Rockwood & Wilkins'

Fractures In Children
[5th Edition]

James H. Beaty
James R. Kasser
CLICK HERE FOR TABLE OF CONTENTS
 Contributing Authors XI Role of the Pediatric Trauma Center 76
Preface xiii Initial Resuscitation and Evaluation 76
Acknowledgments xv Evaluation and Assessment 77
Nonorthopaedic Conditions of the Multiply Injured
Child 80
Orthopaedic Management of the Multiply Injured
SECTION I: GENERAL PRINCIPLES 1 Child 82
Stabilization of Fractures 85
1 The Present Status of Children's Fractures 3 5 Physeal Injuries and Growth Arrest 91
Kaye E. Wil/?ins and Alaric j. Aroojis Hamlet A. Peterson
The Informational Changes 3 Pbyseal Fractures 91
Changes in the Philosophy of Treating Fractures in Complications 104
Children 4 Other Physeal Fractures 105
The Present Status of the Incidence of Fractures in Physeal Arrest 114
Children 5 Complications 128
Etiology of Fractures 12 Results 128
Preventive Programs 17 6 Pathologic Fractures Associated with Tumors
and Unique Conditions of the
2 The Biologic Aspects of Children's
Musculoskeletal System 139
Fractures 21
John P. Dormans and John M. F6mn
Edward W Johnstone and Bruce K Foster
Fractures Associated with Cysts, Tumors, or
The Immature Skeleton 21
Tumor-like Processes 142
Anatomic Regions of the Child's Bones 21 Bone and Fibrous Tissue Diseases 169
The Molecular Bone 29 Congenital Insensitiviry ro Pain 180
Mechanisms of Bone Growth 35 Marrow Disease of Bone 182
Fracture Repair 37 Osteomyelitis 193
The Future of Fracture Repair 42 Pathologic Fractures After Limb Lengthening 197
3 Pain Relief and Related Concerns in Fractures in Conditions that Weaken Bone 197
Children's Fractures 49 Fractures in Neuromuscular Disease 219
Joseph R. Furman 7 Child Abuse 241
Guidelines and Principles of Sedation in Robert M. Camp be!!, Jr.
Children 49 Epidemiology 241
Sedative Medications 54 Historical Overview 241
Regional Anesthesia in the Child with a The Homes at Risk 242
Musculoskeletal Injury 61 The Children at Risk 242
Posroperative Analgesia in the Child with a Sexual Abuse 243
Musculoskeletal Injury 67 Obtaining the History 243
Treatment of Postoperative Nausea 70 Physical Examination 245
Fractures in Child Abuse 249
4 Management of the Multiply Injured Additional Imaging Studies 253
Child 75 Interpreting Imaging Studies in Child Abuse 254
Vernon T Tolo Dating Fractures 256
Incidence of Injuries 75 Laboratory Studies and Consultations 258
Common Mechanisms of Injury 76 The Differential Diagnosis 258

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viii Contents

Osteogenesis Imperfecta 259 Incidence and General Considerations 577

Treatment and Legal Reporting Requirements 260 Extension-Type Supracondylar Fractures 578
The Courtroom 261 Flexion-Type Supracondylar Fracture 616
Prevention of Child Abuse 263 15 The Elbow: Physeal Fractures, Apophyseal
Injuries of the Distal Humerus, Avascular
Necrosis of the Trochlea, and T-Condylar
SECTION II: UPPER EXTREMITY 267 Fractures 625
James H. Beaty and James R. Kassfr
8 Fractures and Dislocations of the Hand and Physeal Fractures 625
Carpus in Children 269 Apophyseal Injuries of the Distal Humerus 663
Thomas J Graham and Peter !V!. Watm Avascular Necrosis of the Trochlea 681
Overview of Pediatric Hand Injuries 269 T-Condylar Fractures 687
Specific Fractures of the Pediatric Hand 278 16 Dislocations of the Elbow 705
Carpal Injuries in Children 341 George H. Thompson
Dislocations of the Hand and Carpus 360
Classification 705
9 Distal Radius and Ulna Fractures 381 Posterior Elbow Dislocations 705
Peter M. Waters Anterior Elbow Dislocations 722
Classification 382 Medial and Lateral Elbow Dislocations 724
Anatomy 382 Divergent Elbow Dislocation 725
Physeal Injuries 385 Proximal Radioulnar Translocation 726
Radial Physeal Stress Fractures 404 Radial Head Dislocation 727
Ulnar Physeal Fractures 405 Isolated Dislocations of the Ulna 732
Ulnar Styloid Fractures 407 Subluxation of the Radial Head (Pulled Elbow
Metaphyseal Fractures 408 Syndrome) 732
Complete Fractures 416 17 Proximal Humerus, Scapula, and
Pediatric Galeazzi Fractures 432 Clavicle 741
10 Injuries to the Shafts of the Radius and Young Kwon and John F. Sarwark
Ulna 443 Fractures of the Proximal Humerus 741
Charles T Price and Gregory A. Mencio Fractures of the Scapula 751
Fractures of the Shafts of the Radius and Ulna 443 Fractures of the Clavicle 757
Plastic Deformation of the Radius and Ulna 475 Fractures of the Humeral Shaft 765
Distal Humeral Diaphyseal Fractures 776
11 Fractures of the Proximal Radius and Supracondylar Process Fractures 783
Ulna 483 Glenohumeral Subluxation and Dislocation 783
Hemy G. Chambers
Fractures of the Proximal Radius 483
Fractures of the Proximal Ulna (Olecranon) 506 SECTION III: SPINE 807
12 Monteggia Fracture-Dislocation in
Children 529 18 Cervical Spine Injuries in Children 809
Earl A. Stanley and Jose F. de la Garza W C. Warner, Jr.
Historical Background 529 Anatomy 810
Anatomy and Biomechanics 532 History 813
Characteristics and Management of Monteggia Symptoms 813
Injuries 535 Evaluation 813
Summary 560 Radiographic Evaluation 814
13 The Elbow Region: General Concepts in the Initial Management of Cervical Spine Injuries 818
Pediatric Patient 563 Spinal Cord Injury without Radiographic
Abnormalities 822
James H. Beaty and James R. Kassfr
Spinal Cord Injury in Children 822
Incidence 563 Neonatal Injury 823
Anatomy 564
Occipital Condylar Fracture 823
Radiographic Findings 570
Atlantooccipital Instability 824
14 Supracondylar Fractures of the Distal Fractures of the Atlas 830
Humerus 577 Atlantoaxial Injuries 831
James R. Kasser and James H. Beaty SubaxiaJ Injuries 839
 Contents ix

19 Fractures of the Thoracic and Lumbar Osgood-Schlatter Lesion 1026

Spine 847 Fractures of the Patella 1029
Randall T Loder and Robert N. Heminger Part II: Intraarticular and Ligamentous Injuries
Anatomy 847 About the Knee 1035
Classification and Mechanism of Injury 848 Osteochondral Fractures 1035
Signs and Symptoms 852 Fracture of the Tibial Spine
Radiographic Findings 853 (Intercondylar Eminence) 1038
Treatment 859 Ligament Injuries 1044
Prognosis and Complications 863 Knee Dislocations 1057
Patellar Dislocations 1059
Meniscal Injuries 1062
Discoid Meniscus 1067
SECTION IV: LOWER EXTREMITY 881 Tibiofibular Dislocations 1068
24 Fractures of the Shaft of the Tibia and
20 Fractures of the Pelvis 883 Fibula 1077
S. Terrance Canale and James H. Beaty Stephen D. Heinrich
Diagnosis 883 Epidemiology 1077
Classification 885 Classification 1079
Applied Anatomy 886 Diaphyseal Fractures of the Tibia and Fibula 1083
Avulsion Fractures 886 Postfracture Immobilization 1099
Fractures of the Pubis or Ishcium 890 Postfracture Rehabilitation 1099
Fractures of the Sacrum 893 Fractures of the Distal Tibial Metaphysis 1099
Fractures of the Coccyx 893 Complications Associated with Diaphyseal
Fractures of the Ipsilateral Rami 895 Tibia/Fibula Fractures 11 0 1
Fractures Near or Subluxation of the Symphysis Special Fractures 1108
Pubis 895 25 Distal Tibial and Fibular Fractures 1121
Fractures Near or Subluxation of the Sacroiliac
R. Jay Cummings
Joint 897
Diagnosis 1122
Unstable Fracture Patterns 897
Mechanism of Injury and Classification 1125
Acetabular Fractures 904
Anatomy 1131
Complications 909
Treatment 1134
21 Fractures and Traumatic Dislocations of the Rehabilitation 1159
Hip in Children 913 Prognosis and Complications 1160
R. Dale Blasier and Laurie 0. Hughes 26 Fractures and Dislocations of the Foot 1169
Fractures of the Hip 913 Thomas P. San Giovanni and Richard H. Gross
Hip Dislocations in Children 929
Anatomy 1170
22 Femoral Shaft Fractures 941 Fractures of the Talus 1172
James R. Kasser and James H. Beaty Osteochondral Fractures of the Talus 1185
Anatomy 941 Subtalar Dislocation 1187
Mechanism of Injtiry 941 Calcaneus 1187
Diagnosis 942 Fractures of the Lesser Tarsal Bones 1195
Radiographic Findings 942 Tarsometatarsal Injuries 1195
Classification 943 Metatarsals 1199
Treatment 943 Fractures of the Base of the Fifth Metatarsal 1202
Complications of Femoral Shaft Fractures 968 Operative Treatment 1206
Special Fractures of the Femoral Shaft 973 Stress Fractures 1206
Fractures of the Phalanges 1208
23 Fractures and Dislocations about the Open Fractures of the Foot 1209
Knee 981 Lawn Mower Injuries and Other Crush
Paul D. Sponsetler and Car! L. Stanitski Injuries 1209
Part I: Extraarticular Fractures 982 Lacerations of the Foot 1214
Distal Femoral Epiphyseal Fractures 982 Puncture Wounds 1215
Fracture of the Proximal Tibial Epiphysis 1011 Lesions that May Resemble Fracture 1215
Avulsion of the Tibial Tubercle 1019 Subject Index J223
 THE PRESENT STATUS OF
CHILDREN'S FRACTURES
KAYE E. WILKINS
ALARIC J. AROOJIS

THE I FORMATIO AL HA GE THE PRES ,NT STATUS Or THE I CIDENCE OF

Single-Authored Texts FRACT RES I CHILDRE
Mulriauthored Texts Incidence Fracrures
Exclusive Children's Fractures Texts Defining the Incidence of Fractures
Multiauthored Children's Fracture Texts Difficulties in Comparing Fracture Srudies
Emergence of Pediacric Orthopaedics Frequency of Childhood Fractures
Specific F racrure Incidences
CHA GES IN TI E PHILOSOPHY OF TREATING
FRACTURES I CHT DREN ETll LOGY OF FRACTURES
Bloum's Nonoperative Axioms Broad Causes
Complications with Operative Intervenrion Fractures Resulting from Accidemal Trauma
Trend Toward Minimal Invasion Summary
Facwrs Creating a Trend Toward Operative Intervention Less Common Etiologies
Changes from Previous Editions
Phases in Developmem of Operative Techniques PREVENTIVE PROGRAMS
Specific Problems with Operative Techniques National Campaigns
Nonoperative Techniques Need w be Maintained Local Community Parricipation

Tn the past generation there have been many changes in how THE INFORMATIONAL CHANGES
fracrutes in children are handled. This has been the result of
many factors. First, there has been a drastic change in the dissem-
Single-Authored Texts
ination of information regarding the management of children's At the turn of the century the major fracture texts were authored
fractures. Second, there has been a change in the philosophy by single individuals who used their own personal experience as
of how fractures are created, with more emphasis on operative their major reference source. In rhe more popular single-auth-
management. Third, there has been a change in the incidence ored texts by Stimson (0), Scudder (9), and Cotton (3), the
offractures in the United States and Europe. Fourth, and finally, trend was to discuss both adult and children's fractures in the
in a modern North American environment, there have been same sections on a geographical basis; for example, fractures
changes in the etiology of fractures in children. Each of these about the elbow. This single-authored text concept continued
factors will be discussed as a separate section in this chapter. into the late I 950s and early I%Os, with the most popular texts
The first twO factors will be discussed briefly. The third and of that period being those by Bohler (2), Key and Conwell (4),
fourth factors will be discussed in more detail. and Watson-Jones (l1).
The whole goal in studying the incidence of children's frac-
tures is to develop preventative strategies. The experience of
others in rhis aspect will be discussed in the [lfth section of this
Mllltiauthored Texts
chapter. With the explosion of orthopaedic knowledge and the develop-
ment of regional anatomic orthopaedic specialization, it became
impossible for one author to produce a fracture text that was
all-encompassing. Thus began rhe trend toward multiauthored
fracrure texts with twO to three editors. The first to stan this
Kaye E. Wilkins: Children's Hospiral, Sanea Rosa Medical Center, San
trend in fracture texts in North America were Charles Rockwood
Anronio, Texas.
Alaric]. Aroojis: Deparrment ofOrrhopaedics, King Edward V11 Memorial and David Green, who produced the first edition of their multi-
Hospital, Bombay, India. authored textbook Fractures in 1975 (7). A year later, Wilson
4 General Principles

had revised Warson-Jones' text with some multiple authors (12). CHANGES IN THE PHILOSOPHY OF
In chis text, Chapter 17, authored by Anthony Carrerall, focused TREATING FRACTURES IN CHILDREN
on children's fractures. The brst edition of Fractures by Rock-
Blount's Nonoperative Axioms
wood and Green did nor include children's fracrures.
Dr. Walrer Blount, in his textbook Fractures in Children, empha-
sized thar because of growth, children's fractures have a grear
Exclusive Children's Fracture Texts
porential to remodel (1). In fact, he outlined the rules of remod-
In Nonh America, one of the pioneers in fracture treatmenr in eling as to what amount of angulation would be accepted in
children was Walter P. Bloum, who in 1955 was the first to children's fracrures. However, he was very opposed to operarive
author a rextbook devoted exclusively to children (1). His philos- intervention. This was especially true in his opinion ofinrramed-
ophy of nonoperative managemenr set the standard for (L'eating ullary fixation of femoral shaft fractures in children:
children's fractures for more than a generation. Almost 20 years 'The operation is unnecessary, however and as such must be
latet, Mercer Rang authored another textbook devoted exclu- condemned. It inrroduces the hazard of an unnecessary anes-
sively to children's fraceures (6). His book has served as a stan- thetic, unnecessary exposure of bone ends, and trauma to the
dard reference for the rreatment of children's fractures to this entire marrow caviry of the femur. There is no reason for doing
day. it" (1).

Multiauthored Children's Fracture Texts Complications with Operative Intervention

Again, it soon became impossible for one person to author a It was his experience that non unions often followed open reduc-
textbook on children's fracrures that covered each fraceure type tions in children. He wenr on to delineate the serious other
and its treatment in suHlcienr detail to satisfy the demands of complications thar he had seen with open reduction, including
the present-day onhopaedic surgeon. Thus evolved the multi- dearh from sepsis. His comment was, "One postoperative osteo-
authored text on children's fractures. The first edition of a rext- myelitis in a lifetime is enough to cure a surgeon of a casual
book of this rype was added as volume ]J] to the twO volumes arrirude roward open reduction."
of Fractures in Adults, edited by Rockwood and Green in 1984 This aversion to operative management of children's fractures
(8). This multiauthored concept of textbooks on cl1i Idren's frac- set the tone for a generation of orthopaedic surgeons.
tures has been followed by many other excellent texts. These
multiauthored textbooks have been well received; they are now
in subsequent editions. These present-day textbooks now serve Trend Toward Minimal Invasion
as a single encompassing reference source for the physician who
Certainly, prior to the mid-1950s, when Bloum published his
treats children's fractures.
textbook (1), operative procedures usually required large inci-
sions and extensive dissection. In the 45 years since rhe publica-
Emergence of Pediatric Orthopaedics tion of his book, there has been a trend toward more operative
i mervention with good results. However, the surgery performed
Consolidation of Information
is minimally invasive, and fixation is often only temporary.
Pediatric Orthopaedic Journals
In the past, information regarding the management of children's Factors Creating a Trend Toward Operative
fractures was interspersed in journals and meetings dealing with Intervention
general onhopaedics. In 1981, TheJournal ofPediatric Orthoped-
ics was established by Lynn Staheli and Roben Hensinger, and it This trend toward more operative intervention has been rhe
contained articles devoted exclusively to onhopaedic conditions result of four factors: (a) improvement in technology; (b) rapid
seen in pediatric patients. It is interesting to note that the first healing allowing minimal and temporary fixation; (c) the finan-
article in cheir first volume was related to trauma, "The Surgical cial and social pressures to limit the hospitalization of children;
Treatment of Partial Closure of the Growth Plate" by Anders and (d) the expectation by rhe public for a perfeCt outcome in
Langenskiold (5). Pa.n B of The Journal ofPediatric Orthopedics every case.
was esrablished in 1992 [Q allow rhe expansion of the number
of articles from non-North American authors.
Improvement in Technology
The use of the image intensifier has greatly improved the ease
Pediatric Fracture Courses
wirh which fractures can be reduced and stabilized internally
The recognition of the uniqueness of children's fractures has with percutaneous methods. Other technical advances such as
stimulated the production of a number of courses organized computed tomography (CT), magnetic resonance imaging
world-wide devoted exclusively to the management of children's (MRI) , and sonographic imaging have expanded the ability to
trauma (see Appendix A). Thus, there has been a concentration better define the fracture patterns. The lise of powered inSTru-
of both spoken and written information regarding children's ments and cannulated screws has improved the accuracy of ap-
fractures in the modern orrhopaedic communiry. plying fixation devices via percutaneous rechniques.
 Chaptel' l: The Prf.fent StiltuS 0/ Children's Fracturl'S 5

Rapid Healing problems become more apparent and thus there often are modi-
ficarions of rhe original rechnique. Thus, it takes a period of
Because children heal and remodel rapidly, in many cases the
rime before the technique becomes relarively complication free.
fixation devices need to be utilized for only a shon period of
time. Children rolerare all rypes of casrs well for short periods
of rime, which allows a minimally stabilized fracture ro be immo- Specific Problems with Operative
bilized until rhere is sufficiem imernal callous ro supplement Techniques
the limited imernal fixarion.
Some of the specific problems rhat have occurred over rhe years
are Iisted as follows:
Minimal Hospitalization
1. Ulnar nerve injulY with mecLolateraJ pin fixarion of supra-
The rising cosrs of hospiralizarion have creared a rrend ro mobi- condylar fracrures (16)
lize children to an ourpariem serring as soon as possible. This 2. High reFracrure rate with external fixation of femoraJ shaFt
has been reinforced by rhe facr rhar in [\vo rhirds of rhe families Fracrures (18)
in rhe U nired Srares both parems are wage earners. 3. Avascular necrosis of rhe femoral head following use of imer-
Cox and Clarke, in evaluaring rhe Fracrure managemem in locking inrramedulialY nails (13,17)
rheir hospiral in Sourhampron, England, found a high incidence
As will be memioned in the following chapters of rhis texr-
of secondary hospiral trearmem for fracrures inirially managed
book dealing with the specific fracrures, rhere have been recent
nonoperarively (J 5). There was a 12% read mission rare ro cor-
changes in the operative technique or posroperative management
recr lare displacemem of fracrures of the radius and disral hume-
ro minimize the developmem of rhese problems.
rus. In addition, 24% of their internal fixation procedures were
to saJvage unacceptable results of nonoperative management. It
was their conclusion thar more selecrive inirial operative imer- Nonoperative Techniques Need To Be
venti on in radial and disral humeral fractures could decrease rhe Maintained
incidence of costly readmissions to the hospital.
UnFonunare!y, with this emphasis on operarive management,
There are borh social and financial pressures ro mobilize the
rhe Facr rhar most children's Fractures can be managed by nonop-
child early. The trend now is ro temporarily surgically srabilize
erarive rechniques becomes obscured. As a resulr, many of the
these fracrures so rhar the patient can be discharged early.
recem orrhopaedic rrainees are not developing good nonopera-
tive rechnical skills.
The Perfect Result Two recem arricles have demonsnated improved resulrs of
rrearing children's fractures by focusing on improvemems of
Modern parents have become very sophisticared and now expecr prior nonoperative methods. Chess and co-workers (J 4) have
a perfecr ourcome For rheir child. They inspect the x-rays, ques- shown that when properly applied, a well-molded shon arm cast
rion the alignment, and expecr rhe alignmem ro be perfect or provides JUSt as good a resulr as a long arm casr in trearing
anatomic. displaced fractures of rhe distal radial metaphysis. The key ro
A common starement made by rhe patient's father is, "He success in using a shorr arm cast is in a careful molding of rhe
has rremendous poremial ro be a great athlete." These pressures casr at rhe Fractures site so rhere is a proper casr index of 0.7 or
often direct rhe rrearing physician roward operarive intervemion Jess. Walker and Rang (21) recently revised the concepr of rreat-
ro obrain a perfecr alignment. ing unsrable fractures of rhe shafts of the radius and ulna wirh
a long arm cast with rhe elbow in extension. This has resulted
Changes from Previous Editions in a lower remanipulation rate.
Conrinued Focus on developing and maintaining nonopera-
The trend roward rhe establishment of surgical intervention can rive skills such as appropriare casr applicarion and proper
be seen in rhe changes in the previous editions of rhis textbook. moulding techniques needs ro be consranrly reemphasized as rhe
In the £1rsr edition (19), velY lirde menrion was made t'egarding mainsray of nearing children's fracrures.
inrramedullary fixation of either Femoral or radial and ulnar shah
fracrures. There was an exrensive discussion of methods of rrac-
rion for femoral shah fracrures and supracondylar fracrures. In THE PRES NT STATUS OF THE
rhe foutth edition (20), the reverse was [[ue. There was consider- INCIDENCE OF FRACTURES IN
able discussion ofinrramedullary flxarion and very liule menrion CHILDR N
regarding naction rechniques.
The incidence of children's Fractmes is exrremely variable. It can
vaty with the child's age, rhe season of the year, cui rural and
Phases in Development of Operative
environmentaJ climates, and the hour of the day, ro name jusr
Techniques
a Few facrors. As a culrure changes from a primarily rural ro
Often, a new procedure is proposed and becomes widely used. an urban seuing, rhe injury parrerns may change as well. Ie is
Inirially, rhere is a wave of enthusiasm for rhe benefirs of [he imporrant ro develop a general picrure of how, when, and why
procedure. However, with more widespread use of a procedure, fractures occur in children.
6 General Principle;

Incidence of Fractures In shorr, che goals for scudying children's fraccures have
changed over che pasc 60 years. Originally, the goal was to iden-
Healing Processes
tifY the most common bones fractured and how chey heal. The
Early reviews primarily developed a knowledge base of fracrure goals of presem scudies are co gather data in an attempt co de-
healing in children. WalkJing's 1934 review demonscraced thac crease the incidence of fractures by establishing preventive pro-
children's fractures heal differently and included such concepts grams.
as me overgrowth of long bones afcer fraccure and the ability of
children's fracrures to remodel significant angular deformicies Defining the Incidence of Fractures
(56). In 1941, Beekman and Sullivan published an excensive
review of me incidence of children's fracrures (24). Their pi- Variations
oneering work-still quoted coday-included a srudy of 2,094 Cultural Differences
long bone fraccures seen over a 1O-year period ac Bellevue Hospi-
cal in New York City. The major purpose of their srudy was co When on.e looks at the incidence of specific fractures within
develop basic principles for creacing children's fraccures. a well-defined group of children, the data are usually concise.
In 1954, two major reports, one by Hanlon and Estes (36) However, when trying to obtain the global or general incidence
and che other by Lichtenberg (47), confirmed the findings of the of injury or fracture patterns for all types of children, there may
previous studies with regard to the general incidence of children's be problems. For instance, Cheng and Shen studied children in
long bone fraccures and cheir ability to heal and readily remodel. Hong Kong who lived in confined high-rise apartments (28).
These initial reviews were mainly stacistical analyses and did noc Their risk of exposure to injury differed from the study by Reed
delve deeply into the crue epidemiology of children's fractures. of children living in the rural environment ofWinnipeg, Canada
In 1965, Wong explored che effect of cultural factors on the (50). Two separate reviews by Laffoy (39) and Westfelt (57)
incidence offractures by comparing Indian, Malay, and Swedish have found that children in a poor sociaJ environment (as defined
children (58). In che 1970s, two other scudies, one by Iqbal (34) by a lower social class or by dependence on public assistance)
and anocher by Reed (50), added more stacistics regarding the had an increased incidence of accidents. In England, children
incidence of the various long bone fracrures. from single-parent families have been found to have higher acci-
dent and infection rates (31).
Preventive Programs Thus, in domestic settings where many people are on. public
assistance or where there is a higher incidence of disruption of
Landin's 1983 report on 8,682 fractures established a trend in
family scructure, social racher chan physical factors may be more
reviewing the incidence of children's fractures (41). He reviewed
of an influence on the incidence of injuries.
the data on all fractures in children that occurred in Malmo,
Sweden, over 30 years, and examined the factors affecting che
incidence of children's fraccures. His study remains a landmark Climatic Differences
on this subject. By studying twO populacions, 30 years apan, he The c1imace may be a strong factor as well. Children in colder
evaluaced whether fraccure patterns were changing, and if so, climaces, with ice and snow, are exposed to risks different from
che reasons for such changes. His initial goal was to escablish those of children living in warmer climates. The exposure time
data for preventive programs, so he focused on fracrures char to oucdoor activities may be grearer for children who live in
produced clean, concise, concrete data. warmer c1imares. For example, me incidence of chronic overuse
In 1997 Landin updaced his work, reemphasizing che stacis- elbow injuries in young baseball players (lictle league elbow) is
tics from his previous publication (40). He felc chat che twofold far greater in the souchern United States rhan in more northern
increase in fraccure race during the 30 years from 1950 co 1979 communities. This is simply because rhere is greater playing or
in Malmo was due mainly co an increased parricipation in spores. exposure time.
In 1999, in cooperation with Tiderius and Duppe, Landin (55)
scudied the incidence in che same age group again in Malmo
Difficulties 1n Comparing Fracture Studies
and found chat the incident race had accually declined by 9%
in che years 1993 co 1994. The only exception was an increase Defining Age Groups
of discal forearm fractures in girls, which he amibuced co cheir
Another problem with comparing srudies is the definition of
increased participacion in sporring evencs.
pediatric age groups. Some use 12 years as a cutoff age; others
Cheng and Shen, in cheir 1993 scudy from Hong Kong, also
extend ir to 16 or 20.
set oue co define che problems of children's fracrures by separat-
ing the incidences into age groups (28). They tried to gacher
epidemiologic daca on which to build prevemive programs. In Inpatient Versus Outpatient Studies
1999 chis study was expanded to include almost 6,500 fraccures Some studies report only fracture victims admitted to a hospital,
in children 16 and younger over a 10-year period (27). The which loads rhem toward the more serious injuries.
fraccure paccerns changed lictle over those 10 years. What did
change was che increased incidence of closed reduccion and per-
Anatomic Location
cutaneous pin flxacion of fractures, with a corresponding de-
crease in open reductions. There was also a marked decrease in Reports vary in the precision of their defined types of fracture
the hospital stay of their patiencs. patterns. I n the older series, reportS were only of the long bone
 CIJaprer 1: Tbe Present Status oj Children's Fractllre)' 7

involved, such as the radius. More recent series have em phasized

a more specific location, separating the radius, for example, inro Annuallncidence/10,000
physeal, distal, shaft, and proximal fracture types.
Thus, in (lying to define rhe exact incidence of fractures, it *------k Boys
500
is difficult to compare series because of culrural, environmental, 1c·· ..* Gi~s
and age differences. In this section, rhese differences were consid-
ered in grouping the results and producing average figures. These
data are presented in an anempt to provide a reasonable and
400 /'*
accurare reflection of the overall incidence of injuries and frac-
rures in all children. 300 I
1*
~:
Frequency of Childhood Fractures
200
In Landin's series from Malmo, Sweden, the chance of a child *
sustaining a fraCture during childhood (birth to age 16) was
100 /. *
42% for boys and 27% for girls (41). When considered on an *.*
annual basis, 2.1 % of all the children (2.6% for boys, 1.7% for
girls) sustained at least one fracture each year. These figures were
*
for all fracrure types and included those treated on an inpatient
0 5 10 15 AGE

basis and an outpatient basis. The overall chance of fracture per FIGURE 1-1. Incidence of fractures by age. Boys peak at 15 years. Girls
peak earlier, at 12 years and then decline. [Reprinted from Landin LA.
year was 1.6% for both girls and boys in a srudy from England Fracture patterns in children. Acta Orthop Scand 1983;54(suppl 202):
of both outpatients and inpatientS by Worlock and StoweI' (59). 13, with permission.]
The chance of a child sustaining a fracture severe enough to
require inpatient treatment during the first 16 years of life is
6.8% (28). Thus, on an annual basis, 0.43% of the children in
an average community will be admined for a fraCture-related Age Groups
problem during the year. Correlation With Incidence of Injuries
In a series of23,915 patients seen at four major hospitals for S[arring with birth and extending [Q age 12, all the major series
injury-related complaints, 4,265 (17.8%) had ftactures (26,32, [hat segregated patients by age group have demonstrated a linear
33,57). Thus, close to 20% of the patients who presem to hospi- increase in the annual incidence of fractures with age (Fig. I-I)
tals with injuries have a fracture. (27,28,34,41,59). There seems co be a peak at 12 years, with
It is intcl'csting to note that in a follow-up study by Tiderius, some decrease unri I age 16, probably relared ro a significant
Landin, and Duppe (55) in the yeaL'S 1993 and 1994, 13 years decrease in the incidence of fracrures in girls over age 12. The
after the tet'mination of the original 30-year study by Landin percentage of injured boys as compared wi[h girls conrinues to
(41), there was almost a 10% decrease in the incidence of frac- increase in the older age groups.
tures in the 0- ro 16-year age group. They attributed this ro less These fracrure sta[istics differ slightly from the incidence of
physical activity on the part of modern-day children coupled overall injuries: the incidence of injuries peaks early, at ages I
with bener prorective SPOrtS equipment and increased traffic ro 2 years (Fig. 1-2) (39). Although there is a high incidence of
safety (e.g., Stronger cars and use of auro restraint systems). The
overall incidence of children's fractures is summarized in Table
1-1.
Thousands
12
"'
..
~
M N
0 "!
0 0

10 '"g
~ ",' M
N

~
M
TABLE 1-1. OVERALL FREQUENCY OF «i
FRACTURES 8
""
g ,
Percentage of children sustaining at least one fracture from a
M
.....
to 16 years of age: boys, 42%; girls, 27%
Percentage of children sustaining a fracture in 1 year:
6

."'
M 0
"'to-
..
.~ ""--
'"

1.6%-2.1% 4 ,.; . "'

.N
,.;

Percentage of children who are hospitalized because of a frac-

ture: during entire childhood (0-16 years), 6.8%; each year, 2
0.43%
Percentage of patients with injuries (all types) who have frac- a
tures: 17.8% <1 yr 1-2 yrs 3-6 yrs 7-12 yts 13-18 yrs
FIGURE 1-2. Injuries per 100,000 children per year. Estimated U.S. in-
Data from references 26, 28, 32, 33, 42, 57, and 59. jury rates in children by age and sex, 1978. (Reprinted from .Ri~ara FP,
Bergman AB, LoGerfo JP, et al. Epidemiology of childhood II1Junes. Am
J Dis Child 1982; 136: 503; with permission.)
8 General Principles

injuries in children ages 1 (0 2, [he incidence of fractures is low. left (0 right overall averages 1.3: 1. In some fractures, however,
Most injuries in children or this age are nononhopaedic enrities especially those of supracondylar bones, lateral condyles, and the
such as head injuries, lacerations, and abrasions. In facr, the distal radius, the incidence is far gteater, increasing ro as much
incidence of lacerations in both sexes peaks at this age (51). as 2.3: 1 for the lateral condyle. In the lower extremity, the
incidence of injuty on the right side is slightly increased (32,
Trauma 41).
The reasons for the predominance of the Jeft upper extremity
In 1962, Kempe and associates (37) called auenrion (0 the high
have been studied, but no definite answers have been found.
incidence of fracrures and other injuries in young children that
Rohl (52) speculated that the right upper extremity is often
were due ro nonaccidenral rrauma. They termed these injuries
being used actively during the injury, so the left assumes the
pan of the barrered child syndrome. Akbarnia and colleagues
role of protection. In a study examining the left-sided predomi-
later defined the specific fracture patterns seen in victims of
nance in the upper extremity, Monensson and Thonell (49)
child abuse (22). Not all fractures in the first year of life can be
questioned patienrs and their parents on atrival ro the emergency
arrributed to abuse, however. In a review of fractures occurring
department about which arm was used for protection and the
in the first year or life, McClelland and Heiple found that fully
position of the fractured extremity at the time of the accident.
44% were from documenred accidental and nonabusive etiolo-
They found two trends: regardless of handedness, the left arm
gies (47). They also nored that 23% of these patients had a
was used more often (0 break the fall, and when exposed ro
generalized condition that predisposed them (0 fractures. Thus,
trauma, the left arm was more likely ro be fractured. The cause
although nonaccidenral trauma remains the leading cause of frac-
tures during the first year of life, other constitutional conditions for this larrer increased incidence in the left side was thought
may predispose children ro fractures from accidenral causes. The ro be due ro either rile increased fragility or immature neuromus-
high incidence or fracrures from nonaccidenral rrauma extends cular coordination of the nondominanr extremity.
(0 age 3 (38).

