Skeletal Atlas of Child Abuse

Springer’s Forensic Laboratory Science Series

Series Editor Ashraf Mozayani, Ph.D.

For further volumes: http://www.springer.com/series/8401 wwwww Skeletal Atlas of Child Abuse

Jennifer C. Love, PhD Forensic Anthropology Director Forensic Anthropology Division Harris County Institute of Forensic Sciences Houston, Texas

Sharon M. Derrick, PhD Agency Coordinator/Forensic Anthropologist Forensic Anthropology Division Harris County Institute of Forensic Sciences Houston, Texas

Jason M. Wiersema, PhD Forensic Anthropologist/Disaster Preparedness Coordinator Forensic Anthropology Division Harris County Institute of Forensic Sciences Houston, Texas Jennifer C. Love Sharon M. Derrick Forensic Anthropology Director Agency Coordinator/Forensic Anthropologist Forensic Anthropology Division Forensic Anthropology Division Harris County Institute of Forensic Sciences Harris County Institute of Forensic Sciences Houston, Texas Houston, Texas [email protected] [email protected]

Jason M. Wiersema Forensic Anthropologist/Disaster Preparedness Coordinator Forensic Anthropology Division Harris County Institute of Forensic Sciences Houston, Texas [email protected]

ISSN 2157-0353 e-ISSN 2157-0361 ISBN 978-1-61779-215-1 e-ISBN 978-1-61779-216-8 DOI 10.1007/978-1-61779-216-8 Springer New York Dordrecht Heidelberg London

Library of Congress Control Number: 2011931280

© Springer Science+Business Media, LLC 2011 All rights reserved. This work may not be translated or copied in whole or in part without the written permission of the publisher (Humana Press, c/o Springer Science+Business Media, LLC, 233 Spring Street, New York, NY 10013, USA), except for brief excerpts in connection with reviews or scholarly analysis. Use in connection with any form of information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed is forbidden. The use in this publication of trade names, trademarks, service marks, and similar terms, even if they are not identified as such, is not to be taken as an expression of opinion as to whether or not they are subject to proprietary rights.

Printed on acid-free paper

Humana Press is part of Springer Science+Business Media (www.springer.com) Dedication

We dedicate this atlas to our spouses, whose support enabled us to be successful in this endeavor. Dalford D. Owens, Jr. – JCL Elbert D. Derrick, III – SMD Alanna E. Koos – JMW wwwww Foreword

Child abuse investigation is one of the most contentious areas of forensic pathology. The forensic pathologist must determine, within a reasonable degree of medical certainty, the cause and manner of death. This opinion must be rendered with a comprehensive knowledge of the case – a knowledge that includes the medical history, scene findings, police investigation, history of terminal events, and a complete autopsy. The autopsy is one component of the overall investigation, and it is imperative that all injuries be thoroughly documented. Although other pathologists may offer alternative opinions regarding the mechanism of injury, or even the cause of death, the actual anatomic findings should never be in question. The collaborative approach taken at the Harris County Institute of Forensic Sciences (HCIFS) reflects this philosophy. The team of forensic anthropologists who work within the office and alongside the pathologists is immeasurably important in completing the requisite documentation. In our experience, anthropologists bring to the autopsy table another dimension of knowledge that is rarely tapped in the medical examiner setting. In this collaborative setting, suspected child abuse deaths are first examined by a forensic pathologist, with complete documentation of soft tissue injuries including visceral injuries, neuropathology, and examination of subcutaneous tissues. A forensic anthropologist is then brought in with the pathologist to take the examination another step, exposing all skeletal elements. The need for additional studies of the exposed elements (including histology and further anthropologic processing) is determined at that time. In this approach, the traditional role of the forensic anthropologist (examination of skeletal remains) is greatly expanded while keeping within the scope of his or her expertise. The value of the collaborative approach between forensic pathologists and anthropologists is perhaps best illustrated by the numerous examples of classic metaphyseal lesions presented in this text. These lesions are difficult – and sometimes impossible – to identify radiographically. They must be sought at autopsy. Only with careful analysis of many cases using the approach described in this text (including abusive injuries, accidental injuries, and deaths from disease) will the true incidence, mechanism, and healing process of these injuries be appreciated. Skeletal Atlas of Child Abuse is an illustrated guide to anthropologists’ role in investigating child abuse. The book offers a fairly comprehensive literature review of injuries within each body region or skeletal element and then illustrates injuries using real case examples. The literature review is presented in a nonbiased manner. The authors walk the reader through published data regarding the mechanics of injuries and the interpretation of injuries, including what the injuries may imply regarding mechanism. Also included is a review of literature that describes limitations of interpretation of a particular injury as being inflicted or accidental. The case examples are provided to demonstrate for the reader effective ways of viewing and then photographically documenting in situ examples of skeletal injuries as well as examples of processed skeletal elements. The abundance of in situ photographs sets this volume apart from the typical anthropology text, and this reflects the close collaboration between pathologists and anthropologists in the HCIFS. Information provided with each case example includes the mechanism of injury, if that can be determined, and describes limitations of interpretation. Information regarding the cause and manner of death is provided for many of the cases, but this determination is not the intent of the illustrations or the thrust of the book. A chapter on natural disease conditions affecting the bones provides a good overview of several conditions that often are invoked as “mimics” of child abuse. This is a good starting point and will be of value to forensic pathologists and anthropologists, as these conditions frequently are suggested as explanations for unexplained injuries in abuse cases. Although isolated skeletal findings may well suggest one of these natural disease processes, differential diagnosis involves analysis of the entire case, including not only anatomic findings, but history – a history including the terminal events, the complete medical history, and birth history in some cases. The pathologist, working in tandem with the anthropologist and investigative personnel, must consider all facets of the case to arrive at a proper cause and manner of death determination and to opine regarding antemortem treatment of the child. This book will serve as a valuable reference for practicing anthropologists, pathologists, and possibly radiologists in recognition of skeletal trauma. Although Skeletal Atlas of Child Abuse focuses on pediatric trauma, much of the information within the text and photographs of this volume is applicable to the analysis of skeletal trauma in general. Additionally, this photographic atlas of bone injury and pathology creates a comprehensive instructional resource for the forensic course classroom or for postgraduate training in the medical examiner office setting.

vii Perhaps the biggest contribution of this book is an implicit statement: forensic anthropology is a science that is most valuable when practiced as an integral component of the autopsy process, rather than a separate discipline unassociated with examination of the “soft tissue.” Examination of skeletal elements in situ as amply illustrated here, preferably in collaboration with the pathologist, allows both disciplines to arrive at a reasoned evaluation of each injury and, hence, of the total case. Forensic pathologists who have come to view anthropologists in their traditional role of analysis of skeletal remains will find this an eye-opening approach. Dwayne A. Wolf, MD, PhD Deputy Chief Medical Examiner Harris County Institute of Forensic Sciences

viii Preface

The Centers for Disease Control and Prevention (CDC) defines child maltreatment as “any act or series of acts of commis- sion or omission by a parent or other caregiver (e.g., clergy, coach, teacher) that results in harm, potential for, or threat of harm to a child.” The CDC further identifies four common types of abuse: physical, sexual, and emotional abuse, and neglect. The 2008 Child Maltreatment report by the US Department of Health and Human Services states that the fatality rate among abused and neglected children is 2.3 per 100,000 children. Eighty percent of the deaths occur in children younger than 3 years. Physical abuse accounts for 22.9% of all child maltreatment fatalities. Despite the frequency of child fatalities attributed to physical abuse, the recognition of child abuse is challenging in the forensic setting. Signatures of nonaccidental injury may be subtle and differentiating accidental from nonaccidental injury difficult. Yet, successful adjudication of a child abuse case often depends on comprehensive documentation of injury, including recognition, documentation, and interpretation of skeletal injury. The goal of this volume is not to showcase all skeletal injury observed in children, but to illustrate common skeletal findings in child abuse fatalities investigated by a medical examiner’s office serving a large urban area. The Harris County Institute of Forensic Sciences (HCIFS) serves a population of approximately 4 million. In 2009, HCIFS certified 4,153 deaths, 3,383 of which required an autopsy. Infants and toddlers (ages birth to 4 years) accounted for 204 of these deaths; 31 were classified as homicide, 59 as natural, 48 as accident, and 66 as undetermined. In 2006, the HCIFS Forensic Anthropology Division was formed with the primary responsibility of providing expertise in skeletal analysis at the request of the medical examiner. The Texas Code of Criminal Procedures permits the involvement of a forensic anthropologist in the attempt to establish the cause and manner of death. Furthermore, under the Texas statute, the autopsy must include the retention of body fluid samples, tissues (including bone), and organs to ascertain the cause of death or whether a crime was committed. During the past 4 years, the HCIFS anthropologists have consulted on 75 cases of suspected child abuse. Typically, a consultation involves a full skeletal examination and the retention of the skeletal element(s) of known or suspected trauma for a complete anthropologic analysis (see Chap. 1). Per protocol, all elements are photographed after processing to document the trauma and the condition of the bone. The photographs taken following standard operational procedure during daily casework are shown in this volume. Also included are photographs of skeletal elements in situ during the autopsy. The purpose of the autopsy photographs is to provide the readers with examples of the trauma when first recognized. The skeletal injuries most commonly encountered from our examination of child abuse fatalities were the impetus for this volume. The text accompanying the images summarizes the current literature explaining the mechanism of each injury. Additionally, skeletal development, most notably of the skull, is included to assist new practitioners with the differentiation of normal developmental features from trauma. The goal of Chap. 7 was not to generate a compendium of infant and childhood conditions that affect the quality of bone, but to familiarize the reader with a few disorders that have been described as possible mimics of child abuse in the literature. Most of the diseases described are rare, and we have no direct experience investigating child fatalities associated with them. However, we feel a basic understanding of these conditions is necessary to adequately analyze skeletal lesions in infants and children and to offer effective testimony in child abuse cases. A forensic anthropology division is relatively rare among medical examiner offices in the United States. Even rarer is the involvement of forensic anthropologists in nondecomposed child abuse cases, such as is the practice of the HCIFS. The numerous child abuse cases investigated by the HCIFS and the strong collaboration between the medical examiners and the forensic anthropologists have led to a large collection of skeletal injury photographs. Given the unique opportunity to analyze a substantial amount of nonaccidental trauma, we feel we have amassed a valuable resource for the medicolegal field and have attempted to share this resource here.

Jennifer C. Love, PhD Sharon M. Derrick, PhD Jason M. Wiersema, PhD

ix wwwww Acknowledgments

This atlas is the result of support from many individuals who generously shared their knowledge and talents, and we are grateful for them. First, we thank Dr. Luis A. Sanchez, Chief Medical Examiner of Harris County Institute of Forensic Sciences (HCIFS). Dr. Sanchez envisioned the HCIFS Forensic Anthropology Division and worked diligently to gain the support of the commissioners of Harris County. Once the division was established, he provided the resources necessary to build a successful laboratory and created an environment in which training, teaching, research, and publication are encouraged. His vision brought the three of us together, enabling us to collaborate on this project. We thank Dr. Dwayne A. Wolf, Deputy Chief Medical Examiner, for securing this atlas within the field of the forensic pathology through his foreword. We also extend our gratitude to Dr. Wolf’s staff of Assistant Deputy Chief and Assistant Medical Examiners. These individuals of the HCIFS Forensic Pathology Division entrusted us with the cases for which they were ultimately responsible and put their confidence in our methods and analysis, although they were initially novel to them. These individuals are: Roger A. Mitchell, Jr., MD Stephen K. Wilson, MD Roger P. Milton, Jr., MD Morna L. Gonsoulin, MD Ana E. Lopez, MD Mary L. Anzalone, MD Albert Y. Chu, MD Kathryn Haden-Pinneri, MD Sara N. Doyle, MD Marissa Feeney, MD Merrill O. Hines III, MD Darshan R. Phatak, MD Pramod Gumpeni, MD Luisa F. Florez, MD Michael Condron, MD We are indebted to Dustin Hatfield, Andre Santos, Desmond Bostick, Erica Schacht, Olyn Taylor, and Fran Daher, who are or were members of the HCIFS Forensic Imaging Division. The quality of the images within this atlas is a direct result of their talents. We specifically acknowledge Desmond Bostick, who patiently retook several of the photographs in a studio setting and then digitally perfected the images. His enthusiasm for the project and striving for perfection were heartening. Furthermore, Dustin Hatfield reviewed the images, tweaking several to ensure they were of adequate quality for publication. We also mention K. Diane Logan, HCIFS Morgue Director, and her staff of autopsy assistants. The morgue staff supported us in many ways, including retaking radiographs and assisting during the skeletal examinations. A special mention of Dr. Deborrah C. Pinto is imperative. Dr. Pinto served as our Forensic Anthropology Fellow during the final phase of this manuscript. She took on the lion’s share of the casework, enabling us to focus on the project. Without Dr. Pinto’s willingness, enthusiasm, and ability to process the incoming casework, this atlas would have been significantly delayed in completion. Finally, we thank the following professors and mentors who shared their knowledge and casework and showed great patience as we learned how to identify, analyze, and interpret nonaccidental trauma in children: Murray K. Marks, PhD – JCL Steven A. Symes, PhD – JCL, JMW D. Gentry Steele, PhD – SMD, JMW Lori Wright, PhD – JMW, SMD David Glassman, PhD – JMW, SMD Turhon Murad, PhD – JMW P. Willey, PhD – JMW

Jennifer C. Love, PhD Sharon M. Derrick, PhD Jason M. Wiersema, PhD

xi wwwww Contents

Chapter 1 Skeletal Examination Method ...... 1

Chapter 2 Skull Fractures ...... 9

Chapter 3 Rib Fractures ...... 39

Chapter 4 Fractures of the Vertebral Column, Sternum, Scapulae, and Clavicles ...... 57

Chapter 5 Long Bone Fractures ...... 69

Chapter 6 Healing and Interpretation ...... 85

Chapter 7 Natural Disease May Mimic Child Abuse ...... 103 Index ...... 117

xiii wwwwwwwwwwwww Skeletal Examination 1 Method Critical to the appropriate interpretation of possible child abuse is consistent and complete documentation of skeletal injury by all practitioners, including radiologists, clinicians, pathologists, and anthropologists [1, 2]. Complete documentation of skeletal injury by anthropologists requires a standardized method for evaluating the entire skeleton in any case in which injury is suspected. The authors employ a method referred to as skeletal examination to evaluate infants and children with medical histories and/or soft tissue injuries suspicious for inflicted trauma. Skeletal examination involves first incising and reflecting the skeletal muscle and periosteum overlying all long bones, scapulae, and ribs to facilitate detailed inspection for traumatic injury in situ, then removing and chemically processing elements with suspected trauma to generate a comprehensive interpretation of the injury. This method is intended to identify occult fractures typically not recognized during standard radiograph surveys or autopsy by providing greater visibility of the appendicular and axial skeleton [3].

Radiographic Examination

The skeletal examination is preceded by the acquisition of a complete set of skeletal radiographs that clearly illustrate the shafts and articular ends of each of the long bones and ribs, as well as the skull. The radiograph views should include anterior-to-posterior and lateral views of the skull; anterior-to-posterior and oblique (from both sides) views of the chest and abdomen; overall anterior-to-posterior views of the extremities taken in anatomic position, thus avoiding the crossing of long bones and obscuring the underlying bone surfaces; and images of each joint taken with a collimated beam. The anthropologist reviews these radiographs as the initial avenue to identify possible fractures, but the radiographs also represent an additional image-based record of the bones and fractures in their anatomic locations (Figs. 1.1–1.3).

J.C. Love et al., Skeletal Atlas of Child Abuse, Springer’s Forensic Laboratory Science Series, 1 DOI 10.1007/978-1-61779-216-8_1, © Springer Science+Business Media, LLC 2011 Fi g u r e 1-2. Close-up radiograph of the wrist and hand of a 5-month-old male. Typically, close-up joint radiographs are taken with a collimated beam to reduce X-ray scatter and to Fi g u r e 1-1. Negative anterior-to-posterior chest radiograph facilitate inspection of bones prior to skeletal examination. showing skeletal elements of the thorax and abdomen of a 5-month-old male. The cause of death was classified as drown- ing and the manner as homicide.

Fi g u r e 1-3. Radiograph of the arm of a 5-month-old male, with improper orientation of the forearm. The proximal ends of the radius and ulna are superimposed, obstructing the metaphysis of the radius.

2 Skeletal Atlas of Child Abuse Skeletal Examination

Ribs

The ribs are evaluated with the child lying supine; the Cushing periosteal elevator is then used to reflect the long bones are examined with the child lying prone. For periosteum to expose fractures and areas of subpe- this reason, the authors advise beginning the skeletal riosteal new bone formation (SPNBF) along the rib bod- examination by evaluating the ribs. Examination of the ies. Special attention should be paid to both the ribs first requires removal of the serous pleural mem- costochondral junctions and to the rib head–vertebral brane adhering to the internal surface of the rib cage. articulations for evidence of disruption of the joints. To Removal of the pleura involves peeling the membrane remove the ribs with suspected trauma, a scalpel cut is laterally and anteriorly from the rib heads to the sternal made through the cartilaginous portion of the rib head rib ends. Following removal of the pleural membrane, at an approximate 45° angle toward the posterior apex the internal intercostal muscles are reflected to provide of the transverse process of the vertebra to which the greater visibility of the rib bodies. A horizontal cut is then rib is attached. Caution should be exercised to prevent made through the periosteum along the long axis of scalpel contact with the delicate cortical bone overly- each rib from the rib heads to the sternal rib ends. A ing the rib head (Figs. 1.4 and 1.5).

Fi g u r e 1-4. Autopsy photograph of ribs prior to skeletal examination. The image shows the left side of the rib cage of a 2-month-old male following removal of the serous pleural membrane but prior to incision of the periosteum. Note that the pleural surface of several ribs is obstructed by muscle.

Skeletal Examination Method 3 Fi g u r e 1-5. Right ribs in situ following reflection of the periosteum. The rib fractures are readily visible once the periosteum is removed. Notice the absence of hemorrhage in the tissue surrounding the fracture, suggesting cardiopulmonary resuscitation fractures (see Chap. 3 for a description of rib fractures).

Long Bones

Examination of the long bones begins with the dece- and expose the underlying bone surface and the dent lying prone with the extremities in anatomic posi- metaphyses. Additional incisions through the perios- tion to prevent crossing of the long bones of the teum often are necessary to fully visualize the epiphyses forearms. Incisions made to examine the subcutaneous and the chondro-osseus junctions (COJs). Caution tissue of the back, buttocks, arms, and legs during the should be exercised during this process to recognize autopsy are extended through the periosteum to the and avoid destruction of adherent SPNBF. Certain long surface of the long bone, and the overlying muscle is bones require additional attention because of their resected with attention given to minimizing the amount specific morphology. For example, the elbow is flexed of resulting soft tissue destruction. Ligaments and ten- during evaluation to provide visibility of the olecranon dons, for example, are cut to facilitate reflection of process of the ulna and the olecranon fossa of the complete muscle bodies rather than focal destruction humerus. Elements with suspected trauma are removed of areas of musculature, which results in unnecessary for analysis, preferably in their entirety. To remove the disfigurement. Reflection of the overlying muscles is fol- element, the attaching ligaments are incised with care lowed by a longitudinal incision through the periosteum, not to cut the cartilaginous epiphysis or the bone. along the shaft of each bone. Caution should be taken Separating the bones by side during collection, pro- not to cut into the cartilaginous epiphyses. A Cushing cessing, and storage helps avoid the confusion associ- periosteal elevator is then used to reflect the periosteum ated with siding subadult bones (Figs. 1.6 and 1.7).

4 Skeletal Atlas of Child Abuse Fi g u r e 1-6. Normal tibial and fibular COJs of a 2-month-old male. The interface between the bone and cartilage is readily visible after the periosteum is removed.

Fi g u r e 1-7. Close-up view of normal tibial and fibular COJs of a 2-month-old male. Note the regular and straight interface between the bone and cartilage.

Skeletal Examination Method 5 Clavicle

The same procedure used to expose the surface of the recommend examining the clavicles after the ribs, long bones is applied to the clavicles. The authors before placing the decedent in the prone position.

Scapula

To evaluate the scapulae, the infraspinatus and periosteum. The periosteum is incised along the same supraspinatus muscles are cut along the medial margin axes, and the periosteal elevator is used to reflect the of the scapula and along the scapular spine. The mus- periosteum in the same fashion as the overlying muscle cles are reflected laterally to expose the underlying tissue.

Documentation and Analysis

Once the bones are exposed, overview photographs The container in which the specimens are processed are taken to document the completeness of the skele- should be closed with a lid or cling wrap to prevent tal examination; then, photographs are taken of each evaporation of the processing solution. The tempera- fracture in situ. As stated earlier, each skeletal element ture of the solution is elevated to a consistent temper- with suspected trauma is removed in its entirety if possi- ature of 60°C for approximately 24 h. The cycle may ble. Artifacts of the autopsy and/or skeletal examina- be repeated if necessary. An incubator facilitates tion are documented in the bench notes as the maintenance of the appropriate temperature and examination proceeds. Detailed bench notes record ensures minimal if any destruction of the bone during which bones were retained and the location of the the process. Fragmented elements are reconstructed suspected fracture(s). prior to analysis. The processed bone is then available Following removal, the suspect elements are pro- for gross inspection. All processed elements are evalu- cessed to remove all adherent soft tissue and to pro- ated in their entirety both grossly and via a stereomi- vide maximum visibility of the bone surfaces. The croscope. An overall photograph of the complete recommended method for processing the elements is array of elements recovered is taken in approximate to first fully submerge them in a solution composed of anatomic position, and subsequent individual photo- one part of concentrated liquid detergent containing graphs are taken of each element and each injury alkaline builders and two parts water, one part detergent. (Figs. 1.8 and 1.9).

6 Skeletal Atlas of Child Abuse Fi g u r e 1-8. Processed skeletal elements. Shown are the ele- examination because of the presence of trauma or suspected ments removed from a 1-month-old male for an anthropo- trauma to the bone. logic analysis. All elements were removed during the skeletal

Skeletal Examination Method 7 Fi g u r e 1-9. Postprocessing view of the right tibia of a 4-month-old male. A healing midshaft fracture of the tibia is observed following processing.

References

1. Cramer KE, Green NE: Child abuse. In Skeletal Trauma in Children. 3. Love JC, Sanchez LA: Recognition of skeletal fractures in Edited by Green NE, Swiontkowski MF. Philadelphia: Saunders; infants: an autopsy technique. J Forensic Sci 2009, 54(6): 2003:587–606. 1443–1446. 2. Kleinman PK (ed): Diagnostic Imaging of Child Abuse, edn 2. St. Louis: Mosby; 1998:110–148.

8 Skeletal Atlas of Child Abuse 2 Skull Fractures Head injury, common in children, is the most frequent cause of death among abused children under 2 years of age [1–5]. Skull fractures reportedly are present in between 2 and 20% of children who present to U.S. hospitals for outpatient evaluation of head injuries [6]. Although head injury and skull fracture statistics generally are not separated from each other in the clinical literature, the leading causes of head injury in children, in decreasing order of frequency, are falls, motor vehicle crashes, pedestrian and bicycle injuries, sports-related trauma, and child abuse [7, 8]. Skull fractures are described in the following bones in order of decreasing frequency: parietal, occipital, frontal, and temporal bones [9–12]. Linear fractures are most common in children, followed by depressed fractures and fractures of the basilar skull [9]. Distinguishing accidental from nonaccidental head trauma is an important component of the forensic autopsy, and the thorough detection and appropriate interpretation of skull fractures is critical to the distinction between nonaccidental and accidental skull fractures. The impression of accidental versus nonaccidental cranial trauma has changed considerably during the past few decades. Skull fractures related to inflicted trauma once were described as simple linear fractures most commonly located on the parieto-occipital region of the skull [11], and more complex depressed, comminuted, and/or diastatic fractures of the skull were simply considered uncommon [11]. The consensus in more recent literature is that simple fractures of the type formerly considered suspicious for inflicted trauma are more or less ambiguous in the absence of other injury, and that complex fractures, particularly of the cranial base, are more suspicious for inflicted trauma [13, 14]. Depressed and complex skull fractures remain highly suspicious for inflicted trauma, but abusive skull fractures are often linear and similar to their accidental counterparts in both location and extent [13, 15, 16]. Fractures are more likely to have resulted from inflicted trauma if any of the following characteristics are present: (1) a stellate configuration, (2) depressed margins, (3) a fracture that crosses a suture, (4) multiple intersecting fractures, or (5) involvement of the skull base [10, 17]. Often it is the constellation of skeletal injuries that provides clarity in distinguishing accidental from nonaccidental trauma, because as many as 50% of children who have inflicted rather than accidental head injury also have evidence of other and/or prior skeletal injury [3, 12, 18]. The American Academy of Pediatrics [19] recommends that all children under 2 years of age whose circumstances of injury are suspicious for nonaccidental injury undergo a full radiographic skeletal survey. The relationship between acute abusive head trauma and prior head injury also has been demonstrated by Ewing-Cobbs et al. [20]. These authors indicated that 40–45% of children diagnosed with acute abusive head trauma have CT or MRI evidence of prior head injury. For this reason, the ability to distinguish healing from acute cranial fractures is important. Most published data regarding the frequency and characteristics of childhood head injury are from a clinical context and thus are based on radiographic interpretation. However, numerous authors have acknowledged the difficulties associated with recognizing and characterizing skull fractures based on radiographs [21, 22]. Normal anatomic features may superimpose fractures, obscuring them in conventional radiographs [21]. Linear fractures that fall in the plane of the CT scan, particularly those of the vertex and basilar skull, also may be overlooked [22]. False positive and/or negative findings may

J.C. Love et al., Skeletal Atlas of Child Abuse, Springer’s Forensic Laboratory Science Series, 9 DOI 10.1007/978-1-61779-216-8_2, © Springer Science+Business Media, LLC 2011 result from incorrect interpretation of unusual suture and detailed interpretation of forces associated with the vascular marking locations and atypical morphologic fracture and the duration of time since it occurred. The features on radiographs [21], suggesting that a signifi- chapter first provides an overview of pediatric cranial cant underrepresentation of childhood skull fractures in fracture types and proceeds with a discussion of pediat- the clinical literature is likely. ric cranial anatomy as it pertains to the interpretation of This chapter describes the manifestation of skeletal skull fracture, a review of the literature regarding the injury to the subadult cranium as seen during the skeletal manifestation of fractures to the various regions of the examination process. Compared with radiologic evalu- skull, and a discussion of the distinctions between acci- ation, this method facilitates a more detailed gross and dental and nonaccidental fractures; it concludes with a microscopic evaluation of suspect cranial bones for the series of recent anthropologic case examples from the presence and types of fractures, as well as a more Harris County Institute of Forensic Sciences (HCIFS).

