Abusive Head Trauma
Rachel P. Berger
Dennis Simon
Jennifer E. Wolford
Michael J. Bell
KEY POINTS
Epidemiology
Abusive head trauma (AHT) is a term that has evolved over the last 40 years to reflect brain injuries that occur as a result of child abuse.
AHT occurs in different cultures and ethnic groups.
Risk factors for AHT include the child’s developmental stage as well as caregiver factors.
Mechanisms of injury include shaking, blunt force trauma, and hypoxia/ischemia.Diagnosis
The history of present illness from the caregiver cannot be relied upon, as the perpetrator may not divulge accurately the circumstances around the events, and other caregivers may not be aware of the incident.
Careful documentation of the history is essential for reporting the incident to authorities.
A rapid, targeted physical examination is essential to begin resuscitative efforts and to document injuries as they are discerned.
Management
Rapid assessment and resuscitation to ensure a patent airway, effective breathing, and sufficient cardiovascular/circulatory support are essential for prevention of secondary injuries.
Intracranial pressure (ICP) and cerebral perfusion pressure (CPP) thresholds are believed to be age dependent, likely affecting clinical goals for young children with AHT.
Seizures are common after AHT and should be detected aggressively and treated.Outcomes
Glasgow Outcome Scale Extended for Pediatrics (GOS E-Peds) is the newly established outcome measure for all pediatric TBI, including children with AHT.
Overall outcomes for AHT are significantly worse than noninflicted TBI in children in several series.
Developmental disabilities after AHT are extremely common and lifelong.Reporting Legal Issues
In all the states of the United States, physicians are mandated to report suspected child abuse and are protected by law from the ramifications of doing so.
Although some institutions have designated Child Protection Teams to evaluate children with suspected abuse. Ultimately, it is the responsibility of the treating physician (often the pediatric intensivists) to ensure that state authorities are notified about any suspected child abuse or AHT.The management of a critically ill child with abusive head trauma (AHT) is among the most challenging aspects of professional practice faced by the intensivist. Unlike almost any other disorder in clinical medicine, the children with AHT are generally brought to medical care with an unclear or patently false history of present illness, making the rapid diagnosis of the brain injury the first hurdle in a long series of challenges in managing these children. The nomenclature of this condition has evolved over the years since the 1974 publication in which Caffey (1) referred to “the whiplash 
shaken infant syndrome.” There have been numerous terms used to describe the constellation of injuries that now is referred to as “abusive head trauma” (2). “Shaken baby syndrome” (3) is probably the most recognizable of these terms, although “inflicted traumatic brain injury,” “inflicted childhood neurotrauma,” “nonaccidental traumatic brain injury,” and “intentional traumatic brain injury” are also used in the literature (4,5). The term AHT represents an improved understanding of the brain injuries that are not due to shaking alone, but can be the result of a combination of mechanisms including shaking, blunt impact, spinal cord injury, and hypoxic-ischemic injury. Use of the term AHT also changes the focus from the mechanism of injury to the abusive etiology of the injury. This review describes the necessary aspects of care of these children for the intensivist by focusing on the brain injury despite the fact that injuries to the abused child can include orthopedic, ophthalmologic, solid organ, and other injuries. For a comprehensive review of the multitrauma patient, the reader is referred to other chapters within this textbook.