Frequency by Season and Time of Day

Gender
Fractures are more common during the summer, when children
The male predominance of injUlY and fracture vierims has been
are out of school and exposed to more vigorous physical activi-
discussed (Figs. 1-1 and 1-2, Table 1-1). For all age groups, the
ties. Four studies from the northern hemisphere have confirmed
overall ratio or boys ro girls who sustain a single fracrure is 2.7: 1
this summertime increase (Fig. 1-3) (27,28,52,59).
(28). In girls, fracture incidence peaks just before adolescence
The mOSt consistent climatic facror appears to be the number
and then decreases during adolescence (28,41,50). In Cheng
of hours of sunshine. Masterson and co-workers (46), in an
and co-workers' 10-year study from Hong Kong (27), the male
eloquent study from Ireland, found a strong positive correlation
incidence in the 12- (0 16-year age group was 83%. The inci-
between monthly sunshine hours and monrhly fracture admis-
dence of fractures in girls steadily declined from their peak in
sions. There was also a weak negative correlation with monrhly
the 0- (0 3-year age group.
rainfall. Overall, the average number of fractures in the summer
In some areas there is little difference in the incidence of
was 2.5 times that in the winter. In days with more sunshine
fractures between boys and girls. For example, during the first
hours than average, the average fracture admission rate was 2.31
2 years of life, the overall incidence of injuries and rractures in
per day; on days with fewer sunshine hours than average, the
both genders is nearly equal. During these first 2 years, the injury
admission rate was 1.07 per day.
rates for foreign body ingestion, poisons, and burns have no
significanr gender differences. With activities in which there is
a male difference in participation, such as with sports equipment
and bicycles, there is a marked increase in the incidence or inju-
ries in boys (27,51). 50
The injury incidence may not be due ro the rate of exposure
alone; behavior may be a major fac(Or. For example, one study
40
found that the incidence of au(O/pedestrian childhood injuries w
peaks in both sexes at ages 5 ro 8 (53). When the total numbet U
z
of street crossings per day was studied, both sexes did so equally, w 30
Cl
but despite this equal exposure, boys had a higher number of (3
injuries. Thus, the difference in the rate between the sexes begins ~
20
(0 develop a male predominance when behaviors change. The

difference in the injury rate between the genders may change in

the ruture as more girls panicipate in activities with increased 10
physical risk (27,51).
J F M A M J J A 5 0 N D
Right Versus Left Frequency FIGURE 1-3. Distribution of children's fractures on a monthly basis.
Note the general increase from May to October. (Reprinted from Reed
In most series, the left upper extremity demonstrates a slight MH. Fractures and dislocations of the extremities in children. J Trauma
bur significant predominance (27,28,32,34,41,51). The ratio of 1977; 17: 353; with permission.)
 Chapter 1: The Present Status of ChiLd/'en 's Fractures 9

In Sweden, the incidence of fractures in the summer had a Long- Term Trends
bimodal pattern that seemed to be influenced by cultural tradi-
Increase in Minor Trauma
tions. In twO large series of both accidents and fractutes in Swe-
Landin's srudy is the only one that has compared the changes
den by Westfelt (57) and Landin (41), the researchers noticed
over a significant time span: his data were collected over 30 years
increases in May and September and significant decreases in
(41). He classified the degree of trauma as slight, moderate, or
June, July, and August. Both writers attributed this to the fact severe. The incidence of all trauma in both boys and girls in-
that children in their region left the cities to spend the summer creased significantly over the 30-year study period, but the inci-
in the countryside. Thus, the decrease in the overall ftacture rate dence of severe trauma increased only slightly. The greatest in-
probably was due to a dectease in the number of children at risk crease was seen in the "slight" categoty. Landin attributed the
remaining in the city. increase in this category to the introduction of subsidized medi-
Masterson and co-workers (46) speculated that because the cal care. Because expense was not a factor, parents were more
rate of growth increases during the summer, the number of phy- inclined in the later years of the study to seek medical attention
seal fractures should also increase, because the physes would be for relatively minor complaints. Physicians, likewise, were more
weaker during this time. For example, the incidence of a slipped inclined to order x-rays. Thus, many of the minor injuries, such
capital femoral epiphysis, which is related to physeal weakness, as torus fractures, which were often ignored in the earlier years,
increases during the summer (23). However, Landin, in his study were seen more often at medical facilities during the later years.
of more than 8,000 fractures of all types, found the overall sea- Likewise, the overall incidence of fractures in Malmo, Swe-
sonal incidence of physeal injuries to be exactly the same as den, (the same city as Landin's original srudy) (41) significantly
nonphyseal injuries (41). decreased (10%) in the more recent years (55).
Age may affect the seasonal variation of fractures. In children The one fracture type that exhibited a true increase over this
ages 0 to 3, no seasonal variations are seen. The number of period was that of the femoral shaft. This increase was thought
fractures in this age group was consistent throughout the year to be influenced by new types of play activities and increased
(38). participation in spons.
Thus, it appears that climate, especially in areas where there
are definite seasonal variacions, influences the incidence of frac- Increase in Child Abuse
tures in all children, especially in the older children. However, The number of fractures due to nonaccidental causes (child
in small children and infanrs, whose acrivities are not seasonally abuse) has risen consistently in the past decades. In Kowal-Vern
dependent, there appears to be no significant seasonal influence. and associates' study of fractures in children ages 0 to 3 (38),
The time of day in which children are most active seems to the number of fractures due to abuse increased almost 150 times
correlate with the peak time for fracture occurrence. In Sweden, from 1984 to 1989. This increase was attributed to a combina-
the incidence peal<ed between 2 and 3 P.M. (57). In a well- tion of improved recognition, better social resources, and an
documented study from Texas by Shank and co-workers (54), increase in the number of cases of child abuse.
the hourly incidence offractures formed a well-defined bell curve
peal<ing at about 6 P.M. (Fig. 1-4). Specific Fracture Incidences
Age Factors
The anatomic areas most often fractured seem to be the same
in the major series, but these rates change with age. For example,
30 / 26
the supracondylar fracture of the humerus is most common in
25 the first decade, with a peak at age 7. Fractures of the femur are
most common in children ages 0 to 3. Fractures of the physis
25
..- -- are more common just before skeletal maturity. This variation
19 19 is best illustrated in Cheng and Shen's data (Fig. 1-5) (28).
20 17
16
.. _._--
Landin found a similar age variability and divided it into
13 six distinct patterns (Fig. 1-6) (41). When he compared these
15 12
11 .. - _. •.. 1-.. _.. ·10 - _ .... -
variability patterns wirh the common etiologies, he found some
correlation. For example, late-peak fractures (distal forearm,
10 7 phalanges, proximal humerus) were closely correlated with sports
6 -_. - _.
'-- ~.
·····5·~--
4 and equipment etiologies. Bimodal pattern fractures (clavicle,
5

0 1/
, ••
1 I
• /
femur, radioulnar, diaphyses) showed an early increase from
lower energy trauma, then a late peak in incidence due to injury
from high- or moderate-energy trauma. Early peak fractures (su-
7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 pracondylar humeral fractures are a classic example) were due
Time of Day mainly to falls from high levels.
FIGURE 1-4. Incidence of children's fractures per time of day. There is
an almost bell-shaped curve with a peak at around 6 P.M. (Reprinted Locations
from Shank LP, Bagg RJ. Wagnon J. Etiology of pediatric fractures: the
fatigue factors in children's fractures. Presented at the National Confer- Early reports of children's fraerures lumped tOgether the areas
ence on Pediatric Trauma, Indianapolis, 1992; with permission.) fractured, and fractures were reponed only as to the long bone
10 Ceneral Principles

35 -

31.18

30 - 28;94-

27.06

25
23.31

20 18.33
17.13
16.2
15.24
15 - -
12.28
11.45 11.26
10.01
10 9.53

6.26
.,e, FIGURE 1-5. The frequency of occurrence of the most com·
5 --., 1-
man fracture areas in children. The frequency of each frac·
3.12
ture pattern differs with the various age groups. The figures

o 0-3 yrs, ('!oj 4·7 yrs. ('!o) 8·11 yrs. ('!o)

~ express the percentage of total fractures for that age group
and represent boys and girls combined. (Reprinted from
12·16 yrs, ('!o) Cheng JC, Shen WY. Limb fracture pattern in different pedi-
_ Forearm Shall
atric age groups: a study of 3,350 children. J Orthop Trauma
• Dls1Il Rldlus Supracondylar Humerus ffiJITJ Tibial Shall
1993;7:17; with permission.)

involved (e,g., radius, humerus, femur) (24,32,34,43,44,48). elbow (mainly supracondylar fractures) in Cheng and Shen's
More recent reports have split fractures into the more specific series (27,28).
areas of the long bone involved (e.g., the distal radius, the radial
neck, the supracondylar area of the humerus) (28,34,41,50,59).
Physeal Injuries
This change in reporring-from the so-called "Iumpers" to the
"splitters"-has produced a more accurate picture of the true The incidence of physeal injuries overall varied from 14.5% (29)
incidence of each specific fracture rype. ro a high of 27.6% (45). To obtain an overall incidence of
physeal fractures, six repons rotaling 6,479 fractures in children
were combined (25,29,45.48,50,59). In this group, 1,404 in-
Single Bones volved the physis, producing an average overall incidence of
21. 7% for physeal fractures (Table 1-4).
In children, fractures in the upper extremiry are much more
common than those in the lower extremity (32,34). Overall, the
radius is the most commonly fractured long bone, followed by Open Fractures
the humerus. In the lower extremity, the tibia is more commonly
The overaJl incidence of open fractures in children is consislent.
fractured than the femur (Table 1-2).
The data were combined from the four reportS in which the
incidence of open fractures was reporred (28,32,45,59). The
incidence in these reports varied from 1.5% to 2,6%. Combined,
Specific Areas Fractured
these repons represented a total of 8,367 fractures with 246
In recent years, five reportS produced by so-called splitters di- open fraerures, resul ti ng in an average incidence of 2.9% (Table
vided fracture types into many anatomic areas (28,34,41,50,59). 1-5).
In trying to reach a global consensus, the author has identified Regional trauma centers often see patients exposed to more
areas common to all the reports but has taken some liberties to severe trauma, so there may be a higher incidence of open frac-
do so. For example, distal radi:tl metaphyseal and physeal frac- tures in these patients. The incidence of open fracrures was 9%
tures were combined to form the distal radius. Likewise, the in a report of patients admitted 1'0 the trauma center of the
carpals, metacarpals, and phalanges were combined ro form the Children's National Medical Centet·, Washington, D.C. (26).
region of the hand and wrist. AI I the fractures around the elbow,
from rhose of the radial neck ro supracondylar fractures, were
Multiple Fractures
grouped as elbow fractures. This grouping allows comparison
of the regional incidence of specific fracture types in children Multiple fractures in children are uncommon: the incidence
(Table 1-3). ranges in the various series from 1.7% to as much as 9.7%. In
The individual repons agreed that the most common area four major reports totaling 5,262 patients, 192 patients had
fractured was the distal radius. The next most common area, more than one fracture (Table 1-6) (28,32,34,59). The inci-
however, varied from the hand in Landin's series (41) to the dence in this multiple series was 3.6%.
 Chapter 1: The Present Status of Children's Fractures 11

Late Peak
TABLE 1-3. INCIDENCE OF SPECIFIC FRACTURE
DISTAL FOREARM TYPES
PHALANGES (HAND, FOOT)
PROXIMAL END OF THE HUMERUS Fracture %
Distal radius and physis "" 23.3
Hand '(carpals," metacarpals, and 20.1
o 5 10 15 age phalanges)
Elbow area (distal humerus and 12.0
Bimodal
proximal radius and ulna)
CLAVICLE Clavicle 6.4
FEMUR
TARSAL·METATARSAL
Radius shaft 6.4
Tibia shaft 6.2
RADIUS-ULNA, DIAPHYSIS
Foot (metatarsals and phalanges) 5.9
Ankle (distal tibia) 4.4
Femur (neck and shaft) 2.3
o 5 10 15 age Humerus (proximal and shaft) 1.4 .
Other 11.6
Rising
Data from references 28,34,'41,50, and 59.
ANKLE
CARPAL-METACARPAL

o 5 10 15 al!e

Early Peak
TABLE 1-4. INCIDENCE OF PHYSEAL
FRACTURES
SUPRACONDYLAR REGION
OF THE HUMERUS Total fractures = 6,477
Number of physeal injuries = 1,404
Precentage of physeal injuries = 21.7%

0 5 10 15 age
Data from references 25, 29, .30, 45, 48, and 59.

Irregular

;vv- TIBIA, DIAPHYSIS

INCIDENCE OF OPEN FRACTURES

TABLE 1-5,
0 5 10 15 age

FIGURE '·6. Patterns of fracture: variations with age. The peak ages Total number of fractures" =8,367
for the various fracture types occur in one of five patterns. [Reprinted Total open fractures = 246
from Landin LA. Fracture patterns in children. Acta Orthop Scand 1983; Percentage = 2.9%
54(suppl 220):80; with permission.]
Data from references 28, 32, 45, and 59.

TABLE '-2. INCIDENCE OF FRACTURES IN

LONG BONES

. BonE! %
TABLE 1-6. INCIDENCE OF MULTIPLE
" Radius 45.1 FRACTURES
Humerus 18.4
Tibia 15.1 Total fractures = 5,262
Clavicle" 13.8 Total number of multiple fractures = 192
Femur 7.6 Percentage = .:1.6%

""Data from references 24, 32, 34, 43, 44, and 48. " Data from references 28, 32, 45, and 58.
12 General PrincipLes

Recurrent Fractures and fracrures resulring from parhologic condirions wil.l be ad-
dressed in larer chaprers of rhis book.
Children with generalized bone dysplasias, such as osteogenesis
imperfecta and other metabolic diseases that produce osteopenia,
are expected to have repeat fractures. In these patients, the etiol- Fractures Resulting from Accidental
ogy of these recurrent fractures is understandable and predict- Trauma
able. However, some children with normal osseous strucwres
are prone to recurrent fractures, for reasons that remain unclear. Accidental trauma can occur in a variery of serrings, some ofren
The incidence of recurrent fractures in children is about 1% overlapping orhers. However, for purposes of simpliciry, frac-
(30). rures can be considered ro occur in rhe following five environ-
Landin and Nilsson (42) found that children who susrained menrs: horne environmenr; school environment; play and recrea-
fractures with relatively little rrauma had a lower mineral coment rional acriviries; moral' vehicle and road accidcnrs; and
in rheir forearms, but they could nor correlare rhis finding I'vjrb uncommon causes such as ice cream cruck, water rubing, and
children who had repear fractures. Thus, in children who seem gunshor and missile injuries.
to be srructurally normal, rhere does nor appear ro be a physical
reason for rheir recurrent fractures. Home Environment

Repeat Fractures Fracrures susrained in rhe home environmenr are defined as

Failure to find a physical cause for repear fracrures shifrs rhe rhose rhar occur in rhe house and surrounding viciniry. These
focus to a psychological or social cause. The one common facror generally occur in a fairly supervised environmenr and are mainly
in accidenr repearers has been a high incidence of dysfuncrional due co falls from furnirure, srairs, fences, and crees.
families (36).]n Sweden, Wesrfelr found rharchildren who were
accident tepearers came from "sociaJly handicapped" families Falls from Heights
(i.e., rhose on public assisrance or rhose wirh a caregiver who Falls call valY in severiry from a simple fall while running, ro a
was an alcoholic) (57). Thus, recmrent fractures are probably fall of grear magnirude, such as from a rhird scory window. In
due more ro behavioral or social causes rhan physical causes. falling from heighrs, adulrs often land on rheir lower exrremiries.
Landin in his follow-up article (40) followed children with repear accounting for rhe high number of lower extremiry fractures.
fracwres (four or more) inro adolescence and adulrhood. He especially rhe calcaneus. Children tend co fall head flrsr, using
found rhese children had a significantly increased incidence of rhe upper exrremiries co break rhe fall. This accounrs for rhe
convicrions for serious criminal offenses when compared wirh larger number of skull and radial fractures in children. Femoral
children wirh only one liferime fracture. fracrures are also more common in children falling from grear
heighrs. In conrrast co adulrs, spinal fracrures are rare in children
who fall from grear heights (61,84,97,100).
ETIOLOGY OF FRACTURES In one srudy, children falling rhree scories or less all survived.
Falls from rhefifrh or sixrh floor resulred in a 50% mortaliry
While studying rhe epidemiology of fracrures, ir is imporranr ro rare (61).
focus on rhe eriology of fractures and rhe serrings in which rhey
occur. ]n rhis age of compurerized gizmos and rhe "need for Injury Rate Increases with Age
speed," children are ofren rhe vicrjms of rhe consumer marker Injuries also can occur from rhe unsupervised use of unsafe play
and unsafe producrs. Fracrures do nor OCCur in a vacuum, and equipmenr, such as trampolines and monkey bars, within rhe
well-researched srudies rhar analyze rhe physical and social envi- home environmenr and will be considered in derail larer. The
ronment in which they occur are exrremely valuable. lr is a overall incidence of franures occurring because of such play
truism rhar children, unforrunarely, learn more from experience acriviry in rhe home environmenr increases wirh age. Only 15%
rhan by educarion, so effons should be made toward nearing a occur in roddlers, but 56% occur during older years (J 10).
safer environmenr for play and recreation. Srudies thar idenrify
risky parrerns of use or unsafe playground behaviol' go a long Social Factors
way in directing specific prevenrive healrh measures. Recom- 1nreresri ngly, a Swedish srudy (I09) showed rhat an increased
mendations can be made to manufacturers regarding modi fica- incidence offracrures in a home environmenr did nor necessarily
rion of a producr, and educarion can be imparted co parenrs, correlate wirh rhe physical amibures or poor safery precaurions
school authorities, healrh-care professionals, physical rrainers, of rhe house. Radler, ir implicared disruprion of rhe family struc-
and children. rure and presence of social handicaps (alcoholism, welfare reeipi-
enrs, ere.) as rhe rrue cause for rhe increase.

Broad Causes
School Environment
Broadly, fracrures can occur due to rhree main causes: accidenral
rrauma, nonaccidenral injury (child abuse), and parhologic con- The supervised environmenrs ar school are generally safe, and
dirions. Because accidental trauma forms the largesr eriologic the overaU annual rare of injury (rocal percenrage of children
group, ir will be addressed in detail here. Nonaccidenral rrauma injured in a single year) in rhe school environmenr ranges from
 Chapter 1: The Present Status of Children's Fractures 13

2.8% to 9.2% (63,81,95,109). True rates may be higher because line skates over the past decade, and several studies have high-
of inaccurate reporting, especially of mild injuries. In one series, lighted their risks and dangers.
the official rate was 5.6%, but when the parents were closely
questioned, the incidence of unreported, trivial injuries was as Bicycle Injuries
much as 15% (71). The annual fracture rate of school injuries Bicycle injuries are a significant cause of mortality and morbidity
is low. Of all injuries sustained by children ar school in a year, for children (92). Bicycle mishaps are the most common causes
only 5% to 10% involved fractures (71,81,95). In Warlock and of serious head injury in children (108). Boys in the 5- to 14-year
Stower's series of children's fractures from England (110), only age group are at greatest risk for bicycle injury (80%). Puranik et
20% occurred at school. A large incidence of injuries (53%) al. (92) studied the profile ofpediatric bicycle injuries in a sample
occurring in school are related to athletics and sporting events of 211 children who were treated for bicycle-related injury at
(81). These injuries are highest in the middle-school children. their trauma center over a 4-year period. They found that bicycle
The peak time of day for injuries at school is in rhe morning, injuries accounted for 18% ofall pediatric trauma patients. Bicy-
which differs from the injury patterns of children in general cle/motor vehicle collisions caused 86% of injuries. Sixty-seven
(81). percent had head injuries and 29% sustained fractures. More
than half of the incidents occurred on the weekend. Sixteen
percent were injured by ejection from a bicycle after losing con-
Play and Recreational Activities
trol, hitting a pothole, or colliding with a fixed object or another
Playground bicycle. Fractures mainly involved the lower extremity, upper
Play is an essential element of a child's life. It enhances physical extremity, skull, ribs, and pelvis in decreasing order of incidence.
development and fosters social interaction. Noncompetitive
sports and recreational activities are enjoyed by all children. Un- Helmet Use Low. More importantly, the study detected that
fortunately, unsupervised or careless use ofsome play equipment the use of safety helmets was disturbingly low «2%). Other
can endanger life and limb. When Matt et al. (86) studied the studies confirm the observation that less than 13% to 15% of
incidence and pattern of injuries to children using public play- children wear helmets while riding bicycles (72,93). The Year
grounds, they found that approximately 1% of children using 2000 Health Objectives call for helmet use by 50% of bicyclists
playgrounds sustained injuries. Sixty-five percent of these chil- (102). Research has shown that legislation, combined with edu-
dren were injured by falling from equipment such as climbing cation and helmet subsidies, is the most effective srraregy to
frames, slides, swings, and monkey bars. They found that chang- increase use of safety helmets in child bicyclists (65). As public
ing playground surfaces from concrete to more impact-absorbing awareness of both the severity and preventability of bicycle-re-
surfaces such as bark reduced the incidence and severity of head lated injuries grows, the goal of safer bicycling practices and
injury but increased the tendency to long bone fractures (40%), lower injury rates can be achieved (92).
bruises, and sprains.
In a study of injuries resulting from playground equipment, Injuries from Bicycle Parts. Bicycle spokes and handle bars
Waltzman et al. (06) found rhar most injuries occurred in boys are also responsible for an increasing number of fractures and
(56%) with a peak incidence in the summer months. Fractures soft tissue injuries in children. D'Souza et al. (70) and Segers
accounted for 61 % of these injuries, 90% of which involved the et at. (94) found that bicycle spoke injuries are typically sustained
upper extremity and were sustained due to falls from playground when the child's foot is caught in the spokes of the rotaring
equipment such as monkey bars and climbing frames. Younger wheel. Out of a total of 130 children with bicycle spoke injuries,
children (1-4 years) were more likely to sustain fractures than 29 children sustained fractures of the tibia, fibula, or foot bone.
older children. In their study, the surface below the equipment Several had lacerations and soft tissue defects. D'Souza et al.
apparently did not influence rhe type or severity of fracture; with (70) suggested that a mesh cover to prevent the toes from enter-
30 of the 79 fracrures occurring on "soft surfaces." ing between rhe spokes and a plastic shield to bridge the gap
Similar observations were made in a study by Lillis and Jaffe between the fork and horizontal upright can substantially de-
(83) in which upper extremiry injuries, especially fractures, ac- crease the incidence of these injuries.
counted for the majority of hospitalizations resulting from inju-
ries on playground equipment. Older children sustained more Skateboarding
injuries on climbing apparatus, whereas younger children sus- Skateboarding and in-line skating have experienced a renewed
tained more injuries on slides. surge in popularity over the past two decades. With the increas-
ing number of participants, high-tech equipment development
Newer Play Devices and vigorous advertising, skateboard and skating injuries are
Other recreational activities enjoyed by children, such as bicy- expected to increase. Because the nature of skateboarding en-
cling, skating, skateboarding, and sledding, are an important compasses both high speed and extreme maneuvers, high-energy
cause of fractures and injuries in children. Several studies have trauma fractures and other injuries can occur, as highlighted by
analyzed rhe incidence and pattern of injuries arising from the several studies (73,89,91). Studies have shown that skate-
unsupervised or cateless use of this equipment and have sug- boarding-related injuries are more severe and have more serious
gested safety precautions and equipment modification to de- consequences than roller-skating or in-line skating injuries (89).
crease the risk of injury. A disturbing trend is the rekindled In a study of skateboarding injuries, Fountain et al. (73) found
enthusiasm toward the use of trampolines, skateboards, and in- that fractures of the upper or lower extremity accounted for 50%
14 emeral Principli'j"

of all skateboarding injuries. Interestingly, more tnan one third Skiing Injuries
of those injured sustained injuries within the first week of skate- Skiing injuries are seasonal in nature and occur with outdoor
boarding. Most injuries occurred in preadolescent boys (75%) winter recreational activity. In a study of major skiing injuries
10 to 16 years of age, and despite traffic legislation, 65% sus- in children and adolescents, Shorter et a!. (96) found greater
tained injuries on public roads, footpaths, and parking lots. Sev- than 90% of injured children to be boys 5 to 18 years of age.
eral organizations have recommended safety guidelines and pre- Sixty percent of the accidents occurred due to collisions with
cautions such as use of helmets, knee and elbow pads, and wrist stationary objects such as trees, poles, and stakes. Most injuries
guards, but such regulations are seldom enforced. occurred in the afternoon, among beginners, and in the first
week of skiing season. Fractures accounted for one third of rhe
Roller Skates and In-Line Skates tOral injuries sustained. The twO main factOrs implicared in
In a study of in-line skate and roller skate injuries in childhood, skiing injuries are excessive speed and loss of control; effective
Jerosch et aI. (78) found that in a group of 1,036 skaters, 60% prevention efforrs should target both of rhese factors.
had sustained injuries. Eight percent of these were fractures,
mosrly involving the elbow, forearm, wrist, and fingers (78%).
Less than 20% used protective devices, and most Jacked knowl- Snowboarding Injuries
edge of the basic techniques of skating, braking, and falling. [n Snowboarding runs a similar risk to skiing. Bladin et a!. (62)
a larger study of 60,730 skating injuries in children, Powell and found that approximarely 60% of snowboarding injuries in-
Tanz (91) found that 68% of the children were preadolescent volved the lower limbs and occurred in novices. The mosr com-
boys with a mean age of 11.8 years. Fracrures were the most mon injuries were sprains (53%) and fractures (26%). Com pared
common injury (65%), and [WO thirds of these involved the with skiers, snow boarders had 21:z times as many fractures, par-
distal forearm. Two and a half percent required hospital admis- ticularly to the upper limb, as well as more ankle injuries such
sions; 90% of these admissions were for a fracture. Similarly, as sprains. The absence of ski poles and the fixed position of
Mitts and Hennrikus (85) found that 75% of in-line skating the feet on the snowboard mean that the upper limbs absorb
fractures in children occurred in the distal forearm as a result the fuJI impact of any fall.
oHalls on the outStretched hand. One in eight children sustained
a fracture during the first attempt at the sporr. The orthopaedic
community has an obligation to educate the public on the need Motor Vehicle Accidents
for wearing wrist guards when using in-line skates or roller skates.
This category includes injuries sustained by occupants ofa motOr
vehicle and victims of vehicle-versus-pedestrian accidents.
Trampoline-Related Injuries
The injury parrerns of children involved in motOr vehicle
Trampolines enjoyed increasing popularity in the 1990s and are
a significant cause of morbidity in children. Several studies have accidents differ from those of adults. In all rypes of motor vehicle
noted a dramatic increase in the number of pediatric trampoline accidents for all ages, children constitute a little over 10% of
injuries (PTIs) during the past 10 years, rightfully deeming it the tOtal number of patients injured (79,101). Of all the persons
as a "national epidemic" (75,98). Furnival et al. (75), in a retro- injured as motor vehicle occupants, only abour 17% to 18% are
spective srudy ofPTIs over a 7 -year period, found that the annual children. Of the victims of vehicle-vets us-pedestrian accidents,
number of PTIs tripled between 1990 and 1997. In contrast to about 29% are children. Of the total number of children in-
other recreational activities in which males constirute the popu- volved in motOr vehicle accidents, 56.4% were vehicle-versus-
lation at risk, PTI patients were predominantly female, with a pedestrian accidents, and 19.6% were vehicle-versus-bicycle ac-
median age of 7 years. Nearly a third of the injuries resulted cidents (69).
from falling off the trampoline. Fractures of the upper and lower The fracture rate of children in motor vehicle accidents is
extremi ries occurred in 45% and were more frequen rly associated less than that of adults. Of the total number of vehicle-versus-
with falls off the trampoline. In another excellent study on PTIs, pedestrian accidents, about 22% of the children sustained frac-
Smith (98) found that there was virtually a 100% increase in tures; 40% of the adults sustained fractures in the same type of
injuries from 1990 to 1995, with an average of greater than accident. This has been attributed to the fact that children are
60,000 injuries per year. Younger children had a higher inci- more likely to "bounce" when hit (69).
dence of upper extremity fractures and other injuries. In a later Children are twice as likely as adults to sustain a femur frac-
study, Smith anL! Shields (99) came up with some interesting ture when struck by a.n automobile, but in adulrs tibia and knee
data. Fractures, especially involving the upper extremity, ac- injuries are more common in the same type of accident. This
counted for 35% of all injuries. Interestingly, more than 50% seems to be related to where the car's bumper strikes the victim
of the injuries occurred under direct adult supervision. More (64,102). MotOr vehicle accidents do produce a high proportion
disturbingly, 73% of the parents were aware of the potential of spinal and pelvic injuries (64).
dangers of trampolines, and 96% of the injuries occurred in the
home backyard. These researchers, along with others (75),
rightly concluded that use of warning labels, public educarion,
Summary
and even direct adult supervision were inadequate in preventing
these injuries and have called for a total ban on the tecreational, The etiologic aspects of children's Fractures are summarized in
school, and competitive pediatric use of rrampolines (57,99). Fig. 1-7 and Table 1-7.
 Chapter I: The Present SttltltS of Children's Fractures 15

350 _

300 -lHHm~9
Motor Vehicle Accidents (MVA

Home

CJ '-Schooi'
Sports
279

250

200

150 --
118
103 ""
100 ""
73 ~!
50
27
.~~
16
3 " 0 o 5 6 1 ~~
o ;;

Infants Toddlers School Children

(Numbers Expressed as Total Patients)
FIGURE 1-7. The incidence of fractures in children expressed as the four common etiologic categories.
Most fractures occur at home. The numbers are expressed as total patients per each age category.
(Reprinted from Worlock P, Stower M. Fracture patterns in Nottingham children. J Pediatr Orthop 1986;
6:656; with permission.)

Less Common Etiologies velociry assault weapons. Mulriple missiles can result from a
shotgun blast or shrapnel from war weapons. Missile injuries
Ice Cream Truck
represent open fracrures with varying degrees ofsoft tissue injUlY.
M ubarak et al. (87) reponed on ice cream cruck-related acci- The incidence of gunshot wounds in children has become in-
delHs in which children, distracted by ice cream crucks, were creasingly common in the United States (l07).
struck by an oncoming vehicle, sustaining pelvic and lower limb
fracrures. The vision of oncoming drivers was often blocked by Gunshot and Firearm Injuries
the large size of the ice cream rruck parked by the curb. In a sad reflecrion of the changing times and the newly pervasive
gun culture, firearms are determined to be second only to motor
vehicles as the leading cause of death in youths. In considering
Water Tubing
the prevalence of firearms in the United States, ir has been esti-
Parmar et al. reponed serious injuries sustained during water mared thar rhere are about 200 million privately owned guns
rubing (the pulling of an inner tube behind a power boat) (90). in the United States and that approximately 40% of U.S. house-
holds comain firearms of some rype (66). The incidence of gun-
shor wounds in children has become increasingly common in
Gunshot (Missile) Wounds: Definition the United States (l07).

