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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
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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
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contained in the material herein.
vi
CONTRIBUTORS vii
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
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
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
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
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
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
CHAPTER 1 — SKELETAL GROWTH, DEVELOPMENT, AND HEALING AS RELATED TO PEDIATRIC TRAUMA 5
A B
callus. The hematoma is eventually replaced by the ingrowth oxygen tension, and more cartilage is formed. Motion at the
of fibrovascular tissue. This developing construct provides fracture site, the presence of a fracture gap, and an intact
structural support to stabilize the bone ends. This primitive soft tissue envelope all encourage the formation of abun-
tissue is eventually replaced through endochondral and in- dant callus (Fig. 1.2C, D). The increased diameter of the
tramembranous bone formation. callus enhances biomechanical stability because the rigidity
Tissue differentiation during the reparative phase is strong- of the bone is proportional to its radius. The callus formed
ly influenced by local mechanical factors. Fracture stability has subsequently undergoes endochondral ossification. Ideal
a critical effect on bone healing. Fracture healing is classically fracture treatment involves enough rigidity to ensure ade-
divided into primary and secondary healing. Primary healing quate vessel ingrowth, followed by progressive loading and
results from rigid stabilization (i.e., plate immobilization) and motion to stimulate ample callus formation.36,40
involves a direct attempt by the cortex to bridge the fracture As the periosteum produces bone beneath it, the perioste-
gap. Bridging occurs through direct haversian remodeling by um is pushed away from the bone and makes a collar of bone
intramembranous bone formation (Fig. 1.2A, B). around the area of injury. Initially, this tissue is more cartilagi-
Secondary healing results from treatment of fractures with nous and fibrous and is not very well ossified. It may not show
less rigid methods (i.e., fracture bracing, casts). In second- up well on a radiograph until the blood supply is adequate
ary healing, more motion at the fracture site leads to lower enough to allow mineralization and conversion to bone.
6 CHAPTER 1 — SKELETAL GROWTH, DEVELOPMENT, AND HEALING AS RELATED TO PEDIATRIC TRAUMA
is controversial because surgical reduction of distal tibial fractures; some investigators have hypothesized that disrup-
fractures was not shown to reduce the incidence of prema- tion of the periosteal sleeve or increasing vascularity of the
ture physeal closure, which still remained high at 43%.54 bone after a fracture increases longitudinal growth.19,23 This
Physeal fracture healing in clinical and basic science studies phenomenon most frequently compensates for fractures
is rapid; almost all fractures heal within 3 weeks. that heal with shortening but occasionally results in the in-
jured limb being longer. The same cells and processes that
govern normal growth are involved in fracture healing.55
DIFFERENCES BETWEEN PEDIATRIC AND Studying growth mechanisms with microarray technology
ADULT FRACTURE HEALING demonstrates the complexity of the genetic response to a
fracture. In a study of femoral overgrowth mechanisms in
One of the primary differences between pediatric and adult a rat model, more than 5000 genes in the proximal femo-
bone is that the periosteum in children is very thick. The ral physis were noted to respond significantly to fractures.
periosteum around the fracture site walls off the hemato- Genes related to vascular development and growth were
ma and is stripped from the bone as bleeding occurs—a downregulated, which casts doubt on the widely held asser-
primary factor in the amount of new bone formed around tion that femoral overgrowth is a consequence of increased
a fracture. The area of bone necrosis on either side of the vascularity in the limb after a fracture.35 It has been postu-
fracture surface must be replaced by viable bone through lated that mechanical factors, such as tension within the
the process of bone resorption and deposition. This process surrounding periosteum, may have some control over the
leads to an initial radiographic appearance of sclerosis at the growth rate.18,19 This is clinically best exemplified by post-
fracture site because new bone is being formed on the exist- traumatic tibia valgus after proximal tibial metaphyseal frac-
ing necrotic bone. The area around the necrotic bone elicits tures in children (the Cozen phenomenon).56–58 Recent
an inflammatory response. Because pediatric bone is more basic science data by Halanski et al59 confirmed that disrup-
vascular than adult bone, the inflammatory (hyperemic) re- tion of the periosteum would accelerate growth. This pat-
sponse is more rapid and significant. Temperatures as high tern of overgrowth is not observed in adult fracture healing,
as 40°C may be noted after major long bone fractures. This and thus, fracture shortening at union will be permanent.
hyperemic inflammatory reaction may also be responsible
for growth stimulation, which may result in overgrowth of GROWTH ARREST LINES OR GROWTH
the bone. The early stage of fracture healing is shorter in a
SLOWDOWN LINES
child than in an adult.14,19
The major reason for the increased speed of healing of In radiographs of bones that were fractured several weeks
children’s fractures is the periosteum, which contributes the to months previously, transverse lines may be seen in the
largest part of new bone formation around a fracture. Chil- metaphyseal region. These lines are usually referred to as
dren have significantly greater osteoblastic activity in this Harris growth arrest lines, or the transverse lines of Park,60
area because bone is already being formed beneath the peri- and are unique to children’s bones after a fracture or injury.