Skull Fracture Types

Skull fractures are separated into four types: linear, The original article describing the ping-pong fracture depressed, diastatic, and basilar. Linear fractures are states a single case and notes that the depression was nondisplaced fractures that take a linear path across not associated with a fracture [32]. Ping-pong fractures the skull and involve the entire cross section of bone. In are seen primarily during the first few months of life and infants and children, linear fractures most often involve are the cranial analog to the greenstick fractures that the bones of the vault, including the parietal, occipital, appear in subadult long bones. Ping-pong fractures and frontal bones. Linear skull fractures result from low- are most commonly associated with short falls and energy transfer associated with blunt trauma over a rarely with birth trauma [31]. Skull fractures associated wide area of the skull [23]. Linear fractures in children with birth trauma are more often depressed than linear may become what are referred to as growing skull frac- and are most often located on the frontal and parietal tures (GSFs) in cases in which progressive enlargement bones [26, 33]. of a skull fracture occurs in association with an underly- Diastatic skull fractures are those in which the sutures ing dural tear or defect [24–26]. GSFs are most common are widened. These fractures may be associated with a in children under 3 years old and are most commonly fracture that transverses the suture, or they may be located on the parietal bone [27, 28]. GSFs also have found in the absence of associated fracture or trauma. been described as rarely occurring in the posterior cra- They are most common in children, because the cranial nial fossa or the orbital roof in children [29]. GSFs some- sutures have not yet fused [34]. Suture diastasis also has times are referred to as leptomeningeal cysts, traumatic been associated with idiopathic brain swelling and an meningocele, cerebrocranial erosion, cephalhydro- array of congenital disorders, including osteogenesis cele, or meningocele because of the associated soft imperfecta [35, 36]. tissue response. These fractures present themselves in Basilar skull fractures are linear fractures involving the association with herniated cerebral tissue, so they are base of the skull. Most basilar skull fractures involve the often easily recognizable. temporal bone [37] and may occur at either the squama Depressed skull fractures are associated with high- or base of the temporal bone, or in the area of the energy transfer to a relatively small area of the skull. occipital condyles. These fractures range in severity from compound com- Crushing head injuries also are relatively common minuted fractures with inwardly displaced fragments among children [38]. These injuries generally involve located at the point of maximum impact force to sim- accidental crushing forces applied to a stationary head ple depressions in the skull without accompanying and are characterized by multiple comminuted and fracture. The parietal bones are the most common intersecting fractures. The forces applied in these injuries location of accidental depressed skull fractures in both generally are slow loading (<200 ms) [38]. Examples of children and adults [11, 30]. Depressed fractures of the crushing head injuries include those resulting from the cranial vault are particularly common among neo- wheel of a car passing over the head or from a televi- nates. These fractures sometimes are referred to as sion or other heavy object being pulled or falling onto ping-pong fractures because they resemble the the head. Plastic deformation often is associated with indented surface of a plastic ping-pong ball [31, 32]. these injuries as a result of the slow-loading forces.

The Pediatric Cranium

The pediatric skull differs significantly in its structure, quency of traumatic injury that characterizes the pediatric mechanics, and anatomy from the adult skull. This distinc- skull. The following paragraphs summarize the anatomic tion has a significant effect on the pattern, type, and fre- and structural characteristics of the pediatric skull.

10 Skeletal Atlas of Child Abuse Pediatric Cranial Anatomy

The primary anatomic differences between the adult sutura mendosa (Fig. 2.2) is the remnant line of fusion and pediatric skull are most evident in the perinatal and between the fetal pars interparietalis and the pars infant skull. These include several features that are not supraoccipitalis. These extend superomedially from the present in the adult skull, including remnant sutures and lateral margins of the pars squama toward the center fontanelles. These features influence the morphology and may extend as much as half the distance between and propagation of fractures in the infant skull [39, 40]. the lateral border and the center of the bone. In the The bones of the pediatric skull are also generally more articulated skull, the sutura mendosa are continuous elastic than those of the adult, a distinction that also is with the mastoid fontanelle, and are often referred to manifest in the form of variation between adult and as the lateral fissures. There typically is a median fissure pediatric skull fractures [23]. Following is a review of the that extends some distance from the superior margin of anatomic characteristics of the pediatric skull that dis- the pars squama into the bone during the perinatal tinguish it from that of the adult. period. This fissure is continuous with the posterior fonta- The neonatal and infant skulls are marked by several nelle. The margins of the pars squama are serrated in developmental sutures and fontanelles that are not infanthood. Vascular and nervous grooves appear on present in the adult skull. The anterior fontanelle is dia- the pars squama during the perinatal period. Fusion of mond shaped and located at the intersection of the the separate components of the occipital bone begins frontal and the right and left parietals, at the landmark during infanthood and continues until the fifth or sixth of bregma in the adult skull (Fig. 2.1). The posterior fonta- year. The sutura mendosa begin to close during the nelle is located at the intersection of the right and left fourth month and generally are closed by the end of parietals and occipital, the landmark of lambda. The the first year, although some have suggested they may sphenoid (anterolateral) fontanelle is located at the remain in some form into the third year of life [45]. The intersection of the temporal squama, sphenoid, parietal, pars lateralis and pars squamous initially are separated and coronal, at the landmark of pterion. The mastoid by the sutura intraoccipitalis posterior, which begins to (posterolateral) fontanelle is located at the intersection fuse by the end of the first year and is completely fused of the parietal, occipital, and temporal bones, at the during the third year of life. The pars lateralis fuses with landmark of asterion. Additionally, several bones of the the pars basilaris between the fifth and seventh years vault, including the frontal, occipital, and temporal of life. bones, are composed of independent segments during The perinatal temporal bone consists of two separate much of the fetal period. The multiple component devel- components: the combined squamotympanic and the opment of the bones results in fetal sutures (present in petromastoid. These elements fuse during the first year the neonatal period) that may cause confusion during of life, along with gradual expansion of the mastoid pro- trauma analysis, including the sutura mendosa, which is cesses and the bony auditory meatus. The lateral growth located on the squamous part of the occipital bone. of the petrous portion generally and the meatus specifi- The perinatal frontal bone consists of two separate cally results in a dramatic change in the orientation of halves, each of which ossifies from a single center, the tympanic membrane. At birth, the membrane is ori- divided vertically by the metopic suture. The opposing ented horizontally and located more inferiorly on the sides of the frontal bone are in contact but unfused in skull. The membrane assumes its more vertical adult ori- infanthood. A widening of the metopic suture located entation by age 4 or 5. The mastoid process grows in near its midpoint is referred to as the metopic fontanelle. length and width according to multiple growth periods Fusion of the metopic suture begins anteriorly at the that vary between males and females. Overall growth bridge of the nose and progresses posteriorly. One-third of the squamous proceeds rapidly until age 4, then of metopic sutures close at 3 months, 60% by 5 months, continues at a slower pace until age 20 [43]. 65% by 7 months, and nearly 100% by 9 months [34], The bones of the face covary in their morphology although some may persist into the fourth year and, in and development in a very complex way [41]. At birth, rare cases, into adulthood [41]. The frontal bone grows the maxilla is very small and its shape is determined into the 16th year of life in males and the 15th year of life largely by the underlying developing deciduous tooth in females [42, 43]. Pneumatization of the frontal sinus buds, whose crypts form noticeable bulges along the begins in the postnatal period, and expansion continues anterior surface. The tooth buds are very near the base until puberty. The mean age of initial visibility of the fron- of the eye orbit, and the maxillary sinuses are present tal sinus on radiograph is between 2 and 6 years [44]. but very small as a result. The alveolar bone is primarily The pediatric parietal bone is a single square-shaped cancellous and continuously remodels as the tooth bone with a prominent eminence located near its cen- buds grow. The overall growth of the maxilla is dictated ter. The eminence increases in prominence during the by two major influences: growth in response to the need first 9 months of life, then begins to flatten as the bone to accommodate more and larger teeth and growth in takes the adult form [43]. The parietal bone reaches its response to the development of the surrounding anat- adult dimensions by about age 16 [43]. The parietal omy, including the eyes and the nose. The maxillary bones are separated from the frontal bone by the coro- sinuses expand from the postnatal period into adult- nal suture and anterior fontanelle. The anterior fonta- hood. Growth of the mandible keeps pace with growth nelle is the largest of the fontanelles and increases of the maxilla, and also is dictated by the growth of the during the first month of life. Thirty-eight percent of ante- dentition. At birth, the mandible consists of two halves rior fontanelles are closed by the end of the first year, divided at a centrally located symphysis. The symphysis and nearly all by 2 years of age [42]. fuses during the first year. The pediatric mandible con- The paired pars lateralis were counted as two compo- sists primarily of trabecular bone wrapped in thin, con- nents, making a total of four components. The bilateral stantly changing cortical bone. The dimensions of the

Skull Fractures 11 mandible, including the depth of the chin, height of the year in conjunction with the completion of the decidu- ramus, angle of the mandible, and bigonial breadth, ous dentition. Growth of the zygomatics proceeds along change significantly during childhood as a result of the with the development of the attached maxilla as it growth of the dentition [45]. grows to accommodate rapid dental development. At birth, the zygomatic bones are triradiate in shape, This process results in a shift in the location of the zygo- with recognizable overall morphology [41]. They achieve maticomaxillary junction and the orientation of the adult proportions, but not size, by the second or third zygomaticomaxillary suture.

Fi g u r e 2-2. Posterior skull. Shown in situ are the suture mendosa (single arrowhead), the mastoid fontanelle (arrow), and the sutura intraoccipitalis posterior (paired arrowheads) of a Fi g u r e 2-1. Anterior fontanelle. Shown in situ is the anterior fonta- 3-month-old male. The cause and manner of death were clas- nelle of a 3-month-old male. The cause of death was classified sified as undetermined. as herpes simplex viral myocarditis, the manner as natural.

Pediatric Cranial Mechanics

Several variables influence both the likelihood and the three-layered structure that characterizes mature pattern of skull fracture, including differences in level of cranial bones (Fig. 2.3). The diploe that separates the force, impact surface area and type, skull cross-sec- inner and outer tables of the bone of the cranial vault is tional thickness, thickness of the scalp and hair, and generally thought to develop in early childhood, impact location and direction [46–48]. Additionally, the although the timing is debated [38, 53]. The develop- structure/morphology of the subadult cranium is distinct ment of the three-layered structure of cranial bone has from that of the adult in several ways that critically influ- implications beyond the mechanical response of the ence its response to traumatic insult [21, 49–52]. This dis- cranial bones to trauma because the meningeal artery tinction is the result of physiologic influences on cranial grooves arise with the development of the diploe, which anatomy related to growth and development. The pri- increases the susceptibility of the meningeal arteries to mary anatomic distinctions between the subadult and damage in adulthood [54]. Another structural distinc- adult skull are the relative dimensions of face and vault, tion between adults and children is the relatively tighter variation associated with the development of the denti- adherence of the dura mater to the intracranial surface tion, the degree of pneumatization of the frontal and in children under 2 years of age relative to adults [55]. paranasal sinuses, and overall changes in the relative Decades of experimental and clinical research have size of the various components of the skull [49]. The attempted to elucidate the biomechanical response of impact of each of these factors is addressed under the skull to impact loads in both adults [56–61] and chil- “Skull Fracture Location.” dren [62, 63]. Gurdjian [58, 59] first argued that skull frac- Specific anatomic differences also exist between the tures initiate at a site remote from the impact rather structure of adult and pediatric cranial bone that can than at the site of impact. This often-cited opinion is influence the manifestation of traumatic injury. For supported by significant recent experimental literature example, the neurocranial bones of infants and very [64, 65]. Researchers suggest that fractures initiate at young children are thinner and may lack the typical sites of outbending surrounding the central area of

12 Skeletal Atlas of Child Abuse inbending (impact site), then travel both toward the fracture. Comparison of their data with published adult center of the impact area and away from the outbend- human data demonstrates that the elastic modulus, ulti- ing area. There is some disagreement in the recent lit- mate stress, and energy absorbed to failure increase erature regarding this theory. Recently, Kroman [61] whereas the ultimate strain decreases with age for cra- used high-speed film to demonstrate that adult skull nial bone, but that these properties increase with age fractures initiate at the site of impact and radiate away. for sutures. The models were subjected to impact load- The impact sites tested in this experiment were located ing; the results demonstrate that the infant skull is compli- on the parietal bone. The same debate is relevant to ant relative to the adult skull, resulting in global cranial the interpretation of pediatric cranial fractures. shape changes in response to impact rather than the Experimental studies of nonhuman cranial bone support more localized response seen in the adult skull. the outbending theory [21, 64]. Baumer et al. [64] found that the pediatric porcine parietal bone fractures in their sample initiated at sites away from the impact site, regardless of age. Recent research investigated the variation in the manner in which pediatric cranial bone responds generally to biomechanical forces [65] and more specifically to impact trauma [21, 64]. Baumer et al. [64] used porcine models to investigate the change in susceptibility of the parietal bone to fracture with age. They found that an increase in impact energy was required to initiate skull fractures with advancing age and the concurrent increase in cross-sectional thickness. They also noted that an impact against a compliant interface resulted in relatively greater fracture damage when impact inten- sity was controlled. Kriewall et al. [66] concluded that age-related changes of pediatric cranial bones, as measured in ash weight, affected the force required to initiate skull fractures. Margulies and Thibault [21] used human and porcine models to evaluate the difference Fi g u r e 2-3. Parietal bone of a 3-month-old female displaying a between adult and subadult cranial bone response to multilayer structure (arrowheads denote separate layers).

Skull Fracture Location

The specific location of fractures on the subadult skull posterior margin of the foramen magnum (including reflects the type and circumstances of injury. The epi- the occipital condyles), the temporal bones in their demiology of cranial fracture changes with age, and entirety, and the sphenoid bone. the resemblance between adult and subadult cranial bone fracture location frequencies increases with age. The adult skull is prone to fracture at anatomic sites that are thin, and fractures are more common in por- tions of the skull that do not have a three-layered structure (i.e., do not have diploe). These areas include the squamous temporal bones, the sphenoid ala, the floor of the middle cranial fossa, the cribriform plate, the roofs of the eye orbits, and the region of the posterior cranial fossa located between the mastoid and dural sinuses (sigmoid and transverse sulci) [41]. The following paragraphs describe the patterns of fracture common to specific regions of the skull and their general etiology. This volume divides the skull into three anatomic regions based on consideration of the fracture types and locations as they relate to trauma type: the vault, facial, and cranial base regions (Fig. 2.4). The vault region includes the frontal bone superior to the frontal sinus, the complete parietals, and the occipital bone from the posterior margin of the foramen magnum posteriorly. The facial region includes the inferior seg- Vault ment of the frontal bone including the frontal sinus; the Face upper margins of the orbits, maxilla, zygomatics, and Basilar skull (cranial base) mandible; and the floor of the anterior cranial fossa, Fi g u r e 2-4. Skull regions. In this volume, the pediatric skull is divided including the orbital roofs. The cranial base includes into the vault (blue), facial (yellow), and cranial base (red) the segment of the occipital bone anterior to the regions to simplify the categorization of fracture locations.

Skull Fractures 13 Vault Fractures

Skull fractures documented in the clinical literature as located fractures, and fractures that cross sutures were associated with nonaccidental childhood injury are more common in the abuse sample than in the acci- most commonly located on the parietals and occipital dental one. Their conclusion is distinct from Hobbs’s [10] [67]. Geddes et al. [68] noted that 18 of the 19 skull frac- in that they found no significant difference between tures identified in a sample of 53 children aged 1 month accidental and abusive fractures in terms of the spe- to 8 years who died as a result of inflicted head trauma cific morphology of depressed, diastatic, nonparietal, were located on either the parietal or the occipital. or complex fractures. In concurrence with Hobbs’s [10] Hobbs [10] listed the following fractures as being more conclusion, Meservy et al. [11] attached greater suspi- common in nonaccidental than accidental injury cases: cion to the presence of multiple fractures, bilateral frac- depressed skull fractures, diastatic fractures wider than tures, and fractures crossing sutures. Of note, the sample 3 mm, nonparietal fractures, fractures having a com- of Meservy et al. [11] comprised children who survived plex configuration, multiple calvarial fractures, bilateral their injuries, and it is likely that the children in Hobbs’s fractures, and fractures that cross sutures. He stated that [10] sample, some of whom were deceased, were the presence of one or more of these features is reason injured more severely as a whole. to suspect abuse, and that most of the cases in his sam- Oon and Yu [69] completed a survey of 50 children ple had two or more of them; however, as Meservy et al. aged 3 months to 4 years who had either accidental or [11] pointed out, he provided no statistical support for nonaccidental fractures on the posterior aspect of the his conclusion. Meservy et al. [11] used a sample of parietal bone extending anteriorly from the lambdoidal radiographs of 134 children under 2 years of age to suture, most frequently in the approximate superior– investigate distinctions between accidental and non- inferior midpoint of the suture. The authors noted a fre- accidental skull fractures. The parietal bone was the quent (32 of 50) association between these fractures and most frequently fractured in both the abuse and acci- Wormian bones, an Inca bone, or accessory posterior dental groups, occurring in 88% of the abused children parietal sutures, arguing for a causal relationship between and 91% of the accidental sample. The authors found the fractures and these anomalies. Figures 2.5–2.46 are that the presence of multiple fractures, bilaterally case examples of pediatric cranial vault fractures.

Fi g u r e 2-6. Postprocessing view of the ectocranial surface of the Fi g u r e 2-5. Linear skull fracture. Shown in situ is a linear skull frac- occipital bone of the individual in Fig. 2.5. The location of ture of the occipital bone in a 2-year-old male. Minimal subpe- the foramen magnum is indicated by the single arrowhead. riosteal new bone formation (SPNBF) extends the length of the Note SPNBF along the fracture line (paired arrowheads) and fracture, with early bridging and rounded fracture margins. early fracture bridging (arrow). The fracture intersects the sutura intraoccipitalis posterior, and its morphology is consistent with an impact against an object with a broad, flat surface area. The cause of death was classified as blunt force head trauma, the manner as undetermined.

14 Skeletal Atlas of Child Abuse Fi g u r e 2-8. Endocranial surface of the occipital bone of the individual in Figs. 2.5–2.7. The fracture intersects the intraoccipital suture at the margin of the foramen magnum (arrowhead).

Fi g u r e 2-7. Postprocessing view of the endocranial surface of the occipital bone of the individual in Figs. 2.5 and 2.6. The fracture intersects the intraoccipital suture (arrowhead) at the margin of the foramen magnum (paired arrowheads). Early fracture bridging is present along the fracture (arrow).

Fi g u r e 2-10. Postprocessing view of the endocranial surface of the posterior skull of the individual in Fig. 2.9. A complex pattern of intersecting fractures that incorporates a portion of the lambdoidal suture is located on the occipital bone (arrowhead). A portion of the fracture is depressed. The fracture Fi g u r e 2-9. Posterior autopsy view of the skull of a 2-year-old pattern is consistent with a posterior-to-anterior-directed female. A complex pattern of perimortem intersecting frac- impact with an object of relatively small surface area. tures is located on the occipital bone. Remote fractures are present on the appendicular and thoracic skeleton. The cause of death was classified as blunt trauma of the head with subdural hematoma and skull fracture, the manner as homicide.

Skull Fractures 15 Fi g u r e 2-11. Postprocessing ectocranial view of a stellate fracture pattern on the superior portion of the occipital bone of the individual in Figs. 2.9 and 2.10. The arrowheads indicate the path of the fracture.

Fi g u r e 2-12. Posterior (a) and lateral (b) autopsy views of the skull of a 6-month-old female. A complex pattern of fractures is visible on the posterior right parietal (arrowheads). The cause of death was classified as blunt force head trauma, the manner as homicide.

Fi g u r e 2-13. Postprocessing view of the right and left parietals and a segment of the occipital bone from the individual in Fig. 2.12. A complex pattern of fracture is located on the right parietal (arrowhead). The fracture is three pronged with radiating fractures extending superior-anteriorly, anterior-inferiorly, and posteriorly from the point of intersection. The two anteriorly radiating fractures terminate within the right parietal bone, and the bone between them is slightly depressed.

16 Skeletal Atlas of Child Abuse Fi g u r e 2-15. Autopsy view of the right side of the skull of a 9-month-old male. A stellate fracture pattern is located on the posterior right parietal (single arrowhead), and a widely separated radiating fracture extends anteriorly to terminate in the coronal suture (paired arrowheads). The cause of death was classified as blunt trauma of the head with skull fractures and subdural hemorrhage, the manner as homicide. Fi g u r e 2-14. Close-up view of the right parietal and occipital bones in Fig. 2.13. An additional linear fracture (arrowhead) extends inferiorly from the lambdoidal suture and is continuous with the aforementioned fracture via the diastatic fracture of the lambdoidal suture. The fracture pattern is consistent with a superior-to-inferior, posterior-to-anterior-directed impact. The fracture margins are sharp, and there is no gross evidence of healing at or near the fracture sites.

Fi g u r e 2-16. Endocranial view of the right parietal bone in the individual in Fig. 2.15. The fracture margins are sharp, with no indication of a healing response. The pattern of fracture is consistent with an impact in a right-to-left direction with an object of relatively small surface area.

Skull Fractures 17 Fi g u r e 2-17. Cranial bones. Shown are right lateral (A), oblique right analysis. The fractures were of both acute and remote origin. frontal (B), posterior (c), and left lateral (d) autopsy views of the The cause of death was classified as blunt trauma of the head skull of a 1-month-old male with multiple visible fractures (arrow- with skull fractures and brain contusions, and the manner as heads). The entire calotte was recovered for anthropologic homicide.

18 Skeletal Atlas of Child Abuse Fi g u r e 2-18. Postprocessing view of the bones retained for analysis eminence, with radiating fractures extending anteriorly, posteri- from the individual in Fig. 2.17. The autopsy cut transects the skull orly, and medially from the impact site. The fracture pattern is through the parietal bones in the coronal plane. A perimortem, consistent with a minimum of one direct blow to the right tri-pronged stellate fracture is located near the right parietal cranium in a right-to-left direction with a relatively broad object.

Fi g u r e 2-19. Postprocessing view of the left parietal bone from the individual in Figs. 2.17 and 2.18. The single arrowheads indicate a remote transparietal fracture across the body of the parietal bone. The fracture extends anteroposteriorly from the coronal suture to the lambdoid suture. Primary new bone formation is present along the fracture margins, and the fracture is partially stabilized. Note that the bone is transected by the autopsy cut (paired arrowheads). An acute fracture also is visible superior to the remote fracture (arrow).

Skull Fractures 19 Fi g u r e 2-20. Postprocessing views of the frontal bone pictured in surface. A depressed fracture is observed near the coronal Fig. 2.18. (a) Ectocranial view showing only a subtle indication suture (arrowhead). of a fracture (arrowhead). (b) Close-up view of the ectocranial

Fi g u r e 2-21. Posterior autopsy view of the skull of a 4-month-old male. A complex fracture pattern is present involving the left parietal and occipital bones near lambda. The fracture is curvilinear and courses through the parietal bone anteriorly and to the left from lambda, then extends posteriorly and inferiorly Fi g u r e 2-22. Postprocessing view of the occipital skull fracture across the lambdoidal suture, terminating in the occipital pictured in Fig. 2.21. The margins of the fractures are sharp, squama just left of and superior to the external occipital protu- without evidence of a healing response. Evidence of previous berance (fracture path indicated by arrowheads). The fracture skeletal injury was located on the ribs and long bones. creates a displaced fragment of parietal bone. The fracture pattern is consistent with an impact to the posterosuperior skull immediately left of lambda with an object of relatively small surface area. Note the diastatic separation of the lambdoidal and sagittal sutures. The cause of death was classified as blunt trauma of the head and the manner as homicide.

20 Skeletal Atlas of Child Abuse Fi g u r e 2-24. Autopsy view of the posterior right side of the skull of a 15-month-old female. A stellate fracture is observed on the occipital bone (arrowhead). The horizontal component of the fracture is located at the level of the sutura mendosa, a developmental suture within the forming occipital squama. The vertical component of the fracture extends inferiorly from the horizontal component and terminates in the sutura intraoccipitalis posterior. The cause of death was classified as complications of blunt trauma of the head with subdural hematoma Fi g u r e 2-23. Close-up postprocessing view of the occipital frac- and skull fracture, the manner as homicide. ture pictured in Fig. 2.22. The photograph illustrates the sharp edges of the fracture and the associated lack of a healing fracture response.

Fi g u r e 2-26. Endocranial view of the occipital skull fractures pictured in Figs. 2.24 and 2.25. The photograph depicts the path (as indicated by arrowheads) of the fracture on the endocranial surface of the occipital bone.

Fi g u r e 2-25. Close-up view of the fracture pictured in Fig. 2.24 (arrowheads mark the fracture). A segment of the skull including a portion of the occipital and right parietal bones was retained for anthropologic analysis.

Skull Fractures 21 Fi g u r e 2-27. Postprocessing view of the cranial segment recovered from the individual in Figs. 2.24–2.26 for anthropologic analysis. Evidence of a healing response is located along the fracture margins.

Fi g u r e 2-28. Healing linear skull fracture. Shown are close-up with fibrous tissue bridging and minimal SPNBF. The fracture postprocessing views of the fracture pictured in Figs. 2.24–2.27. type is consistent with a direct impact to the posterior right skull The fracture is in the initial stage of healing, as shown on the in a posterior-to-anterior direction with an object of relatively endocranial (a) and the ectocranial (b) surfaces. It is open, small surface area.

22 Skeletal Atlas of Child Abuse Fi g u r e 2-29. Autopsy views of the left (a) and right (b) sides of the segments of the right and left parietal, and a segment of the posterior skull of a 4-month-old male. Note the fractures inferior squama of the left temporal was recovered for anthropologic to the lambdoidal suture on both the left and right sides of the analysis. The cause of death was classified as blunt trauma of bone (arrowheads). A specimen including the occipital the head and the manner as homicide. squama, a posterior segment of the left pars lateralis, posterior

Fi g u r e 2-30. Postprocessing views of the ectocranial (a) and lambdoidal suture near asterion superiorly and medially and endocranial (b) surfaces of the occipital bone from the indi- meeting inferior to lambda. Diastatic fractures were identified vidual in Fig. 2.29. Bilateral linear fractures (arrowheads) on the left lambdoidal and left posterior squamosal suture. were identified extending from the right and left sides of the

Skull Fractures 23 Fi g u r e 2-31. Close-up views of the left (a) and right (b) fractures pattern is consistent with a minimum of two blows: one to the of the occipital bone pictured in Figs. 2.29 and 2.30. There is right posterior cranium and one to the left posterior cranium. partial union of both fractures with woven new bone forma- The healing pattern is consistent with a single traumatic event, tion, as well as fracture bridging (arrowheads). The fracture evident by the uniform new woven bone along the fractures.

Fi g u r e 2-32. Postprocessing view of the occipital bone of a 1-month- old female. A segment of the left parietal also was recovered for anthropologic analysis. Three perimortem fractures were noted on the bones of the skull: two on the occipital and one on the left parietal. The first occipital fracture is curvilinear and extends inferomedially from the midpoint of the left half of the lambdoidal suture (arrowhead). The second occipital fracture is linear and extends superomedially from the left sutura intraoccipitalis posteriorly into the squama left of the external protuber- ance (paired arrowheads). The fracture margins are sharp, and there is no bony reaction at or near the fracture sites. The cause of death was classified as hypoxic ischemic encephalopathy due to multiple blunt force injuries, including skull fractures and subarachnoid hemorrhage, and the manner as homicide.

