Patterns of Head Injury in Non Accidental Trauma

Patterns of Head Injury in Non Accidental Trauma

Patterns of Head Injury in Non Accidental Trauma
Lawrence Buadu, MD PhD, Sven Ekholm MD PhD, Ann Lenane MD, Toshio Moritani MD, Akio Hiwatashi MD, PL Westesson MD.
University of Rochester Medical Center, Rochester, New York

Scalp Swelling

Fig 1.

Intracranial Injury (continued)

Fig 6.

Hypoxic Ischemic Injury

Scope of the problem
It is estimated that more than 2000 children in the United States die each year as a result of child
abuse [1]. Many think that the number is actually higher because many child fatalities, that are
actually related to abuse are reported as accidents, homicides or sudden infant death syndrome.
Nonaccidental head injury (NAHI) is largely restricted to children under three years of age, with the
majority occurring during the first year of life [2]. Inflicted head injury is the most common cause of
traumatic death in infancy [2, 3]. With inflicted head injury an accurate history is rarely provided at
presentation. The history provided may be vague or may vary with time [4]. Physical examination,
although useful may provide little insight regarding underlying brain injury. Consequently, the
diagnosis and detection of nonaccidental head injury (NAHI) usually comes to rest on radiologic
imaging. If radiographic indicators of abuse or neglect are missed, it portends grave consequences
for the child who will invariably be returned to a high risk environment. It is therefore crucial for
radiologists to be familiar with the imaging findings of NAHI.

Fig 6. 2 month old female
seizures and apnea. Nonenhanced CT (NECT) shows
the reversal sign with diffuse
and extensive hypodensity of
the cerebral cortices and
relative sparing of the basal
ganglia and cerebellum.

Fig 1. Scout image from a
CT exam in an 8 month old
male with suspected NAHI
head injury shows biparietal
soft tissue swelling (fig 1a.).
Coronal T1 gradient echo
images (fig 1b) show the
biparietal subgaleal hematomas to better advantage.


Fig 2.





Shear Injury

Fig 7.

Educational Goals:
1. Review the common radiological features of NAHI.
2. Highlight the subtle and less apparent indicators of NAHI.

Fig 2 8 month old male with
suspected NAHI (same patient
as fig 1). Axial nonenhanced
CT exam with bone algorithim
shows a linear defect (arrow)
in the right parietal region
(fig 2a) consistent with fracture. A second fracture in the
left parietal region (arrow) is
less apparent. 3D reconstructed images (fig 2b)
depict the right parietal
however, the left parietal
fracture (arrows) is less
apparent due to a smoothing
effect (fig 2c). MIP images
(fig 2d) shows the left parietal
fracture to best advantage.

Biomechanics and Terminology
The various terminologies applied to inflicted head injury in children reflect the evolution in our
understanding of the underlying mechanisms necessary to cause some of the injuries seen. The term
whiplash shaken baby syndrome was originally coined by Caffey to explain the constellation of
findings of subdural and subarachnoid hemorrhages, traction type metaphyseal fractures and retinal
hemorrhages in children [5]. Since then terms like shaken baby syndrome, shaken impact syndrome
and shaken infant syndrome have all been used in an attempt to explain underlying mechanisms of
inflicted head injury infants. Regardless of terminology it is well accepted that most inflicted head
injuries in children are of the dynamic type. Dynamic injuries may occur in either direct contact
trauma or indirect injury. Contact phenomena result in localized distortion or a fracture of the skull, a
focal cortical injury, epidural hematoma or subdural hematoma. In contrast to direct trauma, indirect
injuries are independent of skull deformation and entail inertial loading which occurs with sudden
acceleration or deceleration of the head [6]. Although a contact may occur with this mechanism,
significant life threatening injuries may occur without an impact. Head acceleration or decelerations
results in a variety of strain deformations of the skull and its contents. Shear strain deformation,
which produces disruption at tissue interfaces is the most important mechanism in the production of
intracranial injury. Furthermore the primary injury occurring with these biomechanical forces may
result in other pathophysiologic alterations or secondary injury (e.g. edema, swelling, hypoxic
ischemia, herniation) and produce additional imaging findings.

Scalp Injury (Fig 1)
Scalp injuries are usually the result of direct impact but may not be apparent in inflicted head injuries.
When present, these may manifest as abrasion, bruising, laceration, or a burn; subcutaneous
hemorrhage or edema (caput succedaneum); subgaleal hemorrhage or a subperiosteal hemorrhage
(cephalhematoma). Although CT is well suited to the evaluation of these fluid collections , MR
imaging with its superior soft tissue resolution shows these changes to better advantage (fig 1a & b)

Cranial Injury (Fig 2)
The prevalence of skull fractures in all cases of abuse is 10% to 13% [7]. The radiographic
appearances of skull fractures may be classified into simple and complex categories. CT scan may
show a linear defect on axial sections with bone algorithim (fig 2a) however if the fracture is in the
plane of the scan it can easily be overlooked. 3D reconstructions are helpful but may obscure the
fracture line due to a smoothing effect (fig 2c). Maximum intensity projection images (MIP) are
especially sensitive and depict fractures to best advantage (fig 2d).

