Problems and Challenges with Inflicted Trauma at the Extremes of Life
Moderators: Gregory G. Davis and Roger W. Byard
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
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
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.
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
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 . 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
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)
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 . 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
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' .
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
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 . 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 .
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.
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 
, 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
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