3. Head Trauma in Child Abuse Outline V D

VISUAL DIAGNOSIS
OF
CHILD ABUSE
ON
CD-ROM LECTURE SERIES
3. Head Trauma in Child Abuse
Outline
Abstract
Controversies in Shaken Baby Syndrome/
Shaken Impact Syndrome
Learning Objectives
Outcomes in Shaken Baby Syndrome/Shaken
Impact Syndrome
Incidence and Prevalence
The Biomechanics of Head Injury
Types of Head Injuries
Anatomy and Characteristics of the Infant Head
Types of Extracranial Injuries
Types of Skull Fractures
Types of Intracranial Injuries
Shaken Baby Syndrome/Shaken Impact
Syndrome (SBS/SIS)
Mechanism of Injury
Lesions Seen
Associated Injuries
Retinal Hemorrhages and Shaken Baby
Syndrome
Theories of Etiology of Retinal Hemorrhages
Characteristics of Retinal Hemorrhages
Differential Diagnosis of Retinal
Hemorrhages
Signs and Symptoms of Shaken Baby
Syndrome
Imaging Techniques
Laboratory Studies
Data Collection
1
Visual Diagnosis of Child Abuse on CD-ROM Lecture Series
3. HEAD TRAUMA IN CHILD ABUSE
Abstract
60% of inflicted injury deaths.3 Annegers4 estimated
that in the United States, children between the ages
of 1 year and 15 years die of head trauma-related
injuries at a rate of 10 per 100,000, a rate 5 times
the death rate of childhood leukemia, the next
leading cause of death. In 1985, there were approximately 7,000 brain injury deaths—about 29% of all
injury deaths in this age group.5 In a 1990 study,6
17% of all brain injuries and 56% of serious brain
injuries in children younger than 1 year were caused
by assault. In a 1985 study of 84 head-injured
infants ranging in age from 3 weeks to 11 months,
64% of injuries were attributed to accidents and
36% were the result of abuse.2 In a recent study
of 287 head-injured children younger than 6.5 years
of age, abusive head trauma accounted for 19% of
the total. When restricting the age group to children
younger than 3 years, one third of the head-injured
children had sustained their injuries as a result of
abuse. When injuries subsequent to motor vehicle
crashes were excluded (easily distinguished from
possible abuse), 49% of the head-injured children
had sustained their injury from abuse.7 The mortality
rate in the child abuse group was 13% versus 2%
for the accident group. In another retrospective
review of medical records submitted to the National
Pediatric Trauma Registry during the 10-year period
from 1988 through 1997,8 children categorized as
victims of child abuse were younger (mean age
12.8 months versus 27.5 months for the unintentional trauma group), had a higher mortality rate
than the unintentional group (12.7% versus 2.6%),
and the child abuse survivors were more severely
injured (Injury Severity Scores between 20 and 75
in 22.6% of the child abuse group versus 6.3% in
the unintentional group). Ewing-Cobbs and colleagues9 found a similar age distribution (10.6
months in the abuse group versus 35.6 months
in the accident group).
There is more mortality and morbidity from nonaccidental head trauma than from any other single
cause of child physical abuse. Knowledge of basic
cranial anatomy and the properties of the tissues of
the various layers of the head is necessary to understand how biomechanical forces can affect those tissues. Types of head injuries can be roughly classified
into extracranial injuries, skull injuries, and intracranial injuries. Each of these categories is further subdivided according to the severity and involvement of
the injured structures. Shaken baby syndrome (SBS)
and shaken impact syndrome (SIS) are specific entities produced by specific biomechanical forces and
have characteristic signs and symptoms and physical
and radiologic findings. Shaking and impact lead to
rupture of bridging veins and collection of blood in
the subdural and/or subarachnoid spaces, traumatic,
vascular, hypoxic, and biochemical injuries to the
brain; extensive retinal hemorrhages (RHs); and
diffuse axonal shearing of brain substance. Abusive
head trauma can be distinguished from other etiologies of head injury by careful attention to the history
of the injury, the resulting signs, symptoms, imaging
studies, and clinical course.
Learning Objectives
• To differentiate abusive from non-abusive head
injuries
• To identify the types of scalp injuries associated
with abuse
• To differentiate simple from complex fractures of
the calvarium
• To identify mechanisms of intracranial bleeding
• To define and describe SBS/SIS
• To differentiate abusive and non-abusive
mechanisms of RHs and their significance
• To compare computed tomography (CT) and
magnetic resonance imaging (MRI) for use in
diagnosing head injuries
There are no firm statistics regarding the incidence
of SBS/SIS because there are no central reporting
registries to collect these data. Estimates range
from 600 to 1,400 per year. Shaken baby syndrome/
SIS occurs in babies, usually younger than 1 year,
but has been described in children considerably
older.10,11 Recent papers in the medical literature
have reported confirmed cases of shaking in
adults leading to the same clinical and pathological
findings as in infant shaking cases.12
Incidence and Prevalence
Craniocerebral trauma is the most common cause
of mortality and long-term morbidity in physically
abused children, and it is second only to vehiclerelated injuries as a cause of traumatic mortality in
the United States.1,2 Intracranial injury is found in
2
Visual Diagnosis of Child Abuse on CD-ROM Lecture Series
3. HEAD TRAUMA IN CHILD ABUSE
The subgaleal space is not truly a “space” until
blood or other material separates the overlying
tissue from the skull.
The Biomechanics of Head Injury
Hymel et al13 have advanced the understanding of
biomechanics in head trauma. There are contact
(the head striking or being struck by an object) and
noncontact (acceleration/deceleration) types of
injury. Contact forces cause focal strain that tends
to be limited to the site of impact. Contact can
cause scalp injury and/or skull fracture as well as
more distant injuries, such as hemorrhages and
parenchymal disturbances. Noncontact forces can
cause the brain to deform, causing rupture of
bridging veins and strains within the parenchyma.
The skull is the bony calvarium, with an outer and
inner table surrounding a small marrow cavity.
The epidural space also is a potential space, overlying the dura mater.
The dura mater is a relatively tough membrane
overlying the intracranial contents. Within the dura
runs an extensive network of dural sinuses containing venous blood returned from the brain by the
bridging veins. These are numerous small veins arising from the surface of the brain and connecting
to the dural sinuses. They are fixed to the brain and
to the dura, so that they have no mobility. They run
through the subdural and the subarachnoid spaces.