24 Skeletal Atlas of Child Abuse Fi g u r e 2-33. Left side of the occipital bone pictured in Fig. 2.32. (a) Note the fracture (arrowhead) and a second defect (arrow). The second defect is a remnant of the sutura mendosa. (b) Close-up view of the sutura mendosa (arrowhead).

Fi g u r e 2-34. Fracture located on the left parietal from the case shown in Figs. 2.32 and 2.33. The fracture is linear and extends inferiorly from the sagittal suture to an area immediately posterior to the parietal eminence.

Fi g u r e 2-35. Autopsy view of the superior surface of the skull of a 10-month-old male. The decedent underwent a craniotomy prior to death (note the burr hole indicated by the single arrowhead). The bones were evaluated in situ (the craniotomy defect is indicated by paired arrowheads). Both the cause and manner of death were classified as undetermined.

Skull Fractures 25 Fi g u r e 2-36. Left lateral autopsy view of the skull pictured in Fig. 2.35. The trauma in this case was limited to the anterior, posterior, and right sides of the skull (there were no acute or remote fractures on the left side).

Fi g u r e 2-37. Posteroinferior autopsy views of the skull pictured in relatively broad surface area. (b) The first fracture is vertically Figs. 2.35 and 2.36 (Note an autopsy saw cut bisects the occipi- oriented and extends from the right lambdoidal suture, con- tal). (a) Two acute linear fractures are observed on the occiput: tinuing through the squama, and terminating immediately right one vertically oriented (arrowheads) and one horizontally of the posterior midline of the foramen magnum (arrowheads oriented (arrow). The horizontal fracture extends medially from indicate the fracture path). (c) The fracture bifurcates between the sutura mendosa. The fracture pattern is consistent with a the inferior nuchal line and the foramen magnum, creating a direct impact to the posterior cranium against an object of triangular fragment.

26 Skeletal Atlas of Child Abuse Fi g u r e 2-39. Autopsy view of the right side of the skull shown in Figs. 2.35–2.38. The right side of the skull was the site of the craniotomy (note the burr holes indicated by the arrowheads). The craniotomy defect noted in Fig. 2.35 is visible along the superior Fi g u r e 2-38. Autopsy view of the occipital skull from the case margin of the skull. shown in Figs. 3.35–3.37. The second linear fracture (arrowhead) is horizontally oriented and extends medially from left asterion. Laterally the fracture is diastatic, involving the sutura mendosa.

Fi g u r e 2-41. Autopsy view of the right side of the skull of a 2-month-old male. Note the linear fracture located on the right parietal (arrowheads). No other trauma was noted during the skeletal examination. Segments of the right parietal and the occipital bones were retained for anthropologic analysis. Both the cause and manner of death were classified as undetermined.

Fi g u r e 2-40. Autopsy view of the anterior surface of the skull shown in Figs. 3.35–3.39. The autopsy cut traverses the frontal bone and intersects the craniotomy cut.

Skull Fractures 27 Fi g u r e 2-42. Postprocessing view of the segment of the right parietal recovered from the individual shown in Fig. 2.41. A linear fracture extends from the approximate midpoint of the right squamosal suture posteriorly to the lambdoidal suture Fi g u r e 2-43. Close-up view of the fracture shown in Figs. 2.41 and (arrowheads). The fracture margins are sharp, and there is no 2.42. The quality of the bone in this decedent is abnormally thin evidence of healing. The fracture location and type are consis- and porous. The compromised quality of the bone likely tent with an impact to the right side of the skull with an object decreased its ability to withstand impact, possibly leading to of relatively broad surface area. fracture from forces associated with normal activity. The arrowhead indicates a postmortem fracture (autopsy artifact).

Fi g u r e 2-44. Postprocessed occipital bone segment recovered bone indicated by the arrowheads (b). A remnant sutura men- from the individual shown in Figs. 3.41–3.43. Panel (b) is a close-up dosa (a) is present on the bone and is not of forensic concern of panel (a). Note the areas of abnormally thin translucent (paired arrowheads).

28 Skeletal Atlas of Child Abuse Fi g u r e 2-45. Crushing head injury. (a) Superior view of the horse subsequently stepped onto the side of her head. The calotte. (b) Endocranial surface of the skull base. The 4-year- cause of death was classified as blunt head trauma, the old female was thrown from the back of a horse, and the manner as accident.

Skull Fractures 29 Fi g u r e 2.46. Calotte of the individual pictured in Fig. 2.45. The fracture patterns and deformation are consistent with Shown are the superior (a), endocranial (b), right lateral (c), two opposing forces applied to the skull simultaneously. The and left lateral (d) surfaces. The calotte is marked with two larger fracture pattern of the left posterior calotte is consis- complex patterns of radiating and concentric fractures. One tent with a slow-loading impact with an object of broad sur- of the fracture patterns is large, extends anteriorly and medi- face area, and the small fracture pattern of the right anterior ally from the posterior left quadrant of the calotte, and calotte is consistent with an impact with an object of a rela- involves the left and right parietal, occipital, and frontal tively small surface area. All fracture margins are sharp, with bones. The other fracture pattern is small, located on the no evidence of healing. No additional antemortem or peri- right anterior region of the calotte, and concentrated primar- mortem trauma is observed on the specimen. The quality and ily on the frontal bone. The calotte also is marked with signifi- development of the bone is as expected for the individual’s cant cranial deformation, resulting in artificial plagiocephaly. reported age of 4 years.

30 Skeletal Atlas of Child Abuse Facial Bone Fractures

Maxillofacial injuries/fractures are rare, and less frequent status of the bones of the face and dentition and to the in children than in adults [50–52, 70–72]. Pediatric facial degree of pneumatization of the involved sinuses. fractures account for approximately 5% of all facial Skeletal injuries of the subadult face vary in severity from fractures [71]. The frequency of subadult facial fractures minor fractures to complex fractures involving some is lowest in infancy and increases with age [72]. The low combination of orbital zygomatic and maxillary occurrence of pediatric facial fracture is attributed to complexes. the higher cranial vault-to-facial skeleton ratio in chil- There is a considerable lack of consensus in the litera- dren, the elastic composition of pediatric facial bones, ture as to the primary causes of pediatric facial fracture, the presence of protective thick soft tissues, and the primarily because of the variation in ages of the chil- lack of pneumatization of the paranasal sinuses [73]. dren surveyed. However, most pediatric facial fractures Some authors suggest that facial fractures in children are the result of motor vehicle accidents, followed by may also be underreported because of difficulties asso- sports-related injury, falls, and nonaccidental trauma. ciated with their recognition on radiographs, particu- The number attributed to nonaccidental injury varies larly as a result of the presence of unerupted tooth buds, widely (3.7–61%), with most authors reporting it in the and the minimal pneumatization of the paranasal 10% range [52, 62, 72, 73]. Most fractures involving the sinuses [49, 70]. The pattern of facial bone fracture also subadult face are associated with very high-energy differs between children and adults [49, 70, 72]. This vari- forces and are regularly associated with other neuro- ation is attributed to differences in the developmental cranial injuries [63].

Inferior Frontal Bone Fractures

In young children, particularly those younger than 7 years, the large cranial vault is more exposed than the relatively smaller face to trauma and frontal bone fractures are common [50, 70]. The increased proportion of the cranial vault relative to the face in children has been associated with a higher proportion of upper facial fractures in children, as opposed to the greater proportion of lower facial fractures in adults [74]. In the absence of the frontal sinus, the forces associated with impacts sustained directly to the frontal eminence transfer either superiorly across the body of the frontal bone or posteriorly across the orbital roof, resulting in fractures at these locations [62]. Fractures of the orbital roof are relatively common and often radiographically occult in young children [75]. Greenwald et al. [75] associated isolated orbital roof fractures with younger children (mean age, 2.8 years). Most of these fractures are linear and often associated with relatively minor trauma. The authors used a fall from a height of less than 10 feet as an example of minor trauma. Messinger et al. [76] found that maxillofacial fractures were associated with orbital roof fractures in 30% of a sample of children with an average age of 3.3 years. They concluded that most children with orbital roof fractures do not have associated facial fractures and that each patient in the fracture sample lacked frontal sinus pneumatization. Orbital roof fractures often are characterized as nondisplaced, blow-out, or blow-in [77]. Fi g u r e 2-47. Autopsy view of the endocranial surface of the base Figures 2.47 and 2.48 are photographs of an acute of the skull of a 9-month-old female. Perimortem fractures are orbital roof fracture in a 9-month-old female. located in the anterior and middle fossae. The cause of death was classified as blunt force head trauma with skull fractures and brain injury, the manner as homicide.

Skull Fractures 31 Fi g u r e 2-48. Close-up endocranial view of the anterior cranial fossa in the individual pictured in Fig. 2.47. Note the perimortem fracture of the orbital roof (arrowheads). There is no indication of a healing response along the fracture margins.

Midface, and Orbital Rim Fractures

The reduced proportional emphasis on the orbits rela- or no displacement, medium energy with minimal dis- tive to the adult, in combination with the lack of frontal placement and mild comminution, and high energy sinus pneumatization and the associated tendency with severe displacement and comminution of the toward fracture of the frontal bone and orbital roofs, zygomatic processes and arch [80]. limits the number of orbital rim fractures in children [63]. The reduced anterior protrusion of the nose relative to Midface fractures including the floors of the orbits and the vault is associated with a lower incidence of nasal the maxilla are rare in children, particularly those under bone fractures in children than in adults [81, 82]. Nasal 2 years of age. The frequency of these fractures increases fractures, however, are the most common facial frac- with age-related structural changes of the face, partic- tures among children [81]. Nasal fractures in children ularly sinus pneumatization. Midface fractures in chil- often are limited to the septum rather than the nasal dren generally are associated with high-energy impacts bones. The septum may be either fractured longitudi- such as motor vehicle collisions [70]. Fractures of the nally or dislocated entirely. Asymmetric nose tip defor- midface become increasingly common as develop- mity, characterized by laterally displaced nasal bones ment of the paranasal sinuses progresses [51, 70, 78, 79]. and septum, is sometimes present in newborns and has Fractures to the medial and lateral rims of the orbits been attributed to both birth trauma and an abnormal increase in frequency after age 7, and there is a con- intrauterine position. With the exception of cases in comitant decrease in orbital roof fractures [51, 70]. which the septum is completely dislocated from the sep- Blow-out or trapdoor fractures of the orbital floor gener- tum, the nose tip deformity pattern generally is limited to ally are associated with direct impacts to the eye in chil- newborns. There is considerable debate regarding the dren [79]. These fractures are circular defects in the appropriate means to correct these deformities [82–84]. orbital floor in which one of the fracture margins is dis- Complex fractures such as Le Fort fractures represent placed inferiorly. a very small number of facial fractures in children [51] Zygomatic fractures are more common than other and are exceedingly rare in children less than 2 years midfacial fractures in children [51, 70]. In children, these old [70]. Most of these fractures are present in children fractures often manifest as greenstick fractures of the over 10 years old [79]. The Le Fort classification system is zygomatic bone and/or the lateral eye orbit. Zygomatic used to classify complex facial fractures in the same fractures are categorized as low energy with minimal way for adults and children.

32 Skeletal Atlas of Child Abuse Mandible Fractures

Mandible fractures are second to nasal fractures in their the age of 15 [89]. Fractures of the angle and body frequency among facial fractures in children [62, 70]. regions are relatively less common but increase in fre- Keniry [85] suggests that between 8 and 15% of mandi- quency with age. The common pediatric mandible ble fractures occur in children younger than 15, but fracture pattern is attributed to the thin cortical bone MacLennan [86] found that only 1% of mandible frac- overlying the heavily vascularized medullary bone in the tures occurred in children under 6 years old. The ratio of mandibular condyles in children [70]. An additional dif- bone to tooth tissue is high in children, and the thin cross ference between the adult and pediatric mandible is section of the mandibular cortical bone predisposes the that a single impact to the mandible in children tends to pediatric mandible to greenstick fracture [87, 88]. The cause a single fracture, whereas in adults it tends to condyles are the site most commonly associated with cause multiple fractures. The distinction between the fractures in children, followed by the symphyseal region. adult and subadult mandible fracture pattern ceases Condyle fractures were present in 72% of children with after about age 9 [88]. Figures 2.49–2.51 are photographs mandible fractures in a 1992 study of 220 children under of an acute mandible fracture in a 9-month-old female.

Fi g u r e 2-49. Autopsy view of the maxilla and mandible. An Fi g u r e 2-50. Mandibular fracture. Shown is an inferior view of the incomplete vertical fracture is located near the symphysis mandible of the individual pictured in Fig. 2.49. Note the incom- (arrowheads) of a 9-month-old female. No fractures were plete mandibular fracture (arrowhead). The location and located on or near the condyles. The cause of death was clas- characteristics of the fracture are consistent with an anterior- sified as blunt force head trauma with skull fractures and brain to-posterior-directed impact with an object with a medium to injury, the manner as homicide. wide surface area.

Skull Fractures 33 Fi g u r e 2-51. Anterior view of the mandible and a mirrored view of the posterior surface of the mandible of the individual pictured in Figs. 2.49 and 2.50. A V-shaped fracture pattern is observed on the posteroinferior aspect of the mandible slightly right of the midline. The fracture margins are sharp, and there is no indication of a healing response at the fracture site.

Cranial Base Fractures

In children, cranial base or basilar skull fractures are blow and often manifests as extensive fractures of the most commonly located on the temporal bone and the basioccipital region. A type III fracture is an avulsion anterior occipital bone in the area of the occipital con- injury associated with hyperrotation and lateral bend- dyles. There are three common varieties of temporal ing. In general, basilar skull fractures are associated with basilar skull fractures: longitudinal, transverse, and mixed high-energy transfer from blunt trauma, axial compres- [36]. Longitudinal fractures are the most common and sion, lateral bending, or rotational injury. typically involve the squamous portion of the temporal In a sample of 62 patients under 18 years old with bone. Transverse fractures are less common and travel basilar skull fractures, Liu-Shindo and Hawkins [91] attrib- from the foramen magnum through the inner ear into uted the injury most commonly to pedestrians struck by the middle cranial fossa. The remainder of cranial base motor vehicles (42%), followed by falls (27%), motor fractures share components of both longitudinal and vehicle collisions (23%), and being hit by an object (i.e., transverse fractures, thus are referred to as mixed. baseball bat) (8%). OCFs are rare in children and most Occipital condylar fractures (OCFs) are also subdi- often result from motor vehicle collisions and sporting vided into three varieties: type I, type II, and type III [90]. accidents with other associated head injury [92]. Cranial A type I fracture is associated with axial compression base fractures are difficult to recognize on both CT and resulting in a comminuted fracture of the occipital conventional radiography [54]. Figure 2.52 is a case illus- condyle. A type II fracture is associated with a direct tration of an acute pediatric cranial base fracture.

34 Skeletal Atlas of Child Abuse Fi g u r e 2-52. Autopsy views of the endocranial surface of a response. The cause of death was classified as blunt force 9-month-old female. Note the linear fracture of the squamous head trauma with skull fractures and brain injury, the manner temporal bone indicated by arrowheads (a) and in close-up as homicide. (b). The fractures are devoid of any indication of a healing

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Skull Fractures 37 wwwww 3 Rib Fractures Rib fractures are recognized as strong indicators of nonaccidental injury in infants and children and are more prevalent than any other type of skeletal injury in cases classified as child abuse [1–13]. They remain strong indicators of nonaccidental injury in older children (>18 months) when other types of fractures become more prevalent with accidental injury [1]. Several researchers have found that the average number of rib fractures is significantly higher in cases of nonaccidental injury than in those of accidental injury and that rib fractures often are the only skeletal injury observed in cases classified as child abuse [1, 2]. The consensus among researchers is that regardless of the type of injury, rib fractures are associated with a major traumatic event (i.e., motor vehicle crash), and without an adequate history, nonaccidental injury must be considered a cause [5, 14, 15]. Exceptions include pathologic fractures (see Chap. 7) and rib fractures secondary to organ recovery. The standard method for recovery of the heart and lungs involves a median sternotomy followed by spreading of the ribs. Kleinman and Schlesinger [8] produced rib fractures in the posteromedial region by opening a median sternotomy with a sternal retractor. A median sternotomy with forcible lateral spread of the anterior ribs places excessive force on the posteromedial region of the ribs, increasing the potential to cause posterior rib fractures (see section “Posterior Rib Fractures”).

Rib Fracture Location

The location of a rib fracture is considered a valuable indicator of the mechanism of trauma [2, 3, 7, 8, 16, 17]. However, a literature review of infant rib fracture studies shows there is no standard definition for identifying the regions of a rib. Most simply, the rib is divided into four regions: posterior, posterolateral, anterolateral, and anterior (Fig. 3.1). The posterior region is the area from the medial tip of the rib head to the lateral margin of the rib tubercle. The posterolateral region is the area from the lateral margin of the rib tubercle to the most lateral point of the rib. The anterior and anterolateral regions of the rib span the most lateral point of the rib to the sternal end. In the upper and midrange ribs, the demarcation between the anterior and anterolateral regions is the midpoint that approximately aligns with the middle of the clavicle bone (midclavicular). In the lower- range ribs, the anterolateral and anterior regions of the rib become increasingly smaller. In the 11th and 12th ribs, there is no anterior or anterolateral portion of the rib; the complete rib lies in the posterior region of the thorax.

J.C. Love et al., Skeletal Atlas of Child Abuse, Springer’s Forensic Laboratory Science Series, 39 DOI 10.1007/978-1-61779-216-8_3, © Springer Science+Business Media, LLC 2011 Posterior

Posterolateral

Fi g u r e 3-1. Regions of a rib. The rib typically is divided into four Anterolateral regions. The posterior region is the area from the medial tip of the rib head to the lateral margin of the rib tubercle. The posterolateral region is the area from the lateral margin of the rib tubercle to the most lateral point of the rib. The anterior and anterolateral regions of the rib span from the most lateral point of the rib to the sternal end. The interface of the anterior and Anterior anterolateral regions is the midpoint.

Posterior Rib Fractures

Of the four regions of the rib, fractures located in the significant difference in location of the fracture between posterior region are regarded as the strongest indicator nonaccidental and accidental injury. of nonaccidental injury [2, 3, 7, 8, 15, 16, 18]. Posterior rib Mechanisms postulated to cause posterior rib frac- fractures are often multiple, arranged in a serial pattern, tures include avulsive forces applied to the rib head and bilateral [16]. Kleinman et al. [7] found that of 84 rib and posterior levering of the rib over the transverse pro- fractures identified in 31 infant victims of nonaccidental cess of the thoracic vertebra [2, 8, 15, 19]. The develop- injury, 53 fractures (63%) were located in the posterior ing rib head is primarily hyaline cartilage and is region of the rib. Bulloch et al. [2] conducted a retro- analogous to the metaphysis of a long bone at the spective study of infants treated at two children’s hospi- chondro-osseous interface. The structure is held in tals over a 3-year period and identified 39 cases with place with strong ligamentous attachments. When rib fractures; 32 (82%) of the cases were classified as excessive force is applied to the costovertebral articu- child abuse. The authors found posterior rib fractures lation, an osseous fragment is avulsed from the rib head were more common than anterior ones but found no (Figs. 3.2–3.9) [8].

40 Skeletal Atlas of Child Abuse Fi g u r e 3-3. Avulsion fracture of the rib head. An avulsion fracture of a rib head is shown after processing; the view is of the articulating surface (same individual as shown in Fig. 3.2). Note the exposed trabecular bone of the articulating surface of the rib head. The fracture is similar in structure to a partial classic metaphyseal lesion (see Chap. 5).

Fi g u r e 3-2. Rib head fractures in situ. Rib head fractures (arrows) are shown in situ in a 2-month-old male. Note the absence of hemorrhage at the fracture sites. The cause of death was classified as blunt trauma of the head with skull fractures and subdural hemorrhage, the manner as homicide.

Fi g u r e 3-5. Avulsion fracture of the rib head in situ. An avulsion fracture of a rib head (arrow) is shown in situ in a 2-month-old female. The cause of death was classified as methicillin-resistant Fi g u r e 3-4. Avulsion fracture of the rib head. An avulsion fracture Staphylococcus aureus (MRSA) chest wall abscess with dissem- of a rib head is shown after processing (same individual as inated infection and a contributing factor of chronic stress shown in Fig. 3.2). The cortical bone of the articulating surface of associated with multiple blunt trauma injuries, the manner as the head has been fractured, exposing the trabecular bone. homicide.

Rib Fractures 41 Fi g u r e 3-6. Partial avulsion rib head fracture. This partial avulsion fracture of the rib head was observed in a 2-month-old male; the view is of the pleural surface. The cause and manner of death were classified as undetermined.

Fi g u r e 3-7. Healing rib head fractures in a 2-month-old male. Note the thickened cortical bone (arrows) and the lipping of the bone callus over the articulation surface of the rib head. The cause and manner of death were classified as undetermined.

Fi g u r e 3-9. Rib head fractures in a 4-month-old male who underwent a median sternotomy during organ recovery. Several healing rib fractures and an acute cranial fracture were noted Fi g u r e 3-8. Healing rib head fracture. This healing rib head frac- in the decedent. The rib head fractures were the only acute rib ture (arrow) was observed in an 11-week-old female with mini- fractures observed. Because of the surgical history, organ mal fracture callus formation. A healing fracture of the rib neck recovery could not be excluded as a possible cause of the (arrowhead) also is present. The cause of death was classified fractures. The cause of death was classified as blunt force as blunt force head trauma, the manner as homicide. trauma to the head, the manner as homicide.

42 Skeletal Atlas of Child Abuse Kleinman et al. [7, 8, 16] found that when the chest is the anteroposterior plane. The infant is held facing the forced posteriorly, a classic level 1 lever is formed at or adult with the adult’s palms on the infant’s sides, fingers near the costovertebral articulation point (the rib tuber- on the back, and thumbs near the midline of the chest. cle and vertebral transverse process). The costoverte- Kleinman [16] also postulated that similar forces occur bral ligaments are stronger than the bone, and excessive when the chest is forced onto a broad surface while the forces result in the failure of the rib in the region of the rib back is unsupported. Kleinman and Schlesinger [8] neck and tubercle (Figs. 3.10–3.15). Based on animal reported that posterior rib fractures do not occur when experimentation and assailant testimony, Kleinman [16] the anterior chest is compressed and the back is sup- suggested that posterior rib fractures result when an ported on a broad surface (such as with the administra- infant is held by the chest while the thorax is squeezed in tion of cardiopulmonary resuscitation [CPR]).

Fi g u r e 3-11. Posterior fracture of the rib head (same individual as shown in Fig. 3.10). Note the porotic cortical bone of the rib head (arrow). The hyperporosity reduced the bone’s ability to withstand low-level forces.

Fi g u r e 3-10. Posterior rib fractures. These acute posterior rib fractures (arrows) were found in a 2-month-old female. The cause of death was classified as acute bacterial bronchopneumonia associated with bronchopulmonary dysplasia due to prematurity, the manner as natural. Decreased bone quality has been documented as associated with prematurity in the neonatal period (see Chap. 7). The decedent was born at 27 weeks’ gestation.

Fi g u r e 3-12. Acute incomplete fracture of the rib neck in a 21-month-old female. The fracture was interpreted as a failure Fi g u r e 3-13. Healing fracture of the rib neck in a 2-month-old male. in tension due to posterior levering of the rib over the trans- Note the beginning formation of a fracture callus. The healing verse process of the vertebra. The cause of death was classi- precludes interpreting the direction of forces associated with the fied as blunt trauma of the torso with rib fractures, liver fracture, but the location is consistent with posterior levering of laceration, and traumatic transection of the pancreas, the the rib over the transverse process of the vertebra. The cause manner as homicide. and manner of death were classified as undetermined.

Rib Fractures 43 Fi g u r e 3-14. Healing posterior rib fractures. Shown are healing Fi g u r e 3-15. Healing posterior rib fractures. Shown are healing neck/tubercle fractures of left ribs 8–11 (arrows) observed in an fractures of the rib neck of left ribs 2–4 (arrows; same individual 8-week-old male. The healing precludes interpreting the direc- as shown in Fig. 3.14). Note that the fracture calluses are more tion of forces associated with the fracture, but the location is organized and smaller than those shown in Fig. 3.14, indicating consistent with posterior levering of the ribs over the transverse an older injury (see Chap. 6). process of the vertebrae. The cause of death was classified as blunt trauma of the head with skull fractures and brain contusions, the manner as homicide.

Posterolateral Rib Fractures

Posterolateral rib fractures are less common than poste- Fractures located at the most lateral point of the rib rior rib fractures (Figs. 3.16–3.26) [16]. Posterolateral frac- body (the posterolateral and anterolateral interface) tures are typically observed adjacent to ribs with neck are postulated to be the result of anteroposterior com- fractures [16]. Kleinman et al. [7] studied 31 infants who pression that causes the bone to fail in tension [17]. died with nonaccidental skeletal injuries. Of the 84 total Additionally, the body of the rib (the region that includes rib fractures observed, eight (5%) were identified as the posterolateral, anterolateral, and anterior regions) is posterolateral. vulnerable to direct impacts [2, 19].

44 Skeletal Atlas of Child Abuse Fi g u r e 3-16. Posterior rib fractures in a 21-month-old female. (a–c) impact. The cause of death was classified as blunt trauma of the Note the splaying apart of the bone, especially in panel (b). The head and torso with bilateral rib and scapular fractures, visceral fracture types are consistent with a posterior-to-anterior-directed lacerations, and multiple contusions, the manner as homicide.

Fi g u r e 3-17. Posterolateral/anterolateral rib fractures. Multiple healing posterolateral/anterolateral rib fractures (arrows) are shown in situ in an 8-week-old male; also note the anterior rib fractures (arrowheads). The cause of death was classified as blunt trauma of the head with skull fractures and brain contusions, the manner as homicide.

Fi g u r e 3-18. Healing fractures of left ribs 1–12 from the individual pictured in Fig. 3.17. The rectangle marks the posterolateral/ anterolateral rib fractures marked by arrows in Fig. 3.17. Numerous posterior and anterior healing rib fractures are present as well.

Rib Fractures 45 Fi g u r e 3-19. Healing posterolateral incomplete fracture of the right ninth rib of a 3-year-old female. The fracture was interpreted to be the result of an anterior-to-posterior compression of the chest with posterior levering. The cause of death was classified as multiple blunt trauma of the head, torso, and extremities, with fractures; lacerations of the heart, liver, and mesentery; and subdural hemorrhage. The manner was classi- Fi g u r e 3-20. Close-up of the fracture pictured in Fig. 3.19. Note fied as homicide. the rounded margins and the subperiosteal new bone formation (SPNBF) around the fracture along the pleural surface of the rib (see Chap. 6 for a description of bone healing).

Fi g u r e 3-21. Rib fractures in situ. A healing posterolateral rib fracture (arrow) is shown in situ in an 11-month-old male. The arrowheads indicate additional posterolateral-to-anterolateral fractures. The cause and manner of death were classified as undetermined.

