Shaken Baby Syndrome

adult head injury in road traffic accidents. Following

Guthkelchs paper, the shaken baby syndrome has
become widely accepted as a form of child abuse [1].

Introduction
The diagnosis shaken baby syndrome (SBS) has
been widely accepted for over 30 years, but recent
evidence from biomechanical and clinical observational studies questions the validity of the syndrome.

The Triad of Injuries

The three elements of the triad are encephalopathy,
RH, and SDH.

Retinal Hemorrhages (RHs)

Definition
The diagnosis of SBS is based on the clinical triad
of encephalopathy, retinal hemorrhage (RH), and
subdural hemorrhage (SDH) in infants, usually under
six months of age, who may die unexpectedly or
survive with greater or lesser degrees of neurological damage [1]. The term non-accidental head injury
(NAHI) has been preferred as it has no implications
for mechanism of injury. Other features often associated include a sole carer at the time of collapse and
a clinical history that is incompatible with the severity of the injuries. The diagnosis of inflicted injury
becomes less problematic if there is objective evidence of violence, such as bruises, fractures, or burns,
but objective evidence of trauma has not always been
necessary in making the diagnosis.
Central to the assessment of these cases is whether
the triad of findings can be regarded as diagnostic
of abuse with any degree of certainty. This review
examines the evidence base for each element of
the triad and the current biomechanical evidence
regarding mechanisms of infant head injury and its
pathological investigation.

History
SDH has been associated with child abuse since the
mid-19th century [2]. Kempe described SDH with
multiple skeletal injuries and bruises as the battered child syndrome and Caffey described long bone
fractures and SDH [35], but it is Guthkelch [6]
who developed the hypothesis that the whiplashlike
movements during shaking cause the characteristic
bilateral thin film SDH of the syndrome. He based
his hypothesis, that shaking causes tearing of the
cerebral bridging veins leading to SDH, on the biomechanical studies of Ommaya [7] who was researching

RHs have been regarded as an important indicator

of inflicted injury, but many other causes of retinal bleeding are recognized in infants, for example
after normal birth, raised intracranial pressure, blood
dyscrasias, hemoglobinopathies, extracorporeal membrane oxygenation, cataract surgery, and accidental
trauma [8]. Postmortem indirect ophthalmoscopy has
shown RHs to be more common after natural disease and accidental injury than after inflicted injury
[9]. These authors also noted that infants suspected
to have been abused were more likely to have ophthalmological examination in life than infants with
accidental injuries or natural diseases. This bias readily distorts the true incidence of RH in non-accidental
injury. Indeed Vinchon [10] noted in his study of
infant head injury that In the construct of our study
we could not obviate the circularity bias, and the evaluation of the incidence of RH in child abuse remains a
self-fulfilling prophecy. These authors did, however,
suggest that the extent and nature of retinal bleeds
may be more important as indicators of inflicted head
injury than their existence per se [10].
The main hypotheses for genesis of RH are that
it is the result of venous obstruction, which in turn
may result from compression of the optic nerve
by raised intracranial or intravascular pressure, even
transiently, or that the tissues of the retina are torn
during the act of shaking. This latter hypothesis does
not withstand biomechanical scrutiny [11].

Encephalopathy
This term may be widely interpreted to include a
range of clinical manifestations from feeding difficulties, vomiting, and sleepiness to seizures and
fulminating cerebral edema.
The specific neuropathological features of traumatic brain injury are contusions and traumatic

Shaken Baby Syndrome

(a)

(b)

