Section 3 -

Inflicted Childhood Head Trauma And The Courts Roger W Byard Marks Professor of Pathology, University of Adelaide and Chief Forensic Pathologist, Forensic Science South Australia, Australia

Introduction Assessing inflicted childhood head trauma may be a complex process, as mechanisms may be subtle and injuries may appear relatively non-specific. An additional problem is the lack of experimental data that can be used to evaluate possible mechanisms of injury or to help with estimating the amount of force required to cause a certain lesion. Lethal inflicted injuries in infancy and childhood most often involve the craniocerebral region. The clinical presentations of such injuries are often quite non-specific and involve reduced levels of consciousness in children who were allegedly previously well. Any undiagnosed encephalopathic state in an infant or young child should prompt careful evaluation for inflicted injuries, particularly if there has been associated lethargy, rapidly developing unconsciousness, poor feeding, seizures, apneic episodes or unexplained neurological deficits. Increased intracranial pressure and hydrocephalus may be subsequent findings [1, 2, 3]. Presenting histories are usually falsified to protect the assailant, often including incorrect times frames and spurious stories of falls from low heights. Rather than provide a detailed analysis of specific entities, the following discussion deals with recurrent problems that arise in court. Discussion Infants and young children have anatomic peculiarities of the skull and brain that predispose to particular forms of injury. The head is relatively larger than in later life and is not supported by particularly strong neck muscles. The skull is composed of thin bony plates that are not fused and the base of the skull lacks well-defined ridges. Lack of myelination makes the brain much softer and more friable than in older children and it is surrounded by relatively more cerebrospinal fluid. The combined effect of all of these features is that infant brains are vulnerable to shearing injuries when subjected to accelerative and decelerative forces [4, 5, 6]. Shaken Infant Syndrome (SIS) is a term that has been used when an infant has been gripped firmly by an adult and shaken backwards and forwards in a violent manner resulting in significant brain damage and/or death. The classical findings include thin subdural hemorrhages, subarachnoid hemorrhage, retinal hemorrhage, cerebral edema and evidence of diffuse axonal injury [7]. Considerable debate has, however, occurred in the courts, at scientific meetings and in the literature as to whether SIS exists, and if it does, whether the features in lethal cases indicate severe trauma or not. Conflicting opinions have also been expressed as to the alleged manifestations of shaking, and whether or not the features could be due to impact rather than to shaking alone [8, 9, 10, 11, 12, 13]. Given the likelihood of impact and shaking occurring together, and the difficulty that may occur in attempting to retrospectively distinguish between the two, better generic terms for these types of injuries are craniocerebral trauma and non-accidental head injury (NAHI) [3, 7]. In 2003 Geddes et al. proposed a 'unified hypothesis' in which they asserted that subdural and retinal hemorrhages found in shaken infants were due to hypoxia with brain swelling, rather than to trauma [14]. However, the proposal was considerably weakened by i) the lack of ocular examination in any of the 50 infants and fetuses studied, ii) the fact that only one case manifested a subdural hemorrhage (a case with sepsis and disseminated intravascular coagulation), and iii) that the only microscopic findings were of intradural and not subdural, hemorrhage. Despite these weaknesses, however the hypothesis has been widely cited in courts, along with the assertion that the degree of force necessary to produce the findings in shaking cases was not necessarily great [14, 15, 16]. However, in a Court of Appeal hearing dealing with a series of cases of shaking and inflicted head injury in infants in the United Kingdom in 2005, Geddes was reported as stating that the theory was not 'quite right' and that she 'could no longer support the hypothesis that brain swelling was the cause of subdural haemorrhages and retinal haemorrhages' [17]. It has also been asserted that a lesser degree of force may cause damage to the upper cervical spine, compromising respiratory function resulting in superimposed hypoxic brain injury, possibly with the other features normally attributed to shaking [14, 18]. While it is very important to examine the upper cervical cord in all of these cases, it must be recognised that the triad of cerebral edema, retinal hemorrhages and subdural hemorrhages in obtunded or dead infants does occur with perfectly normal, uninjured cervical spinal cords. Additionally, retinal and subdural hemorrhages are not recognized features of hypoxic-ischemic encephalopathy. Problem continue due to unreliable data in the literature. Early reports of possible inflicted or non-inflicted head injuries in infants often relied completely on the veracity of the presenting history. One result of this acceptance of the initial description of the possible event leading to the fatal injury was a belief that lethal intracranial trauma could occur from falls from very low heights. This continues to be vigorously debated. One study that shed some light on this was the report by Chadwick et al that showed that if the initial history of an injury is accepted unchallenged, the chance of dying from a fall of less than four feet was far greater (eight times) than from a fall of 10 to 45 feet [19]. The obvious conclusion is that more than just a simple fall was involved in children in the first group and that their histories must have been falsified. Infants and young children are surprisingly robust and clearly documented and independently witnessed cases of deaths due to intracranial injury from low falls are lacking. In fact when reliable witnesses have been present, children have only died from falls from buildings when this has exceeded three stories [20]. It is also difficult to extrapolate from models to the living human infant. Animal models suffer from this comparison in that injury patterns in infants are inextricably linked to the shape and physical characteristics of the immature human skull, cranial fossae and brain. There are no animal models that closely replicate the infant brain and skull. Mechanical models may certainly improve our understanding of the mechanism of accelerative and decelerative forces, however, replicating the complex mixture of tissues of different densities and tensile strengths with active and variable blood flow that is found in the human infant brain is extremely difficult. [6, 21, 22, 23, 24, 25] . Another problem that has occurred in pediatric forensic cases has been the lack of complete autopsy examinations including ancillary testing. On occasion this has involved either no examination of the cranial cavity, or failure to obtain formal neuropathological assessment of the brain and cord [26] , and these practices continue. Pediatric cases are usually quite complex and their retrospective assessment may be impossible if appropriate dissections and examinations were not performed at the time of the initial post-mortem. One way of dealing with these problems is to follow established autopsy and death scene examination protocols to ensure that appropriate investigations are being undertaken [27, 28]. Guidelines for the evaluation of expert evidence have been published [29] . References Hobbs CJ. Head injuries. Brit Med J 1989;298:1169-70. Willging JP, Bower CM, Cotton RT. Physical abuse of children. A retrospective review and an otolaryngology perspective. Arch Otolaryngol Head Neck Surg 1992;118:584-90. Byard RW, Cohle SD. Homicide and suicide. Ch 3 In: Sudden Death in Infancy, Childhood and Adolescence. Byard RW. 2nd edition, Cambridge University Press, Cambridge , 2004; pp 77-166. Duhaime A-C, Christian CW, Rorke LB, Zimmerman RA. Nonaccidental head injury in infants - the "shaken-baby syndrome". 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