Skull fractures are contact injuries and may occur
with or without accompanying brain injury. Cranial
impact over a large surface causes linear skull
fractures. Cranial impact over a small area may
result in a depressed skull fracture.
The subdural space, another potential space, lies
beneath the dura mater.
Epidural hemorrhage may occur below a cranial
impact. Subdural hemorrhage may occur as a contact
or a noncontact (acceleration/deceleration) injury.
The piarachnoid membrane is a lacy (spiderweblike) membrane, more delicate than the dura mater,
and following the sulci and gyri of the brain. The
cerebrospinal fluid (CSF) is contained within the
subarachnoid space and circulates throughout the
central nervous system (CNS) with nutritional and
excretory function.
Crushing injuries of the head result from slow,
distributed mechanical loading, allowing severe
strain conditions but inducing minimal cranial
acceleration. Patients with crush injuries to the
head often recover well.
Diffuse brain injuries are primarily the result of
shearing strains created by cranial acceleration,
but contact strains from cranial impact play a significant role in the production of these injuries and are
thought by some14,15 to be of primary importance in
producing the lesions seen in abusive head trauma.
The brain substance (parenchyma) lies beneath
the subarachnoid space. The brain parenchyma is
made up of millions of neurons, the basic cell of
the nervous system. Each neuron has one axon
and several dendrites. Axons carry efferent (outgoing) nerve impulses and dendrites carry afferent
(incoming) nerve impulses. The neurons are
gathered into nerve bundles and tracts going to
the various parts of the body. The gray matter of
the brain consists of the neuron cell bodies and
the white matter consists primarily of the nerve
bundles and tracts. Blood vessels (arterioles,
venules, and capillaries) are everywhere within
the brain substance.
Types of Head Injuries
Anatomy and Characteristics of the
Infant Head
Understanding the anatomy of the infant head is
central to grasping the concepts of injury. In its
most simple terms, the head can be viewed as a
series of layers, each consisting of different types
of tissues. Each of these tissues has unique properties, and they differ from each other in major
ways. Because of this, each of these layers reacts
to trauma in a different manner, leading to differing
manifestations of injury.
A protein-rich material, myelin, is laid down around
the components of the CNS over the first 18 months
of life. This substance makes the brain of an older
child and adult much firmer than the brain of an
infant or young child. The other characteristic of the
infant brain, and another reason for its fragility, is
that the infant brain contains approximately 25%
more water than the brain of an older child and
adult. Pathologists describe the infant brain as
being gelatinous in consistency.
The scalp consists of the skin and its appendages,
subcutaneous tissue, and underlying fascia, the galea.
3
Visual Diagnosis of Child Abuse on CD-ROM Lecture Series
3. HEAD TRAUMA IN CHILD ABUSE
Types of Intracranial Injuries
FIGURE 3-1. TYPES OF EXTRACRANIAL INJURIES
Bleeding within the skull can occur in the
• Epidural space
• Subdural space
• Subarachnoid space
• Brain parenchyma (brain tissue itself)
• Intraventricular space
Bleeding in the epidural space may be due to
venous or arterial injury, but is usually is due to
dural venous tears.16–18 It usually is associated with
a skull fracture.17 An epidural hematoma on CT
appears as a hyperdense, lenticular-shaped extraaxial mass. If it is arterial in origin, it can accumulate
rapidly and, if not diagnosed and treated promptly,
can lead to coma and death. An epidural hematoma
is more often accidental rather than abusive in
origin, but it can be seen as a consequence of
abuse. Prompt medical attention and, in some cases,
evacuation of the hematoma usually results in the
rapid resolution of symptoms and signs and has a
good prognosis.
Types of Extracranial Injuries
• Bruises (visible externally)
• Bruises (intracutaneous and subcutaneous;
not visible externally)
• Lacerations
• Abrasions
Bleeding in the subdural and/or the subarachnoid
spaces is due to the shearing and breaking of the
veins going from the surface of the brain to the
dural sinuses.19 These veins are fixed to the brain
and to the dural membrane. When the brain moves
within the skull, these veins are stretched, and when
they exceed their elasticity, they break and bleed.
• Subgaleal hematomas
• Alopecia (hair loss secondary to hair-pulling)
Types of Skull Fractures
Simple:
Linear—not crossing suture lines
Temporoparietal constitute the
vast majority
Bleeding within the brain substance (parenchyma)
is primarily due to trauma to the brain itself.
Less than 2 mm separation
Complex:
Linear—crossing suture lines
Shaken Baby Syndrome/Shaken Impact
Syndrome (SBS/SIS)
Linear—>2 mm separation
Branching or stellate
Mechanism of Injury
Comminuted (isolated fragments
of bone)
The injuries result from violent shaking and/or
shaking plus impact. Recent data have supported
the concept that shaking and, in many cases,
impact by throwing the child against a surface
and resultant deceleration are the responsible
forces producing the subdural hematoma, subarachnoid bleeding, cerebral trauma, and diffuse
axonal shearing with consequent cerebral edema
leading to raised intracranial pressure.20 There has
been much discussion about whether shaking by
itself is sufficient to produce these injuries or
whether shaking plus impact is required to generate
the forces causing the lesions seen in SBS/SIS. This
Depressed (comminuted with bone
fragments impinging on the brain)
Compound (overlying laceration)
Diastatic (growing)
4
Visual Diagnosis of Child Abuse on CD-ROM Lecture Series
3. HEAD TRAUMA IN CHILD ABUSE
body, particularly the brain. The infant brain, with
much higher water content than an adult brain, is
much softer than an adult brain, having the consistency of gelatin. The absence of myelin, the protein
covering of the nervous tissue, contributes to the
relative softness. These factors make the brain more
easily distorted and compressed within the skull.
discussion really began with the 1987 article from
Duhaime and colleagues15 in which they described
a retrospective study of 48 cases of SBS at their
institution. Of these, 62% had clinical evidence of
blunt trauma to the head (bruising, skull fracture),
and postmortem evidence of blunt trauma was
present in all of the fatal cases. In this article, they
also studied the forces generated when 3 types of
dolls were shaken. Using a strain gauge measuring
forces during shaking, they were unable to demonstrate enough force from shaking to account for the
extent of damage seen in clinical cases. The authors
concluded that impact with rapid deceleration of
the intracranial contents was necessary for these
lesions. This discussion has continued, with some
investigators citing the absence of evidence of
impact in a substantial number of their reported
cases 21,22 The criticism of the required impact theory
cites the crudeness of the doll models used in the
study by Duhaime et al and the fact that no good
data exist to inform us about what magnitude of
forces are required to injure the structures of the
head, particularly the infant brain. There is no way
to obtain experimental evidence to measure the
forces required to produce damage to the infant
brain, and without such information this question
cannot be adequately answered. However, by
comparing data obtained from cases of accidental
head injury, where the histories of injury are known
(such as in motor vehicle crashes [MVCs], where
there is knowledge of the time of the crash, and
ambulance records are detailed as to the condition
of the victims), certain information is available about
the clinical courses, imaging studies, and timing of
injuries, and this can be used to enhance our understanding of abusive head trauma.