Fi g u r e 3-22. Healing complete posterolateral fracture of right rib 6 after processing. The fracture is shown in situ in Fig. 3.21 (arrow). Note the formation of the bone callus (see Chap. 6 for a description of bone healing).

46 Skeletal Atlas of Child Abuse Fi g u r e 3-23. Healing posterolateral rib fracture in left rib 9, an additional rib from the individual pictured in Fig. 3.21. Note that the fracture callus has fully stabilized the fracture (see Chap. 6 for a description of bone healing).

Fi g u r e 3-24. Healing incomplete transverse fracture of the right 12th rib of a 5-year-old female. Note that the rib bows inward at the fracture site (arrow). Although the fracture is located in the anterior region of the rib body, it is classified as a posterior rib fracture because of its position within the torso. The fracture was the only skeletal injury observed in this case and was interpreted as a result of a direct blow to the right back in a posterior-to-anterior direction. The cause of death was classified as blunt force abdominal trauma with jejunal perforation and peritonitis, the manner as homicide.

Fi g u r e 3-26. Postprocessing view of posterior fractures in the ninth rib from the child pictured in Fig. 3.25. The arrows are pointing to two posterolateral fractures. Note the SPNBF at both fracture sites. The more anterior fracture is subtle and observed primarily as a concentrated thickening of the SPNBF. The more posterior Fi g u r e 3-25. Posterolateral rib fractures observed in situ after the fracture was interpreted as a result of posterior levering of the pleura was stripped in a 2-year-old male. The fractures are rib over the transverse process of the vertebra. The subtlety marked by the orange clips. The cause and manner of death and healing of the more anterior fracture preclude interpreta- were classified as undetermined. tion of the associated force.

Rib Fractures 47 Anterolateral Rib Fractures

Anterolateral and anterior rib fractures are considered fracture in this region are the best indicator of the mech- the least indicative of nonaccidental trauma, primarily anism of force – that is, anteroposterior compression or a because these fractures have been associated with direct blow (Figs. 3.27–3.33) [16]. However, healing may CPR [6, 15, 18] (see section “Cardiopulmonary Resus obscure the features of compression and tension failure, citation Fractures”). The morphologic features of an acute precluding determining the mechanism of force.

Fi g u r e 3-28. Close-up of the fracture pictured in Fig. 3.27. Note that the fracture is coated with SPNBF, indicating a relatively short interval between injury and death (see Chap. 6 for a Fi g u r e 3-27. Posterolateral/anterolateral rib fracture. Shown is an description of bone healing and fracture healing rates). incomplete fracture at the posterolateral/anterolateral interface (arrow) observed in a 13-month-old female. The fracture involved only the external surface of the rib and was interpreted as a failure in tension due to anteroposterior compression of the chest. The cause of death was classified as blunt force injuries of the head, the manner as homicide.

Fi g u r e 3-30. Close-up of the fracture pictured in Fig. 3.29. The fracture is a failure in tension along the pleural surface of the rib Fi g u r e 3-29. Incomplete fracture of the anterolateral region of and is interpreted as a result of a direct force applied to the the left seventh rib of the individual pictured in Fig. 3.27. Note bone at the fracture site. the slight deformation of the bone at the fracture site. The fracture type is consistent with a failure in tension along the pleural surface of the rib.

48 Skeletal Atlas of Child Abuse Fi g u r e 3-31. Anterolateral rib fracture. Shown is an incomplete fracture (arrow) of the anterolateral region observed in a 3-year-old female. The cause of death was classified as multi- Fi g u r e 3-32. Close-up of the fracture pictured in Fig. 3.31. The frac- ple blunt trauma of the head, torso, and extremities, with fracture involves primarily the internal surface of the bone. It is clas- tures; lacerations of the heart, liver, and mesentery; and sified as a buckle fracture and is interpreted as resulting from an subdural hemorrhage. The manner was classified as homicide. anterior-to-posterior compression of the chest. Note the SPNBF.

Fi g u r e 3-33. Anterolateral rib fractures. (a) Incomplete fractures as a result of anterior-to-posterior compression of the ribs. The of the right and left third ribs (pleural surface shown) in a 3-year- cause of death was classified as blunt force trauma of the old female. (b) Close-up view of the fractures. The fractures torso, the manner as an accident. (arrows) involve only the pleural surfaces and are interpreted

Anterior Rib Fractures

The anterior region of the rib is vulnerable to direct blows associated with healing rib fractures, and none was as well as anteroposterior compression (Figs. 3.34–3.44). associated with CPR. Smeets et al. [10] reported a single When one considers the anterior region, the fractures of case of a 9-month-old female who presented to the first the sternal face are more informative as to the mecha- aid department of a hospital with a history of a fall nism of trauma. Kleinman et al. [7] found that fractures 2 days prior. During a radiologic examination, posterior of the costochondral junction (CCJ) are analogous to rib fractures, cranial fractures, and classic metaphyseal Salter–Harris type II physeal injury (Figs. 3.38–3.44). The lesions were identified. A sonogram of the chest and fractures involve the chondro-osseous junction, with the abdomen revealed costochondral distraction of the greatest disruption typically occurring along the internal lower left ribs in association with subcutaneous hema- margin of the face (pleural surface). These fractures toma. Based on these findings, a diagnosis of battered may occur without significant involvement of the perios- child syndrome was made. Ng and Hall [20] presented teum, thus resulting in minimal hemorrhage. Furthermore, three case studies (7-, 18-, and 36-month-old children) during the healing process, the fractured sternal face with a total of ten CCJ fractures. The fractures involved reforms in the absence of a callus formation. ribs 6–9, were bilateral in two cases, and were not asso- Weber et al. [15] reviewed 546 autopsies of sudden ciated with CPR. Conversely, Kleinman [16] postulated unexpected death in infancy and found rib fractures that CCJ fractures are a result of depression of the in 24 cases. Four CCJ fractures were found; all were sternum and/or cartilages during CPR.

Rib Fractures 49 Fi g u r e 3-35. Anterior rib fractures. Shown are acute bilateral incomplete fractures (arrows) of the anterior region of the right and left first ribs (view of the inferior surface) observed in the case described in Fig. 3.33.

Fi g u r e 3-34. Healing anterior rib fractures observed in a 2-month- old female. The healing precludes interpretation of the direction of force. The cause of death was classified as blunt force head trauma, the manner as homicide.

Fi g u r e 3-36. Close-up of the fractures pictured in Fig. 3.35. Note that the bone is minimally traumatized (arrows). The injury was not recognized until the periosteum was stripped from the internal surface of the ribs (see Chap. 1 for a description of the Fi g u r e 3-37. Sternal surface of the ribs pictured in Fig. 3.35. Note skeletal examination). that the fracture of the left rib extends onto the sternal surface. The sternal surface of the right rib is normal.

50 Skeletal Atlas of Child Abuse Fi g u r e 3-39. Acute partial fracture of the sternal surface of the left fourth rib of a 3-year-old female. The bone is oriented so that the pleural surface is down. Note that the trabecular bone Fi g u r e 3-38. Normal sternal surface of a rib of a 2-month-old is exposed. The cause of death was classified as multiple blunt male. Note the even texture of the bone and the well-defined trauma of the head, torso, and extremities, with fractures; lac- rim. Lipping of the rim is normal in the midrange ribs of infants erations of the heart, liver, and mesentery; and subdural hem- and should not be mistaken as a rachitic rosary. The cause and orrhage. The manner was classified as homicide. manner of death in this case were classified as undetermined.

Fi g u r e 3-40. Acute partial fracture of the sternal surface of the right sixth rib of a 2-month-old female. The pleural surface is toward the top of the photograph. The lipped rim of the non- Fi g u r e 3-41. Pleural surface of the rib pictured in Fig. 3.40. The fractured area is normal. The cause of death was MRSA chest fracture involves only the rim along the pleural surface. The wall abscess with disseminated infection with the contributory anterior (external) region of the rib is atraumatic. factor of chronic stress associated with multiple blunt trauma injuries. The manner was classified as homicide.

Rib Fractures 51 Fi g u r e 3-42. Healing fracture of the sternal surface observed in a 3-month-old female. Note that the visible trabeculae have begun to thicken. The cause and manner of death were classified as undetermined. Fi g u r e 3-43. Pleural surface of the bone pictured in Fig. 3.42. Note the lacy bone formation along the bone margin (arrow) (see Chap. 6 for a description of bone healing).

Fi g u r e 3-44. Healing fracture of the sternal surface in the 3-year- old female discussed in Fig. 3.39. Note that the sternal surface has begun to reform in the absence of a large encompassing fracture callus.

Cardiopulmonary Resuscitation Fractures

As stated previously, CPR fractures are rare in children. the infant’s chest with both hands and compress it in When they do occur, they typically are located in the an anteroposterior direction. The thumbs are placed midclavicular (anterolateral) region of the rib, are mul- together on the lower half of the sternum, and the fin- tiple and bilateral, are present on the midrange ribs gers are wrapped around the thorax. The two-thumb (third through sixth), and have no to very little hemor- technique is recommended for infants (birth to rhage (Figs. 3.45–3.50) [15, 18]. Additionally, CPR frac- 12 months) and is to be administered by trained medi- tures are not associated with posterior rib fractures. The cal personnel [21]. Reportedly, the two-thumb method direct anterior-to-posterior force in the absence of pos- generates increased pressure compared with the one- terior levering, due to the supported back, protects the hand anterior compression method [21]. The two- posterior and posterolateral regions of the rib. thumb method is very similar to the position Kleinman In 2005, the American Heart Association released [16] documented as described by assailants in child new guidelines for CPR and emergency cardiovascu- abuse cases. To date, no report of rib fractures lar care of pediatric and neonatal patients. The new associated with the two-thumb method has been guidelines require the administrator of CPR to encircle published.

52 Skeletal Atlas of Child Abuse Fi g u r e 3-45. CPR fractures in a 2-month-old female. Shown in situ are CPR fractures (arrows) of left ribs 2–4. Note the lack of hemorrhage. The cause of death was classified as acute bacterial bronchopneumonia associated with bronchopulmonary dysplasia due to prematurity, the manner as natural. Fi g u r e 3-46. Postprocessing view of the CPR fractures shown in Fig. 3.45. The incomplete buckle fractures (arrows) are located in the anterolateral-to-anterior region of the rib and are interpreted as resulting from an anterior-to-posterior compression of the mid- chest. Note the hyperporosity of the anterior region of the ribs. The decrease in density of the cortical bone is consistent with the decedent’s history of prematurity (born at 27 weeks’ gestation).

Fi g u r e 3-48. CPR fracture of the left fifth rib after processing (pictured in situ in Fig. 3.47). The buckle fracture is located on the anterior region of the rib and is interpreted as a result of Fi g u r e 3-47. CPR fractures in a 5-month-old male. Shown in situ anterior-to-posterior compression. A well-healed posterolateral are CPR fractures (arrows) of right ribs 3–6 after the pleura was fracture also was observed in the decedent. The decedent stripped. Note the absence of hemorrhage in the soft tissue had an extensive medical history including extreme prematu- surrounding the fractures. The cause and manner of death rity (delivered at 23 weeks’ gestation). were classified as undetermined.

Rib Fractures 53 Fi g u r e 3-50. CPR fractures of the right third and fourth ribs (pictured in situ in Fig. 3.49). The fractures are located in the Fi g u r e 3-49. CPR fractures in a 2-month-old male. Shown in situ anterior-to-anterolateral region of the rib. The bone appears to are CPR fractures (arrows) of the right third and fourth ribs. have failed in tension on the pleural surface as opposed to the Note the absence of hemorrhage in the tissue surrounding the failure in compression typical of an anterior-to-posterior com- fractures. The cause and manner of death were classified as pression. The decedent received CPR by the local emergency undetermined. medical service (EMS); the two-thumb technique is standard EMS protocol. The type of fracture, failure in tension, may be the result of the two-thumb method. Abnormal bone structure was identified both grossly and histologically, indicating the bone was susceptible to failure under relatively low-level forces.

First Rib Fractures

Fractures of the first rib have received special attention fractures through the subclavian groove, a weak point in the literature (Fig. 3.51) [16, 19, 22, 23]. The first rib is of the rib. They and others postulated that the bone fails uniquely located within the chest. It is positioned under because of muscle contractions associated with violent the shoulder girdle and therefore protected from direct shaking [19, 22, 23]. Vikramaditya [23] reported two blows. The rib is directly united to the sternum by a syn- cases of isolated first rib fractures identified in adoles- chondrosis and has reduced movement at the costo- cents after vigorous activity. The author interpreted the vertebral articulation in comparison with the other ribs. fractures as a result of stress generated from opposing Strouse and Owings [22] stated that the first rib typically forces applied by the scalene and serratus muscles.

54 Skeletal Atlas of Child Abuse Fi g u r e 3-51. Healing left first rib fracture observed in a 2-month-old female. The fracture is in the soft callus formation stage (see Chap. 6). The cause of death was classified as blunt force head trauma, the manner as homicide.

Summary

Rib fractures are considered highly suspicious for nonac- but also are vulnerable to direct impact. Fractures of the cidental injury. The location of a rib fracture is informative rib CCJ also have been reported in cases of nonacci- as to the mechanism of trauma. The rib is conventionally dental injury. Typically, CCJ fractures involve the internal divided into four regions: posterior, posterolateral, anter- margin of the sternal end plate. CPR-related rib fractures olateral, and anterior. Rib fractures in the posterior region normally are incomplete fractures of the pleural surface are postulated to result from anterior-to-posterior con- of the rib at the interface of the anterior and anterolat- striction with posterior levering of the chest. Posterolateral, eral regions. Fractures of the first rib tend to be located anterolateral, and anterior regions of the rib may fracture within the subclavian groove and to be the result of as a result of anterior-to-posterior constriction of the chest opposing muscle constriction rather than direct impact.

References

1. Pandya NK, Baldwin K, Wolfgruber H, et al.: Child abuse and 6. Feldman KW, Brewer DK: Child abuse, cardiopulmonary resus- orthopaedic injury patterns: analysis at a level 1 pediatric citation, and rib fractures. Pediatrics 1984, 73(3):339–342. trauma center. J Pediatr Orthop 2009, 28(6):618–625. 7. Kleinman PK, Marks SC, Nimkin K, et al.: Rib fractures in 31 2. Bulloch B, Schubert CJ, Brophy PD, et al.: Cause and clinical char- abused infants: postmortem radiologic-histopathologic study acteristics of rib fractures in infants. Pediatrics 2000, 105(4):E48. Radiology 1996, 200:807–810. 3. Barsness KA, Cha E, Bensard DD, et al.: The positive predictive 8. Kleinman PK, Schlesinger AE: Mechanical factors associated value of rib fractures as an indicator of nonaccidental trauma with posterior rib fractures: laboratory and case studies. Pediatr in children. J Trauma 2003, 54(6):1107–1110. Radiol 1997, 27:87–91. 4. Spevak MR, Kleinman PK, Belanger PL, et al.: Cardiopulmonary 9. Mandelstam SA, Cook D, Fitzgerald M, Ditchfield MR: resuscitation and rib fractures in infants: a postmortem radio- Complementary use of radiological skeletal survey and bone logic-pathologic study. JAMA 1994, 272(8):617–618. scintigraphy in detection of bony injuries in suspected child abuse. Arch Dis Child 2003, 88(5):387–390. 5. Garcia VF, Gotschall CS, Eichelberger MR, Lowman LM: Rib fractures in children: a marker of severe trauma. J Trauma 1990, 10. Smeets AJ, Robben SGF, Meradji M: Songraphically detected 30(6):695–700. costo-chondral dislocation in an abused child: a new

Rib Fractures 55 sonographic sign to the radiological spectrum of child abuse. 17. Worn MJ: Rib fractures in infancy: establishing the mechanisms Pediatr Radiol 1990, 20:566–567. of cause from the injuries—a literature review. Med Sci Law 2007, 47:200–212. 11. Gunter WM, Symes SA, Berryman HE: Characteristics of child abuse by anteroposterior manual compression versus cardio- 18. Betz P, Liebhardt E: Rib fractures in children—resuscitation or pulmonary resuscitation: case report. Am J Forensic Med Pathol child abuse? Int J Legal Med 1994, 106:215–218. 2000, 21(1):5–10. 19. Schweich P, Fleisher G: Rib fractures in children. Pediatr Emerg 12. Maguire S, Mann M, John N, et al.; Welsh Child Protection Care 1985, 1(4):187–189. Systematic Review Group: Does cardiopulmonary resuscitation 20. Ng CS, Hall CM: Costochondral junction fractures and intra- cause rib fractures in children? A systematic review. Child abdominal trauma in non-accidental injury (child abuse). Abuse Negl 2006, 30(7):739–751. Pediatr Radiol 1998, 28:671–676. 13. Dolinak D: Rib fractures in infants due to cardiopulmonary resus- 21. American Heart Association in collaboration with the citation efforts. Am J Forensic Med Pathol 2007, 28(2):107–110. International Liaison Committee on Resuscitation (ILCOR): 14. Cadzow SP, Armstrong KL: Rib fractures in infants: red alert! The Guidelines 2000 for cardiopulmonary resuscitation and clinical features, investigations and child protection outcomes. emergency cardiovascular care: an international consensus J Paediatr Child Health 2000, 36:322–326. on science. Resuscitation 2000, 46:1–447. 15. Weber MA, Risdon RA, Offiah AC,et al.: Rib fractures identified 22. Strouse PJ, Owings CL: Fractures of the first rib in child abuse at post-mortem examination in sudden unexpected deaths in Radiology 1995, 197:763–765. infancy (SUDI) Forensic Sci Int 2009, 189(1–3):75–81. 23. Vikramaditya PP: Two cases of isolated first rib fractures.Emerg 16. Kleinman PK: Bony thoracic trauma. In Diagnostic Imaging of Med J 2001, 18:498–499. Child Abuse, edn 2. Edited by Kleinman PK. St. Louis: Mosby; 1998:110–148.

56 Skeletal Atlas of Child Abuse Fractures of the Vertebral Column, Sternum, 4 Scapulae, and Clavicles Vertebral, sternal, and scapular fractures are rare in children and are described in the literature as highly specific for child abuse injury [1–7]. However, current research suggests that sternal fracture may actually occur more often as a result of low-force accidental impact [3, 5]. Clavicular fractures are a very common accidental injury in children but may become more suspicious for nonaccidental injury when they occur on the lateral or medial thirds of the shaft or when there are concurrent fractures of the scapula or vertebrae [8–10]. This chapter takes a holistic approach to the torso by describing fractures of the neck, the thoracic skeleton, the pectoral girdles, and the thoracolumbar and sacral regions of the spine. Although the ribs are components of the thoracic skeleton, the common and complex nature of pediatric rib fractures requires a full chapter of detailed description; therefore, these fractures are not discussed here (see Chap. 3). The human vertebral column is a segmented bony structure typically comprising 33 vertebrae cushioned by intervertebral fibrocartilaginous disks and held in place by strong elastic ligaments. The vertebral column extends from the base of the skull to the inferior pelvic aperture, enclosing and protecting the spinal cord, distributing body weight from the head to the lower limbs, and providing stability and flexibility of motion to the torso. The vertebrae are classified by specialized function into five sections: the cervical column (C1–C7), thoracic column (T1–T12), lumbar column (L1–L5), sacrum (S1–S5, usually fused), and coccyx (4 vestigial, usually fused). The cervical column protects the most delicate and vital portion of the spinal cord, provides a bony fulcrum for head movement, and is the attachment site for the neck muscles. The thoracic column is a stabilizing and flexible component of the thoracic skeleton. The robust lumbar column functions as a strong base for transfer of weight to the pelvic girdle and lower limbs and encloses the termination of the spinal cord. At birth the spinal cord terminates at the second or third lumbar vertebra, but by adulthood the termination lies within the vertebral foramen of either the first or second lumbar vertebra. The sacrum articulates superiorly with the fifth lumbar vertebra and laterally with the right and left innominates. The sacrum functions in the transfer of weight from the lumbar region to the lower limbs and encloses the sacral and coccygeal nerve roots. The coccyx is vestigial and small and is variable in presence and number of fused vertebrae. Fractures of the coccyx are not discussed in this chapter. The thoracic skeleton consists of the thoracic vertebral column, the ribs, the sternum, and the costal cartilage that articulates the sternum to the ribs (Figs. 4.1–4.3). The adult sternum is composed of three segments: the manubrium, the corpus sterni, and the xiphoid process. The manubrium is located at the level of the third and fourth thoracic vertebrae and the corpus sterni at the fifth through ninth thoracic vertebrae. The xiphoid process articulates with the inferior corpus sterni and varies in length and ossification. (The characteristics of the immature sternum are somewhat different and are discussed later in reference to pediatric sternal fractures.) The thoracic skeleton encloses and protects the heart and lungs and serves as a large framework for muscle attachments that enable respiration. The flexibility of the bone and cartilage construction of this region allows for expansion and contraction of the thoracic cage during respiratory movement. The right and left pectoral girdles, each comprising one clavicle and scapula, articulate with the manubrium of the sternum through the medial clavicle. The clavicle stabilizes the

J.C. Love et al., Skeletal Atlas of Child Abuse, Springer’s Forensic Laboratory Science Series, 57 DOI 10.1007/978-1-61779-216-8_4, © Springer Science+Business Media, LLC 2011 arm to the thoracic skeleton and holds the glenohumeral the thorax protected by the supraspinatus, infraspinatus, joint in place through ligamentous attachment of the and subscapularis muscles. The anatomy of the pecto- lateral clavicle to the acromion and coracoid process ral girdle provides the mobility required for directional of the scapula. The scapula, which articulates with movement of the arm. the humeral head, slides over the posterior surface of

Fi g u r e 4-2. Autopsy view of the articulated thoracolumbar region of a 2-year-old male. The chest plate and internal organs have been removed as part of the examination procedure. Fi g u r e 4-1. Autopsy view of the articulated clavicles, sternum, and ribs of a 3-year-old female. To provide access to the internal organs, the costal cartilages will be cut to remove a roughly triangular chest plate containing the sternum.

Fi g u r e 4-3. Autopsy view of the articulated right scapula of a 3-year-old male. The supraspinatus and infraspinatus muscles that form a protective cushion for the relatively delicate scapula (arrow) are not reflected from the bone.

58 Skeletal Atlas of Child Abuse Vertebral Fractures

Spinal fractures account for only a small percentage of anterosuperior end plate usually results in a fragment of nonaccidental pediatric fractures (estimated at 1–3%), bone [1, 16]. possibly as a result of the segmented and ligamentous Kemp et al. [7] conducted an in-depth literature construction of the vertebral column, which is particu- review of published studies and case reports of spinal larly flexible in the young child [1, 7, 11–14]. The mecha- trauma identified in child abuse victims less than 18 years nisms associated with spinal fractures are distraction, old. They found reports of 25 child abuse victims with hyperflexion, and/or hyperextension of the vertebral col- nonaccidental spinal injuries: 12 individuals had cervical umn with associated axial loading and rotation [1, 15]. injuries (median age, 5 months), 12 individuals had tho- The vertebral body is the most common site for verte- racolumbar injuries (median age, 13.5 months), and bral fractures [14]. When a portion of the posterior col- one child had cervical, thoracolumbar, and sacrum umn, such as the posterior spinous process, is fractured, injuries (no age given). The type of musculoskeletal inju- it typically is accompanied by a vertebral body frac- ries observed in their review included C2–C3 fractures, ture. Vertebral body fractures have been categorized anterior vertebral dislocation, compression fracture of into three patterns: (1) mild compression deformity with the vertebral body, and bilateral pedicle fractures. The intact end plates; (2) fracture of the anterosuperior end mechanism of injury was confirmed in eight cases. Four plate with no loss of vertebral body height; and (3) a children were shaken, two children were thrown, one combination of compression deformity with anterosu- child was forcefully spanked, and one child with a sacral perior end plate fracture [1, 16]. The fracture of the injury may have been forcibly seated [7].

Neck Fractures

Infants are particularly vulnerable to cervical spine inju- or hyperextension [7]. Bilateral avulsion of the pedicles ries because of the size and weight of the head relative or their synchondroses from the C2 vertebral body to the body (Figs. 4.4–4.6). At this developmental stage, (spondylolysis) and spondylolysis with spondylolisthesis the infant neck flexes at the C2–C3 segment rather (anterior dislocation of a vertebra) are recognized as than at the C5–C6 segment, as is the case in older chil- an injury secondary to hyperextension. This type of neck dren and adults; the vertebral facet joints are underde- fracture in infants and children most frequently is the veloped and horizontally oriented; and the neck result of motor vehicle crash or fall injuries. However, musculature is immature in tone [7]. When suddenly several case reports describing nonaccidental injury subjected to forces of deceleration, the neck may fail have documented bilateral spondylolysis of the C2 ver- in support of the heavy head, resulting in hyperflexion tebra with associated spondylolisthesis [1, 15, 17, 18].

Fi g u r e 4-5. Magnified view of a C1 fracture. A magnified view of the C1 fracture pictured in Fig. 4.4 shows details of the fracture margins where the posterior synchondrosis was in partial fusion Fi g u r e 4-4. Superior view of a fractured C1 vertebra. A nondis- at injury. placed transverse fracture of the posterior synchondrosis is present in the C1 vertebra of a 3-year-old female. The synchondrosis was partially fused at injury. The anterior synchondrosis is open and atraumatic. The cause of death was classified as blunt trauma of the head, neck, torso, and extremities with cervical vertebral fractures and cervicomedullary spinal cord injury, the manner as homicide.

Fractures of the Vertebral Column, Sternum, Scapulae, and Clavicles 59 Fi g u r e 4-6. Superior view of a fractured C2 vertebra. Bilateral transverse fractures are located at the right and left dentoneural junction of the C2 vertebra from the individual pictured in Fig. 4.4 and 4.5. The fracture pattern of the two vertebrae is consistent with a posterior-to-anterior force that dislocated the dens of C2 anteriorly.

Fractures of the Thoracolumbar and Sacral Regions

Nonaccidental fractures of the thoracolumbar region associated with neurologic symptoms, may not be are typically compression fractures of the vertebral bod- acutely painful, and may be difficult to assess on radi- ies resulting from relatively low-energy forces (Fig. 4.7) ography if no CT is performed [11, 20, 22, 23]. Hart et al. [14]. However, the more severe thoracolumbar fracture [20] conducted a retrospective review of 4,876 cases of with listhesis (dislocation) has been described in several pediatric injury presenting at a children’s hospital over a reports of child abuse injuries [12, 14, 19]. Levin et al. [19] 7-year period. Only eight children had documented reviewed plain films, CT scans, and MRI scans of seven sacral fractures, and each patient’s injuries were thoracolumbar fractures with listhesis in child abuse vic- reported as sustained in motor vehicle crashes or falls tims aged 6 months to 7 years. The authors noted that from height. In a review of 89 case files of patients aged the most common location of the fracture was at the 3–16 years with documented thoracolumbar and/or L1–L2 segment. Bode and Newton [12] and Sieradzki sacral injuries sustained in motor vehicle crashes (66%), and Sarwark [14] each reported a single case of child sports activities (21%), and falls (13%), Dogan et al. [21] abuse with thoracolumbar fracture and listhesis. The found that thoracolumbar spine injuries were more fre- level of the fracture was the T12/L1 segment in both quent in children over 9 years of age. The L2–L5 region cases. Eleven of the 12 thoracolumbar injuries reviewed was the most common injury site (29.8% of cases), and by Kemp et al. [7] were located at the T11–T12 segment, the sacrum was the least common injury site (5% of and included compression of the vertebral body with cases). In this study, all the sacral injuries were fractures associated listhesis. of the ala extending from the lateral margin to the lat- Sacral fractures are rarely diagnosed in children, eral border of the neural foramen (zone 1 fracture). comprising an estimated 0.16% of pediatric trauma Zone 1 sacral fractures are typically the result of lateral cases [20, 21]. However, fractures of the sacrum may be compression of the pelvis. All the patients with sacral underreported because most sacral fractures are not fractures were intact neurologically [21].

