1. Shaken Baby Syndrome adult head injury in road traffic accidents. Following
Guthkelch’s paper, the “shaken baby syndrome” has
become widely accepted as a form of child abuse [1].
Introduction
The diagnosis “shaken baby syndrome” (SBS) has
The Triad of Injuries
been widely accepted for over 30 years, but recent The three elements of the triad are encephalopathy,
evidence from biomechanical and clinical observa- RH, and SDH.
tional studies questions the validity of the syndrome.
Retinal Hemorrhages (RHs)
Definition RHs have been regarded as an important indicator
The diagnosis of SBS is based on the clinical triad of inflicted injury, but many other causes of reti-
of encephalopathy, retinal hemorrhage (RH), and nal bleeding are recognized in infants, for example
subdural hemorrhage (SDH) in infants, usually under after normal birth, raised intracranial pressure, blood
six months of age, who may die unexpectedly or dyscrasias, hemoglobinopathies, extracorporeal mem-
survive with greater or lesser degrees of neurolog- brane oxygenation, cataract surgery, and accidental
ical damage [1]. The term non-accidental head injury trauma [8]. Postmortem indirect ophthalmoscopy has
(NAHI) has been preferred as it has no implications shown RHs to be more common after natural dis-
for mechanism of injury. Other features often associ- ease and accidental injury than after inflicted injury
ated include a sole carer at the time of collapse and [9]. These authors also noted that infants suspected
a clinical history that is incompatible with the sever- to have been abused were more likely to have oph-
ity of the injuries. The diagnosis of inflicted injury thalmological examination in life than infants with
becomes less problematic if there is objective evi- accidental injuries or natural diseases. This bias read-
dence of violence, such as bruises, fractures, or burns, ily distorts the true incidence of RH in non-accidental
but objective evidence of trauma has not always been injury. Indeed Vinchon [10] noted in his study of
necessary in making the diagnosis. infant head injury that “In the construct of our study
Central to the assessment of these cases is whether we could not obviate the circularity bias, and the eval-
the triad of findings can be regarded as diagnostic uation of the incidence of RH in child abuse remains a
of abuse with any degree of certainty. This review self-fulfilling prophecy”. These authors did, however,
examines the evidence base for each element of suggest that the extent and nature of retinal bleeds
the triad and the current biomechanical evidence may be more important as indicators of inflicted head
regarding mechanisms of infant head injury and its injury than their existence per se [10].
pathological investigation. 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
History by raised intracranial or intravascular pressure, even
transiently, or that the tissues of the retina are torn
SDH has been associated with child abuse since the during the act of shaking. This latter hypothesis does
mid-19th century [2]. Kempe described SDH with not withstand biomechanical scrutiny [11].
multiple skeletal injuries and bruises as the bat-
tered child syndrome and Caffey described long bone Encephalopathy
fractures and SDH [3–5], but it is Guthkelch [6]
who developed the hypothesis that the whiplash–like This term may be widely interpreted to include a
movements during shaking cause the characteristic range of clinical manifestations from feeding dif-
bilateral thin film SDH of the syndrome. He based ficulties, vomiting, and sleepiness to seizures and
his hypothesis, that shaking causes tearing of the fulminating cerebral edema.
cerebral bridging veins leading to SDH, on the biome- The specific neuropathological features of trau-
chanical studies of Ommaya [7] who was researching matic brain injury are contusions and traumatic

2. 2 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 injury due to the specific intracranial pathophysiology
swelling are frequently seen but are not specific for before the skull bones fuse [19].