Gunshor or missile woul1ds arise from objecrs projected inco Etiology

space by an explosive device. The missiles may be single or multi- In rwo reports from inner-ciry hospitals in the United States
ple. Sil1gle missiles valY from low-velociry hal1dgul1s to high- in rhe 1990s, most injuries resulted from random violence to
16 GenrrrlL PrincipLes

union. Considering the magnitude of many of these injuries,

TABLE 1-7. SUMMARY OF ETIOLOGIC FACTORS
the infection rate for extremity wounds was low (about 7.3%).
IN CHILDREN'S FRACTURES
This low tate was probably due to a vigorous and aggressive
Home environment program of acute wound management (82,101,107). The type
Injuries of missile did not seem to have any relation to the developmem
83% of all children's injuries
of an infection (107).
Fractures
37% of all children's fractures In Lerrs and Miller's 1976 series, one sixth of the patients
School environment had some type of growth disturbance (82). In a third of their
Injuries patients, the missile was only in close proximity to the physis.
Overall rate, 2.8%-9.2% annually In a 1995 report by Washington and co-workers, the incidence
53% related to athletic events
Peak age: middle-school group of missiles affecting the physis was exactly the same (107). How-
Fractures ever, all were a result of a direct injury to the physis by the
Occur in only 5%-10% of all school-related injuries missile. None of their patients with growth arrest had proximiry
About 20% of all children's fractures missile wounds. The higher incidence of growth abnormalities
Motor vehicle accidents (MVA)
in the 1976 series was due to the larger number of shotgun
Injuries
Children only 10% of all MVAs and hunring rifle injuries, which dissipate more of their energy
Of children's MVAs, only 17-18% were occupants; remain- peripheral to the missile track.
der were vehicle/pedestrian or vehicle/bicycle In two of the studies in which patients were followed closely,
Fractures all of the fractures ultimately heaIed (82,107).
Higher incidence of femur fractures in vehide pedestrian
accidents in children
Children have a higher incidence of spinal and pelvic frac- Prevention
tures with MVAs than with other mechanisms In an excellent reporr in 1999, Freed et al. (74) analyzed the
magnitude and implications of the increasing incidence of fire-
arm-related injuries in children. They suggested a product-ori-
ented approach, focusing on the gun, in an attempt to provide
an efficient strategy ofgun control and hence reduce the disturb-
ing trend of firearm-related injuries and death among youths.
innocem bystanders; the prime example was "drive-by shoot-
Rather than modifying behavioral or environmentaI issues,
ings" (101,107). Few were self-inflicted, either volumarily or
which are more complex, chey suggested focusing primarily on
accidentally. In a 1976 report on patiems in a relatively rural
strategies that offset the accessibiliry and design of firearms. In
setting in Canada, almost all the missile injuries were accidemal,
brief, these strategies included the following:
having been caused by the patient or a close friend or relative
(82). Reducing the number of guns in the environment through
In the urban setting, handguns and ri Res are the mosr com- restrictive legislation, gun buy-back programs, gun taxes, and
mon weapons (101,104,107). In rhe rural setting, the most com- physician counseling.
mon weapon is a shotgun (82). The firepower of these weapons Modifying the design of guns to make them more child-proof
has changed over the years. [n one urban hospital reponing and preventing unauthorized and unintended use.
gunshot wounds from 1973 to 1983, most of the injuries were
from .32- or .38-caliber weapons; only 5% were high-caliber or
high-velocity weapons (88). In a larer srudy of gunshot wounds
from the same institution from 1991 to 1994, the incidence of
Falls
injuries from high-caliber and high-velocity weapons (e.g." .357 FaIls can vary in severiry from a simple fall while running, to a
Magnum, AK-47, and other assault rifles) had increased to 35% fall of great magnitude, such as from a third story window. Falls
(108). are often classified as the most common cause of injuries. Falls
In the urban serring, the victims' ages ranged from 1 to 17 are more likely ro be a cause of injury in the younger than in
years, and most of the injuries were in children 12 to 14 (88, the older child. Falls in the home are usually associated with
101,104,107). In the rural setting, the patients were younger; furniture or stairs; outside the home, most falls involve play-
the average age was 9 years (82). ground equipmenr (76,77).
Of 839 children sustaining gunshot wounds, 274 (32.6%) In falling from great heights, adults often land on their lower
involved the extremities (88,101,104,107). Of the gunshot extremities, accounting for the high number of lower exrremiry
wounds that involved the extremities, 51.3% produced signifi- fractures, especially the calcaneus. Children tend to fall head
cant fractures (82,101,107). No single bone seemed to predomi- first, using the upper extremities co break the faJI. This accounts
nate, although a great majority of the fractures were distal to for the larger number of skull and radial fracrures in children.
the elbow (88,101,104,107). Femoral fracrures are also more common in children falling from
great heights. In contrast co adults, spinal fractures are rare in
Complications children who fall from great heights (61,84,97,100). In one
The two most common complications were growth arrest and study, children falling three stories or less all survived (61). Falls
infection. Other complications include delayed union or ma1- from the fifth or sixth floor resulted in a 50% mortaliry rate.
 Chapter /: The Present Status of Children '$ Fractures 17

Intrinsic Causes (115). Recently, the American Academy of Orthopaedic Sur-

geons has produced a program designed to decrease the incidence
Nutrition
of playground injuries. These programs offer background data
In a scudy in Spain, a significanr difference in the fracrure rate
and guidelines for various activities, but their effectiveness has
was found when cities with a high calcium content in their water
not yet been fully srudied.
were compared with those with a lower calcium content. With all
other factors being equal (e.g., fluoride contenr, socioeconomic
background), children who lived in the cities with a lower cal-
Local Community Participation
cium content had a higher fracture rate (I05). To be effective, accident prevention programs require local par-
An increase in the consumption of carbonated beverages has ticipation and cooperation. They must be broad based, and they
been shown to produce an increased incidence of fractures in requite considerable efforr by members of the local community.
adolescents (111). In the United States, one effective program is the New York
Health Department's "Kids Can't Fly" campaign, developed in
Bone Density response ro the large number of injuries and deaths from children
Bone density may be a factor, bur the data are unclear. Landin falling out of apartment house windows in the 1970s (20).
and Nilsson (80) found that the mineral content of the forearms This extensive program consisted of a good reporring system
was lower in children who sustained fractures from mild trauma from hospital emergency rooms, with follow-up by public health
rhan in children who had never sustained fractures. It was not personnel; a strong media campaign to educate the public; a
significantly different, howevet·, in those sustaining fractures door-to-door hazard identification program; and the distribu-
from severe rrauma. This study used measurements of bone den- tion oflow- or no-cost, easily installed window guards to families
sity of the corrical bone in the fOtearms. Cook and co-workers in high-rise apartmems. The city required landlords to provide
(67), using measurements of bone density obtained from trabec- window guards in apartments where children 10 years or
ular bone in the spine and femoral neck, found no difference younger lived. The success of this program was demonstrated
between children who had sustained fractures and those who by a 50% decrease in reponed falls after 3 years and a 96%
had nor. decrease after 7 years 016,120).
Over the past 30 years, Sweden has developed broader based,
community-oriented programs to decrease the incidence of all
Premature Infants types of childhood injuries (I 17). The development of these
Fractures not related to birth trauma reporredly occur in 1% ro pilot programs has been relatively easy in a coumty like Sweden
2% of low-birth-weight or premature infants during their stay because the population is homogeneous, the incidence of poverty
in a neonatal intensive care unit (60). Using a combination of is low, and the government is stable. The Swedish program had
the clinical history, radiographic appearance, and laboratoty a three-pronged approach: injuty surveillance and prevention
data, these infants have been found to have evidence of bone research; establishment of a safer environmem for chi ldren
loss from inadequate calcium and phosphorus intal<e. Correcting through legislative regulation; and a broad-based safety educa-
the metabolic status of rhese 10w-birth-weigJu infants, wirh spe- tion campaign. These programs have produced positive results.
cial emphasis on calcium and phosphorus intake, appears ro Schelp demonstrated a 27% reduction in home accidems in the
decrease the incidence of repeat fractures and to improve the municipality of Falkoping only 3 years after the establishment
radiographic appearance of their bony tissues. Once the meta- of a community-wide campaign (19).
bolic abnormalities are corrected, this temporary deficiency One of the most dramatic changes came in the prevention
seems to have no long-term effects. When premature infants of drowning. In Sweden, 100 children drowned in 1954; by
were followed into later years, there was no difference in their 1988, the number had decreased to 10 (I 17). In the same time
fracture incidence when compared with that of children of nor- period, there was only a 5% decrease in the number of childhood
mal birth weight (68). drownings in the United States. The decrease in drowning did
not result from establishing new, sophisticated emergency medi-
cal services or intensive care units in hospitals; it came by teach-
PREVENTIVE PROGRAMS ing children to swim and promoting the use of life jackets on
toddlers playing near the water. In addition, there was a public
One of the major goals of studying the incidence of fractures is education campaign in the mecUa locally and nationally.
ro identiJY problem areas; it is hoped that by targeting these Effective prevemion programs require local community par-
areas, programs can be designed to decrease the risk [1Ctors. ticipation and education. All the articles, lectures, and pamphlers
in the world cannot help unless local communities make the
necessaty changes to decrease accident risks.
National Campaigns
Several safety programs have been started by national organiza- APPENDIX A: FRACTURE COURSES
tions. The foremost is the American Academy of Pediatrics,
which has committees on accident and poisoning prevention. 1. The 1st Swedish International Seminar on "Treatment of
This group has produced guidelines for athletics (I 14), play- Fractures in Children," Institute for Medical Postgraduate Edu-
grounds (118,121), trampolines (112,113), and skateboards cation, Uppsala, Sweden, May 27-30, 1990
18 General Principles

2. Seminario de Actualizacion, en "Fracturas del Nino," The Present Status of the Incidence of
Madrid, Spain, Ocrober 29-30, 1994 Fractures ill Children
3. Operative Management of Children's Fractures-An In- 22. Akbarnia B, Torg JS, Kirkparrick], et al. ManifeStarions of rhe bar-
teractive Course, The University of Texas Health Science Cen- tcred-child syndrome. J Bone Joint Stlrg {Am} 1974;56: 1159.
ter, San Antonio, Texas, August 8-9, 1997 23. Andren L, Borgstrom KE. Seasonal variation of epiphysiolysis of rhe
4. First Caribbean Children's Fracture Course, Port-au- hip and possihility of causal factor. Acta Orthap Seand 1958;28:22.
24. Beckman F, Sullivan J E. Somc observarions on fractures oflong bones
Prince, Haiti, April 15-18, 1998
in children. Am] Surg 1941 ;51 :722.
5. Third Seminario Imernacional sobre Fracturas en el Nino, 25. Bisgard JD, Martenson L Fractures in children. Surg Gynecol Ob.rtet
Madrid, Spain, October 29-30 19.37;65:464.
26. Buckley SL, Gorscil<lil C, Rohenson W Jr, er al. The relationships of
skeleral injuries wirh rraullla score, injury severiry score, lengrh of
hospital sray, hospira! charges, and mortaliry in children admitted to
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20. Rockwood CA Jr, \'(/i1kins KE, Beaty ]H, eds. Fractures in children, J Trauma 1977;17:351.
4rh ed. Vol II!. Philadelphia: Lippincorr-Raven, 1996. 51. Rivara FP, Bergman AB, LoGerfo Jp, er al. Epidemiology of childhood
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wirh elbow exrension. J Bone Joillt SUig {Br} 1991;73:299. 502.
 ChajJter J: The Present Status of Childrm 's Frrrl'tures 19

52. Rohl L. On fractures rhrough rhe radial condyle of rhe humerus in rance of passive and acrive injury prophylaxis for inline skaring. Knee
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457. 80. Landin LA. Nilsson BE. Bone mineral comenr in children wirh frac-
54. Shank LP, Bagg R], Wagnon]. Etiology of pediauic fractures: rhe WITS. Clin Ortbop 1983;178:292.
farigue factors in children's fractures. Prcsellted ar Narional Confer- 81. lenaway DO, Ambler AG, Beaudoin DE. The epidemiology of
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55. Tiderius C], bndin L, Dtlppe H. Decreasing incidenc~ of fracrtlres 82. Lerrs Rivr, Miller D. Gunshor wounds of rhe exrremiries in children.
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58. Wong PCN. A compararive epidemiologic srudy of fi-actures among 86. 1\1[orr A, Evans R, Rolfe K, er al. Parrcrns of injuries ro children on
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88. Ordog GJ, Prakash A, Wasserberger], er al. Pediarric gun,hor wounds.
] Trauma 1987;27: 1272.
Etiology of Fractures 89. Osberg ]S, Schneps SE, Di Scala C, Li G. Skareboarding: more dan-
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] Pedilltr Ortho! 1988;8:4 I. 90. Parmar P, Lens M, ]arvis]. Injuries caused by warer rubing. J Pediflt/'
61. Barlow B, Neimirska M, Gandhi RP, et al. Ten ye;ns of experience Orthop 1998;18:49.
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70 I. South Med] 1998;91: 1033.
63. Boyce WT, Boyce WT, Sprunger LW, er aI. Epidemiology of injuries 93. Rogers GB. Bicycle helmer use pauerns among children. Pediflt/'ics
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64. Buckley SL, Gorschall C, Roberrson W]r, er al. The rc:larionships of 94. Scgns M]M, Wink 0, Clevers GJ. Bicycle-spoke injuries: a prospec-
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hospiul sray, hospiral charges, and monalirj' in childrcn adl1lirred ro 95. Sheps SB, Evans GO. Epidemiology ofschool injuries: a 2-ycar experi-
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usc following a decade of helmer promorion in Vicroria, Ausrralia-an and adolescenrs. J Traulitfl 1996;40:997.
evaluarion. Areid Anal Prell J996;26:325.
97. Sieben RL, leavirr ]0, French ]H. Fa.lIs as childhood accidents: an
66. Cook 1'], Ludwig]. Gun,' in America. Washingron, DC: Police Foun-
increasing urban risk. Pedifltrics J 971 ;47:886.
darion, 1996.
98. Smirh GA. Injuries to children in rhe unired srares relared ro [['ampo-
67. Cook SO, HardingAF, Morgan El, er al. Associarion of bone mineral
lines, 1990-1995: a narional epidemic. Pediat:rics 1998; I 0 1:406.
density and pediatric fracrtlres.] Pedifltr Orthop 1987;7:424.
99. Smirh GA, Shields B]. Trampoline-relared injuries to children. Arch
68. Dahknburg SL, Bishop N], Lucas A. Pue prerenn infants ar risk for
Pediatr Adou:>'c Med 1998; 152:694.
subscquenr fracrure' Arch Dis Child 1989;64: 1384.
100. Smirh MD, Burrington ]0, Woolf AD. Injmies in children susrained
69. Dcrler RW, Silva J ]r, Holcrofr ]. Pedesrrian accidents: adulr and
in free falls: an analysis of 66 cases.] ji-fluma 1975;15:987.
pediarric injuries.] Emerg Nled 1989:7:5.
101. Srucky W, Loder RT. Exrremiey gunshor wounds in children.] Pedifltr
70. D'Souu LG, Hynes DE, McManus F, er aI. The bicycle spoke injury:
an avoidable accidenr? Foot Ankle 1m 1996; 17: 170. Orthop 1991; 11 :64.
71. Feldman W, Woodward CA, Hodgson C, er al. Prospecrive srudy of 102. Topolcski T, Schlesinger I, Wexler LM, er al. Motor vehicle injuries
school injuries: incidence, eypes, rdared facrors and initial manage- in pediarric rrauma pari ems. Presenred ar rhe American Academy of
mene. Can Med AHoc] 1983; 129: 1279. Orrhopaedic Surgeons Annual Meering, Orlando, 1995.
72. Finvers KA, Strorher RT, Mohradi N. The effecr of bicycling helmers l03. US Public Healrh Service. Healthy People 2000: national health promo-
in prevenring significant bicycle-relared injuries in children. Gin] rion and disease prevention objecrives. Washington, DC: DHSS Publi-
Sport Med 1996;6: 102. cation no. PH58 90-50212, 1990.
73. Fountain]L, Meyers Me. Skareboarding injuries. Sports Med 1996; 104. Valentine], BJocker S, Chang ]HT. Gunshot injuries in children.]
22:360. 'Ji-aumfl 24:952, 1984.
74. Freed LH, Vernick ]S, Hargarrcn SW. Prevenrion of flrearrn-relared 105. Verd VS, Dominguez 5], GOl1ZakL QM, er al. Association berween
injuries and dearhs among yourh. A prodtlcr-orienred approacb. Pedi- calcium conrelH of drinking war,"I" and fracwres in children. An Efp
atr Clin North Am 1998;45:427. Pl'difit/· 1992;37:461.
75. Furnival RA, Sn'eer KA, Schunk ]E. Too many pediarric rrampoline 106. WaJrzman Ml, Shannon M, Bowen AP, er aI' Monkey bar injuries:
injuries. Pediatrics 1999;103:57. complicarions of play. Pediat:rics 1999; I 03:58.
76. GaJlagher SS, Finison K, Guyer B, er a1. The incidence of injuries 107. Washington ER, Lee WA, Ross WA]r. Gunshor wounds to rhe ex-
rtITlong 87,000 Massachtlserrs children and adolescenrs: restllrs of rhe uemiries in children and adolescelHs. Or/hop Clin North Am 1995;
1980-81 sratewide childhood injury prevenrion program surveillance 26:19.
sysrem. Alii] Pub Health 1984;74:1340. 108. Weiss B. Bicycle-rclared head injuries. Clin Sports Med 1999; 13:99.
77. Garrerrson LK, Gallagher SS. Falls in children and yourb. P£'diatr 109. Wesrfelr ]ARN. Fnvironmenral facrors in childhood accidenrs: a pro-
Clin North Am 1985;32: 153. specrive swdy in Goreborg, Sweden. Acta Paediarr 5cand 1982;(suppl
78. ]erosch J, Heidj"nn J. Thorwesren L, er al. Injury p;llll"l"nS in aLcep- 291).
20 General Principles

110. Worlock P, 5rower M. Fracture p<ltterns in Noningham children. J 1 15. American Academy of Pediatrics, Comminee on Accidenr and Poison
Paliatr Orthop 1986;6:656. Prevenrion: skateboard injuries. Ped/an'ics 1989;6: 1070-1071.
Ill. Wyshak C, Frisch RE. Carbonated beverages, dietary calcium, rhe 116. Barlow B, Neimirska M, Gandhi RP, er al. Ten years of experience
dierary calcium/phosphorus ratio, and bone fracrures in girls and boys. with failis from a height in children.] Perlialr 5111g 1983; 18:509.
] Adolesc fJetllth 1994; 15:210. 117. Bergman AB, RivaJa FP. Sweden's experience in reducing childhood
injuries. Pediatrics 1991 ;88:69.
118. Reichddcrfer TE, Overback A, Grecnsher]. Unsafe playgrounds. Pe-
Preventive Programs dintrics 1979;64:962.
119. Scheip l. 'J 'he role of organizations in community participation-pre-
112. American Academv of Pediatrics, Comminee on Accidenc and Poison vention of accidental injuries in a rural Swedish municipality. Soc Sci
Prevcnrion: rramp~lines. Evansron, I\linois, September 1977. Med 1988;26: I087.
113. American Academy of Pediatrics, Comminee on Accident and Poison 120. Spiegel CN, Lindaman FC. Children can't fly: a program ro prevem
Prevenrion: trampolines II. PedinNics 1981;07:438. childhood morbidity and mortality from window falls. Am] Dis Child
114. American Academy of Pediatrics, Comminee on Pediatric Aspects 1977;67:1143.
of Physical Fitness, Recreation and Sporrs: competitive athletics for 121. Werner P. Playground injuries and volunrary product standards for
children of elementary school age. Pediatrics 1981 ;67:928. horne and public playgrounds. Pediatrics 1982;69: 18.
 THE BIOLOGIC ASPECTS OF
CHILDREN'S FRACTURES
EDWARD W. JOHNSTONE
BRUCE K. FOSTER

THE IMMATURE SKELETON MECHANISMS Or BO E GROWTH

Endochondral Ossi ficatjon
A ATOMIC R.EGION OF TH ~ CHILD'S BO ES Regularory Mechanisms in the Physis
Epiphysis Membranous Ossification
Physis Remodeling of Bones
Mewphysis
FRACTURE REPAIR
Diaphysis
Osseous Healing
The Periosteum
Cellular Response ro Trauma
Apophysis
Physeal Healing Patterns
Remodeling of Bones in Children After Injury
TH ' MOL -,CULArZ B E
Molecules of the Carrilage and Bone Mauices HE Ul"URE F FRA TURE REPAIR

THE IMMATURE SKELETO osseous maturation. Salter-Harris type I injuries are common in
infants, and types II, HI, and IV become more common as the
Compared with the relatively static, mature bone of adults, the secondary ossification center enlarges and physeal undulations
changing structure and funnion, both physiologic and biome- develop. Joint injuries, dislocations, and ligamentous disruptions
chanica!, of immature bones make them susceptible ro different are much less common in children; it is more likely thar one of
patterns of failure, Even the types of fracture patterns within a the contiguous physes will be damaged. Changing trabecular
given bone demonstrate temporal (chronobiologic) variations and cortical structures affect metaphyseal and diaphyseal fracrure
that may be correlated with progressive anaromic changes affect- patterns, and the variable size of rhe secondary ossification center
ing the epiphysis, physis, metaphysis, and diapl1ysis at macro- affects susceptibility ro physeal and epiphyseal injuries.
scopic and microscopic levels. The options of treatments available for the treatment of skele-
Skeletal trauma accounts for 10% to 15% of all childhood tal injuries in children are expanding. Most notable is the intro-
injuries (60,128,129,131,171). Fractures of the immature skeJe- duction of growrh facrors, such as rhe bone morphogenic pro-
ron differ from those of the mature skeleton (6,128,129). Frac- teins (BMPs), for the induction of bone formation either in
tures in children are more common and are more likely ro occur non-healing defecrs or for bone fusions. It has become necessary
after seemingly insignificant trauma. Fractures may involve the for the orthopaedic surgeon to have a good knowledge of rhe
various growth mechanisms: Physeal disruptions make up about biological aspects of fracture repair. This chapter covers the basic
15% of all skeletal injuries in chiJdren (128,129,131,132,157). biology of bone growrh and fracture repair, including the roles
Damage involving specific growth regions, sLlch as the physis or of growrh facrors and the extracellular marrix.
epiphyseal ossification center, may lead ro acute or chronic
growth disturbances (127,128,166,190). The pl1ysis is con-
standI' changing, both with active longitudinal and latitudinal
(diametric) growth and in mechanical relation to other compo- ANATOMIC REGIONS OF THE CHILD'S
nents. PhyseaJ fracture patterns vary with the extent of chondro- BON
The major long bones of children can be divided inro four dis-
tincr, constanrly changing anaromic areas: the epiphysis, physis,
f.dward W. Johnstone: Dcp~rrJl)enl of Orrhopaedic Surgery, \X/olllcn's ~nd
metaphysis, and diaphysis (86). Each region is prone ro certain
Childrcn's Hospiral. Adelaide. South Australia.
Bruce K. Foster: Oeparrmenr of Orthopaedic Surgery. Wome,,'s and Chil- patrerns ofinjLIJy; the intrinsic susceptibility changes with ph}'si-
dre,,'s Haspira!. Adelaide. Sourh Auslr~lia. ologic and biomechanical changes during postnaral develop-
22 General Principles

menc. The four regions onglnate and become modified as a

result of the basic endochondral ossification process. Subse-
quently, they are supplemented by membranous bone formation
along the metaphyseal and diaphyseal shafts. Finally, the regions
are remodeled to create mature cortical and trabecular bone.

Epiphysis
At birth, each epiphysis (except the distal femur) consists of a
completely cartilaginous structure at the end of each long bone
(Fig. 2-1), the chondroepiphysis. The corresponding ossifying
structure is the chondro-osseous epiphysis. At a time chatacteris-
tic for each of these chondroepiphyses, a secondary center of
ossificarion forms and gradually enlarges until the cartilaginous
area has been almost completely replaced by bone at skeletal
maturiry. This chondro-osseous rransformation is vascular-de-
pendent (Fig. 2-2). Only arricular carrilage remains at maturity.
As the ossification center expands, it undergoes structural
modifications. The region adjacent to the physis forms a disrinct
subchondral plate parallel to the metaphysis, creating che radio-
graphically characteristic lucent physeal line. The appearance of
the ossification centers differ in cerrain chondroepiphyses, a fac-
tor chac must be considered when diagnosing fractLIres of these
regions. The ossification center imparts increasing rigidiry to the
more resilient epiphyseal cartilage as the secondary osseous tissue
expands (176).
The external surface of an epiphysis is composed of either
FIGURE 2-1. Chondroepiphyses of the distal femur and proximal tibia.
These structures have an extensively developed vascular system (carti- articular cartilage or perichondrium (Fig. 2-3). Muscle fibers,
lage canals) before secondary ossification. tendons, and ligaments may attach directly to the perichon-
drium, which is densely contiguous with rhe underlying hyaline
cartilage. The perichondrium contributes to the continued cen-

FIGURE 2-2. Early formation of the secondary ossification center within the epiphyseal cartilage. This
usually occurs in a region well vascularized by cartilage canals (open arrows). One of the canals sends
a branch into the hypertrophic cells (solid arrow), triggering the ossification process.
 Chapter 2: The Biologic Aspects of Children's Fractures 23

FIGURE 2-3. As the epiphysis matures, the ossifica-

tion center expands and progressively follows the con-
tours of the chondroepiphysis. The epiphyseal surface
is either articular cartilage or perichondrium along the
outer surfaces, as in the medial (solid arrows) and lat-
eral (open arrows) malleoli.

trifugal enlargement of the epiphysis. It also blends impercepti- the physeal conrour. The changing size of the secondary ossifica-
bly into the periosteum. This perichondrial/periosteal tissue con- tion center more effectively demarcates the physeal COntour on
tinuity contributes to the biomechanical strength of the rhe epiphyseal (germinal layer) side. As this center of ossification
epiphyseal/metaphyseal junction at the zone of Ranvier. enlarges cenrrifugally to approach the physis, the originally
When the hyaline cartilage of the chondroepiphysis first spherical shape of the ossification center flattens and gradually
forms, there are no easily demonstrable histologic differences develops a contOur paralleling the metaphyseal COntour. Similar
between the cells of the joint surface and the rest of the epiphy- contOuring also occurs as the ossification center approaches the
seal cartilage. However, at some point, a finite cell population lateral and subarticular regions of the epiphysis (Fig. 2-4). The
becomes stabilized and physiologically different from the re- region of the ossification center juxtaposed to the physis forms
maining epiphyseal canilage. McKibbin (l04) established that a discrete subchondral bone plate that the essential epiphyseal
these twO cartilage types are different physiologically and, by blood vessels must penetrate to reach the physeal germinal zone
implication, biochemically. If a contiguous core of articular and (Fig. 2-5). Damage to this osseous plate in a fracture may cause
hyaline cartilage is removed, turned 180 degrees, and reinserted, localized physeal ischemia.
the rransposed hyaline cartilage eventually will form bone at the If a segment of the epiphyseal vasculature is compromised,
joint surface, whereas the transposed articular cartilage remains whether temporarily or permanently, the zones of cellular
cartilaginous and becomes surrounded by the enlarging second- growth associated with tl1ese particular vessels cannot undergo
ary ossification center. Normally, articular cartilage does not appropriate cell division. In contrast, unaffected regions of the
appear capable of calcification and ossification. As skeletal matu- physis continue longitudinal and latitudinal growth, leaving the
rity is reached, a tide mark progressively develops as a demarca- affected region behind (Figs. 2-6 and 2-7). The growth rates of
tion between the articular and calcified epiphyseal hyaline carti- the cells directly adjacent to rhe affected area are more mechani-
lage. caJJy compromised than cellular areas farther away. The differen-
An important aspect of McKibbin's experiment was an expla- tial rather than uniform growth results in an angular or longitu-
nation of nonunion of certain fractures in which the fragment dinal growth deformity, or both (24,132).
may be rotated, causing the articular surface ro lie against me- Interruption of the metaphyseal circulation has no effect on
taphyseal and epiphyseal bone. Union is unlikely in such a situa- chondrogenesis within the germinal zone or the sequential carti-
tion because the articular surface is incapable of a reparative lage maturation within the hypertrophic zone of the physis (see
osteogenic response, an essential component of bone healing. Fig. 2-6). However, the subsequent transformation of cartilage
to bone (primary spongiosa) is blocked (I82). This causes widen-
ing of the affected area, because more cartilage is added to the
Physis cell columns but none is replaced by invasive metaphyseal vessels
The growth plate, or physis, is the essential structure adding and bone. Once the disrupted metaphyseal circulation is reestab-
bone through endochondral ossification (I2l, 126,130,166). lished, this widened, calcified region of the physis is rapidly
The primary function of the physis is rapid, integrated longitudi- penetrated and ossified, returning the physis ro its normal width.
nal and latitudinal growth. Injuries to this component are unique This is the mechanism seen in growth plate fractures and in
to skeletally immature patients. fractures of the metaphysis. The metaphyseal blood supply is
Because the physeal cartilage remains radiolucent, except for temporarily blocked by separation or impaction, and requires 3
the final stages of physiologic epiphysiodesis, its exact location to 4 weeks for restoration. If the circulatory compromise has
must be inferred from the meraphyseal contour, which follows been caused by a metaphyseal fracture, there also may be a tem-
24 General Prillciples

~ .. ~::".J.•. (~ ; ••: .- ;.:;i.:~~::.:.~~ ..•....

.\~~'''o'': ::t:-\~·o"o·o"o-'::~U"Cr'l~&'i,'
\, ':: ~ "'. ~~., ...• ~': ;) ~:~...
(

'. ;::'~
.
. . >.....':.r""
;. (
, ~

.\\: ~\
'.
A B "'I
\

c
Central Ischemia
FIGURE 2-6. Patterns of response to ischemia of the epiphyseal (A,B)
versus metaphyseal (C,D) circulatory systems. Metaphyseal ischemia is
usually transient; epiphyseal ischemia is usually severe and permanent.

FIGURE 2-4. Distal fibula, showing the variably undulated physis, in-
cluding a mammillary process (arrow). The physeal and epiphyseal carti-
lage turns proximally at the medial region (lappet formation) to partici-
pate in the formation of the distal tibiofibular articulation. Note the
difference in the subarticular subchondral bone, which has formed a
thick plate, compared with the thin, outer subchondral bone.

. /

FIGURE 2-5. Epiphyseal circulation (solid arrows) in a toddler. These

supply the germinal/dividing zones of the physis. The open arrow indi- FIGURE 2-7. Histologic section showing an area of central ischemic
cates the early ossification center. As this area enlarges, it will incorpo- growth arrest (arrow). The infarcted area of cartilage is left behind as
rate the epiphyseal vessels. the rest of the physis continues longitudinal growth.
 Chapter 2: The Biologic Aspects of C!1I"/dl"l'Il 's Fraft/lres 25

poraly halt ro bone form arion in the transielldy ischemic portion .E

of the metaphysis. This leads to an apparent sclerosis when the
bone is compared with the adjacent vascularized metaphysis, A
which undergoes a relative disuse osteoporosis. Compromise of
Pc
the metaphyseal circulation has minimal, if any, effect on physeal p
development, particularly when compared with the major detl·i-
mental effects of epiphyseal circularory compromise.
The effectS of physeal ischemia have been studied extensively
by Trueta and coworkers (180-183). Disrupting the epiphyseal
circulation leads ro either partial or complete cessation of
growrh. The central region seems more sensitive ro ischemia
than the periphery, which may have a variable capaciry ro recover
through continued latitudinal growth (112,125). Ischemic com-
promise leads ro different rates of growth across the affected
physis and significant changes in physeal contour (19). Some
changes may be caused by venous stasis rather than arterial dam-
age (78).

Metaphysis
The metaphysis is a variably contoured flare at each end of the
diaphysis. Its major characteristics are decreased thickness of the
cortical bone and increased trabecular bone in the secondary
spongiosa. Extensive endochondral modeling centrally and pe-
ripherally initially forms rhe primary spongiosa, which then is
remodeled into the more mature secondary spongiosa, a process
that involves osteoclastic and osteoblastic activity. The metaphy-
ses ex.hibit considerable bone turnover compared with other re-
gions of the bone, and this facror is responsible for the increased
uptake of radioneuclides in technetium 99m bone scans (105). FIGURE 2-8. Cortical fenestration (solid arrows) of a metaphysis. Note
The metaphyseal cortex also changes with time. Compared the interdigitation of periosteal (Ps) tissue with the fenestrations. The
with the confluent diaphysis, the metaphyseal cortex is thinner periosteum blends into the periochondrium (Pc). Extensive vascularity
is often present in this region (open arrows). (E, epiphysis; P, physis; Z,
and is more porous (trabecular fenestration; Fig. 2-8). These zone of Ranvier; L, ring of Lacroix.)
cortical feneStrations contain flbrovascular soft tissue elements
that connect the metaphyseal marrow spaces with the subperios-
teal region. The metaphyseal cortex exhibits greater fenestration
near the physis than in the diaphysis, with which it gradually regIOns to abnormal stress and predispose to certain fracture
blends as an increasingly thicker, dense bone (Fig. 2-9). As tem- modes.
poral longitudinal growth continues, conical fenestration be- Although the periosteum is attached relatively loosely to the
comes a less dominant feature, and the overall width of the cortex diaphysis, it is firmly fixed to the metaphysis because of the
increases, creating a greater morphologic transition between the increasingly complex cominuity of fibrous tissue rhrough rhe
juxtaphyseal and juxtadiaphyseal corrices. The metaphyseal re- meraphyseal fenestrarions. Such intermingling of endosteal and
gion does not develop extensive secondary and tertiary haversian interosseous fibrous tissues with the periosteal rissue imparts
systems until the late stages of skeletal maturation. These micro- additional biomechanical strength to the region (170). The peri-
scopic anatomic changes appear to be directly correlated with osteum subsequendy arraches densely into the peripheral physis,
changing fracture patterns and are the reason why torus (buckle) blending into the zone of Ranvier as well as the epiphyseal peri-
fractures are more likely to occur than complete metaphyseal or chondrium. The fenestrated metaphyseal cortex extends to the
epiphyseal/physeal fraCtures. physis as the thin osseous ring of Lacroix.
Anorher microscopic anaromic variarion in rhe metaphysis The meraphysis is rhe sire of exrensive osseous modeling and
occurs at the junction of the primary spongiosa and the hypertro- remodeling, both peripherally and centrally (Fig. 2-10). The
phic region of the physis. In most rapidly growing bones, the metaphyseal cortex is fenestrated, modified trabecular bone on
rrabeculae tend to be longitudinally oriented. However, in which the periosteum deposits membranous bone to thicken the
shorter growing bones, such as the metacarpals and phalanges, cortex progressively. Similar endosteal bone formation occurs.
trabecular formation is predominandy horizontal. As growth de- As this metaphyseal region thickens, the trabecular bone is pro-
celerates in adolescence, a similar horizontal orientation may be gressively invaded by diaphyseal osteon systems, nor unlike os-
seen in the major long bones. These variations in trabecular teons traversing the fracture site in primary bone healing. This
orientation affect the responsiveness of metaphyseal and physeal converts peripheral trabecular (woven or fiber) bone to lamellar
26 GeneraL PrincipLes

\ .
' , As in the diaphysis, there are no significant direct muscle
0 ~L - :Hrachments ro the metaphyseal bone. Instead, muscle fibers pri-
marily blend into the periosteum. The medial diStal femoral
I l.. attachment of the adducror muscles is a significant exception.
'-. ~. Because of extensive remodeling and insertion of muscle and
tendon in this area, the bone often appears irregular and may
be misinrerpreted as showing chronic trauma (i.e., a stress frac-
rure), infection, or a tumor.