osteum as part of normal growth. This already active process These transversely oriented trabeculae occur in bones that
is readily accelerated after a fracture. Periosteal callus bridg- are normally growing rapidly (e.g., femur or tibia) and in
es fractures in children long before the underlying hemato- those in which the trabeculae are predominantly longitudi-
ma forms a cartilage anlage that goes on to ossify. Once cel- nally oriented (Fig. 1.3). When growth deceleration occurs,
lular organization from the hematoma has passed through as happens immediately after a fracture of an extremity, the
the inflammatory process, repair of the bone begins in the bone is, in effect, standing still and making transversely ori-
area of the fracture. In most children, by 10 days to 2 weeks ented trabeculae. The calcified cartilage and bone formed
after the fracture, a rubberlike bone forms around the frac- has increased density and is evident radiographically after
ture and makes it difficult to manipulate. The fracture site further growth. Arrest lines should parallel the physeal con-
is still tender, however, and not yet ready for mobilization of tour if the physis is growing normally. After a fracture, these
the adjacent joints. lines are typically visible 6 to 12 weeks after injury and can
As part of the reparative phase, cartilage formed as the provide the orthopedist with the ability to assess and pre-
hematoma organizes is eventually replaced by bone through dict abnormal growth.60 A specific effort should be made to
the process of endochondral bone formation. Fracture heal- look for these arrest lines during radiographic evaluation of
ing is a recapitulation of bone development that, as noted childhood fractures, especially those involving the physes,
previously, involves a complex interaction of multiple cell because lines that do not parallel the physis indicate an area
types and cellular processes.55 of physeal damage or an osseous bridge.60,61 Arrest lines that
The remodeling phase of fracture healing may continue do not parallel the physis point to an area of abnormal phy-
for some time, particularly in more displaced fractures. The seal growth.
motion of the adjacent joints and the use of the extremity The physes that grow more rapidly (e.g., the distal end of
accelerate remodeling. The stresses and strains of regular the femur or the proximal end of the tibia) have arrest lines
use of the bone directly promote remodeling of the frac- farthest from the physis. In the metaphyseal areas of bones,
tured bone into a bone that closely resembles the original where the slowest growth occurs, transverse trabeculae may
structure. be difficult to see radiographically or may not form at all.
Children also vary from adults as bone overgrowth has Transversely oriented Harris lines may also result from
been seen in pediatric fracture healing. Fractures distant any type of stress on the bone that causes a temporary slow-
from the physis can also result in changes in growth patterns. down in the formation of longitudinally oriented bone.
This is particularly evident in overgrowth after femoral shaft Such stresses include systemic illness, fever, and starvation,
8 CHAPTER 1 — SKELETAL GROWTH, DEVELOPMENT, AND HEALING AS RELATED TO PEDIATRIC TRAUMA
as well as skeletal trauma.62 Similar lines can be seen in immature long bones occurs at the growth plate and along
skeletally immature patients being treated with bisphospho- the shaft.67 Accelerated growth of the injured bone (as well
nates, and are called zebra lines in osteogenesis imperfecta as surrounding bones) can occur, leading to limb length dis-
patients.63,64 crepancy (usually the femur or humerus).68 Growth, howev-
er, can produce deformity if the growth plate is injured or
if trauma has altered muscle forces on an extremity, as may
REMODELING AFTER A FRACTURE IN CHILDHOOD
occur after a spinal cord injury or traumatic brain injury.
The remodeling ability of bone in children may make reduc- Remodeling may occur readily in the plane of a joint
tion accuracy less important than it is in adults. Remodeling is (Fig. 1.5), but it occurs far less readily, if at all, in chil-
a commonly used term in pediatric fracture care, implying dren with rotational deformity or angular deformity not
that the child has the ability to straighten and correct resid- in the plane of the joint.14,65,66,69 Abraham67 studied the
ual deformity with growth. This capability depends not only remodeling potential of immature monkeys and found
on the mechanisms of bone remodeling described earlier that remodeling occurred at the growth plate and along
during the remodeling phase of fracture healing (Wolff’s the concavity of the shaft deformity, with minimal resorp-
law) but also on reorientation of the physis by asymmetric tion on the convexity of the shaft. Diaphyseal remodeling
growth after a fracture (Hueter-Volkmann law or Delpech’s and physeal reorientation with growth contributed simi-
law). Younger children have greater remodeling potential. lar amounts to the degree of remodeling. In femoral shaft
The amount depends on the age of the child, location of the fractures in children, 75% of the remodeling of angular de-
injury in the bone (proximity to the physis), degree of defor- formities takes place in the physis, and 25% comes from
mity, and whether the deformity is in the plane of motion of appositional remodeling of the diaphysis.70 The physis ad-
the adjacent joint.3,65,66 Clinical judgment and experience jacent to a fracture realigns itself with asymmetric growth
are required to guide decision-making regarding defining to become perpendicular to the forces acting through the
“acceptable” reductions, but obtaining the best reduction bone, and most authors believe this is the primary mecha-
possible during initial treatment is advisable because it will nism for remodeling.66
lessen reliance on remodeling. Remodeling does not occur Significant angulation in the midportion of long bones
in displaced intraarticular fractures; thus reduction, usual- is not usually acceptable and does not remodel very well,
ly by open methods, is needed. In children, remodeling is depending on the age of the child. In children younger
often relied on for the treatment of proximal humeral and than 8 years, residual angulation is more acceptable. If the
distal radial injuries because these physes contribute greatly angulation is less than 30 degrees and is within the plane
to the length of the respective segment, and the joints have of the joint, remodeling toward normal alignment can be
wide ranges of motion. Remarkable remodeling has been expected.2,19 The potential for remodeling to an acceptable
documented in cases of these fractures (Fig. 1.4). functional and cosmetic outcome depends on many factors,
The effect of growth on fracture healing usually aids in including which bone is fractured, how close the fracture is
fracture treatment because some angulation and deformity to a joint, the orientation to the joint axis, and the amount
remodels with growth. Remodeling of angular deformities of of growth remaining for the child.66 Side-to-side (bayonet or
CHAPTER 1 — SKELETAL GROWTH, DEVELOPMENT, AND HEALING AS RELATED TO PEDIATRIC TRAUMA 9
A B