trauma. Contusions are very uncommon in infant Damage to the cervical nerve roots has been
brain trauma in the absence of skull fractures. Identifi- documented as part of the pathology of shaking injury
cation of axonal injury now depends on the immuno- [14]. It has not been established that this is the result
cytochemical demonstration of beta amyloid precur- of shaking, as cervical cord displacement resulting
sor protein (BAPP). This is a very sensitive marker of from brain swelling may also cause traction on nerve
interruption of normal axonal flow but may be upreg- roots in the region. Autopsy studies in man and
ulated after hypoxic–ischemic injury and metabolic primates have shown that the spinal cord is displaced
disruption as well as trauma (Figure 1). Distinction during extension and flexion of the neck [20, 21]
of traumatic axonal expression of BAPP from other and it remains a possibility that hyperextension and
flexion could cause traction damage to nerve roots
causes is fraught with difficulty, and depends in part
throughout the length of the spinal cord, but this has
on its distribution [12], [13], [14]. Neuropathological
not been documented in living infants.
studies have shown that in babies who die following
NAHI, the underlying brain pathology is widespread
hypoxic-ischemic injury and not diffuse traumatic Subdural Hemorrhage (SDH)
axonal injury as previously believed [12, 13]. In this
SDH is perhaps the most important and consistent
series axonal injury was seen in a limited distribu- component of the triad. In the acutely sick infant, it
tion in the lower brainstem and in only a minority is frequently the first clinical sign, identified on brain
of cases. Radiological studies have confirmed these scan, to raise the question of abuse. There are no
pathological observations [15]. specific imaging patterns that can distinguish inflicted
This observation is important as traumatic axonal from accidental intracranial injury [22, 23].
injury will lead to immediate loss of function causing Autopsy and imaging studies show that infant
clinical symptoms from the time of trauma. In SDH is usually a thin bilateral film and not a thick,
contrast, hypoxic-ischemic injury and ensuing brain unilateral space occupying clot as seen in traumatic
swelling take variable periods of time to develop SDH in older children and adults [12, 13, 24]. This
and a baby so damaged may not show immediate raises the question of whether the two forms have the
symptoms. Even fatal brain trauma may present with same etiology and anatomical source.
a lucid interval between injury and clinical collapse
[16, 17]. Lucid intervals are more frequently seen Causes of Subdural Hemorrhage. The common-
in infants less than two years of age [18], reflecting est cause of SDH in infants is said to be trauma
the very different responses of the infant brain to [25] although a recent study has shown a significant

3. Shaken Baby Syndrome 3
incidence (26%) of birth-related SDH [26]. Other intracranial damage including retinal and intracranial
causes in infants include benign enlargement of hemorrhage after falls from levels as low as 3 ft [10,
the extracerebral spaces (BEECS), clotting disorders, 17, 30–33]. While most babies may suffer little from
hemorrhagic disease of the newborn, rare metabolic an apparently trivial fall, this is clearly not always
diseases, vascular malformations, and neurosurgical the case.
procedures [25, 27].
Birth-Related SDH
Traumatic SDH Three studies, using magnetic resonance imaging
Proposed traumatic causes of infant SDH are inflicted (MRI), have shown a surprisingly high incidence
injury such as shaking and/or impact and accidental of SDH after birth in asymptomatic infants. Whitby
injuries such as falls. Impact includes blunt impact of identified SDH in the first two days of life in 9%
an object on the head and that resulting from a fall [32], while SDH was seen in up to 46% of otherwise
or striking the moving head on a rigid surface. The normal neonates using higher resolution MRI scan-
biomechanical aspects of these injuries are discussed ning [26, 34]. With regard to method of delivery,
below. The vast majority of cases described as SBS ventouse or instrumental deliveries have been asso-
have evidence of impact [28]. While the pathologist ciated with a higher incidence of intracranial injury
may be able to determine features indicative of [35, 36]. Towner [37] found an increased incidence
impact, it is not, of course, possible to distinguish of intracranial hemorrhage after instrumental delivery
accidental from non-accidental injuries by pathology. with ventouse or forceps and emergency caesarean
section, but the incidence was lower after caesarean
Low-Level Falls section before labor had begun. However, it should
Low-level falls have the potential, albeit only rarely, be noted that all of Looney’s cases followed normal
to cause SDH in infants and young children. Absolute vaginal delivery [26].
