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 6th EDITION

GREEN’S SKELETAL
TRAUMA IN
CHILDREN

Gregory A. Mencio, MD
Neil E. Green Professor and Vice Chairman
Department of Orthopaedics
Vanderbilt University Medical Center
Chief, Pediatric Orthopaedics
Monroe Carell, Jr. Children’s Hospital at Vanderbilt
Nashville, Tennessee

Steven L. Frick, MD
Professor and Vice Chairman
Orthopaedic Surgery
Stanford University School of Medicine,
Stanford, California
Chief, Pediatric Orthopaedics
Orthopaedic Surgery
Lucile Packard Children’s Hospital Stanford,
Stanford, California
Elsevier
1600 John F. Kennedy Blvd.
Ste 1800
Philadelphia, PA 19103-2899

GREEN’S SKELETAL TRAUMA IN CHILDREN, SIXTH EDITION ISBN: 978-0-323-61336-1

Copyright © 2020 by Elsevier, Inc. All rights reserved.

No part of this publication may be reproduced or transmitted in any form or by any means, electronic or
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This book and the individual contributions contained in it are protected under copyright by the Publisher
(other than as may be noted herein).

Notice

Practitioners and researchers must always rely on their own experience and knowledge in evaluating
and using any information, methods, compounds or experiments described herein. Because of rapid
advances in the medical sciences, in particular, independent verification of diagnoses and drug dosages
should be made. To the fullest extent of the law, no responsibility is assumed by Elsevier, authors, editors
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negligence or otherwise, or from any use or operation of any methods, products, instructions, or ideas
contained in the material herein.

Previous editions copyrighted 2015, 2009, 2003, 1998, and 1992.

Library of Congress Control Number: 2019949250

Senior Content Strategist: Belinda Kuhn

Senior Content Development Specialist: Kathryn DeFrancesco
Publishing Services Manager: Shereen Jameel
Project Manager: Rukmani Krishnan
Design Direction: Ryan Cook

Printed in the United States of America

Last digit is the print number: 9 8 7 6 5 4 3 2 1

 Madelyn Anne Mencio
Alyson Mencio Stevens
Marissa Mencio Lichliter

Lisa Kahn Frick

Eric Altman Frick
Rachel Ivy Frick  

We dedicate this book to our teachers, colleagues,

and students.
We single out the memory of our departed colleagues,
Neil Green, MD, and Kathy Cramer, MD.
This book is created to improve the care of the injured
child; Neil and Kathy dedicated their lives
to this goal. Both are fondly remembered and deeply
missed.
Contributors

Alexandre Arkader, MD Eric W. Edmonds, MD, FAOA

Associate Professor of Orthopaedic Surgery Professor of Orthopedic Surgery
Perelman School of Medicine at University of ­Pediatrics University of California San Diego
­Pediatric Orthopedic and Orthopedic Oncology ­Surgeon Director of Orthopedic Research and Sports Medicine
Children’s Hospital of Philadelphia (CHOP) Division of Orthopedic Surgery
Philadelphia, Pennsylvania Rady Children’s Hospital San Diego
San Diego, California
Richard E. Bowen, MD
Clinical Professor John B. Erickson, DO
Orthopaedic Surgery Assistant Professor
David Geffen School of Medicine at UCLA Pediatric Orthopedic Surgery
Los Angeles, California Medical College of Wisconsin
Orthopaedic Institute for Children Milwaukee, Wisconsin
Los Angeles, California
Steven L. Frick, MD
Andrea C. Bracikowski, MD Professor and Vice Chairman
Associate Professor Orthopaedic Surgery
Orthopedics and Rehabilitation Stanford University School of Medicine
Vanderbilt University School of Medicine Stanford, California
Nashville, Tennessee Chief, Pediatric Orthopaedics
Associate Professor Orthopaedic Surgery
Pediatrics Lucile Packard Children’s Hospital Stanford
Vanderbilt Children’s Hospital Stanford, California
Nashville, Tennessee
Associate Professor Christopher Greeley, MD, MS
Emergency Medicine Professor
Vanderbilt University School of Medicine Pediatrics
Nashville, Tennessee Baylor College of Medicine
Houston, Texas
Kevin M. Dale, MD Chief
Assistant Professor of Orthopaedics and Rehabilitation Section of Public Health Pediatrics
Department of Orthopaedic Surgery Texas Children’s Hospital
Vanderbilt University School of Medicine Houston, Texas
Nashville, Tennessee
Nathan L. Grimm, MD
Jaime R. Denning, MD, MS Orthopaedic Surgery Pediatric & Adult
Assistant Professor Sports Medicine Fellow
Orthopaedic Surgery UConn Health Center
Cincinnati Children’s Hospital Medical Center Department of Orthopaedic Surgery
University of Cincinnati School of Medicine Farmington, Connecticut
Cincinnati, Ohio
Christina K. Hardesty, MD
Aleksei B. Dingel, BS Assistant Professor of Orthopaedic Surgery
Research Coordinator Pediatric Orthopaedic Surgery
Department of Orthopaedic Surgery Rainbow Babies and Children’s Hospitals at Case Western
Stanford University School of Medicine Reserve University
Stanford, California Cleveland, Ohio