Lesions Seen
Shaking and the sudden deceleration of the head
at the time of impact do several things
1. The veins that bridge from the brain to the
dura mater, a tough, inelastic membrane inside
of the skull, are stretched and, exceeding their
elasticity, tear open and bleed, creating the
subdural hematoma and/or subarachnoid
hemorrhages common in SBS/SIS.
2. The brain strikes the inner surfaces of the
skull, causing direct trauma to the brain
substance itself and resultant brain swelling
(cerebral edema).
3. Other structures of the brain, the axons, can
be broken, shearing off during the commotion
to the brain causing diffuse axonal shearing
injuries.
4. The lack of oxygen (hypoxia) during shaking
causes further irreversible damage to the
brain substance.
5. Damaged neurons release their intracellular
proteins that cause vasospasm. This adds to the
oxygen deprivation in the brain and also causes
more destruction of adjacent brain cells.23
6. The combined effect of this cascade of injury,
hypoxia, and brain swelling is massive destruction of the brain tissue, causing enormous
increases in intracranial pressure. This causes
compression of the blood vessels, thereby
further decreasing the oxygen supply to
the brain.
The usual trigger for shaking is thought to be inconsolable crying by the infant. Frustrated by attempts
to console the baby, the perpetrator loses control
and grabs the infant, either by the chest, under
the arms, by the arms, or by the neck, and violently
shakes the baby. The duration of the shaking varies,
usually ranging from around 5 seconds to 15 or
20 seconds. It has been estimated by video recordings of a person shaking a doll that the number of
shakes ranges from 2 to 4 per second. During the
shaking, the head rotates wildly on the axis of the
neck creating multiple forces within the head. The
infant stops crying and stops breathing during the
shaking, causing decreased oxygen supply to the
It is these insults to the brain, not the subdural
or subarachnoid blood, that cause the signs,
symptoms, and course of SBS/SIS.
The bleeding in the subdural and subarachnoid
spaces are markers of the tremendous forces
brought to bear on the head during shaking
and/or impact.
5
Visual Diagnosis of Child Abuse on CD-ROM Lecture Series
3. HEAD TRAUMA IN CHILD ABUSE
Associated Injuries
single fresh hemorrhage in 1 eye. Kanter,29 however,
reported on 54 children, 45 of whom had had a
traumatic event prior to resuscitation. Six had RHs,
5 of whom were victims of abusive head trauma.
The one child with RHs after CPR with no preceding
traumatic event had had a seizure at home, arterial
hypertension in the hospital, and subsequently died.
There was no description, however, of the type
and extent of the RHs. His conclusion was that
RHs should not be attributed to CPR. Gilliland and
Luckenbach30 performed postmortem examinations
of the eyes of 169 children. One hundred thirty-one
had resuscitation for 30 minutes or more. No RHs
were found in 99 children, 70 of whom had had
resuscitation. Retinal hemorrhages were found in
70 children, 61 of whom had been resuscitated.
Of these 61, 56 had craniocerebral trauma, both
intentional and unintentional, 3 had CNS causes
of death (tumor, infection), and 1 had sepsis—all
conditions known to be associated with RHs. One
died of undetermined causes. The authors concluded that no case in this study was found to
support the hypothesis that RHs are caused by
CPR. Odum et al31 examined the retinas of 43
hospitalized children who had received at least
1 minute of CPR. One patient with a coagulation
defect had small punctate RHs that were morphologically different from the RHs found in SBS/SIS.
Fackler et al32 produced cardiac arrest in 6 newborn
piglets, followed by controlled mechanical CPR for
50 minutes. After sacrificing the animals, postmortem examinations of the eyes revealed no RHs.
The overwhelming conclusion from all of these
studies is that CPR is rarely, if ever, associated
with the production of RHs and that classic
Purtscher’s retinopathy is distinctly different from
the retinopathy of SBS/SIS.
Bruising and/or skeletal injuries are associated
with some cases of SBS but not all.7,85 Posterior
rib fractures, classic metaphyseal lesions of the
long bones, and other associated fractures of
abuse should be sought by skeletal survey.
Retinal Hemorrhages and Shaken
Baby Syndrome
THEORIES OF ETIOLOGY OF RETINAL HEMORRHAGES
The pathogenesis of RHs is the subject of controversy.
There are 3 major etiologic theories advanced by
those studying the phenomenon. The first suggests
that they are due to increased intracranial pressure
arising from transmission of cardiothoracic pressure
(Purtscher’s retinopathy). This condition is a hemorrhagic retinal angiopathy characterized by preretinal hemorrhages and RHs, retinal exudates, and
decreased visual acuity. It has been described in
adults following a sudden compression of the
thoracic cage and is postulated to be the result
of transmission of an acute increase in intravascular pressure to the head and eyes giving rise to
RHs.24,25 There has been only one pediatric case of
Purtscher’s retinopathy reported in the literature26
prior to the 1975 report of Tomsai and Rosman27
who described Purtscher’s retinopathy in 2 battered
children with clinical signs of traumatic brain injury.
These cases were seen and treated before CT head
scans came into common usage and were probably
SBS/SIS. The RHs as described in this paper are not
classic Purtscher’s retinopathy, which is associated
with cotton-wool exudates and superficial
hemorrhages.
