to be a signiicant cause of septic arthritis in toddlers, is rarely seen today because of H. inluenzae immunization. Kingella kingae is considered to be responsible for an increasing incidence of infection in this population. The identiication of infection caused by this organism in children between the ages of 6 months and 4 years has been facilitated by improved culture techniques, speciically inoculating joint luid into aerobic blood culture bottles.

Osteomyelitis In the child presenting with a limp, if infection has settled into bone, it is usually the result of hematogenous spread.3,64 S. aureus continues to be the most common offending organism, and a methicillin-resistant subset is becoming more common. The clinical picture varies with the age of

the patient. In toddlers and children osteomyelitis may manifest with localized swelling, pain, or pseudoparalysis and may be associated with the sudden onset of fever and a toxic state. In older adolescents the course may be more indolent, resulting in a delay in the diagnosis of hematogenous osteomyelitis. Evidence of deep localized soft tissue swelling is often the earliest radiographic sign of osteomyelitis in toddlers. Destruction of bone, commonly in the metaphyseal region, usually is not appreciated until several days have passed.

Diskitis Infection of the intervertebral disk may interfere with normal walking as a result of the associated back pain.17,64,66,84 In fact, the child may have stopped walking altogether. During the clinical examination, if asked to perform a task that requires bending downward (e.g., picking up an object from the loor), the child either will refuse to do so or will hold the lower back straight and bend only at the hips in an effort to prevent spinal motion. Although the patient may not appear ill, the ESR is elevated in approximately 80% of patients with diskitis. Blood culture results may be positive and, if so, usually show S. aureus to be the causative organism. This can be veriied by needle or open biopsy, but because S. aureus is so commonly found, biopsy normally is not necessary and currently is not recommended as a routine diagnostic procedure. Early in the course of the infection, radiographs may be unremarkable. However, as the disease progresses over several days to weeks, radiographs may demonstrate narrowing of the disk space and irregularities in the vertebral end-plate (Fig. 6-6). MRI shows marked inlammatory changes in the disk and adjacent end-plates. Scintigraphy can help corroborate the initial diagnosis and facilitate localizing the infection.16 To enhance the sensitivity of scintigraphy for early diskitis or vertebral osteomyelitis, single photon emission computed tomography (SPECT) images of the spine may be speciically requested. These images recreate scintigraphic images of the spine in axial, coronal, and sagittal planes and allow for improved visualization of subtle uptake in the inlamed vertebral regions. The child with diskitis or vertebral osteomyelitis should be treated with systemic antibiotic therapy, which results in more rapid resolution of the symptoms than oral antibiotics alone or no antimicrobial therapy at all. The need for immobilization varies. Bed rest alone may sufice for some children; a brace or a cast may be needed for others. Diskitis and vertebral osteomyelitis were at one time thought to be distinct entities, but MRI studies subsequently showed that they probably represent different stages of a similar infectious process. Infectious spondylitis encompasses the entire spectrum of infection involving the disk space and vertebrae.66

Pauciarticular Juvenile Arthritis Pauciarticular juvenile arthritis,64,71 the most common type of juvenile arthritis, usually leads to a mild limp in children approximately 2 years of age. The disease affects girls four times more often than boys. The most commonly involved joints of the lower extremity are the subtalar, ankle, and knee joints. Discomfort is accompanied by limited joint range of motion, mild swelling, and warmth. Laboratory values (WBC count, ESR, and rheumatoid factors) may be

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FIGURE 6-6 A, A 2-year-old boy with a 3-week history of low back pain. He would not allow lexion of his lumbar spine. B, Lateral radiograph of lumbar spine demonstrates narrowing of the L3-4 disk space. C, Bone scan shows reaction in the L3-4 region.

normal, and in 50% of cases the antinuclear antibody test result may also be negative. As the condition progresses, however, these values may change. If joint swelling persists and the laboratory values relect the likelihood of the disorder, the child should be referred to a pediatric rheumatologist. Most children with pauciarticular arthritis do not need orthopaedic intervention and are able to return to normal function with appropriate medical treatment.

noted previously) and examination are often necessary. The patient has limited range of motion of the ankle and knee joints, hyperrelexia, clonus, and some degree of spastic gait. Radiographs are unremarkable in most cases, and other diagnostic studies usually are not necessary. Although the orthopaedist may be the irst to make the diagnosis of cerebral palsy, the patient and parents should be referred to a pediatric neurologist if further explanation or treatment of the underlying neurologic condition is needed.

Neurologic Disorders

Muscular Dystrophy

An underlying neurologic disorder should be considered if the child has always had an abnormal gait or if the child did not begin ambulating within the normal time frame. Most toddlers start walking at approximately 12 months of age, but the normal range extends to 18 months of age. Beyond this age would be regarded as an abnormal delay in walking. A cause for the limp may be found in the prenatal, perinatal, or postnatal history. It is important to note the following: any dificulties associated with the pregnancy or delivery; a history of prematurity, low birth weight, failure to thrive, or perinatal infections; or a need for ventilatory assistance after birth.

Gait abnormalities caused by this uncommon condition are usually irst noted in boys between 2 and 5 years of age. The child may have a history of delayed ambulation and current problems such as stumbling, falling, and dificulty climbing stairs. Clinical examination may demonstrate proximal muscle weakness, Gowers sign, and toe-walking (see Fig. 6-2). The child may also have pseudohypertrophy of the calf. Measuring the patient’s serum creatine phosphokinase level helps to conirm the diagnosis of muscular dystrophy.

Cerebral Palsy Gait disturbance in patients with cerebral palsy is usually caused by muscle spasticity or poor balance, and the severity of the limp depends on the degree of neurologic involvement.ǁ In severe cases, the diagnosis of cerebral palsy has usually been made before the orthopaedist is asked to evaluate the patient’s abnormal gait. The diagnostic challenge is posed by the child with mild cerebral palsy who has not been previously diagnosed with the neurologic disorder and whose muscle imbalance and limp are minor. In these children, a thorough history (with emphasis on the concerns ǁ

References 9, 18, 35, 37, 59, 73, 81, 91.

Anatomic Disorders Developmental Dysplasia of the Hip DDH causes a painless limp in the toddler.3,63-65 In DDH, the femoral head is partially or completely displaced from the acetabulum. The parents often report that the child did not start walking until age 14 to 15 months (a slight delay from the expected 12 months of age, but still within the normal time frame). The child may have a shortened lower extremity and may exhibit one-sided toe-walking, along with a limp, during ambulation (see Video 16-3). If the condition is bilateral, the child may have a swayback appearance and walk with a waddle (Fig. 6-7). An abductor lurch to the

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A

B

FIGURE 6-7 A, A 5-year-old boy with bilateral developmental dislocation of the hips. The patient has excessive lumbar lordosis (swayback). B, Radiograph in same boy shows bilateral hip dislocations.

affected side (Trendelenburg gait) is readily evident. When the child stands on the affected extremity, the pelvis sags to the contralateral side, and the patient tries to compensate by leaning over the affected hip (Trendelenburg sign). During examination when the child is in the supine position, restricted abduction of the affected hip (compared with the normal contralateral hip) may be noted and mild lexion contracture may be present. A radiograph of the pelvis of children 6 months old or older readily veriies the diagnosis of DDH. CT, MRI, and ultrasound evaluations are not necessary because they do not provide any additional worthwhile information in the ambulatory toddler. In some individuals, hip pain and limp secondary to hip dysplasia may not become clinically apparent until adolescence. Before these manifestations, the patient or parents may have been unaware of the presence of any hip disorder. The common presenting complaint is an aching discomfort in the hip, groin, or thigh region after extended physical activity. The clinical examination may be negative or may reveal mild loss of hip range of motion. The diagnosis is conirmed with standing radiographs of the pelvis.

Coxa Vara Congenital or developmental coxa vara is a painless disorder that is similar in clinical presentation to DDH.3,65 If the condition is unilateral, the patient may have an abductor lurch resulting from functional weakness of the abductor muscles (Trendelenburg gait). If the disorder is bilateral, the patient may have a waddling gait. During examination when the patient is in the supine position, hip abduction is limited, and the child usually has increased external rotation and decreased internal rotation of the hip. The diagnosis is readily conirmed with radiographs of the hip, which show a decrease in the angle between the femoral neck and shaft and a vertical orientation of the physis (Fig. 6-8).

Legg-Calvé-Perthes Disease Legg-Calvé-Perthes disease is most prevalent in children between 4 and 12 years of age, but it can be seen in younger children, as well as in adolescents who have not yet reached

FIGURE 6-8 Coxa vara involving the right hip of a 7-year-old girl. The femoral neck–shaft angle is diminished, and the inclination of the physis is nearly vertical.

skeletal maturity.32,62 The disorder affects boys four times more often than girls. Affected children most often present with a limp that is exacerbated by vigorous physical activities and alleviated by rest. Pain is often a minor complaint, usually worse after activities and late in the day, and occasionally children have night pain. Pain may be localized to the groin or hip and is often referred to the thigh or knee. In the earlier phases of the disorder, the child has an antalgic limp during ambulation because of the discomfort. Findings on clinical examination depend on the severity of the disorder. Patients with mild disease may have only a slight loss of hip motion. Those with more severe disease have greater loss of range of motion (particularly abduction and internal rotation), and the patient experiences discomfort during passive range of motion. The primary initial radiographic signs of this disorder are a slight lateralization of the femoral head in the acetabulum

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FIGURE 6-9 Early Legg-Calvé-Perthes disease. Slight lateralization of the left femoral head in the acetabulum (A) is evident. When compared with the lateral radiograph of the normal right hip (B), relative increased density of the left ossiic nucleus (C) is noted.

and a slightly smaller ossiic nucleus (Fig. 6-9). In approximately one third of cases, a subchondral lucency in the femoral head is seen on the frog-leg lateral view. Later, as the disease progresses, collapse and fragmentation of the femoral epiphysis occur. Radiographic changes may not be apparent early in the course of Legg-Calvé-Perthes disease. In these patients, MRI and scintigraphy are effective in diagnosing the disorder.47,85

Slipped Capital Femoral Epiphysis SCFE, one of the more common adolescent hip disorders, occurs when the capital femoral epiphysis displaces posteriorly and medially on the femoral neck.6,12,21 Slippage can occur acutely or gradually and is usually seen in boys between 12 and 15 years of age or in girls between 10 and 13 years of age. Boys are affected more often than girls. On presentation, the patient (typically overweight) complains of constant, mild pain in the hip, groin, thigh, or knee and walks with an antalgic gait. If the slippage is chronic and stable, the symptoms may have been present for several months. On clinical examination, pain is elicited on passive motion of the joint, and loss of range of motion in internal rotation and abduction is noted. When the hip is lexed, the lower extremity often rotates externally as a result of the orientation of the capital epiphysis on the femoral neck. Less often, patients present with the sudden onset of severe pain and an inability to walk because of acute slippage of the epiphysis. This unstable condition is similar to an acute fracture and is associated with an increased incidence of avascular necrosis.51 In patients with SCFE, radiographs of the hips conirm the diagnosis (Fig. 6-10). A lateral view is mandatory because an anteroposterior radiograph may not clearly demonstrate the subtle changes of mild slippage. Both hips should be examined, given that many patients are affected bilaterally. Other imaging studies (e.g., CT, MRI, bone scan) are not necessary for diagnosing SCFE.

Chondrolysis Chondrolysis is an uncommon hip disorder that is seen most often in African Americans, in girls, and in adolescents 12 to 14 years of age.22 It is frequently associated with SCFE (with a reported incidence of up to 8%), but the exact cause is not known.88 The most common patient complaint is insidious hip or groin pain, similar to that of SCFE or hip

FIGURE 6-10 Lateral radiograph of the hips in a 12-year-old boy shows a mild slipped capital femoral epiphysis on the right.

dysplasia. The patient has an antalgic limp, and clinical examination usually reveals limitation of joint motion in all directions. Results of laboratory tests usually are negative. Radiographs demonstrate osteopenia secondary to joint disuse, narrowing of the joint space compared with the contralateral side (>2 mm difference), and subchondral lucencies (Fig. 6-11). Scintigraphy shows increased uptake on both sides of the joint, but the signiicance of this inding is unclear. To lessen the joint synovitis that accompanies chondrolysis, treatment consists of extended rest (non– weight bearing) of the affected extremity and exercises to improve and maintain joint range of motion.

Osteochondritis Dissecans Osteochondritis dissecans is most frequently seen in adolescents.3 Although the knee is most commonly affected, the hip and ankle joints can also be involved. A tunnel projection of the knee provides the best radiographic view of the defect and demonstrates its classic position on the lateral aspect of the medial femoral condyle.

Discoid Meniscus This disorder of the lateral meniscus is usually seen in children between 8 and 12 years of age, but it may also affect younger children between 3 and 8 years of age.1,15,70,76 Most patients have no history of antecedent trauma.

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FIGURE 6-11 Anteroposterior pelvic radiograph of an 11-year-old girl shows chondrolysis involving the right hip. The classic indings include osteopenia secondary to joint disuse, narrowing of the joint space, and subchondral lucencies.

Accompanying the child’s limp may be intermittent swelling of the knee, inability to extend the joint fully, and a clicking sensation. Tenderness may be elicited on the lateral joint line. Radiographs are usually unremarkable, but in some cases they may show widening of the lateral joint space with lattening of the lateral femoral condyle. MRI establishes the diagnosis of discoid meniscus.15,70,76

Toddler’s Fracture

FIGURE 6-12 Radiograph obtained 12 days after onset of a limp in a toddler shows a tibial fracture. Periosteal new bone formation is evident in the vicinity of the linear fracture.

A spiral fracture of the tibia, without concomitant ibular fracture, may result from a torsion type of injury to the lower extremity3,36,61 (Fig. 6-12). However, parents may not recall a history of trauma. The child presents with a limp or may resist any weight bearing on the affected extremity. Initial radiographs may appear normal. When follow-up radiographs are obtained 1 to 2 weeks later, some degree of subperiosteal new bone formation is normally seen. In most cases, the patient is treated only with short-term immobilization.

Tarsal Coalitions As cartilaginous tarsal coalitions in the hindfoot begin to ossify, clinical symptoms appear.46,78,90 Contracture of the peroneal muscles is common, resulting in a stiff, everted latfoot. Oblique radiographs of the feet show the calcaneonavicular coalitions (Fig. 6-13). A radiograph of the subtalar joint (Harris view) may be helpful in showing a talocalcaneal coalition. In most cases, however, CT of the hindfoot is required to diagnose subtalar coalitions33,79 (Fig. 6-14).

Overuse Syndromes As children become more involved in organized sports, overuse injuries appear with greater frequency.10,30,60,64 The most commonly affected joint is the knee, in which patellar tendinitis or apophysitis of the tibial tubercle (OsgoodSchlatter disease) arises. On clinical examination, point tenderness on palpation helps conirm the presence of these disorders. In cases of apophysitis, radiographs may reveal fragmentation of the tibial tubercle. Physical activities that result in repetitive loading of the lower extremities can lead to stress fractures of the tibia or ibula. Radiographs may appear normal, may show a subtle sclerotic line, or may

FIGURE 6-13 Top, Oblique radiograph of the foot demonstrates a calcaneonavicular coalition. Bottom, Postoperative oblique radiograph demonstrates a resected coalition in which a fat graft was interposed.

CHAPTER 6 The Limping Child

FIGURE 6-14 Computed tomography scan of the hindfoot of both lower extremities demonstrates a subtalar coalition on the left.

demonstrate periosteal reaction. If a stress fracture is suspected, scintigraphy is helpful in conirming the diagnosis. During the acute phase of overuse injuries, treatment consists of rest, ice, and antiinlammatory medications. For long-term alleviation, the patient may need to change activities, equipment, or training programs.

Limb Length Discrepancy Gradually progressive limb length discrepancies may become apparent in children between 4 and 10 years of age. To maintain a level pelvis and smooth gait pattern, the child may toe-walk on the shorter leg.38,74 The best clinical method to measure the discrepancy accurately is to have the child stand with the shorter extremity on blocks until the pelvis is level. To determine radiographically which part of the leg is responsible for the limb length discrepancy requires a standing ilm (long cassette) of the entire lower extremity. Careful scrutiny of this radiograph may reveal indings such as a mild congenitally short femur, a physeal abnormality after a remote infection, or a mild ibular hemimelia.

Neoplasms to Consider in the Limping Child Most primary bone tumors are detected before the age of 20 years.3,27,63,64,75 They are often diagnosed on plain radiographs, but some, such as leukemia or Ewing sarcoma, may be dificult to recognize. In children younger than 5 years of age, metastatic lesions, such as neuroblastoma or leukemia, should be considered in the differential diagnosis of neoplasms. In older children benign tumors such as osteoid osteoma, simple bone cysts, and osteochondromas are most often diagnosed; however, malignant tumors such as lymphomas and Hodgkin disease can also occur. Tumors involving the central nervous system (CNS) can also cause a child to limp. Deterioration of gait or loss of previously achieved motor milestones suggests a CNS tumor or neuromuscular disease.

Leukemia Acute leukemia is the most common cancer in children younger than 16 years of age; the incidence peaks between

89

FIGURE 6-15 Computed tomography scan of the fourth lumbar vertebra demonstrates an osteoid osteoma of the right-side posterior element. The patient had low back discomfort and walked with a limp on the right lower extremity.

2 and 5 years of age.55,67,75 Generalized symptoms include lethargy, pallor, fever, bruising, and bleeding. In approximately 20% of cases, the child presents with musculoskeletal complaints. Lymphoblastic leukemia is the form that most frequently causes bony changes. The patient may have a painful limp, and the pain originating from bone involvement may be described as discomfort in an adjacent joint.86 The clinical presentation—with the exception of bruising, bleeding, and hepatosplenomegaly—may be similar to that of arthritis, cellulitis, septic arthritis, or osteomyelitis. The presence of joint symptoms and bone pain, along with skin bruising, bleeding, and hepatosplenomegaly, should lead the clinician to include leukemia in the differential diagnosis. Laboratory tests may reveal anemia, an elevated or depressed peripheral leukocyte count, and an elevated ESR. Initial radiographs may be unremarkable, or transverse zones of lucent metaphyseal bands adjacent to the growth plate may be seen. Results of scintigraphy are often negative. If a thorough evaluation is nondiagnostic but the clinician still suspects leukemia, the patient should be referred to a pediatric hematologist for bone marrow studies.