vi
 CONTRIBUTORS vii

Ginger E. Holt, MD Steven Lovejoy, BS, MD

Professor and Vice Chair, Orthopaedic Surgery Assistant Professor
Vanderbilt University Medical Center Pediatric Orthopedic Surgery
Nashville, Tennessee Vanderbilt Children’s Hospital
Nashville, Tennessee
Elizabeth W. Hubbard, MD
Assistant Professor of Orthopaedic Surgery Jeffrey E. Martus, MD, MS
Duke University School of Medicine Associate Professor
Durham, North Carolina Pediatric Orthopaedic Surgery
Vanderbilt University Medical Center
Megan E. Johnson, MD Nashville, Tennessee
Assistant Professor
Orthopaedics Gregory A. Mencio, MD
Vanderbilt University Medical Center Neil E. Green Professor and Vice Chairman
Nashville, Tennessee Department of Orthopaedics
Vanderbilt University Medical Center
Sheila M. Jones, MD Chief, Pediatric Orthopaedics
Medical Director, Pediatric Emergency Department Monroe Carell, Jr. Children’s Hospital at Vanderbilt
Centennial Women’s & Children’s Hospital Nashville, Tennessee
Nashville, Tennessee
Adjunct Assistant Professor of Pediatrics Amirhossein Misaghi, MD
Vanderbilt Children’s Hospital Orthopedic Surgeon
Nashville, Tennessee CHOC (Children’s Hospital of Orange County)
Orange, California
Kevin E. Klingele, MD
Chief James F. Mooney III, MD
Orthopedic Surgery Chief of Staff
Nationwide Children’s Hospital Medical Affairs
Columbus, Ohio Shriners Hospital for Children-Springfield
Springfield, Massachusetts
Scott H. Kozin, MD
Clinical Professor Robert F. Murphy, MD
Orthopedics Surgery Assistant Professor
Lewis Katz School of Medicine Department of Orthopaedics
Temple University Medical University of South Carolina
Philadelphia, Pennsylvania Charleston, South Carolina
Clinical Professor
Orthopaedic Surgery Unni G. Narayanan, MBBS, MSc, FRCS(C)
Sidney Kimmel Medical College Professor
Thomas Jefferson University Department of Surgery & Rehabilitation Sciences
Philadelphia, Pennsylvania Institute
Chief of Staff University of Toronto
Shriners Hospital for Children Divisions of Orthopaedic Surgery and Child Health
Philadelphia, Pennsylvania Evaluative Sciences
The Hospital for Sick Children
Ying Li, MD Toronto, Ontario
Associate Professor Canada
Department of Orthopaedic Surgery
C.S. Mott Children’s Hospital James P. Norris IV, MD
Ann Arbor, Michigan Clinical Instructor
Orthopaedic Surgery
Kristin Livingston, MD Vanderbilt University Medical Center
Assistant Professor of Orthopaedic Surgery Nashville, Tennessee
University of California, San Francisco
San Francisco, California Shital N. Parikh, MD
Professor
Raymond W. Liu, MD Orthopaedic Surgery
Associate Professor and Victor M. Goldberg Endowed Cincinnati Children’s Hospital Medical Center
Chair in Orthopaedics University of Cincinnati School of Medicine
Pediatric Orthopaedic Surgery Cincinnati, Ohio
Rainbow Babies and Children’s Hospitals at Case Western
Reserve University
Cleveland, Ohio
viii CONTRIBUTORS

Anthony I. Riccio, MD Jeffrey Shilt, MD

Associate Professor of Orthopaedic Surgery Chief of Community Surgery
University of Texas Southwestern Medical Center The Woodlands
Dallas, Texas Texas Children’s Hospital
The Woodlands, Texas
Associate Professor
Sanjeev Sabharwal, MD, MPH
Department of Orthopaedics & Scoliosis Surgery
Professor
Baylor School of Medicine
Orthopedics
Houston, Texas
University of California
Medical Director of Motion Analysis & Human
San Francisco
­Performance
Oakland, California
Texas Children’s Hospital
Houston, Texas
Walter Samora, MD
Assistant Professor
Eric D. Shirley, MD
Orthopedic Surgery
Pediatric Orthopaedic Surgeon
Nationwide Children’s Hospital
Pediatric Orthopaedic Associates
Columbus, Ohio
Woodstock, Georgia

Brian Scannell, MD
Mauricio Silva, MD
Associate Professor
Medical Director
Department of Orthopaedic Surgery
Orthopaedic Institute for Children
Atrium Health
Los Angeles, California
Charlotte, North Carolina
Clinical Professor
Physician
UCLA-Orthopaedic Hospital Department of Orthopaedic
OrthoCarolina
Surgery
Charlotte, North Carolina
David Geffen School of Medicine
University of California Los Angeles
Jonathan G. Schoenecker, MD, PhD Los Angeles, California
Associate Professor and Mast Chair of Pediatric Trauma
and Hip Surgery
Louise Z. Spierre, MD
Vanderbilt University Medical Center
Director Pediatric Rehabilitation
Monroe Carell, Jr. Children’s Hospital at Vanderbilt
Wolfson Children’s Hospital
Nashville, Tennessee
Assistant Professor
Department of Pediatrics
Herbert S. Schwartz, MD University of Florida Health Science Center
Professor and Chair Emeritus Jacksonville, Florida
Orthopaedic Surgery
Vanderbilt University Medical Center
Chris Stutz, MD
Nashville, Tennessee
Assistant Professor
Orthopedic, Hand, and Microvascular Surgery
Kevin G. Shea, MD Texas Scottish Rite Hospital for Children
Orthopedic Surgeon Dallas, Texas
Sports Medicine
Stanford University
George H. Thompson, MD
Stanford, California
Director
Professor
Division of Pediatric Orthopaedic Surgery
Orthopaedics
Rainbow Babies and Children’s Hospital
Stanford University
Cleveland, Ohio
Stanford, California
Professor, Orthopaedic Surgery and Pediatrics
Case Western Reserve University
Cleveland, Ohio
 CONTRIBUTORS ix