Transverse Lines of Park and Harris

Many bones exhibit rransversely orienred, dense trabecular linear
bone patterns within the metaphysis. These lines usually dupli-
cate the contiguous physeal COntour. They may appear after
trauma, particularly when the child has been immobilized in
bed (e.g., rraction for femotal fracture), and they also may appear
after genetalized illnesses or even localized processes within the
bone (e.g., osteomyelitis) (1,62,137,138). The lines result from
a temporalY slowdown of notmal longitudinal growth after in-
jury or illness, and they often are called Harris growth slowdown
or arrest lines (Fig. 2-11). Because of the slowdown, the trabecu-
lae of the primary spongiosa become more uansversely than
longitudinally oriented, creating a temporary thickening in the
FIGURE 2-9. Section of distal tibia showing the transition (solid ar·
rows) of cortical bone from the dense, remodeled diaphysis (diamonds) primary spongiosa adjacent ro the physis. Once the normal lon-
to the fenestrated metaphysis (open arrows). Note the progressive girudinal growth tatc resumes, longitudinal trabecular orienta-
change from a relatively thin periosteum over the diaphysis to a much
tion is restored. The thickened, transversely oriented osseous
thicker one at the metaphysis.
plate is left behind, ro be gradually remodeled as primary spongi-
osa becomes secondary spongiosa.
Usually, transverse lines are distributed relatively symmerri-
cally through the skeleron and occupy identical sites in the corre-
(osteonal) bone, which has differenr biomechanical capaCities,
sponding bones on the twO sides of the body. They are thickest
and thus progressively rransforms metaphyseal correx into dia-
physeal cortex as longitudinal growth conrinues. A rorus (buckle) in metaphyses that grow most rapidly, such as the distal femur
ftacture is most likely ro occur in a metaphyseal region with a and proximal tibia. In the metaphyses with slowest growth, they
trabecular, fenestrated, compressible cortex. may not form at all, or they are exceedingly thin and lie at the
very end of the shaft, directly under the provisional zone of
calcification. These transverse lines parallel the contours of the
physeal pl'Ovisional zone of calcification. \'V'hen several transverse
lines are present, they tend to be parallel. The lines nearest the
end of the shaFt ordinarily are the thickest and wideSt; lines away
from the physes tend to be thinner and less distinct and are
usually broken and irregular. As they eventually become part of
the elongating diaphysis, they disappear completely with endos-
teal remodeling.
Park 037,138) found that temporary longitudinal growth
arrest of a bone was a prerequisire for rhe formarion of a trans-
verse line. During this initial phase of growth sroppage Ot slow-
down, a chin, transverse, osseous template was formed along [he
zone of prolifetative cartilage. When longitudinal growth in the
proliferating cartilage resumed (the recovery phase), the process
became visible radiographically as a transverse line.
More rapidly growing bones are associated with longitudi-
nally oriented trabeculae in the juxtaphyseal region; slower grow-
ing bones, particularly the proximal radius, metacarpals, meta-
FIGURE 2-10. Extensive modeling and remodeling of the medial (M) tatsals, and phalanges, normally have a greater amount of
versus the lateral (L) cortex of the distal femur may create irregularities rransvetscly oriented primary spungiosa (118), making trans-
that have been misinterpreted as fracture, stress fracture, infection,
and tumor. Note the well·formed subchondral bone at the periphery verse septa a normal finding. These particular bones do nor have
of the epiphyseal ossification center. a sufficient diFference in the orientation of trabeculae ro manifest
 rhapter 2: The BioLogic Aspects of ChiLc/reJi '$ FracllI res 27

A B
FIGURE 2-11. Histologic section (A) and x-ray study (B) of a distal femur showing a typical Harris line
(arrows). This formed during an acute illness and chemotherapy for leukemia. The child then resumed
a more normal pattern of growth until her death from leukemia about 14 months later.

transverse lines on radiographs. However, if growth slows in rhat characterisrically lacks haversian systems. The neonatal fem-
the rapidly growing areas normally characterized by longirudinal oral diaphysis appears to be rhe only area exhibiring any signifi-
orientation of trabeculae (e.g., distal femur), then more primary cant change from this feral osseous state to a more marure bone
spongiosa bone is formed in a transverse orientation (127). This with osteon sysrems (lamellar bone) before binh (Fig. 2-12).
bone can be quite thick, and probably relates co the duration Periosreum-mediated, membranous, apposirional bone for-
of the biologic stress. Once normal rates of longitudinal growth mation wirh concomirant endosreal remodeling leads to enlarge-
and trabecular orientation are reestablished, rhe rransversely ori· ment of the overall diamerer of the shaft, variably increased widrh
ented sepral, juxraphyseaJ plare is a contrasr ro the preexisting of rhe diaphyseal cortices, and formation of the marrow cavity.
longitudinally oriented rrabeculae and appears on radiographs Marure, lamellar bone with intrinsic bue constantly remodeling
as a specific transverse line. As remodeling occurs, with migration osteonal paccerns progressively becomes rhe dominant fearure
of the epiphysis away from this region, and with conversion of (Fig. 2-13).
primalY spongiosa to secondary spongiosa, there is a gradual The developing diaphyseal bone in a neonare or young child is
breakup of this transverse trabecular orientation. extremely vascular. When analyzed in cross section, it appears
much less dense than rhe maturing bone of older children, ado-
Useful to Assess Growth After Injury lescents, and adults. Subsequent growth leads to increased com-
These biologic marker lines are important in analyzing the effects plexity of the haversian (osteonaJ) systems and rhe formation
of a fracture on growrh. They can be measured and rhe sides of increasing amounts of extracellular marrix, causing a relative
compared ro corroborate femoral overgrowrh after diaphyseal decrease in cross-sectional porosity and an increase in hardness,
fracrure and eccentric overgrowth medially after proximal ribial factors rhat constantly change the child's suscepribiliry to differ-
metaphyseal fracrure. A line that converges toward a physis sug- ent fracmre parrerns. Certain bones, especially the tibia, exhibit
gests localized growrh damage rhar may resulr in an osseous a significant decrease in vascularity as the bone macures; rhis
bridge and the risk of angular defOl·mity. factor affects rhe rare of healing and risk of nonunion.
The vascularity of the developing skeleton consrantly
Diaphysis changes. In experimental studies, significant chronobiologic
changes in flow patterns were found in the developing canine
The diaphysis consticutes rhe major ponion of each long bone. tibia and femur (89,90,105,106,161). In parricular, there was a
It is principally a product of periosteal, membranous osseous dramaric decrease in tibial circulation with increasing skeletal
tissue apposition on the original endochondral model. This leads maturation. This also occurs in humans, which helps to explain
to the gradual replacement of the endochondral!y derived pri- the increasing delay in fracture healing and the increased inci-
malY ossification center and primary spongiosa; rhe larter is re- dence of nonunion of the tibia in adolescents and adults. A poor
placed by secondalY spongiosa in the metaphyseal region. At vascular response could impair rhe early, crucial stages of callus
birth, the diaphysis is composed of laminar ((-etal, woven) bone formation.
28 Gmeral Principles

A .'

FIGURE 2-12. Sections of the femur at the level of the lesser

trochanter at birth (A) and age 7 years (8). At birth, some corti-
cal thickening and osteon remodeling is evident laterally; the
rest of the cortex is irregular. By age 7 years, extensive thicken-
ing and remodeling of the cortex has taken place. B

A B
FIGURE 2-13. Transverse sections ofthe tibial diaphysis in a neonate (A) and at age 2 years (8). A thick
periosteum is evident in A (open arrows), in association with a rapidly forming anterior cortex. At age
2 years, new subperiosteal (membranous) bone is being added to the cortex (solid arrow).
 Chapter 2: The Biologic Aspects of Children's Fractures 29

Other researchers have suggested that adequate vascularity usually remains intact on the concave (compression) side of an
was a major factor in fracture heaJing,(150,151,184,190,194), injlllY. This intact periosteal hinge or sleeve may lessen the extenr
but they did not consider chronobiologic changes in blood flow of displacemenr of the fracture fragments, and it also can be
patterns. used to assist in the reduction, because the intact portion con-
tributes to the intrinsic stability. Because the periosteum allows
The Periosteum some tissue continuity across the fracture, the subperiosteal new
bone that it forms quickly, bridges the fracture gap and leads
A child's periosteum is thicker, is more readily elevated from to more rapid long-term stability. The periosteum may be specif-
the diaphyseal and metaphyseal bone, and exhibits greater os- ically damaged, with or without concomitant injury to the con-
teogenic potential than that of an adult (126). The periosteum tiguous bone. Such avulsion injuries may lead to the formation
is loosely attached to much of the shaft of the bone, but it of ectopic bone (120). In contrast, severe disruption of the peri-
attaches densely into the physeal periphelY (the zone of Ranvier; osteum, as in an open injury, may impair the fracture healing
Fig. 2-14) through intricate collagen meshworks, thereby playing response. Complete loss of a bone segment, with the periosteal
a role in fracture mechanics and treatment of growth mechanism sleeve reasonably intact, may be followed by complete reforma-
injuries (170). The thicker, stronger, more biologically active tion of the missing bone (16).
periosteum affects fracture displacement, reduction, and the rate
The periosteum, rather than the bone itself, serves as the
of subperiosteal callus formation. It also may serve as an effective
origin for most muscle fibers along the metaphysis and diaphysis.
internal restraint in closed reductions.
This mechanism allows coordinated growth of bone and muscle
Because of its contiguity with the underlying bone, the perios-
units; this would be impossible if all the muscle tissue attached
teum is usuaJly injured to some extent in all fractures in children.
directly to the developing bone or cartilage. Exceptions include
However, because the periosteum more easily separates from the
the attachment of muscle fibers near the linea aspera and into
bone in children, there is much less likelihood of complete
the medial distal femoral metaphysis. The latter pattern of direct
circumferential rupture. A significanr porrion of the periosteum
metaphyseal osseous attachment may be associated with signifi-
cant irregularity of cortical and trabecular bone. Radiographs
of this area often are misinterpreted as showing a neoplastic,
osteomyelitic, or traumatic response, even though they exhibit
only a variation of skeletal development.

Apophysis
Because of the differi ng histologic composition of the tibial tu-
berosity (fibrocartilage instead of columnar cartilage; Fig. 2-15),
failure patterns differ from those in ocher physes. This area devel-
ops primarily as a tensile-responsive structure (i.e., an apophysis).
However, the introduction of an osseous secondary ossiflcation
center initially in the distal tuberosiry interposes osseous tissue,
which tends to fail in tension and which may lead to avulsion
of parr of this ossification center (Fig. 2-16). Healing of the
displaced fragment to the underlying undisplaced secondary cen-
ter creates rhe symptomaric reactive overgrowth known as an
Osgood-Schlatter lesion (119,123). Similarly, in adolescents, ex-
cessive tensile srress may avulse the entire tuberosiry during the
late stages of closure (124).

THE MOLECULAR BONE

Molecule of the Cartilage and Bone
Matrices
The Cartilage Matrix

FIGURE 2·14. Simulated type 1 epiphyseal (E) displacement from the

The cartilage marrix is synthesized by chondrocytes. The main
metaphysis (M). Note the thick periosteum (arrow) and its contiguity constituents of the cartilaginous matrix are collagens (mainly
with the cartilage of the epiphysis (radiopaque here because of the type II) and proteoglycans. AJrhough collagen type II provides
cartilage and air contrast). In the body, however, the similar soft tissue
radiodensities of cartilage, ligament, muscle, and so forth blend to- structural srrength, rhe proteoglycans have structural and regula-
gether, making them radiolucent. tory effects. The structural effects of proteoglycans arise through
30 Genna! PrincipleJ

", ...,
\
, \
I." , .'
"," I,..
\
• I,
\
II,

, I \ \'
\
-\
\
\ \ \
,\

A B

,,

FIGURE 2-15. Histology of a typical apophysis,

the tibial tuberosity (tubercle). A: Attenuated
columnar cartilage adjacent to the main proxi-
mal tibial physis. B: Fibrocartilage and minimal
hypertrophic matrix in the mid-tuberosity re-
gion. C: Fibrocartilage and membranous ossifi-
c cation in the distal end of the tuberosity,

binding ro the collagen components and the water-binding

properties rhat provides resilience ro compression. RegularolY

~'1'~~~
effecrs include growth facror interactions, cell matrix interac-
tions, and regulation of collagen fibril size. Specific molecules
expressed and their functions are listed in Table 2-1.

&~
W'?I
";'-'~:' ...... ~ ...... :.
. ~_ a.,...-:"'
.... '" '. -' •• ' ,',' ,;;};
The Bone Matrix
Except for a small percentage of molecules from the circulation
.. ~l:::-.t.;~···..c--,"'".• ,.... 77;. and preexistent matrices thar may become entrapped, the bone
}.:·is~:~l;¥f~·>I.··:··~t matrix is almost entirely synthesized by osteoblasts. The compo-
::.. .~~'t'...,l:-"·"",'v~~
:':' :\\o;.l"\~
~-'I
.,...~ ... -:' -:',:1 )'~4~ "~:'"
sition of the bone matrix was ourlined by Buckwalter and associ-
r:.. '. ".r.'. ·.'''<'.ii?~A Ossicle
t

. ',:1' ~~::·.i6~7~? " ,

ates (20). Briefly, bone marrix is a composite material composed
;r~~<:f·':..~~~;(;. . .~.~ ~:: t of an inorganic (mineral) portion and an organic porrion. The
"t:.~ .v~~~/r;'1-!J /1
LI'> II' ~ """.;r .Jl.~ /f(~
':"~~' ~ "~I
. ' '. I
composite Structure provides physical strength and resilience to
~",;,:::,~;~~~ fracture. Bone with deficient inorganic mineral content is plia-

~~/;f/1~Fl'/;;¥f::(i;,'<separalion
' ';'.' J1 ,/':,,-;,/V
ble, and bone with deficient organic content is britde.

~
The composition of living bone is 60% to 70% inorganic
•
. "'~~v~lfl
~; ~.\
~,
. ..·1I1JO/:P:/''''
''.1
Tuberosity
componenrs, 5% to 8% water, and the remainder is organic
(76). The inorganic porrion is mainly hydroxyapatite, with some
~/~\t.4'::·'A carbonate and acid phosphate groups. It has also been suggested
c ~~~l:'\':l<l' thar bone crystals do nOt contain hydroxyl groups and should
Physis
be termed apatite rather than hydroxyapatite (20). The organic
FIGURE 2-16_ Avulsion (tension) failure of the developing ossification porrion is composed of collagen type I (90%) and noncoUage-
center of an apophysis. The degree of displacement determines the
likelihood of healing and the symptoms and size of the final lump, nous proteins. The noncollagenous prOtein portion includes a
typical of an Osgood-Schlatter injury. /lumber of proteins and proteoglycans rhar perform strucrural
 C!Japter 2: The Biologic Aspects of Child/'en S Fractures 31

TABLE 2-1. MATRIX MOLECULES OF CARTILAGE

Component Site of Expression Within Physis and Proposed Functions

Collagens
Collagen II (fibril) Predominate collagen of all Imparts strength, site of initial
cartilage mineralization (113, 143)
Collagen IX Proliferative zone of the Associates with the surface of the
physis collagen II fibril (78)
Collagen X (short Hypertrophic cartilage Minera'lization (52, 71, 80)
chain collagen)
Collagen XI (fibril) Proliferative and Collagen fibril size (191)
hypertrophic zone of the
physis
Proteog Iyca ns
Aggrecan Throughout cartilage Imparts resistance to compression.
Forms aggregates with hyaluronic
acid and link proteins (23, 113,
159)
Decorin (DS-PG2) Within chondrocytes and Collagen fibril size and TGF-j3
the Interterritorial activity (7, 67, 744)
capsules of the upper
proliferative
chondrocytes
Biglycan (DS-PG1) Territorial capsules of the TGF-,B activity (67)
upper proliferative
chondrocytes
Fibromodulin Collagen fibril diameter and binding
of cells to the matrix (66)
Matrix Gla protein Cartilage Inhibits mineralization (92)

and regu]arory funcrions. Acrual molecules and funcrions are

oudined in Table 2-2 and in rhe following secrion.

Matrix Constituents
Alrhough ir is nor a complere lisr, rhe following provides an TABLE 2-2. COMPOSITION OF BONE
example of rhe major proreins found wirhin bone and canilage
marrices. Component Proposed Functions

Collagens
Collagens Collagen I Imparts strength, site of initial
Collagens are a Family of proreins coded by ar leasr 19 disrincr mineralization
genes. Members are expressed in mosr tissues. Collagens have a Collagen V Provide the inner core of the
rriple helical region rhar arise from rhe repeared winding of collagen fibril (8, 46)
Collagen VI Cell attachment
rhree collagen molecules around a common axis. Collagens are Collagen XII Collagen fibril size
symhesized as a propepride rhar is ohen glycosylared. Collagen Proteoglycans
is secrered From cells and is processed in rhe extracellular space. Decorin (DS-PG2) Collagen fibril size, TGF-,B activity
The processed collagen forms inw subunirs rhar rhen undergo (162, 163)
Biglycan (DS-PG1) Collagen fibril assembly, TGF-,B
flbt-illogenesis (Fig. 2-17). The facr rhar rhe final fiber is com-
activity (164, 195)
posed of many individual molecules accounts for rhe observed Fibromodulin Collagen fibril diameter, binding
dominant negarive murarions rhar can be observed wirhin rhe of cells to matrix molecules (66)
collagen family (74). The incorporarion of individual molecules Osteocalcin (bone Binds hydroxyapatite (146, 587)
thar comain murarions rhar afFecr rhe packing of rhe peprides Gla protein)
Matrix Gla protein Controls mineralization (92, 146)
inro rhe rriple helix can disrurb rhe srrucrure of rhe whole fiber.
Osteonectin Binds calcium (11)
The molecular srrucrures rhar arise are in rhe form of fibrils or Osteopontin Cell attachment (102).
Ilerlike srrucrures. [n realiry, rhe mulrimeric fibet·s observed in
vivo arc ofrell composed of a number of difterenr collagens (5).
32 Gel/eml Principles

11' terminal Propetide : ••- - - - Mature Collagen Molecule - - -•• : C terminal Propetide
,,, ,
,
, :,
' ..- - - - - - - - - - - - - -..... ,
Triple helical region :
'

1 fibrillogenesis

FIGURE 2-17. Collagens are synthesized as a pro peptide that is often glycosylated (not shown). The
collagen molecule has a triple helical region that arises from the repeated winding of three collagen
molecules around a common axisis. The processed collagen forms into subunits that then undergo fibril-
logenesis.

Collagen [ype [ is the main collagen found in bone and other and bigJycan have side chains ofdermatan sulfate, and betaglycan
tissues. It is composed of twO 0'1 (I) and one O'2(I) polypep[ides. has chondroitin and heparin sulfate chains. Fibromodulin has
The collagen eype I flbets aet as si[es for initial mineralization side chains of Im'atan sulfate. The territorial capsules of the
and provide tensile strength to [he bone. Mutations in the pro- chondrocytes in the upper proliferative region of the physis s[ains
peptides can cause a variety of phenoeypes affec[ing mineraliza- for biglycan, the inrerrerritOrial matrix stains for decorin (7).
tion and bone fragiliey, the mos[ severe being osteogenesis imper- These proteoglycans have a structural role but are also known
fecta. In contrast, collagen type II is a triple helical molecule to inreract with growch factOrs (7,67,144).

ma[ is composed of [hree 0'1 (II) polypeptides and is expressed

wi[hin cartilage. It is the main fibril-forming collagen in cani- Other Noncollagenous Proteins
lage. Mutations cause Langer-SaJdino achondrogenesis and Osteocalcin is also known as bone Cia protein. It has [hree
spondyloepiphyseaJ dysplasia congenita (27,45). residues of gamma-carboxyglutamic acid chat enable it to bind
Other collagen eypes, such as V, IX and Xl, associate with to hydroxyapatite. It is thought to playa role in mineralization

the collagen fibers. They may influence coHagen diame[ers and of the bone matrix (146,147), but tne exact mechanism and
interact with other matrix molecules. Mu[ations in eypes IX funccion are undetermined (35,63).
and Xl can result in a number of clinical manifestations (134). Osteonectin has the ability to bind calcium and collagen type
Collagen type X is associated with the matrix of hypenrophic I, and may enable the process of mineralization thac is initiated
chondrocytes and is involved with the mineraliza[ion process on che colJagen type [ fibers (II).
(80,81,139). Mutation causes spondylometaphyseal dysplasia Osteopontin is thought to be critically involved with [he
(74), but the deletion of the encoding gene resulTs in mild binding of osteoclasts (70,149), cells that degrade to the bone
matrix (103).
changes (73,155).
Matrix Cia protein is an inhibitor of calcification. The carti-
lage of mice lacking this protein undergoes sponraneous calcifi-
Proteoglycans cation (93).
Proteoglycans are present in large amounts within all connective
tissues. Pro[eoglycans are proteins [h.at have ei[her one or a num-
ber of polysaccharide chains linked to a prorein core. The poly- Growth Factors
sacch.aride's glycosaminoglycan side chains are either heparin, Within an individual, cell-to-cell communication occurs be-
heparin sulfate, chondroitin sulfate, derma tan sulfate, or kera[an tween neighboring cells and between cells that are separa[ed by
sulfate. The glycosaminoglycans differ in the composi[ion of an almost complete body length. Communication signals take
their cons[ituenr disaccharide structures. They can combine with me form of diffusible molecules which pass between the cells or
other molecules within [he mauix to form macromolecular by cell surface-bound receptor-ligand interactions (88,193). In
structures (49) (Fig. 2-18). addition, neighboring celJs can pass information betw'een one
Proceoglycans are a critical component of cartilage and bone another via their gap junctions (48). These channels enable the
(23,113,144). The pro[eoglycans presem in the physis include passage of small molecules, including calcium ions, bet\veen
latge proteoglycans like aggrecan as well as smaller pro[eoglycans neighboring cells. Calcium is a key second messenger that pro-
such as decorin, biglycan, and possibly, flbromodulin. Decorin vokes a number of cellular events (lID).
 Chapter 2: The Biologic Aspects of Children:( Fractl/res 33

Aggrecan (macromolecular form)

Aggrecan
(monomer)
+- Glycosaminoglycan
side chains

Decorin L Biglycan t--

FIGURE 2-18. Proteoglycans are proteins, which have either one or a number of polysaccharide (glyco-
saminoglycan) chains linked to a protein core. Aggrecan is present in cartilage and has the ability to
form macromolecular structures with hyaluronic acid and link protein. Decorin and biglycan are present
in bone and cartilage matrix.

Hormones are a group of diverse molecules that are secreted skeletal deformities including Pfeiffer's syndrome (FGFRI),
by endocrine glands and are transporred to their effect target Crouzon's and Jackson-Weiss syndromes (FGFR2), and achon-
tissues by body fluids. They coordinate body functions in com- droplasia (FGFR3).
plex otganisms. Hormones can be in the form of amino acid To date, the fibroblast growth factor family comprises at least
derivatives (e.g., epinephrine) polypeptides (e.g., somatotropin nine members including acidic fibroblast growth factor (FGF-
or growth hormone), glycoproteins (e.g., foUicie-stimulating I), basic fibroblast growth factor (FGF-2) (10,15,47,97,111,
hormone), steroids (e.g., testosterone), or fa try acids (e.g., prosta- 156,172,174,199). Additional fibroblast growth factors exist
glandins). that have far less homology. FGF-I and FGF-2 are present in
Growth factors and hormones may circulate in a free form the extracellular matrix of bone (64).
or be bound to carrier molecules or the extracellular matrix The FGFs are also complicated by the presence of alternative
(136). The binding of growth factors and hormones to other forms of the specific forms of FGF-l and FGF-2. FGF-l is
molecules may result in inhibition of the degradation, delivery, rypically 140 amino acids in length, but larger forms of 160 and
and controlling of activity. Many gtowth factors, including the 154 amino acids have been identified (27,43,53,61). FGF-2 is
fibroblast growth factors, transforming growth factor-13 (TGF- normaJly translated as an 155 amino acid molecule, bur through
/3), and insulin-like growth factors, can be bound to the matrix. the use of alternative start codons, another three higher molecu-
Cell activation usually requires the factors to bind to receprors lar weight forms have been identified.
on the cell surface, although a number of hydrophobic hormones The acidic and basic forms ofFGFs are well conserved across
pass directly through the outer membrane and bind to intracellu- species. Comparing the amino acid composition of FGF-l and
lar receptors (31,44,99,116) (Fig. 2-19). FGF-2 from different species, Hearn found a 92% sequence
A degree of redundancy often exists in that a gene knockout identiry between human and bovine acidic fibroblast growth
for one particular growth factor may result in only slight changes factor. Only 2/l55 and 3/155 amino acids differ in human and
in the phenorype observed. A good example is the double mutant bovine, and human and ovine, forms of basic fibroblast growth
ofBMP-5 and 7, which is lethal during embryonic development, factor, respectively (65).
but a null muration in either one has little effect (169). Six receptor molecules have been identified so far. FGF tecep-
rors can be divided into twO groups by the relative affiniry of
the ligands ro thei r receprors.
Fibroblast Growth Factors
The biologic effects of the fibroblast growth factors are wide- Transforming Growth Factor
spread. Fibroblast growth factors are angiogenic and can influ- The TGF-13 superfamily is composed of more than 24 members
ence mitosis and differentiation in many cell types. The receptors (68). They are subdivided inro families including TGF-I3, in-
to these growth factors have been implicated in a number of hibin, decapenraplegic protein/vegetal hemisphere 1 (DPP/
34 General Principles

Growth Factor Growth Factor

(Inactive) (active)
Binding Proteins

. Sequestered Activated
i.at cell surface Receptor Binding Protein
potentates cell
altachmel1t~__~

FIGURE 2-19. The figure shows aspects of growth factor interactions. Any particular growth factor will
possess only a subset of such interactions. Growth factors may require activation (e.g., TGF-,B). Binding
proteins may sequester or protect the growth factor. The binding protein may also potentate the binding
of the growth factor to the surface receptor (e.g., FGF and heparin). Cells may also sequester the growth
factor at the cell surface.

Vgl), and mUllerian-inhibiring subsrance. Members of rhe TGF-,B may bind to cellular receprors, of which there are ar
TGF-,B and the DPPlVgl families have critical funcrions in the least nine. However, mosr of the acrions are mediated rhrough
developmem of the skeJeron, its growth and maintenance, and twO receptors termed recepror ! and 2. Receprors 1 and 2 ,Ire
fracture repair. The bone morphogenic proreins (except for members of the serinelrhreonine kinase family (l00). TGF-,B
BMP-1) are members of rhe DPPlVgl family and are discussed receptor type 3 is a membrane-bound pwteoglycan termed be-
in the nexr secrion. raglycan. Beraglycan is thoughr ro act as a TGF-,B cell surface
All TGF-,B family members except TGF-,B4 are syll[hesi7.ed reservoir and is nor involved wirh signal transduction itself. Be-
as large precursor forms rhar are processed ro acrive forms. The raglycan has rhe possibility of binding FGF rhrough the heparin
acrive form is either a heterodimer or homodimer. It is rhoughr sulfate chains and may present TGF-,B in conjunCtion with FGF
thar the pro-region may eirher help in rhe folding of rhe proreins ro the cell (l00). TGF-,B also binds ro the small proteoglycans:
during symhesis or comrol activity. In the case ofTGF-,B!, the biglycan, decorin, and fibromodulin (67). The small proteogly-
pro-region and a second glycoprorein can also bind ro rhe active cans bind TGF-,B through rhe leucine-rich repeats in rheir pro-
facror ro form a latent complex. Members of the TGF-,B family tein cores and are thoughr to sequester TGF-,B in rhe matrix.
are highly expressed in bone (TGF-,Bl,TBG-,B2). Imporrant in They also compere wirh betaglycan in binding TGF-,B. Decorin
fracmre repair, TGF-,Bl and TG F-$2 are also released in large has the ability to negatively regulate rhe activity ofTGF-,B (13,
quantities during platelet activation. 160).
Aparr from rhe presence of rhe growrh facror irself, rhe pres-
ence or absence of rhe latenr complex conuols rhe activity of Bone Morphogenic Proteins
TGF-,Bl. TGF-,B members can also be sequestered in the marrix. The bone morphogenic proteins and their onhopaedic relevance
The active TGF-,Bl complex call be released from the latell[ have recently been reviewed by Schmitt and colleagues (160).
complex by extreme pH or by catalytic methods. This is particu- The bone morphogenic prOteins (excepr BMP-1) represent a
larly imporrall[ in fracture repair and bone remodeling. The group of relared growth f:1Ctors that have critical roles in the
acrivation oflarell[ TGF-,B is likely to be critical in the induerion cell proliferation and differentiation of a number of cell types
of fracrure repair and osteoblast function. including mesenchymal cells, chondrocytes, and osteoblasts (28,
The acrive TGF-,B molecules may also be bound and their 82,83,J 86). They have roles in embryo and feral developmenr,
activity COntrolled by a number of matrix molecules, including bone growth, and fracture repair. They also include a number
beraglycan and decorin (l 00,197). A1rernatively, the active of growrh facrors (BMP-2, BMP-7) (OP-I), which are being
 Chflpter 2: The Biologil-" Aspect; Ill" Children)- Fra(furei 35

proposed for the rrearment of fraermes and rhe esrablishment rhe periosteum. Similarly, membrane-derived bones may grow
of bone fusions. and elongare by an endochondral process (126,130).
BMPs exisr as glycosylated dimers. Thineen have been identi-
fied so far, bur owing ro sequence homology, only BMP-2
Endochondral Ossification
rhrough 9 can be classed as members of rhe TGF-,B family.
Parricular BMPs produce ecrapic canilage or bone when im- Endochondral ossification is rhe process by which bone forms
planred subcuraneously (2,188). Like the orher growrh facrors via a canilaginous inrermediare. The physis besr reAeers rhis
discussed so far, rhe BMPs have a number of binding proreins process. Physes are remporary carrilaginous rissue siruared be-
borh in the inrracellular marrix and on rhe cell surface. A secrered rween the primary and secondalY ossification cencers of all long
glycoprorein rermed noggin can bind and inacrivare BMPs (50). bones. From 9 to 10 weeks' gestational age ro skeletal maruri ey
Chordin is a similar protein rhat mosr likely has a similar func- at 15 ro 17 years, they are responsible for the longirudinal growth
rion (142). It has been proposed thar these proreins control of bone. The physis can be divided inro at least three zones.
BMP acriviey and may also serve as a mechanism for esrablishing The reserve zone is situated on rhe epiphyseal side and conrains
gradienrs of BMPs across rhe embryo during developmenr. Ac- small, spherical cells randomly disrribured rhroughout rhe zone.
rive BMPs bind ro hererorerrameric serinelrhreonine kinase re- In the adjacent proliferarive zone, chondrocyres undergo mirosis
ceprors. The nonacrivated receprors exisr as eype 1 and 2 recepror and are organized imo columns running parallel to rhe axis of
proteins, rhe eype 2 recepror aurophosphorylares. Once rhe li- bone growth. Cells in the proliferative zone mature and eventu-
gand binds, the rwo receprors are brought rogether and the re- ally increase ro 5 ro 10 times rheir volwne in rhe hypertrophic
cepror eype I porrion is phosphorylated. Only afrer the recepror region. Marrix vesicles are also deposited wirhin rhe longirudinal
eype 1 is phospholylared is a cellular response achieved. Intracel- septa of the physis. Matrix vesicles are membrane-encapsulared
lular activarion is via the inrracellular proreins termed SMADs srrucrures rhar are thoughr to concentrate calcium and phos-
(rhe humor equivalent of rhe MAD (mothers againsr decapen- phare. Enzymes such as alkaline phospharase conven organic
raplegic) prorein), but orher inhibirors can srill come inro play. phosphares ro inorganic phosphate. The longirudinal septum
Exposure of the cell ro a number of other growth facrors (includ- around rhe rerminal hypenrophic chondrocyres mineralizes, and
ing cer-l) can inhibit the acrivarion of the cell by BMPs (140, this mineralized man'ix forms the templare for new bone deposi-
160). rion in rhe meraphysis (Fig. 2-20).
Associared with rhese changes in cellular arrangemenr and
volume, rhe matrix in rhe physis also undergoes a continual
Angiogenic Growth Factors modification in contenr. The two major macromolecules of car-
Angiogenic facrors are growth facrors that promote neovasculari- rilage marrix produced by rhe chondrocytes are rhe proreoglycans
zation. They are critical in fraerure repair. The invasion of the (predominantly aggrecan with lesser amounts of decorin, bigly-
metaphyseal vascular supply is crucial ro endochondral ossifica- can, and fibromodulin) and rhe collagens (rypes II, IX, X, and
rion, and fracrure repair does nor occur without an adequate XI). The major change in physeal proreoglycan srrucrure occurs
vascular supply. Ir is probably nor by accidenr rhat a number as chondrocytes organize into columns in the proliferative zone.
of angiogenic facrors such as TGF-,B and FGF-2 are sequestered Addirional variation occurs in the hypenrophic region, where
in the bone marrix. Angiogenic facrars act directly or indirectly the glycosaminoglycan sulfarion parrern demonsrrares differ-
on endothelial cells, promoting proliferation and migrarion of ences between the pericellular and exrracellular spaces and rhe
rhe cells into areas in which rhey are released. Angiogenic facrors appearance of a uniq ue collagen (eype 10) is observed. The small
acring indirectly by recruiting macrophages monocyres, in rum, proreoglycans-decorin, biglycan, and fibromodulin-are also
release their own direct-acting angiogenic facrors (165). differenrially expressed across rhe physis, alrhough derailed srud-
Direcr-aering angiogenic facrors include plateler-derived en- ies of rhese proteoglycans have nor been done (see Table 2-1).
dothelial growth facrors (PDEGFs), TGF-,B, and FGF-2 ro name The cellular changes and associated marrix alterations are
bur a few. Indirect aering angiogenic facrors include TGF-,B and geared roward producing a microenvironmenr within the hyper-
rumor necrosis facror-a (TNF-a). rrophic zone of the physis, which is conducive ro marrix mineral-
izanon.