Osteoid Osteoma This benign bone-forming lesion primarily affects individuals younger than 30 years of age.2,28,39,40 However, osteoid osteoma is rare in children younger than 5 years of age and is particularly dificult to diagnose in toddlers who are just beginning to walk.37 The most common clinical manifestations of osteoid osteomas are localized pain and a limp.28 Radiographs may reveal a small (2000 msec) and short TE (50 degrees)

spine’s anatomy.733 It also remains a useful tool postoperatively (particularly with three-dimensional reconstruction) for assessing bone fusion mass if pseudarthrosis is suspected, for evaluating changes in spinal rotation, and for verifying pedicle screw placement.# In addition, CT-myelography affords improved evaluation of the spinal cord when retained metal implants limit the effectiveness of MRI.

Treatment

FIGURE 12-21 Moire topographic photograph. This surfaceimaging system produces an image that can be read in the same way as contour lines on a map. (From Stokes IA, Moreland MS: Concordance of back surface asymmetry and spine shape in idiopathic scoliosis, Spine 14:73, 1989.)

neurologic indings such as ataxia, weakness, and progressive foot deformities; patients with unusually rapid curve progression or excessive thoracic kyphosis; or patients requiring surgery who have left thoracic curves or asymmetric abdominal relexes. Curves greater than 70 degrees do not increase the likelihood of inding a spinal cord anomaly.556 Routine preoperative MRI is not indicated for typical AIS if indings on the neurologic examination are normal.175,556,689,833

Computed Tomography Although CT may clearly demonstrate congenital abnormalities in the spine, it is rarely needed in the routine assessment of individuals with idiopathic scoliosis. However, with the emerging use of vertebral column resection (VCR) in those with extremely severe AIS, preoperative threedimensional CT imaging is indicated to clarify the deformed

Most adolescents with idiopathic scoliosis do not require treatment because of the low probability that their curves will progress.16,455 Treatment is warranted only for patients whose scoliotic curves are at substantial risk of worsening over time or for those with severe curves at initial evaluation. A clear understanding of the risk factors discussed earlier in the natural history section is useful in determining which patients need treatment, regardless of whether they are skeletally immature or mature. In selecting treatment, the physician must consider the adolescent’s remaining growth potential, the severity of the curve at the time of detection, and the pattern and location of the scoliosis. The cosmetic appearance and social factors that may have an impact on treatment also enter into the decision-making process. The treatment choices available are observation, nonsurgical intervention, and surgical intervention, and it is imperative that physicians know which options are appropriate for each individual patient (Table 12-2 provides general guidelines). Actively growing adolescents (Risser grade 2 or lower) with curves between 30 and 45 degrees should start brace therapy at the time of the initial visit.653 In very immature patients (Risser grade 0 and premenarchal if female) with curves exceeding 25 degrees, bracing should be started immediately.456,653 In most cases, growing adolescents with curves exceeding 45 to 50 degrees require operative stabilization because other forms of treatment are ineffective in controlling or correcting the scoliosis. Skeletally mature individuals with curves exceeding 50 to 55 degrees are also at risk for continued curve progression and should be considered for surgical treatment.811 Possible exceptions include patients with well-balanced double curves less than 60 degrees whose clinical appearance is acceptable to them. Continued observation would be necessary to document progression of the scoliosis, which would necessitate surgery.

#

References 154, 225, 287, 407, 418, 440, 619, 847, 848.

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Observation In general, no treatment is needed for curves less than 25 degrees, regardless of the patient’s maturity. Follow-up examinations are necessary, with the interval between visits depending on the patient’s maturity and the size of the curve. For example, a premenarchal Risser grade 0 adolescent with an initial curve measuring 24 degrees should undergo follow-up examinations every 3 to 4 months, and a brace may be needed if the curve progresses. For more skeletally mature patients (Risser grade 3 or higher), longer intervals between visits (e.g., 6 months) are appropriate because curve progression usually occurs at a slower rate, if at all. Clearly, predetermined guidelines do not apply to all cases, and follow-up must be individualized. The magnitude of the patient’s curve at initial evaluation helps determine the frequency of follow-up visits. In general, for growing children with small curves (45 degrees) in a growing adolescent cannot be effectively controlled by a brace and that these patients need surgical treatment. Even if progression could be controlled with a brace, the cosmetic appearance associated with these large curves is often unacceptable because of excessive trunk shift and rib prominence. An exception to this general rule involves very immature adolescents with large curves (approximately 50 degrees) who have not yet reached their PHV. These patients may beneit from bracing to delay curve progression until greater maturity is reached; this may avoid the need for additional anterior spinal fusion to prevent the crankshaft phenomenon. In addition, bracing is not indicated for patients who ind wearing an orthosis to be emotionally intolerable, although appropriate psychological counseling may result in eventual acceptance of a brace by an adolescent. Extreme thoracic hypokyphosis precludes the use of an orthosis. In these cases, normal positioning of the pads within the brace could exacerbate the rib deformity. If the hypokyphosis is 20 degrees or less, corrective pads should be lateralized to

CHAPTER 12 Scoliosis

eliminate any anteriorly directed derotation forces. Finally, skeletally mature adolescents (Risser grade 4 or 5 and, if female, 2 years postmenarchal) should not be treated with braces. Relative contraindications to bracing include a high thoracic or cervicothoracic curve, which ordinarily does not respond to orthotic treatment, and male sex. A relative lack of effectiveness of bracing in boys has been documented, in part because of extremely poor compliance.359,867 Comparison of Orthoses. Numerous reports in the literature attest to the effectiveness of brace treatment.*a In most of these studies, bracing was considered effective if the curve remained within 5 to 6 degrees of its original magnitude on completion of treatment. Some of these studies included low-risk patients (Risser grades 3 to 5, curves 75 degrees) are best analyzed with traction ilms because the mechanics of the bend ilms is minimized for these large and stiff curves.603 The push-prone radiograph was shown to be the best preoperative indicator of lexibility for predicting the inal lumbar curve measurement in patients undergoing selective thoracic fusion for Lenke type 1B and 1C curves.189 Signiicant study using the fulcrum bend test has demonstrated that for the thoracic curve, this test best predicts the status of the thoracic curve following posterior spinal fusion and instrumentation.227,298,466,467 Neurologic Status. If a subtle neurologic abnormality (e.g., asymmetric abdominal relexes) is detected in an otherwise normal individual, MRI of the entire spinal canal should be considered to rule out syrinx, cord tethering, or diastematomyelia.864 Preoperative MRI should also be performed in patients with left thoracic curves and in those in whom the typical apical lordotic sagittal deformity is absent because of the association with intracanal abnormalities.231,482,571,616,681 The MRI study can be ordered when surgery is scheduled. Studies have demonstrated that excessive rotation or kyphosis in the thoracic spine is an indication to perform MRI.175,636 Rib Deformities. The rotational deformity inherent in AIS is often seen most by families and is generally mild to moderate with rare occurrence of the razorback deformity (it is more common in nonidiopathic conditions such as neuroibromatosis). Suggested indications for thoracoplasty include a preoperative rib prominence exceeding 10 degrees (measured from a tangential radiograph with the patient bent forward 90 degrees), preoperative curves greater than 60 degrees, and lexibility less than 20%.295 Surgeon preference and experience play a large role in determining the indications for thoracoplasty; however, the general trend has been less use of this procedure because of improved methods for direct vertebral rotation (DVR). Nonetheless, Professor Suk, the developer of the DVR technique, continues to perform thoracoplasty in all patients with AIS. In addition to improving the patient’s cosmetic appearance, partial resection of three to ive apical ribs provides bone graft in amounts suficient to obviate an iliac crest graft.40,256,295,668,746 A percutaneous thoracoplasty technique has resulted in excellent correction but some loss of coronal plane correction.859 Because some studies report a decline in pulmonary function following thoracoplasty, this technique is contraindicated in patients with compromised preoperative pulmonary or cardiac status. More recent studies have demonstrated an early decline in pulmonary function test results without longlasting effects when compared with a cohort that did not undergo thoracoplasty.134,411,746,859

235

Future Growth Potential. Correction of scoliosis by posterior spinal instrumentation and fusion is usually maintained over time and is not adversely affected by any remaining anterior spinal growth; however, the crankshaft phenomenon (resumption of the curve secondary to anterior growth in patients with posterior fusion) can still occur. Dubousset coined the term when he observed that the entire spine and trunk gradually rotated and deformed as the anterior portion of the spine continued to grow and twist around the axis of the fusion mass (in a manner similar to an automobile crankshaft)196 (Fig. 12-33). Methods to prevent this phenomenon include careful assessment of the growth remaining, the use of anterior fusion when appropriate, and greater use of and correction with pedicle screw ixation. Although its severity is dificult to quantify, the crankshaft phenomenon can best be appreciated by examining serial clinical photographs that demonstrate progressive changes in rib deformities, narrowing of the chest, and imbalance in the thoracic and lumbar spine. Radiographs can also demonstrate progressive changes over time, such as alterations in curve size, rotation, and rib–vertebral angle difference; translation of the apical vertebra toward the chest wall on the convexity; and changes in the vertical inclination of the instrumentation. Radiographic changes of more than 10 degrees in curve size, apical vertebral rotation, and the rib–vertebral angle difference are all thought to relect progression of the deformity secondary to the crankshaft phenomenon.288,405,671 However, during the irst 6 to 12 months

FIGURE 12-33 Crankshaft phenomenon in an 11-year-old girl 1 year after undergoing posterior spinal fusion with instrumentation consisting of all pedicle screws. She grew 7 cm since surgery and has had a trunk shift to the right with a signiicantly worse clinical rotational deformity as shown here.

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after surgery, it is important to not automatically assume that changes in radiographic measurements are a result of the crankshaft phenomenon; these changes are often due to stress relaxation of the spine, gradual maturation of the fusion mass, and realignment of the curve. For female adolescents in need of surgery who have not yet reached their PHV, who are premenarchal, and whose triradiate cartilage remains open, strong consideration should be given to combining anterior and posterior fusion to prevent the crankshaft phenomenon.191,405,673,697 For anterior spinal fusion, a conventional open thoracotomy approach has been compared with the newer, less invasive videoassisted thoracoscopic surgery (VATS).316,503,549,737,804 Advantages of VATS include muscle sparing, improved cosmetic results (less scarring), greater access to the entire length of the thoracic spine, and less effect on pulmonary function than with open thoracotomy. Instruments are used through multiple intercostal portals to resect disk material, perform anterior release, and insert bone graft. However, surgeons require extensive training in the VATS technique. Some reports suggest that stiff posterior constructs, particularly when screws are used at nearly every level in the segment fused, may be strong enough to prevent the crankshaft phenomenon in immature patients, thus avoiding the need for anterior fusion.100,412,759 More research is needed to prove the effectiveness of this approach. Transfusion Requirements. Several procedures are available to reduce the need for homologous blood transfusions in patients undergoing posterior spinal instrumentation for scoliosis, including controlled hypotensive anesthesia, autologous blood predonation of 1 or 2 units, acute normovolemic hemodilution, intraoperative and postoperative salvage of lost blood, intraoperative use of antiibrinolytics, and transfusion decisions based on clinical judgment rather than on a predetermined hemoglobin value. Various combinations of these methods have been shown to signiicantly reduce exposure of patients to homologous blood products during scoliosis surgery.¶a The combination of predonated autologous blood, hypotensive anesthesia, and intraoperative salvage of lost blood is probably the one used most frequently for healthy individuals with idiopathic scoliosis.520,532 Intraoperative salvage of lost blood, the most expensive of the available techniques, is most effective when blood loss is expected to exceed 1000 mL. Acute normovolemic hemodilution appears to be a satisfactory alternative to the use of predonated autologous blood.143,567 The antiibrinolytic agent ε-aminocaproic acid (Amicar) is reportedly a safe, effective, and inexpensive method of reducing perioperative blood loss in patients with scoliosis.174,241 We generally prefer tranexamic acid (TXA), which has also been shown to reduce intraoperative and postoperative blood loss during posterior spinal fusion and instrumentation for AIS in a matched cohort.856 The response to TXA depends on the dose administered, with a higher loading dose of 20 mg/kg followed by a 10-mg/kg/hr infusion appearing to have a greater effect.270

¶a

References 20, 142, 143, 229, 240, 241, 253, 329, 350, 393, 520, 532, 567, 598, 701, 703, 788.

Bone Grafting. The primary goal of scoliosis surgery is to achieve a solid arthrodesis, which is enhanced by meticulous cleaning of soft tissue from the spine, facetectomies, decortication, and adequate bone grafting. Although autogenous iliac crest bone grafting has previously been the standard,133,801 signiicant postoperative pain at the donor site persists and remains the greatest problem with the use of autogenous grafting.274,707 Because of these postoperative symptoms, alternative bone graft substitutes have been sought.67,333,430,431,860 Numerous studies of successful fusions using allografts of frozen, bank-stored bone as a substitute for autogenous bone have been reported34,75,190,214,274,730 without an increase in pseudarthrosis rates.190,214 To minimize the risk of transmitting human immunodeiciency virus, hepatitis virus, and any other potential viral pathogens, the donor blood and tissue are tested at the site of recovery, and testing is usually continued throughout the harvesting process. Freeze-dried cancellous bone is usually exposed to low-dose gamma radiation to sterilize all nonsystemic bacterial and fungal contaminants. Bone morphogenetic protein has become popular for use in single-level lumbar spinal fusions but has yet to become cost-effective for routine use in multisegment scoliosis fusions.5,99,496,606,789 The authors’ preferred technique is to perform thorough stripping of the spine, followed by aggressive facetectomies, decortications of the spine, and the use of allograft bone, without any pseudarthrosis in individuals with AIS being documented in the past 8 years. Spinal Cord Monitoring. Spinal cord monitoring using both spinal somatosensory evoked potentials (SSEPs) and motor evoked potentials (MEPs) is the standard of care during scoliosis surgery and is critical to the safety of any spine deformity surgery. SSEPs record the sensory function of the spinal cord and provide continuous monitoring throughout the procedure.#a This test may, however, be adversely affected by changes in anesthetic level and perfusion, and critical changes tend to lag behind MEPs. With impending neurologic deicit, MEPs are used to monitor the anterior spinal cord motor tracts and are ideally performed by applying a stimulus to the motor cortex of the brain (transcranial MEPs [tcMEPs]).59,263,575,680,726,754 This provides direct stimulation of the motor cortex, which then travels through the anterior column tracts with responses noted in the upper and lower extremity musculature (Fig. 12-34). When MEPs are used in conjunction with SSEPs, the chance of unrecognized injury to the spinal cord is minimized. A large multicenter study of 1121 patients demonstrated that 38 (3.4%) had a critical change on monitoring when tcMEPs and SSEPs were used. Hypotension was responsible for nine changes (corrected by elevating blood pressure), whereas three were due to segmental vessel ligation. The tcMEP/ SSEP combination did not miss any patient with a transient motor or sensory deicit.679 Similar studies have demonstrated excellent results with combined multimodal intraoperative neuromonitoring during AIS surgery.230,584,767,868 Although total intravenous anesthesia with propofol is necessary to obtain good tcMEP data, other techniques to assist in obtaining good monitoring data have

#a

References 25, 123-125, 307, 468, 527, 555, 579.

CHAPTER 12 Scoliosis

FIGURE 12-34 Output of a typical response when using transcranial motor evoked potentials (tcMEPs). The left extremities (left) and right extremities (right) are shown. The red response is the baseline data, whereas the green notes the latest output from the most recent “run” of tcMEPs. The muscle group in the upper extremity is the abductor pollicis brevis, and the lower extremities are evaluated with three muscle groups—the tibialis anterior (LTA and RTA), the soleus (LSOL and RSOL), and the abductor hallucis (LAH and RAH). Note that the most recent amplitudes (green) are the same as the baseline (red) in all muscle groups demonstrating good responses.

been evaluated.370,481,868 The current increase in the use of thoracic pedicle screws for ixation points has led some surgeons to use triggered electromyographic (EMG) monitoring; however, this has been relatively unreliable in the thoracic region without clearly identiied thresholds to indicate when medial screw penetration is seen.620 The wake-up test, a gross evaluation of motor function, is no longer used routinely if spinal cord monitoring is available and results are normal throughout surgery. The wake-up test can be performed if changes in SSEPs or MEPs are noted during correction of the spine because spinal cord injury may exist even when monitored variables return to baseline.552 The authors generally do not perform this test during AIS surgery because irst, a “normal” wake-up test does not provide a detailed examination and strength testing is not possible and, second, even if normal, tcMEP/SSEP monitoring can indicate some stress or subclinical deicit in the spinal cord that may become a permanent deicit with continued surgery. For this test the anesthesiologist allows the patient to regain partial consciousness and motor function during the surgical procedure.285 Intraoperative neuromonitoring is especially useful when intraoperative traction is used because critical changes develop in a third of patients during surgery and are related to having a thoracic curve, a larger Cobb angle, and a rigid curve. A stepwise response to these changes, including removal of the traction, resulted in overall good results, and the presence of MEP recordings at the completion of the surgery was associated with normal neurologic function.432

237

Postoperative Pain Management. Patient-controlled analgesia (PCA) and epidural analgesia are the two methods used regularly for the management of postoperative pain. PCA provides safe and effective analgesia in children as young as 5 years. It allows the patient to self-administer small, preprogrammed doses of opioids via a pump connected to the patient’s intravenous tubing.485 This enables the patient to titrate an opioid blood level in direct response to the changing intensity of pain. The built-in safety mechanism of PCA systems prevents oversedation. In addition, PCA devices can deliver a continuous infusion so that therapeutic levels of analgesia are maintained during sleep. The use of epidural analgesia for scoliosis surgery has become increasingly popular because it provides excellent pain relief; however, meticulous attention to detail is required.*b At the end of the surgical procedure but before closure, the surgeon inserts an epidural catheter. The catheter is tunneled lateral to the incision and is usually left in place for 48 to 72 hours. Low-dose opioids are infused to provide effective analgesia, usually under the direction of pain management teams experienced in this technique. Close monitoring of the patient’s respiratory status and the use of pulse oximetry are necessary for 24 hours after the infusion has been discontinued. Postoperative pulmonary toileting is optimized with this technique. Ketorolac, an injectable nonsteroidal antiinlammatory drug, is effective for the short-term management of moderate to severe postoperative pain. It is often used in conjunction with opioids because the combination provides more effective analgesia than either drug alone does. Although its use has been associated with pseudarthrosis after adult low back surgery,262,488 this problem has not been demonstrated in large series of patients with AIS undergoing surgical correction.740,803 Antibiotic Prophylaxis for Dental Procedures. Antibiotic prophylaxis for dental procedures in patients with spinal instrumentation is a controversial issue.631 Currently, no scientiic evidence supports the position that antibiotics should be given during routine dental care. Streptococcus viridans, the predominant bacterium in normal human oral lora and the most common organism isolated from blood after dental procedures, has not been reported in delayed deep wound infections following spinal instrumentation. In those in whom early postoperative wound infections develop, Staphylococcus aureus is the predominant organism. Yet S. aureus accounts for only 0.005% of the normal oral lora and is rarely isolated after dental procedures.166 Guidelines similar to those provided in the advisory statement issued by the AAOS regarding antibiotic prophylaxis for dental patients with total joint replacement should be used for those who have undergone spinal instrumentation.19 If antibiotic prophylaxis is given, the following regimen is recommended: patients who are not allergic to penicillin can be treated with cephalexin, cephradine, or amoxicillin, 2 g orally 1 hour before the dental procedure; patients who are allergic to penicillin should receive clindamycin, 600 mg orally 1 hour before the dental procedure.