Rachel M. Thompson, MD Dan A. Zlotolow, MD

Assistant Professor-in-Residence Adjunct Clinical Associate Professor of Orthopaedics
Orthopaedic Surgery The Hospital for Special Surgery
UCLA/OIC New York, New York
Los Angeles, California Attending Physician
Shriners Hospital for Children
Philadelphia, Pennsylvania
Preface

The second edition of Skeletal Trauma in Children provided In the fifth edition, we added chapters on Casting Tech-
the reader with advanced analysis and recommendation for niques and Nerve Injury and Repair. We felt that the for-
the full spectrum of musculoskeletal injuries in children. mer was a useful addition because the vast majority of frac-
We added more advanced forms of fracture care than were tures in children are still best treated by casting, splinting,
available in the first edition and provided expanded refer- and/or immobilization, and we wanted this edition to be
ence lists and treatment recommendations based on greater a more comprehensive tool for individuals treating injured
analysis of outcome. children. The Nerve Injury and Repair in Children chapter
The recognition that children’s diaphyseal fractures are was also thought to add to the scope of the book because
not always best treated by nonoperative means was clearly nerve repair is more often appropriately indicated in in-
explained in the chapters of the second edition. Additional jured children than it is in adults with corresponding better
treatment options for diaphyseal fractures involving mini- functional outcomes. Finally, we added levels of evidence to
mal surgical incisions were spelled out in detail. For exam- the reference list to help readers easily identify the research
ple, the morbidity coming from traditional traction and cast design of the cited references and note those that, because
treatment of femur fractures was clearly described. The risk of a higher-quality research design, should impact practice
of complications from operative management of long bone decisions the most.
fractures, such as overgrowth, infection, and nonunion, The sixth edition adds updated chapters with a focus on
were detailed. The second edition added new chapters on innovative, evolving techniques for pediatric fracture care,
the assessment of outcome of musculoskeletal injury, which such as expanded use of minimally invasive bridge plating
has proved to be a widely used reference in the pediatric and elastic nailing, while providing methods and tips for
musculoskeletal injury community. In fact, evidence ob- modern application of tried-and-true principles of closed
tained by this relatively new field has provided much of the treatment for children’s fractures. Newly developed surgi-
rationale for more invasive treatment of skeletal injuries in cal approaches, such as surgical hip dislocation approaches
children. for pediatric hip injuries and arthroscopically assisted tech-
In the third edition, we added two new chapters. The niques for pediatric intraarticular injuries, are reviewed.
chapter on Anesthesia and Analgesia for the Ambulato- As in the first five editions, we did not spend much time
ry Management of Children’s Fractures stems from our reviewing treatment of historical interest only. We updated
long-standing academic interest in the best ways to manage the treatment of all musculoskeletal injuries in this volume
pain in children while achieving safe and accurate reduc- to continue to enable the reader to find quickly and review
tion. As is the tradition of this book with management of the details about what is considered to be the current best
individual injuries, we provided descriptors for the full spec- method of treatment for individual pediatric musculoskel-
trum of options with recommended treatment. Second, we etal injuries. Our contributors again labored many hun-
added a chapter on Rehabilitation of the Child with Multi- dreds of hours individually and in teams to provide you,
ple Injuries. This chapter has proved to be a useful refer- the reader, with this current compendium. Most important,
ence in defining the role of rehabilitation services in obtain- organizing the material in a way that is useful to working
ing optimum outcomes for children with multiple injuries, surgeons should provide the orthopedic surgeon with more
especially those with a concomitant head injury. confidence and result in better outcomes for children with
In the fourth edition, we expanded the detail in the musculoskeletal injuries.
­Rehabilitation chapter and Anesthesia chapter and added
material on new methods of internal fixation, both indica- Gregory A. Mencio, MD
tions and results. In addition, a new chapter on Sports Inju- Steven L. Frick, MD
ries was added.