Figure 1 (a) Acute axonal injury. Bands of BAPP expression in an infarcted area of brain in acute hypoxic-ischemic
injury. (b) Axonal swellings expressing BAPP restricted to the pontine cortico-spinal tracts, considered to indicate traumatic
damage

axonal injury. Hypoxic-ischemic injury and brain

swelling are frequently seen but are not specific for
trauma. Contusions are very uncommon in infant
brain trauma in the absence of skull fractures. Identification of axonal injury now depends on the immunocytochemical demonstration of beta amyloid precursor protein (BAPP). This is a very sensitive marker of
interruption of normal axonal flow but may be upregulated after hypoxicischemic injury and metabolic
disruption as well as trauma (Figure 1). Distinction
of traumatic axonal expression of BAPP from other
causes is fraught with difficulty, and depends in part
on its distribution [12], [13], [14]. Neuropathological
studies have shown that in babies who die following
NAHI, the underlying brain pathology is widespread
hypoxic-ischemic injury and not diffuse traumatic
axonal injury as previously believed [12, 13]. In this
series axonal injury was seen in a limited distribution in the lower brainstem and in only a minority
of cases. Radiological studies have confirmed these
pathological observations [15].
This observation is important as traumatic axonal
injury will lead to immediate loss of function causing
clinical symptoms from the time of trauma. In
contrast, hypoxic-ischemic injury and ensuing brain
swelling take variable periods of time to develop
and a baby so damaged may not show immediate
symptoms. Even fatal brain trauma may present with
a lucid interval between injury and clinical collapse
[16, 17]. Lucid intervals are more frequently seen
in infants less than two years of age [18], reflecting
the very different responses of the infant brain to

injury due to the specific intracranial pathophysiology

before the skull bones fuse [19].
Damage to the cervical nerve roots has been
documented as part of the pathology of shaking injury
[14]. It has not been established that this is the result
of shaking, as cervical cord displacement resulting
from brain swelling may also cause traction on nerve
roots in the region. Autopsy studies in man and
primates have shown that the spinal cord is displaced
during extension and flexion of the neck [20, 21]
and it remains a possibility that hyperextension and
flexion could cause traction damage to nerve roots
throughout the length of the spinal cord, but this has
not been documented in living infants.

Subdural Hemorrhage (SDH)

SDH is perhaps the most important and consistent
component of the triad. In the acutely sick infant, it
is frequently the first clinical sign, identified on brain
scan, to raise the question of abuse. There are no
specific imaging patterns that can distinguish inflicted
from accidental intracranial injury [22, 23].
Autopsy and imaging studies show that infant
SDH is usually a thin bilateral film and not a thick,
unilateral space occupying clot as seen in traumatic
SDH in older children and adults [12, 13, 24]. This
raises the question of whether the two forms have the
same etiology and anatomical source.
Causes of Subdural Hemorrhage. The commonest cause of SDH in infants is said to be trauma
[25] although a recent study has shown a significant

Shaken Baby Syndrome

incidence (26%) of birth-related SDH [26]. Other
causes in infants include benign enlargement of
the extracerebral spaces (BEECS), clotting disorders,
hemorrhagic disease of the newborn, rare metabolic
diseases, vascular malformations, and neurosurgical
procedures [25, 27].
Traumatic SDH
Proposed traumatic causes of infant SDH are inflicted
injury such as shaking and/or impact and accidental
injuries such as falls. Impact includes blunt impact of
an object on the head and that resulting from a fall
or striking the moving head on a rigid surface. The
biomechanical aspects of these injuries are discussed
below. The vast majority of cases described as SBS
have evidence of impact [28]. While the pathologist
may be able to determine features indicative of
impact, it is not, of course, possible to distinguish
accidental from non-accidental injuries by pathology.
Low-Level Falls
Low-level falls have the potential, albeit only rarely,
to cause SDH in infants and young children. Absolute
height is not as important a criterion for injury as
the exact nature of the fall for a particular infant,
in a particular circumstance [29]. The effects of
twisting, rotation, or crushing of the structures of the
neck are crucial in terms of outcome. Biomechanical
studies show that falls even from low levels of
34 ft can generate far greater forces in the head
than shaking [11]. There are a number of case series
demonstrating that infants and children may suffer