60 Skeletal Atlas of Child Abuse Fi g u r e 4-7. Healed compression fracture of the T6 vertebra of a 3-year-old individual. The vertebral body is compressed through the vertical plane, creating a lip along the superior and inferior anterior margins (arrow). The cause of death was classified as complications of blunt trauma of the head with subdural hematoma, the manner as homicide.

Fractures of the Sternum

The sternum is composed of at least four centers of ossifi- body. The authors concluded that although fractures of cation (sternebrae) at birth (Fig. 4.8). The manubrium the sternum are uncommon in children, they are not cannot be identified in isolation until the child is approxi- highly specific for nonaccidental injury. mately 1 year of age [24]. All the sternebrae are usually Ferguson et al. [5] conducted a retrospective study formed by 6 years of age and are fused into a single of sternal fractures treated at a children’s hospital over bone, the corpus sterni, by late adolescence [24]. The a 40-month period. They reviewed the hospital records flexibility associated with the late development of the of children who received a plain radiograph or CT scan sternum has been cited as one of the reasons for the rarity of the thorax after trauma. Twelve cases with sternal of documented pediatric sternal fractures and the likeli- fractures were identified; the age range was 5 years to hood that sternal fractures are associated with significant 12 years. None of the sternal fractures was sustained in blunt force injury to the thorax [1, 25]. Kleinman [1] stated a motor vehicle crash, and all were isolated injuries with- that in the absence of a significant traumatic event, ster- out associated fractures. Eleven of the 12 fractures were nal fractures should be considered suspicious for inflicted nondisplaced fractures of the anterior cortical bone of injury. However, several researchers have found sternal the first and second sternebrae. Seven fractures resulted fractures resulting from relatively minor trauma. from direct blows to the sternum, and five resulted from Hechter et al. [3] reported that pediatric sternal frac- hyperflexion of the torso. One direct blow resulted in a tures may be underdiagnosed, and therefore underre- fracture at the manubriosternal joint and a posterior dis- ported, because of difficulty in obtaining a clear image placement of the corpus sterni. All 12 injuries were acci- of the immature sternum in standard radiographic view. dental and occurred during common activity, such as a They stated that each sternebra must receive a dedi- fall from a trampoline or bouncy structure (four cases), cated radiographic view to eliminate or diagnose frac- a fall from a bicycle (four cases), a fall from a 5- to 6-ft tures of the sternebrae. The authors conducted a height (two cases), and a fall from a standing position retrospective review of radiographic and clinical charts (two cases). of all documented sternal fractures observed at a large In a published case study, DeFriend and Franklin [26] pediatric hospital over an 11-year period. They found 12 described two cases in which children sustained similar documented fractures: four in children under 3 years fractures of the proximal region of the corpus sterni dur- and 8 in children over 3 years of age. Ten of the 12 frac- ing a fall from a swing. One child, an 8-year-old, fell tures were the result of accidental injury. The other two directly onto her chest. The other child, a 7-year-old, fell fractures, one in a 1-year-old and one in a 2-year-old, onto her back, and her legs went up over her shoulders, were suspicious for nonaccidental injury, but the cir- causing hyperflexion of her torso. cumstances of injury were not determined. The most There appears to be consensus in the current litera- common location of sternal fractures in the 12 cases ture that sternal fractures are rare in children but are not was the proximal region of the corpus sterni, followed specific for child abuse in the absence of other suspi- by the manubrium and the lower region of the corpus cious injuries. Pediatric sternal fractures occur most fre- sterni. The most common mechanism of injury was a quently in the proximal region of the corpus sterni, are direct blow to the sternum. In nine cases, there were no rarely displaced, and are often the result of accidental associated fractures of the thorax or other regions of the injury at relatively low levels of force.

Fractures of the Vertebral Column, Sternum, Scapulae, and Clavicles 61 Fi g u r e 4-8. Sternal development of a 6-month-old male in radiographic view. The sternum is composed of at least four centers of ossification (sternebrae) at birth. The manubrium cannot be identified in isolation until the child is approximately 1 year of age.

Fractures of the Scapula

Scapular fractures in adults are relatively uncommon shaking, similar to the mechanism associated with clas- and are typically caused by a direct impact of signifi- sic metaphyseal lesions of long bones. cant force [27]. Several mechanisms may result in frac- The most common location of nonaccidental scapu- ture of the adult scapula: (1) a direct downward impact lar fractures is the middle third of the acromion, although to the shoulder, fracturing the acromion; (2) a direct fractures of the coracoid and inferior glenoid margin also impact to a flexed elbow, transmitting force to and have been documented [1]. In concordance with the fracturing the glenoid rim; (3) a direct impact to the lat- conclusions of Kogutt et al. [25], Kleinman [1] theorized eral shoulder, causing a stellate glenoid fracture; (4) a that nonaccidental scapular fractures are likely a result direct blow to the superior aspect of the shoulder, frac- of indirect forces generated by violent traction and tor- turing the coracoid; and (5) forceful muscular contrac- sion of the humerus. His theory is based on the anatomic tions, resulting in avulsion fracture of the acromion or structure of the shoulder and the concomitant pattern of the coracoid [27]. Pediatric scapular fractures also are fractures observed in abused children. The acromio- uncommon and are recognized as highly specific for clavicular and coracoclavicular ligament attachments nonaccidental injury. However, it has been postulated to the clavicle create a stable unit with the predilection that scapular fractures in infants and young children are for the bone to fail along the two scapular processes. more likely the result of indirect forces than direct impact Several researchers have reported avulsive fractures [1, 4, 25, 28]. of the acromion resulting from muscle spasms in pediat- Scapular fractures are considered highly specific for ric cases similar to those documented in adults. Kalideen child abuse and are documented most often in chil- and Satyapal [29] prospectively studied 171 neonates dren with typical child abuse fracture patterns involving with tetanus over a 5-year period and found ten patients the posterior region of the upper ribs and the pectoral with bilateral symmetric avulsive fracture of the right girdle [1, 4, 25, 28]. In an early paper on child abuse and left acromions. Tetanus results in muscle hypertonia fractures, Kogutt et al. [25] reviewed the case histories and spontaneous contraction of agonist/antagonist and radiographs of 100 infants and children diagnosed muscles. In the shoulder, the deltoid muscle abducts with “battered child syndrome” at a teaching hospital against the concomitant adduction forces, resulting in from 1967 to 1971. The age of the patients ranged from the avulsion of the acromion. Coote et al. [28] reported 6 weeks to 8 years. Skeletal fractures were visible on a case of bilateral acromial fractures in a patient with radiograph in 52 (55%) of the cases, with multiple frac- malignant infantile osteopetrosis. The fractures were tures occurring in 22 (23%) of the cases. In the three noted on chest films taken a day after the patient had scapular fractures documented, the authors observed two witnessed seizures. The authors stated that the two types of fracture: transverse blade fracture acute deltoid muscle contraction against the weak (Figs. 4.9–4.13) and acromial process fragmentation. bone resulted in the avulsive acromial fractures at the Kogutt et al. [25] suggested that transverse blade deltoid muscle attachment sites. These findings support fracture results from direct impact and acromion frag- the theory that acromial fractures in children may occur mentation is caused by severe twisting of the arm or through indirect avulsive forces.

62 Skeletal Atlas of Child Abuse Fi g u r e 4-10. Magnified view of a lateral border scapular fracture. This view of the left scapula pictured in Fig. 4.9 shows callus formation at the margins of the lateral border transverse fracture. The direction of force cannot be determined because of healing, but fractures at this location typically occur as the result of a direct impact to the scapular blade. Fi g u r e 4-9. Scapular blade fractures. Two healing incomplete transverse fractures, one on the medial border and one on the lateral border (arrows), are present in the left scapula of a 3-year-old female. The cause of death was classified as multiple blunt trauma of the head, torso, and extremities with fractures; lacerations of the heart, liver, and mesentery; and subdural hemorrhage. The manner was classified as homicide.

Fi g u r e 4-12. Posteromedial fractures of the right and left scapu- Fi g u r e 4-11. Magnified view of a medial border scapular frac- lae of a 21-month-old female. The infraspinous processes are ture. This view of the left scapula pictured in Figs. 4.9 and 4.10 buckled and the medial border of the right scapula is splayed shows rounding of the margins and subperiosteal new bone apart. The fractures (arrows) are consistent with a posterior-to- formation (SPNBF) around the transverse fracture at the medial anterior impact to the back. The cause of death was classified border (arrow). The direction of force cannot be determined as blunt trauma of the torso and head with bilateral rib and because of healing, but fractures at this location typically scapular fractures, visceral lacerations, and multiple contu- occur as the result of a direct impact to the scapular blade. sions; the manner was classified as homicide.

Fractures of the Vertebral Column, Sternum, Scapulae, and Clavicles 63 Fi g u r e 4-13. Posterior view of bilateral scapular fractures. This posterior view of the right and left scapulae pictured in Fig. 4.12 shows the location and extent of the fractures on the posterior blade surfaces (arrows).

Fractures of the Clavicle

Although the clavicle is classified as a long bone, it does [9, 30]. In the absence of an accidental cause, a medial not contain a medullary cavity. The medial articular clavicle fracture in an infant or young child, as is the end is approximately triangular in shape, and the lateral case in sternal fracture, may increase suspicion of non- articular end is relatively flat. The shaft and articular accidental injury. ends form a double curvature (S shape). The clavicle is Clavicle fractures also may result from birth trauma; located just under the skin at the root of the neck, leav- typically these injuries are group I fractures of the mid- ing it relatively unprotected from impact. Because it is shaft [34]. Current research shows that fractures during connected to the acromial and coracoid processes of birth may not be clearly associated with a traumatic the scapula by ligamentous attachment, the clavicle birth event or be the result of congenital skeletal pathol- also may be injured by an impact to the glenohumeral ogy. Beall and Ross [35] conducted a retrospective joint. Falls, sports injuries, and motor vehicle crashes study of all deliveries at a large urban teaching hospital often result in clavicle fractures, which are reported as from January 1996 to March 1999 to observe the inci- the most common pediatric fracture [9, 30]. dence of birth-related clavicle fracture and to quantify The S shape of the clavicle is divided into thirds for the association of clavicle fracture with shoulder dysto- mechanical classification of fractures by location [9, 31, cia. Shoulder dystocia is the inability of the infant to pass 32]. Group I fractures are those of the middle one third, through the birth canal in a timely manner because the group II fractures are of the lateral third (Figs. 4.13–4.18), shoulders are wedged within the pelvic girdle. Shoulder and group III fractures are of the medial third. The mid- dystocia traditionally has been associated with clavicle clavicular shaft contains a weak spot, which is a prod- fractures [35]. The researchers found 26 clavicle frac- uct of the double-curvature shape, and this is the most ture cases among the 4,297 births (5%). In these cases, frequent site of accidental clavicular fractures (group I clavicle fracture was significantly associated with fractures). Group I fractures typically result from direct increased maternal age and birthweight greater than impact to the lateral shoulder, as may occur in a fall. 4,000 g, but not with documented shoulder dystocia Group II fractures and group III fractures are those of events. the lateral third and medial third, respectively. Neer [32] As further supporting evidence, Groenendaal and further categorized group II fractures into five types Hukkelhoven [36] concluded from an extensive retro- based on the relationship of the fracture to the coraco- spective study of neonate fractures in the Netherlands clavicular ligaments. Group II fractures in an infant or that clavicle fractures may be sustained during birth young child with no history of major accidental trauma without a documented birth trauma event. The authors are more suspicious for nonaccidental injury, because researched the incidence of unexplained clavicle frac- fracture of the lateral third of the clavicle typically is tures in full-term neonate admissions during the perina- caused by a direct blow to the top of the shoulder tal period to ten neonatal intensive care units and 60% [9, 10]. Impact to the top of the shoulder is unlikely to of the level 2 hospitals in the Netherlands from 1997 to occur in a short fall. Group III fractures are categorized 2004. The study data were accessed from The into five types based on the severity of the fracture (e.g., Netherlands Perinatal Registry. Documented birth degree of displacement, involvement of the articular trauma and/or congenital bone disease cases were surface, epiphyseal separation, and comminution). excluded. Of the 158,035 full-term births recorded, 1,174 Group III fractures of the medial third are the least com- had fractures and 227 of the fractures were unexplained mon clavicular injury [33]. Medial clavicular fractures by birth trauma. Clavicle fractures were noted in 212 of are caused by direct impact to the anterior chest, which the 227 unexplained fracture cases; the additional 15 may occur through several accidental mechanisms fractures were humeral (12) and femoral (3).

64 Skeletal Atlas of Child Abuse Fi g u r e 4-14. Osteopenic left clavicle of a 1-month-old female with a complete oblique fracture of the lateral third of the shaft. SPNBF is present on the acromial end and on the shaft adjacent to the fracture. The fracture likely is a result of hyperrotation of the clavicle during birth. The cause of death was classified as sudden infant death syndrome, the manner as Fi g u r e 4-15. Magnified view of a clavicular fracture. This view of natural. the oblique fracture described in Fig. 4.14 shows the fracture margins and SPNBF on the acromial end and shaft. Note the normal absence of a medullary cavity in the clavicular shaft.

Fi g u r e 4-17. Remodeled clavicular fracture. A remodeled fracture callus is present on the lateral third of the right clavicular shaft of a 12-month-old female (arrow). The cause of death was classified as multiple blunt force injuries and malnutrition, the manner as homicide.

Fi g u r e 4-16. Stereomicroscopic view of the inferior surface of the clavicular fracture described in Figs. 4.14 and 4.15. Note the rounded fracture margins and early soft callus formation (arrow).

Fi g u r e 4-18. Clavicle injury associated with humeral fracture. SPNBF is present on the lateral third of the left clavicle of a 3-year-old male (arrow). The injury is associated with a complete fracture of the left proximal humerus. The cause of death was classified as blunt trauma of the head, the manner as homicide.

Fractures of the Vertebral Column, Sternum, Scapulae, and Clavicles 65 Summary

Fractures of the neck, sternum, scapula, lateral or abuse injury, as previously thought. Scapular fracture is medial clavicle, and the thoracolumbar and sacral highly specific for nonaccidental injury and may be the regions of the spine are uncommon in infants and result of abnormal forces generated during shaking or young children. Without an explanatory history of acci- abnormal rotation or traction of the arm. Although frac- dental trauma, these fractures may raise suspicions of ture at the clavicle midshaft is a very common pediat- child abuse injury. Infants are at higher risk for C1–C2 ric injury, fractures of the lateral or medial third of the fractures because of their immature neck structures, clavicle are more suspicious for nonaccidental injury. but the most common type and site of pediatric verte- Birth trauma is a possible mechanism for clavicle injury bral fracture are vertebral body compression fractures and is a consideration when healing clavicle fractures in the thoracolumbar region. Fractures of the immature are observed during the infant postmortem skeletal sternum are rare but may not be as specific to child examination.

References

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Fractures of the Vertebral Column, Sternum, Scapulae, and Clavicles 67 wwwww 5 Long Bone Fractures Fractures occurring in the humerus, ulna, radius, femur, tibia, and fibula are collectively categorized as long bone fractures. Long bone fractures are further classified by type and location. Interpretation of the forces associated with the fracture depends on the location, type, and extent of the fracture. Common long bone fracture types include spiral, oblique, transverse, torus (or buckle), greenstick, and classic metaphyseal lesion (CML) [1]. A spiral fracture circles the shaft and typically results from a rotational force. An oblique fracture crosses the bone diagonal to the long axis, and a transverse fracture crosses the bone at a right angle to the long axis. A torus (or buckle) fracture, in which the cortical bone balloons out, is typically the result of a compression force loading through the long axis of the bone. A greenstick fracture is an incomplete fracture, most often an incomplete transverse fracture, and is commonly found in children as a result of the increased elasticity of the developing bone. CML is a fracture of the physeal plate of a long bone. In terms of location, a developing long bone is conventionally divided into four regions: the shaft (or diaphysis), metaphysis, physis, and epiphysis. The shaft, the tubular midsec- tion of the bone, is subdivided into three regions: the mid, distal, and proximal one third. The metaphyses are the flared regions of the proximal and distal ends of the long bone. At the transition between the shaft and the metaphysis, the cortical bone thins and the density of the trabecular bone increases. The physis is the proximal or distal surface (end plate) of the long bone at the chondro-osseous interface. The epiphysis is the cartilaginous end of the bone containing the secondary ossification site.

Classic Metaphyseal Lesions

The CML is considered the long bone fracture with the greatest specificity for nonaccidental injury (Figs. 5.1 and 5.2) [2, 3]. A CML is a transmetaphyseal disruption of trabeculae of the primary spongiosa (the mineralized cartilage in the developing metaphysis) (Fig. 5.3). It occurs when indirect torsional or tractional forces are applied to an extremity during pulling and/or twisting of an infant’s arm or leg, or flailing of unsupported limbs during shaking. The delicate nature of the immature trabeculae, the loose attachment of the periosteum to the diaphysis, and the firm attachment of the perichondrium to the epiphysis all contribute to the bone failing at the specific location [2, 4–7]. The loose periosteum transmits most of the dynamic force associated with the trauma to the metaphysis, where the trabeculae of the primary spongiosa are weaker than the cartilage of the epiphysis [2, 4]. CMLs are most common during the first and second years of life, when the trabeculae of the primary spongiosa are elongating rapidly, making them vulnerable to torsional and tractional forces (Figs. 5.4 and 5.5) [2]. Historically, CMLs have been called bucket handle or corner fractures. The terminol- ogy is based on the radiologic appearance of the fractures. The series of microfractures through the primary spongiosa cause the physeal surface of the bone to separate from the metaphysis, creating a fragment of bone that remains adhered to the epiphysis.

J.C. Love et al., Skeletal Atlas of Child Abuse, Springer’s Forensic Laboratory Science Series, 69 DOI 10.1007/978-1-61779-216-8_5, © Springer Science+Business Media, LLC 2011 Typically the fragment is thicker along the periphery The reported infrequency of CMLs may reflect the dif- and thinner in the middle (Figs. 5.6 and 5.7). ficulties associated with recognizing the fracture rather Radiologically, the fracture appears as a line or a trans- than their true occurrence. A CML is radiologically sub- lucency through the metaphysis that dips deeper into tle; the fracture is rarely displaced, there is minimal hem- the metaphysis at the edges of the bone, creating the orrhage associated with it, and little to no fracture callus bucket handle or corner fracture appearance [8–10]. forms during the healing process [2]. In fact, Lonergan A CML is considered highly suspicious for nonacci- et al. [12] reported that CMLs often are radiologically dental injury, primarily because the forces associated occult. CMLs also are difficult to recognize during a with the fracture are not generated by accidental falls standard autopsy procedure. Figures 5.8 and 5.9 show a [2, 4, 6]. Kleinman and Marks [9] performed a histologic normal chondro-osseous interface and an acute CML and radiologic examination of 31 deceased victims of after the periosteum was removed. Prior to the skeletal child abuse and found 64 CMLs. The authors reported examination, the fracture shown in Fig. 5.9 was not rec- the most common sites for a CML were the proximal ognized, radiologically or grossly (see Chap. 1). Kleinman and distal tibia and the distal femur. Worlock et al. [5] et al. [8], recognizing the difficulty associated with iden- retrospectively compared the medical records of 35 tifying a CML radiologically, have advocated the children with nonaccidental skeletal injury with those of removal of seemingly normal high-risk metaphyses for 826 children with accidental skeletal injury. The records histopathologic examination in decedents with even documented 17 CMLs; all were observed in cases of low-level suspicion of nonaccidental injury. nonaccidental injury in which the child was under the As the CML heals, the exposed trabeculae become age of 18 months. The authors concluded that CMLs are rounded and thickened. Eventually, the physeal sur- uncommon, making up only 17% of the fractures face reforms. (The healing process of CMLs is discussed recorded in the nonaccidental injury cases, but that in detail in Chap. 6.) Figure 5.10 shows a radiograph of they are specific for nonaccidental injury. Conversely, a healing CML. Figure 5.11 shows the same fracture Caffey [11] noted that birth trauma, especially breech after processing. Figures 5.12–5.17 show CMLs at various delivery, may result in a CML. stages of healing.

Fi g u r e 5-1. Normal physeal surface of a 21-month-old female, after processing. Notice the smooth, regular quality of the Fi g u r e 5-2. Complete CML of the proximal fibula of a 1-month- bone. The cause of death was classified as blunt trauma of the old male. Note the exposed trabeculae. The cause of death torso and head with bilateral rib and scapular fractures, visceral was classified as blunt trauma of the head with skull fractures lacerations, and multiple contusions, the manner as homicide. and brain contusions, the manner as homicide.

70 Skeletal Atlas of Child Abuse Fi g u r e 5-4. Complete CMLs of the right and left distal radii of a 2-month-old male. The cause of death was classified as blunt trauma of the head with skull fractures and subdural hemorrhage, the manner as homicide.

Fi g u r e 5-5. Partial CML of the left distal tibia of a 2-month-old female. Note the fractures through the remaining physeal surface. The cause of death was classified as methicillin-resistant Staphylococcus aureus chest wall abscess with disseminated infection and a contributing factor of chronic stress associated with multiple blunt trauma injuries; the manner was classified as homicide.

Fi g u r e 5-3. Partial CML of the proximal tibia of a 1-month-old male. (a, b) Note the partial separation of the physis from the metaphysis through the primary spongiosa. (c) The physeal surface with the trauma along the posterior margin (the arrow is pointing to the tibial tuberosity of the anterior surface). The cause of death was classified as blunt trauma of the head with skull fractures and brain contusions, the manner as homicide.

Long Bone Fractures 71 Fi g u r e 5-6. Classic metaphyseal lesion. Notice that a small disk of bone remains attached to the epiphysis. The bone fragment Fi g u r e 5-7. Complete CML. Shown is a partially processed proxi- is thicker at the periphery of the bone. mal tibia of a 2-month-old female (same individual as pictured in Fig. 5.5). Note the thin disk of bone adhered to the epiphysis that becomes thicker at the periphery (arrow).

Fi g u r e 5-8. Normal metaphyses in situ. (a) The chondro-osseous junction (COJ; arrow) after the muscle has been reflected. b ( ) The COJ after the periosteum has been removed (arrow). Note the COJ is uniform and straight.

72 Skeletal Atlas of Child Abuse Fi g u r e 5-9. Complete CML. A CML of the right proximal fibula the injury. The cause and manner of death were classified of a 1-month-old male (a) and a close-up (b) are shown in situ. as undetermined. Note the absence of hemorrhage in the soft tissue surrounding

Fi g u r e 5-10. Radiograph showing healing CMLs of the distal ulna and radius of a 3-month-old female. Note the frayed appearance of the distal end of both bones (arrows). The cause and manner of death were classified as undetermined.

Long Bone Fractures 73 Fi g u r e 5-11. Processed ulnar CML shown in Fig. 5.10. Note the thickened trabeculae of the reforming physeal surface (a) and the bony spiculae extending from the bone collar (b).

Fi g u r e 5-12. Healing CML of the right proximal fibula of a 2-year- old male. The decedent survived in the hospital for 3 weeks after the date of the injury. Note the thickened trabeculae Fi g u r e 5-13. Healing CML of the proximal humerus of a 3-year- (arrow). The cause of death was classified as blunt force head old female. The trabeculae are thickened and rounded. The trauma, the manner as homicide. cause of death was classified as multiple blunt trauma of the head, torso, and extremities with fractures; lacerations of the heart, liver, and mesentery; and subdural hemorrhage. The manner was classified as homicide.

74 Skeletal Atlas of Child Abuse Fi g u r e 5-14. Healing CML of the distal fibula of a 2-month-old male. The cause of death was classified as blunt trauma of the head with skull fractures and subdural hemorrhage, the manner as homicide.

Fi g u r e 5-15. Healing partial CML of the distal fibula of a 21-month- old female. The healing pattern suggests the fracture was incomplete. The cause of death was classified as blunt trauma of the torso and head with bilateral rib and scapular fractures, visceral lacerations, and multiple contusions; the manner was classified as homicide.

Fi g u r e 5-16. Healing CML with involvement of the metaphysis trabecular bone of the fractured metaphysis. (c) Radiograph of and epiphysis in a 12-month-old female. (a) Note that the the injury (arrow). The cause of death was classified as multiple fracture callus extends above the physeal surface. (b) Exposed blunt force injuries and malnutrition, the manner as homicide.

Long Bone Fractures 75 Fi g u r e 5-17. Possible healing CML of the fibula of a 2-year-old male. Note that the metaphyseal surface appears hyperporo- tic. The cause of death was classified as blunt force head trauma, the manner as homicide.

Shaft, Metaphyseal, and Epiphyseal Fractures

Reconstructing the mechanism of force from the loca- identified five types (Fig. 5.28). Three of the fracture tion and type of fracture has been a focus of much types involve only the cartilage, one of which parallels research. Researchers have described relationships the physeal surface (type I). Fracture types II and IV dip between fractures of the shaft, metaphysis, and epi- into the metaphysis in a manner similar to that of the physis and the type of forces applied to the bone [6, 7, CML. Kleinman [14] theorized that given the shared fea- 13]. Johnson [7] classified four types of long bone fractures between CMLs and epiphyseal separations, the tures and described the force associated with each. forces associated with each are similar and the type of He stated that spiral fractures are caused by a twisting fracture depends on the magnitude of the force. or torsional force (Figs. 5.18 and 5.19), oblique fractures However, the authors of this text hypothesize that the by a levering or bending force (Fig. 5.20), transverse robustness of the trabeculae of the primary spongiosa is fractures by a direct impact (Figs. 5.21 and 5.22), and a contributing factor. CMLs are more common in infants buckle or torus fractures by compression (Figs. 5.23– and very young children, in whom the trabeculae of the 5.25). Pierce et al. [6] added that buckle or torus frac- rapidly elongating long bones are more vulnerable to tures are most common at the metaphysis–diaphysis traumatic forces [5]. In contrast, Salter–Harris fractures interface. They stated that the predilection results from are more common in older children with robust trabec- the structural transition from the dense cortical bone of ulae resulting from the slower growth rate. However, the diaphysis to the dense trabecular bone of the Jones et al. [15] presented two cases of nonaccidental metaphysis, creating an area more susceptible to fail- physeal injury of the proximal femora in infants (9 and ure in compression. 3 months old). The authors described the mechanism of Epiphyseal separations, in contrast to CMLs, are injury as a combination of traction and torque of the primarily cartilaginous injuries, although they may extend femur resulting from simultaneously pulling and exter- into the bone (Figs. 5.26 and 5.27). Epiphyseal separa- nally rotating the extremity. They inferred that physeal tion occurs more often with accidental injury, especially separation occurs because the ligamentum teres is in older children. Salter and Harris [13] studied more resistant to stress than is the fibrous anchoring ring these fractures experimentally induced in rabbits and of the physis.