shaken infant syndrome.” There have been numerous terms used to describe the constellation of injuries that now is referred to as “abusive head trauma” (2). “Shaken baby syndrome” (3) is probably the most recognizable of these terms, although “inflicted traumatic brain injury,” “inflicted childhood neurotrauma,” “nonaccidental traumatic brain injury,” and “intentional traumatic brain injury” are also used in the literature (4,5). The term AHT represents an improved understanding of the brain injuries that are not due to shaking alone, but can be the result of a combination of mechanisms including shaking, blunt impact, spinal cord injury, and hypoxic-ischemic injury. Use of the term AHT also changes the focus from the mechanism of injury to the abusive etiology of the injury. This review describes the necessary aspects of care of these children for the intensivist by focusing on the brain injury despite the fact that injuries to the abused child can include orthopedic, ophthalmologic, solid organ, and other injuries. For a comprehensive review of the multitrauma patient, the reader is referred to other chapters within this textbook.EPIDEMIOLOGY
AHT is the leading cause of death from child abuse and the most common cause of severe traumatic brain injury (TBI) in infants. The incidence of AHT in the United States and Canada has been measured in multiple studies using different types of case ascertainment. Overall, the data demonstrate similar results regardless of the methodology, but suggest a lower rate of AHT in Canada than in the United States (6,7,8,9,10,11). Two active surveillance studies demonstrated an incidence of 29.7 (95% CI: 22.9-36.7) per 100,000 children less than 1 year of age in the United States and 14.1 (95% CI: 11.8-16.5) per 100,000 children less than 1 year of age in Canada. Small studies from Mexico and Estonia demonstrate that AHT is not unique to developed countries. All studies may ultimately underestimate the 
true incidence of the condition (12,13). Because of the vague nature of symptoms in mild cases of AHT, clinicians may miss the diagnosis of AHT in infants and young children who present without a history of trauma and with soft neurologic signs such as vomiting or fussiness(14). Even the most severe cases of AHT may only be diagnosed at autopsy (14), and of course, AHT may be misclassified as noninflicted TBI.
true incidence of the condition (12,13). Because of the vague nature of symptoms in mild cases of AHT, clinicians may miss the diagnosis of AHT in infants and young children who present without a history of trauma and with soft neurologic signs such as vomiting or fussiness(14). Even the most severe cases of AHT may only be diagnosed at autopsy (14), and of course, AHT may be misclassified as noninflicted TBI.Risk Factors
Risk factors for AHT include those intrinsic to the child and 
to the caregiver. There is a unique age distribution for AHT, with peak incidence rates in the first year of life (mean age of 2-8 months in several reports) (7,8,11). Importantly, however, approximately 25% of children with AHT are older than 1 year of age, and it should be a part of the differential diagnosis in all young children because of the potentially grave consequences of misdiagnosis. AHT is thought to be associated with the peak period of crying during development, as this is the most commonly identified trigger (15,16). In addition to these child-based risk factors, circumstances related specifically to caregivers also contribute to the risk of AHT. Stress—both for communities as well as for individuals—may be the most pervasive of these risks. Studies have demonstrated that military deployment (17), natural disaster (18), and economic stress (8) can all affect the rate of AHT in communities. Specifically, there is an increased incidence of AHT in children on public insurance, which may integrate a number of these factors. On an individual basis, circumstances that decrease a parent’s ability to deal with perceived stresses— including young parental age, poor impulse control, lower levels of maternal education, substance and alcohol abuse, and mental illness, including postpartum depression—can all increase the risk of AHT (19). While it is critically important to recognize these risk factors, the absence of these conditions does not remove the possibility, and hence concern for, AHT in one’s clinical differential diagnosis.
to the caregiver. There is a unique age distribution for AHT, with peak incidence rates in the first year of life (mean age of 2-8 months in several reports) (7,8,11). Importantly, however, approximately 25% of children with AHT are older than 1 year of age, and it should be a part of the differential diagnosis in all young children because of the potentially grave consequences of misdiagnosis. AHT is thought to be associated with the peak period of crying during development, as this is the most commonly identified trigger (15,16). In addition to these child-based risk factors, circumstances related specifically to caregivers also contribute to the risk of AHT. Stress—both for communities as well as for individuals—may be the most pervasive of these risks. Studies have demonstrated that military deployment (17), natural disaster (18), and economic stress (8) can all affect the rate of AHT in communities. Specifically, there is an increased incidence of AHT in children on public insurance, which may integrate a number of these factors. On an individual basis, circumstances that decrease a parent’s ability to deal with perceived stresses— including young parental age, poor impulse control, lower levels of maternal education, substance and alcohol abuse, and mental illness, including postpartum depression—can all increase the risk of AHT (19). While it is critically important to recognize these risk factors, the absence of these conditions does not remove the possibility, and hence concern for, AHT in one’s clinical differential diagnosis.Mechanisms of Injury
The mechanisms of injury in AHT are among the most controversial topics in pediatrics but likely include a combination of shaking, blunt force trauma, hypoxic-ischemic injury, and 
spinal cord injury. In his seminal paper, Caffey (1) described the unexplained occurrence of 23 long bone fractures in six children who also demonstrated subdural hematomas. In these cases, a nursemaid admitted to shaking the victims while holding them by the arms and trunk (1). Subsequently, there have been multiple studies to support the hypothesis that shaking is an important mechanism of injury in many cases of AHT (20,21,22,23,24,25,26). The effect of shear force is most observable within the orbit, as a study in neonatal pigs demonstrated that extensive multilayer retinal hemorrhages and retinoschisis can be caused by shear forces on the retina and macula (27). Retinal hemorrhages rarely, if ever, occur in noninflicted TBI, and when present, do not have the same depth or affected area as retinal hemorrhages seen in AHT (27,28,29). Shaking injury may also explain some instances of subdural hematomas in AHT, with the proposed mechanism of tearing of bridging veins as the brain is rapidly moved within the cranial vault (14,30,31,32).