intracranial damage including retinal and intracranial

hemorrhage after falls from levels as low as 3 ft [10,
17, 3033]. While most babies may suffer little from
an apparently trivial fall, this is clearly not always
the case.
Birth-Related SDH
Three studies, using magnetic resonance imaging
(MRI), have shown a surprisingly high incidence
of SDH after birth in asymptomatic infants. Whitby
identified SDH in the first two days of life in 9%
[32], while SDH was seen in up to 46% of otherwise
normal neonates using higher resolution MRI scanning [26, 34]. With regard to method of delivery,
ventouse or instrumental deliveries have been associated with a higher incidence of intracranial injury
[35, 36]. Towner [37] found an increased incidence
of intracranial hemorrhage after instrumental delivery
with ventouse or forceps and emergency caesarean
section, but the incidence was lower after caesarean
section before labor had begun. However, it should
be noted that all of Looneys cases followed normal
vaginal delivery [26].
While neonates with SDH may be asymptomatic
[26, 35] they may also have signs in the neonatal
period including unexplained apnoea, dusky episodes,
hypotonia, seizures, and lethargy [38].
Sources of SDH. Traditional belief is that in SBS
the SDH results from tearing of the superficial bridging veins as they cross from the brain to the dural
sinuses [6] (Figure 2). This has never been proved.

Figure 2 Infant bridging veins may be visualized by opening the skull very carefully, but they are readily torn in normal
autopsy procedures. (Picture courtesy of Dr P. Lantz)

Shaken Baby Syndrome

Indeed it is very difficult to find documented evidence

of torn bridging veins at surgery or at autopsy. Cushing, who operated on neonates with SDH and subsequently performed the autopsies wrote In two of
the cases I have examined I have satisfied myself that
such ruptures were present. A positive statement, however, cannot be given even for these cases, since the
dissection and exposure, difficult enough under any
circumstances, owing to the delicacy of the vessels is
the more so when they are obscured by extravasated
blood [39]. More recently Maxeiner [40] addressed
the problem by injecting radio-opaque dye into the
veins at autopsy to assess their integrity after removing the top of the head in one piece, hard-boiled egg
style. This approach is not widely used as it destroys
much of the brain and injection pressures need to be
carefully monitored if the veins are not to be ruptured
artifactually.
Volpe [41] said that SDH was by no means
always traumatic and suggested that in neonates
without tentorial tears the bleeding may arise from
the tributary veins of the dural sinuses. Autopsy
studies from the older literature show bridging vein
rupture is uncommon, Craig described 62 neonatal
SDH, of which only 3 had torn bridging veins,
all of those with overriding sutures [42]. Larroche
described 700 autopsies 18% with SDH. [43] She
noted an association with hypoxic-ischemic injury
(Figure 3). She did not identify torn veins.
If SDH does not arise from torn bridging veins,
what other sources may there be? Two obvious

Figure 3

alternative sites of origin exist, the dura itself and

the old subdural membranes (Figure 4).
Dural Hemorrhage
The dura is composed of two leaflets, the periosteal
and the meningeal dura, separated by a thin vascular
channel, which widens to form the large dural sinuses
[44]. There are particularly extensive venous sinuses
in the posterior falx, [45] a frequent site of high signal
on brain scans in asphyxiated infants. Bleeding into
the falx is well recognized in asphyxiated infants
[46]. It has long been acknowledged that optic
nerve sheath hemorrhage arises from the dura [47]
and more recently the dura was proposed as the
source of intracranial SDH in infants [48] (Figure 5).
Careful microscopic examination of the dura confirms
that intradural bleeding is common in asphyxiated
infants, particularly in the dural folds of the falx and
tentorium close to the large venous sinuses [49]. In
some cases intradural bleeding leaks out on to the
subdural surface leading to macroscopically evident
subdural haematoma [50].
Healing Subdural Membranes
Healing of SDH is by formation of a thin, vascular membrane consisting of fibroblasts, macrophages,
which often contain altered blood products, and wide
thin-walled capillaries with a potential to rebleed
[51] (Figure 6). It is uncommon in infants to see a
double layered membrane around a localized mass
of resolving clot, as seen in the elderly, probably
because the infant SDH usually forms as a thin film