x
 PREFACE xi

Levels of Evidence for Primary Research Question1

Types of Studies

Therapeutic Studies— Prognostic Studies— Diagnostic Studies— Economic and

Investigating the Results of Investigating the Effect of Investigating Decision Analyses—
Treatment A Patient Characteristic A Diagnostic Developing An
on the Outcome of Dis- Test Economic or
ease Decision Model
Level I • H igh-quality randomized con- • H igh-quality prospective • Testing of previously • S ensible costs and alterna-
trolled trial with statistically study4 (all patients were developed diagnostic tives; values obtained from
significant difference or no enrolled at the same point criteria in series of con- many studies; multiway
statistically significant differ- in their disease with ≥80% secutive patients (with sensitivity analyses
ence but narrow confidence follow-up of enrolled pa- universally applied refer- • Systematic review2 of
intervals tients) ence “gold” standard) Level I studies
• Systematic review2 of Level I • Systematic review2 of Level • Systematic review2 of
randomized controlled trials I studies Level I studies
(and study results were ho-
mogeneous3)
Level II • Lesser-quality randomized • R etrospective6 study • D evelopment of diag- • S ensible costs and alter-
controlled trial (e.g., <80% • U  ntreated controls from a nostic criteria on basis of natives; values obtained
follow-up, no blinding, or im- randomized controlled trial consecutive patients (with from limited studies; multi-
proper randomization) • Lesser-quality prospective universally applied refer- way sensitivity analyses
• Prospective4 comparative study (e.g., patients en- ence “gold” standard) • Systematic review2 of
study5 rolled at different points in • Systematic review2 of Level II studies
• Systematic review2 of Level II their disease or <80% fol- Level II studies
studies or Level I studies with low-up)
inconsistent results • Systematic review2 of Level
II studies
Level III • C ase-control study7 • Case-control study7 • Study of nonconsec- • A nalyses based on limit-
• R  etrospective6 comparative utive patients (without ed alternatives and costs;
study5 consistently applied ref- poor estimates
• Systematic review2 of Level III erence “gold” standard) • Systematic review2 of Level
studies • Systematic review2 of III studies
Level III studies
Level IV • Case series8 • Case series • C
 ase-control study • No sensitivity analyses
• P oor reference standard
Level V • Expert opinion • Expert opinion • Expert opinion • Expert opinion

1A complete assessment of the quality of individual studies requires critical appraisal of all aspects of the study design.
2A combination of results from two or more prior studies.
3Studies provided consistent results.
4Study was started before the first patient enrolled.
5Patients treated one way (e.g., with cemented hip arthroplasty) compared with patients treated another way (e.g., with cement-less hip

arthroplasty) at the same institution.

6Study was started after the first patient enrolled.
7Patients identified for the study on the basis of their outcome (e.g., failed total hip arthroplasty), called “cases,” are compared with those

who did not have the outcome (e.g., had a successful total hip arthroplasty), called “controls.”
8Patients treated one way with no comparison group of patients treated another way.

From the Journal of Bone and Joint Surgery (jbjs.org). Originally adapted from material published by the Centre for Evidence-Based
Medicine, Oxford, UK. For more information, please see www.cebm.net.
Acknowledgments

Many individuals at Elsevier provided an important role in Drs. Frank Bassett, J. Leonard Goldner, James Urbaniak,
the development, writing, and editing of this text. We would and Robert Fitch at Duke University Medical Center and
like to particularly thank Katie DeFrancesco for her efforts Dan Spengler at Vanderbilt. Finally, I would like to thank
to oversee preparation of the sixth edition. We would be Drs. Steven Lovejoy, Jeffrey Martus, Jonathan Schoenecker,
­remiss not to acknowledge the significant contributions by Christopher Stutz, Megan Johnson, Kevin Dale, and David
Dr Mark Swiontkowski as co-editor of the previous 5 editions Ebenezer, current and former partners at Monroe Carell Jr.
of Skeletal Trauma in Children and whose shared vision Children’s Hospital at Vanderbilt for the expertise, enthu-
along with Dr Green was foundational in the development siasm, and skill they display daily in managing all aspects of
of this text. pediatric orthopedic trauma. Their commitment to excel-
I, Gregory Mencio, acknowledge that my editorial con- lence in patient care, orthopedic education, and scholarly
tribution to this text is based on the knowledge and expe- exchange continues to make coming to work a fulfilling
rience that I have gained from my practice at Vanderbilt experience.
University Medical Center since 1991. In particular, I want I, Steve Frick, want to acknowledge the mentorship pro-
to thank Dr. Neil Green, with whom I had the pleasure of vided me by many orthopedic surgeons during my career,
working for more than 25 years at Vanderbilt. Dr. Green including Drs. Green and Swiontkowski, and Dr. Mencio for
was a great surgeon, tremendous partner, outstanding role the opportunity to assist with this edition. Learning from
model, and loyal friend. He was an educator par excellence Drs. Edward Hanley Jr., Jeffrey Kneisl, James Kellam, Mi-
and a superb surgeon who has had a major influence on chael Bosse, Stephen Sims, Scott Mubarak, Dennis Wenger,
the evolution of pediatric orthopedic trauma care. I am Peter Newton, Henry Chambers, and Douglas Wallace pre-
grateful to Mark Swiontkowski for his friendship over the pared me for a career taking care of injured patients. Thanks
years and guidance in coediting the fifth edition of ­Skeletal to my professional colleagues at Carolinas Medical Center,
Trauma in Children and to Steve Frick for his support and Nemours Children’s Hospital, and Stanford University and
collaboration as coeditor on this edition of the book. I the dedicated members of the Pediatric Orthopaedic Soci-
would also like to recognize the many other mentors who ety of North America for providing ongoing dialogue and
have had meaningful impact on my career, including research to improve our care for injured children.