MECHA ISMS OF BONE GROWTH Regulatory Mechanisms In the Physis

Hormones, for example, normal growrh hormone, have a global
Because bone is rigid, it cannot grow by incernal expansion and effecr on physcal funerion rhroughour rhe body, bur many
bone growth is achieved by adding newly synrhesized bone ro growrh facrors aer locally. The action of rhese growrh facrors
existing bone by two mechanisms: endochondral ossification and have ofren been derermined in vitro and in vivo and can ofren
imramembranous ossification. These mechanisms are named by present conAiering resulrs due ro experimental design and
the intermediare srructures, that must be passed ro form rhe models used. Mosr invesrigations have concenrrared on rhe effeer
bone. The producrion of any parricular bone after inirial differ- of single or, in some cases, two growrh facrors. However, it is
enciation may involve discrete, juxtaposed, or incerspersed areas likely rhar endochondral ossification is conrrolled by a large
of each basic parrern. Endochondral-derived bones generally number of growrh facrors whose acriviry is controlled by a large
have membranous ossification by aJJpositional bone growrh from number of binding proreins borh wirhin rhe marrix and on rhe
36 Cenerrll Principles

Zones

Acts as a source of stem cells for the

Resting

J production of the chondrocyte columns below.

Chondrocytes undergo mitosis, and

while doing so produce a matrix of
predominately collagen type II, and
Proliferative various proteoglycans. Non-collagenous
proteins are also produced that organize
the matrix and regulate the mineralization
process.

The chondrocytes undergo a rapid

increase in size and produce
Hypertrophic collagen X. Mineralization occurs
between the chondrocyte columns.
Most chondrocytes undergo apoptosis.

FIGURE 2-20. The figure shows the process of endochondral ossification within the physis. Although
not as organized, endochondral ossification follows a similar pattern during fracture repair.

chondrocyte surface. Cellular response is determined by parallel in achondroplasia, conseant activation ofFGF receptor (FGFR3)
processing of the intracellular signals that are induced by a num- is inhibirory (87,95). FGF/heparin sulfate interaerion is probable
ber of active growth factors binding to their speciflc receptors. in the differentiation of the physeal chondrocytes because the
Presented is an outline of the likely actions of a number of key cominuous exposure of FGF-2 inhibits chondrocyte differemia-
growth factors on endochondral ossification. It is not complete, tion in vitro and inhibitOts of glycosaminoglycan sulfation (in-
and the models will continue to change. cluding heparin sulfate) restOte the diffcrcmiation process. Addi-
BMP-2 and 7 promote proliferation and matrix synthesis in tional sulfate permits glycosaminoglycan sulfation and returns
undifferentiated chondrocytes (40,84). J t is believed thar once the effect of FGF-2 (30).
the chondrocytes start differentiating, the expression of noggin Vitamin 0 metabolites and parathyroid hormone have roles
inhibits the continual outgrowth of the undifferentiated chon- in calcium mobilization within the body, but they also influence
drocytes (18). The prechondrocytes may also respond to growth endochondral ossification. Parathyroid hormone and pararhy-
hotmone (117,133). Once the chondrocyte has lost itS resting roid hormone-related protein (PTHrp) can inhibit the matura-
phenorype, insulin like growth factOr-l (IGF-1) may act as a (ion of chondroc)'tes. It is posrulated that physcal chondrocytes
stimularor of proliferation and differentiation (117,176). EGF regulate the local production of PTHrp by secreting a protein
can augmenr IGF stimulation by increasing the exptession of (Indian Hedgehog). This protein stimulates the chondrocyte co
the IGF-1 receptOr (12). Although the chondrocytes synrhesize produce PTHrp, which slows the maturation of proliferative
large quantities of matrix moJecules, they also synthesize FGF- chond rocytes co hypertrophic form (85,187). Expression of the
1, FGF-2, TGF-,B, and a number ofehe BMPs (16,25,29). These mRNA for BMP-6 peaks before mineralization (25) (Fig. 2-21).
molecules can ace in an aurocrine manner, but many are seques- AI(hough the chondroc)'tes of the physis will proliferate and
tered intO ehe newly forming cartilage marrix. FGF-2 in low form a cartilaginolls matrix with only the epiphyseal vascular
doses is mirogenic for the chondrocyees (94); however, as occurs supply, the metaphyseal vessels are critical for the mineraJization
 Chapter 2: The Biologic Aspects of Children j. Fractures 37

Intramembranous ossificarion occurs when osreoprogeniror

BMP-7 cells are formed from the overlying tissue. The osteoprogenitor
BMP-2 cells continue ro differentiate into osteoblasrs, which produce a
Growth Hormone marrix rhar undergoes mineralizarion.

IGF-l Remodeling of Bones

FGFI The first bone to be laid down either from the physis or in the
FGFII fracture callus is woven bone, which is remodeled to lamellar
TGF-fJ bone. AJrhough cancellous bone can be remodeled and obrain
Growth Hormone its nutrients from rhe surface, corrical bone is remodeled into a
IL-l complex structure of osreons thar together form rhe corrical
Vitamin D bone. Osteons are [lIbular structures that interconnecr. They
EGF (stimulates IGF receptor) consist of layers of ordered lamellar bone around a cenrral canal.
The central canal con rains blood vessels, lymphatics, and in some
IGF-l cases, nerves (20).
PTH, PTHrp Bone is constandy remodeled by osreoclasts and osreoblasts.
FGFII The bone is encapsulated by bone-lining cells rhat have the po-
TGF-fJ renrial to become activated osteoblasts. The bone-lining cells,
like osreocytes, have slender cellular processes thar make conract
IL-l with the osreocytes wirhin rhe mineralized bone. Osteocyres are
Vitamin D rhought to arise from osreoblasrs rhar have become entrapped
during bone formation. Jr has been proposed thar the bone-
lining cells need to erode the osteoid rhat covers rhe underling
FIGURE 2-21. Growth factors that control or influence maturation and bone for osreoclasts to bind 007,108). Osteoclasts are bone-
proliferation are shown. See the text for specific actions. degrading cells rhat are produced from rhe hematopoietic path-
way. On activation, they bind to rhe surface of the bone and
secrete enzymes into the space beneath. The space is acidic and
conrains many proteolytic and bone degrading enzymes (98).
process (183). Metaphyseal vascular invasion occurs at the hy- The acidic pH and proteases are thought to release and acrivare
perrrophic-metaphyseaJ inrerface. The endorheliaJ cells mosr rhe sequestered TGF-,B, resulring tn rhe differentiarion and acti-
likely invade as a consequence of angiogenic facrors presenr in vation of rhe bone-lining cells ro os reo blasts and OntO osteocyres
the marrix or secrered by the chondrocytes rhemselves. Both (41,42,101). The osreoblasts rhen lay down new osteoid, and
TGF-,B and FCh are known to be angiogenic. It is interesting subsequent mineralization results in bone. AJd10ugh ir is usually
that an oversupply of FGF-2 infused inro the physis induces accepred rhat rhe osteoblast activiry and osteoclast acrivit)' are
vascular invasion from rhe metaphysis only; even if the FGF-2 linked, discussion srill exists about the signals that derermine
is presenr at the epiphyseal side of the physis, rhe epiphyseal rhe equilibrium thar is required ro keep the bone densiry ar
vessel will not invade (4). Although it is often stated thar rhe functional levels. The osreocytes may be rhe mechanosensory
metaphyseal vessels provide the necessary nutrients for the min- sysrem. Osreocytes also possess cellular processes thar connecr
eralizarion process, it is possible that they provide additional osteocytes to one another and to rhe bone-lining cells above (32)
growth facrors that initiate the mineralizarion process. (Fig. 2-22). It is possible thar the osreocytes are responsible for
The vascular supply also brings osteoblasts, osreoclasts, and sensing bone srress; if undue stress is derected, they favor bone
orher cell rypes. The osteoclasts degrade the mi neraJized carrilage deposirion, whereas if a lack of srress is derected, they favor bone
marrix while osreoblasts lay down new bone that is also rich in resOrptIon.
growth facrors such as TGF-,B, FGf-2 and the BMPs.

FRACTURE R PAIR
Membranous Ossification
All axial and appendicular skdetal e1emenrs are involved in sec- Injuries ro rhe developing skeleton may involve osseous, fibrous,
ondary membranous ossification. The diaphyseal correx of devel- and carrilaginous tissues. Healing of rhese tissues differs, depend-
oping tubular bone is progressively formed (modeled) by the ing on both the rype of rissue and rhe remporal marurarion.
periosteum and modified (remodeled) by rhe re-formation of
osteons. This peripheral periosteal process of membrane-derived
ossification is extensive and rapid in fracture healing in infants
Osseous Healing
and young children. The replacement process also may be seen The progressive changes of the normal process of osseous fracture
when portions of the developing metaphysis or diaphysis are healing, wherher in rhe diaphysis, metaphysis, or epiphyseal ossi-
removed for use as bone grafts. ficarion cellter, may be grouped convenienrly inro a series of
38 G'eII<"rfz! Principles

Pre-osteoclast

Bone erosion releases sequested

growth factors such as TGF - fJ
that stimulate osteoblast
differentiation and proliferation.
Bone lining cells degrade
the osteoid covering the Osteobfasts lay down new
bone, and in doing so osteoid that willfater
expose sites for mineralize.
osteoclasts to bind.
Osteoclast

Osteocytes may act as meclJanosensory

devices that determine stress levels
within the bone. Bone is remodeled to
form a structure that reflects its stress load.
-+----- Osteocytes'

FIGURE 2-22. Osteoclasts and osteoblasts constantly remodel bone. Osteocytes exist within the bone.
Bone-lining cells need to erode the osteoid that covers the underling bone for osteoclasts to bind.
Osteoclasts bind to the surface of the bone and secrete enzymes into the space beneath. The acidic pH
and proteases are thought to release and activate the sequestered TGF-,B that results in the differentia-
tion and activation of the pre-osteoblasts to osteoblasts. The osteoblasts then lay down new osteoid,
and subsequent mineralization results in bone.

phases that occur in a reasonably chronologic sequence (104, and fixed in close proximity. Secondary osreonal union occurs
152,154). Several facrars that influence bone healing can be if cortical bone is laid down berween two segments of fracrured
idenritied from clinical observation as well as experimenral work, cortical bone before callus formarion. NonosreonaJ union occurs
and these facrors must be raken inro accounr when rrearing child- through endosteal and periosteal callus formation (58).
hood fracrures on a rational basis, Many experimenrs have been Fracture repair in rhe immature skeJeran can be divided inra
performed on animals, alrhough because of differences in macro- three closely inrcgrated, but sequenrial, phases: the inflammaralY
scopic and microscopic bone strucrure and skeletal homeosraric phase, the reparative phase, and the remodeling phase (Fig. 2-
mechanisms, they may respond differently rhan skeletally imma- 23). In children, the remodeling phase is temporally much more
rure humans (137,148,168,171,175,185,196). Funhermore, extensive and physiologically more active (depending on rhe
mosr experimenrs have been performed on skeletally marure ani- child's age) than the comparable phase in adulrs. The remodeling
mals, and such data are not always relevanr ra fracrure healing plusc is furrher modified by the effects of the physis responding
in the developing skeleran. In addition, certain areas of rhe devel-
to changing joint reaction forces and biologic stresses to alrer
oping skeleran, particularly the physis and epiphyseal hyaline
angular growth dynamics. This occurs even when the fracrure
cartilage, probably do nor heal by classic callus formation. In
is mid-diaphyseal.
fact, when rhis rype of osseous (callus) repair occurs in rhese
cartilaginous regions, significanr growth deformiries may resulr
owing ra formarion of an osseous bridge berween the secondary
ossificarion center and rhe metaphysis (see Chaprer 5). Cellular Response to Trauma
As in adults, rhere are rhree basic mechanisms of fracrure Inflammatory Phase
repair: primary osteonal, secondary osreonal and nonosreonal.
PrimalY osreonal fracture he,tling occurs when cortical bone is Immediarely after a fracture through any of the osseous portions
laid down wirhour any intermediate, and therefore hardly any of rhe developing skeleron (diaphysis, metaphysis, or epiphyseal
callus forms; ir is only possible if cortical bone is repositioned ossification cenrer), several cellular processes begin.
 Chapter 2: The BioLogic Aspects of Children J' Pram/res 39

Non-Osteoneal Healing Process

Monocytes • Mesenchymal cells

Macrophages
PD ECGF ---~)- Neovascularization

~
. TGF-~etc..
Recruitment
(

. '. .~
. '
";" ~.,
~
.~'
~ , ~'
. \~Platelets
Removal of necrosed tISsue Coagulation ~ .. Hemorrhage
and synthesIs of a matrix 'C: ,
permissive for chondrogenesis - : : : : -
and osteoblast mediated
bone formation.
-=:.
"'.--:::::-'~
Cell necrosIs
.~ ~'" -
-===-
A

Recruitment
Mesenchymal cells
Mesenchymal cells " " ' - -

(
t
Fibroblast Osteoblast
• ,.~?; ~ .,~ ~..... t.;:,-~,.; r$~) _, ;" ~~

... <:!~ ._. ~. ,) .L)I ,~. /~"'~~l ~

Collagen I and III
t -'j

1
Chondrogenesis

t
Endochondral Intramembranous
ossification ossification

c
FIGURE 2-23. The figure demonstrates the three phases of fracture repair (A) inflammatory phase, (B)
reparative phase, and (e) remodeling phase. The inflammatory cells remove the debris from the fracture
site and, together with the fibroblastic cells, develop the site into a matrix that will support the cells
that enable new bone to be formed. The mesenchymal cells are recruited by the release of growth
factors in the fracture site. The mesenchymal cells may differentiate into osteoblasts that produce bone
in a membranous fashion. Alternately the mesenchymal cell may become chondrogenic and produce
bone by the endochondral pathway. Remodeling begins with resorption of mechanically unnecessary,
inefficient portions of the callus and the subsequent orientation of trabecular bone along the lines of
stress.
40 General Principles

Hematoma Formation mation of the woven bone of the provisional (primary) callus.
Bleeding of the damaged periosteum, contiguous bone, and soft Initial invasion and cell division are around the damaged bone
tissues stans the process of repair through the release of growth ends but proceed centrifugally away from the fracture site, thus
factors, cytokines, and posteoglandins. If the fracture is localized placing the most mature repair process closest to the fracture
to the maturing diaphysis, there is bleeding from the haversian site. However, bone formation occurs only in the presence of
systems, as well as from the multiple small blood vessels of the an intact, functional microvascular supply. If the vascular supply
microcirculatory systems of the endosteal and periosteal surfaces is deficient, then this modulation of cartilaginous to osseous
and contiguous soft tissue anastomoses (56). In the region of tissue cannot readily occur.
the metaphysis, this bleeding may be extensive because of the
anastomotic ramifications of the peripheral and centtal metaphy-
Reparative Phase
seal vascular systems. A hematoma accumulates within the med-
ullary canal at the fracture site, beneath the elevated periosteum. Cellular Organisation
and extraperiosteally whenever the periosteum is disrupted dur- The fracture hematoma is the area in which the early stages
ing the fracture. In contrast to adults, the periosteum strips away of healing occur (145). Osteogenic cells proliferate from the
easily from the underlying bone in children, allowing the fracture periosteum to form an external callus and, to a lesser extem,
hematoma to dissect along the diaphysis and metaphysis; this is from the endosteum to form an internal callus. However, when
evident in the subsequent amount of new bone formation along the periosteum is severely disrupted, healing cells must differen-
the shaft. tiate from the ingrowth of undifferentiated mesenchymal cells
However, the dense attachments of the periosteum into the throughout the hematoma. By 10 to 14 days in a child, the
zone of Ranvier limit subperiosteal hematoma formation to the fracture callus consists of a thick, enveloping mass of peripheral
metaphysis and diaphysis. Because the perichondrium is densely osteogenic tissue that is beginning to be evident radiographically.
attached, this type of hemorrhagic response is uncharacteristic This new bone is primarily woven (fiber) bone (l 0 1,114,150,
of the epiphyseal ossification center, thus limiting its contribu- 151).
tions to callus formation and any inttinsic stabilization effect. The next step in osseous fracture healing is cellular organiza-
Further, because of the partially or completely intracapsular na- tion (33). Duting this stage, the circumferential tissues serve
ture of some epiphyses, propagation of a fracture into the joint primarily as a fibrous scaffold ovet which cells migrate and orient
allows decompression of some of rhe bleeding into the joinr, to induce a stable tepair. This pluripotential mesenchyme is
again limiring rhe porential volume for eventual callus forma- theoretically capable of modulation into cartilage, bone, or fi-
tion. brous tissue (54,57,135). The mesenchymal cells are tecruited
Coagulation and plateler activarion stop rhe blood loss but by the release of growth factors in the fracture site. Members of
also produce both inflammatory mediatots and angiogenic fac- the BMP family, and possibly their inhibitors, are likely to be
tors. Endothelial cells respond and increase the vascular perme- involved in the recruitment and differentiation of the mesenchy-
ability, and allow the passage of leukocytes, monocyres, and mal cells. The mesenchymal cells may differentiate into osteo-
macrophages into the fracture site. Neovascularization is also blasts that produce bone in a membranous fashion or may be-
initiated. Angiogenic factors like platelet-derived growth factor come chondrogenic and produce bone by the endochondral
(PDGF) and TGF-p, also promote osteoblast recruitment and pathway. Both mechanisms usually are present in a fracture cal-
activation. lus, and the degree to which each is ptesent depends on the type
of bone, age, degree of fixation, level of bone loss, and ttauma.
Local Necrosis In children, because of the osteoblastic activity, the periosteum
The blood supply is temporarily disrupted for a few millimeters contributes significantly to new bone formation by accentuating
on either side of the fracture, creating juxtaposed, avascular tra- the normal process of membtanous ossification to supplement
becular and cortical bone (55) and producing local necrosis. It the cellular otganization within the hematoma, which is going
is likely that the necrosis also results in the release of sequestered through a cartilaginous phase (58,59). The region around the
growth factors (e.g., IGF-l, TGF-I3, FGF-l, and FGF-2) from fracture site thus repeats the process of endochondral ossifica-
the bone. These growth factors may help in promoting differen- tion, in close juxtaposition to membranous ossification from the
tiation of the surrounding mesenchymal cells into bone-forming elevated periosteum. Similar processes occur within the medul-
cells. lary cavity. An integral part of the reparative process at this stage
The inflammatory cells remove the debris from the fracture is microvascular invasion, which occurs very readily in children
site and, with the fibroblastic cells, develop the site into a matrix because of the state of vascularity within and without the bone
that will support the cells that enable new bone to be formed. and surrounding soft tissues (26) . Vessels come from the petios-
This initial matrix often contains collagens rype I, III, and V. teal region as well as from the nutrient artery and endosteal
vessels.
Organization of Hematoma Until this bone goes through the final stages of maturation,
The initial cellular repair process involves organization of the it is still biologically plastic and, if not protected, may gradually
fracture hematoma (39,55,62,69). Fibrovascular tissue replaces deform, especially in an active young child after early release
the clot with a matrix rich in collagens 1, III, and V. This matrix from an immobilization device. Even in a cast, this plasticity
allows chondrogenesis or imramembranous bone formation. may allow deformation from isometric muscle activity.
Such mechanisms eventually lead to mineralization and the for- Clinical union is attained when the fracture sire no longer
 Chapter 2: The Biologic Aspects 0/ Chiidren J' Fmetures 41

moves and is noc painful co anempts at manipulation, although tem that must be replaced. This is a much longer sequence of
it is by no means tescored co its original strength at this time. events and is not a major method of bone repair in children,
With time, the primary caUus is gradually replaced. This is en- except when the fracture involves densely cortical regions such
hanced in the child because appositional growth and increasing as the femora.! or tibial shafts. McKibbin (104) presented an
diameter envelop rhe original fracture region, the canilage and extensive discussion of this process, which is sometimes refetred
woven bone have been replaced by mature, lamellar bone, and to as primary bone union because no imermediate cells are in-
the fracrure has consolidated and essencially returned co most volved.
of its normal biologic standards and response co stress.

Physeal Healing Patterns

Remodeling Phase
The physis has a limited ability to repair; it primarily heals by
The last phase (remodeling) begins with resorption of mechani- increased endochondral bone and cartilage formation, and grad-
cally unnecessary, inefficient portions of the callus and the subse- ual reinvasion by the disrupted metaphyseal vessels to replace the
quent orientation of trabecular bone along the lines of stress. temporarily widened physis eventua.!ly. Very little experimental
The remodeling phase is the longest of the three phases and in work, mostly in rats, has been directed at assessing the posrrrau-
children may continue uncil (and beyond) skeletal maruration matic cellular response patterns of the physis (17).
in response co constantly changing stress patterns imposed by Depending on the level of cellular injury within the physis,
concillued skeletal growth and development. Initially, new bone three types ofchandro-osseous heaLing may occur. First, when the
is laid down by both the fracture callus and the more extensive fracture occurs through the cell columns, hea.!ing occurs primar-
but confluent subperiosteal tissue. This bone is randomly ori- ily by continued, relarively rapid increases in the number of cells
ented and cannot withstand all biologic stresses imposed on it. within the columns, causing moderate widening of the physis.
However, as the bone grows diamerrica.lly in the diaphyseal or Because there are some small epiphyseal vessels in this region,
metaphyseal regions, this new bone is gradually and increasingly some damaged rissue may be resorbed early in the healing pro-
incorporated into the preexisting cortica.! bone, aJigned in accord cess. These vessels also exhibit a hyperemic response, increasing
with predominant stress patterns, and replaced by physiologic ceJlular proliferation rates, especially in the peripheral zone of
remodeling processes. The degree of remodeling and progressive Ranvier. The metaphyseal response parallels this, in that an in-
replacement of fracture callus is greater in younger children, who creased rare of bone replacement of the hypertrophic chondro-
have an immense capacity for growth and change. cyte also occurs. Once the level of fracture fibrosis and debris
The criticaJ step berween the reparative and remodeling within the physis is encountered, the vessels rapidly invade to
phases is the establishment of an intact bony bridge berween reach the rest of the maturing cell columns. These cellular re-
the fragments. Because this involves the joining of separated sponse parrerns lead to restoration of normal anatomy within 3
segments of hard tissue, the whole system must become immo- to 4 weeks (153).
bile. Once the bridge has been established-provided that ade- Second, when the fracture occurs through the transition of
quate, continued mechanicaJ protection is given-subsequent hypertrophic cells to primalY spongiosa (the mosr commonly
biologic failure is unlikely. If the two or more fracture fragments involved cellular level), there may be marked separation, with
remain connected by the periosteum or related material, as is the gap filled by hemorrhagic and fibroblastic tissue. This region
likely in a child, it is easy co see how reparative activity could may progressively form disorganized cartilaginous tissue, nor un-
be conducted from one side to the other relatively easily and like the initial, disorganized cartilaginous callus around a diaphy-
rapidly. seal fracture. Meanwhile, cellular proliferation, cell column for-
The intact bone must then readapt co functional demands. mation, hypertrophy, and calcification continue on the
This is much easier in children, whose skelecons are actively and epiphyseal side of the disorganized callus, leading to widening of
continually remodeling in response to stress, than in adults, who the physis. A vascular invasion of the remnants of hypertrophic,
have more static skelecons. The processes of replacement and calcified cartilage also rapidly occurs on the metaphyseal side of
repair are continuous and concomitant in the normally develop- the fracture. However, once metaphyseaJ vessel invasion reaches
ing skeletOn. The mechanisms involved in fracture healing essen- the disorganized carrilaginous callus, vascular-mediated bone re-
tially are no different than most of the active maturational pro- placement is temporarily slowed, because there is no pattern of
cesses. These processes are much more acrive in children and cell columns to invade in an organized fashion. As the callus
are more active in the metaphysis than in the diaphysis. cartilage matures and calcifies, the metaphyseal vessels begin to
The fracture remodeling process differs in cortical or cancel- invade and replace the cartilage wirh bone irregularly (21). This
lous bone. Both involve a process of simultaneous bone remova.! caJIus may be variably thick, depending on the degree oflongitu-
and replacement by the osteoclasts and osteoblasts through the dina.! and lateraJ displacement and periostea.! continuity with the
accompanying blood vessels. In cancellous bone of the metaphy- physeal periphery. The caJius is replaced at different rates, and
sis or the endosteal surface of the diaphysis, the cells are never the invading metaphyseaJ vessels reach the norma.! cell columns,
very far away from blood vessels, and the whole process of appo- which have been maturing in a normal sequence but without
sirion and replacement may occur on rhe surface of the trabecu- osseous replacement. This widened physis is rapidly invaded by
lae. However, in compact bone, the more deeply placed cells the vessels and replaced by primary spongiosa, and normal phy-
require the presence of an adequately funcrioning perfusion sys- sea.! width is progressively restored.
42 ("eneral Principles

The callus in the subperiosteal region contributes [0 early taphyseal bone, and thereby enhances the risk of forming an
stabiliry. This region heals by vascular invasion of the callus [0 osseous bridge between the two regions.
form trabecular bone between the original metaphyseal cortex
and the subperiosteal membranous bone forming cominuously
external [0 the metaphyseal cartilaginous callus. These three mi- Remodeling of Bones in Children After
croscopic bone regions progressively merge and remodel, making Injury
the region srrong biomechanically. With further growth and In a growing child, the normal process of bone remodeling in
remodeling, this coalescem bone is completely replaced. These the diaphysis and metaphysis (particularly the latter) may realign
initial cellular replacemem processes in both metaphyseal and initially malunited fragments, making absolutely accurate ana-
physeal regions probably take 3 [0 6 weeks. However, remodel- tomic reduction less imporram than in a comparable injury in
ing may cominue for months to years, and it enhances the capac- an adult. However, although some residual angular deformities
ity for spontaneous correction of many residual deformities. undergo spontaneous correction, accurate anatOmic reduction
Third, when the injury extends across all cell layers of the should be the goal whenever possible (51,122,129). Bone and
physis, the repair processes differ slightly. Fibrous tissue initially cartilage generally remodel in response to normal stresses of body
fills the gap between separated physeal components, whereas weight, muscle action, and joint reaction forces, as well as inuin-
rypical callus formation occurs in the contiguous metaphyseal sic control mechanisms such as the periosteum, The potemial
spongiosa or epiphyseal ossification cemer. If large surfaces of for spontaneous, complete correction is grearer if the child is
nonossified epiphyseal cartilage also are involved, fibrous tissue younger, the fracture site is closer to the physis, and there is
initially forms in the intervening region. The reparative response relativc alignmem of the angulation in the normal plane of mo-
shows irregular healing of the epiphyseal and physeal cartilage, tion of the joint. This is particularly evident in fractures involv-
with loss of normal cellular architecture. Within the central phy- ing hinge joims such as the knee, ankJe, elbow, or wrist, in which
seal regions, diametric expansion of cell columns is minimal, so corrections are relatively rapid if the angulation is in the normal
closure of a large defect by physeal cartilage is unlikely. The gap plane of motion. However, spomaneous correction of angular
will remain fibrous, but with the potemial to ossify. Toward the deformities is unlikely in other directions (relative [0 normal
physeal periphery, diametric expansion is more likely, but still joint motion), such as a cubirus varus deformiry following a
may not lead to closure of large cartilage gaps by progressive supracondylar fracture of the humerus. Similarly, rotational de-
replacemem of fibrous tissue. This replacement process essen- ftrmities usual0' do not correct spontaneously.
tially requires the germinal and hypertrophic cell regions [0 dia-
metrically expand by cell division, maturation, and matrix ex-
pansion. The imervening fibrous tissue may disappear through
Growth Stimulation
growth, but only if the gap is narrow. Because blood supply is Fracrures may stimulate longitudinal growth by increasing the
minimal in this region, the fibrous tissue similarly is not well blood supply to the metaphysis, physis, and epiphysis, and at
vascularized, and significam cell modulation, especially [0 osteo- least on an experimemal basis, by disrupting the periosteum and
blastic tissue, is less likely in the short term. However, the larger its physiologic restraint on the rates of longirudinal growth of
the gap filled with fibrous tissue and the longer the time from the physes (34). Such increased growth may make the bone
fracture [0 ske!'etal maturiry, the greater the likelihood of devel- longer than it would have been without an injury (9,36,184).
oping sufficient vasculariry to commence an osteoblastic re- Eccclltl'ic overgrowth may also occur; this is particularly evident
sponse and to form an osseous bridge. Further, in young children in tibia valgum following an incomplete fracture of the proximal
with minimal epiphyseal ossification, the blood supply [0 the tibial metaphysis.
physeal germinal region is nO( as well defined, whereas once the
ossification center expands and forms a subchondral plate over
the germinal region, microvasculariry probably increases and the THE FUTURE OF FRACTURE REPAIR
chances for vascularization and ossification of the fibrous region
increase. This explains the delayed appearance of the osseous Bone grafts contain bone growth factors rhat normally induce
bridge. bone formarion and have the appropriare osteoconducrive ma-
If accurate anatOmic reduction is performed, a thin gap trix. Autogenic grafts also contain osreogenic cells. Bone grafts
should be present rhat should fill in with minimal fibrous tissue, are effecrive, but there are difficulties in obtaining safe and relia-
allowing progressive replacement of the tissue by diametric ex- ble tissue. Although rhe mechanisms of fracrure repair are nor
pansion of the physis and comiguous epiphysis. However, if the fully understood, the level of understanding has enabled key
fragment has been partially or completely devascularized by molecules to be targeted as therapeutic in controlling and pro-
either the initial trauma or subsequem dissection [0 effect an moring fracrure repair. Filler compounds have been developed
open reduction, cellular growth and diametric and longitudinal that either stimulate mesenchymal cells, leading to new bone
expansion may not occur. This increases the chances of cellular formation (osrcoinductive) or enable the bone-forming cells to
disorganization, fibrosis, and evemual osteoblastic response. infilrrate and incorporare ,into bone (osteoconductive).
Failure to correct anatOmic displacement, especially in Salter- Specific growth Factors have been targered for their abiliry
Harris rype 4 growth mechanism injuries, increases the possibil- to promote bone formation. Two growth factors (BMP-2 and
iry of apposition of the epiphyseal ossification center and me- Ostegenic Prorein-1) (BMP-7) show grear promise for their abil-
 C/.Iapln 2.' The BioLogic Aspects vI Children J' Fraflures 43

iry to promote fraceure repair (83,84,90,96,173,192). A number 9. Bisgard JD. Longirudinal overgrowrh of long bones wirh special refer-
ences ro fracrures. Sttrg G)'Ileco! Obsta 1936;62;823-835.
of others, such as TGF-,B, IGF, PDGFs, and FGF-2, also may
10. Bohlen P, Baird A, Esch F, et al. Isolarion and partial molecular
prove to be useful. characteriurion of piruitary fibroblast growth facror. Proc Nat! Acad
TGF-,B plays a major role in fracture repair by promoting Sci USA 1984;81:5364-5368.
proliferation and differentiation of the mesenchymal cells. Exog- 11. Bolander ME, Young MF, Fisher LW, er al. Osteonectin cDNA se-
enous TGF-,B administration can initiate the repair process and quence reveals porenrial binding regions for calcium and hydroxyapa.
rire and shows homologies wirh borh a basemenr membrane prorein
callus formation in uninjured bone (75). The addition ofTGF-
(SPARC) and a serine proreinase inhibitor (ovomucoid). hoc Nat!
,B to fractures promotes wound repair and results in a larget, Acad Sci USA 1998;85;2919-2923.
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in non healing bone defects. PDGF also increases callus size but insulin-like growrh facror-! in rhe regulation of growth plare chondro-
does not improve the fracture mechanically (l15). Growth hor- cyres. Exp Cell Res 1997;234;1-6.
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on fracture repair. Although growth hormone produces inconsis- mental kidney disease. Nature 1992;360;361-364.
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many reviews on the use of growth factors for fracture repair growth facror-beta is produced by chondrocytes and acrivated by ex-
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 PAIN RELIEF AND RELATED
CONCERNS IN CHILDREN'S
FRACTURES
JOSEPH R. FURMAN