The theory of increased cardiothoracic pressure
causing transmitted intravascular pressure to the
head and resultant RHs led clinicians to consider
the possibility of cardiopulmonary resuscitation
(CPR) causing such a chain of events. Goetting and
Sowa28 reported on 20 children who had received
CPR, 2 of whom had RHs. One of those children,
a 2-year-old, had been immersed in water, resuscitated by emergency medical personnel en route to
the hospital, and remained in a coma for 4 days
until death. Autopsy showed no preceding traumatic
events. No information was given as to the brain
findings but one can assume there was cerebral
edema giving rise to raised intracranial pressure
before death. The case, an infant of 1.5 months,
died of sudden infant death syndrome and had a
A second theory concerning RHs holds that they
are the result of increased intracranial pressure. In
1975, Khan and Frenkel33 attributed RHs to acute
intracranial hypertension following cerebral injury,
resulting in retinal venous hypertension. Lambert
et al34 stated that “it seems likely that a sudden
rise in intracranial pressure significantly contributed
to [the occurrence of RHs] in our patient.” Older
accounts in the adult literature claim intracranial
hypertension to be responsible for intraocular
hemorrhage.35,36 In 1993, Munger and colleagues37
examined the eyes of 12 infants with RHs who
had died subsequent to suspected violent shaking.
Ten had subdural hematomas and cerebral edema;
6
Visual Diagnosis of Child Abuse on CD-ROM Lecture Series
3. HEAD TRAUMA IN CHILD ABUSE
9 had subarachnoid bleeding. Retinal detachment,
with the formation of retinal folds, was found in 5.
The authors leaned toward the concept of increased
intracranial pressure as the pathogenetic mechanism.
any other cause.1,2,7,10,15,38,44,46-51 Retinal hemorrhages
in SBS/SIS usually involve the posterior pole in the
nerve fiber and ganglion cell layers, but may involve
any retinal layer. They usually are flame-shaped
rather than dot-, blot-, or boat-shaped hemorrhages
typical of intraretinal or preretinal hemorrhages.46,39
The time of resolution of RHs varies, ranging from
10 days to several months.50
If RHs are caused solely by increased intracranial
pressure, one would expect to see them in accidental head trauma to the same extent as in inflicted
head injury. Johnson et al38 reported on 140 children
whose head injuries were thought to be accidental
(MVCs and long falls in 90%). Retinal hemorrhages
were seen in only 2 patients, both of whom were
in the back seat of a motor vehicle impacted from
the side. These data are borne out in numerous
other studies,1,7,11,30,39,40 and clinical experience has
instructed that most children with head injuries
who have increased intracranial pressure do not
often have RHs.
Although RHs are the most commonly found ocular
lesion in SBS/SIS, other ocular lesions also may be
seen. These include retinal detachment, optic nerve
injury, and cupping of the optic nerve secondary to
raised intracranial pressure.
DIFFERENTIAL DIAGNOSIS OF RETINAL HEMORRHAGES
Vaginal delivery—Occurring in 40% of children
delivered vaginally, these fine petechial preretinal
hemorrhages usually resolve within 10 to 14 days
of delivery leaving no residual.
A third theory—traumatic retinoschisis—suggests
that the forces of shaking are responsible for the
RHs in SBS/SIS. According to this theory, one of
the effects of shaking is to make the lens move
forward and back within the ocular fluids.41 Elner
and associates 42 believed that the full-thickness
hemorrhagic retinal necrosis in 5 of their study
subjects and retinoschisis and perimacular folds
in 4 suggested that severe anteroposterior acceleration-deceleration forces directly produced retinal
injuries in abused children who die of blunt head
injury, and further that blunt head trauma may be
necessary to produce significant vitreoretinal traction
resulting in the constellation of severe retinal
injuries seen in such children. Gaynon et al43
suggest that retinal folds may be a hallmark of
shaking injuries in child abuse victims.
Bleeding disorders—Isolated RHs in coagulopathies
have not been described. When they occur in
patients with bleeding or clotting disorders, they
are associated with other sites of bleeding.
Arteriovenous malformations—Arteriovenous malformations are extremely rare in infancy and, when
present, are seldom associated with RHs.
Increased intracranial pressure—This is present in
most cases of SBS/SIS, but current thinking is that
if increased intracranial pressure caused RHs, they
would be present in all cases of increased intracranial pressure secondary to all causes. This is not
supported by medical literature describing accidental head trauma with increased intracranial pressure.
Retinal hemorrhages have not been found as the
result of seizures in childhood.44,45
Meningitis—Increasingly rare in pediatrics, it is not
likely meningitis would be overlooked after clinical
assessment, culturing, and examination of CSF.
CHARACTERISTICS OF RETINAL HEMORRHAGES
Accidental head trauma—Recent literature on
the incidence of RHs in accidental head trauma
indicates that RHs are seldom seen in cases of
accidental origin.
Retinal hemorrhages seen in SBS/SIS are many in
number, are distributed widely over the entire retina,
are not associated with papilledema, and involve
multiple layers of the retina. Retinal hemorrhages
seen in other conditions usually are closer to the
surface, so-called preretinal hemorrhages, and
resolve quickly. The incidence of RHs in SBS/SIS
is reported to be between 50% to 100% depending
on the series reported, and they may be unilateral
or bilateral, although they more commonly are bilateral. Retinal hemorrhages are overwhelmingly more
common as the result of abusive head trauma than
Signs and Symptoms of Shaken
Baby Syndrome
Symptoms and physical findings vary depending
on the length and severity of the shaking and
whether the infant was thrown onto a surface.
The syndrome can be seen as a continuum from
a short duration of shaking with little or no impact,
7
Visual Diagnosis of Child Abuse on CD-ROM Lecture Series
3. HEAD TRAUMA IN CHILD ABUSE
to severe, prolonged shaking and major impact. The
resulting signs and symptoms may run the gamut
from decreased responsiveness, irritability, lethargy,
and limpness—through convulsions, vomiting from
increased intracranial pressure, increased respiratory
rate, hypothermia, and bradycardia—to coma with
fixed and dilated pupils—to death. All of the
symptoms are caused by generalized brain swelling,
increased intracranial pressure, and, in most cases,
diffuse axonal shearing. These are the direct result
of trauma and anoxia, and the signs and symptoms
begin almost immediately after the shaking and
reach their peak within 4 to 6 hours.52,53
COMPARISON OF CT AND MRI IN HEAD INJURIES
Advantages of CT
Delineates subarachnoid hemorrhage better than MRI
Better imaging of cranial injuries
Ease of performance in unstable patients
Advantages of MRI
Better in subacute and chronic cases
Better for deep cerebral injuries
Able to determine age of extracerebral fluid
Will detect smaller subdural hematomas
LABORATORY STUDIES
IMAGING TECHNIQUES
Children with head trauma severe enough to be
admitted to the hospital also should have laboratory
studies to support diagnoses of associated trauma
in other organ systems, anticipate hematological
and biochemical alterations sometimes attendant
to head trauma, and seek the manifestations of
their neurological status. These studies are displayed
in Table 3-1.