xii
 Skeletal Growth, Development,
and Healing as Related to
Pediatric Trauma 1
Brian Scannell | Steven L. Frick

INTRODUCTION which can be seen in plastic deformation and “greenstick”

fractures in the forearm, should usually be corrected.1,2
Consideration of growth potential is the major difference Bone healing in children is generally rapid, primarily be-
in treating injuries in children as compared with adults. cause of the thickened, extremely osteogenic periosteum.
Pediatric skeletal trauma can result in enhanced or dimin- The age of the patient directly affects the rate of healing of
ished growth. Future growth is usually helpful because any fracture: the younger the child, the more rapidly the
some angular and length deformities can correct them- fracture heals. The periosteum thins as the child grows old-
selves as the child grows. Loss of growth potential can be er and has less osteogenic capability. Injuries to the growth
one of the more difficult problems to treat. Adult bone plate heal more rapidly than shaft fractures do. Physeal in-
is dynamic; it is constantly involved in bone turnover and juries, in almost all parts of the body, heal in approximately
remodeling in response to aging and changes in stress 3 weeks.3
on the skeleton. The pediatric skeleton not only remod- Treatment of trauma to the pediatric skeleton is generally
els in response to alterations in stress but also grows in straightforward. Dislocations and ligamentous injuries are
length and width and changes shape, alignment, and ro- uncommon in children in comparison with adults because
tation as it matures. Understanding growth potential and the physis and bones in children are usually weaker mechan-
the changing forces after skeletal trauma in children are ical links in the system and thus more susceptible to injury.
important in determining the appropriate treatment for Ligamentous injuries may occur, especially in older chil-
injured bones. dren, as physiologic physeodeses begin to occur, resulting
The following are the most common clinical questions in in more secure attachments of the epiphyseal and metaph-
caring for children with fractures: (1) is the physis injured yseal regions.4,5 Most injuries, though, are simple fracture
with an accompanying risk of growth disturbance, and (2) patterns caused by low-velocity trauma such as falls. In most
is the length and alignment of the fracture acceptable or cases, closed reduction followed by a short period of immo-
unacceptable (i.e., will it improve with growth enough that bilization restores normal function to a pediatric extremity.
function and cosmesis will not be adversely affected)? If the However, a number of pitfalls can make treatment of pe-
answer is no, a reduction is indicated. The response to these diatric fractures, particularly fractures of the growth plate,
two questions requires knowledge of normal growth mech- difficult and demanding.
anisms and studies of fractures in children (the science),
whereas applying this knowledge to an individual patient
and making decisions about how to care for the fracture re- HISTORY, DIAGNOSIS, AND INJURY
quire an assessment of multiple factors related to the child MECHANISMS
and the fracture (the art).
Principles of fracture treatment are the same for all In infants, skeletal trauma may be related to the birthing
ages—the goal is to achieve restoration of normal length, process or may be the only sign of child abuse because young
alignment, rotation, and the anatomic reduction of artic- children are at higher risk for abuse.6 The presenting sign
ular surfaces. In children, attempting to preserve normal may be deformity, swelling, or lack of movement in an ex-
growth potential is also critical; thus, assessment of the in- tremity. Caregivers should be questioned about the circum-
tegrity and alignment of the physis is important. Although stances of the injury, and a lack of a plausible mechanism of
some angulation is acceptable when treating fractures in injury should prompt an evaluation for nonaccidental trau-
children, it is best to keep the amount of angulation as small ma. Radiographs of an infant can be difficult to obtain and
as possible by closed fracture treatment methods, regardless interpret, especially those of bones in the elbow and hip re-
of the patient’s age. On the other hand, multiple attempts gion, which may require comparison views. Anteroposterior
at anatomic reduction in a child, particularly in fractures and lateral views, including the joints above and below the
involving the physis, may cause harm and should be avoid- injured area, constitute a minimal radiographic evaluation.
ed. The small amount of angulation associated with torus Usually, routine radiographs coupled with a good physical
or so-called buckle fractures in children is almost always examination can establish the diagnosis. Arthrograms, ultra-
acceptable. Marked bowing that causes clinical deformity, sonography, or magnetic resonance imaging (MRI) can be