*bReferences 26, 204, 373, 464, 485, 687, 736, 769.

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Posterior Spinal Instrumentation Exposure of the spine for posterior instrumentation must be meticulous and thorough, regardless of the implant system selected (see Plate 12-1 on page 292). Harrington Instrumentation. Harrington developed his technique in the late 1950s and irst reported it in 1962.292,293 In this system, hooks apply distraction forces to the concave side of the spinal curve via a ratchet mechanism. Compression force is applied to the convex side of the thoracic curve at the base of the transverse processes, with the amount of force adjusted by tightening nuts on a threaded rod. Long-term follow-up studies have reported that approximately 30% to 40% of curve correction is maintained through the years with Harrington instrumentation.†b However, minimal, three-dimensional correction of the spine was achieved because distraction forces lattened the spine and the implants provided insuficient stability to allow brace-free postoperative mobilization. The technique is detailed in the second edition of Tachdjian’s Pediatric Orthopaedics.755 Multiple-Hook Segmental Instrumentation. The CD instrumentation system was developed in France by Cotrel and Dubousset and was introduced in the United States in the mid-1980s (Fig. 12-35).147 The system revolutionized posterior instrumentation for idiopathic scoliosis by enhancing the surgeon’s ability to improve the three-dimensional orientation of the spine. This was accomplished through the “derotation maneuver” popularized by Dubousset,37,148 whereby the contoured rod is secured to the spine with various hooks and rotated 90 degrees to bring the concave spine posterior and medial for correction. This maneuver, which continues to be used today, improves the sagittal contour, achieves signiicant curve correction, and improves the rotation or translation of the spine. The second rod increases the construct’s strength and torsional stability, particularly when rigidly united to the irst rod via a rodconnecting device. Numerous reports have documenteded signiicant improvement in the correction of idiopathic scoliosis with CD instrumentation. Rib deformities were reduced, curve correction in the range of 48% to 69% was achieved and maintained, and nearly normal sagittal alignment was restored.‡b The ability to preserve lumbar lordosis in curves requiring long fusion to L3 or L4 avoided the long-term “lat back” problems that occurred with Harrington distraction instrumentation. The TSRH instrumentation system was introduced in 1988 and, like the CD system, uses multiple hooks and screws to attach smooth, precontoured rods to the spine.32,345 Once the system is assembled, selective compression, distraction, and rotation maneuvers can be performed to correct the spinal deformity. These maneuvers follow the principles introduced by Cotrel and Dubousset148 and have resulted in outcomes similar to those with CD instrumentation.72,634,718 The technique of a multiple-hook system is †b

References 160, 178, 304, 328, 458, 507, 576, 817. References 71, 87, 154, 236, 276, 328, 399, 401, 420, 421, 422, 601, 612, 633, 654, 696, 793, 812, 842, 848.

‡b

FIGURE 12-35 Cotrel-Dubousset (CD) instrumentation. The irst contoured rod is secured to the concave side of the spine with multiple hooks and is rotated 90 degrees. This maneuver improves the sagittal contour and achieves signiicant correction of the curve. Placement of the second rod increases the construct’s strength. CD instrumentation uses numerous hooks but no sublaminar wires.

illustrated in Plate 12-2 on page 294 on the accompanying website. Pedicle Screws. The use of pedicle screws has dramatically changed the operative treatment of all spinal deformity, including AIS. The use of pedicle screw ixation for correction of deformity was irst described in the lumbar spine in the mid-1990s.38,289,749 These studies demonstrated that pedicle screws provide greater ability to obtain and maintain coronal plane correction of the thoracolumbar or lumbar curves in individuals with double major idiopathic scoliosis. When compared with hooks, initial correction was 72% versus 60% with hooks, and less loss of correction occurred at follow-up (5% versus 13%).38 Signiicant improvement in LIV tilt (82% versus 50%) and translation (50% versus 23%) was seen when compared with hooks.289 Pedicle screws placed in the lumbar spine for pediatric spinal deformity have a very good track record, with few complications.76,91,212,453,677 The improved correction of deformity and maintenance of the correction achieved with

CHAPTER 12 Scoliosis

A

C

239

B

FIGURE 12-36 Thoracic pedicle screw ixation. A, Preoperative posteroanterior (left) and lateral (right) radiographs of a 13-year-old girl with a double thoracic (Lenke type 2A) curve pattern. The main thoracic curve measures 62 degrees, and the upper thoracic curve measures 40 degrees. B, Supine-bending radiographs to the left (left) and to the right (right) demonstrate improvement of the main thoracic curve to 37 degrees and the upper thoracic curve to 36 degrees. C, Postoperative posteroanterior (left) and lateral (right) radiographs demonstrate excellent coronal correction and maintenance of the sagittal proile.

lumbar pedicle screws led to their use in the thoracic spine (Fig. 12-36). Suk and coauthors irst reported the routine use of pedicle screws in the thoracic spine for spinal deformity surgery in 1995 and achieved improved coronal plane correction in the screw group (72%) versus hooks (55%) and hybrids (66%).750 The initial reports of their safety demonstrated overall good results, with a pedicle screw breech rate of between 1.5% and 15% and few neurologic complications.2,52,186,395,748 The learning curve is steep, and greater surgeon experience leads to improved accuracy.2,669 Reports of improved correction of spinal deformity have led to fairly enthusiastic adoption of the technique by surgeons, with overall improved radiographic correction when

compared with more traditional hook constructs.§b The improved coronal plane correction achieved with pedicle screw ixation can be attributed to several factors. First, surgeons generally place pedicle screws at more levels than when hooks or other anchors are used; second, the threecolumn ixation of the spine provides better “grip” of the vertebrae, so correction maneuvers yield greater improvement in the spinal deformity; third, the use of procedures to mobilize the spine has expanded and included greater use of Ponte-style or Smith-Petersen osteotomies, concave and convex rib osteotomies, and for very severe curves, use of §b

References 100, 380, 381, 395, 440, 605, 715, 729, 752, 798.

240

SECTION II Anatomic Disorders

the VCR procedure; and inally, with improved ixation, the surgeon can use a number of correction strategies, including the traditional rod rotation maneuver, segmental distraction or compression, and segmental in situ bending. Fixation of each vertebra in the instrumented segment may be an important factor when coronal plane correction with thoracic pedicle screws is analyzed. However, the appropriate screw “density” (the number of pedicles illed with pedicle screws relative to the total number that are available) is not well known, and early studies demonstrated conlicting results, with some showing a positive effect with improved coronal correction136 and others demonstrating no difference between high and low screw density.69 In North America, longer-term follow-up has demonstrated maintenance of correction with nearly 70% coronal plane correction.411 Perhaps the greatest advantage of thoracic pedicle screws is improved axial plane correction. Lee and associates described a DVR maneuver in which the concave and convex screws in the juxtaapical vertebrae were rotated opposite the direction of the rod rotation maneuver.410 With CT they demonstrated better apical rotation in the group that underwent DVR than in those who did not (42.5% versus 2.4%). The technique of apical derotation can be performed via a number of methods, and all have demonstrated some success in improving the rotational deformity in a variety of AIS curves.185,330,331 Use of this technique may obviate the need for thoracoplasty and the associated detrimental effect on pulmonary function (see Plate 12-3 on page 297).156,354 However, care in maintaining thoracic kyphosis when performing these DVRs is necessary to avoid creation of lordosis as one pushes anteriorly on the spine. This loss of thoracic kyphosis is accompanied by a loss of lumbar lordosis.550 Large-diameter rods with an accentuated thoracic kyphosis contour help maintain the thoracic kyphosis with the posterior approach,512 whereas the anterior approach maintains kyphosis because correction of the coronal plane is achieved with shortening of the anterior column.734 It is important to preserve the tension band of the soft tissues proximal to the planned instrumented levels to prevent junctional kyphosis, which has been reported with the use of pedicle screws.306 Surgical treatment of spinal deformity has three main aspects. The irst is to grab onto the spine with anchors strategically placed on the spine, typically with pedicle screws today. The second is to mobilize the spine when necessary through a variety of techniques, including intraoperative traction, multiple Ponte-style osteotomies, or even resection procedures. Finally, once the anchor points are placed and the spine is lexible (either inherently so or following mobilization techniques), a variety of surgical techniques can be used to improve the spinal deformity. Thoracic pedicle screws can be placed in several ways, but generally two main methods are used: freehand, in which the screws are placed without the use of luoroscopic guidance, and image guided, in which the screws are inserted under the guidance of some radiographic imaging modality.379 Freehand Technique. The freehand technique relies on a thorough understanding of pedicle anatomy in the thoracic spine, including the anatomic landmarks for the starting point and the trajectory and general guidelines with regard

to the width, height, and depth of the pedicles in the various regions of the thoracic spine.‖b In addition, an understanding of the surrounding anatomic structures laterally and medially is important to avoid injury.439,735 In general, the width of the thoracic pedicle is smaller in the proximal part of the thoracic spine, on the concavity of the upper and main thoracic curves, and with greater curve magnitude. The spinal cord is positioned adjacent to the concave pedicles with less than 1 mm of epidural space, as compared with 3 to 5 mm on the convex side.439 At the apex of a right thoracic scoliosis, the aorta is positioned more lateral and posterior to the vertebral body than in a normal, straight spine.439,735 The combination of narrow pedicles, dural sac proximity medially, and aorta proximity laterally makes safe screw placement challenging on the concavity of these thoracic curves. The most challenging pedicles are those in the proximal part of the thoracic spine, especially on the concave aspect. The freehand technique entails identifying the starting point for screw insertion, decorticating that level with a burr, entering the cancellous channel with a pedicle inder, and traveling down the pedicle via manual pressure. The channel is then probed to ensure that all ive walls (anterior, medial, lateral, superior, and inferior) of the pedicle are intact, followed by tapping the pedicle, reprobing to ensure maintenance of the pedicle walls, and placing the screw. Fluoroscopy or plain radiography is then used to check the position of the screws. Kim and co-workers reported on 3204 screws placed in the thoracic spine for spinal deformity and randomly analyzed 577 screws with CT imaging.379 They demonstrated that 6.2% of the screws had moderate cortical perforation, including 1.7% with medial wall violation; however, no neurologic or vascular complications occurred. Pedicle screws have been placed successfully in patients with severe deformities and scoliosis curves greater than 90 degrees, with a thoracic pedicle screw accuracy rate of 96.3% and no neurologic complications.395 Image-Guided Techniques. A variety of image guidance techniques have been described, from plain radiography following guidewire placement to continuous stepwise luoroscopic evaluation299,398,748 to true surgical navigation using preoperative or intraoperative CT scanning and intraoperative computer navigation.¶b Suk and colleagues described a method in which anatomic landmarks are used to identify the starting point and guidewires are drilled into the center of the pedicle, which are then visualized on a plain PA radiograph.748 Based on these radiographic images, adjustments are made in the position of the guidewires before placing the screws. A review of their experience in placing 4604 thoracic pedicle screws in 462 patients demonstrated that 1.5% of the screws were malpositioned in 10.4% of the patients, with only 4 screws (0.09%) placed medially. One patient experienced transient paraparesis, and three had dural tears. True image guidance systems rely on either a preoperative or an intraoperative CT scan to deine the spinal anatomy (initial data acquisition), followed intraoperatively by image-to-patient registration. Surgical navigation is then performed during placement of the pedicle screws. ‖b

References 391, 557, 577, 581, 582, 790, 791, 880, 881. References 6, 247, 280, 355, 402, 618, 866.

¶b

CHAPTER 12 Scoliosis

Early results demonstrated similar or improved screw accuracy when compared with more conventional imaging.247,280,402,406,618 One study reported that a potentially unsafe screw was 3.8 times less likely to be inserted with navigation and that the chance of a signiicant medial breach was 7.6 times higher without navigation.786 Alternatively, CT imaging may be used to conirm accurate screw placement, although the systems currently available provide less detail than a typical CT scanner found in radiology suites does. All these image guidance techniques expose the patient and surgeon to increased radiation, which may have long-term effects.346,660,709 Other Methods of Assessing Screw Placement. Other methods to determine safe and accurate screw placement include EMG stimulation, which has produced reliable results and clear guidelines when lumbar pedicle screws are within the pedicle.137,427,690 The premise of this technique is that when the electrical current is passed through a completely intraosseous pedicle screw, it will not result in a triggered EMG peripheral response. With greater stimulus intensity, however, even a well-placed screw will trigger a peripheral response, so guidelines have been established based on the level of stimulation required to elicit a response: greater than 8 mA deines a screw completely within the pedicle; between 4 and 8 mA is intermediate, which means that the screw should be removed and the medial wall probed; and less than 4 mA indicates a strong likelihood of a pedicle wall defect. Although good success has been achieved in the lumbar spine, studies involving the thoracic spine have not been able to clearly deine threshold values for determining a safe screw.433,620,624 The technique of EMG stimulation for ascertaining thoracic pedicle screw placement is technician dependent and takes some experience to perform. It should serve only as an adjunct to thorough understanding of the pedicle anatomy, meticulous surgical technique, and good imaging. The improved radiographic correction seen with the use of thoracic pedicle screws has not been directly associated with improved clinical outcomes. Comparisons of thoracic pedicle screws and hook constructs or a hybrid construct (hooks proximally and screws distally) have demonstrated no difference in 2-year postoperative scores and little or no correlation between coronal plane correction in AIS and the SRS outcome instrument.158 The advantages of improved radiographic correction when using thoracic pedicle screws for the treatment of spinal deformity must be weighed against the risk and cost of these implants. In most series the incidence of the most feared complications—neurologic injury and major injury to soft tissue structures, including the great vessels—is very low (74 degrees) at the start of treatment showed the most signiicant loss of correction after brace discontinuance, with the result that there was little overall correction.90 This inding suggests that orthotic management is perhaps not indicated for a deformity of large magnitude without some previous correction of the deformity—by casting, for example. Although smaller deformities can be maintained at a smaller magnitude with orthotic treatment, greater deformities need greater initial correction to be stabilized, thus requiring a more aggressive treatment approach. Brace treatment is used relatively infrequently at our institution because of the generally benign larger magnitude of deformity at presentation, and the problem of brace it and compliance in an adolescent already with self-image deicit. For immature patients, the Milwaukee brace is used most frequently, regardless of the curve pattern, because we have found the use of a TLSO less effective.

CHAPTER 13 Kyphosis

Cast Treatment When passive correction is less than 40%, as determined from a hyperextension lateral radiograph over a bolster or on clinical examination, brace treatment is not likely to be effective. Antigravity or localizer casts can be applied in serial fashion to produce more correction of the kyphosis (Fig. 13-7).80,99 This treatment regimen, used extensively in

A

Europe, entails applying two or three casts (changed every 2 to 3 months) in an attempt to progressively correct the deformity. After the 6- to 9-month period of casting, the patient is treated with a Milwaukee or other type of retention brace to maintain the correction during the remainder of growth. With such a regimen, not only is the deformity improved by as much as 40%, but there also is less loss of correction. In a 2-year follow-up French study,71 the loss of

FIGURE 13-6 A and B, Milwaukee brace treatment of hyperkyphosis. The posterior pads can be progressively bent into more correction.

B

A

313

B

C

FIGURE 13-7 A, A 16-year-old boy with Scheuermann kyphosis measuring 75 degrees and signiicant cosmetic concern. B, After 6 months of serial Risser casting, the deformity was reduced to 48 degrees. C, At 18 years of age, the kyphosis measured 54 degrees. The patient wore a Milwaukee brace part time for 1 year after cast correction.

314

SECTION II Anatomic Disorders

correction averaged just 7 degrees, whereas in a 3-year follow-up series reported by Ponte and associates, only 4 degrees of correction was lost.80 The European experience with cast treatment has led to the following observations: (1) The long-term goal of controlling the deformity so that the curve ultimately ends up in a physiologic range (100 degrees).73 Only in such a patient would the choice of surgical approach (anterior and posterior versus posterior alone) be modiied or dictated by the preoperative pulmonary status.

Surgical Approach Patients younger than 16 years treated by posterior fusion for Scheuermann kyphosis can have a gradual postoperative improvement in kyphosis attributed to remodeling of the anterior vertebral wedging.31 The posterior-only approach originally was recommended for immature patients (

LOW GRADE 60

Type 6

Retroverted pelvis Unbalanced spine

C7

Balanced pelvis (Type 4)

C7

Balanced spine (Type 5)

C7

Unbalanced pelvis (Type 6)

FIGURE 14-1 Classiication according to the Spinal Deformity Study Group.99

330

SECTION II Anatomic Disorders

B

A

FIGURE 14-2 A, High dysplastic spondylolisthesis. The L5-S1 facet is congenitally dysplastic. Listhesis and kyphosis occur with facet subluxation. This patient was in neurologic crisis from severe listhesis, without a pars elongation or defect. B, When the L5 body is displaced well forward of the sacrum, it is projected on an anteroposterior radiograph as an upside-down Napoleon’s hat (arrowheads).