In most instances of moderate to severe head
injury, the first imaging modality should be CT
scanning without contrast because it is readily
available in most hospitals and can be performed
safely with life support systems operating during
the procedure. Bone windows should be employed
along with the standard scan. Plain radiographs of
the skull will usually show existing skull fractures
more clearly than CT. Magnetic resonance imaging
is ordinarily used as a confirmatory test rather than
an initial one due to the longer scan times and
need for life support, but MRI gives superior detail
in showing parenchymal changes and smaller
subdural hematomas.
A recent study54 examining coagulopathy in pediatric
abusive head trauma found that there were prothrombin time prolongations in 54% of patients
with parenchymal damage and in 20% of those
without demonstrable parenchymal damage. Other
coagulation markers (partial thromboplastin time,
platelet counts, and fibrinogen levels) also were
altered. The authors hypothesize that these abnormalities in coagulation elements are due to tissue
Although head injury may capture the attention
of providers because of the altered levels of consciousness resulting from it, trauma to other parts
of the body must be considered during the initial
assessment. Computed tomography scans of the
abdominal viscera are valuable when there are
reasons to believe that intra-abdominal injury may
coexist with head injury.
TABLE 3-1. LABORATORY STUDIES
• CBC with morphology, serial hematocrits
• Serum electrolytes, BUN, creatinine, serum and urine
osmolality
Skeletal surveys are recommended in serious head
trauma in children younger than 3 years because
the diagnosis of abuse may be made or supported
if unsuspected or occult traumatic injuries are found
in other parts of the appendicular skeleton. Such
accompanying skeletal fractures are seen in roughly
half of the cases of abusive head injury. Posterior
rib fractures are present in some cases of shaken
infants and can be demonstrated either with bone
scintigraphy for fresh fractures or with follow-up
thoracic films in 10 to 14 days to see callus formation at the site of the fractures.
• Urinalysis
• Liver function studies (AST, ALT, alkaline phosphatase)
• Serum and urinary amylase
• Creatine phosphokinase (CPK)
• Cultures of blood, urine, cerebrospinal fluid (if safe
to perform lumbar puncture)
• PT, PTT, TT, platelet count, fibrinogen, and FDP
• Stool for blood
• Arterial blood gases
8
Visual Diagnosis of Child Abuse on CD-ROM Lecture Series
3. HEAD TRAUMA IN CHILD ABUSE
presence of bruises on the back, thighs, or in the
perineum also should be noted. Photodocumentation of such injuries is highly desirable.
factor release from damaged parenchymal cells that,
when complexed with factor VII, activate coagulation
via the extrinsic pathway, leading to disseminated
intravascular coagulation.
The examination of the fundi is of utmost
importance. This should be carried out ideally
by pupillary dilation and indirect ophthalmoscopy,
or at the very least by direct ophthalmoscopy.
Although RHs are the most common finding in
child abuse, other lesions also may be seen. These
include retinal detachment, optic nerve injury, and
cupping of the optic nerve (papilledema secondary
to raised intracranial pressure).
DATA COLLECTION
While a child with a serious head injury is being
evaluated and treated medically, it is crucial for a
detailed, analytical—but not challenging or accusatory—history to be obtained from the caretakers.
The person collecting the history should ideally be
someone with experience in child abuse cases and
one who does not have immediate responsibility
for the medical treatment required by the child. It
is the rule that abusing parents will tell a misleading
story about how the “accident” happened and are
sometimes quite inventive in describing the event.
Thus the skill of interviewing becomes an important
foundation on which to build the diagnostic formulation. Gentle probing, with inquiries and request
for clarification on questionable portions of the
history, sometimes called “the Columbo Approach,”
often will elucidate the mechanism of injury and
show discrepancies in the history. The history of the
pregnancy, labor and delivery, neonatal course, as
well as a history of family diseases is important,
with particular attention to bleeding and clotting
disorders, neurological diseases, metabolic and
bone disease, or other genetic conditions of the
family. This comprehensive evaluation will save
returning to the caretakers for missing data as the
case ages. The medical history of the child, including
previous injuries and serious illnesses or hospitalizations, along with a review of systems should be
obtained. Exploration of the social milieu with attention to the living arrangements and the relationships
of household members should be done.
Controversies in Shaken Baby
Syndrome/Shaken Impact Syndrome
Shaking versus shaking plus impact—In 1987,
Duhaime et al15 reported on 48 cases of SBS in
which two thirds of the subjects had external
evidence of head trauma, and all of the infants
who died had external trauma. Using 3 doll models
implanted with accelerometers to measure the
forces developed during shaking, Duhaime and
colleagues concluded that shaking alone was
insufficient to produce the forces seen in the
injuries. In 1968, Ommaya and colleagues55 showed
that subdural hematomas could be experimentally
produced in rhesus monkeys by rotational displacement of the head on the neck alone, without significant direct head impact. Gennarelli et al56
confirmed this in 1982 and concluded that “it is
apparent that nothing need strike the head in order
for acute subdural hematomas to occur. It is sufficient that the head undergo the appropriate acceleration strain-rate conditions, since in this animal
model nothing strikes the head. Thus those mechanical events that result from an object contacting
the head are not necessary for acute subdural
hematoma (ASDH). Although impact to the head
is certainly the most common cause of clinical
ASDH, it is the acceleration induced by the impact
and not the head contact per se that causes the
ASDH.” Others, however, believe that shaking in
and of itself is sufficient to cause the lesions seen
in SBS.7,21,22,42,51,57–64 The major problem in this controversy is that no one has been able to devise a
model that even closely approximates the head
and neck of the human infant. There are so many
properties of the scalp, skull, meninges, brain, blood
vessels, and neck musculature that are unknown
In conducting a physical examination of the child
with a head injury, there is the risk of overlooking
less urgently compromised organ systems. Bleeding
visceral organs are the most glaring and potentially
disastrous omissions, but overlooking cutaneous
injuries can deprive the diagnostician of important
clinical data because of the fleeting nature of these
injuries. Likewise, inspection of the oral cavity looking for intraoral lesions and a search for hidden
head lesions under the hair should be done. The
neck should be carefully inspected for signs of
injury (strangulation, hand or finger bruising). The
9
Visual Diagnosis of Child Abuse on CD-ROM Lecture Series
3. HEAD TRAUMA IN CHILD ABUSE
and variable from infant to infant that an attempt
to determine the amount of force required to produce particular injuries is difficult.
setting and in the courts. The so-called lucid interval
in adults has been described in the adult medical
literature and refers to that period of time between
a significant head injury and the onset of signs and
symptoms commensurate with the seriousness of
the head injury. A comparable phenomenon has not
been described in children in the pediatric literature.