height is not as important a criterion for injury as While neonates with SDH may be asymptomatic
the exact nature of the fall for a particular infant, [26, 35] they may also have signs in the neonatal
in a particular circumstance [29]. The effects of period including unexplained apnoea, dusky episodes,
twisting, rotation, or crushing of the structures of the hypotonia, seizures, and lethargy [38].
neck are crucial in terms of outcome. Biomechanical
studies show that falls even from low levels of Sources of SDH. Traditional belief is that in SBS
3–4 ft can generate far greater forces in the head the SDH results from tearing of the superficial bridg-
than shaking [11]. There are a number of case series ing veins as they cross from the brain to the dural
demonstrating that infants and children may suffer 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)

4. 4 Shaken Baby Syndrome
Indeed it is very difficult to find documented evidence alternative sites of origin exist, the dura itself and
of torn bridging veins at surgery or at autopsy. Cush- the old subdural membranes (Figure 4).
ing, who operated on neonates with SDH and sub-
sequently performed the autopsies wrote “In two of Dural Hemorrhage
the cases I have examined I have satisfied myself that The dura is composed of two leaflets, the periosteal
such ruptures were present. A positive statement, how- and the meningeal dura, separated by a thin vascular
ever, cannot be given even for these cases, since the channel, which widens to form the large dural sinuses
dissection and exposure, difficult enough under any [44]. There are particularly extensive venous sinuses
circumstances, owing to the delicacy of the vessels is in the posterior falx, [45] a frequent site of high signal
the more so when they are obscured by extravasated on brain scans in asphyxiated infants. Bleeding into
blood” [39]. More recently Maxeiner [40] addressed the falx is well recognized in asphyxiated infants
the problem by injecting radio-opaque dye into the [46]. It has long been acknowledged that optic
veins at autopsy to assess their integrity after remov- nerve sheath hemorrhage arises from the dura [47]
ing the top of the head in one piece, hard-boiled egg and more recently the dura was proposed as the
source of intracranial SDH in infants [48] (Figure 5).
style. This approach is not widely used as it destroys
Careful microscopic examination of the dura confirms
much of the brain and injection pressures need to be
that intradural bleeding is common in asphyxiated
carefully monitored if the veins are not to be ruptured
infants, particularly in the dural folds of the falx and
artifactually.
tentorium close to the large venous sinuses [49]. In
Volpe [41] said that SDH was by no means some cases intradural bleeding leaks out on to the
always traumatic and suggested that in neonates subdural surface leading to macroscopically evident
without tentorial tears the bleeding may arise from subdural haematoma [50].
the tributary veins of the dural sinuses. Autopsy
studies from the older literature show bridging vein Healing Subdural Membranes
rupture is uncommon, Craig described 62 neonatal Healing of SDH is by formation of a thin, vascu-
SDH, of which only 3 had torn bridging veins, lar membrane consisting of fibroblasts, macrophages,
all of those with overriding sutures [42]. Larroche which often contain altered blood products, and wide
described 700 autopsies 18% with SDH. [43] She thin-walled capillaries with a potential to rebleed
noted an association with hypoxic-ischemic injury [51] (Figure 6). It is uncommon in infants to see a
(Figure 3). She did not identify torn veins. double layered membrane around a localized mass
If SDH does not arise from torn bridging veins, of resolving clot, as seen in the elderly, probably
what other sources may there be? Two obvious because the infant SDH usually forms as a thin film
Figure 3 Fresh subdural blood seen after birth asphyxia. (Picture courtesy of Dr I. Scheimberg)

5. Shaken Baby Syndrome 5
Arachnoid Superior sagittal sinus Intradural fluid channel
granulation
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 and be influenced by the method of treatment of
required to identify the membranes radiologically the acute hematoma. Surgical evacuation or tap-
[52]. In some cases, acute SDH leads to accumu- ping may prevent later reaccumulation of fluid [53,
lation of fluid in the subdural space. The reasons 54]. The period of time for redevelopment of sub-
for this are unknown. Fluid collections may result dural fluid collections may be long, between 15
from immaturity of the arachnoid granulations and and 111 days [55]. It is likely that an important
impaired cerebrospinal fluid (CSF) absorption [22], contribution to chronic subdural fluid accumulation is

6. 6 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 sub- Distribution. In the first few days after bleeding,
dural membrane [56, 57]. subdural blood sediments under the influence of
There is little information regarding the potential gravity and undergoes secondary redistribution to the
for birth-related SDH to evolve into chronic fluid most dependent part, the posterior falx and tentorium
collections. Whitby followed nine cases with a repeat [59]. Radiological studies show that subdural blood
scan at one month; none had developed a chronic tracks down around the spinal cord [60] and, if the
collection [35]. Rooks followed 18 cases for up to 3 spine of babies with intracranial SDH is examined at
months, one developed a further subdural bleed [34]. autopsy, blood is regularly seen in the subdural space
However these studies could not identify membranes and around sacral nerve roots in the most dependent
as contrast was not used. Chronic membranes have parts of the dural sac (Figure 7).
