This document is a de-identified extract from medical reports prepared in 1999 by Dr Mark Donohoe in selected and typical cases of alleged shaking and injuries to infants. It's purpose is to provide a framework for assessing assumptions and evidence required for determining that particular injuries were caused by intentional and violent shaking. A companion document, an assessment of the "quality of evidence" in the research so far published (to late 1998) in the peer-reviewed medical literature, is currently under consideration for journal publication, and cannot be included with this document (September 2001). This document is accompanied by the literature references reviewed for SBS/NAI and Terson's syndrome. Feedback on this document (with version number and date) is welcome. Please email the author at <email@example.com>.
"shaken baby syndrome"
question which needs to be answered is the
assessment of a child with subdural haemorrhages
with or without retinal haemorrhages is not,
"could this be a case of shaken baby
syndrome?", because this is clearly one
possibility. The questions which need to be
answered would appear to be:
This report is intended as an aid to answering these questions in a particular case.
issues and evidence for SBS
As with all "swings of a pendulum", however, there are associated dangers of such increased surveillance for abuse. The most obvious risk is that cases not associated with abuse will be incorrectly assumed to be abuse, and that the totality of evidence in cases will be ignored in favour of apparently "incriminating" evidence. I say this because it is, even in theory, impossible to attain perfection in the correct attribution of cause of injury. In the past, actual abuse cases were missed as a result. Now, cases unrelated to abuse are occasionally incorrectly attributed to abuse. The medical tests which are supportive of the diagnosis of non-accidental injury (NAI) have been pushed by many advocates as being proof of NAI generally, and SBS in particular.
The diagnosis of NAI and SBS rests on a number of factors, including medical and social history, family circumstances, medical examination, a wide range of test results, and the results of investigations and interviews by experienced multi-disciplinary teams. The diagnosis of NAI or SBS cannot ever rest upon the results of a few isolated investigations alone, as has been the case in recent years.
are two main reasons for pursuing suspected
NAI vigorously, namely:
the medical profession may well be acting
in the interests of the child by assuming
NAI even when it has not occurred, one must
recognise the potential for harm to the family
and child where such assumptions prove to
be incorrect. The decision on whether or not
NAI has occurred, and who is responsible for
it if it has occurred, must be made by the
legal process, and such judgements must be
dispassionate and based on evidence, rather
than assertion by those wishing to protect
the child. While it is self-evident that the
safety and rights of the child must be protected
in every case, the rights of the parents and
carers cannot be ignored or forgotten in so
doing. There is a clear risk in assuming that
abuse has occurred in cases where the evidence
is weak, and where alternative opinions have
not been adequately pursued and excluded.
cases which I have so far reviewed would never
have been investigated for potential abuse
had it not been for the medical findings,
as there was no evidence of or suggestion
of abuse. In such cases, NAI has been assumed
where other alternative explanations not only
exist, but are arguably more likely than NAI.
the tendency of the medical profession to
ignore the possibility of adverse reactions
to vaccines, especially those containing thiomersal
(a mercury preservative), is important.
more than half of the cases I have reviewed,
there is an apparent temporal relationship
between the injury and prior vaccination with
thiomersal-containing polyvalent vaccines
or multiple simultaneous vaccinations. The
vaccine typically leads to pyrexia and crying
immediately following vaccination, and the
infant is given paracetamol (acetaminophen)
at increasing doses for control of crying
and pyrexia in the following days. In most
of these cases, a broad spectrum antibiotic
has also been prescribed in the same period.
has been suggested that the alternative explanation
should be preferred, namely that the vaccination
itself caused no injury, but induced crying
which lasted for days, leading to frustration
and eventual shaking by a parent or carer.
Even if this is accepted, it raises a most
interesting issue of ultimate causation. Had
the vaccine(s) not been administered, the
adverse reaction and crying would not have
occurred, and there would have been no risk
or likelihood of shaking or injury of any
type. The acceptance of such crying and pyrexia
as a "normal and expected" consequence
of polyvalent vaccinations in up to 20% of
infants does nothing to address the consequences
of the crying and the increased risk of injury
to the child from such a common event. It
is disingenuous to argue that "the disease
would have been worse than the vaccination",
because the disease may or may not have occurred,
and is a part of normal life of a child, whereas
vaccination is a procedure requiring informed
If one identifiable risk of vaccination is that of shaking and injury following prolonged crying (assuming that shaking did occur as a result of the vaccine-induced crying), then this needs to be conveyed to parents of children being vaccinated as part of the informed consent. If they are made aware of the potential for prolonged crying and pyrexia, and are told of the risks associated with shaking which may be a consequence of this crying, then the risk itself may be reduced. Thus, it is arguable that vaccination is an independent predictor (or risk factor) for neurological injuries in infants, whether it is directly causative or predisposes to other outcomes which are causative. A recognition of the association (direct or indirect) may allow for action and warnings which may decrease the likelihood of adverse outcomes.
