Article

Abusive head trauma.

Department of Pediatrics, Kempe Child Protection Team, The Children's Hospital, 13123 E. 16th Avenue, Box 138, Denver, CO 80045, USA.
Pediatric Clinics of North America (Impact Factor: 2.2). 05/2009; 56(2):317-31. DOI: 10.1016/j.pcl.2009.02.001
Source: PubMed

ABSTRACT Child physical abuse that results in injury to the head or brain has been described using many terms, including battered child syndrome, whiplash injuries, shaken infant or shaken impact syndrome, and nonmechanistic terms such as abusive head trauma or nonaccidental trauma. These injuries sustained by child abuse victims are discussed in detail in this article, including information about diagnosis, management and outcomes. The use of forensics, the use imaging studies, and associated injuries are also detailed.

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    ABSTRACT: Infants with abusive head trauma (AHT) have diffuse brain damage with potentially fatal brain swelling. The pathogenesis of the brain damage remains unclear. We hypothesize that brain damage in AHT is due to hypoxic-ischemic injury with hypoxic-ischemic encephalopathy (HIE) rather than primary traumatic brain injury (TBI) with traumatic diffuse axonal injury (tDAI). We studied brain tissue of AHT victims. Primary outcome measure was the presence of primary traumatic versus hypoxic-ischemic brain injury. The diagnosis of tDAI followed a standardized semiquantitative diagnostic approach yielding a 4-tiered grading scheme (definite, possible, improbable, and none). In addition, results of quantitative immunohistochemical analysis in a subgroup of AHT victims with instant death were compared with matched SIDS controls. In our cohort of 50 AHT victims, none had definite tDAI (no tDAI in 30, tDAI possible in 2, and tDAI improbable in 18). Instead, all AHT victims showed morphological findings indicative of HIE. Furthermore, the subgroup with instant death showed significantly higher counts of damaged axons with accumulation of amyloid precursor protein (APP) in the brainstem adjacent to the central pattern generator of respiratory activity (CPG) (odds ratio adjusted for age, sex, brain weight, and APP-count in other regions = 3.1; 95 % confidence interval = 1.2 to 7.7; p = 0.015). AHT victims in our cohort do not have diffuse TBI or tDAI. Instead, our findings indicate that the encephalopathy in AHT is the due to hypoxic-ischemic injury probably as the result of respiratory arrest due to local damage to parts of the CPG in the brainstem.
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