Gum 1 ES AND PRI CIPLES OF S DATIO Barbiturates

CHlLDRE Propofol
Definitions REGIONAL ANESTHESIA IN THE CHILD WlTH A
Monitoring MUSCULOSKELETAL INJURY
Parienr Assessment Regional Anesthetic Agent
Oral Intake Precaurions Local Anestheric Toxicity
Hemodynamic Status Intravenous Regional Anesthesia
Coexisting Nonmusculoskeletal Injuries Local Infilrration Anesthesia: HematOma Block
Status of rhe Airway Femoral Nerve Block
Treatment Facility
POSTOPERATIVE A ALGE IA I THE CHILD
SEDATIVE MEDICATIONS WITH A MUSCU OSKEL TAL INJURY
Nirrous Oxide Posroperative Analgesia With Opioids
Ketamine Posroperative Analgesia Wirh Nonsteroidal Antiinflammarory
Benzodiazepi nes Drugs
Opioids Postoperative Analgesia With Local Anesrhetic Agents
Chloral Hydrare TREATMENT OF POSTOPERATIVE AU$EA

Providing pain relief is one of rhe many imporrant pans of rhe of postoperative nausea. The author hopes that the orthopaedic
management of children's fractures. In addition, because having practitioner will find this chapter of significant benefit, not only
a fracture reduced is nor only painful but also frightening to in the emergency room setting bur also in the office and on the
many children, providing young parients with adequate sedation hospital ward.
and amnesia are additional welcome elements of good care.
However, rhe correct use of any of the available medicarions for
obraining these goals muSt involve an appropriate undemanding GUIDELINES A D PRINCIPLES OF
of proper dose, desired effects, and untowaJd side effects. The SEDATION IN CHILDREN
purpose of this chapter is to provide a thorough source of infor-
mation regarding safe and effective analgesia and sedation for Definitions
children with fractUres. This chapter discusses the concept of
The practitioner must recognize that sedation describes a contin-
sedation and its definitions, the various medications used to
uum ranging from neal" wal<efulness to complete loss of con-
achieve the sedation state, and the various medications used to
sciousness (Fig. 3-1). Terms used to describe various stages along
achieve analgesia, including both systemic medications and local
this continuum have included conscious sedation, deep sedation,
anesthetics. Intravenous regional anesthesia (Bier Blocks), hema-
and general anesthesia (63).
toma blocks, and femoral nerve blocks (for femur fractures) are
Sttictly speaking, the term conscious sedation means a phar-
discussed in depth. The management of postoperative pain is
macologically controlled altered state of consciousness in which
discussed, along with the treatment of the troublesome side effect
patients maintain their ability to respond purposefully to verbal
commands. For nonverbal patients or young infants, conscious
sedation implies the ability to respond purposefully to physical
stimulation, not simply by reflex withdrawal to pain. U nfortLI-
Joseph R. Furman: Stat Anesthesia, San Antonio, Texas. nately, most physician and nursing personnel tend to use the
50 General flriJlicipies

Protective reflexes maintained : Loss of reflexes TABLE 3·1. RECOMMENDED DISCHARGE

Patent airway _ 1 ____ Unable to maintain airway CRITERIA AFTER SEDATION
Responds appropriately : Impaired response
I 1. Cardiovascular function and airway patency are satisfactory
I
1 and stable.
Conscious I
I
2. The patient is easily arousable, and protective reflexes are
sedation I intact.
Awake or 3. The patient can talk (if age appropriate).
"sedation 4. The patient can sit up unaided (if age appropriate).
analgesia" 5. For a very young or handicapped child incapable of the usu-
ally expected responses, the presedation level of responsive-
ness or a level as close as possible to the normal level for that
child should be achieved.
6. The state of hydration is adequate. *
FIGURE 3-1. Sedation and analgesia for procedures is a continuum.
(Reproduced with permission from American Society of Anesthesiolo- * Adequate hydration may be achieved with intravenous fluids.
gists from ASA 1997 Annual Refresher Course lectures. Sedation and There is no specific requirement that children be ablEi to tolerate
Analgesia in Pediatric Patients for Procedures Outside the Operating oral fluids before discharge from a treatment facility. Children
Room. Richard F. Kaplan, M.D. No. 221) who are nauseated, or actively vomiting should be treated and
observed until this problem resolves (see sect'ion on treatment of
postoperative nausea).
Guidelines for monitoring and management of pediatric patients
during and after sedation for diagnostic and therapeutic
term "conscious sedation" w mean anything shon of a general procedures. Pediatrics 1992;89:1110-1115, with permission.
anesthetic. For such reasons, the consensus of the 1996 report
by rhe American Society of Anesrhesiologists Task Force on
Sedarion and Analgesia by Non-Anesthesiologim (l08) is that
the term conscious sedarion, alrhough in common usage, is im-
precise. This reporr recommends replacing the term conscious
sedation wirh the more descriprive rerm sedarion/analgesia (Fig. of qualified personnel who are competenr in rhe use of moniror-
3-1). Whatever rhe preferred term, the important point w recog- ing devices, and capable of recognizing the clinical signs of airway
nize is that the safesr level of sedation is rhat which permits or hemodynamic instability. AJthough skill in ar least pediauic
purposeful response ro verbal or physical stimulation. Ir is at basic life support is necessary (63,119), training in pediatric
rhis level of sedarion rhat the risk of hypovenrilarion, apnea, or advanced life support (PALS) is cerrainly desirable. In the au-
cardiovascular instability is minimal. Unforrunarely, and realisri- thor's opinion, rhis training should be considered absolurely nec-
cally speaking, such relarively lighr levels of sedation are wtally essary. The orrhopaedic surgeon must always demand, and have
inadequare for the performance of a painful procedure such as available, skilled health professionals, either physicians or nurses,
rhe reducrion of a fracrure. AJso the younger and less cooperarive co assisr in obsenTing the parient and rhe monitors during proce-
the parient, rhe less likely thar so-called conscious sedation can dures requiring medications rhar arc known ro depress respira-
realistically be achieved ar aJI (92). Therefore, it is very likely wry or cardiovascular funcrion. Having one person performing
thar for orrhopaedic procedures, chiJdren may have w be sedated borh the surgical procedure and moniroring the patient is a
w levels at which they are nor easily responsive w verbal stimula- practice rhar should be strongly discouraged in all bur the mosr
tion, and as such, at increased risk for respirarolY and cardiovas- desperare circumstances.
cular compromise. Even in children in whom lighr levels of Oxygenarion, venrilarion, and circularion are the three pa-
sedarion ([[ue conscious sedation) is possible, uninrended overse- rameters rhat require careful assessment. For the most parr, mon-
darion may occur wirhour warning. Oversedation may lead w iroring remperarure is usually of minimal imporrance. The major
(a) loss of rhe airway, (b) impaired protective reflexes leading w exceptions, of course, are children who arrive in the hospiral
the possibility of aspirarion of gasrric conrents, and (c) cardiopul- either severely hyporhermic or febrile.
monary arresr (Fig. 3-1). Ir is for rhese reasons thar careful moni- Moniroring oxygenation requires conrinuous pulse oxime[Jy
roring of sedared parjents as prescribed in standard guidelines and conrinual visual inspection of the patient. Nore rhar the
(l08) is absolutely imperarive. term continuous moniroring refers ro a constanr measuremenr
undertaken for a period of time wirhout interruprion. Conrinual
moniroring refers w an assessment taken at frequent regular
Monitoring intervals.
Obviously, rhe purpose for moniwring sedated patients is w The value of pulse oximetry as an early detecror of impeding
provide timely derecrion and correction of abnormaliries in re- hypoxemia has been well demonstrated (34). The problem with
spiratory and cardiovascular function. The monitoring process relying on visual inspection alone w derermine adequacy of oxy-
begins before the administration of any sedarive medicarions. genation is rhat cyanosis is both a late and variable sign of hypo-
Moniwrjng conrinues unabared ulHil the patient returns ro base- xemia. Demonstrable cyanosis requires rhe presence of ar leasr
line presedation level of consciousness and is ready for discharge. 5 g of desaturared hemoglobin per deciliter. Therefore, for exam-
Acceprable discharge criteria are noted later (Table 3-1). ple, a parient with a hemoglobin level of 10 g/dL would rheoreri-
Of viral importance ro the moniroring process is the presence cally nor even appear cyanotic unril rhe oxygen saturation level
 Chapter 3: Pain ReLiefand ReLated Concerns in Children '5 Fractures 51

(Spoz) plummets to 50%. For this same reason, a severely ane-

TABLE 3-2. NORMAL VALUES FOR HEART RATE
mic patient may never develop visible cyanosis even at profound
BY AGE
levels of hypoxemia. To add to a potentially confusing situation,
the ambient light (especially fluorescent light) in many clinical Range
environments may make any patient appear cyanotic (33). Age (beats/min)
Therefore, pulse oximetry is essential in all heavily sedated pa- Newborn 110-1'50
tients to detect abnormalities of oxygenation rapidly. 1-11 months 80~150
Note, however, that the pulse oximeter is not perfect. Factors 2 yeilrs 85-125
that affect the accuracy of the pulse oximeter include patient 4 75-115
movement (33), direct bright light on the probe (21), and mal- 6 65-110
8 60-110
position of the probe (9). CorreCt probe placement, shielding
the probe site from bright light, and gende restraint of the moni-
toring site should improve the dependability of this aJJ-impor-
Rasch DK, webster DE. Clinical manual of
pediatric anesthesia.
New York: McGraw-Hili, 1994:16, with permission.
tant monitor.
Monitoring ventilation goes hand in hand with monitoring
oxygenation. Monitoring ventilation requires close obsetvation
of the patient and either intermirrent or continuous auscultation
of breath sounds. A sedated ch ild's head may flex forward easily,
producing airway obstruction as the child begins to fall asleep Auscultation with the precordial stethoscope is valuable in the
(33). Maintaining patients in the so-called sniffing position helps monitoring of both ventilation (breath sounds) and circulation
prevent airway obstruction (Fig. 3-2). The sniffing position con- (hean sounds). Its use is encouraged in the monitoring of deeply
sists of elevating the patient's head with pads under the occiput, sedated patients (63).
keeping the shoulders flat on the table, and ex.tending the head Monitoring circulation for most sedated children consists of
at the atlanto-occipital joint (I 34). Children younger than 3 intermirrent determination of heart rate and blood pressure (63).
years of age have a relatively large head in proportion to the size For children, normal values for heart rate and blood pressure
of their trunk and do not require padding under the occiput vary with age (Tables 3-2 and 3-3). A simple formula for calcu-
(35). Along with continual assessment of the child's head posi- lating the normal systolic blood pressure and lower limit of nor-
tion, any restraining devices should be checked and rechecked mal for systolic blood pressure in children by age is worth memo-
to ensure that they are not contributing to either airway obstruc- rizing (Table 3-4). Electrocardiographic (ECG) monitoring is
tion or restriction of chest movement (63). especially important for the child with an underlying histOly of
a significant cardiac dysrythmia or known ECG abnormality
such as long QT syndrome, or history ofWol ff- Parkinson-Whi te
syndrome. In the absence of monitor artifact, the pulse oximeter
provides continuous assessment of heart rate. Deeply sedated
children should have blood pressure and hean rate and respira-

TABLE 3-3. NORMAL VALUES FOR BLOOD

PRESSURE BY AGE

Blood Pressure (mm Hg)

Age SystoliC Diastolic

Full-term infa nt 60 (45)* 35
3-10 day 70-75 (50) 40
6 mo 95(55) 45
4 yr 98 57
6 yr 110 60
8 yr 112 60
12 yr 115 65
16 yr 120 65

* The .numbers in 'parentheses refer to mean arterial blood

pressure.
Steward DJ: Manual of pediatric athesthesia. New York: Churchill:
FIGURE 3-2. The sniffing position. In an adult or in an older child, a Livingstone. 1990:24, and Rasch DK, Webster .DE. Clinical Manual
folded sheet or towel under the occiput, plus moderate head extension of Pediatric Anesthesia. New York: McGraw-Hili, 1994:17, with
at the atlanto-occiptal joint, helps to maintain an open airway. In a permission.
child younger than 3 years of age, the relatively large head size in
proportion to the trunk makes occipital padding unncessary (35).
52 General Priniciples

before elective surgery, and solid food to 8 hours before elective

TABLE 3-4. CALCULATION OF NORMAL BLOOD
surgery (50).
PRESSURE BY AGE
Emergency patienrs are definitely at risk for aspiration (143).
80 + (2 x ilge in years) = normal systolic BP for age Sedatives depress the protecrive reflexes (63). Caution is neces-
70 + (2 x age in years) sary to avoid the morbidity and possible mortality of aspiration
= lower limit of normal, systolic BP for age
pneumol1la.
It is known rhat in trauma parients, the time interval between
Rasch DK" Webster DE. Clinical Manual of Pediatric Anesthesia.
New York: McGraw-Hili; 1994:197, with permission. last oral inrake and time of injury is a cricical factor in the
retention of gastric contents (99). It is clear that children injured
within I to 2 hours after eating presenr with large gastric volumes
(19). Although fasting cal1 reduce an injured child's gastric vol-
ume (95), it is not clear how long of a fast is ideal. Also, in the
presence of pain, anxiety, and wirh the administration of opioid
tory rare rneasurernenrs determined and recorded ar leasr ar 5-
pain relievers, all of which may occur in the patient with a
minure inrervals (63). For children under conscious sedarion
fracrure, gastric emptying may be radically slowed (57). If the
(sedarion/analgesia), the frequency of vital sign determination
procedure can wait, it is safe to say rhat a fasting period is in
is ar rhe diSCI'erion of rhe physician (63).
order. Starting inrravenous fluids to prevent dehydration is im-
Ir is imporranr to emphasize again rhar monitoring rhe pa-
portant. Note that ar present, chere is no reliable method of
tient must conrinue unril rhe patienr meets preset discharge crire-
assessing the volume of gastric conrenrs, alrhough differenr
ria (Table 3-1) (63). Often, when a surgical procedure is over
methods have been suggested (55). Patient hunger on presenta-
and parienrs are no longer being actively stimulated, uninren-
tiona I deep sedation wirh resulring airway obstruction and apnea tion for surgical treatment is noc a good indicator of an empry
may occur. Therefore, ir is essential ro remain vigilanr until sromach (95).
the parienr recovers completely from their sedative medications. In the author's opinion, the safest recommendations regard-
Note thar the time to recovery varies depending on rhe amounr ing sedarion of patients with a pocenrial full stomach are as
and rype of sedative medication given, and rhis poinr should follows:
be r:Jlcen inro account when planning a sedacion regimen. The
1. If possible, postpone the procedure, even for as little as 4
durarion of aerion of particular sedarives and sedative combina-
hours.
tions are discussed separately.
2. Use the lighrest effective level of sedation. Titrate sedacion
to effect, and avoid large bolus doses of medicarions.
Patient Assessment 3. Consider the administrariol1 of medications to reduce gascric
Only afrer careful parienr assessmenr can rhe pracrjrioner decide volume (metoclopramide) or to increase gastric pH (hista-
whether sedarion in an emergency room setting, where rile air- mine-2-recepror blockers). These medications, when indi-
way is unconrrolled and unprorecred, is feasible and safe. Admin- cated, should be administered intravenously I hour before
isrering sedarive medicarions wirhour flrsr evaluaring a parienr sedative medications are given. The appropriate dose of met-
is an invirarion for disasrer. 11' is imporrant first to be aware oclopramide (Reglan) is 0.15 mg/kg. The usual adulr dose
of rhe child's medical hisrory, previous allergic or adverse drug for metoclopramide is 10 mg, which should be more chan
reacrions, currenr medicarions, and presence of coexisring dis- sufficient for any child. Famoridine (Pepcid), a histamine-
eases before proceeding wirh deliberare alreration of a parienr's 2-receptor blocker, may be given in a dose of 0.3 to 0.4 mg/
srare of consciousness (63). In addirion to rhese basic details, kg intravenously, with a maximum dose of 20 mg.
rhe patienr wirh musculoskelcral injuries has ro be evaluared for 4. Within 15 minutes of administering sedation, consider rhe
rime of last oral inrake, hemodynamic srarus, presence of other use of oral nonpaniculace alHacids (Bicitra, sodium citrate)
injuries, and status of the airway. to raise gasrric pH. Unfortunarely, these medications are nor
velY palatable.
Oral Intake Precautions 5. Note that pregnancy, morbid obesity, gastroesophageal re-
In rhe management of elecrive parients, significanr pulmonary flux, bowel obsuucrion, and increased intracranial pressure
aspiration is rare in pediatrics (143). al1 magnifY rhe risk of regurgitation and aspiration of gastric
Note rhar for e1eerive patienrs, multiple studies suppOrt and contents. Therefore, additional caution is necessary in man-
encourage the liberal inrake of clear liquids up unril 2 ro 3 hours aging patiems with any of these conditions. Patients with
before scheduled surgery in othelwise healthy children (32,95, coexisting bowel obsrrucrion should nor be sedated, and pa-
122,129). Acceptable clear liquids are appJe juice, water, sugar tients with increased intracranial pressure should not be se-
water, and gelatin. Milk (including breast milk), milk products, dated without the input and knowledge of the :mending neu-
and juices with pulp are not clear liquids. For elective patients, rosurgical staff.
most pediatric al1esthesiologisrs now adhere to the so-called 2- 6. If treatment cannot wait and the surgical procedure or the
4-6-8 rule regarding oral inrake. This rule restricts clear fluids patient is not amenable to regional ancsrhesia, the safest ap-
to 2 hours before elective surgery, breast milk to 4 hours before proach is a general anesthetic with a rapid sequence induction
elective surgery, baby formula (cow's milk formula) to 6 hours and a protected airway (endorrache:d ruhe). This approach
 Chapter 3: Pain Reliefand Relaied Concerns in Children's Fractures 53

is also safest for uncooperative children who urgently need

TABLE 3·5. AIRWAY MANAGEMENT
a computed tomography (Cf) scan, an magnetic resonance EQUIPMENT
imaging (MRI) scan, or other detailed diagnostic studies.
Ventilation Face Masks*
Infant, child, small adult, medium adult, large adult
Hemodynamic Status Breathing bag and valve set
Oral airways
The magnitude of blood loss from a child's injuries is not always Infant, child, small adult, medium adult, large adult
readily apparent. In children, long bone fractures and head inju- Nasa I airvyays
ries may easily have associated large concealed hemorrhages (140, Small, medium, large
153). It is important to assess the patient's volume status accu- Laryngoscope handles
Laryngoscope blades
rately before administering sedative medications. In a hypovo- "Straight (Miller) No.1, 2, 3
lemic child, sedatives may interfere with catecholamine- Curved (Macintosh) No.1, 2, 3
mediated compensatory mechanisms and produce profound he- Endotracheal tubes
modynamic instabiliry, leading to cardiovascular collapse. 2.5-,-6.0 uncuffed
6.0-8.0.cuffed
Note that in an injured child, blood pressure monitoring
Appropriate-sized styletsfor endotracheal tubes
alone does not provide a good indication of the patient's under- (must be lubricatecf before insertion)
lying volume status (105,155). Children maintain a normal Appropriate-sized suction catheters for endotracheal tubes
blood pressute for their age in the face of large intravascular Yankauer-type suction
volume deficits (155). More reliable signs of ongoing hypovo- Nasogastric tubes
(10-18 French)
lemia in children include sinus tachycardia, mottling, cool ex-
Nebulizer set-up for treatment of bronchospasm
tremities, poor urine output (less than 1 to 2 mLlkg/h), and
altered state of consciousness. Each of these signs can imply
* The correct-sized ventilation face mask will fit over the child's
poor perfusion of different organ systems [skin, musculoskeletal face from the br.idge of.-the nose to the c1eft.of the chin. This
system, kidneys, and central nervous system (CNS), respec- guideline' is also correct when using patient-administered nitrous
oxide analgesia. .
tively). Volume replacement, not sedation, should be the initial . Guidelines for monitoring and management of pediatric patients
goal in the management of hypovolemic children. during and after sedation for diagnostic and therapeutic
procedures. Pediatrics, 1992;89: i 110-1115, with permission.

Coexisting Nonmusculoske1etal Injuries

Serious head injury accounts for 70% of pediatric trauma deaths
(30,105). Respiratory deptession from sedation, with resultant
hypercapnia and hypoxia, may aggravate an underlying closed
head injury and worsen its prognosis (153). In addition, any
pharmacologic change in the parient's state of consciousness may
confuse the neurologic evaluation. Other injuries to major body
cavities or injuries associated with major blood loss should be
assessed carefully before any sedative medicarions are adminis- TABLE 3-6. VASCULAR ACCESS EQUIPMENT
tered.
Intravenous catheters
(24-16 gauge)*
Status of the Airway Intraosseous bone-marrow needle
Intravenous tubing
A tenuous airway can easily become a completely obstructed Pedi.atric drip (60 dropslmL)
airway in a sedated child. There are common problems in chil- Pediatric burette-type
dren associated with airway obstruction. For example, children Adult drip (10 drips/mL)
Intravenous fluids
with large tonsils and adenoids may have Obstructive sleep apnea Lactated Ringer's
(89). Obstructive sleep apnea, which is associated with a history Normal.s.aline
of loud snoring and daytime sleepiness, may be acutely exacer- Miscellaneous equipment
bated with the administration of sedative medications (36). Tourniquets "
Alcohol wipes
Othet potentially dangerous problems include micrognathia
Arm boards
(shorr jaw), limited abiliry to open the mouth, and limited move-
ment of the neck, either congenital or acquired (12).
* In resuscitation situations, no more tl1an90 sec should be spent
attempting to gain peripheral venous access. If attempts have
been' unsuccessful, then central venous· cannula"tinn, intraosseoUs
Treatment Facility cannulation, or peripheral.venous cutdown should be done
according to the E!.xpertise of available personnel.
What about the medical faciliry where the child is receIving (Guidelines for monitoring and management of pediatric patients
during and after sedation for diagnostic and therape'utic
treatment? On-site resuscitation equipment, including equip- procedures. Pediatrics, 1992;89:1110-1115, with permission.
ment for airway management (Table 3-5) and equipment for
vascular access (Table 3-6) must be available for children of all
54 General Priniciples

ages and sizes (63). In addition, a positive pressure oxygen deliv- Ketamine
ery system capable of delivering at least 90% oxygen for at least
Ketamine, which is structuraJly related to phencyclidine, was
60 minutes must also be readily available (63). A working sucrion
first synrhesized in 1963. Developed to produce the "anesrhetic
appararus (63) must be easily accessible ro handle patient secre-
state (analgesia, amnesia, loss of consciousness and immobility)"
tions, as well as for unexpecred regutgitation and vomiting.
without total CNS depression, it was approved for general clini-
These recommendations are essentiaJ for patient safety and for
cal use in 1970 (31,157).
optimum patient cate.
The commercial prepJration ofketamine is a racemic mi.xture
of twO optical isomers with differing activity (157). Ketamine
is typicaJly administered intravenously or intramuscularly (59,
SEDATIVE MEDICATIONS 136). RectaJ (118), oraJ (64,145), and intr:masaJ adminisrration
(54) have been described in the literature.
Having now considered the preliminary step of patient assess-
Ketamine is metabolized in the liver, primarily by N-methyla-
ment, the practitioner must now decide which sedative or seda-
tion to norketamine. Norketamine has about one third the seda-
tives co use. The ideal sedative should be easy ro administer,
tive and analgesic potency ofketamine. As such, ketamine should
quick in onset, devoid of side effects, and rapid in termination
be administered cautiously or in reduced doses to patients with
of effects. The abundance of refetences in the literarure excolling
impaired hepatic function.
the virrues of differenr sedative drugs and drug combinations is
Intravenous ketamine, I to 2 mg/kg, produces unconscious-
the best indicaror that we do not yet have the ideal sedative.
ness wi th in 30 co 60 seconds (136). PeaJ{ plasma concen rrations
Each of the drugs that is discussed has only some of the properties
occur wirhin 1 minute. Return of consciousness occurs within
of an ideal sedative medication. Also, patients demonstrate great
10 to 15 minures, although complete recovelY may be delayed
variability in response co medications. It is imporrant ro treat
(136). Dose requirements and recovelY rimes from ketamine are
each patienr as an individuaJ and to not expect to be able ro fit
age relared (24,87).
every child wirh a fracrure inro any particular sedation regimen.
Ketamine has been found co have interactions at multiple
For patients who cannot be adequately sedated, the orthopaedic
binding sites, including N-methyl-D-asparrate (NMDA) and
surgeon should consult an anesthesiologist for provision of a
non-NMDA recepcors, nicotinic and muscarinic cholinergic re-
brief, well-conrrolJed general anesthetic.
ceptors and opioid recepcors (83). Agonist actions of ketamine
on opioid receptors play only a minor role in its analgesic effects
Nitrous Oxide (83). Note that naloxone, a narcotic antagonist rhat is further
discussed in rhe section on opioids, does nor reverse the anaJgesic
Self-administered 50% nitrous oxide (50% nitrous oxide and
effect of ketamine (83). The psychotomimetic effects of keta-
50% oxygen) has been found ro be moderately useful in provid-
mine, however, may involve interacrion wirh a specific subclass
ing sedation and analgesia for the reduction of children's frac-
of opioid receptors known as kappa receptors (83). For analgesia,
tures. Evans and co-workers (45) found it to be comparable in
the main sire of action is the NMDA receptor. The reader is
efficacy to intramuscular meperidine (2 mg/kg) and prometha-
referred to other sources for further informarion on this topic
zine (I mg/kg). However, in a different srudy, Hennrikus and
(83).
co-workers noted that 46% of their patienrs experienced signifi-
cant pain with nitrous oxide alone as a sedative and analgesic
for fracture reduction (67). Patients with completely displaced
Central Nervous System Effects of Ketamine
radius and ulna fractures had a statistically higher incidence of
failure to achieve analgesia (67). Willi the addition of a hema- Ketamine produces a state known as dissociative anesthesia. Dis-
toma block (discussed in a subsequent section), Hennrikus and sociative anesthesia refers to a cataleptic state characterized by
his coinvestigators were able co obrajn a 97% incidence of ade- functional and electrophysiologic dissociation between the thaJa-
quate sedation and analgesia (66). This srudy does illustrate the moneocortical and limbic systems (I 57). Patients keep their eyes
important point that where possible, the use of regional anesthe- open and exhibit a slow nystagmic gaze. Corneal and pupillary
sia, in combination with aJmost any sedation regimen is an excel- reflexes remain intact. Generalized hypertonicity may be present.
lent way to enhance pain relief and co minimize the need for Even though ketamine has effects on nicorinic acetylcholine re-
systemic sedative and analgesics. ceptors in skeletal muscle, this effect is of minor significance,
In generaJ, nirrous oxide is a weak sedative and analgesic. It because ketamine increases muscle tone by central mechanisms
does have the advantages of rapid onset, relative ease of utiliza- (83). Patients receiving ketamine may exhibit purposeful move-
tion, and rapid termination of effects (88). Because it diffuses ments bur not necessarily in response ro surgical stimulation
rapidly into enclosed air-filled spaces, its use is conrraindicated in (157).
patients with bowel obstruction or pneumothorax (88). Nitrous Ketamine's anaJgesic effect is inrense and may ourlast its seda-
oxide is aJso contraindicated in patients with aJtered intracraniaJ tive effect (59). In one study of minor surgical procedures with
compliance (88). keramine anesthesia, no additionaJ analgesics were required for
Alrhough nitrous oxide is perhaps a useful part of the sedation 24 hours posroperatively (69). Amnesia persisrs for about one
armamentarium, this aurhor does not believe that the literature hour after apparent recovelY from ketamine (136).
supports the use of nitrous oxide aJone as a reliable sedative and Emergence phenomena are relatively rare in children, al-
anaJgesic for pediatric orthopedic procedures. though young adulrs are especially susceprible to this problem
 Chapter 3: Pain Relief and Related Concerns in Children's Fractures 55

(69). Changes in mood and body image, out-oE-body experi- never be given in an unmonitored setting, such as a patient's
ences, floating sensations and frank delirium are all possible room on a regular hospital ward, or a clinic that does not have
(157). Emergence phenomena result from misinterpretation of appropriate monitoring and resuscitation equipment (see the
auditory and visual stimuli at the neurologic level (157). Al- first parr of this chapter).
though usually terminating within 24 hours (136), prolonged
emergence phenomena lasting as long as 10 to 12 months have
been reported in children (102). An increased incidence of emer- Cardiovascular Effects of Ketamine
gence reactions is seen in patients older than 16 years, female Ketamine stimulates rhe sympathetic nervous system and leads
patients, patients who have received doses of intravenous keta- to the release of endogenous catecholamines. Through such an
mine above 2 mg/kg, and patients with a history of abnormal effect, ketamine produces a dose-dependent increase in heart
personalities (157). There is no evidence that emergence in a rate and blood pressure (144), and therefore, it is useful in the
quiet environmenr decreases the incidence of this problem (157). operating room in patients with mild hypovolemia. As a byprod-
Benzodiazepines (e.g., diazepam and midazolam) are the most uct of its sympathetic stimulation, ketamine produces bronchod-
effective treatment for ketamine-induced delirium and halluci- ilation, and as such, it has been useful in the anesthetic manage-
nations (157). In fact, the administration of a benzodiazepine ment of patients with asthma (88). However, because ketamine
3 to 5 minutes before ketamine is effective in almost entirely is a direct myocardial depressant, its administration to patients
eliminating the possibility of emergence delirium (88). who are profoundly hypovolemic, and whose sympathetic ner-
Transient diplopia (31), ataxia (60), and disequilibrium (60) vous system is already maximaJiy stimulated, will lead to cardio-
may occur after ketamine use. Early attempts at ambulation vascular collapse. The reader is reminded that any sedation given
should be discouraged (60). Ketamine does not induce seizures to a hypovolemic parient must be administered very judiciously
and is not necessarily conuaindicated in patients with an under- and preferably after the volume srarus is corrected.
lying seizure disorder (157).
Ketamine is contraindicated in patients with increased intra-
cranial pressure or with abnormal intracerebral compliance. Review of Relevant Literature (Ketamine)
Thus, parients who have sustained a head injury as part of their
In 1990, Green and co-workers reviewed a collective experience
ongoing trauma should not receive this drug (144). It is inrerest-
of nearly 12,000 children sedated with ketamine for various
ing to note that there are some reportS actually suggesting that
there is a neuroprotective effect for ketamine (83). However, procedures (60,61). In 1998, Green and coworkers (62) pub-
lished their experience with 1,022 pediatric patients aged 15
the recommendation that ketamine be avoided in head-injured
patients still stands firm for now. years and younger sedated with ketamine 4 mg/kg intramuscu-
larly for a variery of emergency room procedures, consisting
mainly of laceration repairs and fracture reductions. From this
Respiratory Effects of Ketamine group of patients, the authors reported twO cases of apnea, four
Ketamine can have some potentially troublesome effects on the cases of lalyngospasm, one case of respiratory depression, and
airway. It causes the production of increased salivary and tra- seven cases of partial airway obstruction (e.g., airway malalign-
cheobronchial secretions, which can lead to coughing, laryngo- ment) responding co repositioning of the head. They also re-
spasm, and airway obstruction. This problem may be especially ported a 6.7% incidence of vomiting but no cases of aspiration.
treacherous in patients with an ongoing respiratory infection. In an interesting study by Kennedy and colleagues (81), inn'ave-
Glycopyrrolate (Robinul), an antisialogogue, should be adminis- nous ketamine combined with midazolam (Versed) was com-
tered 3 to 5 minutes before ketamine (at the same time that the pared with fentanyl combined with midazolam in the manage-
benzodiazepine is given) to ameliorate this problem (88). The ment of pediatric fractures. This particular study is further
dose for glycopyrrolate is 5 to 10 ,ug/kg, given intravenously. discussed later.
For large children, a dose of 0.2 mg (200 ,ug) of glycopyrroJate
given intravenously is sufficient. Unless there is some other
strong indication for its use, ketamine should be avoided in ~ AUTHOR'S PREFERRED METHOD
patients with ongoing infections of the respiratolY tract. ,~ OF TREATMENT
Although ketamine does not usually produce significant
depression of ventilation (136), apnea has been teported with Salient points regarding the safe use ofketamine are summarized
its administration (37). Apnea is more likely to occur when the in Table 3-7. Monitoring and procedural guidelines for deeply
drug is given intravenously in rapid boluses (37) or in combina- sedared patients (63) should be followed whenever ketamine is
tion with other respiratOry depressants (136). However, there used. If used intramuscularly, the dose should be limited to 4
are reports of apnea in otherwise healthy children sedated in the mg/kg. If the drug is used intravenously, the total dose should
emergency department with intramuscular ketamine alone in be limited to 2 mg/kg. The reader is reminded to use glycopyrro-
the usual recommended dosage (96,126). late, and to consider strongly the administration of midazolam
In addition, ketamine does not protect against aspiration of (Versed) 0.05 to 0.1 mg/kg for the prevention of agitation and
gastric contents (26,141). In this regard, ketamine is no different delirium. Note that there is an increased risk of respiratory
from any other sedative and analgesic except maybe for self- depression whenever more than one sedative medication is ad-
administered 50% nitrous oxide in oxygen. Ketamine should ministered. Note also [hat no reversal drug exists for ketamine.
56 GmeraL PrillicipLes

is 4.8 minutes for mida20lam versus 1.6 minutes For diazepam

TABLE 3-7. KETAMINE IN PEDIATRIC
(25). Thetefore, when titrating midazolam for sedation, it is
SEDATION
important ro wait 5 minutes between doses.
I. Methods of Administration and Dosage
A. 1M, 4 mg/kg
B. IV, 1-2 mg/kg Central Nervous System Effects
C. PO, 6-10 mg/kg
D. Rectal, 5-10 mg/kg Anxiolysis and centrally mediated relaxation of skeletal muscle
II. Contraindications rone is presumed ro occur from a benzodiazepine-induced in-
A. Altered state of consciousness
B. Increased intracranial pressure
crease in the availabiliry of glycine inhibitory neurotransmitter
C. Active upper respiratory infections (increased quantity of (33). Facilitating the action of the inhibirory neurotransmitter
secretions and possible increased risk of laryngospasm) gamma-aminobutyric acid (GABA) is responsible for the seda-
D. Full"stomilch tive eFFects of benzodiazepines (133). It remains unclear what
E. Prior unfavorable experience with ketamine
the site of action is for the production of amnesia (33).
F. Patients> 16 yr old (increased incidence of emergence
phenomena)
Note that midazolam and diazepam produce direct depres-
III. Advantages sion of the central respiratolY drive (54) and that apnea may
A. Provides sedation, amnesia, intense analgesia occur (l8,72,113), especially after parenteral administration of
B. Sympathetic-mediated activity may be beneficial for chil- these drugs. Although it is generally considered very safe, orally
dren with asthma.
administered midazolam has been reported to produce airway
IV. Disadvantages
A. Increases production of saliva and tracheobronchial se- obstruction in a child with congenital airway anomalies (85). In
cretions. Coadministration of glycopyrrolate 0.01 mg/kg general, the incidence of respiratory complications increases with
recommended. the presence of major vital organ disease (72). However, even
B. Potential for loss of the airway from: in healthy adult volumeers, inrravenous sedation with midazo-
1. Laryngospasm secondary to increased secretions
lam (0.1 mg/kg) can depress the vemilarory response to hypoxia
2. Aspiration from laryngeal incompetence
3, Apnea (3). Concomitant administration of opioids (72,133,161)
C. Emergence phenomena: Rare in young children. No ad- greatly increases rhe risk of respiratory complications. Therefore,
vantage to quiet environment. Midazolam may help, but extra vigilance and careful titration of medications to effect are
may contribute to oversedation. even more Important when using more than one sedative or
analgesic medication.