SS > 40°

PI > 45°

A

B

FIGURE 14-3 A, Primary sacral dome deformity. There is mild kyphosis and translation with normal posterior elements (note isthmic spondylolysis at L4-5). B, A high pelvic incidence (PI ) associated with a primary sacral dome deformity or pars defect may produce listhesis as a result of abnormal vertical shear (arrow) at L5-S1. SS, Sacral slope.

Isthmic Spondylolisthesis (Wiltse Type II) The isthmic type of spondylolisthesis (termed acquired traumatic in the Marchetti-Bartolozzi classiication) is a more common and benign form that rarely produces signiicant neurologic indings or gait disturbance (Fig. 14-4). Pars stress fracture, or spondylolysis, is fairly common, reported

to be 4.4% at 6 years of age and 6% at 18 years.51 A study of lumbar spine computed tomography (CT) scans in asymptomatic patients has noted rates in the general population of 5.7% and 3.1% of spondylolysis and spondylolisthesis, respectively.5 Spondylolysis is most prevalent at L5, accounting for 87% of all stress fractures, followed by lysis at L4 (10%) and L3 (3%).154 Both familial and racial

CHAPTER 14 Other Anatomic Disorders of the Spine

SS < 40°

PI < 45°

B

A

C

D

E

F

FIGURE 14-4 A, Isthmic spondylolysis beginning as a stress fracture of the pars. B, In patients with a lower pelvic incidence (PI) and sacral slope (SS), spondylolysis may occur as a result of extension (the nutcracker mechanism) on the L5 pars. C, Lateral radiograph in a 4-year-old child with back pain. There is a pars defect and 13% listhesis. D, Bone scan demonstrating unilateral hot lysis on the left. E, Single-photon emission computed tomography scan demonstrating same active lysis. F, Although orthotic management eliminated the symptoms, the listhesis increased to 29% over a period of 4 years. Monitoring was continued.

331

332

SECTION II Anatomic Disorders

predispositions toward isthmic spondylolisthesis have been observed.51,182,204,209 The incidence of isthmic spondylolisthesis seems to stabilize in adulthood, during which the degenerative type of spondylolisthesis predominates. Acquired pars defects appear to have mechanical causes. The pars region is the weakest area of the neural arch and is susceptible to fatigue fracture.32 Histologic analyses of fetal and stillborn vertebrae have conirmed trabecular and cortical irregularity of the lumbosacral pars interarticularis caused by ossiic nucleus irregularity.158 This histologic peculiarity may act as a stress riser in the lower lumbar vertebrae. Equally important may be anatomic parameters restricting excursion of the lumbosacral facets. In particular, spondylolytic specimens from the Hamann-Todd collection at the Cleveland Museum of Natural History have demonstrated that the pars of L5 is subject to increased contact stress during normal extension movement. This has been found in specimens in which the lumbar interfacet transverse distance does not increase appropriately between L4 and S1, thus limiting facet glide during the extension of L4-5 and L5-S1 and pinching the pars from above and below, producing a fatigue fracture.200 This supports the proposed “nutcracker” mechanism of spondylolysis and is seen in patients with a relatively low pelvic incidence and sacral slope (see Fig. 14-4, B and later, “Radiographic Findings”), who consequently have a relatively horizontal L5 disk.151 Pars defects have not been observed in newborns or nonambulatory patients, thus supporting the MarchettiBartolozzi contention that this form of spondylolisthesis is more accurately termed acquired. Pars lysis or elongation does not occur in primates that do not have an upright bipedal gait.208 The presence of lumbar lordosis, which is unique to humans, is thought to be necessary for spondylolisthesis to occur. Both lexion and extension forces have been implicated in the production of these stress fractures.40,49,200 The increased incidence of isthmic spondylolytic defects in athletes who perform repetitive lumbar hyperextension (e.g., gymnasts, football linemen, cricket bowlers) conirms this mechanism.39,85,171,192 Spondylolisthesis occurs more frequently if L5 has short transverse processes and is high riding relative to the iliac crest. This susceptibility to spondylolisthesis may occur because the L5 vertebral body is hypermobile when it is not anchored deeply in the pelvis, with strong ligaments attached to longer transverse processes.49,127,136 An acquired isthmic spondylolysis in a juvenile patient can progress to a listhesis as a result of shear forces during upright gait, as described for patients with the shear mechanism of spondylolysis.151 An anterior force on L5 is produced and increases as the spine is lexed, especially in patients with an increased PI and SS (see Fig. 14-3, B). The posterior muscle attachments that act on the laminae and spinous process hold this part of the neural arch in place and thus tend to separate or distract the spondylolysis further. With a strong anterior delection force, a slip between the sacral apophysis and end-plate may also occur and allow anterior translation and rotation of the slipping vertebra.160 Thus, an acquired isthmic spondylolysis in a growing child can progress to a signiicant spondylolisthesis, even in the absence of congenital dysplasia of the lumbosacral facets.

Other Types of Spondylolisthesis Degenerative spondylolisthesis, which occurs in adults, will not be discussed in this chapter. Similarly, traumatic spondylolisthesis, a rare condition resulting from signiicant spinal trauma, is more appropriately discussed under the management of spinal injuries. Pathologic spondylolisthesis is treated in the same fashion as nonpathologic spondylolisthesis of the same grade and severity or in conjunction with a global thoracolumbar deformity associated with a syndrome or skeletal dysplasia.115,123 Treatment must take into account that the underlying bone pathology or abnormal connective tissue may make pseudarthrosis more likely and treatment failure more frequent.

Clinical Features The age at onset is probably the most important determinant of symptoms and the need for treatment. The more severe dysplastic types usually present at an earlier age because of greater instability of the lumbosacral junction, producing neurologic symptoms. Children may not have pain but demonstrate deformity and gait abnormalities from lumbosacral instability as the only neurologic signs.86,128 Spondylolysis is generally manifested as low back pain only. This is not surprising considering that the lysis produced by a stress fracture in, for example, an adolescent gymnast produces no slippage and hence no neurologic risk. Pain may radiate to the buttocks and posterior of the thighs from mechanical instability, and it is usually aggravated by lexion and extension activities. Mechanical low back pain symptoms are always a cause for suspicion in a child or adolescent and mandate radiography, especially in a susceptible athlete or dancer. Physical examination may actually be normal in patients with spondylolysis or a low-grade (45 years) have not found predictive value in the age, percentage of slippage, lumbar index (lordosis), or slip angle at initial evaluation.8,53,163 Only Seitsalo and co-workers have found prognostic value in the initial percentage of slippage.170 The adolescent growth spurt continues to be a period of interest because signiicant progression of translation or kyphotic deformity is uncommon after maturity in a patient with mild deformity ( 20 degrees) is also present. The L5 body will appear to be falling off the anterior edge of the sacrum, with a trapezoidal deformity of L5 and rounding off of the sacrum indicating chronicity. Spondyloptosis, the end stage of the process, exists when the L5 body lies in the front of the sacrum and below a horizontal line from the top of the sacral dome (Fig. 14-16). More importantly, however, is the determination of the spinopelvic parameters to differentiate between whether

CHAPTER 14 Other Anatomic Disorders of the Spine

A

343

B

FIGURE 14-14 A, Ferguson view L5-S1, 1 year following L5-S1 instrumentation and posterolateral fusion for symptomatic spondylolisthesis (low grade). Unilateral fusion on the left has not fully relieved the patient’s pain. No fusion between L5 and the sacrum can be seen on the right, and lysis around the S1 screw indicates implant loosening and pseudarthrosis. B, Radiographic appearance in an 18-year-old man being reevaluated for new onset of back pain 3 years after successful L5-S1 fusion for low-grade spondylolisthesis. An L4 stress fracture can be seen above the fusion mass (arrow).

A

B

FIGURE 14-15 A, Follow-up of the patient in Figure 14-8, age 14. No treatment was given. Because of slip progression, surgery was recommended. B, The slip was stabilized by transsacral ixation after partial postural reduction. At 2 years postoperatively, she continued a high level of activity.

the pelvis is balanced or retroverted (unbalanced) and whether the spine is balanced or unbalanced (positive C7 plumbline anterior to the femoral heads; see Figs. 14-1 and 14-10).99,117 Based on the outcome of reduction for highgrade slips, the importance of these distinctions in spinopelvic parameters is now accepted, with evidence to support reduction techniques for cases with a retroverted (unbalanced) pelvis featuring low SS and high PT, along with the PI more than 60 degrees or an L5 incidence more than 45 degrees.99,102,152

The need for reduction to achieve solid fusion, neurologic stabilization and resolution, and prevention of later progression or recurrence has not been conirmed to date because of a lack of high-level evidence studies and the inding that there has so far been no demonstrable difference in clinical outcomes of patients treated in situ versus with reduction.§

§

References 18, 43, 80, 122, 147, 148, 174, 193.

344

SECTION II Anatomic Disorders

A

D

B

E

C

F

FIGURE 14-16 A, Lateral radiograph of grade V spondylolisthesis (spondyloptosis). B, The patient was unable to stand with the right knee extended because of severe right hamstring spasm. Note the drop of the pelvis on the right. C, Marked olisthetic scoliosis and limitation of forward bending preoperatively. D, She underwent in situ posterolateral fusion. Within 6 months, symptoms were dramatically improved. At 12 years postoperatively, her fusion was solid. Note the improved slip angle occurring spontaneously with fusion in situ only. E and F, Excellent mobility 12 years postoperatively. The patient is asymptomatic.

However, the retrospective multicenter study of Labelle and associates102 demonstrating the restoration of sacropelvic balance following repositioning (reduction) of L5, and indirectly improving the outcome by this restoration because of the better quality of life for balanced patients, may now change attitudes toward the value of at least partial reduction. Lumbosacral kyphosis, the key deformity, can be corrected by a variety of means, from traction and corrective casting to posterior instrumented reductions with pedicle screw instrumentation or the use of sublaminar wiring (Video 14-1).‖ Proponents of reduction have maintained

‖

References 3, 15, 17, 18, 24, 38, 41, 43, 69, 79, 108, 121, 125, 126, 155, 165, 168, 174.

that the incidence of pseudarthrosis and slip progression is decreased by biomechanical restoration of lumbosacral alignment and that reduction may produce orthopaedic decompression of stretched nerve roots and dura.12,43,44,130,145 Also, improved sagittal plane balance and reduction in lumbar hyperlordosis are achieved if the reduction is maintained.19,100,102 A selective approach to surgical reduction based on the concept of spinopelvic balance discussed earlier has now been suggested.78,99,117 Retrospective data have suggested that reduction of the unbalanced pelvis leads to clinically signiicant improvements in SS, PT, and L5 incidence angle (slip angle) and corresponding improvement in the normal spine sagittal proile. On the other hand, reduction of the preoperatively balanced pelvis yields relatively no change in these parameters and therefore theoretically provides little

CHAPTER 14 Other Anatomic Disorders of the Spine

345

Table 14-2 Recommended Treatment for Spondylolisthesis

Type*

Neurologic Signs Present?

Treatment Initial

Recurrence or Progression

No

↓ Activity, NSAID, TLSO, SSE

PLF in situ or repair

5—retroverted pelvis, balanced spine 6—retroverted pelvis, unbalanced spine

No Yes No Yes

Same as lysis Same as lysis Consider PLF in situ ± IF Decompress + PLF in situ + IF Consider PLF in situ + IF ± PR ± L5-S1 IF PLF + IF + PR + L5-S1 IF Same as type 4 + decompress Same as type 5 Same as type 5 + decompress

PLF in situ PLF in situ ± IF grade 2 PLF + IF + PR + L5-S1 IF

4—balanced pelvis

No No No Yes No

Lysis Low grade 1 (nutcracker) 2 3 (shear)

PLF ± IF ± PR ± L5-S1 IF

IF, Internal ixation; L5-S1 IF, TLIF or transsacral ixation; NSAID, nonsteroidal antiinlammatory drug; PLF, posterolateral fusion; PR, partial reduction; SSE, spine stabilization exercises; TLSO, thoracolumbosacral orthosis. *Based on Spinal Deformity Study Group classiication, as presented by Labelle and co-workers.100

beneit.99,102 Based on these indings, a tentative treatment algorithm for the surgical treatment of spondylolisthesis has been proposed (Table 14-2). With the exception of complete spondyloptosis, all reductions are partial—again, primarily out of respect for the risk of neurologic complication—with emphasis on the correction of the slip angle and an improved L5 incidence (see Figs. 14-9 and 14-10, B).

Surgical Methods: High-Grade Spondylolisthesis In Situ Fusion Versus Reduction. Posterolateral in situ fusion without decompression remains a valid option even for the most severe slips, particularly as an index procedure (see Fig. 14-16). Numerous reports have documented satisfactory results from in situ L4-S1 fusion with respect to relieving symptoms and restoring normal activity, and this has been achieved without signiicant morbidity, thus discounting some of the proposed beneits of reduction.¶ Gait abnormalities, including the lexed hip–lexed knee posture, resolve after surgical stabilization.172 As noted, proponents of reduction emphasize the restoration of global sagittal plane alignment.102,122 The increased risk for pseudarthrosis or progressive slip, the other frequently cited drawbacks of in situ treatment, may also be ameliorated by reduction. As with lower grade slips, pseudarthrosis by itself does not condemn the patient to a poor outcome, but a poor outcome is more likely with nonunion.106,110,131,138,141 The incidence of pseudarthrosis is variable (0% to 45%).# Similarly, progressive L5 translation and lumbosacral kyphosis have been mentioned as problems after in situ fusion, even though reports of nonprogression are generally reassuring.52,70,88,146,148 Radiographic slip progression caused by presumed bending of a fusion mass occurs without clinical outcome suffering.16,64,107,125,170,173 To resolve this debate and achieve fusion with an in situ technique—circumferential in situ fusion—may produce the best result with the least morbidity by achieving a 100% fusion rate, eliminating progression via anterior column

support and avoiding neurologic risk by acute reduction.73,190 A single Finnish institution has provided the intermediateterm follow-up of operatively treated high-grade spondylolisthesis patients. At 17-year follow-up, circumferential in situ fusion provided a lower rate of kyphosis progression and better Scoliosis Research Society (SRS) and Oswestry disability scores compared with posterolateral or anterior in situ fusion alone.73,105 A second study of overlapping patient populations comparing circumferential in situ fusion with circumferential fusion after reduction actually demonstrated improved disability scores in the in situ fusion group despite a modest improvement in slip angle in the reduction group.147 Thus, the need for reduction of high-grade spondylolisthesis remains unproven because the performance of reduction must result in a higher fusion rate and elimination of slip progression to justify the higher morbidity and complication rates.148 Partial reduction with circumferential fusion is a compromise procedure to achieve solid fusion without neural deicit and to restore sagittal balance.18,108,152 It is clear that reduction is associated with increased complications, primarily neurologic. A review of 4 years’ experience of the surgical treatment for spondylolisthesis from 2004 to 2008 by SRS members demonstrated a ivefold increase in the rate of neurologic injury when reduction was undertaken, with those undergoing reduction reporting a 10% neurologic injury rate versus 2.1% of those fused in situ.56 This was in agreement with previous reports that cited rates of neurologic deicits of from 0% to 27%.*a To assess reducibility of the lumbosacral kyphosis and degree of translation preoperatively, hyperextension radiographs obtained with the patient positioned over a bolster are useful. If satisfactory reduction of the slip angle is achieved by simple hyperextension, an in situ fusion can be performed, followed by casting or some form of internal ixation to maintain this postural reduction.24,64,121,165 A cast may be applied several days after in situ surgery and is best done with the patient awake so that neurologic function can be monitored during reduction maneuvers. Reduction

¶

References 33, 52, 64, 70, 74, 84, 88, 138, 144, 170, 206. References 16, 52, 64, 70, 88, 110, 130, 131, 144, 148.

#

*aReferences 16, 38, 73, 111, 133, 150, 155, 180.

346

SECTION II Anatomic Disorders

A

B

D

C

FIGURE 14-17 Traction-reduction casting for spondylolisthesis. A, The patient is placed in cervical-pelvic traction on the Risser table, and the hips are allowed to hyperextend. B, A sling is placed under the sacrum to translate it forward. The direction of pull is toward the feet to make the anterior translation force perpendicular to the sacrum. Additional hyperextension can be achieved by dropping the leg supports further as the cast is applied and the sacrum elevated. C, View from the foot of the table. D, Diagram showing reduction forces.

includes hyperextension of the lower extremities and pelvis combined with anterior translation of the sacrum, usually by a posteriorly placed, anteriorly directed force (e.g., pelvic slings, pressure localizers; Fig. 14-17).121,165 Such cast application requires an experienced cast application team with an appropriate Risser table and the patient must be prepared for a period of up to 9 months—4 months recumbent in a double-pantaloon cast—to maintain the reduction by such external positioning.41,64,165 A 20% to 45% pseudarthrosis rate for fusion has been reported, and progression of listhesis despite solid fusion occurs in up to 26% of patients.†a Postural reduction of the spondylolisthesis, internally ixed by instrumentation, is intended to improve these results, with the added beneit of restoration of trunk height and sagittal balance, along with a higher rate of fusion as a result of the improvement in alignment. The beneit to the patient in not being immobilized in a pantaloon spica cast for several months is also self-evident.

Historical methods of preoperative reduction (halo femoral traction, serial casting) have been supplanted by postural (hyperextension) or intraoperative methods, and are now stabilized by internal ixation in some form.17,41,121,165 Anterior fusion, notwithstanding its European proponents, carries its own set of complications as a result of the transperitoneal approach, including hemorrhage from proximity of the great vessels and, in the male, retrograde ejaculation.165,190 Posterior pedicle screw ixation permits reducing the slip angle by direct extension of the L5-S1 segment, as well as in translating the listhetic segment posteriorly (Fig. 14-18); however, the problem is that up to a 65% incidence of neurologic complications and a 30% incidence of implant failure have also been reported.‡a Complete reduction, as opposed to partial, has been shown to increase tension on the L5 roots, making partial reduction more attractive, especially if decompression is carried out prior to reduction.12,18,108, 145, 159 Acute

†a

‡a

References 16, 17, 107, 125, 131, 170, 173.