and assumptions regarding allegation of SBS
In this document, I address each of these statements separately, and attempt to assess the evidence for and against each statement.
Spontaneous subdural haemorrhage (SDH) does
not occur in a normal, healthy infant.
is clear evidence that SDH can be caused by
anatomical, infectious and biochemical disorders
which cause no obvious symptoms prior to the
intracranial bleeding. In such circumstances,
the infant appears "normal and healthy"
(although probably not robustly healthy) despite
the underlying, predisposing pathology.
disorders, predisposing to SDH, include:
list is not intended to be exhaustive. It
is also possible that more than one predisposing
factor existed, and that it was a combination
of factors which led to the intracranial haemorrhage.
For example, a mild factor XIII deficiency,
when combined with malabsorption or Reye's
an infant under six months, such disorders
may be asymptomatic, or may simply result
in a non-specific failure to thrive. In some
of these diseases, the first presentation
is that of an intracranial bleed. It is only
possible to exclude these other causes by
careful history taking,
is my view, based on the cases I have reviewed,
that there is a tendency to assume that NAI
has occurred in infants with SDH and RH, and
as a consequence of that assumption, there
is a general failure in the first instance
to pursue other potential causes or contributions
to the injury as
once the allegation of abuse has been made,
and police or welfare services have become
involved, there is a general unwillingness
to consider any other plausible causes of
the injury. In a sense, the parents or carer
are assumed to be guilty, and have no logical
way of "proving" their
SDH combined with retinal haemorrhage (RH)
is pathognomonic of "non-accidental injury"
The combination of SDH and RH strongly support a diagnosis of NAI, but in no way constitute proof that NAI occurred. The value of the diagnosis of SDH and RH is that their presence can markedly increase the confidence of a diagnosis of NAI, given other circumstances or findings which may indicate NAI. Even if we assume that all non-accidental injuries involving shaking or blunt trauma to the head of babies cause subdural haemorrhage and retinal haemorrhage, it does not follow that all cases of SDH and RH are caused by NAI. One must know what other diseases or circumstances may cause SDH and RH. Since the mechanism of RH is unknown (Riffenburgh 1991), it is important that the specific hallmarks of NAI be delineated, as proposed recently (Rohrbach 1997).
(1997) has stated,"Intraretinal haemorrhages
alone are typical, though not pathognomonic
for the 'battered-child syndrome'". According
to Rohrbach, the combination of the following
provides increased certainty of NAI, although
there are clearly shortcomings in this single
ophthalmologists examining the infant needs
to be questioned as to whether the changes
seen in the particular case match these proposed
Conditions apart from NAI which may result in SD and RH include: bleeding disorders; meningitis; septicaemia; leukaemia; galactosaemia; hypertension; and Henoch-Schonlein purpura.
RH may also occur simply as a consequence of the intracranial bleeding. A number of papers which deal with the mechanism of the RH have suggested that the increasing intracranial pressure and subarachnoid haemorrhage lead to retinal haemorrhages (Jacobi 1986), and these may be accompanied by SDH. In fact, this association is known as "Terson's syndrome". A number of papers (Giangiacomo 1985, Weingeist 1986, Jacobi 1986,Keithahn 1993, Poepel 1994) point out the similarities between Terson's syndrome and the retinopathy of shaken baby syndrome, with some suggesting that SBS should be considered in the differential diagnosis of Terson's syndrome.
Thus, there are other plausible and reasonable explanations for the combination of SDH and RH in an infant. Any of the factors listed above as potential causes of SDH must be considered a plausible cause of the RH as well.
The presence of SDH and RH is insufficient to prove any particular cause. It is likely that the majority of cases in which SDH and RH are found in infants under one year of age are NAI, but this is a statistical association. In any given case, these findings are only supportive of NAI. The case must stand or fall on other factors which would lead one to suspect NAI.