Other Systemic Effects

With careful titration, significant hemodynamic changes are un-
Benzodiazepines
usual with midazolam (113). Loss of protective airway reHexes
Initial imerest in the use of benzodiazepines developed when is also unlikely under these circumstances (13) as long as the
these drugs were noted to exert taming effects in animals (33). physician pays careful attemion to the effects of each incremental
Ben20diazepines provide anxiolysis, hypnosis, cenrraJly mediated dose on the patient's state of consciousness. Caution is always
(40) relaxation of muscle tone, anregracle and retrograde amne- urged if the patient's stomach is Full. Slurring of speech is a
sia, and anticonvulsant activity (113). Benzodiazcpines have no rypical sign of sedation with benzodiazepines (113). Children
analgesic activity and require supplementation For painful proce- may also exhibit loss of anxiety, unsolicited smiling, and even
dures (33). laughter.
In reporting their experience with 2,617 children sedated for
endoscopic procedures, Massanari and co-workers (91) nored
Pharmacology that 36 patients exhibited paradoxical reactions to midazolam,
including inconsolable crying, combativeness, and agitation.
Midazolam (Versed) is the primary ben20diazepine used For pe-
The authors of this study were able to treat these reactions with
diatric sedation. It oFFers several advantages over other benzodi-
flumazenil, a benzodiazepine antagonist, which is further dis-
azepines (58). It is water soluble and, therefore, usually rela-
tively painless on injection (113,158). It does occasionally cause cussed below.
discomfort on injection, although the pain is not as severe as
that with diazepam (Valium). At physiologic pH, mida20lam
Review of Relevant Literature (Midazolam)
becomes highly lipid soluble, facilitating transport into the CNS
and onset of sedative effects (l58). Initial recovery, which is due In children, midazolam can be administered by oral, nasal, sub-
to redistribution of the drug away from the CNS, occurs in lingual, intravenous, intramuscular, and rectal routes (88). A
about 30 minutes. The elimination half-life of mida20lam is liquid oral formulation, whose concentration is 2 mg midazo-
significantly shorrer than that of diazepam (58). On a milli- lam/mL, now exists in the United States. It is marketed as Versed
gram-per-milligram basis, midazolam is at least twO ro three Syrup 2 mg/mL and is manuFactured by Hoffman-LaRoche
times as potent as diazepam (56). Electroencephalographic pharmaceuticals. lf this formulation is not available at a partiCL1-
(EEG) studies indicate that the blood-brain equilibration time lar location, rhen the practitioner can order the paremeral form
 Chrlprn 3: J)ain Re/ielrT/ul Relared COllcerm iii Chi/dreils Fractures 57

this amount is usually limited ro 20 ro 25 mg. Note that analgesic

TABLE 3-8. BENZODIAZEPINES IN PEDIATRIC
SEDATION supplementation in the form of either local anesthetics, opioids,
or both is required for painful procedures. Patients who receive
I. Method of Administration parenteral benzodiazepines must be monirored with pulse ox-
A. Diazepam: 0.1 to 0.3 mg/kg IV or PO. 1M administration imetry, because oxygen desaruration may occur (125).
should be avoided because it is painful.
B. Midazolam
1. PO, 0.5-0.75 mg/kg Drug reversal
2. Nasal, * 0.3-0.4 mg/kg
3. 1M, 0.03-0.1 mg/kg Flumazenil (Romazicon) reverses the sedative effects ofbenzodi-
4. IV, 0.05-0.1 mg/kg azepines (76,82,107). The flumazenil dose for children is 10
II. Contra indications ttg/kg intravenously. Flumazenil administration may then be
A. Previous unfavorable experience with benzodiazepines
continued at 5 ttg/kg/minute until the child awakens, or uneil
B. (?) Early pregnancy (possible teratogenicity)
C. Altered state oT consciousness a total dose of 1 mg has been given (77). The elimination half-
III. Advantages life of flumazenil is 30 minutes, compared with 1 ro 2 hours
A. Generally provide excellent sedation and amnesia for midazolam. Patients who receive flumazenil should be ob-
B. Revers;ble if necessary (fILJmazenil, 10 ,ug/kg) up to a total served fot at least 2 hours before discharge ro ensure that rese-
dose of 1.0 mg)
dation from the original benzodiazepine does not occur. In the
IV. Disadvantages
A. No analgesic effect author's opinion, the use of flumazenil should be limited to
B. Respiratory depression, especially with parente'ral admin- , situations of relative or absolute benzodiazepine overdose leading
istration to respirato'y or hemodynamic compromise. Routinely reversing
C. Combination with narcotics may lead to oversedation or benzodiazepines is both unnecessary and, in the absence of per-
respi ratory arrest
sistene monitoring, potentially dangerous.

* Many children find the intranasal administration of midazolam

to be very unpleasant..This method of administering midazolam is
not recommended. ~ AUTHOR'S PREFERRED METHOD
,~ 0 F TREATMENT
Salient points regarding the use of midazolam and orher benzo-
diazepines are summarized in Table 3-9. AJthough supplemental

(usually the 5 mg/mL concentration) ro be mixed in 5 ro 10

mL of a sweet-tasting syrup (l06). Acetaminophen syrup or
ibuprofen syrup are useful vehicles for mixing parenteral midazo- TABLE 3·9. OPIOIDS IN PEDIATRIC SEDATION
lam, keeping in mind the appropriate pediatric doses of acet-
aminophen and ibuprofen (Table 3-8). The author's personal I. Method of Administration
preference is to mix the midazolam in 3 ro 5 mL of Tylenol A. Morphine: 0.05-0.1 mg/kg 1M or IV
B. Meperidine: 0.5~1.0 mg/kg 1M or IV
syrup. For nasal administration, which the author does not rec-
C. Fentanyl: In increments of 0.001 mg/kg IV (maximum
ommend, rhe parenteral preparation is used with no additives. total dose, 0.004-0.005 mg/kg)
The reason for discouraging the use of nasal midazoJam is be- D. Nalbuphine: 0.1 mg/kg 1M or IV
cause most children find its administration ro be very unpleasant. Patients younger than 3 mo old should be given no more than
In one study, 84% of children given intranasal midazolam cried half of these doses initially. IV titration to desired effect is the
ideal way to administer all sedative medications.
in response to administration of the medication (80). Although
II. Contraindications
sublingual administration is a good idea from a pharmacologic A. Altered state of consciousness
point of view (see discussion under morphine), it requires a B. Previous unfavorable experience. (excludes that medica-
degree of patient cooperation that may be difficult to reliably tion only)
obtain in children. In other words, an uncooperative child may C. Sedation for nonpainful procedure
III. Advantages
be unwilling or unable to hold a medication under his or her
A. Provide excellent analgesia
tongue. B. Reversible if necessary (naloxone 0.001-0.005 mg/kg IV
Hennes and colleagues (65) have used oral midazolam to titrated to effect)
allay the anxiety of children requiring laceration repair in the IV. Disadvantages
emcrgency department. Farovich and Jacobs (47) also noted de- A. Risk of respiratory depression and apnea
B. Increased risk of respiratory depression and apnea when
creased anxiety in children requiring laceration repair after oral combined with other sedatives
midazolam versus in a comrol group that received only a placebo. C. No amnestic effects
Note that if the practitioner decides to use orally administered V. Additional Side Effects (more likely when used in recurrent
midazolam, the appropriate dose is 0.5 to 0.75 mg/kg (48) and doses for treatment of pain)
Nausea, vomiting, pruritus, constipation, decreased gas-
a waiting period of 10 ro 30 minuees is required for onset of
tric motility
effects. The maximum amount of midazolam that should be
administcrcd orally has not been determined, but in practice,
58 General Prilliciples

analgesia is required for painful procedures, such as rhe reducrion (38). The overall incidence of true allergic reactions ro opioids
offractures, the anxiolysis and amnesia thar midazolam produces is very small (38).
make ir an excellent medicarion for children wirh onhopaedic
injuries. Careful inrravenous rirrarion of midazolam in incre-
ments of 0.05 mg/kg may be undertaken, combined wirh a re- Meperidine
gional anesrhetic block (Bier block, hemaroma block, for exam- The use of meperidine (Demerol) parallels that of morphine.
ple) for pain relief. The aurhor believes rhar oral midazolam, The initial intravenous or intramuscular dose is 0.5 ro 1.0 mg/
with irs mandarory 10- ro 30-minute wairing period. and with kg. Again, the dose should be reduced by at least one half in
its lack of titratability ro effect, is probably best reserved for use infants younger rhan 3 months of age (114). Normeperidine, a
as a preoperative medicarion before elecrive surgical procedures. meraboJic breal<down product of meperidine, has been associ-
Also, for emergency patients, intravenous rirration is the besr ated wirh seizures, agitation, rremors, and myoclonus (68,78).
and most efficienr way ro achieve desirable levels of parient seda- Meperidine is nor recommended for patients wirh an underlying
tion and cooperation. The combination of midazolam and seizure disorder. Accumulation of normeperidine is more likely
opioids is discussed in the nexr seerion. in siruarions of prolonged meperidine adminisrrarion. There-
fore, meperidine should be used cauriously, if ar all, in rhe trcar-
ment of chronic pain (33). As wirh morphine, meperidine may
Opioids produce hypotension due ro various mechanisms (8). Hisramine
Opioids include all exogenous subsrances, narural or synrheric, release has also been reponed wirh meperidine (8).
rhar bind to specific receprors and produce morphine-like effecrs
(38). There are several rypes and subrypes of opioid receprors
(8,138). Opioids vary in rheir respecrive affini ry for recepror Fentanyl
rypes, accounting for rhe difference in side effeers. Opioids are Fentanyl is a synthetic narcoric 100 rimes more porent rhan
classified as pure recepror agonisrs (e.g., morphine, meperidine, morphine and 1,000 rimes more porent rhan meperidine on a
fenranyl), agonisr-anragonisrs (e.g., nalbuphine), or pure anrago- milligram-per-milligram basis. Fenranyl is highly lipid soluble
nisrs (e.g., naloxone) (38). and rapidly penerrares rhe CNS (8). When adminisrercd in low
doses, irs durarion of aerion is from 30 ro 45 minures. For seda-
rion, fentanyl is given intravenously in increments of 0.5 ro 1
Opioid Agonists
,ug/kg. The maximum roral dose is 4 ro 5 ,ug/kg (33). As a
All opioid agonisrs produce dose-dependent respirarOlY depres- preoperarive medication, fentanyJ is availabJe in an oral raspberry
sion and apnea (138). Nausea and vomiring occur because oE flavored lollipop known as rhe Fentanyl Oralet (88). Currently
direer srimularion of the chemorecepror rrigger zone in rhe floor available sizes for the Oraler are 200 ,ug, 300 ,ug, and 400 ,ug.
of rhe founh ventricle of the medulla oblongata (138). As a preoperarive medicarion, rhe recommended dose ranges
from 10 ro 20 ,ug/kg. Troublesome side eEfcers ofrhis prepara-
rion include nausea and vomiring, prurirus, and oxygen desatura-
Morphine rion (121).
Morphine is a well-known analgesic. It is usually administered Reonser of respirarOlY depression up ro 4 hours after fentanyJ
administration has been reponed (131). Glotric closure (5), and
intravenously or intramuscularly, although sublingual and reeral
muscular rigidiry (6,120,128) can occur, especially, aJrhough
routes have been described (33). Oral morphine is usually used
nor exclusively, with adminisrrarion of higher doses. Respirarory
for long-term pain control in patients with severe, chronic pain.
arresr may occur, especially wirh rhe coadminisrrarion of orher
Renal administration of morphine is not recommended because
sedarives (61). For rhese reasons, fentanyl should be ri rrated
ir has been associated wirh delayed absorption, deJayed respira-
rory depression, and death (33,58). In general, rectally adminis- slowly ro effect.
rered medications are absorbed unpredictably (135) and access
of the medication ro the reeral mucosa may be variabJy impeded
Opioid Agonist-Antagonists
by reeral srool content.
The usual starting dose for intravenous or intramuscular mor- A so-called ceiling effecr or limir on rhe degree of respirarolY
phine is 0.05 ro 0.1 mg/kg. In infanrs younger [han 3 momhs depression has been demonstrated for various opioid agonisr-
old, the dose should be reduced by at leasr one half because of anragonists, including nalbuphine (116) and burorphanol (149).
increased susceptibiliry ro respirarory depression (14). Mor- Nalbuphine and morphine have rhe same analgesic porency on
phine should be reserved for painful procedures lasting a[ leasr a milligram-per-milligram basis (114). Nalbuphine has a shoner
30 minutes (33). Morphine is nor very lipid soluble, and its eliminarion half-life (73). Opioid agonisr-antagonists have no
delay in leaving the CNS accounts for a potential durarion of particular advantage over properly dosed opioids (38). The
aerion of3 to 4 hours (8,33). Hyporension secondary ro vasodila- major problem with opioid agonist-antagonists is that rheir ceil-
tion, histamine release, or vagally mediated bradycardia can ing effect on respirarolY depression is often accompanied by a
occur even with the administrarion of smalJ doses of morphine ceiling etTen for analgesia (138). Also, agonist-anragonisls re-
(8). Hisramine release along the course of [he vein inro which duce the analgesic effectiveness of pure agonists (e.g., morphine,
the morphine is adminisrered is nor by itself an allergic reacrion meperidine, fenranyl, codeine) if additional analgesia is required
 Chapter 3: Pain Relief and Related Concerns in Children s Fractures 59

(38). In patients who ate receiving opioids on a long-term basis, dures in children, a combination of a benzodiazepine and a nar-
adminisrration of opioid agonist-antagonists can precipitate cotic is probably ideal (110,127,161), as long as the principles
acute withdrawal symptoms (38). of careful titt'ation and close patient monitoring are observed.

Drug Reversal With Opioid Antagonists • AUTHOR'S PREFERRED METHOD

Naloxone (Narcan), which has no agonist activity of its own, ,~ OF TREATMENT
displaces opioids from opioid receptors (138). Note that rapid
reversal of narcotic effects may precipitate severe hypertension, Salient points regarding the use of opioids as well as opioid and
pulmonary edema, ventricular or supraventricular irritability, benzodiazepine combinations for pediatric sedation are summa-
seizures, and cardiac arrest (7,44). Dysphoria, nausea, and vom- rized in Tables 3-10 and 3-11. Opioid and benzodiazepine com-
iting may also occur. Acute narcotic withdrawal in this situation binations provide amnesia, analgesia, and sedarion. The tradeoff
reflects sympathetic nervous system stimulation from abrupt re- is that of additive respiratOry depression and additive depression
versal of analgesia and sudden perception of pain (8). Therefore, of protective airway reflexes. In borh elective and emergent situa-
naloxone should be titrated to effect (telief of respiratOry depres- tions, rhe practitioner must
sion) in incremems of 1 to 5 ,ug/kg intravenously. Naloxone 1. Thoroughly evaluate the patient, as has been discussed earlier
has a duration of action of 30 to 45 minutes, and resedation is in the chapter.
possible. Close patient observation is required, and supplemental 2. Follow standard practice guidelines for deep sedation (63).
naloxone doses may be necessary. Current dosage tecommenda- 3. Pay careful attention to dosing limits (Table 3-11).
tions in cases of frank opioid intoxication are significantly higher 4. Be cerrain rhat both flumazenil and naloxone are available.
(43). Caution is always advised against precipitating acute nar- These medications are to be used strictly for the treatment of
cotic withdrawal. The first priority in the treatment of narcotic absolute or relative overdose ofbenzodiazepines and opioids,
overdose is a patent, weJl-maintained airway. respectively. Do not use these medications to expedite dis-
Similar to the situation with flumazenil for reversal of benw- charge from the emergency room.
diazepines, the author believes that the routine use of naloxone
to reverse narcotic sedative medications is unwarranted and, for
reasons noted earlier, potentiaJly dangerous. Naloxone use Midazolam and Ketamine Compared With
should be reserved for situations of ailway compromise brought Midazolam and Fentanyl
on by telative opioid overdose, and it should never be urilized as While studying a group of 260 children berween the ages of 5
a way of expediting patient discharge after a procedure requiring and 15 presenting for the emergency room reduction of frac-
sedation.

Review of Relevant Literature (Opioids)

With careful monitOring and judicious administration, combi- TABLE 3-10. FENTANYL AND MIDAZOLAM IN
PEDIATRIC SEDATION"
nations of opioids for analgesia and benwdiazepines for amnesia
and anxiolysis are probably the most useful sedatives in existence i. Method of Administration
today for the management of children's fractures. Varela and IV titration to effect
co-workers (150) reported exceJlent patient and physician satis- A. Midazolam: In increments of 0.05 mg/kg to a maximum
0f 0.1 mg/kg. Wait 5 min b.etween doses.
faction using intravenous meperidine and midazolam for intra-
B. Fentanyl: Begin 5 m.in after last midazolam dose.. Give
venous sedation for the closed reduction offractures in children. in increments of O.OO.lmg/kg to a maximum of 0.003
In this particular investigation, the average meperidine dose was mg/kg. Wait 2 to 3 min between doses..
1.47 mg/kg and the average midazolam dose was 0.11 mg/kg. II. Contra indications _
There were no episodes of apnea or cardiorespiratory complica- A. Altered state of consciousness
B. Previous unfavorable experience with either medication
tions. These investigators stress that careful patient monitoring
C. Specific contraindicationsto benzddiazepines or
is importam, not only during but after the procedure as well. opioids (see Tables 3-9 and 3-10).
lmravenous morphine 0.1 mg/kg plus midawlam 0.1 mg/kg III. Advantages -
is another useful sedation mixture for children with fractures, A. Provides sedation, amnesia (midazolam), and analgesia
especially when combined with a hematoma block (personal (fentanyl)
B. Reversible if necessary (see Tables 3-9 and 3-10).
communication, ). Edeen, M.D.). The hematOma block is dis- IV. Oisadvantilges
cussed later in the chapter. With this particular approach, the A. Additive- respiratory depressant effects
midazolam is administered first, followed by the morphine about B. Additive depressant effects on protective airway
5 minutes later. The hematoma block is performed, and the reflexes with increased risk for regurgitation and
fracture is then reduced. Again, careful patient monitOring as aspiration of gastric contents'
previously outlined is essential to good care.
In the absence of specific contraindications, including ten- * An'excellent review of the advantages -and problems associated
with this drug regimen is provided by Yasterandcolleagues 135,
uous ailway status, unstable hemodynamic status, or histOry of
specific aJlergic reactions, for the petformance of painful proce-
60 General PrinicipleJ

gospasm. Vomiting occurred more often in the group taking

TABLE 3-11. CHLORAL HYDRATE IN PEDIATRIC
SEDATION
ketamine, and group taJ(jng the ketamine had a longer mean
time to recovery and discharge.
I. Method of Administration This is a very detailed study thar looks very closely at two
20 to 75 mg/kg orally or rectally (maximum single dose, 1.0 viable regimens for sedation of children with fractures. Again,
g. If a second dose is given, the maximum total dose is
either 100 mg/kg or 2.0 g, whichever is lower).
with careful monitOring and careful attention to drug tin'ation,
Ik Contra indications the practirioner may wish to ny both to determine which is
A. Compromised hepatic function more useful in their individual practice. The authors of this
B. History of obstructive sleep apnea* study favor the ketamine and midazolam regimen and provide
C. Previous unfavorable experience with chloral hydrate
good evidence for their conclusions (81).
III. Advantages
No specific advantages for sedation and treatment of
children with fractures
IV. Disadvantages Pediatric Cocktail
A. Prolonged time to peak effect (as long as 60 min)
8; Difficult to titrate
The so-called pediatric cockcail (OPT) or "lyric" cockcail is a
C. Prolonged observation period required mixture of meperidine (Oemerol) and two phenothiazines: pro-
methazine (Phenergan), and chlorpromazine (Thorazine). For
* Caution is required when using any sedative medication in multiple reasons, this sedative regimen should be avoided. Pro-
patients with obstructive sleep apnea. longed and profound sedation occur, often far outlasting the
procedure for which the sedation was intended. One study has
reported a mean total recovelY time of 19 hours, plus or minus
15 hours, in children receiving OPT in the emergency depart-
ment (142). Orthostatic hypotension is possible, because pro-
methazine and chlorpromazine are alpha-adrenergic blockers
[Ures, Kennedy and coworkers (81) compared the effeCtiveness of (33). Severe respiratory depression and death, both during and
two regimens for sedation and analgesia. For tne first reduction after the procedure, have occurred in patients sedated with DPT.
attempt in each patient, all of the children initially received All three medications in this mixture lower rl1e seizure threshold,
midazolam 0.1 mg/kg (maximum dose of 2.5 mg) at 3-minure and phenothiazines can produce dystonic reacrions (33). Note
intervals until either objective signs of onset of drug effect devel- that there is no reversal agem for phenothiazine overdose.
oped (slurred speech, glassy eyes) or unril three doses of midazo-
lam were given. One minute after the administration of the last
dose of midazolam, half the patients began receiving fentanyl,
titrated in increments of 0.5 ,ug/kg until either a decreased re- • AUTHOR'S PREFERRED METHOD
sponse to verbal or painful stimulation was noted, or a maximum ,~ OF TREATMENT
dose of2 ,ug/kg had been administered. The maximum amount
of fentanyl used was 100 ,ug. The otner half of the patients, The author strongly believes rhat the use of the pediatric cocktail
instead of receiving femanyl, were given ketamine, titrated in should be abandoned (127),
incremems of 0.5 ,ug/kg, using the same criteria as for femanyl
to determine onset of effecL Ketamine tirration continued, if
Chloral Hydrate
necessary, until a maximum amount of2 ,ug/kg had been given.
All of tne patients who were given ketamine also received glyco- Of greatest use in sedating children for nonpainful diagnostic
pyrrolate, 5 ,ug/kg as an anrisiaJogogue. Additional amouncs of procedures such as radiographic studies, chloral hydrate is ad-
midazolam and the study drug were given if analgesia and seda- ministered in a dose of 20 to 75 mg/kg orally or rectally. The
tion were judged to be insun:;cient or if additional reduction maximum single dose is 1 g, If more than one dose has to be
attempts were necessary. Treatmenr failures occurred in those given, the upper limit for the rotal dose is either 100 mg/kg or
parienrs who experienced significant adverse drug effects or who 2 g, whichever is lower.
obrained insufficient sedation and analgesia. Although, theoretically, rectal dosing should be more effi-
Patient distress was quamified using various behavioral scales. ciene, because of the lack of a first pass hepatic effect (135), 30
The reader is referred to the article itself for more derailed infor- ro 60 minutes may elapse before chloral hydrate rakes effeer no
mation about the measurement process (81). Whereas preseda- marter how it is administered. Children receiving chloral hydrate
tion scores were basically the same for both groups, during frac- musr be observed for at least several nours. Respirarory depres-
ture reduction, rhe investigatOrs reported a significantly Jower sion is unusual, but children with sleep apnea and adenotonsillar
score of patient distress for the children receiving midazolam hypertrophy may be particularly vulnerable ro airway obstruc-
and ketamine than for rhose receiving midazolam and fentanyl tion after sedation with chloral hydrate (16). At least one death
(81). In general, tne ketamine and midazolam combination was has been reported following its use (74), These problems empha-
favored by parents and by the involved orthopaedic surgeons size that even sedatives thought to have little risk of producing
(81). On the other hand, however, C\.vo patienrs receiving mida- respirarory depression must be administered under properly su-
zolam and ketamine required brief assisted ventilation with a pervised conditions (63) and with strict adherence ro dosage
bag, valve, and mask apparatus, and one patient developed lalyn- guidelines.
 Chapcer 3: Pain Relief and ReLated Concerns in ChiLdren:r Fractures 61

~ AUTHOR'S PREFERRED METHOD not be used in the management of children with fractures in an
,~ OF TREATMENT emergency room setting. First and foremosr, ir is easy to sud-
denly lose the airway in a patient given propofol. Therefore, this
Chloral hydrare is of minimal use in rhe sedation and treatment drug has really should be administered by an anesthesiologisr
of patients with fractures. It provides no analgesia, and ir lacks (79). Second, the drug provides no analgesic effecr and, rhere-
the rapidity of onser and rirrarability of intravenous opioids and fore, has ro be combined with an opioid, which, in turn, will
benzodiazepines. The pracritioner should be familiar with rhis inrensify rhe respiratory depressanr effects of propofol. Third,
medicarion, however, because it remains in common use for in children, the administrarion of propofol is associated wirh
nonpainful pediatric procedures. Salient features regarding its opisthotOnic posturing and myoclonus (88), which is certainly
adminisrration are summarized in Table 3-12. nor helpful in the reduction of a fracrure. Propofol has vasodila-
tory and negarive inorropic effects, which can lead to hypoten-
sion (88). Finally, there is some concern thar propofol may be
Barbiturates associated with seiwres (88), although Momora and co-workers
In general, barbirurates have a lower margin ofsafety than benzo- (97) have used propofol to Stop seiwre activity from local anes-
diazepines (132). In addition, barbiturates seem to lower the theric overdose.
pain threshold, and are therefore a poor choice for producing
sedarion in the presence of a painful condition, such as a fracture • AUTHOR'S PREFERRED METHOD
(132). With these points in mind, barbiturates should nOt be ,~ OF TREATMENT
used for sedating children with fractures.
Regarding children with fractures, propofo] should be reserved
Propofol for administration in the operating room as part of a regimen
of general anesthesia by an anesthesiologist.
Propofol is a substituted isopropyl phenol rhat is a rapid-acting
intravenous anesthetic (136). Because it is virtually insoluble in
aqueous solutions, it has to be dissolved in lecithin-containing REGIONAL A ESTHESIA IN THE CHILD
formularions. The orthopaedist may have seen this whirish medi- WITH A MUSCULOSKELETAL INJURY
carion administered by the anesrhesiologisr in the operating
room, where it has gained the popular name of "milk of am- Within the limitations and guidelines that are discussed later,
nesia." the use of regional anesthesia ro relieve pain in children with
Propofol has a fasr onset of action, owing to its high lipid musculoskeletal injuries is reasonable and worthwhile.
solubility, and an exrremely short durarion of action. Awakening
is rapid, wirh litde to no "hangover" effect as seen with other Regional Anesthetic Agents
drugs (136). Ir also has antiemetic effects (88). Regional or local anesthetic medications prevent nerve impulse
However, rhere are several reasons for which d1e drug should propagation by interfering with the function of rhe sodium chan-
nel on the axonal membrane (139). Commonly used local anes-
rhetics have either an amino amide or amino esret linkage in
their molecular structure (146). Amino amide local anesthetics
include lidocaine (Xylocaine), bupivacaine (Marcaine, Sen-
TABLE 3-12. MANIFESTATIONS OF LOCAL
ANESTHETIC TOXICITY· sorcaine), mepivacaine, prilocaine, etidocaine, and the relarively
new agent ropivacaine. Amino ester local anesthetics include
1. Numbness of the lips and tongue, metallic taste in the mouth. procaine (Novocain), chloroprocaine, tetracaine, benzocaine,
2. Lightheadedness
and cocaine.
3. Visual and auditory disturbances (double vision and tinnitus)
4. Shivering, muscle twitching, tremors (initiar tremors may in- Medications within each group have important intrinsic dif-
volve the muscles of the face and distal parts of the extremi- ferences in potency, durarion of action, and porential for roxicity
ties) (36,146). For example. lidocaine is significantly less toxic a drug
5. Unconsciousness than bupivacaine bur it also has a shorrer durarion of action.
6. Convulsions
7. Coma An important feature of ropivacaine is that even rhough its dura-
8. Respiratory arrest tion of action is similar to bupivacaine, ir produces Jess CNS
9. Cardiovascular depression and collapse toxicity and less cardiac toxicity (123). Durarion of acrion for
rhe various local anesrhetic medications is also determined in
* With gradual incr~ases in plasma concentration, these signs and part by the type of regional block performed. For example, single
symptoms may occur.in order as listed. With the sudden dose brachial plexus blocks tend to have a far longer duration
development of high plasma concentrations of a local anesthetie
agent, the first manifestation of toxicity may be a convulsion, than do single dose epidural or subarachnoid blocks (36).
respiratory arrest, or cardiovascular collapse. In young children, or
in children who are heavily sedated, subjective evidence of
impending local anesthetic toxicity (manifestations 1, 2, 3) may be Local Anesthetic Toxicity
difficult to elicit..
Ar least three types of adverse reactions can occur from local
anesrheric agents. Clinically, the most important is systemic tox-
62 General Prinicipln

icity of rhe CNS and cardiovascular sysrem from relarive over-

TABLE 3-14. MAXIMUM RECOMMENDED
dose inro rhe circulation. This type of reacrion is nor a medica-
DOSES OF COMMONLY USED
rion allergy bur simply a Function of placing roo much LOCAL ANESTHETICS IN
medicarion inro rhe bJoodsrream. Note rhat in rhe presence of CHILDREN
a major artery, even a few drops of local anesrhetic can lead
Injection Dose
ro seizure acrivity. An example of rhis problem is seen in the
(mglkg)
performance of stellare ganglion blocks in rhe neck for rhe man-
agement of reflex symparheric dystrophy of rhe upper extremity, With
where rhe verrebral anery can be accidentally entered during Agent 'Plain Epinephrine*
administration of the medication. Lidocainet (Xylocaine) 5 7
In mosr cases, however, the severity of systemic toxicity is Bupivacaine+ (Marcaine, 2.5 3
directly relared ro rhe concentrarion of local anesthetic in rhe Sensorcaine)
bloodsrream (Table 3-13) (36). Seizures and cardiac arrest may Mepivacaine (Carbocaine) 4 7
be rhe initial manifesrarions of systemic roxicity in patients who Prilocaine§ 5.5 8.5
rapidly arrain a high serum level of medication (42,98,109).
Agents with greater intrinsic potency, such as bupivacaine and * The addition of epinephrine (vasoconstrictor) reduces the rate of
local anesthetic absorption into the bloodstream, permitting use
etidocaine, require lower levels for producrion of symptoms (36). of a higher dose.
Dysrhyrhmias and cardiovascular toxiciry may be especially se- t For IV regional anesthesia (Bier blocks), the maXimum lidocaine
dose is 3 mg/kg. Preservative-free lidocaine witho'ut epinephrine
vere with bupivacaine, and resuscitarion of rhese parients may should be used for either Bier blocks or hematoma blocks.
be prolonged and difficulr (2,36). * Owing to its cardiotoxicity, bupivacaine should never be used for
IV regional anesthesia or for hematoma blocks.
The prevention and rrearment of acure local anesrheric sys- § Of the amide local anesthetics, prilocaine is the least likely to

temic toxiciry are outlined in Table 3-14. produce eNS and cardiovascular toxicity. However, a byproduct of
prilocaine metabolism may lead to severe methemoglobinemia in
A1rhough rhe potenrial for CNS roxicity may be diminished young children. Prilocaine is, therefore, contraindicated in children'
wirh barbirurares or benzodiazepines, given either as premedic- younget'than 6 mo old.
ations or during rrearmenr of convulsions, rhese measures do
nor alrer rhe cardiotoxic rhreshold of local anesrhetic agents.