76 Skeletal Atlas of Child Abuse Fi g u r e 5-18. Spiral fracture of the right humerus of a 1-month-old male. The cause of death was classified as blunt trauma of the head with skull fractures and brain contusions, the manner as homicide.

Fi g u r e 5-19. Spiral fracture of tibial shaft observed in a 4-month- old male. Note the early formation of a fracture callus. The Fi g u r e 5-20. Vertical ulnar fracture. Shown is an incomplete verti- cause of death was classified as blunt force head trauma, the cal fracture of the ulnar midshaft observed in a 14-month-old manner as homicide. male (a) and a close-up (b). The cause of death was classified as blunt force head trauma, the manner as homicide.

Long Bone Fractures 77 Fi g u r e 5-21. Transverse humeral fracture. (a–c) Transverse fracture family, the decedent’s left arm was shut in a car door. Note the with anterior/posterior compression located on the left proxi- early formation of a fracture callus. The cause of death was clas- mal humeral shaft of a 3-year-old male. According to the child’s sified as blunt trauma of the head, the manner as homicide.

Fi g u r e 5-23. Torus ulnar fracture. Shown is a torus fracture of the proximal ulna (arrow) of a 14-month-old male. The cause of death was classified as blunt force head trauma, the manner as homicide.

Fi g u r e 5-22. Transverse ulnar fracture. Shown is an incomplete transverse fracture of the ulnar shaft of a 3-year-old female (a) and a close-up of the fracture (b; same individual as shown in Fig. 5.13). Note the early signs of healing, rounded fracture margins, and minimal subperiosteal new bone formation (SPNBF).

78 Skeletal Atlas of Child Abuse Fi g u r e 5-24. Torus ulnar fracture. Shown are a torus fracture (arrow) of the distal ulnar shaft of a 16-month-old female (a) and a close-up of the fracture (b). Panel (b) shows the posterior surface of the bone. The cause of death was classified as blunt force head trauma, the manner as homicide.

Fi g u r e 5-25. Healing fracture of the left distal radial shaft of a 2-year-old female. The cause of death was classified as blunt trauma of the head with subdural hematoma and skull fracture, the manner as homicide.

Fi g u r e 5-26. Epiphyseal fracture. Shown is an epiphyseal fracture and the fracture callus (arrows) were not visible until the bone of a 12-month-old female, before processing (a) and after pro- was processed. The cause of death was classified as multiple cessing (b). The extension of the fracture into the metaphysis blunt force injuries and malnutrition, the manner as homicide.

Long Bone Fractures 79 Fi g u r e 5-27. Humeral condylar fracture. (a, b) Fracture of the indicating healing in the absence of a fracture callus and lateral condyle of the right humerus of a 12-month-old SPNBF. The fracture of the epiphysis was not noted prior to female. Panel (b) shows the distal physeal surface. Note the processing. The cause and manner of death were classified as rounded fracture margins and the thickened trabecular bone, undetermined.

Fi g u r e 5-28. Salter–Harris classification system. The five fracture Type III involves only the cartilaginous epiphysis. Type IV involves types of the Salter–Harris classification system are shown. Type I both the epiphysis and metaphysis. Type V is a crushing injury is a cartilaginous fracture that parallels but typically does not involving the interface of the cartilage and bone. involve the metaphysis. Type II involves a metaphyseal fragment.

80 Skeletal Atlas of Child Abuse Accidental Versus Nonaccidental Injury

The distinction between accidental and nonaccidental 13 years and identified 429 fractures. The most common injury cannot be made on fracture type alone, because bone fractured was the humerus, followed by the femur no long bone fracture type is pathognomonic for non- and the tibia. Loder and Bookout [21] reviewed 75 cases accidental injury [16–19]. Differentiating accidental from of battered children with fractures (average age of the nonaccidental long bone fractures depends on the age study sample was 16 months). The most common frac- and developmental stage of the child and the history of ture occurred in the skull, followed by the tibia. the traumatic event as well as the type and location of Additionally, researchers have searched for trends in the fracture [6, 12, 18–20]. Several researchers have fracture types among nonaccidental injuries. Worlock emphasized the importance of considering the age of et al. [5] performed a retrospective comparison of frac- the patient when diagnosing nonaccidental injury [5–17, ture patterns observed in accidental and nonacciden- 21–26]. As mentioned previously, Worlock et al. [5] retro- tal trauma in children under the age of 5 years and spectively compared nonaccidental to accidental long found spiral humeral fractures were significantly more bone fractures and found that one in eight children common in the group with nonaccidental trauma under the age of 18 months who sustain a fracture is a (P < 0.001). Beals and Tufts [29] conducted a retrospec- victim of child abuse. Pandya et al. [24] compared skel- tive review of medical charts and radiographs of chil- etal injury patterns of 500 child abuse victims with 985 dren under the age of 4 years with femoral fractures accidental injury cases (aged birth to 48 months) and treated at the University of Oregon Health Sciences found that the odds of a tibial/fibular fracture were 12.8 Center over a 22-year period. The authors found that times, humeral fracture 2.3 times, and femoral fracture fractures of the subtrochanteric level and CMLs of the 1.8 times more likely the result of child abuse if the child distal physis were more common in victims of nonacci- was under 18 months of age. Conversely, in children dental injury. Additionally, Arkader et al. [30] examined 18 months of age and older, the occurrence of humeral the occurrence of complete metaphyseal fractures of and femoral fractures was 3.4 and 3.3 times more likely the distal femur recorded by two level 1 trauma centers the result of an accidental injury. In a literature review, over a 10-year period. They found 29 fractures, 20 of Pierce et al. [6] found that among infants, 40–80% of which occurred in infants. Fifteen of the 20 fractures were long bone fractures are from abuse. Coffey et al. [27] confirmed to be the result of child abuse or highly suspi- conducted a retrospective study of patients treated at cious for abuse. The five fractures resulting from acciden- a regional pediatric trauma center and found that 67% tal injury were the result of birth trauma, a fall from a of lower-extremity fractures in patients less than swing, being dropped by a sibling, a fall from a bed, and 18 months of age were linked to child abuse whereas a motor vehicle accident (Fig. 5.29). As mentioned ear- only 1% of lower-extremity fractures in patients 18 months lier, Loder and Bookout [21] reviewed 75 cases of bat- of age and older were linked to abuse. tered children with a total of 154 fractures and found the Researchers have studied the occurrence of most common long bone fracture was transverse nonaccidental fractures by long bone in an attempt to shaft fractures, followed by CMLs. Rewers et al. [31] identify trends; however, there is no consensus. Kemp conducted a review of the cases with documented et al. [19] conducted a thorough literature review with femoral fractures entered into the Colorado Trauma the goal of distinguishing fractures resulting from acci- Register over a 4-year period. They found that among dental and nonaccidental injuries. The authors included children younger than 3 years, falls were the most com- studies that reported skeletal trauma in children less mon cause of femoral fractures, followed by nonacci- than 18 years of age and found that the probability of dental injury. The nonaccidental femoral fractures abuse given a humeral fracture was between 0.48 and tended to be more distal and to have a combined 0.54 and that of a femoral fracture was between 0.28 shaft–distal metaphysis pattern. and 0.43. Loder and Feinberg [25] conducted a retro- As noted earlier, humeral and tibial fractures are spective review to examine the demographic and injury common in nonaccidental injury; however, these frac- characteristics of children hospitalized with nonacci- tures are common in accidental injury as well. Of dental injury. Using the 2000 Healthcare Cost and humeral fractures, shaft and supracondylar (Fig. 5.30) Utilization Project Kids’ Inpatient Database of child fractures are reported frequently in cases of accidental abuse cases, the authors identified 1,794 cases with injury in infants and children [19]. Humeral shaft frac- musculoskeletal trauma and a diagnostic coding of tures have been documented as birth trauma, most abuse. These cases were broken down into four groups often associated with macrosomic and breech presen- based on age: infants (birth to 1 year), toddlers tation [32]. Hymel and Jenny [33] reported two cases of (1–2 years), children (3–12 years), and adolescents accidental spiral humeral shaft fractures occurring in (13–20 years). Forty-nine percent of all the fractures infants when they were rolled onto their outstretched occurred in the infant group. The most common loca- arm by a caregiver. Furthermore, Shaw et al. [34] con- tion of a fracture was the skull, followed by the humerus ducted a retrospective study during which four and the femur. King et al. [28] reviewed the charts and physicians independently reviewed the medical charts radiographs of 189 battered children aged 1 month to of patients younger than 3 years who were treated

Long Bone Fractures 81 for humeral shaft fractures (N = 34). Based on the charts, the physicians ranked each case as probable not abuse, probable abuse, or indeterminate. Of the 34 cases, 62% were unanimously ranked or ranked by three of the four physicians as probable not abuse, and 20% were ranked as probable abuse by one or more of the physicians. The remainder of the cases (18%) were ranked as indeterminate by two or more of the physicians. Kemp et al. [19] reviewed 32 published studies of child abuse victims younger than 18 years and found that supracondylar fractures were reported to be more likely associated with accidental injury, specifically falls. Worlock et al. [5] found that in the 35 infants and toddlers with nonaccidental injuries (150 total fractures), only one fracture was identified as supracondylar. Of the 116 infants and toddlers with accidental injuries (135 fractures), 13 fractures were identified as supracondylar. Despite reporting a lower occurrence of supracondylar fractures in nonaccidental cases than accidental cases (3:70), Strait et al. [22] cautioned against dismiss- ing supracondylar fractures as accidental based on fracture type alone. Accidental tibial fractures require special attention. Fi g u r e 5-29. Healing torus fracture. Shown is a healing torus frac- Childhood accidental spiral tibial (CAST) fractures typi- ture (arrow) of the distal femoral metaphysis observed in a cally are isolated spiral fractures located on the mid 1-month-old female. Note the frayed appearance of the and distal regions of the tibial shaft that occur with rel- periphery of the physeal surface; the physeal surface is intact. atively low levels of force. Often the spiral fracture is The cause of death was classified as hypoxic–ischemic oriented superolaterally to inferomedially. CAST frac- encephalopathy due to multiple blunt force injuries, including tures are most common in children aged 2–6 years. The skull fractures and subarachnoid hemorrhage; the manner mechanism is a torque or rotational force applied to was classified as homicide. the lower extremity associated with a fall or an immobilized foot [35]. CAST fractures are easily recognized on radiographs. Toddler fractures, which are considered a subset of CAST fractures, are nondisplaced oblique or spiral fractures of the distal tibia that are difficult to recognize on radiographs [8]. Mellick and Ressor [35] conducted a 14-month prospective study during which ten CAST fractures were recognized, as well as a retrospective study of 5 years of social work service records of child abuse cases. Of the ten fractures examined during the prospective study, nine were a result of accidental injury and were found in children ranging in age from 21 to 44 months. Only one fracture resulted from nonaccidental injury; the infant was 9 months old (nonambulatory). During the retrospective study of the child abuse cases, 33 cases were found with skeletal injury, only three of which were CAST fractures. Of the three CAST fractures, one was in a 2-month-old who on subsequent hospital visits had rib fractures. The other two cases involved a 19-month- old and a 17-month-old, and the suspicion of child abuse and neglect was based on an inability to exclude child abuse and a previous allegation of leav- ing the child unattended. Of interest, Schwend et al. [26] found that spiral femoral shaft fractures were com- Fi g u r e 5-30. Supracondylar humeral fracture observed in a mon in ambulatory children and described them as 3-year-old female. Note the SPNBF along the shaft proximal to analogous to toddler fractures. They stated that femo- the fracture. The cause of death was multiple blunt trauma of ral shaft fractures may occur at relatively low-energy the head, torso, and extremities with fractures; lacerations of levels, including low-level simple falls, and are nonspe- the heart, liver, and mesentery; and subdural hemorrhage. The cific for nonaccidental injury. manner was classified as homicide.

82 Skeletal Atlas of Child Abuse Summary

Long bone fractures are highly variable in type and is pathognomonic for nonaccidental injury. The age of location. The mechanism of the injury often can be the child, inconsistencies between history and clinical reconstructed from the features of the fracture. The con- presentation, delay in treatment, and injuries of various sensus among researchers is that no long bone fracture ages often are more telling than the fracture itself.

References

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Long Bone Fractures 83 wwwww Healing and 6 Interpretation The ultimate goal of skeletal injury analysis in cases of suspected child abuse is to reconstruct the child’s life history with regard to the number, extent, and timing of the traumatic episodes. Recognizing and interpreting fracture distribution patterns throughout the body enable the anthropologist to move from the myopic assessment of the isolated fracture to the comprehensive evaluation of the inflicted injury that may have multiregional involvement. In turn, assessment of the stage(s) of healing observed throughout the skeleton often leads to an estimate of the minimum number of traumatic episodes and the age(s) of the injury. However, variation in healing rates associated with the type of bone injured and the extent of the initial injury must be recognized.

Healing

Conventionally, bone healing is broken into three phases: inflammation, reparation, and remodeling. The inflammation phase begins immediately following the trauma as a result of bleeding from the damaged periosteum, bone, and surrounding soft tissues. The hemorrhage leads to formation of a hematoma, which may be intramedullary, subperiosteal, or extraperiosteal, depending on the extent of the injury. The disruption of the vessels of the Haversian and Volkmann systems interrupts the blood supply to the osteocytes adjacent to the fracture site, resulting in a focal avascular trabecular and cortical bone. Necrosis of the bone, cartilage, and soft tissue occurs at the avascularized areas. With time, the hematoma is vascularized and inflammatory cells migrate into the injury site. The initial cellular repair processes are organization of the fracture hematoma and resorption of the necrotic tissues. Fibrovascular tissue replaces the clot. The collagen fibers eventually are mineralized to form the woven bone of the primary callus [1–5]. During the reparation phase, new bone is formed through two processes, endochondral and membranous; meanwhile, the necrotic bone of the fracture ends continues to be resorbed. Endochondral bone formation occurs within the hematoma, and membranous bone formation occurs under the periosteum. The organizing hematoma serves primarily as a fibrin scaffold that supports the repair cells. The repair cells are of mesenchymal origin and are pluripotent, forming collagen, cartilage, and bone. Initially, cartilage forms within the organizing hematoma, now referred to as the fracture callus. With time, the cartilage is resorbed and replaced by bone. The newly formed bone is highly disorganized woven bone. Concomitantly, the cells of the cambium layer of the periosteum and endosteum proliferate and begin to deposit bone matrix. The bone matrix envelops the forming callus. As the cartilage and bone form, the fracture becomes increasingly more stable; however, it remains vulnerable to deformation during this phase [3, 4]. McKibbin [5] and Chapman [4] described the formation of a medullary callus as part of the healing process. They stated that formation of the medullary callus occurs later in the healing process, forms in the absence of a cartilage model, and appears to be unaf- fected or possibly stimulated by motion at the fracture site. The primary function of the medullary fracture callus is to replace the fracture gap.

J.C. Love et al., Skeletal Atlas of Child Abuse, Springer’s Forensic Laboratory Science Series, 85 DOI 10.1007/978-1-61779-216-8_6, © Springer Science+Business Media, LLC 2011 The final phase of healing is the remodeling phase, Healing of physeal injuries follows a reparative course during which the disorganized woven bone is replaced different from that of shaft and metaphyseal fractures. with organized mature bone. Osteoclasts remove the To understand the repair mechanisms, an understand- superfluous and poorly organized woven bone, whereas ing of normal growth and development is necessary. osteoblasts form mature bone that is organized in accor- Growth at the epiphysis occurs through endochondral dance to biomechanical forces. Most likely, bone for- ossification. The epiphysis consists of hyaline cartilage, mation and resorption are controlled by piezoelectricity and at the furthest point from the physeal plate the cells [3]. When the bone is subjected to stress – compressive, are in a resting state. As the cells progress from the rest- tensile, or shearing – electropositivity occurs along the ing state to ossification, they transition through several more convex surface and electronegativity occurs phases. Histologically, the transition is broken down into along the more concave surface. Electropositivity five zones: (1) resting, (2) proliferation, (3) hypertrophic appears to favor bone formation, and electronegativity cartilage, (4) calcified cartilage, and (5) ossification favors bone resorption. Ultimately, the bone will return (Fig. 6.2). In the resting zone, the chondrocytes are dis- to its original contour or an altered form that enables organized. In the proliferative zone, the chondrocytes the bone to sustain normal biomechanical forces [3, 4]. divide rapidly and organize to form columns of stacked Subperiosteal new bone formation (SPNBF) is the cells. The columns are oriented parallel to the long axis bone formed by the cambium layer of the periosteum, of the bone. In the hypertrophic cartilage zone, the as mentioned earlier. It requires special attention in chondrocytes become enlarged through the accumu- infants and children because occasionally it is the only lation of glycogen, and the lacunar wall is resorbed, evidence of injury observed [2]. At very low levels of resulting in a thin septum between the cells. Some of the force, the periosteum may be disturbed in the absence lacunae become confluent. In the calcified cartilage of a fracture, causing SPNBF to occur (Fig. 6.1). When a zone, the chondrocytes die and the thin septum of the fracture does occur, the weakly attached periosteum chondrocytes becomes calcified by deposits of hydroxy- enables the hematoma to spread along the diaphysis apatite. In the ossification zone, blood capillaries and and metaphysis, leading to diffuse new bone formation osteoprogenitor cells originating from the periosteum [3]. SPNBF also is laid down in response to frostbite, burns, invade the cavities left by the chondrocytes. The osteo- and infection and as a function of normal growth and progenitor cells give rise to osteoblasts, which deposit development [2, 6, 7]. Using high-detailed postmortem bone matrix over the calcified cartilage [2, 8, 9]. skeletal radiologic surveys, Kwon et al. [7] studied 101 When the physeal plate is injured, the blood supply neonates and infants who had died of sudden infant to the ossification zone is disrupted, interrupting the ossi- death syndrome. The authors found SPNBF in 35% of the fication of the matrix. In the absence of ossification, the sample. SPNBF peaked at ages 2–3 months, was uncom- hypertrophic and calcified cartilage zones thicken. mon in infants younger than 1 month and those older Kleinman et al. [10] compared the thickness of the than 4 months, and did not exceed 2 mm in thickness. hypertrophic zones in traumatized distal tibiae to atrau- SPNBF was found more commonly on the bones of the matic distal tibiae and found it to be significantly greater lower extremities and bilaterally. Johnson [6] stated that at the site of injury. The authors found the thickening SPNBF due to normal growth and development occurs may be focal or diffuse, and they theorized the involve- most often in infants less than 4 months old. He also ment is a reflection of the extent of the initial injury. described pathologic SPNBF as typically layered, When the thickening is focal, normal bone formation greater than 2 mm in thickness, having a convex border, adjacent to the injury site creates the appearance of and extending into the distal metaphyseal and periphy- cartilaginous extensions into the physeal plate. Finally, seal regions. Kleinman [2] found that the quantity, thick- the authors warned that diffuse hypertrophic thickening ness, density, and longitudinal extension of SPNBF is observed in several pathologic conditions, such as correlate to the severity of the injury and increase with rickets and mucolipidosis II. movement at the fracture site.

Fi g u r e 6-1. Subperiosteal new bone formation. Shown is the inferior surface of a rib angle of a 2-month-old male. Note the SPNBF in the absence of a fracture. The cause and manner of death were classified as undetermined.

86 Skeletal Atlas of Child Abuse Fi g u r e 6-2. Thin section of the costochondral junction of a rib of a 2-year-old male. The five zones of endochondral bone formation are labeled as follows: R resting zone; P proliferation zone; H hypertrophic cartilage zone; C calcified cartilage zone;O ossification zone.

Stages and Rates of Healing

In the dry bone under gross examination, the three The remodeling stage spans from the late conversion phases of healing often are broken into four stages: of the woven bone to lamellar bone to the reforming of induction, soft callus formation, hard callus formation, the normal contour of the bone and reconstitution of and remodeling. The induction stage spans from the the medullary cavity (Figs. 6.11 and 6.12). The fracture moment of injury until SPNBF is observed at the fracture line may be visible during the early remodeling phase. site (Figs. 6.3 and 6.4). Rounding of the fracture margins According to Chapman [4], this phase may last through- as a result of osteoclastic resorption occurs during this out the growth and development of the child. Kleinman stage and is typically observed at 4–7 days post injury [2]. [2] found that the stage typically peaks around 1 year. However, in very young infants, SPNBF may be observed Islam et al. [12] examined 707 radiographs of forearm prior to rounding of fracture margins (Fig 6.5). fracture in 141 patients, who ranged in age from 1 to The soft callus formation stage spans from the gross 17 years, with a mean age of 8 years. The results of the recognition of SPNBF to initial bridging of the fracture study are listed in Fig. 6.13. This study presented a pic- line. The fracture line is first bridged with fibrous matrix ture of the healing rate in subadults; however, the sensi- and then with primary woven bone (Figs. 6.6–6.8). The tivity of feature detection was affected by the variable fibrous bridge typically disintegrates during the macera- interval between follow-up radiographs and the effects tion process, but the SPNBF remains. During this stage, of the external stabilizing cast on the clarity of the the callus is disorganized. Radiologically, SPNBF typically radiographs. is observed 10–14 days post injury in children and The healing rate of physeal injuries is much less defined. 7–10 days in infants. SPNBF has been documented There is a substantial paucity of research on physeal heal- 4 days after injury in neonates with birth trauma [2]. The ing rates, most likely because of the difficulties associated peak period for bridging of the fracture line is 14–21 days with recognizing healing classic metaphyseal lesions in children [2]. (CMLs; see Chap. 5). SPNBF and callus formation typically During the hard callus stage, the fracture callus fully do not occur with the healing of physeal injuries, and bridges the fracture, the fracture line is in the process of extensions of cartilage into the primary spongiosa are obliteration, and the woven bone is replaced by lamellar subtle [2, 10]. Kleinman [2] stated that a CML becomes bone, commonly termed consolidation (Figs. 6.9 and 6.10). inconspicuous by 4–8 weeks after the date of injury. During this stage, the osteoclasts are still active but most Grossly, the fractured physeal surface transitions from of the hematoma and inflammatory tissue is resorbed sharp trabeculae to rounded thickened trabeculae to [2]. Salter [11] gave a rough rule of thumb for aging reformation of the physeal surface (Figs. 6.14–6.18). Thus consolidating femoral fractures: 3 weeks at birth, 8 weeks far, these gross changes have not been correlated to the at 8 years, 12 weeks at 12 years, and 20 weeks at age of injury. However, the rate of healing most likely ³20 years of age. Kleinman [2] stated that the hard cal- depends on the growth rate at the specific site as well as lus stage may range from 14 to 90 days in children, but the extent of the injury, the age and health status of the the peak period is 21–42 days. individual, and whether the injury was repetitive [2, 10].

Healing and Interpretation 87 Fi g u r e 6-3. Early induction stage. Shown are acute posterior rib fractures of a 2-month-old female. Note there is an absence of healing, the fracture margins are sharp, and there is no SPNBF. The cause of death was classified as acute bacterial bronchopneumonia associated with bronchopulmonary dysplasia due to prematurity, the manner as natural.

Fi g u r e 6-4. Late induction stage. Shown is a healing fracture of the right ulnar shaft of a 3-year-old female. Note the rounding of the fracture margins with no definitive SPNBF. The cause of death was classified as multiple blunt trauma of the head, torso, and extremities with fractures; laceration of the heart, liver, and mesentery; and subdural hemorrhage. The manner was classified as homicide.

88 Skeletal Atlas of Child Abuse Fi g u r e 6-5. Healing radial fracture of a 9-month-old female. Note the sharp edges of the fracture surrounded by SPNBF. The cause of death was classified as blunt force head trauma with skull fractures and brain injury, the manner as homicide.

Fi g u r e 6-6. Early soft callus formation stage. Shown is a healing lateral rib fracture of a 13-month-old female. Note the thin layer of SPNBF forming along the pleural surface of the rib (arrowheads). The cause of death was classified as blunt injuries of the head, the manner as homicide.

Fi g u r e 6-7. Soft callus formation stage. Shown are healing lateral rib fractures of a 2-month-old male. Note that the SPNBF is thicker and nearly completely surrounds the shaft. The cause of death was classified as blunt trauma of the head with skull fractures and brain contusions, the manner as homicide.

Healing and Interpretation 89 Fi g u r e 6-8. Late soft callus formation stage. Shown are healing lateral rib fractures of the same individual pictured in Fig. 6.7. Note that the fracture calluses are large and consist primarily of woven bone. In situ, the calluses bridged the fractures, but after processing, the fractures remain open.

Fi g u r e 6-9. Early hard callus formation. Shown is a healing posterior rib fracture of a 2-year-old female. Note that the fracture callus is still disorganized and the fracture line is still visible, but there is complete union of the fracture. The cause of death was classified as multiple blunt force injuries of the torso, the manner as homicide.

Fi g u r e 6-10. Late hard callus formation stage. Shown is a healing posterolateral rib fracture of the same individual pictured in Fig. 6.9. Note that the fracture line is still somewhat visible as the woven bone is being consolidated into lamellar bone.

90 Skeletal Atlas of Child Abuse Fi g u r e 6-11. Early remodeling stage. Shown are healing posterior rib fractures of the same individual pictured in Fig. 6.7. Note the loss of the fracture line and the consolidation of the disorganized callus.

Fi g u r e 6-12. Remodeling stage. Shown are healing posterior rib fractures of the same individual pictured in Fig. 6.7. Note the organization of the bone callus into lamellar bone and the reduction of the callus as the normal contour of the bone is reestablished.

Healing and Interpretation 91 RADIOLOGIC CHANGES OBSERVED IN HEALING FOREARM LONG BONE FRACTURES FeatureTime since Status Patients, % (n/n) Injury, wk Rounding of fracture margins1Present60 (42/70)

SPNBF < 2Absent100 (0/22) 4Present 100 (33/33) SPNBF incorporation in cortex 3Present 0 (0/66)

10 Present58 (31/53) Fracture margin resorption 2Occurred9 (11/177) 4–6 Occurred 56 (84/150) 7Occurred1 (1/96) Decrease in fracture gap8Occurred 91 (86/95) Sclerosis of fracture margin 2 Present6 (7/117) 4–6 Present 85 (128/150) 11 Present0 (0/18) Calcified callus 2 Present 15 (18/117) 4 Present 100 (sample size not given) Density of callus (equal to 10 Present 90 (26/29) surrounding cortical bone) Bridging 8 Partial50 (sample size not given) 10 Complete 40 (12/30) Remodeling 4 Present1 patient 8 Present 95 (91/96)

Fi g u r e 6-13. Radiologic changes observed in healing forearm long bone fractures (data from Islam et al. [12]).