Fresh subdural blood seen after birth asphyxia. (Picture courtesy of Dr I. Scheimberg)

Shaken Baby Syndrome

Arachnoid
granulation

Superior sagittal sinus

Intradural fluid channel

Lateral lacuna of
sagittal sinus

Dura

Inner dural plexus

Subarachnoid
space

Cortical
draining vein

Arachnoid barrier
membrane

Falx

Figure 4 Diagram representing a coronal slice through the brain and dura indicating the intradural sinuses and their
relationship to cortical surface veins, arachnoid granulations, and intradural fluid channels

(a)

(b)

Figure 5 (a) The dura is thickened and congested and there is patchy subarachnoid and subdural blood. Autopsy 44 h
after collapse following choking episode. (Courtesy of Dr I. Sheimberg.) (b) H & E stained section of falx showing it to
be destroyed by massive acute bleeding

rather than as a mass lesion. Contrast injection is

required to identify the membranes radiologically
[52]. In some cases, acute SDH leads to accumulation of fluid in the subdural space. The reasons
for this are unknown. Fluid collections may result
from immaturity of the arachnoid granulations and
impaired cerebrospinal fluid (CSF) absorption [22],

and be influenced by the method of treatment of

the acute hematoma. Surgical evacuation or tapping may prevent later reaccumulation of fluid [53,
54]. The period of time for redevelopment of subdural fluid collections may be long, between 15
and 111 days [55]. It is likely that an important
contribution to chronic subdural fluid accumulation is

Shaken Baby Syndrome

(a)

(b)

(c)

Figure 6 (a) Dural surface showing a very thin yellow-brown membrane, which has partly lifted during removal of the
brain. Head injury four weeks prior to death. (b) H & E stained section of acute bleed overlying a chronic membrane, which
consists of some six layers of fibroblasts between which are macrophages and new capillaries (three days after collapse
with acute SDH) (c) Same section stained with CD34 to show endothelial cells. Note capillaries growing into the fresh clot

repeated rebleeding and oozing from a chronic subdural membrane [56, 57].
There is little information regarding the potential
for birth-related SDH to evolve into chronic fluid
collections. Whitby followed nine cases with a repeat
scan at one month; none had developed a chronic
collection [35]. Rooks followed 18 cases for up to 3
months, one developed a further subdural bleed [34].
However these studies could not identify membranes
as contrast was not used. Chronic membranes have
been seen at autopsy in up to 31% of infants dying
unexpectedly without previous clinical evidence of
chronic SDH [58]. In view of the potential for acute
accidental SDH to evolve into a chronic collection
several months later [55], it would appear likely that
the same pattern would follow birth-related SDH. At
this time, we simply have insufficient information.

Distribution. In the first few days after bleeding,

subdural blood sediments under the influence of
gravity and undergoes secondary redistribution to the
most dependent part, the posterior falx and tentorium
[59]. Radiological studies show that subdural blood
tracks down around the spinal cord [60] and, if the
spine of babies with intracranial SDH is examined at
autopsy, blood is regularly seen in the subdural space
and around sacral nerve roots in the most dependent
parts of the dural sac (Figure 7).

Differential Diagnosis of SBS

The most common causes of the triad are impact,
birth-related SDH, BEECS, coagulopathies, apnoea,
asphyxia and choking, acute life-threatening events

Shaken Baby Syndrome

(a)

(b)

Figure 7 (a) A collection of fresh subdural blood at the dorsal aspect of the sacral spinal cord. Baby died within hours
of inflicted abdominal injury with acute and chronic subdural hemorrhage. (b) Microscope section showing an elliptical
collection of fresh blood dorsal to the spinal cord. The blood is within a chronic subdural membrane indicated by the iron
pigment, stained here by Perls stain. Baby died three weeks after traumatic subdural hemorrhage

(ALTEs), osteogenesis imperfecta, osteopenia of

prematurity, and metabolic diseases [14, 28, 61,
62, 63].