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 Differential Diagnosis of SBS
accidental SDH to evolve into a chronic collection
several months later [55], it would appear likely that The most common causes of the triad are impact,
the same pattern would follow birth-related SDH. At birth-related SDH, BEECS, coagulopathies, apnoea,
this time, we simply have insufficient information. asphyxia and choking, acute life-threatening events

7. Shaken Baby Syndrome 7
(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 Perl’s stain. Baby died three weeks after traumatic subdural hemorrhage
(ALTEs), osteogenesis imperfecta, osteopenia of Biomechanics
prematurity, and metabolic diseases [14, 28, 61,
62, 63]. Biomechanics is the application of principles of
physics to biological systems and has been the main-
stay of research into motor vehicle safety for six
Choking/Asphyxia decades. It was just such research into noncontact
head injury from rear-end shunts that stimulated
In a considerable number of cases, vomiting and/or Guthkelch to formulate his hypothesis for SBS in
reflux are described at the time of collapse, and 1971 [6]. Ommaya [7] had caused concussion, SDH,
in some there is a history of feeding difficulties, and white matter shearing injury (diffuse axonal
gastroesophageal reflux, and choking or apnoeic injury) in primates by whiplash. Guthkelch suggested
episodes [14, 62]. SBS is commonly diagnosed in the that the rotational forces of shaking would cause
first three months of life, the age of peak incidence of tearing of bridging veins and bilateral subdural bleed-
sudden infant death syndrome. Inhalation of feed or ing, although Ommaya himself warned that “It is
vomit may play a part in sudden infant death [64] and improbable that the high speed and severity of the
awake apnoea is associated with gastroesophageal single whiplash produced in our animal model could
reflux [65]. The physiological response to aspiration be achieved by a single manual shake or even a short
may be dramatic; foreign material on the larynx series of manual shaking of an infant in one episode”.
causes laryngospasm, which is associated with startle, More recent studies using “crash test dummies”
cessation of respiration, hypoxaemia, bradycardia, indicate that impact generates far more force than
and a doubling of blood flow to the brain [66]. shaking (Figure 9) and that impact is required to
These circumstances, with or even without vigorous produce SDH [68]. Cory and Jones [69] generated
resuscitation, may cause reperfusion injury and a pre- forces that exceeded the injury threshold for concus-
existing healing subdural membrane may bleed. The sion, but not for SDH or axonal injury. Their adult
dura itself may become hemorrhagic and ooze blood shaker volunteers fatigued after 10 seconds. While
into the subdural space (Figure 8). As long ago as they concluded that “It cannot be categorically stated,
1905, Cushing suggested that coughing, choking, and from a biomechanical perspective, that pure shak-
venous congestion may explain some forms of infant ing cannot cause fatal head injuries in an infant”,
SDH [39], a hypothesis recently revived by Geddes, they noted that in their experiments there were chin
[48, 67]. and occipital contacts at the extremes of the shaking

8. 8 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)
125
100 From adult male’s arms
76.2 cm
Inflicted slamming
style impacts onto
75 surfaces noted
50.8 cm
Bed – mattress
Leather sofa
50
25.4 cm
25
Free fall impacts onto
carpeted stairs
(fall heights noted)
0
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 It is likely that the forces required to cause intracra-
expressed their concerns regarding the difficulties in nial injury will also damage the weak infant neck
extrapolating to human infants the findings in both [71]. In road traffic accidents, infants who suffer sin-
dummy and animal models. Biomechanical studies gle severe hyperextension forces have cervical frac-
have shown that falls and impact to the head pro- tures, dislocations, spinal cord injury, and torn nerve
duce significant rotational forces when the impacting roots, not SDH [72–74].