Fi g u r e 6-15. Early healing CML on the right proximal fibula of a 2-year-old male. Note the area of thickened trabeculae (arrow). The cause of death was classified as blunt force head Fi g u r e 6-14. Acute CML of the right proximal fibula of a 1-month- old male. Note the sharply defined trabeculae. The cause of trauma, the manner as homicide. death was classified as blunt trauma of the head with skull fractures and brain contusions, the manner as homicide.

92 Skeletal Atlas of Child Abuse Fi g u r e 6-17. Healing CML of the left distal tibia of a 2-month-old male. Note the reforming of the physeal plate. The cause of death was classified as blunt trauma of the head with skull fractures and subdural hemorrhage, the manner as homicide.

Fi g u r e 6-16. Healing CML of the left distal tibia of a 3-month-old female. Note the increased thickening of the exposed trabeculae. The cause and manner of death were classified as undetermined.

Fi g u r e 6-18. Healing CML of the left distal fibula observed in a 21-month- old female. The original fracture most likely was incomplete and involved the lateral region only. Note the porotic but reforming physeal plate. The cause of death was classified as blunt trauma of the torso and head with bilateral rib and scapular fractures, visceral lacerations, and multiple contusions; the manner was classified as homicide.

Healing and Interpretation 93 Healing of the Skull

Gross examination of processed bone reveals that osteoclastic craniectomy for sagittal synostosis. Using woven bone bridges fractures in the skull in a manner radiographs, they found that reossification did not occur similar to that of other parts of the skeleton, but large at the craniectomy edges but rather as small bone fracture calluses typically do not form. The woven bone islands that developed between the separated margins deposited does not exceed the thickness of the bone of the surgical cuts. These islands of bone expanded to (Figs. 6.19–6.21). Concurrently, a very thin layer of SPNBF join the fragment margins. The authors found initial reo- blankets the bone affected by the hematoma ssification started at 2 weeks postoperation in all patients (Fig. 6.22). and was completed by 6 months in infants 6 months old Research has shown that the dura mater is active as and younger at the time of surgery, 12–18 months in a regulator of calvarial ossification in infants and chil- infants 7–12 months old, and 2 years in young children dren less than 2 years of age [13, 14]. The fibrous mem- (>12 months). In young children, the authors found a brane allows for more effective reossification of defects tendency for the formation of persistent pseudo-sutures in the calvaria of children than in that of adults. at the surgical sites. Of note, during the procedure the Greenwald et al. [14] suggested that it is the differential surgeons obtained hemostasis of the bone fragments expression of growth factors and extracellular matrix using bone wax. One of the most common complica- molecules that distinguishes the osteogenic propensity tions associated with bone wax is inhibition of osteogen- of adult and subadult dura mater. The authors were esis [18]. Therefore, the healing rates reported by Hassler able to demonstrate a relatively greater rate of prolif- and Zentner [16] may be slightly slower than expected eration of dural cells as well as significantly higher rates in the absence of bone wax. Paige et al. [17], studying of production of proliferating cell nuclear antigen, trans- healing of frontal orbital advancement procedures per- forming growth factor b1, basic fibroblast growth factor formed in children with sagittal synostosis, also found a 2, alkaline phosphatase, osteocalcin, and collagen Ia direct correlation between the age of the child and the gene expression in young children. Calcified bone nod- completeness of skull regeneration. In a retrospective ules arose from the immature dural cultures but did not study, the authors reviewed the medical charts of 81 grow from the adult dural cell cultures. patients who underwent the procedure. The median The increased healing rate of cranial defects in infants age of the group was 12 months. The authors found clo- and children is well described in the surgical literature sure of the surgical sites occurred within the first postop- [15–17], and surgeons have taken advantage of this erative year, but there was an increased prevalence in characteristic of the infant skull for many years. Hassler the formation of bone closure defects in patients and Zentner [16] studied infants who underwent radical 9 months and older at the time of the surgery.

Fi g u r e 6-19. Healing linear transparietal skull fracture of a 2-month-old male (same individual as pictured in Fig. 6.7). Note that the fracture is bridged with woven bone in the absence of a callus swell.

94 Skeletal Atlas of Child Abuse Fi g u r e 6-20. Healing occipital skull fractures of a 4-month-old (ectocranial surface). Note the bridging of the fracture in the male. The decedent survived in the hospital for 37 days absence of a callus swell. The cause of death was classified as after the date of injury. (a) Ectocranial surface of the occiput. blunt trauma of the head, the manner as homicide. (b) Endocranial surface. (c) Close-up of the right fracture

Fi g u r e 6-21. Healing lambdoidal diastatic fracture of the individual pictured in Fig. 6.20. Note the lacy bone layered on the suture digitations (arrows).

Fi g u r e 6-22. Healing linear parietal fracture (endocranial surface) of a 9-month-old female. Note the roughened raised SPNBF (arrowheads). The SPNBF is encroaching on the fracture from the outer limits of the hematoma. The cause of death was classified as blunt force head trauma with skull fractures and brain injury, the manner as homicide.

Healing and Interpretation 95 Healing Rate

As stated previously, the rate of healing depends on the from whom these ribs were removed was 8 weeks old at age of the individual [19]. Fractures in infants and chil- the time of death. He was born at 38 weeks’ gestation dren heal much faster than those in adults for the fol- and spent 9 days in the neonatal intensive care unit for lowing reasons: Immature bones are more woven than supplemental oxygen and a small patent foramen mature ones and have a propensity to incompletely fail ovale. He was discharged in good condition. During the in compression rather than tension. Incomplete com- autopsy, the infant was noted to be malnourished with pression fractures initially are more stable and require features consistent with dehydration and severe stress less callus formation during the healing process [1]. reaction. Despite the poor health status of the infant, Immature bones are more vascular and capable of a several of the ribs progressed to the remodeling stage greater hyperemic response than mature bones, allow- within 8 weeks. ing the inflammatory response to occur more rapidly. When repetitive injury occurs, it can slow the healing The osteogenic environment in infants and children rate and cause an exuberant callus to form (Figs. 6.24– enables the periosteum to contribute immediately and 6.26) [2, 5]. Kleinman [2] stated that the term repetitive immensely to the formation of new bone [1, 3]. In chil- injury should be reserved for additional injury to a single dren, there also is a higher concentration of trabecular fracture site. Repetitive injury should not be used to bone adjacent to thick cortical bone. Ogden [3] theo- describe the presence of fractures of various ages seen rized that this medullary bone may respond faster than throughout the body. He also stated that any fracture lamellar bone to injury, improving the fracture healing that is not stabilized either externally or internally is at rate in children. Furthermore, he stated that the perios- significant risk for repetitive injury, even in the absence teum is stronger in children than adults and is more likely of an assault. When repetitive injury occurs after an ini- to remain intact and coordinate the osteogenic tial period of healing, the newly formed blood vessels of response. Figure 6.23 demonstrates how quickly an the hematoma are torn, reinitiating the inflammatory infant heals, even with compromised health. The infant response, leading to additional callus formation.

Fi g u r e 6-23. Multiple rib fractures in various stages of healing observed in an 8-week-old infant. A total of 45 healing rib fractures were observed and represented a minimum of four traumatic episodes. The healing stages are described as open fractures with initial primary bone formation, open fractures with large calluses of primary bone, stabilized fractures with organizing bone calluses, and reducing calluses. The cause of death was classified as blunt trauma of the head with skull fractures and brain contusions, the manner as homicide.

96 Skeletal Atlas of Child Abuse Fi g u r e 6-24. Exuberant fracture callus observed on an anterior rib fracture in a 6-year-old male. The decedent had a history of repeated blunt force trauma to the chest over a 2-week period. The cause of death was classified as multiple blunt force trauma, the manner as homicide.

Fi g u r e 6-25. Healing humeral fracture. (a, b) Healing humeral was classified as methicillin-resistant Staphylococcus aureus fracture with exuberant callus formation of a 2-month-old chest wall abscess with disseminated infection and a contrib- female. Panel (b) shows the posterior surface of the distal por- uting factor of chronic stress associated with multiple blunt tion of the callus. Note the large cloaca. The cause of death trauma injuries; the manner was classified as homicide.

Fi g u r e 6-26. Posterior rib fracture of a 14-month-old male. Note what appears to be a secondary deposit of bone callus, suggesting a possible repeat injury (arrowhead). The cause of death was classified as blunt head trauma, the manner as homicide.

Healing and Interpretation 97 Interpretation

Forces associated with nonaccidental injury often affect rib fractures were located in the posterior and postero- multiple bones in separate regions of the body. A good lateral regions. At the fracture sites, the ribs were buckled example is the violent shaking of an infant, which gen- or splayed apart. The fractures in the anterior and anter- erates compression and posterior levering of the chest olateral regions of the ribs were simple, consisting pri- as well as flailing of the limbs. Figure 6.27 shows the distri- marily of incomplete failure in compression. The right and bution of healing fractures observed in a 3-month-old left scapulae were fractured along the medial border at female. A total of 25 rib fractures and 15 long bone frac- the level of the scapular spine. The infraspinous processes tures were found on the decedent. All fractures were along the medial margin of the right and left scapulae healing. Based on the healing stages observed in the were buckled, and the internal and external surfaces of ribs, a minimum of two traumatic episodes were identi- the medial border of the right scapula were splayed fied (Fig. 6.28). The type and distribution of the rib apart. The fractures observed in the decedent were in fractures – posterior, posterolateral, and at the chondro- two stages of healing: soft callus formation with minimal osseous junction – and CMLs of nearly every long bone SPNBF and acute with sharp margins and no bony reac- are consistent with constriction and posterior levering of tion. The types and distribution pattern of the fractures the chest and uniform flailing of the limbs. The fracture were consistent with a posterior-to-anterior-directed distribution suggests violent shaking. force applied while the anterior chest was supported by Figures 6.29–6.32 show rib and scapular fractures a broad surface. The uniformity of the fracture types and observed on a 21-month-old female. A total of 51 frac- the healing stages suggest a similar force was applied on tures were observed on the decedent. The more severe two separate occasions within a relatively short period.

Fi g u r e 6-28. Posterior rib fractures demonstrating two stages of healing. The fractures were observed in the same individual Fi g u r e 6-27. Distribution pattern of fractures of a 3-month-old represented in Fig. 6.25. (a) Fracture in the soft callus formation female. The blue dots mark the location of the fractures. The stage. Note that the fracture is open, with minimal SPNBF. cause and manner of death were classified as undetermined (b) Fracture in the remodeling stage. (skeletal diagram adapted from Buikstra and Ubelaker [20]).

98 Skeletal Atlas of Child Abuse Fi g u r e 6-29. Posterior and posterolateral rib fractures. (a–c) Posterior and posterolateral rib fractures of a 21-month-old female. Note the splaying apart of the bone, especially in panel (b), and the buckling, most notable in panel (c). The fracture types were observed bilaterally in all ribs except right and left rib 12. The fracture types and distribution are consistent with a posterior-to-anterior impact. The cause of death was classified as blunt trauma of the torso and head with bilateral rib and scapular fractures, visceral lacerations, and multiple contusions; the manner was classified as homicide.

Healing and Interpretation 99 Fi g u r e 6-31. Incomplete compression fractures observed in the Fi g u r e 6-30. Lateral rib fracture of the individual pictured in anterior region of the rib of the individual pictured in Fig. 6.27. Fig. 6.29. Note the buckling of the cortical bone, resulting from Note the subtle fracture with SPNBF (right arrow) in comparison a force directed parallel to the anterior/posterior plane of the with the absence of a healing response at the fracture site, bone. indicated by the left arrow.

Fi g u r e 6-32. Scapular fractures observed in the individual pictured in Fig. 6.29. (a) Note the bilateral uniformity (arrows), suggesting that a single impact caused both fractures. (b) Also note the splaying apart of the bone, most notable at the arrow.

100 Skeletal Atlas of Child Abuse Summary

Recognition of various stages of healing and fracture contribute significantly to the investigation of the case. distribution patterns is critical to the successful recon- Identifying the trauma vector of each fracture and struction of the traumatic event(s). Providing an estima- then, when appropriate, associating the individual tion of the minimum number of traumatic episodes forces with a single action enable a comprehensive and a timeline based on the stage(s) of healing can reconstruction of the inflicted injury.

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Healing and Interpretation 101 wwwww Natural Disease May 7 Mimic Child Abuse The skeletal system, one of the ten major organ systems of the human body, is integral to routine body functions. The bones, tendons, and ligaments provide support, protection of visceral organs, and leverage for movement. The bones of the skeleton also store and release necessary minerals, such as calcium, magnesium, and phosphorus, into the bloodstream. Because of the skeleton’s participation in these vital functions, natural disease conditions that significantly affect the health, growth, and development of the soft tissues frequently also produce a pathologic skeletal response. Bone reactions to the stresses of premature birth, various disease syndromes, and genetic and congenital disorders can be seen grossly on the postmortem pediatric skeletal examination. Bone involvement in natural disease frequently is observed as osteopenia, osteoporosis, or osteomalacia, although certain syndromes produce a hyperostotic (proliferative) cortical bone response. Weakened bone, whether it is delicately thin (osteopenia) or delicately soft (osteomalacia), is predisposed to pathologic fracture. Although less prevalent, hyperostotic bone response to disease may resemble a healed fracture or a healing fracture callus. These findings on skeletal examination may raise the suspicion for child abuse injuries. Osteopenia and osteomalacia are the most common bone reactions to prematurity and natural disease in the developing infant skeletion. Rauch and Schoenau [1] described osteopenia and osteomalacia as the result of two types of deficiencies: (1) an apposition/ resorption deficiency in which either an insufficient amount of osteoid is synthesized and deposited by the osteoblasts or there is pathologically increased resorption of the osteoid by the osteoclasts and (2) an insufficient amount of mineral incorporated into the osteoid. The first type of deficiency leads to osteopenia and may progress to osteoporosis. A reduction in the formation of osteoid and/or increased resorption of the osteoid results in fewer trabeculae and a thinner cortex. Cartilage typically is not affected and continues to develop normally. The authors maintain that because pediatric osteoporosis cannot be accurately measured by bone density radiography, osteoporosis should be diagnosed only in the presence of pathologic fractures, which indicate that bone mass is inadequately low and cannot withstand normal mechanical requirements. The second type of deficiency leads to osteomalacia. Incorporation of mineral into the osteoid is disturbed, causing a reduction in the average mineral content of the developing bone. The bone becomes relatively soft, and the trabeculae have a “washed out” appearance on radiograph. Cartilage is usually also affected by this deficiency, and the metaphyses of the affected elements have characteristic widened and irregular borders in radiographic view. Many natural conditions that produce an abnormal bone response, especially those with a genetic or congenital etiology, are so multifocal and life-threatening that they are diagnosed quickly during pregnancy or shortly after birth (the perinatal period). The symptoms of others, particularly certain metabolic diseases, usually prompt the pediatri- cian to order a battery of diagnostic tests that result in a timely diagnosis and treatment. However, when a condition that results in pathologic bone is not severe or even apparent in the perinatal period and/or a clinical diagnosis is not obtained prior to the death of an infant or young child, child abuse may be suspected. Although not meant as a comprehensive review of all such disorders, this chapter presents 11 examples of natural conditions commonly described in the literature as possible mimics of bone response to inflicted injury [2–10]. The published incidence statistics for these conditions vary by resource because they are not public health-related reportable diseases. Concomitantly, the

J.C. Love et al., Skeletal Atlas of Child Abuse, Springer’s Forensic Laboratory Science Series, 103 DOI 10.1007/978-1-61779-216-8_7, © Springer Science+Business Media, LLC 2011 prevalence in cases under medical examiner/coroner in this chapter are of bone specimens in which the jurisdiction also is unclear. In our experience and case- response to natural disease may have some features work, the cause of death in medicolegal cases rarely that are similar in appearance to child abuse injury; specifies the clinical names for these conditions, result- however, not all the conditions described in the text are ing in underreporting. Thus, the photographs presented pictured.

Sequelae of Prematurity

The World Health Organization defines premature birth be hard to assess, the condition may occur in up to 57% as childbirth prior to 37 weeks’ gestation [11]. Prematurity of infants with a birthweight of less than 1,000 g. The carries a substantial risk for infant mortality. Globally, an authors also noted that poor mineralization is very com- estimated 28% of all infant deaths within the first week of mon in infants born weighing less than 1,500 g. James life are the result of premature birth. In the United States et al. [12] used PA to measure the bone mineral content and other developed nations, the prognosis for survival of the forearm in 17 infants at 40 weeks postconception. of premature infants, even those as young as They also took a blood sample from each infant and 22–25 weeks’ gestation, has improved greatly because assayed it for alkaline phosphatase activity. The of access to advances in perinatal medicine. Currently, researchers found that bone mineral content was sig- infants born at 32 weeks’ gestation in developed nations nificantly correlated with infant size. The premature have a survival rate comparable with that of infants infants were shorter, weighed less, and had a lower born at term [11]. Despite the improved survivability, bone mineral content than their term counterparts. however, premature infants remain at risk for long-term Because premature infants typically are smaller at comorbidities resulting from their original premature 40 weeks than a term infant, size was removed from the condition (sequelae of prematurity). Bone fragility and statistical analysis. Even when the calculations were fracturing are possible sequelae of prematurity that adjusted for size, the premature infants had a signifi- may be mistaken for inflicted injury (Figs. 7.1–7.3). cantly lower bone mineral content than the term infants Poor prenatal nutritional status, early separation from in the study. However, Horsman et al. [17] found in a maternal hormones, substrate deficiency related to study of 58 infants measured at later dates of postcon- inadequate postpartum nutritional supplementation, ception (65–100 weeks) that there is a “catch-up” treatment drug side effects (e.g., from corticosteroids), period of mineralization between 40 and 60 weeks that lack of mechanical stimulation of the skeleton, and results in normalization of the bone density. severe systemic disease all are recognized as contribut- Rauch and Schoenau [1] stated that the physical ing factors in the development of bone fragility of pre- density of the long bone diaphysis of all infants, whether maturity [1, 12]. However, substrate deficiency is a premature or term births, decreases by about 30% dur- fundamental and common factor in premature infants ing the first 6 months postpartum. This decrease is a result that is known to be a significant detriment to bone of the expansion of the marrow cavity, which occurs at health. Supplementation of the premature infant diet a faster rate than the increase in the cross-sectional usually is required to prevent substrate deficiency area of the cortical bone. This process resolves later in because breast milk contains low levels of calcium and the premature infant than it does in the term infant. phosphate [13]. When premature infants are fed unsup- Therefore, the authors contended that comparison of plemented breast milk, they experience low plasma measured differences of physical density between the concentrations of phosphate and raised calcium excre- premature and term infant at the same postconception tion levels in the urine. Their bodies do not have enough age may not actually be evidence of long-term bone phosphate to support metabolism and overall growth, disease in the healthy premature infant. so phosphate is pulled from the skeleton. The calcium in Improvements in maternal health and prenatal fol- the skeleton then lacks sufficient phosphorus to use as a low-up, nutritional supplementation, and adjusted pro- building block for bone growth and is excreted as waste. tocols that reduce the amount of time spent immobilized Bone apposition and mineralization slow, resulting in on the ventilator likely have reduced the incidence of fragility. severe bone responses in the typical premature infant Several published studies from the 1980s compared born in the hospital since the 1980s [1]. However, radiologic bone density, bone mineral content as because our forensic casework reflects only the pre assessed through photon absorptiometry (PA), and mature infants with poor outcomes, bone fragility due serum calcium and phosphorus levels of premature and to sequelae of prematurity, usually exacerbated by term infants [12–17]. Brooke and Lucas [13] reported immobility during a long hospitalization, is a very common that although radiologic evidence of osteopenia may observation.

104 Skeletal Atlas of Child Abuse Fi g u r e 7-1. Osteoporotic rib from a 2-month-old individual born prematurely. Note the porosity on the internal surface of the rib body at the sternal end. The cause of death was classified as acute bacterial bronchopneumonia associated with bronchopulmonary dysplasia due to prematurity, the manner as natural.

Fi g u r e 7-2. Osteoporosis in a premature male. The osteoporotic sternal end of the right seventh rib is pictured. The 3-month-old male was born at 33 weeks’ gestation, remained in the hospital postnatally for 2 months, and then was released home. After 1 week at home, the individual returned to the hospital and died during a subsequent 28-day hospital stay. The cause of death was classified as blunt force head trauma with skull fractures, the manner as undetermined.

Fi g u r e 7-3. Osteopenic rib of a premature male with an extensive medical history. The sternal end of the left fourth rib from a 5-month-old male with an extensive medical history following premature birth shows marked fragility of the cortex with exposure of the trabeculae. The cause of death was classified as complications of extreme prematurity, the manner as natural.

Natural Disease May Mimic Child Abuse 105 Osteogenesis Imperfecta

Osteogenesis imperfecta (OI) is a broad term that refers be observed in an infant or child with OI: osteoporosis, to the skeletal system’s response to a disorder of the con- cranial suture ossicles (Wormian bones), blue sclerae, nective tissue in which type 1 collagen is of abnormal hearing impairment, triangular positioning of facial fea- quality or is produced in reduced quantity. Type 1 colla- tures, crumbling teeth, and joint laxity. The limbs may be gen is a structural protein essential to the development bowed, and multiple fractures and fenestrations related and maintenance of the bones, dentin, organ capsules, to bone fragility may occur throughout the skeleton (see fascia, corneas, sclera, tendons, meninges, and skin [18, Figs. 7.5 and 7.6). In some cases, the clinical signs of OI 19]. OI is caused by missense mutations (point mutations are more subtly expressed, and blue sclerae also may that result in a codon that codes for an amino acid dif- be observed in children who have thin sclerae but do ferent from the one required) in the code for type 1 pro- not have OI [7]. Differentiation between OI and inflicted collagen (COL1A1 and COL1A2). These mutations may injury in the clinical setting may be complicated in mild be inherited as an autosomal dominant allele or an cases, particularly when the collagen or DNA sequenc- autosomal recessive allele (rare), or may occur as spon- ing test results are inconclusive [7]. However, classic taneous mutations in the infant’s genome. OI is classified metaphyseal lesions (CML), which are highly suspicious into types I–IV, based on the mode of inheritance and for inflicted injury, are not typically reported in clinically the severity of the phenotypic expression (Fig. 7.4). The diagnosed OI without severe loss of distal long bone most severe cases typically are lethal in the perinatal mass [7, 18]. Plotkin [19] estimated the prevalence of OI period [18]. A suite of major clinical features may at 1 in 20,000 live births.

CLASSIFICATION OF OSTEOGENESIS IMPERFECTA Type Description Clinical Features Inheritance I Mild Variable bone fragility, blue sclerae, stature Autosomal dominant near normal without bowing of long bones, possible hearing loss, high pain tolerance, possible easy bruising, variable dental involvement II Most severe Extreme bone fragility, usually lethal in fetal or Autosomal dominant or new perinatal period, in utero fractures and growth mutation; in rare cases, the retardation, blue sclerae, deformation of long inheritance may be bones, beaded ribs autosomal recessive III Severe Fragile bone, chronic bone pain, possible in Autosomal dominant or new utero fractures, cranial deformities (triangular mutation; in rare cases, the face), progressive deformation of long bones, inheritance may be reduced stature, pale blue-gray or normal autosomal recessive sclerae, joint hyperlaxity, vertigo, possible dental involvement IV Undefined Fragile bone in infancy with possible dental Autosomal dominant involvement; effects on stature and scleral hue are not yet well-defined

Fi g u r e 7-4. Classification of OI (adapted from Ablin et al. [18] and Plotkin [19]).

Syndromes Resembling Osteogenesis Imperfecta

Disorders that resemble OI in phenotype but originate production of structural proteins. The mutations causing through different genetic mutations are described in SROI may be inherited or of congenital origin and usu- the literature and are sometimes listed as OI types V–VII, ally occur in recessive autosomal alleles [19]. As in OI, brittle bone diseases, or syndromes resembling OI (SROI). the morbidity and mortality of SROI depend on the SROI may be caused by posttranslational modifications severity of the phenotypic expression because the (as in posttranslational loss of cartilage-associated effects of these disorders on the skeleton do not typi- protein [CRTAP]) or by other mutations that affect the cally resolve with time and growth and development.

106 Skeletal Atlas of Child Abuse Fi g u r e 7-5. Poor cranial bone quality. The multiple fenestrations visible in the cranial specimens from a 3-month-old male are typical of the poor bone quality characteristic of OI or SROI. Note the remnant sutura mendosa (arrow). The cause and manner of death were classified as undetermined.

Fi g u r e 7-6. Magnified view of poor cranial bone quality. A magnified view of the cranial specimens pictured in Fig. 7.5 shows the delicate bone surfaces and the open fenestrations. Note the remnant sutura mendosa (arrow).

Infantile Cortical Hyperostosis (Caffey Disease)

Infantile cortical hyperostosis, commonly referred to as and variable expressivity, placing it in the same family of Caffey disease because it was defined by Caffey and collagen disorders as OI. Silverman [20] in 1945, is a disease of bone proliferation The clinical presentation of Caffey disease is charac- that presents in fetuses and young infants. The fetal terized by initial fever and soft tissue inflammation and form, possibly inherited as an autosomal recessive trait, swelling. Three pathologic phases have been described is severe and frequently fatal. The infantile forms, usually – early, subacute, and late [21] – that roughly corre- benign and self-limiting, do not typically result in mortal- spond to the three stages of fracture healing – ity or permanent health deficits. The infantile forms are inflammation, repair, and remodeling – particularly as categorized into two types: heritable and sporadic. observed in cases of repetitive injury. In the early phase Both types initiate osteogenic changes that may be of Caffey disease, there is an acute intraperiosteal confused clinically and radiographically with bone inflammatory reaction with swelling and thickening of response to trauma [21–23]. In the event an infant with the periosteum. During the subacute phase, the perios- undiagnosed Caffey disease receives a postmortem teum continues to thicken and undergoes increased skeletal examination, cortical hyperostosis must be dif- subperiosteal new bone formation (SPNBF). As the phase ferentiated from healing trauma. progresses, osteoblastic activity produces exuberant The etiology of sporadic infantile Caffey disease is and hyperplastic lamellar bone layers that thicken the not well defined. This form of the disease typically pres- bone cortex. Fibrosis of the bone marrow may develop. ents at 9–11 weeks of age. Multiple explanations for the Disorganized bone also may be deposited in the periph- development of the disease include an inflammatory eral soft tissues and form bony bridges between long response trigger, infection by a latent virus, or an allergic bones. In the late phase, the underlying original cortex is reaction. Cortical hyperostosis also has been observed removed by osteoclastic activity, resulting in a com- in infants receiving therapeutic doses of prostaglandin E plete turnover of the cortical bone and reshaping of the in preparation for surgery [21, 24]. element. Over time, active bone proliferation slows, The heritable infantile form typically presents at peripheral bone is removed from the soft tissue, and as approximately 6–8 weeks of age and has been reported the disease self-resolves, additional cortical remodeling as following an autosomal dominant pattern of inheri- occurs. On postmortem skeletal examination, the bone tance within families [21, 23, 25, 26]. These studies show response may resemble the exuberant bony callus of a that Caffey disease may result from a heterozygous mis- healing fracture responding to repetitive injury. Caffey sense mutation in COL1A1 with incomplete penetrance disease typically resolves before 2 years of age [21].