spinal cord injury. In his seminal paper, Caffey (1) described the unexplained occurrence of 23 long bone fractures in six children who also demonstrated subdural hematomas. In these cases, a nursemaid admitted to shaking the victims while holding them by the arms and trunk (1). Subsequently, there have been multiple studies to support the hypothesis that shaking is an important mechanism of injury in many cases of AHT (20,21,22,23,24,25,26). The effect of shear force is most observable within the orbit, as a study in neonatal pigs demonstrated that extensive multilayer retinal hemorrhages and retinoschisis can be caused by shear forces on the retina and macula (27). Retinal hemorrhages rarely, if ever, occur in noninflicted TBI, and when present, do not have the same depth or affected area as retinal hemorrhages seen in AHT (27,28,29). Shaking injury may also explain some instances of subdural hematomas in AHT, with the proposed mechanism of tearing of bridging veins as the brain is rapidly moved within the cranial vault (14,30,31,32).Blunt force trauma, either alone or in combination with shaking, is another potential mechanism of injury, with biomechanical studies demonstrating significantly greater rotational force when shaking is combined with blunt impact (3,33,34). Whether or not blunt force trauma is required to produce the forces necessary to cause severe (or fatal) brain injury has been the subject of much debate. An early biomechanical study suggested that shaking alone did not result in sufficient forces to cause such injuries (34)—findings supported by two postmortem studies (34,35). Geddes and colleagues (35) studied 14 cases of fatal AHT and found that while all cases had evidence of blunt force trauma, the evidence for this mechanism was only found in postmortem examination in half of the cases. In contrast, in two studies evaluating AHT cases where there were confessions by perpetrators, a significant proportion found no evidence of an impact (20,26). More contemporary experimental models (including porcine models of repetitive acceleration-deceleration and finite element model predictions) have suggested that previous models may have underestimated the complexity of the biomechanical forces in play as well as age-dependent differences in injury potential (36,37,38). Further evaluation of these and other models will likely improve our understanding of the complex interplay between the forces that are applied in AHT.
Hypoxic-ischemic damage to the brain in AHT has been widely observed. An intriguing study compared serum biomarkers of neuronal injury in patients with AHT, noninflicted TBI, and hypoxic-ischemic injury and found that the biochemical profile seen in AHT was more similar to that of patients with hypoxic-ischemic injury, demonstrating late peak biomarker concentrations that would be consistent with ongoing cell death (39,40). It has been theorized that hypoxia-ischemia may result from a delay in seeking medical attention after an incident of abuse by a perpetrator. However, the possible linkage between injury to the brain stem and upper spinal cord injury with the development of apnea and hypoxic injury has been proposed. A recent magnetic resonance imaging (MRI) study suggests that subdural hematomas within the cervical spinal cord are frequently observed with nonfatal AHT, but not in children with noninflicted TBI (41). Others have emphasized that damage to the respiratory centers in the cervicomedullary junction may play a role in the development of hypoxia-related injuries after AHT (41,42,43,44).
DIAGNOSIS
As mentioned earlier, the history provided by the caregiver in cases of AHT
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