In one study, Willman and colleagues53 reviewed the
case histories of 95 fatally injured children 16 years
of age and younger. The head injuries were all accidental and involved blunt, non-penetrating forces.
All cases had been witnessed, and the time of injury
ascertained. Injuries included subdural hematoma;
subarachnoid hematoma; extradural hematoma;
cerebral, cerebellar, or brainstem contusions; skull
fractures; and cerebral edema. Thirty cases had CT
scans. The shortest interval between injury and CT
scans demonstrating severe brain swelling was 1
hour, 17 minutes. Six cases showed evidence of
mild swelling among those with head CT scan
performed less than 3 hours post-injury. In only
1 case of a CT scan being done in less than
3 hours was there no brain swelling. Computed
tomography scans done later than 3 hours after
injury demonstrated various degrees of brain
swelling. In only 1 case was there a “lucid interval”:
an 11-year-old boy with an epidural hemorrhage
who died of a surgical complication.
Neck injuries—Cervical spine injuries occur in 1%
to 2% of most large series of abusive head injuries.
It is surprising that this incidence is not higher, given
the large acceleration-deceleration forces applied
to the head and by reflection to the cervical spine
and neck musculature. In autopsy and clinical
appraisals of children dying from SBS/SIS, there
is little reporting of significant neck and cervical
spine injuries. Hadley and colleagues65 reported
subdural and epidural bleeding in 6 fatally injured
infants. Feldman et al66 sought to determine the
utility of MRI screening for cervical spine and cord
abnormalities in 12 cases of abusive head trauma.
In this series, 5 children had died of their head
injuries and 4 of them had small subdural or subarachnoid hemorrhages at the level of the cervical
spine. Magnetic resonance imaging had not identified any of these lesions. The authors questioned
the efficacy of screening MRIs as a method for
detecting cervical injuries in children with head
injuries. Two cases of cervical spine injury, suffered
as the result of hyperflexion of the neck, were
reported by Rooks et al.67 By more careful attention
to head injuries, it may be found there are more
injuries than have been reported in the past.
Serious head injuries resulting from falls—Many
cases of abusive head trauma have histories of
short falls as the reason for the head injury.
However, there is a vast literature demonstrating
that short falls (less than 10 feet) rarely, if ever,
produce life-threatening head injuries, except in
the cases of epidural hematomas. These latter
intracranial injuries are easily distinguished from
subdural and subarachnoid hematomas on CT
and/or MRI imaging studies.68–79
Outcomes in Shaken Baby Syndrome/
Shaken Impact Syndrome
There are too few studies analyzing outcome of
SBS/SIS, but those that do indicate that long-term
morbidity is high.80–83 The most common sequelae
include tetraplegia, hemiplegia, blindness, cognitive
impairment, neurobehavioral disorders, hemiparesis,
and psychomotor delay. Spasticity, lack of coordination, and ataxia are the most common forms
of psychomotor impairments.84 The few long-term
follow-up studies lead to the conclusion that the
full implication of such injuries takes more than
5 years to appreciate.
The “lucid interval” and the time of injury to onset
of signs and symptoms—This phenomenon has
been the subject of argument both in the hospital
10
Visual Diagnosis of Child Abuse on CD-ROM Lecture Series
3. HEAD TRAUMA IN CHILD ABUSE
References
18. Barkovich A. Destructive brain disorders in childhood. In:
Barkovich A, ed. Pediatric Neuroimaging. 2nd ed. New York,
NY: Raven Press; 1995:107–175
1. Duhaime AC, Alario AJ, Lewander WJ, et al. Head injury
in very young children: mechanisms, injury types, and
ophthalmologic findings in 100 hospitalized patients
younger than 2 years of age. Pediatrics. 1992;90:179–185
19. Yamashima T, Friede RL. Why do bridging veins rupture into
the virtual subdural space? J Neurol Neurosurg Psychiatry.
1984;47:121–127
2. Billmire E, Myers P. Serious head injury in infants: accident
or abuse? Pediatrics. 1985;75:340–342
20. Duhaime AC, Christian CW, Rorke LB, Zimmerman RA.
Nonaccidental head injury in infants—the “shaken-baby
syndrome”. N Engl J Med. 1998;338(25):1822–1829
3. Weston JT. The pathology of child abuse and neglect. In:
Kempe CH, Helfer RE, eds. The Battered Child. Chicago, IL:
University of Chicago Press; 1980:241–271
21. Alexander R, Sato Y, Smith W, Bennett T. Incidence of
impact trauma with cranial injuries ascribed to shaking.
Am J Dis Child. 1990;144(6):724–726
4. Annegers J. The epidemiology of head trauma in children.
In: Shapiro K, ed. Pediatric Head Trauma. Mt. Kisko, NY:
Futura Publishing; 1983:1–10
22. Gilliland MG, Folberg R. Shaken babies—some have
no impact injuries [see comments]. J Forensic Sci.
1996;41(1):114–116
5. Kraus J, Fife D, Cox P, Ramstein K, Conroy C. Incidence,
severity and external causes of pediatric head injury. Am J
Dis Child. 1986;140:687–693
6. Kraus J, Rock A, Hemyari P. Brain injuries among infants,
children, adolescents and young adults. Am J Dis Child.
1990;144:684–691
23. Zauner A, Bullock R. The role of excitatory amino acids in
severe brain trauma: opportunities for therapy: a review.
In: Bandak F, Eppinger R, Ommaya A, eds. Traumatic Brain
Injury. Bioscience and Mechanics. Larchmont, NY: Mary Ann
Liebert, Inc.; 1996:97–104
7. Reece RM, Sege R. Childhood head injuries: accidental or
inflicted? [see comments]. Arch Pediatr Adolesc Med.
2000;154(1):11–15
24. Marr W, Marr E. Some observations on Purtscher’s disease:
traumatic retinal angiopathy. Am J Ophthalmol.