With rapid and appropriare rrearmenr, rhe fatality rare from

TABLE 3-13. PREVENTION AND TREATMENT OF local anesrhetic convulsions should be greatly decteased (36).
ACUTE LOCAL ANESTHETIC Ie is absolutely essential ro sray wirhin accepted dose limits
SYSTEMIC TOXICITY when using any local anestheric (Table 3-15). To aid in dose
Preventive Measures calculations, a simple formula for convening percent concenrta-
rion to milligrams to millilirer is provided in Table 3-16.
1. Ensure ava,ilability of oxygen administration equipment, air-
way equipment, suction equipment, and medications for AJrhough rare, rrue immune-mediared allergic reacrions ro
treatment of seizures (diazepam or midaiolam, thiopental, local anesrherics are possible, more commonly wirh amino esrers
succinylcholine). rhan wirh amino amides (22,52). The reader is referred to other
2. Ensure co'nstant verbal contact with patient (for symptoms of sources for the derailed managemenr of allergic or anaphylacric
toxicity) and monitor cardiovascular signs and oxygen satura-
tion. reacrions (28,100).
, 3. Personaily' prepare the dose of local anesthetic and ensure it' Local nerve damage and reversible skeleraJ muscle changes
is within the accepted dosage range. have been reported from rhe use of local anesrherics (36).
4. Give the anesthetic slowly, and fractionate the dose.

Treatment Intravenous Regional Anesthesia

1. Establish a clear airway; suction if required.
2. Give oxygen by face mask. Begin artificial ventilation if neces- Intravenous regional anesthesia was firsr described by Augusr
sary. Bier in 1908 (15). Although ir declined in popularity as brachial
3. Give diazepam 0.1-0.3 mg/kg IV in incremental doses until
convulsions cease. Midazolam (0.05-0.1 mg/kg) may be used
instead, also in increments until convulsions cease.
4. Thiopental in increments of 1-2 mg/kg IV may be used to
control the seizures.
TABLE 3-15. CONVERSION FORMULA FROM %
5. Succinylcholine (1 mg/kg IV) may be used if there is inade-
CONCENTRATION TO
quate control of ventilation with the other medications. Arti- '
MILLIGRAMS/MILLILITER
ficial ventilation and possibly·endotracheal intubation are re-
quired after using succinylcholine. ' Percentage concentration x 10 = Number of mg/mL
6. Use advanced cardiac life-support measures as necessary to
support the cardiovascular system (more likely with local an- Examples: 0.25% bupivacaine has 2.5 mg bupivaca'ine/mL;
esthetics of increased potency, such as bupivacaine). 2% lidocaine has 20 mg lidocaine/mL.
 Chapter 3: Pain Reliefand Related Concerns in Children's Fractures 63

TABLE 3-16. PARENTAL OPIOID DOSING

SCHEDULE FOR ANALGESIA IN
CHILDREN*

IMt: Morphine, 0.1 ~0.15 mg/kg q 3-4 h

Meperidine, 1.0-1.5 mg/kg q 3-4 h

IV: Morphine, 0.05-0.1 rhg/kg. q 2 h

Meperidine, 0.5-1.0 mg/kg q 2 h

* Infants < 3 mo old should be dosed in increments of one third

to one half because of increased risk of respiratory depression.
t Intramuscular dosing should rarely be used.
Adapted from Roger, l.and Mora, M. Acute postoperative and
chronic pain in children. In Rasch, D.K. and Webster D.E. eds.:
Clinical manual of pediatric anesthesia. New York: McGraw-Hili,
1994:297, with permission,
FIGURE 3-3. Intravenous infusion for fluids, sedative medications, and
if necessary, resuscitative medications has been started in the contralat-
eral hand. A pulse oximeter probe is present on the patient's index
finger.

plexus blocks were developed, it was revived in 1963, when its

safe and successful use for the reduerion of forearm fracrures in 1. Confirm the immediate availability of a funerioning posi-
adults was reported (70). Since then, mulriple reporrs have ar- tive-pressure oxygen delivery system, as well as appropriate
rested to its usefulness in the rreatment of upper limb injuries airway management equipment (Table 3-5) (63). Also, con-
in adults and children (10,17,29,46,53,104,147). firm the immediare availability of medications for the rreat-
The mechanism of action is uncertain. It may involve borh ment of anesthetic-induced convulsions (Table 3-13).
direer transport of local anesthetic to major nerve trunks or rhe 2. Start an intravenous infusion in the contralateral arm (Fig.
blockade of small nerve endings (53). 3-3). A patent intravenous line is of paramount imporrance
Intravenous regional anesthesia is reliable, wirh a higher suc- in treating the complicarions of this block. Obtain a baseline
cess rate than other approaches to upper extremity blocks (53). ser of vital signs, including systolic and diastolic blood pres-
Orher advantages include its simplicity, rapidity of onset, and sure. Monitor pulse oximetry (Fig. 3-3) as well as the ECC
rapidity of recovery. Rapidity of recovery may be considered continuously (Fig. 3-4).
borh an advantage as well as a disadvantage, because, with local
anestheric alone, the analgesic effect is lost once rhe tourniquet
is deflated. A recent report in adulrs examined the addition of
rhe nonsteroidal antiinflammatory medication ketorolac (Tora-
dol) to the local anesthetic solurion for intravenous regional
anesrhesia and found thar patients did obtain prolonged analge-
sia after the tourniquer was released (124). However, no pediatric
studies have been performed on this drug combination.
Intravenous regional anesthesia is unsuitable for lesions above
rhe elbow (71). In addition, if the fracture involves the supracon-
dylar area of rhe humerus, the cuff may limit the degree of
hyperflexion needed to produce an adequate reduction. Intra-
venous regional anesthesia is contraindicared in patients with
underlying heart block, known hypersensitivity to local anes-
thetic agents, and seizure disorders (71). Although not tOtally
contraindicated, caution is urged when using rhis technique
in patients with underlying hemoglobinopathies such as sickle
cell disease.

•
\...~
AUTHOR'S PREFERRED METHOD
OF TREATMENT --
FIGURE 3-4. Continuous display of the electrocardiogram (top wave-
form) and continuous display of the plethysmographic tracing from
The basic steps involved in performing an intravenous regional the pulse oximeter (second line). Intermittent blood pressure reading
block are as follows: is displayed.
64 Genna/ I'rinicipLes

3. Selecr an appropriare rourniqueL An orrhopaedic rourni-

quet rhar can be fasrened securely should be used. Because
Velcro may become less adhesive wirh time, check the
tenacity of the rourniquet before use. As an added safety
measure, the rourniquet may be covered with strong adhe-
sive tape or an Ace bandage after application. The rourni-
quet should fully encircle rhe arm and overlap back on
itself by at least 6 cm (personal communication, K.E.
Wilkins, M.D.). The arm may be minimally padded
with cast padding underneath the rourniquet (17). If a
pneumatic rourniquet is used, the physician must be
familiar with the location of the rourniquet pressure gauge
(Fig. 3-5) (29) and valves, because these features may
vary in location from model ro model. Narrow-cuffed
double rourniquets may nOt effectively occlude arterial
Aow, and their use has been discouraged (71). Tourniquer
discomfon should not be a problem during shorr proce-
FIGURE 3-6. Venipuncture for administration of local anesthetic has
dures. If this problem develops, a second tourniquet can been performed with a butterfly needle. An intravenous catheter may
be applied distaUy over rhe anesrhetized area of the be more secure than a needle, which can become dislodged from within
arm. the vein.

4. Palpate rhe radial pulse of the injured limb.

5. Place and secure a shorr 22-gauge cannula in a vein on
rhe dorsum of the hand of the fracrured limb. A 23-gauge
burrerfly needle may also be used (Fig. 3-6). Note that al-
though ir may be possible ro "rhread" a butrerfly needle
securely into a large vein, burrerfly needJes may stiU slip our vein or even an antecubital vein can be used. However, the
of the vein more easily rhan a plastic intravenous catheter. use of proximaJ veins in the arm may result in a less effective
The author recommends the use of intravenous catheters block (71).
whenever possible. If a distal vein is unavailable, a proximal 6. Wirh the courniquer deflated, exsanguinate the limb by
vertically elevating it above the level of rhe hearr for 60
seconds.
7. Rapidly inflare the rourniquer to a pressure of 225 to 250
mm Hg or 150 mm Hg above rhe patienr's syscolic blood
pressure (51). Check for disappearance of the radial pulse.
Cross-clamping rhe tubing of the cuff after inflation is dis-
couraged (71), because it might prevent detection of a smaJ I
leak. Constant observation of the cuff pressure gauge is rec-
ommended.
8. Lower the extremity and slowly inject the local anesrhetic.
It is recommended that this injection be done over a
period of 60 seconds. A concenrration of 0.5% plain
lidocaine (5 mg/mL) is used (Fig. 3-7). Bupivacaine is
contraindicared for rhis block because of irs cardiocoxicity.
To prevent thrombophlebitis, the local anesthetic solution
must be free of any additives or preservatives (71). In
different studies, the recommended dose of lidocaine has
varied from 1.5 co 3.0 mg/kg 00,17,29,46,53,104,147).
A dose of 1.5 mg/kg appears to bc safc and effecrive,
and may produce a decreased incidence of complications
(17). One srudy has recommended a maximum lidocaine
dose of 100 mg for this block (46). The skin of the
extremity becomes motrled as the drug is injected. The
patienr, unless he or she is very sedated, and the parents,
if they are watching, should be warned that rhe extremity
will look and feel scrangely (personal communicarion,
FIGURE 3-5. Tourniquet controls may vary in position from model to K.E. Wilkins, M.D.). Analgesia and muscle relaxarion
model. It is imperative for the practitioner to be aware of the function
of each of the controls to avoid accidental premature deflation of the develop within 5 minures of injection (71). Note that
tourniquet. for fractures ar the wrist, placement of a regular penrose
 Chapter 3: Pain Reliefand Related Concerns in Children's Fractures 65

FIGURE 3-9. Hematoma block performed with the last 2 mL of the

intravenous lidocaine solution to enhance analgesia at the fracture site.
FIGURE 3-7. Preservative-free 0.5% lidocaine without epinephrine for
intravenous regional anesthesia.

12. Release the cuff at the end of the operation, or at the

end of a 15-minute interval, whichever is longer. Cuff
deflation, followed by immediate reinflation, as a method
of delaying systemic absorption of local anesthetic is im-
drain tourniquet around the distal forearm may improve
practical because it cannot be done rapidly enough to
distribution of the local anesthetic solution at the fr~crure
prevent significant entry of local anesthetic into the general
site (Fig. 3-8) (personal communication, K.E. Wilkins,
circulation (71).
M.D.).
13. Monitor the patient closely for at least 15 minutes for any
9. To improve analgesia for fracture redunion, the last 2 mL
complications related to the block. The treatment of local
of local anesthetic solution may be injected directly into
the fracture hematoma (Fig. 3-9) (personal communication,
K.E. Wilkins, M.D.). The technique of local infiltration
anesthesia, or hematoma block, is discussed further in a
subsequent section of this chapter.
10. Perform the surgical procedure (Fig. 3-10).
11. Leave the cuff inflated for at least 15 minutes (71), even if
the surgical procedure takes less time.

FIGURE 3-8. Penrose drain tourniquet on the forearm to improve dis- FIGURE 3-10. Fracture reduction under appropriately monitored seda-
tribution of local anesthetic at the fracture site. tion and intravenous regional anesthesia.
66 General Priniciple.f

anesthetic-induced systemic toxiciry has been discussed

(Table 3-13).
] 4. Ofcourse, depending on whatever sedation has been admin-
istered, the patient should be monitOred until discharge cri-
teria are met (Table 3-1)
An assistant must be presem to watch the patient, the tOurni-
quet, and the monitOrs at all times.

Local Infiltration Anesthesia: Hematoma

Blod{
HematOma block has been successfully used in the treatment of
distal forearm fractures (27,94). This simple technique involves
injecting local anesthetic intO the fracture hematOma, the loca-
tion of which is confirmed by aspirating blood into the syringe
(Fig. 3-9). When done alone, 1% lidocaine in a dose of] to 2
mg/kg is used (94). As indicated earlier, when combined with
a Bier block, the last I to 2 mL of local anesthetic solution
are used. Although the medication is rapidly absorbed imo the
circulation, the resulting systemic blood levels of 10caJ anesthetic
are well below those required for eNS tOxiciry (94). Hematoma
blocks may be used in patients who have received a regional
block yet still have residual pain at the fracture site.
AJioto and co-workers (4) have described the use of an inuaar-
tiCLdar hematOma block for the manipulative reduction of ankle
fractures in a popuJation group that included both children and
adults. The youngest patient in their study group who received
a hematOma block was 12 years old. The technique they describe
consisted of a direct injection of 2% lidocaine 1 mg/kg (the
amhors used 2 mg lidocaine per pound) intO the tibiotalar joim
space. Absolute sterile technique was used, with the skin overly-
ing the fracture site being prepared with a povodine-iodine
preparation. A 22- or 25-gauge needle was used for the injection
of the local anesthetic solution. The authors of this investigation
recommend directing the needle in a slightly cephalad direction
to avoid injury to the talar and tibial articLilar surfaces. Aspiration
of blood was used to confirm ently into the intraarricular space.
The injection was performed only if no resistance was encoun-
tered. A minimum of ] 5 minutes was aJlowed to pass after the
injection, during which time the patient was closely obstl"ved
and monitOred for any evidence of local anesthetic systemic tOx-
iciry (see earliet). The injection was considered adequate if the
patient was subsequently able to elevate the injured limb off the
bed withom assistance and petfotm active ankle dorsiflexion
and plantarflexion. The authors of this investigation found the
intraarricular ankle hematOma block to be safe, effective, and
well tOlerated by patients (4). Although some of their patiems
tolerated the injection and the subsequent fracture reduction
without the use of any other supplementaJ analgesics or sedatives,
most children would probably require the same rype of sedation
that would be used before performing a Bier block or a hema-
tOma block of the upper extremiry. FIGURE 3-11. Barbotage. When performing a hematoma block, the
local anesthetic is given by barbotage. A: Half the anesthetic is injected
in the hematoma. B: The blood from the hematoma is withdrawn until
• AUTHOR'S PREFERRED METHOD the original volume is regained. C: This mixed material is repeatedly
\..~~ OF TREATMENT injected and reaspirated until the anesthetic is dispersed in the hema-
toma. The final aspirate should contain a volume equal to the original
anesthetic. Thus, the final volume of fluid in the hematoma has not
Full aseptic technique, including adequate skin preparation and been increased.
the use of sterile gloves, is recommended. The incidence ofinfec-
 Chapter 3: fain ReLie/and ReLated Concerm ill Children's FraCtures 67

cial in order to minimize side effects from anyone particular

approach (e.g., the use of NSA1DS to decrease the incidence of
nausea, vomiting, or even respiratory depression from opioids).
The end point is to make patients comfortable while minimizing
adverse reaC[ions.

Postoperative Analgesia With Opioids

Opioids have long been the mainstay of postoperative analgesia.
It is important for the practitioner to understand the rationale
Medial Lateral behind different dosage regimens to maximize pain relief for the
FIGURE 3-12. Section of right thigh immediately below the inguinal patient.
ligament, showing femoral nerve under cover of fascia iliaca and its
block by a barrage technique. (Reproduced with permission from Anes-
thesia, 1977, Volume 32, page 577. Analgesia in Patients with Fractured
Shaft of Femur. F.R. Berry, M.D.) Intermittent Dosing
AJthough commonly used, traditional intermittent as-needed
dosing of intramuscular and intravenous opioids (Table 3-17)
makes little pharmacologic sense for control of severe pain (49,
tion from introduction of a needle into the hematoma is greatly 148). Wide variations in plasma opioid levels occur, leading to
decreased if antiseptic precautions are taken (75). The hematoma periods of sedation alternaring with prolonged periods of no
is localized by aspirating blood into the syringe. The local anes- pain relief at all (49). In addition, for pediatric care, intramuscu-
thetic solution is given gradually by alternate injection (barbo- lar dosing is a particularly poor choice (148), because children
tage) of a small amount of medication and withdrawal of a small often chose to hide their pain rather than risk having to undergo
amount of hematoma until all of the medication has been given an injection. The end result with intermittent dosing, especially
(Fig. 3-11). In the case of the intraarticular hematoma block at
the ankle (4), a slow direct injection is used, with careful ECC
monitoring for any evidence of dysrhyrhmias.
Reported complications with hematoma blocks in the upper
extremiry include compartment syndrome (162), temporary pa- TABLE 3-17. PATIENT·CONTROLLED
ralysis of the anterior interosseous nerve (162), and increased ANALGESIA IN CHILDREN
incidence of carpal tunnel syndrome (84).
Loading dose: Morphine, 0.025-0.05 mg/kg
Maintenance dose: Morphine, 0,01-0.02 mg/kg
Lockout interval: 6-10 min
Femoral Nerve Block 4-hr maximum: Morphine, 0.4 mg/kg/4 h
Treatment of Side Effects
Berty (14) has described a technique of rapid analgesia for pa-
Pruritus
tients with a fracture of the femoral shaft using 1 % lidocaine Diphenhydramine (0.5 mg/kg IV) OR
with 200,000 epinephrine or 1.5% lidocaine with 1: 200,000 Low-dosenaloxone (0.5-1.0 ,ug/hr)
epinephrine deposited at the femoral nerve, just below the ingui- Nausea/vomiting
nal ligament (Fig. 3-12). As always, the anesthetic dose should Metoclophramide (0.1 mg/kg IV) OR
Droperidol (10-30 ,ug/kg IV or 1M) OR
remain within accepted limits. For lidocaine with epinephrine, Ondansetron (0.15 mg/kg IV over 15 min)
7 mg/kg is the permissible dose limit. Low-dose naloxone as for pruritus
Cooperation and tolerance among young children for re- Urinary retention «1 mUkg/h in the face of adequate fluidin-
gional blocks varies, so careful patient selection is advised. take)
Low-dose naloxone infusion as above
Respiratory depression
Vital signs: specify parameters that require treatment and
method for contracting responsible physician.
POSTOPERATIVE ANALGESIA IN THE Stop PCA pump.
CHILD WITH A MUSCULOSKEL TAL Give 100% oxygen and maintain the airway.
Give naloxone (1-5 I.£g/kg IV bolus). Repeat as needed.
INJURY Consider naloxone infusion (3-5 ,ug/kg/h).

Safe and effective postoperative analgesia in children with mus-

Rogers J, Moro M. Acute postoperative and chronic pain in
culoskeletal injuries can be accomplished with opioids, nonste- children. In. Rasch ORe and Webster DE, eds. Clinical manual of
roidal antiinflammatory agents (NSAlDS), or local anesthetic pediatric anesthesia. New York, McGraw-hili, 1994:298, with
permission.
agents.
Simultaneous use of more than one modaliry may be bendi-
68 General Priniciples

with imramuscular narcotics, is unnecessalY undertreatment of individuals, alrhough careful assessment of each individual situa-
paIn. tion is required.
When compared with tradirional inrermittent dosing, im-
proved pain conn'oJ and greater parient satisfaction have been
Patient-Controlled Analgesia demonstrated (J 1). Note that further improvement in pain relief
Patient-controlled analgesia (PCA) is a sensible approach ro the may be achieved with rhe addition of a continuous background
problems inherent with imermirrent as-needed dosing of opioids in fusion of opioids to maintain the plasma concentrations of
(49). With PCA, intravenous self-ritration of small doses of the analgesic during sleep. However, adding a background infu-
opioids ar frequent intervals eliminates rhe wide variations in sion may increase the risk of opioid-associated nausea, sedation,
plasma drug levels seen with imermirrent dosing (49). It also and hypoxemia (39,159).
aJlows patients to gain control over their pain managemem (23), Conceivably, for younger chi Idren or for chiJdren othelwise
which may be of psychological importance to the parimt's well- unreJiably capable of pushing rhe button on the PCA cord, "par-
being. em-controlled analgesia" may be useful. The author has used
PCA was first evaluated in adolescents in 1987, after several this approach in a patient as young as 1 1/2 years of age. In this
years of successful use in adulrs (23). Since then, this modality particular situation, however, the parents were very motivated
has been used for children as young as 6 years of age (11). and inrelligent, and had done this before for their child after
Depending on rhe intelligence and cooperative ability of rbe another surgical procedure. In general, PCA is safest when only
child, it is conceivable that PCA could be used for younger the patient is opel'ating the device.

TABLE 3-18. DOSING SCHEDULES AND FORMULATIONS FOR ORAL OPIOIDS IN CHILDREN

Agent Dose Pediatric Formulations·

Codeinet 0.5-1.0 mg/kg q 4 to 6 h (max. single dose, 15 mg/5 mL oral solution

60 mg)
Codeine with acetaminophen (Tyl,enol with 0.5-1.0 mg/kg codeine q 4 to 6 h + 10-15 12. mg codeine + 120 mg acetaminophen/5
Codeine, Phenaphen with Codeine, mg/kg acetaminophen q 4 to 6 h mL solution
Capital with Codeine) Tylenol (300 mg) + Codeine tablets #1: 7.5
mg, #2: 15 mg, #3: 30 mg, #4: 60 mg
Hydrocodone with acetaminophen (Lortab, Adult dose: hydrocodone 5-10 mg q 4 to 6 2.5 mg hydrocodone/5 mL +
Anexsia, .Co-Gesic, DuoCet, Hy-Phen, h. acetaminophen 120 mg/5 mL (Lortab
Vicodin) Children (only antitussive dose is Liquid)
published): 0.6 mg/kg day divided in
three to four doses/day.
<2 yr: Do not exceed 1.25 mg/dose.
2-12 yr: Do notexceed 5 mg/single dose.
>12 yr: Do not exceed 10 mg/single dose.
Meperidine .(Meperidine HCI, Demerol HCI)t 1.1-1.8 mg/kg q 3 to 4 h 50 mg meperidine/5mL solution
Max. single dose 100 mg
Morphine (morphine sulfate, Raxanol)t 0.2-0.4 mg/kg q 4 h (Adult dose is 10-30 10 10 mU5 mL and 20 mg/5mL solution
mg q 4 h) Absorption from the GI tract is
variable.
Hydromorphone (Dilaudid, Hydromorphone Optimum pediatric dosage for analgesia 5 mg hydromorphone/5 mL solution
HCI)t not established.
Antitussive dose is:
6-12 yr: 0.5 mg q 3-4 h
> 12 yr: 1 mg q 3-4 h
Oxycodoneand Aspirin:j: (Percodan-Demi)t§ 6-12 yr: ~ tablet q 6 h Oxycodone§ + 325 mg aspirin
>12 yr. ~ tablet q 6 h

* This table does not provide an exhaustive list of all available oral opioids and oral opioid/nonsteroidal anti·inflammatory drug combinations. A
complete discussion and complete lists of all respective formulations may be found in AHFS Drug Information '94.
t Denotes a schedule I drug, for which a triplicate prescription is required.
:j: Owing to an assoCiation with Reye's syndrome, medications containing aspirin should be expressly avoided in children with flulike symptoms or
children with chickenpox.
§ Percodan-Demi contains 2.25 mg oxycodone hydrochloride and 0.19 mg oxycodone terephthalate + 325 mg aspirin;
Adapted from Opiate Agonists. In McEvoy CK, Litvak K, WeishOH, Jr, eds. AHFS Drug Information '94. Bethesda, MD American Society of HospitaJ
Pharmacists; 1994; Taketomo, C.K., Hodding JHJ, Kraus, OM: Pediatric dosage handbook, 2nd ed. Hudson, OH. Lexi-Comp, 1993: Ragers J., and Moro,
M.: Acute Postoperative and Chronic Pain in Children. In Rasch, DK, Webster DE (eds.): Clinical Manual of Pediatric Anesthesia. New York: McGraw-
Hill, 1994, with permission.
 Chaptel' 3: Pain Reliefand ReLated Concerm in Children 5 Fractures 69

Parameters that musr be considered are the loading dose, the based on patient response. The use ofNSAIDS (see the following
maintenance dose, and the lockout intervaJ (the period during seccion) as parr of the anaJgesic regimen may be helpful in reduc-
which no further adminisrration of medication will occur despite ing or eliminating rroublesome opioid-related side effects.
attempts ro do so by the patient), and the 4-hour maximum
dose (Table 3-18). For PCA, morphine is more effective than
Other Modes of Opioid Administration
meperidine (J 51). Opioids orher than morphine should be used
only for patients aJlergic ro morphine (20), or for whom mor- EpiduraJ opioids are being used in children after major surgelY
phine produces inrolerable side effecrs. Whenever possible, rhe with excellent results (112). The author encourages close cooper-
persistent use of one medication helps avoid dosing errors (20). ation between surgeons and anesthesiologists ro avail children
The use of rhe PCA pump should be explained ro patients of this modaliry of analgesia whenever feasible.
preoperatively. Effective use of a loading dose will avoid the
problem of having ro play catch-up with out-of-control levels
Postoperative Analgesia With Nonsteroidal
of pain.
Antiinflammatory Drugs
Mishaps have occurred with PCA pumps due to program-
ming errors (156), so ward personnel must be (Otally familiar NSAIDs have moderately good analgesic properties (148). Un-
with the equipment. Treatment of opioid-re1ated side effects is like opioids, which produce analgesia by effects on CNS recep-
outlined in Table 3-18. tors, NSAIDs act peripherally by inhibiting prostaglandin syn-
thesis and decreasing inflammation (137,152). Inflammarory
mechanisms play an important parr in the pathogenesis of post-
Oral Administration of Opioids
operative pain (148), and therefore, the use of NSAIDs maJ<es
Oral dosing of opioids is exrremely useful for the continued good sense in the postoperative setting. AJso, aJthough NSAIDs
managemenc of diminishing posroperacive pain, once oral anal- have some rroubling side effeccs of their own, they do not pro-
gesics are rolerated. SeveraJ oraJ analgesics are available, and their duce respirarolY depression, nausea, and vomiting, which are
appropriate use is summarized in Table 3-19. None of these some of the bothersome features ofopioids. Thus, using NSAIDs
medications is devoid of side effects, including mood changes, either as an adjunct or as a substitute for opioids where feasible
nausea, vomiting, constipation, dizziness, and prurirus. The oc- should decrease or eliminate the possibiliry of drug-induced nau-
currence and degree of side effecrs vary from patient ro patient, sea, vomiting, or respirarory depression in the surgical patient
so the physician should be prepared ro change dosing regimens (148).

TABLE 3-19. DOSING SCHEDULES AND FORMULATIONS FOR NSAIDS IN CHILDREN

Agent Dose Formulations *

Ibuprofen (oral) 5-10 mg/kg q 6 h (published dose is for treatment of 100 mg/5 mL suspension
fever, not specifically for analgesia) Tablets: 200, 300,400,600,800 mg
Naproxen (oral) 5-7.5 mg/kg q 12 h 125 mg/5 mL suspension
Tablets: 250, 375, 500 mg
Ketorolac (1M, IV) 0.5 mg/kg q 6 h Injectable 30 mg/mL
Choline Magnesium 50 mg/kg/day 500 mg salicylate/5 mL solution
Trisalicylate (Trilisate) (oral}t Divided into 2 or 3 doses (maximum daily dose, 2.25 g) Tabl.ets: 500, 750, ;000 mg
Salsalatelf (oral) (Disalcid) Pediatric dose not published; adult maintenance dose is Tablets: 500, 750 mg
2-4 g/day. .
Acetaminophen:!: (oral, rectal} 10-15 mg/kg q 4-6 h 80 mg/0.8 mL drops
80 mg chewable tablets
160 mg/5 mL solution
325, 500 mg-tablets
120-, 325-, 650-mg suppositories

* An exhaustive listing of available formulations for NSAIDs may be found in AHFS Drug Information '94.
t Although they are salicylates, choline magnesium trisalicylate and salsalate do not crossreact with aspirin and may be used in patients allergic to
aspirin.As many as 28% of children with asthma may be in this group of patients. Owing to an association with Reye's syndrome, saficylates should
be avoided in children with. flu-Uke symptoms or chickenpox.
* Acetaminophen is considered a member of this class of medications, even though it mainly acts centrally and it only very weakly inhibits
prostaglandin synthesis. Acetaminophen also does not crossreact with aspirin and may be used in patients allergic to aspirin.
(Adapted from Nonsteroidal Anti-Inflammatory Agents. In McEvoy, GK, Litvak, K, and Welsh, OH, Jr. eds. AHFS Drug Information '94. aethesda, MD:
American Society of Hospital Pharmacists, 1994; Walson, P.O., and Mortensen, M.E.: Pharmacokinetics of common analgesiCS, anti-inflammatori.es
and antipyretics in children. Clin Pharmacokinet 17:116-137,1989, with permission.
70 General Priniciplej

Potential side effects of this class of drugs include platelet

TABLE 3-20. PHARMACOLOGIC APPROACH TO
dysfunction, gastritis, and acute renal dysfunction (93,152). A
POSTOPERATIVE NAUSEA *
history of sensitivity to aspirin or a history of nasal polyps may
be associated with potentially fatal cross-sensitiviry to other Agent Dosage Route
NSAIDs (1,137). In children with asthma, the prevalence of
Promethazine 0.25-0.5 mg/kg IV or per rectum
aspirin sensitivity may be as high as 28% OIl). Therefore, asth- (Phenergan)
matic children should probably receive only those NSAIDs that Metoclopramide 0.1 mg/kg (maximum IV
do not cross-react with aspirin. These medications include acet- (Regian) dose, 5 mg)
aminophen, salsalate (Disalcid), and choline magnesium trisali- Ondansetron 0.15 mg/kg (maximum IV
(Zofran) dose, 4 mg)
eylate (Trilisate) (30) (Table 3-19).
In a child with a chronic underlying bleeding disorder,
* Additional helpful measures include ensuring adequate IV
NSAIDs are not necessarily contraindicated. Consultation with hydration, avoiding forced oral fluids until the patient is hungry,
the child's hematologist is advised regarding the use of specific and avoiding forced early ambulatien, especially when opioids are
given for pain relief.
medications in this class.
Ketorolac, unlike other NSAIDs, can be administered not
only orally but also intravenously and intramuscularly. A loading
dose of 1.0 mg!kg may provide similar analgesia as 0.1 mgt
kg of morphine (90). The pharmacology of ketorolac has been
extensively reviewed (86), and both its mode of action and
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