forces are not aligned through the center of gravity
of the head, due to hinging of the head on the Investigation of Shaken Baby Syndrome
neck. Shaking is not necessary to cause rotational
acceleration. SBS or NAHI is most likely to occur in an infant
Neck injuries may be underreported in babies dying suddenly under the age of six months. Autopsy
dying after severe abuse [70]. In Ommaya’s study, should be performed with careful consideration of
11 of 19 primates had neck injuries; these were adult this diagnosis and appropriate steps taken to support
animals with mature neck structure and musculature. or exclude it. The records of pregnancy and delivery

9. Shaken Baby Syndrome 9
must be carefully studied to look for any evidence of evidence of intradural bleeding and rupture onto
complications that could mimic NAHI. These include the subdural surface. This may be the source of
pregnancy disorders such as oligohydramnios, fetal significant subdural blood.
hypokinesia, and prematurity, which lead to osteope- The brain must be fixed for detailed histological
nia and predispose to fractures. The birth history and examination.
method of delivery are important as SDH may arise In all of these cases, the time between collapse
at this time while being entirely asymptomatic in and death may play a significant part in the final
the neonatal period. Head circumference charts are pathology. A baby who has collapsed and becomes
important; head circumference measurements taken at apnoeic with subsequent cardiopulmonary rescusci-
birth and in the subsequent weeks may reflect abnor- tation (CPR) and ventilation will be shocked and
mal head growth, which can indicate an accumulating suffer multiorgan failure with altered clotting, loss
subdural fluid collection and a propensity to rebleed. of integrity of vessels and membranes, oozing of
The clinical history may give clues to other prob- blood into intracranial compartments, including the
lems in the early weeks of life. Vomiting, feeding subarachnoid and subdural spaces, and development
problems, and apnoeic episodes and ALTEs may of the “respirator brain”.
indicate difficulties with coordination of breathing, Review of the brain imaging in life is essential
sucking and swallowing, and vulnerability to chok- in assessing, as far as possible, just how much
ing. Any event that threatens life may also potentially hemorrhage occurred at the time of collapse and how
end it. much may be the result of subsequent secondary
The history of the baby’s terminal collapse must changes. It is recognized that SDH may continue to
also be carefully examined. Parents may describe bleed after initial onset [75] especially if a baby is
events that reveal a cause for collapse. In any other very sick. Finding a large clot at autopsy may suggest
field of medicine, the clinical history is regarded as traumatic rupture of a large vessel, but comparison
the cornerstone of diagnosis and it should not be with early brain scans may indicate that the bleed was
disregarded without serious critical evaluation. only minor at the outset, indicating a slower oozing
The autopsy can reveal evidence of trauma such process with different implications for causation. It
as deep bruises and fractures not seen in clinical is becoming increasingly obvious that not all SDH
examination. The examination of the intracranial arises from traumatic rupture of blood vessels.
contents is paramount. The scalp and skull require
careful examination for evidence of bruising and Acknowledgment
fractures. Suture separation due to raised intracranial
pressure and wormian bones can be mistaken for I would like to thank Dr Irene Scheimberg and Dr Pat Lantz
fractures. When the cranium is opened, the presence for providing pictures and Dr Chris Van Ee for valuable
of any intracranial bleeding must be noted. Unclotted discussion and for preparing Figure 8.
blood may escape from the subdural space as the
skull is opened and be mistaken for bleeding from the References
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