References 3, 15, 18, 38, 44, 56, 69, 79, 104, 126, 155, 159, 174.

CHAPTER 14 Other Anatomic Disorders of the Spine

A

B

347

C

D FIGURE 14-18 A to C,Instrumented reduction of lumbosacral kyphosis using distraction, extension, and posterior translation forces creates a deiciency of the anterior column. D, Interbody support with compression to secure the cage or graft is necessary to prevent L5-S1 disk collapse.

reduction of the slip angle produces an anterior column deiciency at L5-S1 by virtue of distraction and lordosis (see Fig. 14-18). Adding anterior column support is associated with improved implant performance, stability, and correction.108,130,131 Some authors have suggested that with the avoidance of a decompression and by retaining the posterior elements, they have not found the need for an anterior graft, perhaps because of the retained posterior bone for fusion.159 However, for most authors, the addition of anterior fusion by a ibular dowel, interdisk graft or cage, or addition of posterior interbody fusion is the solution to loss of ixation with recurrence.§a The indications for instrumented reduction of highgrade spondylolisthesis (and spondyloptosis) are evolving. When successfully accomplished without neurologic complications, instrumented reduction improves global sagittal §a

References 13, 15, 41, 69, 79, 104, 108, 121, 131, 155, 175, 176.

alignment, provides decompression of the dural sac and nerve roots, and allows early mobilization of the patient. It should be supplemented with anterior support to prevent loss of sacral ixation and recurrence of kyphosis and achieve a high rate of fusion. Thus, instrumented reduction may require two operative procedures, anterior and posterior, and if anterior support fusion is attempted by a posterior interbody technique, transcanal surgery is necessary, with retraction of nerve roots already stretched by the deformity. The technical expertise needed to perform the multiple intraoperative steps in instrumented reduction safely is probably the most important aspect in achieving a result that exceeds that of an in situ treatment, with or without instrumentation. However, as noted, it is still generally unproven that the clinical outcome of an instrumented reduction exceeds that of a successful in situ fusion for most, if not all, cases of high-grade listhesis.147,193

348

SECTION II Anatomic Disorders

Alternative Instrumented Reduction Techniques Other reduction options for the treatment of high-grade spondylolisthesis and spondyloptosis exist; these include postural reduction with in situ ixation via screws or a ibular graft from the sacrum to L5 through a posterior approach,1,12,13,150,176 L5 vertebrectomy with posterior L4-S1 ixation-fusion, reduction via posterior instrumentation of L4-S1 followed by later removal of L4 instrumentation to preserve motion at L4-5, and even intrasacral forms of ixation.58,59,83,155 These techniques involve, in the irst method, postural reduction (usually partial) of the slip angle and in situ ixation, with or without decompressive sacroplasty, to provide neurologic safety and in the second method, reduction only after total decompression by complete removal of the L5 vertebra to provide anatomic space for complete realignment. The neurologic risk and technical dificulty of attempted instrumented reduction for spondyloptosis inspired Gaines to develop the two-stage L5 vertebrectomy and posterior L4-S1 ixation as the solution to this challenging deformity.58,59 In a irst-stage procedure, the L5 vertebra is excised via a transperitoneal approach, thus making acute reduction of L4 on S1 possible. The posterior procedure includes decompression by removal of the L4 and L5 posterior elements, followed by L4-S1 pedicle ixation and posterolateral grafting. In Gaines’ series, all patients had anatomic reduction, with resolution of gait disturbance and back and leg pain. However, instrumentation failure, permanent L5 root deicits, and retrograde ejaculation were noted.58 In view of the neurologic safety and fusion success of one-stage transsacral ixation, the indication for the more extensive Gaines procedure to deal with high-grade spondylolisthesis or spondyloptosis deformity remains elusive.13 The Bohlman posterior decompression with in situ ixation is probably best suited to patients with preoperative motor or cauda equina deicit and 100% or greater listhesis— in other words, patients who arguably have the highest neurologic risk with reduction because the deicit already exists.13,176 Decompression by sacroplasty (Fig. 14-19), indicated by the presence of bowel or bladder deicit, is followed by ibular dowel grafting from the sacral pedicle or body to the L5 body situated directly anteriorly (Fig. 14-20). Transsacral ixation can be augmented by pedicle screw ixation, thereby achieving bony arthrodesis and internal ixation in situ after postural reduction (see Fig. 14-20, D).1,12 With this approach, all patients have been reported to recover neurologic function, and 90% achieved solid fusion.12,150,176 Because the neural elements are adequately decompressed by sacroplasty, no additional reduction is necessary, and in situ arthrodesis is achieved by combining posterolateral fusion with L5-S1 ibular fusion. Postural reduction by pelvic hyperextension and transsacral ixation in patients without neural deicit (other than hamstring or sphincter spasm) has produced sagittal plane realignment with safety and solid fusion in a one-stage procedure (Fig. 14-21).1,12,150 Prone hyperextension under anesthesia, with care taken to support the abdomen by positioning on chest rolls only and elevation of the lower extremities to position L5-S1 in extension, achieves the partial reduction. A posterior Wiltse approach (see Fig. 14-12) provides adequate access to the L4 pedicles and

FIGURE 14-19 Removal of the posterosuperior dome of the sacrum to decompress the dural sac and nerve roots (sacroplasty). A high-speed burr from each side is useful once retraction of the dural sac and root exposes the prominent sacral dome.

sacrum, and the L5-S1 segment is transixed in the reduced position by S1 pedicle screws directed ventromedially to engage the L5 body anterior to the sacrum. A Bohlman dowel can be added by retracting the dural sac medially once the transsacral screws are in place. Additional anterior alar exposure, lateral to the L5-S1 facet, provides a fusion surface for the anteriorly placed iliac crest graft between the L5 transverse process and ala. A lap of alar bone can be elevated and turned ventrally and cephalad to engage the L5 transverse process also. The instrumentation is then completed by connecting bilateral L4 pedicle screws to the S1 transsacral screws with short rods, and the construct is then compressed (see Figs. 14-15 and 14-21). The method thus achieves partial reduction, correction of the lumbosacral kyphosis, and near-circumferential arthrodesis by virtue of the intervertebral, posterolateral, and even anterolateral alar grafting. There is minimal neurologic risk because the only reduction attempted is passive and postural. If the listhesis is rigid and the kyphosis not partially reducible—an unlikely occurrence in the adolescent population—sacroplasty can be performed to remove obstruction to reduction, as described in Bohlman’s original method.13,138,176 Additional instrumentation to supplement these techniques and/or replace the ibular dowel rod have recently been introduced. In an effort to avoid the morbidity of a ibular autograft, several authors have described custom screws, including the use of two hollow modular anchorages (HMAs), which can be illed with cancellous bone graft to aid in fusion. These are combined with standard L4-S1 instrumentation posteriorly.103 Another innovation includes cannulated, custom, 10-mm compression screws to provide compression between the sacrum and L5, which are introduced after decompression of the posterior elements of

CHAPTER 14 Other Anatomic Disorders of the Spine

349

L5-S2 and dissection of the sacral nerve roots. This can be combined with a sacral dome resection and placement of bone graft into the L5-S1 interbody space, which is then compressed with a lag screw head for the compression screw to create circumferential fusion.14

Lumbar Disk Herniation

A

A herniated lumbar disk must be considered in the differential diagnosis of low back pain in children and adolescents, and especially if leg pain dominates the clinical picture. However common this entity may be in adults, disk protrusion or herniation is an infrequent but nonetheless possible cause of signiicant morbidity in the pediatric and adolescent populations. Thus, in the evaluation of a pediatric patient with low back pain and unremarkable plain radiographic studies of the lumbar spine, the possibility of a herniated lumbar disk must be considered.

B

L4–ala grafts

Incidence Dowel

C

Although the actual incidence of lumbar disk herniation in the pediatric age group is unknown, a 1% incidence in children under 18 has been reported.42,201 A herniated lumbar disk was irst described in a 12-year-old child by Wahren in 1945.198 Increasing physician awareness and the widespread use of MRI may lead to a higher incidence being reported. There does not appear to be a gender predilection for herniated disks in children. A number of investigators have reported a slight preponderance in boys, thought to be caused by delayed maturity, which exposes the immature spine to abnormal stress for a longer period.28,35,46,47,71

D

FIGURE 14-20 A, Laminectomy and sacroplasty to decompress the dura. B and C, Spondylolisthesis is stabilized with a ibula dowel placed from the sacral body (medial to the S1 pedicle) into the center of the L5 body immediately ventrally. An additional L4-ala bone graft is also added (C). D, A pedicle screw construct to augment the dowel is created by placing bilateral screws from the S1 pedicle into the L5 body, parallel to the dowel, and connecting them to L4 pedicle screws.

A

Causes Lumbar disk herniation in children and adolescents has been attributed primarily to trauma, especially in patients with predisposing congenital spinal stenosis or an abnormally

B

C

FIGURE 14-21 A, An 11-year-old girl with severe hamstring tightness and an awkward gait, worsening for 6 months. There is a high dysplastic type 5 (Spinal Deformity Study Group) spondylolisthesis with a 30-degree slip angle and isthmic lysis producing no neurologic deicit other than the gait disturbance. B, Three years after postural reduction and transsacral ixation with posterolateral and L5-alar grafting. The slip angle is reduced to less than 8 degrees. C, Ferguson view, 3 years postoperatively. Solid bilateral L4-S1 fusion is apparent. The patient is asymptomatic.

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SECTION II Anatomic Disorders

narrow lumbar canal. Up to 70% of patients with herniated disks report antecedent trauma, either an acute event that is well remembered or cumulative repetitive trauma exacerbated by a less traumatic event.28,35,142 Certain competitive athletic events associated with back injuries—for example, football, gymnastics, and cheerleading—are the same types of activities that predispose a patient to spondylolysis and are frequently reported by patients with herniated disks. The association of congenital anomalies of the lumbar spine with disk herniation is also well known.35,46,98,139 Sacralization of L5 or lumbarization of S1 is commonly described, although these anomalies are so ubiquitous in the population that their relationship to lumbar disk herniation may be coincidental. More important is anteroposterior canal narrowing, which can often be detected on the initial lateral lumbar spine radiograph and is conirmed with CT (Fig. 14-22).46 The smaller canal leaves less room available for nerve roots after disk herniation and therefore increases the likelihood of symptoms from an intruding soft herniation. A familial predisposition to disk herniation has been suggested.134,195,211 An increased prevalence of disk herniation in irst-degree relatives has been reported, and as many as

A

Clinical Features Pediatric disk herniation differs from the condition in adults primarily because symptoms are intermittent and without dramatic neurologic indings. The diagnosis is frequently delayed, by an average of 10 months, because the initial complaint, back pain, is often not accompanied by sciatica, and thus when plain radiographs are found to be normal, no further investigation is undertaken.177 Increasing and nonresolving back pain with sciatica is an indication for MRI. In addition, the teenager will describe back stiffness as a result of spasm and splinting by the paraspinous muscles, which may be noted as an abnormal posture or limp. The most revealing symptom in the presciatic stage is the presence of increased back pain with the Valsalva maneuver (e.g., straining, coughing) or any type of lexion maneuver. Another typical inding in an adolescent with a herniated disk is the relative absence of neurologic signs. Motor

C

B

D

92% of adolescents with disk herniation have a history of low-back pain or sciatica. Although genetic and environmental factors must be considered together, a familial predisposition to disk disease is likely among adolescents with disk herniation.

E

FIGURE 14-22 A and B, Initial plain radiographs of an obese 12-year-old girl with stiff, lexed scoliosis and severe back pain. The congenitally stenotic spinal canal is suggested by the very short pedicles. C, MRI scan showing central disk protrusion. The canal is severely compromised at L4-5. D, Lateral MRI scan showing disk herniation at L5-S1, as well as at L4-5. E, CT myelogram showing severe canal encroachment with short pedicles at L4-S1. This patient was treated by two-level diskectomy because of her severe pain and postural disturbance.

CHAPTER 14 Other Anatomic Disorders of the Spine

from the originating disk space. The need to treat congenital spinal stenosis can also be determined preoperatively.60 CT myelography can similarly be used to visualize a herniated disk. The reported advantage of CT lies in the evaluation of bony lesions, speciically a slipped vertebral apophysis, which is often associated with central disk herniation. MRI has been reported to be inferior to CT in the diagnosis of slipped vertebral apophysis, which would have therapeutic implications in that the preoperative diagnosis of slipped vertebral apophysis is invaluable in planning the surgical approach.47,48 The obvious disadvantage of CT myelography is that it is an invasive study that requires radiation. Its routine use is probably unnecessary unless MRI demonstrates an unusually large central herniation that has migrated cephalic or caudal to the posterior aspect of the adjacent vertebra, suggesting a possible apophyseal avulsion, or when MRI is severely artifactually degraded because of the presence of stainless steel implants (see Fig. 14-23).4,34 As in adults, the L4-5 and L5-S1 disks account for approximately 95% of all herniated disks in children and adolescents.‖a Because physical examination is unreliable in identifying the level of herniation in the pediatric population, the most important use of MRI (or CT myelography) is to locate the precise anatomic level of herniation. In addition, if MRI of the lower lumbar canal fails to reveal a herniated disk or other lesion, evaluation of the nerve roots and conus medullaris by MRI becomes mandatory to rule out other intraspinal neoplasms as the source of the back pain.

weakness or bowel and bladder dysfunction are rare and except for a positive straight-leg raising test, there may be essentially no neurologic indings. On the other hand, dysesthesia or motor weakness not necessarily conforming to the level of disk herniation has been noted in 41% and 21% of patients, respectively.25 Relex abnormalities are uncommon, with less than 50% of patients having an absent or decreased deep tendon relex. Postural changes may also include an irritative or olisthetic type of scoliosis (see Fig. 14-22, A), similar to that seen in a spondylolytic crisis, which again may be the only sign of a neurologic problem. The lack of neurologic indings is attributed to the increased canal size and lexibility of the adolescent spine, which allow the dura to move away and accommodate intruding disk material without affecting the nerve roots.61,139 Because of accommodation, there may be a discrepancy between the level of herniation and subsequent neurologic indings, if any.28,46 Radiographic evaluation is mandatory to identify the level of herniation correctly.

Radiographic Findings Plain radiographs of the lumbar spine are an important screening evaluation of any patient with low back pain. Standing AP and lateral ilms will help eliminate certain inlammatory or tumorlike conditions, and oblique radiographs will rule out spondylolysis. Typically, plain radiographs show loss of lumbar lordosis on the lateral ilm. Other structural abnormalities may be present, including spina biida occulta, sacralization of L5 or lumbarization of S1, and the presence of six lumbar vertebrae.35,46,139 Disk space narrowing, with or without lipping of the vertebral margins or small avulsion fragments posterior to a vertebral body, may indicate chronicity or the presence of a slipped lumbar apophysis. Spinal canal narrowing may also be suspected from lateral radiographs (see Fig. 14-22). In at least 50% of patients with a herniated disk, however, plain radiographs will be unremarkable. MRI is the procedure of choice to diagnose disk herniation.34 This study not only demonstrates the herniated disk but also can be used to evaluate nerve roots and accurately shows stenosis and narrowing of the disk space (Fig. 14-23). Free disk fragments can be identiied in the canal as separate

A

B

351

Treatment Treatment of herniated lumbar disks in children and adolescents is not unlike that for adults in that the initial treatment should be nonoperative. Exceptions are patients with a progressive, well-documented neurologic deicit and those with a massive central herniation producing signiicant neurologic compromise, such as bowel and bladder dysfunction. Nonoperative management has traditionally included rest, muscle relaxants and analgesics, and heat and physical ‖a

C

References 28, 35, 46, 61, 139, 142, 156.

D

FIGURE 14-23 A, Radiograph in a 17-year-old girl who had undergone posterior spinal fusion of T5-L3 for double major scoliosis 3 years previously. She complained of sciatica and severe back pain. B and C, Myelography was performed because of the presence of stainless steel implants and revealed a left-sided L4-5 disk herniation (white arrows in B). D, Axial CT section showing a left-sided disk at L4-5 (arrow). Because the patient had already undergone a long spinal fusion to L3, epidural steroids were used in an attempt to avoid surgical treatment at L4-5.