1962;54:693–705
8. DiScala C, Sege R, Li G, Reece RM. Child abuse and
unintentional injuries: a 10–year retrospective [see
comments]. Arch Pediatr Adolesc Med. 2000;154(1):16–22
25. Purtscher O. Noch unbekannte Befun nach Schaeltrauma.
Ber Dtsch Ophthalmol Ges. 1910;36:294–301
26. Morgan O. A case of crush injury to the chest associated
with ocular complication. Trans Ophthalmol Soc UK.
1945;65:366–369
9. Ewing-Cobbs L, Kramer L, Prasad M, et al. Neuroimaging,
physical, and developmental findings after inflicted and
noninflicted traumatic brain injury in young children.
Pediatrics. 1998;102(2 Pt 1):300–307
27. Tomsai L, Rosman N. Purtscher retinopathy in the battered
child syndrome. Am J Dis Child. 1975;129:1335–1337
10. Ludwig S, Warman M. Shaken baby syndrome: a review of
20 cases. Ann Emerg Med. 1984;13(2):104–107
28. Goetting M, Sowa B. Retinal hemorrhage after cardiopulmonary resuscitation in children: an etiologic re-evaluation.
Pediatrics. 1990;85:585–588
11. Duhaime AC. Head trauma. Thousand Oaks, CA: Sage
Publications, Inc; 1997
29. Kanter R. Retinal hemorrhage after cardiopulmonary
resuscitation or child abuse? J Pediatr. 1986;108:430–432
12. Pounder DJ. Shaken adult syndrome. Am J Forensic Med
Pathol. 1997;18(4):321–324
30. Gilliland MGF, Luckenbach MW. Are retinal hemorrhages
found after resuscitation attempts? A study of the eyes of
169 children. Am J Forensic Med Pathol. 1993;14:187–192
13. Hymel KP, Bandak FA, Partington MD, Winston KR. Abusive
head trauma? A biomechnics-based approach. Child
Maltreatment. 1998;3(2):116–128
31. Odum A, Christ E, Kerr N, et al. Prevalence of retinal
hemorrhages in pediatric patients after in-hospital cardiopulmonary resuscitation: a prospective study. Pediatrics.
1997;99(6):E3
14. Ommaya AK, Hirsch AE. Tolerance for cerebral concussion
from head impact and whiplash in primates. J Biomech.
1971;4:13–23
15. Duhaime AC, Gennarelli TA, Thibault LE, Bruce DA,
Margulies SS, Wiser R. The shaken baby syndrome. A
clinical, pathological, and biomechanical study.
J Neurosurg. 1987;66(3):409–415
32. Fackler J, Berkowitz I, Green R. Retinal hemorrhages in
newborn piglets following cardiopulmonary resuscitation.
Am J Dis Child. 1992;146:1294–1296
16. Schutzman S, Barnes P, Mantello M, Scott R. Epidural
hematoma in children. Ann Emerg Med. 1993;22:535–541
33. Khan SG, Frenkel M. Intravitreal hemorrhage associated
with rapid increase in intracranial pressure (Terson’s
syndrome). Am J Ophthalmol. 1975;80(1):37–43
17. Shugerman RP, Paez A, Grossman DC, Feldman KW,
Grady MS. Epidural hemorrhage: is it abuse? Pediatrics.
1996;97(5):664–668
34. Lambert SR, Johnson TE, Hoyt CS. Optic nerve sheath
and retinal hemorrhages associated with the shaken baby
syndrome. Arch Ophthalmol. 1986;104(10):1509–1512
11
Visual Diagnosis of Child Abuse on CD-ROM Lecture Series
3. HEAD TRAUMA IN CHILD ABUSE
35. McCrae M, Teasell R, Canny C. Bilateral retinal detachments
associated with Terson’s syndrome. Retina. 1994;14:467–469
52. Gilliland MGF. Interval duration between injury and severe
symptoms in nonaccidental head trauma in infants and
young children. J Forensic Sci. 1998;43(3):723–725
36. Muller P, Deck J. Intraocular and optic nerve sheath
hemorrhage in cases of sudden intracranial hypertension.
J Neurosurg. 1974;41:160–166
53. Willman KY, Bank DE, Senac M, Chadwick DL. Restricting
the time of injury in fatal inflicted head injuries. Child Abuse
Negl1997;21(10):929–940
37. Munger CE, Peiffer RL, Bouldin TW, Kylstra JA, Thompson RL.
Ocular and associated neuropathologic observations in
suspected whiplash shaken infant syndrome. A retrospective study of 12 cases. Am J Forensic Med Pathol.
1993;14(3):193–200
54. Hymel KP, Abshire TC, Luckey DW, Jenny C. Coagulopathy
in pediatric abusive head trauma. Pediatrics. 1997;99(3):
371–375
55. Ommaya AK, Faas F, Yarnell P. Whiplash injury and brain
damage: an experimental study. JAMA. 1968;204(4):
285–289
38. Johnson D, Braun D, Friendly D. Accidental head trauma
and retinal hemorrhage. Neurosurgery. 1993;33:231–235
39. Betz P, Puschel K, Miltner E, Lignitz E, Eisenmenger W.
Morphometric analysis of retinal hemorrhages in the
shaken baby syndrome. Forensic Sci Int. 1996;78:71–80
56. Gennarelli TA, Thibault LE, Adams JH, Graham DI,
Thompson CJ, Marcincin RP. Diffuse axonal injury and traumatic coma in the primate. Ann Neurol.
1982;12(6):564–574
40. Elder JE, Taylor RG, Klug GL. Retinal haemorrhages in
accidental head trauma in childhood. J Paediatr Child
Health. 1991;27:286–289
57. Kirschner RH. The pathology of child abuse. In: Helfer ME,
Kempe RS, Krugman RD, editors. The Battered Child. 5 ed.