1
2 CHAPTER 1 — SKELETAL GROWTH, DEVELOPMENT, AND HEALING AS RELATED TO PEDIATRIC TRAUMA

useful as a diagnostic aid when radiographs are confusing.3,7 when treating very young children with fractures.6,16 Care
Additionally, a skeletal survey can be used in the young pa- must be taken to ensure that the child is checked for signs of
tient because unsuspected fractures may be present up to abuse on the initial assessment and for possible subsequent
20% of the time.8 injuries during follow-up. Repeating a skeletal survey at 2 to
Children with multiple trauma or head injuries or both 3 weeks is strongly recommended in young patients to in-
can have occult axial fractures and physeal injuries that crease diagnostic yield in patients with suspected abuse inju-
may not be suspected or may be difficult to diagnose, even ries.17 Parents or guardians of children who are not brought
with a good physical examination. This is more commonly back for follow-up appointments for fractures should be con-
seen in patients with a lower Glasgow Coma Scale and high- tacted and asked to schedule a return visit.
er Injury Severity Score.9 In these children, historically, a
bone scan assisted in diagnosing fractures unidentified by
routine screening radiographs10; however, they can be dif- FORMATION OF BONE
ficult to obtain in multiply injured children. More recently,
radiographic skeletal surveys and multiplanar imaging with Embryonic bone forms through either membranous or en-
computed tomography or MRI are favored for identifying dochondral ossification. In the former, mesenchymal cells
occult injuries.11 proliferate to form membranes primarily in the region in
Fractures through the growth plate in children can be which flat bones are fabricated.18,19 Endochondral ossifi-
difficult to interpret if the fracture is not displaced. A thor- cation is bony replacement of a cartilage model and is the
ough physical examination can usually identify this type of mode of formation of long bones.
injury; the sign is swelling and maximal tenderness occur-
ring over the injured physis, which occurs most commonly
MEMBRANOUS BONE FORMATION
at the distal end of the radius or fibula. Palpation at or distal
to the tip of the lateral malleolus usually identifies a liga- Membranous bone formation increases the diameter of long
mentous injury; swelling and tenderness at the growth plate bones and is responsible for the creation of flat bones such
may suggest a fracture undetected by radiographs. However, as the scapula, skull, and, in part, the clavicle and pelvis.
studies evaluating children with lateral ankle pain after in- Flat bones are formed as mesenchymal cells condense into
jury but normal radiographs were not found to frequently sheets that eventually differentiate into osteoblasts. Surface
have a physeal fracture by ultrasound5 or MRI.12 Another cells become the periosteum. Primary bone is remodeled
recent MRI study challenges the perception that distal fibu- and transformed into cancellous bone, to which the peri-
lar physeal injuries are common after twisting ankle injuries osteum adds a compact cortical bone cover. This type of
in skeletally immature patients.4 Often, a small metaphyseal growth is independent of a cartilage model.
fragment on the radiograph suggests physeal injury. Repeat- As endochondral ossification lengthens bones, prolifera-
ed radiographs in 1 to 2 weeks can confirm the physeal inju- tion of bone occurs beneath the periosteum through mem-
ry because the healing physis appears wider, and periosteal branous bone formation, thus enlarging the diameter of the
reaction may be seen. diaphysis in long bones. This type of bone formation is also
Each age group has typical injury mechanisms and com- apparent in subperiosteal infection and after bone injury
mon fractures. Most infants and newborns (≤12 months of when periosteal bone forms around a fracture hematoma
age) sustain fractures by having someone else injure them. (Fig. 1.1). The osteogenic periosteum of children contrib-
When children are older, walking and running, accidental utes to rapid healing because the callus and periosteal new
injuries are more common. Children most commonly frac- bone increase the diameter of the bone and provide early
ture the forearm, usually the distal end of the radius.13–15 biomechanical strength.
Clavicle fractures are common in infancy and in the pre-
school age group, but their incidence decreases with increas-
ENDOCHONDRAL OSSIFICATION
ing age. Elbow hyperextension in early and midchildhood
predisposes children in these age groups to supracondylar Endochondral ossification requires the presence of a carti-
humerus fractures. Forearm fractures, although common in lage anlage. Early in gestation, mesenchymal cells aggregate
young children, show a progressive increase into the teen- to form models of the future long bones. A cartilage model
age years. develops, and the peripheral cells organize into a perichon-
Most injuries occur when the child falls. Severe, high-en- drium.18,19 Cartilage cells enlarge and degenerate, and the
ergy injuries are less common in children and are frequently matrix surrounding them calcifies. This calcification begins
caused by automobiles, lawn mowers, or motorcycles/all-ter- in the center of the diaphysis and becomes the primary os-
rain vehicles. As a child approaches the midteens, injuries sification center. Vascular buds enter the ossification center
are much like those of an adult. The age at which the growth and transport new mesenchymal cells capable of differenti-
plates close varies greatly and depends on hereditary factors ating into osteoblasts, chondroclasts, and osteoclasts. These
and hormonal variation. Skeletal age is an important factor cells align themselves on the calcified cartilage and deposit
in the consideration of injuries in children, in that the clos- bone. Primary cancellous bone is thus formed, and ossifica-
er the child is to the end of growth, the less prominent the tion expands toward the metaphyseal regions.
role of the growth plate in treatment of the injury and the Long bone growth continues as the terminal ends of the
less the remodeling potential. Healing capacity is inversely cartilage model keep growing in length by cartilage cell pro-
related to age. liferation, hypertrophy, and production of extracellular ma-
Finally, child abuse must be considered in all children’s in- trix. This growth continues in this manner until after birth,
juries, and, as noted earlier, it should especially be considered when secondary ossification centers (epiphyses) develop.
 CHAPTER 1 — SKELETAL GROWTH, DEVELOPMENT, AND HEALING AS RELATED TO PEDIATRIC TRAUMA 3

(growth spurts) occurring after prolonged periods of stasis.