Choking/Asphyxia
In a considerable number of cases, vomiting and/or
reflux are described at the time of collapse, and
in some there is a history of feeding difficulties,
gastroesophageal reflux, and choking or apnoeic
episodes [14, 62]. SBS is commonly diagnosed in the
first three months of life, the age of peak incidence of
sudden infant death syndrome. Inhalation of feed or
vomit may play a part in sudden infant death [64] and
awake apnoea is associated with gastroesophageal
reflux [65]. The physiological response to aspiration
may be dramatic; foreign material on the larynx
causes laryngospasm, which is associated with startle,
cessation of respiration, hypoxaemia, bradycardia,
and a doubling of blood flow to the brain [66].
These circumstances, with or even without vigorous
resuscitation, may cause reperfusion injury and a preexisting healing subdural membrane may bleed. The
dura itself may become hemorrhagic and ooze blood
into the subdural space (Figure 8). As long ago as
1905, Cushing suggested that coughing, choking, and
venous congestion may explain some forms of infant
SDH [39], a hypothesis recently revived by Geddes,
[48, 67].

Biomechanics
Biomechanics is the application of principles of
physics to biological systems and has been the mainstay of research into motor vehicle safety for six
decades. It was just such research into noncontact
head injury from rear-end shunts that stimulated
Guthkelch to formulate his hypothesis for SBS in
1971 [6]. Ommaya [7] had caused concussion, SDH,
and white matter shearing injury (diffuse axonal
injury) in primates by whiplash. Guthkelch suggested
that the rotational forces of shaking would cause
tearing of bridging veins and bilateral subdural bleeding, although Ommaya himself warned that It is
improbable that the high speed and severity of the
single whiplash produced in our animal model could
be achieved by a single manual shake or even a short
series of manual shaking of an infant in one episode.
More recent studies using crash test dummies
indicate that impact generates far more force than
shaking (Figure 9) and that impact is required to
produce SDH [68]. Cory and Jones [69] generated
forces that exceeded the injury threshold for concussion, but not for SDH or axonal injury. Their adult
shaker volunteers fatigued after 10 seconds. While
they concluded that It cannot be categorically stated,
from a biomechanical perspective, that pure shaking cannot cause fatal head injuries in an infant,
they noted that in their experiments there were chin
and occipital contacts at the extremes of the shaking

Shaken Baby Syndrome

(a)

(b)

Figure 8 (a) Cortical vein thrombosis. Infant died 10 days after collapse following two choking episodes. Several surface
veins are thrombosed (arrows). (b) Section of thrombosed vein shows a network of new capillaries growing into the
periphery of the thrombus (CD31)

Peak head acceleration (g)

Bed mattress

25.4 cm

50

50.8 cm

75

Inflicted slamming
style impacts onto
surfaces noted

Leather sofa

76.2 cm

100

From adult males arms

125

25

Free fall impacts onto

carpeted stairs
(fall heights noted)

Figure 9 Comparative forces generated by dropping or shaking and slamming a dummy representing a six-month-old
infant (C Van Ee, personal communication 2007)

motion that could have caused impact. These authors

expressed their concerns regarding the difficulties in
extrapolating to human infants the findings in both
dummy and animal models. Biomechanical studies
have shown that falls and impact to the head produce significant rotational forces when the impacting
forces are not aligned through the center of gravity
of the head, due to hinging of the head on the
neck. Shaking is not necessary to cause rotational
acceleration.
Neck injuries may be underreported in babies
dying after severe abuse [70]. In Ommayas study,
11 of 19 primates had neck injuries; these were adult
animals with mature neck structure and musculature.