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SECTION II Anatomic Disorders

therapy. Although bed rest, with or without traction, has been a traditional modality for adults, there is little objective evidence that bed rest is actually required to achieve the decreased activity that is an essential part of nonoperative management. Relative immobilization of the lumbar spine can be achieved with various orthotic devices, which are better accepted by the patient and parents because they allow the patient at least to attend school and take care of normal daily activities. There is little enthusiasm for the traditional complete bed rest regimen, and for patients who are in severe pain we usually proceed to some type of corset or lumbar orthosis to immobilize the lumbar spine. The use of other modalities (e.g., ultrasound, transcutaneous nerve stimulators) under the supervision of a physical therapist may be valuable; however, there is little evidence that such treatment signiicantly improves the clinical course. The use of epidural steroids is controversial. Prospective studies of epidural steroid injections for acute disk herniation or radicular pain have not demonstrated a long-term beneit in adults.29,30,149 Although epidural steroids combined with local anesthetic can provide acute relief of pain, there is no evidence that sciatica, which is generally predictive of an extruded disk fragment in the absence of back pain, is improved by epidural steroids. Because back pain, muscle spasm, and sciatica can be relieved with other nonoperative methods already mentioned, epidural steroids appear to have a limited role in the management of herniated lumbar disks in adolescents. Possible indications for their use would be as a temporizing modality in a patient with acute severe back pain and as a symptomatic modality in patients for whom surgery is not a treatment option or is extremely unattractive.25 An example of the latter might be a patient who has previously undergone spinal fusion to correct a deformity of the low lumbar spine and in whom a disk herniates at the next unfused level (see Fig. 14-23). In these patients, the risk of producing additional degenerative changes after surgical treatment of a disk below a long fusion is high, and thus prolonged nonoperative treatment in an effort to avoid any surgery would be appropriate. The natural history of disk herniation with sciatica is generally good in that spontaneous resolution of symptoms without intervention can be expected over time.202 At least 50% of young patients do well with nonoperative treatment on long-term follow-up.28,211 Most patients can return to sports competition, although some will have recurrent back or leg pain. The challenge for the treating physician is to determine as quickly as possible at which point nonoperative treatment is unsuccessful to avoid unnecessary delay in surgical treatment. Indications for surgery include failure of nonoperative management and persistence of symptoms after an appropriate period of nonoperative management and rarely when neurologic deicit is progressive. The dificulty with the decision in the former situation is that given enough time, symptoms of sciatica in particular will resolve. On the other hand, the uniformly good early results after disk excision make it inappropriate to withhold surgery in the presence of severe and persistent symptoms. Although no deinitive formula for operative intervention is possible, a patient who is clearly incapacitated or disabled by back or leg pain and who is not improving with a regimen of rest, immobilization, analgesics and muscle relaxants, and other physical

therapy modalities should be considered a candidate for surgery within 1 month of the onset of treatment. Any patient who appears to have deteriorating neurologic indings should undergo expedient disk excision. The operative technique for open diskectomy in young patients does not differ from that used in adults.77,179 Patients should be placed in the knee-chest position to increase access to the lumbar interspaces. Accurate placement of the incision is important because minimizing exposure enhances early recovery and rehabilitation. The appropriate interspace, based on preoperative imaging studies, should be identiied with localizing radiographs. Aided by a lamina spreader, the ligamentum lavum is excised, and enough lamina is removed to allow exposure of the lateral aspect of the nerve root. It is usually unnecessary to resect bone from the intervertebral facet joint and if the patient has a central herniation, bilateral laminotomies should be performed to remove protruding disk material from both sides of the canal adequately. Inasmuch as adolescents have no preexisting disk degeneration, only the fragments protruding into the canal need to be excised because the residual tissue in the disk space is normal. If the protruding disk material is attached in any way to the posterior longitudinal ligament or the cartilaginous endplate, this should be carefully incised to remove the protruding material. Lateral exposure and foraminal decompression are necessary only if the nerve root is not freely mobile and without tension after evacuation of disk fragments from the canal. Assuming that the intervertebral joints have not been violated, there is no need to combine spinal fusion at the level of diskectomy. Patients can be mobilized rapidly on the day after surgery, with back supports for symptomatic relief only. Early range-of-motion strengthening exercises are recommended, and patients should be seen by rehabilitation personnel as indicated. The results of surgery are generally gratifying in that sciatic pain is reduced or vanishes almost immediately, and back pain resolves quickly. Relex abnormalities and straightleg raising tension may require additional time to resolve. The long-term results of disk excision are unfortunately not as good as the immediate short-term results in that varying residual back discomfort and sometimes leg pain can return in a quarter to a third of patients.46,98,156,177 Of patients with good or excellent results, 15% to 28% initially may need repeat surgery.142,177 Transient symptoms may return in 29% of patients monitored for up to 10 years.139 From these longer term studies, therefore, the prospect for relief of symptoms after diskectomy is somewhat guarded, despite the initial results being gratifying. Thus, vigorous nonoperative treatment before proceeding to operative management continues to be the initial recommendation.28,35,139,187 In contrast, many patients who undergo surgery have had symptoms for longer than 5 months before surgery, and this is clearly too long to wait before operative intervention. The key to managing herniated lumbar disks in adolescents, as in adults, is to proceed to operative management relatively quickly once it has been recognized that the patient is not improving with maximal nonoperative therapy because the results of surgical treatment, in the short and long terms, are much improved the shorter the duration of symptoms before surgery.

CHAPTER 14 Other Anatomic Disorders of the Spine

Slipped Vertebral Apophysis Avulsion of a bony fragment from the posterior caudal or cephalic rim of the vertebral body into the spinal canal produces what amounts to a large central disk herniation.26,48,67,178 First reported in 1954, the signs and symptoms are essentially the same as those of a herniated lumbar disk, although the entity is probably much rarer.4 Instead of herniation of disk material through the annulus and posterior longitudinal ligament into the canal, this lesion involves separation of the partially ossiied rim of the posterior vertebral apophysis at its osteocartilaginous junction, with varying amounts of posterior displacement of the apophysis and contiguous disk. As with herniated nucleus pulposus, trauma, as a single event or as a cumulative process in sports such as weightlifting, gymnastics, or wrestling, is accepted as the cause of fracture of the osteocartilaginous junction.26,67,178 Extreme lexion of the spine combined with rotation appears to increase the risk for ring apophyseal avulsion.82,93,112,114,164 The central herniated disk adjacent to the superior or inferior rim of the vertebra whose ring has been avulsed protrudes posteriorly, whereas the avulsed rim fragment stays attached to the posterior vertebral body by a periosteal sleeve. Typically, the posterior longitudinal ligament remains intact. Most apophyseal avulsions in adolescents involve the L4-5 or L5-S1 levels, with the most frequent avulsions originating from the inferior rim of L4 or the superior rim of the S1 body.4,48,164,178 Lumbar apophyseal avulsions occur predominantly in males, again explained by the fact that boys reach skeletal maturity at a later age than girls and therefore have a longer period of exposure to trauma before maturity. Because of the activities associated with this lesion (e.g., weightlifting, wrestling) there appears to be an increased risk of the lumbar lexion placing repetitive stress on the lower lumbar spine.

Clinical Features Patients with a slipped vertebral apophysis have essentially the same symptoms as those with herniated lumbar disks. The most prominent complaint is intermittent but progressive low back pain, with or without sciatica; others include paraspinal muscle spasm and limitation of back motion and straight-leg raising, but minimal or no neurologic indings. Patients describe back stiffness and have a peculiar gait because of the abnormally decreased lumbar motion. Pain is exacerbated by activities such as lifting or straining when coughing or sneezing. Sciatica may or may not be present initially, but may develop later during the course of the disorder. Limited straight-leg raising is common and is usually bilateral because of the central nature of the herniation. Postural scoliosis does not tend to be as prominent, as with herniated nucleus pulposus. Sensory and relex indings are uncommon but have been observed.

Radiographic Findings Fracture of the vertebral ring apophysis can be seen on a lateral radiograph of the lumbar spine as a small bony fragment posterior to the vertebral body from which it has been avulsed. CT myelography is the radiographic study of choice in that the canal obstruction is easily seen on lateral views

353

and axial sections. The large central fragment of bone displaced into the canal and the defect in the vertebral rim are best seen on axial CT views. Frequently, the amount of canal encroachment is dramatic, with almost complete occlusion of the spinal canal by the avulsed fragment and attached disk. Three types of fracture morphology have been described, according to the age of the patient and size of the bony fragment avulsed with the rim of the apophysis.185 Types I and II fractures are seen in younger patients and are central in their origin from the vertebral body, with type II having a larger bony fragment than type I. Type III lesions occur in older teenagers and young adults and are more lateral in location than midline. Differentiation among these types is accomplished by evaluating the axial sections of a CT study and noting the size of the fragment and amount of canal encroachment.

Treatment Because an avulsion fracture of the vertebral apophysis involves a large central intrusion of bone, cartilage, and disk into the spinal canal, most patients are treated operatively to remove this mass, with good results. Short-term results with nonoperative treatment can be good, but no long-term results of nonoperative treatment are available for these patients.96 Reports of young patients with spinal stenosis associated with central disk herniation and calciication have suggested that this pathology may result from a ring apophyseal fracture at an earlier age.48,164 The decision regarding operative treatment depends primarily on the presence or absence of neurologic indings and amount of canal encroachment by the avulsed apophysis. In a sense, this is the same as treatment of a herniated disk. In patients without indings and a capacious spinal canal, nonoperative management is appropriate, and a good outcome has been reported in the short term.48 When operative treatment is indicated because of neurologic progression or failure of symptoms to resolve, the amount of the herniated material must be taken into consideration when planning the surgical approach. Generally, because of the size of the lesion, a limited approach does not allow safe or complete removal of the entire mass of disk and bone. A bilateral laminotomy approach with excision of the inferior portion of the lamina above is necessary to gain full access to the canal and allow elevation of the thecal sac and nerve roots off the anterior mass protruding posteriorly. The mass may be as thick as 1 cm, composed of bone superiorly and cartilage and disk inferiorly, and extend across the entire anterior canal. Thus, a more extensile exposure of the canal than what is typical for a herniated nucleus pulposus is necessary.96 Excision of fragments early in the course of the condition is generally easier than in a more chronic case, in which nerve roots and dural adhesions to the protruding mass make safe excision of the mass dificult. Symptoms resolve immediately after successful excision of these lesions. The postoperative course and rehabilitation are similar to those for patients with herniated disks. Return to normal activities is based on the return of full back lexibility and rehabilitation to normal strength. In follow-up beyond 2 years, most patients can return to essentially normal activities, including sports.48,67,114,164,178,185

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SECTION II Anatomic Disorders

Incomplete removal of protruding material or excessive retraction placed on a nerve root during excision can obviously compromise the result. The essential difference between a slipped vertebral apophysis and the more common herniated nucleus pulposus is determined by careful scrutiny of the plain radiographs and visualization of the small bony fragment in the spinal canal posterior to the vertebral body from which it originated. In addition, if a large central disk herniation is seen on MRI, at least a few CT axial sections should be obtained through the vertebral body immediately adjacent to the disk to search for a posterior apophyseal rim avulsion or bony defect. By evaluating the spinal canal in this fashion preoperatively, the surgeon should be able to plan the appropriate exposure to deal with the intraspinal pathology.

Transitional Vertebra (Bertolotti) Syndrome Approximately 4% to 6% of the general population has a partially sacralized, or transitional, vertebra at the

A

lumbosacral junction.189 This common anomaly is an enlarged transverse process (or processes) that articulates with the sacrum or pelvis as a neoarticulation. In bilateral cases in which L5 is assimilated into the sacrum, there may be an association with mechanical low back pain, originally described by Bertolotti in the Italian radiology literature in 1917 and subsequently debated as a cause of accelerated degenerative disk problems at an adjacent level. The occurrence of so-called facetogenic pain has been described in unilateral cases, with pain in the low back area, buttock, and proximal aspect of the thigh thought to be secondary to degenerative changes in the neoarticulation.90,162 In one reported case, a teenager had pain on the side contralateral to the abnormal articulation. Excessive stress on the normal facet, caused by the abnormal facet being ankylosed to the sacrum, was thought to be the pain generator.21 Our experience with unilateral transitional vertebra syndrome is similar in that the pain is usually reported on the side opposite the neoarticulation (Fig. 14-24). The patients are typically active teenagers and have low back and buttock pain that is activity related at irst, but may become more continuous, with sciatic-type complaints leading to further

B

D

C

E

FIGURE 14-24 A, 16-year-old girl with a 3-year history of unrelenting left-sided low back pain, with radiation to the buttock. An enlarged transverse process of L5 articulating with the sacral ala on the right is noted. B to D, Three-dimensional reconstructed CT scans of the neoarticulation on the right side (B), with no abnormality on the left (C). E, The patient improved clinically within 6 months after resection of the neoarticulation.

CHAPTER 14 Other Anatomic Disorders of the Spine

A

355

B

FIGURE 14-25 Radiographs (A) and CT reconstruction (B) of a 16-year-old boy evaluated after 6 months of left-sided back pain from a football injury. The solid and massive fusion between the transverse process and sacrum on the side ipsilateral to the pain, with no evidence of an articulation, seemed to indicate that completion of the L5-S1 fusion by simple bilateral facet arthrodesis in situ was beneicial. In short-term follow-up, the patient showed mild improvement.

imaging to rule out diskogenic or other sources of pain. Patients often exhibit restriction in side bending and hyperextension as a result of pain. Although the transitional vertebra may have been diagnosed by plain radiographs, this inding may be more or less ignored because of the relative frequency of what is often considered a nonpathologic coincidental inding.45,55,120 As a consequence of the presumed increased stress on the normal facet, these patients do not respond well to physical therapy because motion adds progressive asymmetric stress from the restricted mobility of the transitional segment. Lack of degenerative changes in the abnormal articulation can be postulated by the fact that bone scans are often normal.90 In Brault’s report, the abnormal side was hot whereas the contralateral painful facet was normal, as conirmed by MRI.21 Our patients have also demonstrated positive bone scans at the neoarticulation and no changes in the painful contralateral side. These indings probably do not clarify the cause or treatment recommendations because they can support either surgical remedy, fusion or resection. Treatment should be initially conservative, although patients referred to us have generally undergone previous therapy and nonoperative modalities, including medication, and are thus considered to represent a failure of nonoperative methods. It is not unusual for patients to have been symptomatic for 2 to 3 years before referral. Injection of the painful facet with local anesthetic and steroid is a logical diagnostic step and frequently produces temporary resolution, although the effect will eventually wear off and pain will recur.21,90,162 Unfortunately, a good response to facet injection does not necessarily predict a positive surgical outcome.162 The choice of resection of the abnormal articulation versus completion of fusion of the transitional vertebra

cannot be accurately analyzed because of the uncommon nature of the condition and the uncertainty of the cause. Sufice it to say that both methods are reported to relieve the symptoms, which our experience has supported. Resection of the abnormal transverse process and neoarticulation has the potential of restoring mobility by releasing the ankylosed abnormal side, thus permitting the nondegenerated normal facet to return to a healthy state. The resection is done through a standard posterior approach to the lumbosacral junction. It entails removing the often extensive bony connection between the L5 transverse process and the sacrum or iliac wing with a burr and Kerrison rongeur and carefully protecting and unrooing the L5 nerve root. The resected bony surfaces are then treated with bone wax, hopefully to prevent re-formation. In patients with a massive fusion between the transverse process and sacrum (Fig. 14-25), simple completion of the fusion on the contralateral painful side seems equally logical and certainly simple. We have taken this approach in one patient, with improvement in symptoms after 3 months, the time that it may have taken for all movement at the transitional segment to cease. Unfortunately, follow-up is limited, so this method, as well as the resection option, must be analyzed from a short-term perspective only.

Acknowledgment The following colleagues kindly contributed material to this chapter: Jose Luis Beguiristan, Alvin H. Crawford, and Robert G. Viere.

References For References, see expertconsult.com.

CHAPTER 14 Other Anatomic Disorders of the Spine

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51. Fredrickson BE, Baker D, McHolick WJ, et al: The natural history of spondylolysis and spondylolisthesis, J Bone Joint Surg Am 66:699, 1984. 52. Freeman BL 3rd, Donati NL: Spinal arthrodesis for severe spondylolisthesis in children and adolescents. A long-term follow-up study, J Bone Joint Surg Am 71:594, 1989. 53. Frennered AK, Danielson BI, Nachemson AL: Natural history of symptomatic isthmic low-grade spondylolisthesis in children and adolescents: a seven-year follow-up study, J Pediatr Orthop 11:209, 1991. 54. Frennered AK, Danielson BI, Nachemson AL, et al: Midterm follow-up of young patients fused in situ for spondylolisthesis, Spine 16:409, 1991. 55. Frymoyer JW, Gordon SL: Research perspectives in low-back pain. Report of a 1988 workshop, Spine 14:1384, 1989. 56. Fu KM, Smith JS, Polly DW Jr, et al: Morbidity and mortality in the surgical treatment of six hundred ive pediatric patients with isthmic or dysplastic spondylolisthesis, Spine (Phila Pa 1976) 36:308, 2011. 57. Fujii K, Katoh S, Sairyo K, et al: Union of defects in the pars interarticularis of the lumbar spine in children and adolescents. The radiological outcome after conservative treatment, J Bone Joint Surg Br 86:225, 2004. 58. Gaines RW: L5 vertebrectomy for the surgical treatment of spondyloptosis: thirty cases in 25 years, Spine 30(Suppl):S66, 2005. 59. Gaines RWJ: The L5 vertebrectomy approach for the treatment of spondyloptosis. In Bridwell KH, DeWald RL, editors: The textbook of spinal surgery, Philadelphia, 1997, Lippincott-Raven, p 1357. 60. Gibson MJ, Szypryt EP, Buckley JH, et al: Magnetic resonance imaging of adolescent disc herniation, J Bone Joint Surg Br 69:699, 1987. 61. Giroux JC, Leclercq TA: Lumbar disc excision in the second decade, Spine 7:168, 1982. 62. Giudici F, Minoia L, Archetti M, et al: Long-term results of the direct repair of spondylolisthesis, Eur Spine J 20(Suppl 1):S115, 2011. 63. Glavas P, Mac-Thiong JM, Parent S, et al: Assessment of lumbosacral kyphosis in spondylolisthesis: a computer-assisted reliability study of six measurement techniques, Eur Spine J 18:212, 2009. 64. Grzegorzewski A, Kumar SJ: In situ posterolateral spine arthrodesis for grades III, IV, and V spondylolisthesis in children and adolescents, J Pediatr Orthop 20:506, 2000. 65. Hambly M, Lee CK, Gutteling E, et al: Tension band wiring–bone grafting for spondylolysis and spondylolisthesis. A clinical and biomechanical study, Spine 14:455, 1989. 66. Hammerberg KW: New concepts on the pathogenesis and classiication of spondylolisthesis, Spine 30(6 Suppl):S4, 2005. 67. Handel SF, Twiford TW Jr, Reigel DH, et al: Posterior lumbar apophyseal fractures, Radiology 130:629, 1979. 68. Hanson DS, Bridwell KH, Rhee JM, et al: Correlation of pelvic incidence with low- and high-grade isthmic spondylolisthesis, Spine 27:2026, 2002. 69. Harms J, Jeszensky D, Stoltze D, et al: True spondylolisthesis reduction and monosegmental fusion in spondylolisthesis. In Bridwell KH, DeWald RL, editors: The textbook of spinal surgery, Philadelphia, 1997, Lippincott-Raven, p 1337. 70. Harris IE, Weinstein SL: Long-term follow-up of patients with grade-III and IV spondylolisthesis. Treatment with and without posterior fusion, J Bone Joint Surg Am 69:960, 1987. 71. Hashimoto K, Fujita K, Kojimoto H, et al: Lumbar disc herniation in children, J Pediatr Orthop 10:394, 1990. 72. Hefti F, Seelig W, Morscher E: Repair of lumbar spondylolysis with a hook-screw, Int Orthop 16:81, 1992. 73. Helenius I, Lamberg T, Osterman K, et al: Posterolateral, anterior, or circumferential fusion in situ for high-grade spondylolisthesis