Growth in length occurs only at the physis and can occur
through three mechanisms: an increase in the number of
cells, an increase in the size of cells, or an increase in the
amount of extracellular matrix. The physis responds to var-
ious growth-regulating hormones (e.g., growth hormone,
thyroxine, estrogen, and testosterone), parathyroid hor-
mone, and corticosteroids, as well as the peptide-signaling
proteins—transforming growth factor β (TGF-β), platelet-de-
rived growth factor (PDGF), and bone morphogenetic pro-
teins (BMPs)—and immunoregulatory cytokines (interleu-
kin-1 [IL-1] and IL-6).22–26 Further research is still needed
to better understand these growth pathways. However, re-
cently it was suggested that differential expression of gene
pathways specifically for BMP-2 and BMP-6 may contribute
to further physeal growth.27
Local paracrine regulators have recently been identified
as critical in controlling bone development and remodeling.
An important feedback loop controlling chondrocyte devel-
opment involves Indian hedgehog protein (Ihh) and para-
thyroid hormone-related peptide. These paracrine factors
control the decision for chondrocytes to leave the prolifera-
tive pool and undergo hypertrophic differentiation.28,29 Fi-
broblast growth factor (FGF) signaling also appears crucial
A B in regulating chondrocyte proliferation and differentiation
in the physis and appears to have an opposite effect from
Fig. 1.1 (A) Radiograph of a healing supracondylar fracture illustrat- the BMPs, decreasing chondrocyte proliferation, increasing
ing the periosteum stripped (arrow) to nearly the midshaft of the hu- production of Ihh, and accelerating differentiation of hy-
merus. The bridging periosteal bone stabilizes this fracture in about 3
pertrophic chondrocytes.29 An example of abnormal growth
weeks. (B) The large periosteal involucrum surrounds the former bone
(sequestrum) in a femur with osteomyelitis. The periosteum can be
related to FGF signaling is in achondroplasia. A gene muta-
stimulated to remanufacture an entire cortex around this area, such tion affecting FGF receptor 3 suppresses proliferation and
that when the sequestered bone is removed, the periosteal bone will maturation of growth plate chondrocytes, causing decreased
form a new (larger-diameter) femoral diaphysis. growth plate size and decreased bone elongation.30 Thyrox-
ine is also involved in the cellular and molecular events of
The mass of cartilage found between the epiphyseal and terminal chondrocyte differentiation and morphogenesis of
diaphyseal bones in later postnatal development thins to be- columnar cartilage.31
come the epiphyseal plate, which continues as the principal Diurnal variation in the growth of bone has been shown
contributor to the growth (in length) of long bones until to reflect the levels of the different hormones, and animal
maturation is reached. The girth of the long bone is provid- studies suggest mechanical factors may also be critical be-
ed by the cambium layer of the periosteum.13,18 Successive cause 90% of growth occurred during periods of recum-
surfaces of compact bone are added to the exterior while re- bency in a study of growth in sheep.21 Physeal growth is
modeling by resorption of the interior (endosteal) surface slowed by excessive compression and accelerated by distrac-
takes place. tion, recognized in the American literature as the Hueter-
Once the physis is established between the epiphysis and Volkmann law,32 but noted earlier by Delpech in 1829.33
metaphysis, the periosteal ring becomes relatively firmly at- This theory affects growth but also fracture healing, which
tached at the level of the zone of hypertrophied cells. This is one of many differences between pediatric and adult frac-
periphyseal periosteal collar is referred to as the fibrous ring ture healing.
of LaCroix.3,13,18 The zone of Ranvier, the cellular segment Growth in length ceases at skeletal maturity with fusion of
responsible for growth in diameter of the physis,13 is located the physes and occurs at different times in individual bones;
in the same area. The periosteum is firmly attached at this it also varies based on gender, hereditary factors, and hor-
level. Even when the periosteum is torn over the metaphysis mone levels. Physiologic physiodesis is the normal, gradual
or diaphysis, it usually remains attached at the physis. replacement of the growth plate by bone during adoles-
cence, and physeal closure is induced at skeletal maturity by
estrogen levels in both males and females.28
REGULATION OF GROWTH AND
DEVELOPMENT
BIOLOGY OF FRACTURE HEALING
Factors affecting skeletal growth vary and are incompletely
understood. Although commonly used growth curve charts Fracture healing is usually divided into three stages: (1)
suggest that growth is smoothly continuous throughout inflammatory, (2) reparative, and (3) remodeling. Fracture
childhood, a saltation and stasis model of human growth healing involves both membranous and endochondral os-
is now recognized,20,21 with bursts of growth in length sification. Injuries to the pediatric skeleton always involve
4 CHAPTER 1 — SKELETAL GROWTH, DEVELOPMENT, AND HEALING AS RELATED TO PEDIATRIC TRAUMA