Chicago, IL: The University of Chicago Press; 1997:248–295
41. Greenwald M, Weiss A, Oesterle C, Friendly D. Traumatic
retinoschisis in battered babies. Ophthalmology. 1986;93:
618–625
58. Budenz D, Farber M, Mirchandani H, Park H, Rorke LB.
Ocular and optic nerve hemorrhages in abused infants with
intra–cranial injuries. Ophthalmology. 1994;101:559–565
42. Elner SG, Elner VM, Arnall M, Albert DM. Ocular and
associated systemic findings in suspected child abuse: a
necropsy study. Arch Ophthalmol. 1990;108:1094–1101
59. Frank Y, Zimmerman R, Leeds N. Neurological manifestations in abused children who have been shaken. Dev Med
Child Neurol. 1985;27:312–316
43. Gaynon MW, Koh K, Marmor MF, Frankel LR. Retinal folds
in the shaken baby syndrome. Am J Ophthalmol. 1988;
106(4):423–425
60. Giangiacomo J, Khan J, Levine C, Thompson V. Sequential
cranial computed tomography in infants with retinal hemorrhages. Ophthalmology. 1988;95:295–299
44. Levin A. Ocular manifestations of child abuse. In: Reece R,
Ludwig S, eds. Child Abuse: Medical Diagnosis and
Management. Baltimore, MD: Lippincott Williams and
Wilkins; 2001
61. Kleinman PK, Barnes PD. Head trauma. In: Kleinman PK,
ed. Diagnostic Imaging of Child Abuse. 2nd ed. St. Louis,
MO: Mosby; 1998:285–342
45. Sandramouli S, Robinson R, Tsaloumas M, Willshaw H.
Retinal hemorrhages and convulsions. Arch Dis Child.
1997;76:449–451
62. Riffenburgh R, Sathyavagiswaran L. Ocular findings at
autopsy of child abuse victims. Ophthalmology. 1991;98:
1519–1524
46. Annable W. Ocular manifestations of child abuse. In: Reece
R, editor. Child Abuse: Medical Diagnosis and Management.
Malvern, PA: Lea and Febiger; 1994:138–49
63. Wilkinson WS, Han DP, Rappley MD, Owings CL. Retinal
hemorrhage predicts neurologic injury in the shaken baby
syndrome. Arch Ophthalmol. 1989;107(10):1472–1474
47. Buys YM, Levin AV, Enzenauer RW, Elder JE, Letourneau MA,
Humphreys RP, et al. Retinal findings after head trauma in
infants and young children. Ophthalmology. 1992;99(11):
1718–1723
64. Zepp F, Bruhl K, Zimmer B, Schumacher R. Battered child
syndrome: cerebral ultrasound and CT findings after
vigorous shaking. Neuropediatrics. 1992;23:188–191
48. Eisenbrey A. Retinal haemorrhages in the battered child.
Child’s Brain. 1979;5:40–44
65. Hadley MN, Sonntag VK, Rekate HL, Murphy A. The infant
whiplash-shake injury syndrome: a clinical and pathological
study. Neurosurgery. 1989;24(4):536–540
49. Han DP, Wilkinson WS. Late ophthalmic manifestations
of the shaken baby syndrome. J Pediatr Ophthalmol
Strabismus. 1990;27(6):299–303
66. Feldman K, Weinberger E, Milstein J, Fligner C. Cervical
spine MRI in abused infants. Child Abuse Negl. 1997;21:
199–205
50. Levin A. Ocular manifestations of child abuse. Ophthalmol
Clin North Am. 1990;3:249–264
67. Rooks V, Sisler C, Burton B. Cervical spine injury in child
abuse: report of two cases. Pediatr Radiol.
1998;28:193–195
51. Zimmerman RA, Bilaniuk LT, Bruce D, Dolinskas C, Obrist W,
Kuhl D. Computed tomography of craniocerebral injury in
the abused child. Radiology. 1979;130:687–690
68. Barlow B, Niemirska M, Gandhi RP, Leblanc W. Ten years
of experience with falls from a height in children. J Pediatr
Surg. 1983;18(4):509–511
12
Visual Diagnosis of Child Abuse on CD-ROM Lecture Series
3. HEAD TRAUMA IN CHILD ABUSE
69. Chadwick DL, Chin S, Salerno C, Landsverk J, Kitchen L.
Deaths from falls in children: how far is fatal? J Trauma.
1991;31(10):1353–1355
79. Smith MD, Burrington JD, Woolf AD. Injuries in children
sustained in free falls: an analysis of 66 cases. J Trauma.
1975;15(11):987–991
70. Helfer RE, Slovis TL, Black M. Injuries resulting when small
children fall out of bed. Pediatrics. 1977;60:533–535
80. Bonnier C, Nassagne M, Evrard P. Outcome and prognosis
of whiplash shaken infant syndrome: late consequences
after a symptom–free interval. Dev Med Child Neurol.
1995;37:943–56
71. Joffe M, Ludwig S. Stairway injuries in children. Pediatrics.
1988;82(3 Pt 2):457–461
81. Duhaime AC, Christian C, Moss E, Seidl T. Long–term
outcome in infants with the shaking-impact syndrome.
Pediatr Neurosurg. 1996;24(6):292–298
72. Kravitz H, Driessen G, Gomberg R, Korach A. Accidental
falls from elevated surfaces in infants from birth to one
year of age. Pediatrics. 1969;44(suppl):869–876
82. Fischer H, Allasio D. Permanently damaged: long–term
follow-up of shaken babies. Clin Pediatr. 1994;33:696
73. Lehman D, Schonfeld N. Falls from heights: a problem not
just in the Northeast. Pediatrics. 1993;92:121–124
83. Haviland J, Russell R. Outcome after severe non-accidental
head injury. Arch Dis Child. 1997;77:505–507
74. Lyons TJ, Oates RK. Falling out of bed, a relatively benign
occurrence. Pediatrics. 1993;92:125–127
84. Wharton R, Rosenberg S, Sheridan R, Ryan D. Long–term
medical consequences of physical abuse. In: Reece R, ed.
Treatment of Child Abuse: Common Ground for Mental
Health, Medical and Legal Professionals. Baltimore, MD:
Johns Hopkins University Press; 2000:117–134
75. Meller JL, Shermeta DW. Falls in urban children. A problem
revisited. Am J Dis Child. 1987;141(12):1271–1275
76. Musemeche CA, Barthel M, Cosentino C, Reynolds M.
Pediatric falls from heights. J Trauma. 1991;31(10):
1347–1349
85. Atwal GS, Rutty GN, Carter N, Green MA. Bruising in
non–accidental head injured children; a retrospective study
of the prevalence, distribution and pathological associations
in 24 cases. Forensic Sci Int. 1998;96(2–3):215–230
77. Nimityongskul P, Anderson L. The likelihood of injuries
when children fall out of bed. J Pediatr Orthop. 1987;7:
184–186
78. Selbst SM, Baker MD, Shames M. Bunk bed injuries.
Am J Dis Child. 1990;144(6):721–723
13