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97. Komatsubara S, Sairyo K, Katoh S, et al: High-grade slippage of the lumbar spine in a rat model of spondylolisthesis: effects of cyclooxygenase-2 inhibitor on its deformity, Spine (Phila Pa 1976) 31:E528, 2006. 98. Kurihara A, Kataoka O: Lumbar disc herniation in children and adolescents. A review of 70 operated cases and their minimum 5-year follow-up studies, Spine 5:443, 1980. 99. Labelle H, Mac-Thiong JM, Roussouly P: Spinopelvic sagittal balance of spondylolisthesis: a review and classiication, Eur Spine J 20(Suppl 5):641, 2011. 100. Labelle H, Roussouly P, Berthonnaud E, et al: The importance of spinopelvic balance in L5-S1 developmental spondylolisthesis: a review of pertinent radiologic measurements, Spine 30:S27, 2005. 101. Labelle H, Roussouly P, Berthonnaud E, et al: Spondylolisthesis, pelvic incidence, and spinopelvic balance: a correlation study, Spine 29:2049, 2004. 102. Labelle H, Roussouly P, Chopin D, et al: Spinopelvic alignment after surgical correction for developmental spondylolisthesis, Eur Spine J 17:1170, 2008. 103. Lakshmanan P, Ahuja S, Lewis M, et al: Transsacral screw ixation for high-grade spondylolisthesis, Spine J 9:1024, 2009. 104. Lamartina C, Zavatsky JM, Petruzzi M, et al: Novel concepts in the evaluation and treatment of high-dysplastic spondylolisthesis, Eur Spine J 18(Suppl 1):133, 2009. 105. Lamberg T, Remes V, Helenius I, et al: Uninstrumented in situ fusion for high-grade childhood and adolescent isthmic spondylolisthesis: long-term outcome, J Bone Joint Surg Am 89:512, 2007. 106. Lauerman WC, Bradford DS, Ogilvie JW, et al: Results of lumbar pseudarthrosis repair, J Spinal Disord 5:149, 1992. 107. Laurent LE, Osterman K: Operative treatment of spondylolisthesis in young patients, Clin Orthop Relat Res 117:85, 1976. 108. Laursen M, Thomsen K, Eiskjaer SP, et al: Functional outcome after partial reduction and 360 degree fusion in grade III-V spondylolisthesis in adolescent and adult patients, J Spinal Disord 12:300, 1999. 109. Legaye J, Duval-Beaupere G, Hecquet J, et al: Pelvic incidence: a fundamental pelvic parameter for three-dimensional regulation of spinal sagittal curves, Eur Spine J 7:99, 1998. 110. Lenke LG, Bridwell KH, Bullis D, et al: Results of in situ fusion for isthmic spondylolisthesis, J Spinal Disord 5:433, 1992. 111. Lindholm TS, Ragni P, Ylikoski M, et al: Lumbar isthmic spondylolisthesis in children and adolescents. Radiologic evaluation and results of operative treatment, Spine (Phila Pa 1976) 15:1350, 1990. 112. Lippitt AB: Fracture of a vertebral body end-plate and disk protrusion causing subarachnoid block in an adolescent, Clin Orthop Relat Res 116:112, 1976. 113. Lowe RW, Hayes TD, Kaye J, et al: Standing roentgenograms in spondylolisthesis, Clin Orthop Relat Res 117:80, 1976. 114. Lowrey JJ: Dislocated lumbar vertebral epiphysis in adolescent children. Report of three cases, J Neurosurg 38:232, 1973. 115. Lubicky JP: Unusual spondylolisthesis, Spine 30(Suppl):S82, 2005. 116. Mac-Thiong JM, Duong L, Parent S, et al: Reliability of the Spinal Deformity Study Group classiication of lumbosacral spondylolisthesis, Spine (Phila Pa 1976) 37:E95, 2011. 117. Mac-Thiong JM, Labelle H: A proposal for a surgical classiication of pediatric lumbosacral spondylolisthesis based on current literature, Eur Spine J 15:1425, 2006. 118. Mac-Thiong JM, Labelle H, Parent S, et al: Reliability and development of a new classiication of lumbosacral spondylolisthesis, Scoliosis 3:19, 2008. 119. Mac-Thiong JM, Wang Z, de Guise JA, et al: Postural model of sagittal spinopelvic alignment and its relevance for lumbosacral developmental spondylolisthesis, Spine (Phila Pa 1976) 33:2316, 2008.

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120. MacLean JG, Tucker JK, Latham JB: Radiographic appearances in lumbar disc prolapse, J Bone Joint Surg Br 72:917, 1990. 121. Marchetti PG, Bartolozzi P: Classiication of spondylolisthesis as a guideline for treatment. In Bridwell KH, DeWald RL, editors: The textbook of spinal surgery, Philadelphia, 1997, LippincottRaven, p 1211. 122. Mardjetko S, Albert T, Andersson G, et al: Spine/SRS spondylolisthesis summary statement, Spine 30(Suppl):S3, 2005. 123. Martin RP, Deane RH, Collett V: Spondylolysis in children who have osteopetrosis, J Bone Joint Surg Am 79:1685, 1997. 124. Marty C, Boisaubert B, Descamps H, et al: The sagittal anatomy of the sacrum among young adults, infants, and spondylolisthesis patients, Eur Spine J 11:119, 2002. 125. McPhee IB, O’Brien JP: Reduction of severe spondylolisthesis. A preliminary report, Spine 4:430, 1979. 126. McQueen MM, Court-Brown C, Scott JH: Stabilisation of spondylolisthesis using Dwyer instrumentation, J Bone Joint Surg Br 68:185, 1986. 127. Meyerding HW: Spondylolisthesis, Surg Gynecol Obstet 54:371, 1932. 128. Meyers LL, Dobson SR, Wiegand D, et al: Mechanical instability as a cause of gait disturbance in high-grade spondylolisthesis: a pre- and postoperative three-dimensional gait analysis, J Pediatr Orthop 19:672, 1999. 129. Miller SF, Congeni J, Swanson K: Long-term functional and anatomical follow-up of early detected spondylolysis in young athletes, Am J Sports Med 32:928, 2004. 130. Molinari RW, Bridwell KH, Lenke LG, et al: Anterior column support in surgery for high-grade, isthmic spondylolisthesis, Clin Orthop Relat Res 394:109, 2002. 131. Molinari RW, Bridwell KH, Lenke LG, et al: Complications in the surgical treatment of pediatric high-grade, isthmic dysplastic spondylolisthesis. A comparison of three surgical approaches, Spine 24:1701, 1999. 132. Morscher E, Gerber B, Fasel J: Surgical treatment of spondylolisthesis by bone grafting and direct stabilization of spondylolysis by means of a hook screw, Arch Orthop Trauma Surg 103:175, 1984. 133. Muschik M, Zippel H, Perka C: Surgical management of severe spondylolisthesis in children and adolescents. Anterior fusion in situ versus anterior spondylodesis with posterior transpedicular instrumentation and reduction, Spine (Phila Pa 1976) 22:2036, 1997. 134. Nelson CL, Janecki CJ, Gildenberg PL, et al: Disc protrusions in the young, Clin Orthop Relat Res 88:142, 1972. 135. Neugebauer FI: The classic: a new contribution to the history and etiology of spondylolisthesis by F.L. Neugebauer, Clin Orthop Relat Res 117:4, 1976. 136. Newman PH: The etiology of spondylolisthesis, J Bone Joint Surg Br 45:39, 1963. 137. Newman PH: A clinical syndrome associated with severe lumbosacral subluxation, J Bone Joint Surg Br 47:472, 1965. 138. Newton PO, Johnston II CE: Analysis and treatment of poor outcomes following in situ arthrodesis in adolescent spondylolisthesis, J Pediatr Orthop 17:754, 1997. 139. O’Connell JEA: Intervertebral disc protrusions in children and adolescents, Br J Surg 47:611, 1960. 140. O’Sullivan PB, Phyty GD, Twomey LT, et al: Evaluation of speciic stabilizing exercise in the treatment of chronic low back pain with radiologic diagnosis of spondylolysis or spondylolisthesis, Spine 22:2959, 1997. 141. Ogilvie JW: Complications in spondylolisthesis surgery, Spine 30(Suppl):S97, 2005. 142. Papagelopoulos PJ, Shaughnessy WJ, Ebersold MJ, et al: Longterm outcome of lumbar discectomy in children and adolescents sixteen years of age or younger, J Bone Joint Surg Am 80:689, 1998.

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143. Pedersen AK, Hagen R: Spondylolysis and spondylolisthesis. Treatment by internal ixation and bone-grafting of the defect, J Bone Joint Surg Am 70:15, 1988. 144. Peek RD, Wiltse LL, Reynolds JB, et al: In situ arthrodesis without decompression for Grade-III or IV isthmic spondylolisthesis in adults who have severe sciatica, J Bone Joint Surg Am 71:62, 1989. 145. Petraco DM, Spivak JM, Cappadona JG, et al: An anatomic evaluation of L5 nerve stretch in spondylolisthesis reduction, Spine 21:1133, 1996. 146. Pizzutillo PD, Hummer CD 3rd: Nonoperative treatment for painful adolescent spondylolysis or spondylolisthesis, J Pediatr Orthop 9:538, 1989. 147. Poussa M, Remes V, Lamberg T, et al: Treatment of severe spondylolisthesis in adolescence with reduction or fusion in situ: longterm clinical, radiologic, and functional outcome, Spine (Phila Pa 1976) 31:583, 2006. 148. Poussa M, Schlenzka D, Seitsalo S, et al: Surgical treatment of severe isthmic spondylolisthesis in adolescents. Reduction or fusion in situ, Spine 18:894, 1993. 149. Power RA, Taylor GJ, Fyfe IS: Lumbar epidural injection of steroid in acute prolapsed intervertebral discs. A prospective study, Spine 17:453, 1992. 150. Roca J, Ubierna MT, Caceres E, et al: One-stage decompression and posterolateral and interbody fusion for severe spondylolisthesis. An analysis of 14 patients, Spine 24:709, 1999. 151. Roussouly P, Gollogly S, Berthonnaud E, et al: Sagittal alignment of the spine and pelvis in the presence of L5-S1 isthmic lysis and low-grade spondylolisthesis, Spine (Phila Pa 1976) 31:2484, 2006. 152. Roussouly P, Meyrat RB: High-grade spondylolisthesis: partial reduction. In Bridwell KH, DeWald RL, editors: Textbook of spinal surgery, ed 3, Philadelphia, 2011, Lippincott Williams & Wilkins, p 638. 153. Roussouly P, Transfeldt E, Berthonnaud E, et al: Changes in spinal and pelvic parameters after high-grade isthmic spondylolisthesis, Eur Spine J 10(Supp 1), 2001. 154. Rowe G: Etiology of the separate neural arch, J Bone Joint Surg Am 35:102, 1953. 155. Ruf M, Koch H, Melcher RP, et al: Anatomic reduction and monosegmental fusion in high-grade developmental spondylolisthesis, Spine (Phila Pa 1976) 31:269, 2006. 156. Russwurm H, Bjerkreim I, Ronglan E: Lumbar intervertebral disc herniation in the young, Acta Orthop Scand 49:158, 1978. 157. Saal JA: Dynamic muscular stabilization in the nonoperative treatment of lumbar pain syndromes, Orthop Rev 19:691, 1990. 158. Sagi HC, Jarvis JG, Uhthoff HK: Histomorphic analysis of the development of the pars interarticularis and its association with isthmic spondylolysis, Spine 23:1635, 1998. 159. Sailhan F, Gollogly S, Roussouly P: The radiographic results and neurologic complications of instrumented reduction and fusion of high-grade spondylolisthesis without decompression of the neural elements: a retrospective review of 44 patients, Spine (Phila Pa 1976) 31:161, 2006. 160. Sairyo K, Goel VK, Grobler LJ, et al: The pathomechanism of isthmic lumbar spondylolisthesis. A biomechanical study in immature calf spines, Spine 23:1442, 1998. 161. Sairyo K, Katoh S, Ikata T, et al: Development of spondylolytic olisthesis in adolescents, Spine J 1:171, 2001. 162. Santavirta S, Tallroth K, Ylinen P, et al: Surgical treatment of Bertolotti’s syndrome. Follow-up of 16 patients, Arch Orthop Trauma Surg 112:82, 1993. 163. Saraste H: Long-term clinical and radiological follow-up of spondylolysis and spondylolisthesis, J Pediatr Orthop 7:631, 1987. 164. Savini R, Di Silvestre M, Gargiulo G, et al: Posterior lumbar apophyseal fractures, Spine 16:1118, 1991.

165. Scaglietti O, Frontino G, Bartolozzi P: Technique of anatomical reduction of lumbar spondylolisthesis and its surgical stabilization, Clin Orthop Relat Res 117:165, 1976. 166. Schoenecker PL: Developmental spondylolisthesis without lysis. In Bridwell KH, DeWald RL, editors: The textbook of spinal surgery, Philadelphia, 1997, Lippincott-Raven, p 1255. 167. Schoenecker PL, Cole HO, Herring JA, et al: Cauda equina syndrome after in situ arthrodesis for severe spondylolisthesis at the lumbosacral junction, J Bone Joint Surg Am 72:369, 1990. 168. Schwend RM, Waters PM, Hey LA, et al: Treatment of severe spondylolisthesis in children by reduction and L4-S4 posterior segmental hyperextension ixation, J Pediatr Orthop 12:703, 1992. 169. Seitsalo S: Operative and conservative treatment of moderate spondylolisthesis in young patients, J Bone Joint Surg Br 72:908, 1990. 170. Seitsalo S, Osterman K, Hyvarinen H, et al: Severe spondylolisthesis in children and adolescents. A long-term review of fusion in situ, J Bone Joint Surg Br 72:259, 1990. 171. Shaffer B, Wiesel S, Lauerman W: Spondylolisthesis in the elite football player: an epidemiologic study in the NCAA and NFL, J Spinal Disord 10:365, 1997. 172. Shelokov A, Haideri N, Roach J: Residual gait abnormalities in surgically treated spondylolisthesis, Spine 18:2201, 1993. 173. Sherman FC, Rosenthal RK, Hall JE: Spine fusion for spondylolysis and spondylolisthesis in children, Spine 4:59, 1979. 174. Shuflebarger HL: High-grade isthmic dysplastic spondylolisthesis: monosegmental surgical treatment. Presented at the 33rd Annual Meeting of the Scoliosis Research Society, New Orleans, March 17-22, 1998. 175. Shuflebarger HL, Geck MJ: High-grade isthmic dysplastic spondylolisthesis: monosegmental surgical treatment, Spine 30(Suppl):S42, 2005. 176. Smith MD, Bohlman HH: Spondylolisthesis treated by a singlestage operation combining decompression with in situ posterolateral and anterior fusion. An analysis of eleven patients who had long-term follow-up, J Bone Joint Surg Am 72:415, 1990. 177. Smorgick Y, Floman Y, Millgram MA, et al: Mid- to long-term outcome of disc excision in adolescent disc herniation, Spine J 6:380, 2006. 178. Sovio OM, Bell HM, Beauchamp RD, et al: Fracture of the lumbar vertebral apophysis, J Pediatr Orthop 5:550, 1985. 179. Spencer DL, Bernstein AJ: Lumbar intervertebral disc surgery. In Bridwell KH, DeWald RL, editors: The textbook of spinal surgery, Philadelphia, 1997, Lippincott-Raven, p 1547. 180. Stanton RP, Meehan P, Lovell WW: Surgical fusion in childhood spondylolisthesis, J Pediatr Orthop 5:411, 1985. 181. Steiner ME, Micheli LJ: Treatment of symptomatic spondylolysis and spondylolisthesis with the modiied Boston brace, Spine 10:937, 1985. 182. Stewart TD: The age of incidence of neural arch defects in Alaskan natives considered from the standpoint of etiology, J Bone Joint Surg Am 35:937, 1953. 183. Taillard WF: Les spondylolisthesis, Paris, 1957, Masson. 184. Takahashi K, Yamagata M, Takayanagi K, et al: Changes of the sacrum in severe spondylolisthesis: a possible key pathology of the disorder, J Orthop Sci 5:18, 2000. 185. Takata K, Inoue S, Takahashi K, et al: Fracture of the posterior margin of a lumbar vertebral body, J Bone Joint Surg Am 70:589, 1988. 186. Tanguay F, Mac-Thiong JM, Wang Z, et al: Developmental spondylolisthesis: is slip angle related to quality of life? Stud Health Technol Inform 158:182, 2010. 187. Taylor TFK: Lumbar intervertebral disc prolapse in children and adolescents, J Bone Joint Surg Br 64:135, 1982. 188. Terai T, Sairyo K, Goel VK, et al: Biomechanical rationale of sacral rounding deformity in pediatric spondylolisthesis: a clinical and biomechanical study, Arch Orthop Trauma Surg 131:1187, 2011.

CHAPTER 14 Other Anatomic Disorders of the Spine

189. Tini PG, Wieser C, Zinn WM: The transitional vertebra of the lumbosacral spine: its radiological classiication, incidence, prevalence, and clinical signiicance, Rheumatol Rehabil 16:180, 1977. 190. Tiusanen H, Schlenzka D, Seitsalo S, et al: Results of a trial of anterior or circumferential lumbar fusion in the treatment of severe isthmic spondylolisthesis in young patients, J Pediatr Orthop B 5:190, 1996. 191. Tokuhashi Y, Matsuzaki H: Repair of defects in spondylolysis by segmental pedicular screw hook ixation. A preliminary report, Spine 21:2041, 1996. 192. Toueg CW, Mac-Thiong JM, Grimard G, et al: Prevalence of spondylolisthesis in a population of gymnasts, Stud Health Technol Inform 158:132, 2010. 193. Transfeldt EE, Mehbod AA: Evidence-based medicine analysis of isthmic spondylolisthesis treatment including reduction versus fusion in situ for high-grade slips, Spine (Phila Pa 1976) 32(Suppl):S126, 2007. 194. VanDam BE: Nonoperative treatment and surgical repair of lumbar spondylolysis. In Bridwell KH, DeWald RL, editors: The textbook of spinal surgery, Philadelphia, 1997, Lippincott-Raven, p 1263. 195. Varlotta GP, Brown MD, Kelsey JL, et al: Familial predisposition for herniation of a lumbar disc in patients who are less than twenty-one years old, J Bone Joint Surg Am 73:124, 1991. 196. Vaz G, Roussouly P, Berthonnaud E, et al: Sagittal morphology and equilibrium of pelvis and spine, Eur Spine J 11:80, 2002. 197. Vialle R, Dauzac C, Khouri N, et al: Sacral and lumbar-pelvic morphology in high-grade spondylolisthesis, Orthopedics 30:642, 2007. 198. Wahren H: Herniated nucleus pulposus in a child of twelve years, Acta Orthop Scand 73:40, 1945.