a variable amount of surrounding soft tissue injury. Unlike Pediatric bone is more vascular than that of an adult and
the soft tissues, which heal by replacement of the injured is able to generate a greater hyperemic and inflammatory
tissue with collagen scar tissue, bone heals by replacing the response. The more mature (less porous) the cortex, the
area that is injured with normal bony tissue. slower the vascular response to injury. Vasodilatation and
The blood supply to the bone is an important part of frac- the cellular inflammatory response begin shortly after a frac-
ture healing, and significant soft tissue injury delays healing ture, and the injured area is filled with inflammatory cells
because the blood supply to bone enters at sites of soft tis- such as polymorphonuclear leukocytes and macrophages.
sue attachment. The normal process of fracture healing in The hematoma and inflammatory response also incite the
any part of the bone follows a set chronologic order. Any of release of molecules such as growth factors and cytokines
these phases may be disrupted or delayed by excessive adja- from the platelets.37 In the initial phase of fracture healing,
cent soft tissue injury. after the hematoma has formed, a scaffolding of fibrovascu-
lar tissue replaces the clot with collagen fibers. These fibers
eventually become the collagen of the woven bone of the
INFLAMMATORY PHASE
primary callus that forms around the fracture.
The inflammatory phase of fracture healing “sets the stage” The primary callus is later ossified as the microvascular
for cartilage and bone formation by supplying the building supply returns to the area. However, the bone, for at least a
blocks necessary for repair and remodeling. When bone is in- millimeter or two directly adjacent to the fracture site, loses
jured, the bone, periosteum, and soft tissue (mostly muscle) its blood supply early in the inflammatory stage. After ini-
around the fracture begin to bleed. Hematomas form at the tial reabsorption of the dead bone along the fracture line,
fracture site, both inside and outside the bone. The hemato- the fracture line in children usually becomes more visible
ma may dissect along the periosteum, which is easily elevated radiographically 2 or 3 weeks after injury. The dead bone at
or was elevated at the time that the fracture was maximally the fracture surface is revascularized in a process that occurs
displaced. The more severe the soft tissue injury, the more faster in more vascular areas such as the metaphysis (as com-
displaced the fracture; in addition, the more the periosteum pared with the diaphysis).
is torn, the larger the area that fills with the hematoma. The The vascular response aids in initiating the cellular re-
role of a hematoma is to serve as a source of signaling agents sponse to the fracture. A number of TGF-β subtypes help
capable of initiating cellular events critical to fracture healing. mediate cellular and tissue responses to inflammation and
This also explains why some minimally displaced or greenstick tissue repair.37 During the inflammatory phase of fracture
fractures (minimal to no hematoma) may be slow to heal. healing, TGF-β from the extracellular matrix of bone and
Research has focused on factors controlling fracture heal- also from platelets controls the mesenchymal precursor cells
ing in two groups: peptide-signaling proteins (TGF-β, FGF, that may form osteoblasts and osteoclasts. The maximal cel-
PDGF, and BMPs) and immunoregulatory cytokines (IL-1 lular response is ongoing within 24 hours of injury and oc-
and IL-6).25 The peptide-signaling proteins are derived from curs first in the subperiosteal region of the fracture.38,39
platelets and extracellular bone matrix and are critical for Osteogenic induction is stimulation by growth factors to
regulation of cell proliferation and mesenchymal stem cell convert the multipotential cells into osteoprogenitor cells.
differentiation. TGF-β is a multifunctional growth factor The osteoprogenitor cells on the undersurface of the peri-
that controls tissue differentiation in fracture repair. FGFs osteum help form periosteal bone. The osteogenic cells that
increase the proliferation of osteoblasts and chondrocytes originate from the periosteum help manufacture the exter-
and may stimulate the formation of new blood vessels. PDGF nal callus. Endochondral bone formation from the endos-
acts on mesenchymal cell precursors to stimulate osteoblast teal areas combines with subperiosteal bone formation to
differentiation. BMPs are a class of proteins produced in the bridge the fracture.
early stages of fracture repair and strongly stimulate endo- The subperiosteal callus in children initially stabilizes the
chondral ossification. The sole criterion for BMP classifica- area so that the external callus may clinically heal the frac-
tion is the induction of bone formation in a standard in vivo ture by the end of the reparative phase. During remodeling,
rodent assay, and at least 14 BMPs, grouped in the TGF su- this callus decreases and is replaced with the endochondral
perfamily of growth and differentiation factors, have been ossified bone that has formed at the fracture surface.
identified. BMPs are present in bone matrix in a form that
allows for presentation to marrow stromal cells to induce
REPARATIVE PHASE
differentiation into osteoblasts. Furthermore, osteoblasts have
been shown to synthesize and secrete BMPs. Cells that syn- The reparative phase of fracture healing is highlighted by
thesize new bone during fractures also have been shown the development of new blood vessels and the onset of carti-
to be targets of BMPs and to possess BMP receptors. BMPs lage formation. The surrounding soft tissue provides vascu-
(BMP 2, 3, 4, 5, and 8) and BMP receptors are upregulated lar ingrowth initially to the periosteal area and subsequently
in the periosteum as early as 3 days after fracture.34 to the endosteal area. Before the fracture, the cortical blood
Studies utilizing microarray analysis of the genetic response supply was primarily from endosteal bone and branched out
to a fracture demonstrate that the genomic response to a radially from inside the medullary canal. During the repar-
fracture is complex and involves thousands of genes, includ- ative phase, most of the blood supply to the cortex arises
ing the BMPs and other growth factors noted earlier, as well from outside the bone rather than inside.
as immunoregulatory cytokines.10,34–36 The immunoregula- Rat models of fracture healing reveal that intramembra-
tory cytokines are released from inflammatory cells present nous and endochondral bone formation is initiated during
in the hematoma and serve to regulate the early events in the first 10 days. Inflammatory mediators in the fracture he-
fracture healing. matoma recruit chondrocytes capable of producing fracture
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