Natural Disease May Mimic Child Abuse 107 Caffey disease predilects the diaphysis of the long wrists and hands, rarely are involved. The incidence of bones (including the clavicles), mandible, and ribs, but Caffey disease is unclear, as it appears to be relatively also may affect the scapulae asymmetrically [21, 26]. rare but cases may be difficult to diagnose. Diagnosed Other elements, such as the vertebrae and bones of the cases also may be underreported.

Hypophosphatasia (Rathbun Syndrome)

Hypophosphatasia, also known as Rathbun syndrome (Figs. 7.7–7.10). Mortality is high; approximately 50% of [27], is an inherited or congenital metabolic disorder patients diagnosed with infantile hypophosphatasia do (inborn error of metabolism) that results in defective not survive [30]. bone mineralization. This disorder is believed to be The childhood form is somewhat less severe, although caused by a missense mutation in the autosomal reces- debilitating, and may be the result of compound sive gene ALPL, which codes for tissue-nonspecific alka- heterozygosity in which there are two heterogeneous line phosphatase (TNSALP) [28, 29]. The mutation results recessive alleles present at a particular locus [28]. in a serum deficiency of the enzyme. Hypophosphatasia Childhood hypophosphatasia may present with bone is a relatively rare disorder; an estimated incidence of 1 pain and/or pathologic fracture in a child who has per 100,000 births was published in 1957 [30]. experienced a delay in walking. The child may be short Hypophosphatasia has been classified into six forms in stature and ambulate with a shuffling gait. Bone based on the age when skeletal involvement occurs. inflammation and osteomyelitis may develop without Two of the forms – the infantile and childhood forms – documented traumatic injury. Often there is premature may mimic child abuse. Infantile hypophosphatasia typi- loss of the deciduous teeth, particularly the incisors. cally manifests with symptoms prior to 6 months of age. Rachitic ribs and long bone metaphyses with radiolu- The infant may present with weight loss, vomiting, and cent projections that extend from the epiphyseal plate hypotonia (reduced muscle tone). Blue sclera of the into the metaphysis may be observed on radiographic eyes may be observed, similar to the documented char- examination. The projections at the long bone meta- acteristic of OI. Laboratory studies typically reveal cal- physes are distinct radiographically from the poorly ossi- cium in the urine and abnormally high levels of calcium fied epiphyses and flared metaphyses commonly in the blood. Osteopenia with pathologic fracture, pre- observed in rickets but may resemble the focal thicken- mature craniosynostosis, irregularity of the long bone ing of healing metaphyseal injury [28, 31, 32]. The overall metaphyses, and “beading” of the ribs at the costo- presentation of the child may be suspicious for chronic chondral junction (similar to the rachitic ribs observed in inflicted injury if further testing is not completed and a rickets) often are observed on radiographic examination diagnosis rendered prior to death.

Fi g u r e 7-7. Osteoporotic left femur. The distal left femur from a 3-year-old male dis- plays cortical bone porosity and fenestrations. The individual died approximately 1 year after a debilitating head injury that resulted in encephalomalacia. The cause of death was classified as complications of blunt trauma of the head with subdural hematoma, the manner as homicide.

108 Skeletal Atlas of Child Abuse Fi g u r e 7-8. Transverse view of an osteoporotic left femur. This transverse view of the midshaft of the left femur pictured in Fig. 7.7 shows the sparse trabeculae and delicate cortical bone indicative of reduced bone quality.

Fi g u r e 7-9. Transverse view of an osteoporotic femur from a 5-year-old female. The trabeculae are sparse, and the cortical bone is relatively poor in quality. The individual spent 4 years as a quadriplegic following a motor vehicle crash. The cause of death was classified as asphyxia due to the detachment of a ventilator from the tracheos- tomy used to treat quadriplegia following blunt impact trauma with cervical spine injury; the manner was classified as an accident.

Fi g u r e 7-10. Healed fracture of the osteoporotic right femur pictured in Fig. 7.9. The shaft retains a slight anteroposterior bend from the fracture. An involucrum with large cloacae is present along the posterior surface, consistent with osteomyelitis (arrow).

Natural Disease May Mimic Child Abuse 109 Menkes Disease

The molecular basis of Menkes disease is an X chromo- room clinicians’ suspicions for inflicted injury. In both some-linked recessive trait that causes abnormal cop- cases, the infants subsequently were diagnosed with per metabolism, impaired absorption in the intestines, Menkes disease. In the first case, the infant was hospital- and concomitant copper deficiency. Because of the ized at 3 months with pneumonia, upper gastrointestinal impaired metabolism, copper accumulates in the duo- bleeding, and seizure. At 9 months, he again was hospi- denum, kidney, spleen, pancreas, and skeletal muscle. talized with seizures. A cerebral CT scan suggested sub- Copper deficiency during growth and development dural hematoma. A radiographic skeletal survey showed results in nerve sheath demyelination and interferes with metaphyseal spurs at the distal long bones. A prelimi- neurodevelopment. The estimated international inci- nary diagnosis of “shaken baby” syndrome was investi- dence of Menkes disease ranges from 1 in 50,000 to 1 in gated, but eventually the correct diagnosis of Menkes 250,000 births [33]. disease was obtained. In the second case, a 3-month- Menkes disease presents almost exclusively in males, old infant presented to the hospital with seizures. MRI of because female carriers typically are asymptomatic. the head showed bilateral subdural hematomas. Infants with Menkes disease appear generally healthy A radiographic skeletal survey showed anterior flaring from birth until approximately 8 weeks of age, when of the ribs and metaphyseal spurs of the distal femur, clinical manifestations begin to arise, including loss of ulna, and radius. Biochemical and genetic studies con- developmental milestones, hypotonia, seizures, inguinal firmed Menkes disease in this case. hernia, failure to thrive, abnormally kinky hair, and loose Very early recognition of Menkes disease in the peri- skin. Skeletal involvement in Menkes disease includes natal period, followed by subcutaneous copper injec- abnormal development of the sternum and sternal ribs tions, has produced some success in achieving normal that results in a “sunken” chest, osteoporosis with multi- neurodevelopment. However, although there are milder ple fractures (see Figs. 7.7–7.10), diaphyseal periosteal variants, classic Menkes disease usually results in the reaction, metaphyseal spurring and widening, sutural child’s death by about 3 years of age [36]. Although ossicles, and scalloping of the posterior portion of the Menkes disease is relatively rare, in the absence of a vertebral bodies [33]. Arita et al. [34] and Bacopoulou clinical diagnosis, familiarity with the skeletal manifesta- et al. [35] reported separate cases in which male infants tions of Menkes disease may inform the postmortem had radiologic results that increased the emergency skeletal examination.

Mucolipidosis Type II

Mucolipidosis is a metabolic disorder of lysosomal stor- breathing, generalized hypotonia, frequent otitis age inherited as an autosomal recessive allele. In this dis- media, thick skin, epicanthal folds, prominent abdo- order, there is a functional deficiency of lysosomal men with umbilical hernia, a flat midface with enzymes that results in abnormal vacuolization and inclu- depressed nasal bridge and small orbits, widening of sions in the cytoplasm of mesenchymal cells, particularly the rib bodies, kyphosis, concavities of the anterior ver- the fibroblasts. In addition to producing valvular heart dis- tebral bodies, pelvic dysplasia, joint limitation, diaphy- ease, mucolipidosis type II severely affects the trabecular seal expansion of the long bones with periosteal and cartilage structures of the skeletal system [37, 38]. cloaking, short hands and fingers, and clubbing of the The disorder is slowly progressive from birth and typically feet. Although some symptoms may be present at birth fatal prior to 10 years of age. The most common mecha- or shortly thereafter, the full clinical picture that includes nism of death is respiratory insufficiency due to mucosal many of the skeletal anomalies is not completely thickening, congestive heart failure, and gradual stiffen- apparent until the infant is close to 12 months of age ing of the rib cage. Reported global incidence estimates [37]. Therefore, despite the severe morbidity associ- range from 1 in 123,500 to 1 in 625,500 live births [37]. ated with this disorder, it is possible that a clear diagno- Clinical symptoms of mucolipidosis type II include sis of mucolipidosis type II may not be made prior to developmental delay and failure to thrive, noisy death and a subsequent postmortem examination.

110 Skeletal Atlas of Child Abuse Sickle Cell Disease

Sickle cell disease (SCD) is a heritable disorder that may experience symptoms of the disorder, although it does result in sudden pediatric death from pulmonary dis- occur [39, 40]. tress. The hemoglobin-b gene (HBB) codes for the b-pep- SCD also may produce skeletal lesions as a result of tide chain of adult hemoglobin, b-globin. A mutation in sickle cell crises [41]. Acute and chronic bone infarcts HBB that produces the hemoglobin variant Hb S is the (death of cellular elements of the bone marrow), med- most common cause of SCD. In this variant, the amino ullary sclerosis, bone necrosis, periostitis, and sterile acid valine is substituted for glutamic acid. This substitu- osteomyelitis with development of cloacae (see tion causes aggregation of the hemoglobin molecules Figs. 7.7–7.10) are all discussed in the literature [42, 43]. when they release oxygen. The red blood cells become Kepron et al. [42] reported an autopsy case of a 5-year- rigidly sickle-shaped and clump together, forming block- old boy who experienced “multifocal epiphyseal sepa- ages in the blood vessels. Additionally, anemia devel- rations due to microinfarction and hemorrhage of the ops because the abnormal red blood cells are destroyed underlying bone.” The separations were accompanied at a higher rate than is normal in humans. SCD is an by marrow fibrosis, subperiosteal hemorrhage, and autosomal recessive disorder. Individuals who have one SPNBF. The authors assert that on radiograph and during copy of the normal HBB gene and one copy of the the skeletal examination, the epiphyseal separations mutated gene have sickle cell trait and are less likely to resembled CML.

Hypovitaminosis D and Rickets

Vitamin D enhances absorption of calcium and phos- resulting in further risk for demineralization and fractures phorus from the small intestine (see section “Short Bowel [46]. The term rickets refers to the clinically and radio- Syndrome”) and has a role in the maturation of osteo- graphically recognized metabolic bone disease that clasts that resorb calcium from the bones. Several disor- may ensue when hypovitaminosis D is not treated ders that cause malabsorption of nutrients, as well as promptly. poor dietary intake and even certain demographic Infants and children with congenital or untreated characteristics of the individual, may result in insufficient hypovitaminosis D are particularly susceptible to rickets vitamin D levels (hypovitaminosis D). because of the nutritional needs of active skeletal Vitamin D status is measured most accurately through growth and development. The findings of rickets include analysis of serum 25-hydroxyvitamin D concentration. diffuse bone rarefaction and osteomalacia, craniota- A concentration of less than 11 ng/mL indicates hypovi- bes, bowing of the weight-bearing long bones after the taminosis D. However, Heaney et al. [44] demonstrated child begins to walk, softening of the ribs with flaring of that maximum calcium absorption occurs at levels the sternal ends, fraying and cupping of the metaphyses greater than 32 ng/mL. Vitamin D is available from exog- of the distal long bones on radiograph, and pathologic enous sources (absorption through diet and supple- fractures with delayed healing (Figs. 7.11–7.14) [9, 45]. mentation) but also may be synthesized endogenously. Metaphyseal changes in the long bones are usually The skin acts as the major source of endogenous vita- bilateral and appear radiographically as a separation min D production. A proper diet that includes vitamin between the epiphysis and metaphysis. This finding is D-supplemented milk and minimal exposure to sunlight caused by demineralization in the calcified cartilage typically provide sufficient access to vitamin D in healthy zone. The lack of mineralization at this location results in individuals. However, dark skin pigmentation, residence an area of diminished radiolucency that imitates a wide above the 35° latitude in winter, breastfeeding without separation between the epiphysis and metaphysis [47]. vitamin D supplementation, and copious use of high- Also as a consequence of the demineralization, the SPF sunscreen may decrease the amount of serum cartilage at the metaphysis loses normal columnar 25-hydroxyvitamin D concentration and are risk factors organization, resulting in the characteristic frayed and for hypovitaminosis D [45]. Hypovitaminosis D is associ- cupped appearance. Keller and Barnes [9] reported ated with osteomalacia caused by lack of sufficient that although the affected metaphyses may become calcium and phosphorus uptake for bone health and increasingly sclerotic and malformed, they are usually with elevated parathyroid hormone levels, which may asymptomatic and resolve quickly with treatment of the initiate increased movement of calcium from bone, hypovitaminosis D.

Natural Disease May Mimic Child Abuse 111 Fi g u r e 7-11. Comparison of typical and atypical development The cortical bone is slightly brittle, flaky, and easily chipped. On of the physeal surface. (a) Normal development of the physeal radiograph, the metaphyses appear frayed. The atypical qual- surface is shown in the left ulna, fibula, and radius from a ity and morphology of the bone in the 3-month-old individual is 2-month-old individual. (b, c) In comparison, note the flared dissimilar to that produced by a metabolic disease such as hypo- tal metaphyses in the left and right distal ulnae from a 3-month- vitaminosis D. The cause of death was classified as undeter- old male with atypical bone development and quality. The mined, the manner as undetermined (co-sleeping). physeal surfaces are deep, cup-shaped, and macroporotic.

Fi g u r e 7-12. Comparison of typical and atypical development are compared. Note the smooth, slightly convex surface with of the distal left radius. The normal physeal surface of the distal intact rim in panel (a) and the porous, rugged, slightly concave left radius from a 5-month-old individual (a) and the atypical surface with chipped rim (arrow) in panel (b). surface from the 3-month-old male (b) described in Fig. 7.11

112 Skeletal Atlas of Child Abuse Fi g u r e 7-13. Atypical development and bone quality of the rib the atypical surface (b) of the 3-month-old individual described sternal end surface in a 3-month-old male. The normally in Fig. 7.11. Note the surface porosity and brittle rim in developed sternal end surface (a) is dense compared with panel (b).

Fi g u r e 7-14. Healing fracture of the left sixth rib in a 3-month-old male. A fracture of the midclavicular region of the sixth rib is in the early hard callus stage of healing (arrow). The individual, described in Fig. 7.11, has atypical bone quality that may be symptomatic of a metabolic disease. Although the stage of fracture healing is consistent with approximately 3–4 weeks postinjury in an infant, pathologic conditions may affect skeletal growth and development and the rate of bone healing. Birth trauma is not excluded as the possible cause of the fracture in this 3-month-old individual.

Metabolic Bone Disease in Short Bowel Syndrome and Biliary Atresia

Bone response to malabsorption of nutrients follows a patient concurrently in pediatric cases. The etiology pattern similar to that of rickets in both short bowel syn- and health ramifications of these two disorders are dis- drome and biliary atresia, disorders that may affect the cussed in this section.

Short Bowel Syndrome

Short bowel syndrome occurs when there is functional Skeletal growth, development, and maintenance or anatomic loss of small intestine surface area to the depend on the skeletal system’s access to appropriate extent that the capacity of the bowel to absorb nutri- amounts of calcium, magnesium, and phosphorus. ents is compromised. This disorder is characterized by Approximately 30–35% of total dietary calcium and diarrhea, steatorrhea (abnormal amount of fat in the magnesium are absorbed in the small intestine. Although feces), malabsorption, electrolyte imbalances, and the duodenum is the site of active calcium transport, pas- malnutrition [48]. In children, short bowel syndrome usu- sive calcium transport occurs throughout the small intes- ally is the result of necrotizing enterocolitis, in which the tine. Because of the longer period during which the intestinal tissue dies; intestinal atresia (blockage or clo- contents are in the jejunum and ileum, these regions sure of the intestine); intestinal volvulus (obstruction of absorb a larger proportion of the total calcium. Magnesium the intestine by twisting); congenital short small bowel; also is absorbed throughout the small intestine, but the congenital abdominal wall defects; or meconium peri- maximum absorption takes place in the proximal section tonitis [49]. of the small intestine. Approximately 65% of dietary

Natural Disease May Mimic Child Abuse 113 phosphorus is absorbed by the small intestine through a available in sufficient quantity for use by the body. Even passive diffusional process stimulated when the concen- with total or supplemented parenteral nutrition, inade- tration of phosphorus in the lumen exceeds 47 mg/L [50]. quate absorption may occur, growth and development In short bowel syndrome patients, the absorptive surface of the skeleton slows, and overall bone density decreases. area of the small intestine is so reduced that the essential Radiographic findings include osteopenia, osteoporosis, minerals of calcium, magnesium, and phosphorus, as and irregularities of the distal metaphyses of the long well as other important nutrients and fluids, are not made bones (Fig. 7.15).

Fi g u r e 7-15. Short bowel syndrome. The distal right and left ulnae of a 6-month-old infant with friable ossified metaphyseal rings, poor bone quality, and marked porosity are pictured. The cause of death was classified as short bowel syndrome with cholestasis and hepatic fibrosis due to partial small bowel resection and administration of parenteral nutrition for treatment of necrotizing enterocolitis associated with prematurity; the manner was classified as natural.

Biliary Atresia

The pathogenesis of biliary atresia is poorly understood. age is essential to prevent death. Estimates of incidence Various etiologies have been proposed that describe range from 1 per 10,000 to 1 per 15,000 live births in the possible infectious origins and genetic anomalies [51]. United States [52]. Infants with biliary atresia may present with jaundice Skeletal findings of biliary atresia patients on radio- that persists longer than 2 weeks postbirth, dark urine, graphic examination include osteopenia, metaphyseal light stools, firm hepatomegaly, and splenomegaly. flaring, rachitic ribs, and pathologic fractures. DeRusso Biliary atresia has been classified into three types (I–III). et al. [53] describe three cases of infants with previously Up to 90% of pediatric cases fall into the type III cate- diagnosed biliary atresia in which the skeletal findings in gory, involving closure or destruction of the right and left the emergency department raised suspicion of child hepatic ducts to the level of the hepatic port. In these abuse and resulted in investigation by child protective cases, the ducts are typically open the first few weeks services. Katayama et al. [54] reported 13 biliary atresia after birth but become inflamed and are progressively cases in which radiologic manifestations of bone destroyed, resulting in cholestasis (reduced bile forma- involvement were found, including fractures, rachitic tion and flow). Surgical treatment prior to 2 months of ribs, and irregularities of the distal metaphyses.

Summary

Bone response to prematurity and/or natural disease bone, frayed metaphyseal surfaces, or callus-mimicking may result in osteopenia, osteoporosis, osteomalacia, or bone formation are likely to raise suspicions of inflicted proliferative bone formation in infants and young chil- injury. It is important to include natural disease as a dif- dren. In the absence of a clear clinical diagnosis prior to ferential in the postmortem diagnostic process in pedi- the postmortem examination, fractures of delicate atric cases.

114 Skeletal Atlas of Child Abuse References

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116 Skeletal Atlas of Child Abuse Index A D American Academy of Pediatrics, 9 Depressed skull fractures, 10 Avulsion fracture, scapula, 62 Diastatic fractures, 10, 14 B E Basilar skull fractures, 10 Exuberant fracture, 96, 97 Battered child syndrome, 62 Biliary atresia, 114 F Birth trauma, 64 Fracture distribution patterns, 85 Bone mineral content, 104 Fracture healing CML, 93 C costochondral junction, 86, 87 Caffey disease, 107–108 endochondral bone formation, 86, 87 Callus formation, 96 epiphysis, 86 Catch-up mineralization, 104 forearm long bone fractures, 87, 92 Cervical vertebral fractures, 59 hard callus formation stage, 87, 90 Child abuse, mimics healing rate, 96–97 biliary atresia, 114 hematoma, 85 cartilage, 103 hypertrophic and calcified cartilage zones, 87 hypophosphatasia (see Rathbun syndrome) induction stage, 87, 88 hypovitaminosis D, 111–113 inflammation phase, 85 infantile cortical hyperostosis (see Caffey disease) medullary callus, 85 Menkes disease, 110 radial fracture, 87, 89 mucolipidosis type II, 110 remodeling phase, 86 osteogenesis imperfecta remodeling stage, 87, 91 autosomal dominant allele, 106 reparation phase, 85 classification, 106 right proximal fibula, 87, 92 cranial bone quality, 106, 107 skull, 94–95 syndromes, 106 soft callus formation stage, 87–90 type 1 collagen, 106 subperiosteal new bone formation, 86 osteomalacia, 103 Fracture interpretation, 98–100 osteopenia, 103 rickets, 111–113 H SCD, 111 Humeral fracture, 96, 97 sequelae of prematurity, 104–105 short bowel syndrome, 113–114 L Childhood accidental spiral tibial (CAST) Long bone fractures fractures, 82 accidental vs. nonaccidental injury, 81–82 Classic metaphyseal lesions (CML), 93 CML bony spiculae, 70, 74 bony spiculae, 70, 74 bucket handle, 69 bucket handle, 69 chondro-osseous junction, 70, 72 chondro-osseous junction, 70, 72 corner fractures, 69 corner fractures, 69 distal fibula, 70, 75, 76 distal fibula, 70, 75, 76 distal radii, 69, 71 distal radii, 69, 71 distal tibia, 69, 71 distal tibia, 69, 71 distal ulna, 70, 73 distal ulna, 70, 73 epiphysis, 70, 72 epiphysis, 70, 72 metaphysis and epiphysis, 70, 75 metaphysis and epiphysis, 70, 75 nonaccidental injury, 69, 70 nonaccidental injury, 69, 70 physeal surface, 70, 74 physeal surface, 70, 74 primary spongiosa, 69, 71 primary spongiosa, 69, 71 proximal humerus, 70, 74 proximal humerus, 70, 74 right proximal fibula, 70, 73, 74 right proximal fibula, 70, 73, 74 Clavicles, fracture, 64–65 greenstick fracture, 69

J.C. Love et al., Skeletal Atlas of Child Abuse, Springer’s Forensic Laboratory Science Series, 117 DOI 10.1007/978-1-61779-216-8, © Springer Science+Business Media, LLC 2011 Long bone fractures (Continued) location, 39–40 shaft, metaphyseal, and epiphyseal fracture, 76, 79 posterior rib fractures humeral condylar fracture, 76, 80 avulsion fracture, 40–42 location, 76 bronchopneumonia, 40, 43 oblique fractures, 76, 77 callus, 40, 43 primarily cartilaginous injuries, 76, 79, 80 cardiopulmonary resuscitation, 43 Salter–Harris classification system, 76, 80 hyaline cartilage, 40 spiral fractures, 76, 77 median sternotomy, 40, 42 torus ulnar fracture, 76, 78, 79 MRSA, 40, 41 transverse humeral fracture, 76, 78 neck/tubercle fractures, 40, 44 transverse ulnar fracture, 76, 78 porotic cortical bone, 40, 43 type, 76 subdural hemorrhage, 40, 41 vertebral transverse process, 43 M posterolateral rib fractures Methicillin- resistant staphylococcus aureus (MRSA), 40, 41 anterior rib fractures, 44, 45, 47 Mucolipidosis type II, 110 anterior-to-posterior compression, chest, 44, 46 Multiple rib fractures, 96 anteroposterior compression, 44 peritonitis, 44, 47 N pleura, 44, 47 Neonate fractures, 64 subperiosteal new bone formation, 44, 46 Nonaccidental scapular fractures, 62 visceral lacerations, 44, 45 O S Occipital bone, 13 Salter–Harris classification system, 76, 80 Osteogenesis imperfecta Scapula, fracture autosomal dominant allele, 106 acromial process fragmentation, 62 classification, 106 acromioclavicular and coracoclavicular ligament, 62 cranial bone quality, 106, 107 autopsy view, 57, 58 syndromes, 106 battered child syndrome, 62 type 1 collagen, 106 bilateral acromial fractures, 62 Osteomalacia, 103 lateral border scapular fracture, 62, 63 Osteopenia, 103 posteromedial fractures, 62, 63 stellate glenoid fracture, 62 P subperiosteal new bone formation, 62, 63 Pectoral girdles, 57 transverse blade fracture, 62 Pediatric cranial mechanics, 12–13 Short bowel syndrome, 113–114 Perinatal frontal bone, 11 Sickle cell disease (SCD), 111 Physeal injury, healing, 86 Skeletal examination method Posterior rib fracture, 96, 97 clavicle, 6 Prenatal nutritional status, 104 documentation and analysis adherent soft tissue removal, 6 R artifacts, 6 Rathbun syndrome, 108–109 midshaft fracture, tibia, 6, 8 Repetitive injury, fracture, 96 skeletal elements, 6–7 Rib fractures long bones, 4–5 anterior rib fractures radiographic examination, 1–2 battered child syndrome, 49 ribs, 3–4 bilateral incomplete fractures, 49, 50 scapula, 6 chondro-osseous junction, 49 Skull fractures costochondral junction, 49 accidental vs. nonaccidental cranial trauma, 9 healing, 49, 50 causes, 9 lacy bone formation, 49, 52 cranial base fractures, 34–35 MRSA chest wall abscess, 49, 51 definition, 9 periosteum, 49, 50 facial bone fractures pleural surface, 49, 51 inferior frontal bone fractures, 31–32 sternal surface, 49–52 mandible fractures, 33–34 trabeculae, 49, 52 maxillofacial injuries, 31 anterolateral rib fractures, 48–49 midface, and orbital rim fractures, 32 cardiopulmonary resuscitation fractures, 52–54 pediatric facial fractures, 31 first rib fractures, 54–55 forensic autopsy, 9

118 Index location, 13 parietal bone, 14, 17 pediatric cranial anatomy, 11–12 perimortem, 14, 19, 24 pediatric cranial mechanics, 12–13 posteroinferior autopsy views, 14, 26 types, 10 remote transparietal fracture, 14, 19 U.S. hospitals, 9 sagittal suture, 14, 25 vault fractures stellate fracture pattern, 14, 16, 17 anthropologic analysis, 14, 21, 22, 27 sutura mendosa, 14, 21, 25, 27 autopsy artifact, 14, 28 Sternal development, 62 bilateral linear fractures, 14, 23 Sternum, fracture, 61–62 blunt force head trauma, 14–16 bone formation, 14, 24 T calotte, 14, 30 Temporal bone, 10 complex fracture pattern, 14, 20 Toddler fractures, 82 cranial bones, 14, 18 craniotomy, 14, 25, 27 V crushing head injury, 14, 29 Vertebral body compression fractures, 66 diastatic fractures, 14 Vertebral column fractures ectocranial surface, 14, 20 adult sternum, 57 foramen magnum, 14–15 autopsy view, 57, 58 frontal bone, 14, 20 classification, 57, 59 head trauma, 14 intervertebral fibrocartilaginous disks, 57 lambdoidal suture, 14, 15, 17 neck fractures, 59–60 linear skull fracture, 14, 22 pectoral girdles, 57 nonparietal fractures, 14 posterior spinous process, 59 occipital skull fracture, 14, 20, 21 thoracic skeleton, 57 occipital squama, 14, 22 thoracolumbar and sacral regions, 60–61

Index 119