3 In the absence of evidence of identifiable external trauma, SDH and RH are only caused by violent "acceleration/deceleration" actions caused by an adult, known as "shaken baby syndrome". Most studies show a high proportion of NAIs are associated with other signs of trauma or abuse, either in the damaged infant or in other family members. In a recent British retrospective study (Jayawant 1998), about 60% showed signs of other trauma (bruising, fractures, resolving old SDH, etc). Other authors have suggested similar or higher percentages as showing signs of trauma or abuse, especially in cases of severe cerebral damage and death (Alexander 1990, Duhaime 1987, Lancon 1998).
As noted above, factors which may cause or contribute to SDH or SAH in an infant are likely to cause RH as well. A recent study (Jayawant 1998) noted an 80% association between SDH and RH, suggesting that RH is not an independent risk predictor, but a marker of severity and extensiveness of intracranial bleeding.
A number of authors (Duhaime 1987, Lancon 1998, Closset 1992) have suggested that shaking without impact does not generate sufficient forces to cause the types of injuries seen in SBS cases. Many others disagree, holding that shearing forces tend to rupture the fragile veins across the dural space. These other authors propose ways in which shaking with a rotatory component, possibly at particular frequencies, or with rapid deceleration caused by soft impact (eg pillow, etc), could cause such shearing.
In fact, if this view of rotation at particular frequencies is correct, it is likely that the forces required to cause the damage observed may be less important than had previously been thought.
is no case definition for SBS, and this tends
to cause problems in deciding if a particular
case is one of SBS. Many authors have taken
the view that any unexplained presentation
of SDH and RH in an infant is NAI until proven
otherwise. While useful as a medical "rule
of thumb", it should be noted that this
leads to a reversal of the burden of proof
if applied in a legal setting, and can result
in the assumption of guilt in blameless carers.
If all unexplained cases are defined as NAI
or SBS, then the circular definition results
in carers having to prove their innocence,
which is logically impossible for this condition.
The essential ingredient of SBS would appear to be strong evidence of shaking and NAI. The majority of studies, however, assume that all unexplained cases of SDH and RH are SBS and NAI, and do not determine the degree of confidence that the assumption is correct. In addition, the actions said to be required to cause NAI have changed over time from fore-aft shaking with impact, to severe and prolonged fore-aft shaking without impact, to rotatory acceleration-deceleration without impact, and more recently to rotatory acceleration-deceleration with soft object impact.
Without a clear case definition, and without a means of proving whether an unobserved carer performed the particular actions required, the attribution of unexplained SDH and RH to SBS is neither provable nor disprovable. It is not a question which can be scientifically decided with current knowledge and techniques, and does not meet Popper's test of a valid scientific hypothesis (that an experiment can be defined which could disprove the hypothesis, were it to be incorrect). The diagnosis rests on the presence of sufficient "other factors" which would raise suspicion of NAI, and the clinical, ophthalmological and radiographic findings become supportive, rather than diagnostic, in such circumstances.
SBS must be intentional, or at least they
would appear intentional to any dispassionate
There are few data or cases in which the precise actions or forces used to create the injuries have been determined or observed. The lack of observational or experimental data make it impossible to determine what an independent, dispassionate observer would perceive.
It may be a reasonable assumption that the rareness of the SBS-type injury (estimated incidence in Britain at less than one in 4,000 children per year - Jayawant 1998) would imply excessive force. This may be a false assumption, however, if the damage arises from a particular type of action, rather than simply being a function of applied force. Rhythmic rotation of the baby at a particular frequency, for example, would be expected to lead to an amplification of applied force and relative motion between brain and skull in the infant. Such shaking may appear to be benign, yet cause significant damage to the dural vessels.
The diagnosis of "shaken baby syndrome"
can be made confidently on the basis of clinical
and x-ray assessment alone.
Nine factors suggesting NAI are identified in children who have suffered SDH, namely:
Social and Family Issues
Investigations and clinical findings
Of the nine proposed key factors in identification of NAI, the number found in any particular case may be important in determining likelihood of SBS/NAI.
the severity of shaking required to cause
these findings would have been obvious, and
was unrelated to any shaking or corporal punishment
admitted to by family members.
[Retinal hemorrhage in the infant as an indication
of shaken baby trauma] Schmidt US, Mittelviefhaus
K, Hansen LL Klin Monatsbl Augenheilkd 1997
Dec 211:6 354-8
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