It is likely that the forces required to cause intracranial injury will also damage the weak infant neck
[71]. In road traffic accidents, infants who suffer single severe hyperextension forces have cervical fractures, dislocations, spinal cord injury, and torn nerve
roots, not SDH [7274].

Investigation of Shaken Baby Syndrome

SBS or NAHI is most likely to occur in an infant
dying suddenly under the age of six months. Autopsy
should be performed with careful consideration of
this diagnosis and appropriate steps taken to support
or exclude it. The records of pregnancy and delivery

Shaken Baby Syndrome

must be carefully studied to look for any evidence of
complications that could mimic NAHI. These include
pregnancy disorders such as oligohydramnios, fetal
hypokinesia, and prematurity, which lead to osteopenia and predispose to fractures. The birth history and
method of delivery are important as SDH may arise
at this time while being entirely asymptomatic in
the neonatal period. Head circumference charts are
important; head circumference measurements taken at
birth and in the subsequent weeks may reflect abnormal head growth, which can indicate an accumulating
subdural fluid collection and a propensity to rebleed.
The clinical history may give clues to other problems in the early weeks of life. Vomiting, feeding
problems, and apnoeic episodes and ALTEs may
indicate difficulties with coordination of breathing,
sucking and swallowing, and vulnerability to choking. Any event that threatens life may also potentially
end it.
The history of the babys terminal collapse must
also be carefully examined. Parents may describe
events that reveal a cause for collapse. In any other
field of medicine, the clinical history is regarded as
the cornerstone of diagnosis and it should not be
disregarded without serious critical evaluation.
The autopsy can reveal evidence of trauma such
as deep bruises and fractures not seen in clinical
examination. The examination of the intracranial
contents is paramount. The scalp and skull require
careful examination for evidence of bruising and
fractures. Suture separation due to raised intracranial
pressure and wormian bones can be mistaken for
fractures. When the cranium is opened, the presence
of any intracranial bleeding must be noted. Unclotted
blood may escape from the subdural space as the
skull is opened and be mistaken for bleeding from the
dural sinuses. It is important to note the volume and
nature of blood and the presence of xanthochromia,
indicating older bleeding. As the cranium is opened,
the bridging veins should be visualized and their
integrity assessed. If there is a question of bridging
vein rupture, histological examination may assist in
establishing this. The dural sinuses and draining veins
should be examined for evidence of thrombosis.
The dura must be carefully examined for evidence
of older bleeding. A chronic subdural membrane may
be thin and patchy and represented only by patches
of light brown discoloration. Multiple samples should
be taken from the dura, including the falx and
tentorium, for histological examination to look for

evidence of intradural bleeding and rupture onto

the subdural surface. This may be the source of
significant subdural blood.
The brain must be fixed for detailed histological
examination.
In all of these cases, the time between collapse
and death may play a significant part in the final
pathology. A baby who has collapsed and becomes
apnoeic with subsequent cardiopulmonary rescuscitation (CPR) and ventilation will be shocked and
suffer multiorgan failure with altered clotting, loss
of integrity of vessels and membranes, oozing of
blood into intracranial compartments, including the
subarachnoid and subdural spaces, and development
of the respirator brain.
Review of the brain imaging in life is essential
in assessing, as far as possible, just how much
hemorrhage occurred at the time of collapse and how
much may be the result of subsequent secondary
changes. It is recognized that SDH may continue to
bleed after initial onset [75] especially if a baby is
very sick. Finding a large clot at autopsy may suggest
traumatic rupture of a large vessel, but comparison
with early brain scans may indicate that the bleed was
only minor at the outset, indicating a slower oozing
process with different implications for causation. It
is becoming increasingly obvious that not all SDH
arises from traumatic rupture of blood vessels.

Acknowledgment
I would like to thank Dr Irene Scheimberg and Dr Pat Lantz
for providing pictures and Dr Chris Van Ee for valuable
discussion and for preparing Figure 8.

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