Subdural hemorrhage in infancy: keep an open mind

Abstract

In North America and the United Kingdom, putative cases of pediatric head injury are often disputed in the criminal justice system. The main issues that often arise are whether, in a specific case, the neuropathologic and ocular findings are due to: abusive head trauma [1], an accidental fall [2], or a natural condition that has mimicked a head injury. In general, there are four general types of natural/ non-traumatic mimics that are proposed as alternate explanations in cases of pediatric head injury. Two of these alternate explanations are non-controversial and are widely accepted as non-traumatic causes of subdural hemorrhage: coagulopathy (e.g., vitamin K deficiency, primary disorders of hemostasis) and selected rare diseases or conditions (e.g., cerebral venous thrombosis, glutaric aciduria, mitochondrial disorders). Indeed, the past few years has seen an increasing number of case reports of non-traumatic subdural hemorrhage (Table 1). The latest contribution by Guddat et al. [3] expands this list to include acquired coagulopathy, complicating neonatal giant cell hepatitis. The publication of clinicopathologic case reports on proposed mimics of pediatric head injury is an important and welcome contribution to forensic medicine. Pathologists and clinicians should be encouraged to publish such cases to improve our understanding of these often complex and difficult cases. Furthermore, the main medicolegal value of a published evidence-base of relevant counterexamples is the ability to identify what ancillary laboratory testing should be undertaken in unclear cases (e.g., testing for hemophilia A in male infants with unexplained subdural hemorrhage) [4]. In addition to the widely accepted mimics of pediatric head injury, there are two other possibilities that are controversial and not widely accepted as alternate explanations. These are best considered hypotheses that are the topic of debate in the literature and the courts: (1) hypoxic dural vascular injury and (2) rebleeding of a chronic subdural hemorrhage. The hypoxic dural vascular injury hypothesis was initiated by Geddes [5] and later modified and expanded by others [6]. The hypothesis indicates that endothelial cells of meningeal blood vessels (largely dural venous structures) are damaged by a hypoxic insult while simultaneously congested/distended, leading to the extravasation of blood. Thus, blood accumulates in subdural space. Although not widely accepted, upper airway obstruction from choking on vomitus or food has been proposed as a causal mechanism. There is essentially no direct observational evidence to support this hypothesis. However, there is some evidence to support that subdural/subarachnoid hemorrhage in critically ill neonates is explained by this mechanism [6]. In critically ill neonates, subdural hemorrhage can occur due to extension of blood from extensive intradural hemorrhage caused by a hypoxic-septic insult to the dura. However, it seems unlikely that this mechanism can explain subdural hemorrhage significantly beyond the neonatal period, since there is often no or slight intradural hemorrhage in cases of older infants and children with subdural hemorrhage. In addition, subdural hemorrhage is not part of the classical pathology of hypoxic encephalopathy following drowning or cardiac arrest from a variety of causes [7]. On balance, unless there is extensive intradural and subdural hemorrhage in a neonate with hypoxia, this hypothesis is unlikely M. S. Pollanen Centre for Forensic Science and Medicine, University of Toronto, Toronto, ON, Canada