355.e5

199. Wang Z, Parent S, Mac-Thiong JM, et al: Inluence of sacral morphology in developmental spondylolisthesis, Spine (Phila Pa 1976) 33:2185, 2008. 200. Ward CV, Latimer B: Human evolution and the development of spondylolysis, Spine 30:1808, 2005. 201. Webb JH: Protruded lumbar intervertebral discs in children, JAMA 154:1153, 1954. 202. Weber H: Lumbar disc herniation. A controlled, prospective study with ten years of observation, Spine 8:131, 1983. 203. Whitesides TE Jr, Horton WC, Hutton WC, et al: Spondylolytic spondylolisthesis: a study of pelvic and lumbosacral parameters of possible etiologic effect in two genetically and geographically distinct groups with high occurrence, Spine 30(Suppl):S12, 2005. 204. Wiltse L: Etiology of spondylolisthesis, Clin Orthop 10:48, 1957. 205. Wiltse LL, Bateman JG, Hutchinson RH, et al: The paraspinal sacrospinalis-splitting approach to the lumbar spine, J Bone Joint Surg Am 50:919, 1968. 206. Wiltse LL, Jackson DW: Treatment of spondylolisthesis and spondylolysis in children, Clin Orthop Relat Res 117:92, 1976. 207. Wiltse LL, Newman PH, Macnab I: Classiication of spondylolisis and spondylolisthesis, Clin Orthop Relat Res 117:23, 1976. 208. Wiltse LL, Widell EH Jr, Jackson DW: Fatigue fracture: the basic lesion is isthmic spondylolisthesis, J Bone Joint Surg Am 57:17, 1975. 209. Wynne-Davies R, Scott JH: Inheritance and spondylolisthesis: a radiographic family survey, J Bone Joint Surg Br 61:301, 1979. 210. Yue WM, Brodner W, Gaines RW: Abnormal spinal anatomy in 27 cases of surgically corrected spondyloptosis: proximal sacral endplate damage as a possible cause of spondyloptosis, Spine 30(Suppl):S22, 2005. 211. Zamani MH, MacEwen GD: Herniation of the lumbar disc in children and adolescents, J Pediatr Orthop 2:528, 1982.

CHAPTER 15

Disorders of the Upper Extremity Chapter Outline Introduction 356 Principles of Dressing and Splinting 364 Principles of Acute Care 378 Principles of Reconstruction 384 Congenital Anomalies 388 Juvenile Arthritis and Other Noninfectious Inlammatory Conditions 452 Infections 461 Neonatal Brachial Plexus Palsy 464 Tumors of the Upper Limb 471 Microsurgery 474

Introduction Very few congenital anomalies of the upper limb can be restored to normal function and appearance. The goals of treatment are therefore to maximize functional potential, preserve sensation, and minimize scarring. The surgeon should offer support, irst to the family and later to the child, to help them cope with the impact of knowing that even with today’s medical technology, the limb cannot be restored to normal. Surgical intervention should be undertaken only when the intended procedure is to be done for the child, not merely to the child, and when the goals are clearly understood by the family and, when possible, the child. Some surgical indications for common congenital conditions are straightforward, and the literature detailing the techniques is abundant. Surgery for other, less common conditions requires careful, sometimes creative preoperative planning and the ability to change these plans intraoperatively in an acceptable fashion if aberrant anatomy precludes a beneicial outcome. In general, the goal of surgical treatment of congenital upper limb anomalies is to position the hands so that bimanual activity within the ield of vision is possible. Preservation of joint motion, when possible, is desirable to allow the greatest reach of the limbs, especially with regard to reaching the face and perineum. Because hand function requires intact sensation, scars should be placed carefully and peripheral nerves protected throughout the limb. Position, motion, and strength for grasp and release are the goals of surgery on the nondominant hand, which will stabilize objects for manipulation by the dominant hand. Position, motion, and strength for pinch and ine motor function are the goals of surgery on the dominant hand. 356

Christine Ho

Embryology The upper limb bud appears along the crest of Wolf (Fig. 15-1) at approximately 23 days of gestation. Mesodermal proliferation within the limb bud depends on a critical vascular structure that grows with the limb and supplies nutrients and oxygenation. The limb bud is innervated from its inception by nerves derived from the neuroectoderm. The leading edge of the limb bud ectoderm is a thickened ridge called the apical ectodermal ridge (AER) (Fig. 15-2). It functions as an advancing mobile command center and contains the “architectural blueprint” for the limb’s structure. The AER is programmed to allow sequential transcription of crucial segments of DNA. The time-linked sequence of genetic transcription directed by the AER controls the proximodistal differentiation of limb structures. A number of ibroblast growth factors are involved in maintaining outward growth. Genetically encoded limb anomalies are “blueprint” variations and are built into the limb construction process. Differentiation of the underlying mesodermal substrate occurs through the interplay of concentration gradients of growth factors and cellular mediators. On the caudal edge of the limb bud, a zone of polarizing activity (Fig. 15-3) has been identiied as being crucial to the craniocaudal orientation of the limb. The Hox gene family plays a role in this radioulnar (or tibioibular) orientation of the limb. The WNT7 group of genes plays a role in dorsoventral patterning. The increasing number of clinically recognized conditions that can be mapped to speciic gene mutations is contributing to a better understanding of the control of the three axes of limb development. Vascular ingrowth supplying the advancing progress zone (Fig. 15-4) of undifferentiated mesodermal cells is critical to the development of limbs of normal length and size. Disruption of this vascular support limits the amount of mesodermal substrate and results in the spectrum of transverse limb deiciencies known as symbrachydactyly (Fig. 15-5). The inal act of the AER is programmed self-destruction through a gene that codes for an endonuclease. This gene triggers a process known as apoptosis (Fig. 15-6), or programmed cell death. Dissolution of the interdigital webbing occurs at the end of the embryonic period, at approximately 56 days of gestation. The limbs continue to grow during the fetal period. A requirement for normal prenatal development is a protected uterine environment. Congenital limb abnormalities may also be due to teratologic, deforming, or disruptive inluences on development. Teratogenic agents may affect development at the genetic transcription stage or may interfere with posttranscription growth factors. Physical forces may cause deformation of the growing embryo or fetus or

CHAPTER 15 Disorders of the Upper Extremity

357

disruption of normal development; an example of the latter is the amnion disruption sequence (amniotic band syndrome; Fig. 15-7). Associated anomalies correlating with the timing of development of other organ systems may occur in a child with an upper limb abnormality. Recognized associations include anomalies of the heart, thoracic contents, spine, and kidneys, all of which develop concomitantly with the upper limb. Known hereditary associations also include hematopoietic and gastrointestinal conditions and lower limb anomalies (Fig. 15-8).

History and Examination Pertinent History The history taking begins with asking the parents to describe the child’s problem. This description may bring into focus a more speciic inquiry. The expanded description of the problem should include any functional limitations in ageappropriate activities and—elicited by gentle inquiry—the emotional status of the family and child in dealing with the deformity. An offer of occupational therapy to assist in activities of daily living (ADLs) and referral to support networks of families with similar children or to psychological counseling can be made at this juncture. Questions about the pregnancy should elicit information about previous pregnancies and miscarriages (a clue to

FIGURE 15-1 The upper limb bud. Forming slightly ahead of its inferior counterpart, the upper limb begins to develop during the fourth fetal week at the same time as the heart and other organs, as well as closure of the vertebral mass. This is shown well in this image from Nilsson’s classic book Behold Man. (From Nilsson L: Behold man, Boston, 1973, Little Brown, p 53.)

FIGURE 15-2 The apical epidermal ridge (arrowheads), an early condensation of the leading edge of the limb bud, is shown well on this scanning electron micrograph. (From the University of North Carolina School of Medicine: Embryo images: normal & abnormal mammalian development. http://www.med.unc.edu/ embryo_images/unit.)

A FIGURE 15-3 A, The zone of polarizing activity (ZPA) is shown well in this image of a chicken embryo and is the source of cellular mediators that direct development of the limb. (From Riddle RD, Tabin C: How limbs develop, Sci Am 280:78, 1999.) Continued

SECTION II Anatomic Disorders

358

ANTERIOR-POSTERIOR Metacarpals

Anterior Radius

II Digits

Wing limb bud

Zone of polarizing activity (ZPA)

IV

Ulna

Humerus

III

Normal wing

Posterior

III IV

Transplanted ZPA

Mirror image duplication from graft

Normal development

II

ZPA

IV Donor

Recipient

Grafted wing

III

PROXIMAL-DISTAL

Only humerus develops

Early wing limb bud Apical ectodermal ridge (AER)

AER removed

AER

AER removed

Later wing limb bud

Humerus develops, radius and ulna form

Early wing limb bud AER

B

AER replaced by bead soaked in a fibroblast growth factor

Normal wing

FIGURE 15-3, cont’d B, Classic experiments have demonstrated the basic chemical signaling that occurs from the ZPA and apical ectodermal ridge during limb development.

CHAPTER 15 Disorders of the Upper Extremity

FIGURE 15-4 Progress zone. The rapidly growing mesoderm surrounds a central vessel and lies directly under the zone of polarizing activity. (From the University of North Carolina School of Medicine: Embryo images: normal & abnormal mammalian development. http:// www.med.unc.edu/embryo_images/ unit-mslimb/mslimb_htms/mslimb018a.htm.)

A

D

B

359

FIGURE 15-6 Apoptosis. Controlled death of interdigital cells allows formation of the normal web space of the adult. Failure of this process results in syndactyly.

C

E

FIGURE 15-5 Symbrachydactyly is a spectrum of congenital hand deformities characterized by unilateral involvement and lack of a hereditary history. In some cases, chest wall abnormalities and Möbius syndrome may be present. A popular embryologic theory is that these cases may be the result of a subclavian artery disruption sequence occurring during the irst 3 to 5 weeks of intrauterine life. This diagnosis is the third most common congenital anomaly seen in the hand clinic at the Texas Scottish Rite Hospital for Children; it is exceeded in frequency only by polydactyly and syndactyly. The four symbrachydactyly types include the short-inger type (A), the atypical cleft type (B), the monodactylous type (C), and the peromelic type (D). The Poland syndrome of absence of the sternal head of the pectoralis major (E) can occasionally be seen with rib cage defects and is associated with symbrachydactyly.

360

SECTION II Anatomic Disorders

FIGURE 15-7 Band syndrome. Deep constriction is seen in the region of the junction of the middle and distal thirds of the calf.

FIGURE 15-9 Typical facial appearance of a child with FreemanSheldon syndrome.

The pertinent family history for a child with a limb abnormality includes questions about similar anomalies in the families of both parents.

Physical Examination

FIGURE 15-8 Thrombocytopenia–absent radius syndrome. The forearms of these children have a large, fan-shaped muscle that spans the arm from the deltoid tuberosity to the carpus and may be important as a component of deformity in patients with radial clubhand.

possible genetic conditions); illnesses and exposure to disease, chemicals, radiation, or drugs during the pregnancy; dificulties with the pregnancy, such as leakage of amniotic luid or premature labor; and any antenatal testing such as amniocentesis or chorionic villus sampling and the reason for the testing. Information elicited about the delivery includes the infant’s gestational age, birth weight, Apgar scores, condition at delivery, and anything abnormal about the placenta or umbilical cord. (A single umbilical artery is abnormal and is one of the abnormalities in the VACTERL association [vertebral abnormalities, anal atresia, cardiac abnormalities, tracheoesophageal istula and/or esophageal atresia, renal agenesis and dysplasia, and limb defects; see Box 15-4].) Information to be obtained about the newborn period includes any extended hospital stay, diagnostic tests or treatment required, bleeding problems or the need for blood transfusions, nutritional status, and attainment of appropriate developmental milestones.

The physical examination is focused by the complaint but includes inspection of the entire child. The examiner should pay special attention to overall muscle tone while handling the child. A loppy infant may be morphologically normal but developmentally delayed. An appreciation of the appropriate relexes according to the age of the child helps the examiner detect central nervous system dysfunction. Craniofacial features such as premature closure of sutures, abnormal head shape, facial asymmetry, crumpled or abnormal ears, and micrognathia suggest syndromes associated with limb abnormalities. As the observer becomes more familiar with the dysmorphic features, other facial features characteristic of syndromes will be recognized (Fig. 15-9). The neck and chest should be palpated for symmetry and integrity of the clavicle and ribs, the presence and bulk of the pectoralis and latissimus musculature, and symmetry of the breast tissue. The lower limbs are checked for stability of the hips, length, and symmetry, and any deformity is noted. The spinal examination includes a check of alignment and range of motion (ROM) of the neck and palpation of the dorsal spinal elements. Any cutaneous manifestation of spinal dysraphism, such as a hairy patch or dimple, should be investigated (Fig. 15-10). Examination of the limbs includes observation and documentation of all pertinent indings. The limbs can be inspected before the examiner evaluates the active and passive ROM of all joints. Any asymmetry in size should be noted. Motor examination includes observation of active ROM, palpation of muscle bulk, assessment of any musculotendinous contractures or spasticity, and in older children,

CHAPTER 15 Disorders of the Upper Extremity

FIGURE 15-10 A sacral dimple is a sign of potential vertebral and spinal cord abnormalities.

evaluation of strength and measurement of strength grades. Any anomalies should be noted in anatomic descriptive terms and by classiied or named conditions if the diagnosis is clear. Pejorative terms such as lobster claw or clubhand should be avoided in favor of simpler descriptive terms such as cleft, deviated, bowed, or angled. Assessment of sensation may be inferred from the texture, temperature, presence of sweat and papillary ridges, and integration of the limb or digit into function. Discrete sensory testing is impossible in a young child but usually possible in older children. Asymmetry in the size of limbs or parts of limbs may be a clue to asymmetric neural innervation of the limb, vascular or neural malformation, or a possible underlying tumor. In the case of anomalous formation of limb structures, the examination should focus on both the appearance and function of the limb. Observation of the child while using the limb in developmentally appropriate activities is important. A description of the functional limitations, such as an inability to touch the mouth with the hands or to bring the feet into a plantigrade position, should be included in the record to provide a clearer picture of the abnormality. The examination of the child may need to be repeated to obtain a clear picture of the problem and the potential treatment. Establishing rapport with an older child is important in formulating a plan for treatment and may take more than one visit. Having several small, washable, nonlatex toys available for the child to play with is helpful for observing active ROM of the upper limbs and ine motor dexterity (Fig. 15-11). White coats tend to provoke conditioned negative behavior and thus make examination of the child more dificult. Examining a young child is very different from examining an older child or adult. Tricks of the trade include using toys, decoys, diversions, and patience.

Timing of Surgical Procedures Rational timing of hand procedures in children depends on the parent, the child, the procedure, the surgeon, the hand itself, and the anesthesiologist. All must be ready for the procedure to achieve the best result. A logical approach

361

FIGURE 15-11 Toys—the secret diagnostic weapon of the pediatric hand surgeon.

makes decision making easier for the surgeon and parent and leads to a better result for the patient.

The Parent Especially in children with a congenital deformity, the attitude of the parents must be one of cooperation. Parents need to work through a bereavement process by mourning loss of the “perfect baby” that they had anticipated before birth. The time required for family members to experience this bereavement is variable. The grief process may lead to unrealistic expectations of the surgical procedure and the surgeon. The parent and the surgeon must be patient and allow grieving to take its course. This is one reason why all but the most trivial reconstructive surgical procedures on a child’s hand are best deferred until after the irst 6 months of life. Bradbury lists three stages of the grieving process.1 Denial. In the denial phase, the parent tends to minimize the impact of the deicit: “There’s nothing my child can’t do!” Anger. This phase is important for the surgeon to recognize in the parent because the anger may be directed toward the surgeon or may focus on the obstetrician’s failure to make a prenatal diagnosis. With a diagnosis such as Erb palsy, the parent may be unable to get past the assignment of blame. Before reconstructive surgery the parent must understand that the only real solution is not “what if ” but “what now.” Before this the parent is not capable of understanding informed consent. Distress. In the distress phase parents experience feelings of guilt, anxiety about future pregnancies, and loss of control. It may be helpful to discuss with the parents the time of fetal development when the deformity occurred. Genetic counseling for the parents may be useful. At times, parents may seek to abdicate their responsibility for decisions until the child is an adult and can decide for himself or herself. This is inappropriate and should be strongly discouraged.

362

SECTION II Anatomic Disorders

Table 15-1 Cooperation Milestones in Children

Table 15-2 Growth of the Hand

Age

Milestones

Age

Infants (30 degrees), whereas nighttime splinting prevents progression of mild contractures (60°

Beta Angle 3 months

Pavlik harness

IIc

43°-49°

>77°

Acetabular deiciency

Pavlik harness

IId

43°-49°

>77°

Everted labrum

Pavlik harness

III

77°

Everted labrum

Pavlik harness

IV

Unmeasurable

Unmeasurable

Dislocated

Pavlik harness/closed vs. open reduction

Normal

None

Delayed ossiication

Variable

Lateralization

Pavlik harness

Dislocated

Pavlik harness/closed vs. open reduction

Simplified Classification I >60°

19° (6-13 years) >25° (≥14 years)

Ib

Normal

15°-19° (6-13 years) 20°-25° (≥14 years)

IIa

Moderate deformity of femoral head, femoral neck, or acetabulum

Same as class I

III

Dysplasia without subluxation