Intracranial Injury
Extra-axial (Figs 3,4)
Extra-axial lesions are usually hemorrhagic in nature. Hemorrhage can be epidural, subdural or
subarachnoid. Epidural hematomas (EDH) are infrequently encountered in infancy and are
particularly uncommon in cases of abuse. They are usually the result of direct impact injuries and
are often associated with skull fractures [8]. In contrast, nonaccidental subdural hemorrhage is
much more common, usually caused by high energy, angular or rotational acceleration
deceleration forces delivered during shaking or shaking impact assaults. Shear strain forces result
in disruption of delicate cortical bridging veins as they leave the cortical surfaces to enter the dural
venous sinuses. The injury most frequently involves the cortical venous structures draining into
the superior sagittal sinus. Consequently, the smallest and earliest collections are encountered in
the interhemispheric regions over the cerebral cortices. Because the underlying mechanisms are
similar there is a high association of retinal hemorrhages in nonaccidental trauma with SDH.
Acute subdural collections are hyperdense on CT. However, subacute or chronic subdural
hematomas tend to be of low or mixed attenuation on CT and are better delineated on MR
imaging (fig 3a & b). The mechanism of subarachnoid hemorrhage (SAH) is similar to that of
SDH resulting from the disruption of cortical veins occurring with angular accelerations or
decelerations of the head. In contrast to its high sensitivity for detecting SDH, MRI is relatively
insensitive to the presence of hyperacute or acute SAH. Fluid attenuated Inversion Recovery
(FLAIR) imaging is, however, quite sensitive and has resulted in improved detection of SAH (fig



Intra-axial (Fig 5)
Most intra-axial lesions in contrast to extra-axial lesions are nonhemorrhagic although hemorrhagic
lesions can occur (fig 5). Nonhemorrhagic intra-axial lesions which are more difficult to identify early
in their course and are responsible for most deaths from inflicted head injury [9]. Nonhemorrhagic
intra-axial lesions may present as diffuse pathologic alterations like hyperemic cerebral swelling,
diffuse cerebral edema or hypoxic ischemic injury. More focal manifestations include focal infarcts or
axonal injury.

Diffuse Cerebral Edema
Brain edema is the most profound pathologic alteration encountered with inflicted brain injury, yet the
most poorly understood. Brain edema a consequence of increased brain water (cytotoxic and
vasogenic) may occur as a reponse to direct focal injury such as cerebral contusion or diffuse primary
injury such as diffuse axonal injury (DAI). Furthermore, vascular occlusion due to cerebral brain stem
herniation as well as pressure necrosis may lead to cerebral edema. CT images obtained immediately
after the traumatic event often show no evidence of swelling or edema. Swelling or edema may
become manifest on CT within a few hours with extensive loss of gray-white differentiation and diffuse
hypodensity. These findings carry a poor clinical outcome regardless of the clinical grade.

Hypoxic Ischemic Injury (Fig 6)

Fig 7. 14 day old male infant
with new onset focal seizures,
fever and swelling on the right
forehead. Axial CT shows a
focus of hemorrhage over the
left temporal tip (arrow)
(fig 7a). Axial T1 and T2weighted images confirm the
presence of hemorrhage at
the right temporal tip (fig 7b &
c). Diffusion weighted image
shows two punctuate foci of
restricted diffusion (arrows) in
the left parietal lobe most
consistent with axonal injury
(fig 7d). ADC values (not
shown) were diminished.

There is a tendency for profoundly injured infants to develop CT manifestations of brain edema that
primarily involves the cerebral cortex and subcortical white matter but apparently spares the basal
ganglia, thalami brainstem and cerebellum. This finding is often associated with subdural hematoma
and can be unilateral or bilateral. Cohen and colleagues [10] coined the term reversal sign to
describe this phenomenon (fig 6). The pathogenesis of the reversal sign is not entirely understood but
experimental studies appear to indicate that cerebral cortical gray matter is particularly sensitive to
hypoxic ischemic injury. Bird and associates suggest that the peripheral low density with relative
central high density is related to the passive congestion and distension of deep medullary veins
because of partial venous outflow form obstruction from the increased intracranial pressure [11].



Shear Injury (Fig 7)
Shear injury of the white matter generally referred to as diffuse axonal injury results from angular
acceleration during shaking or blunt impact trauma. Histologically the lesion is characterized by
axonal swelling or the so called retraction balls. Lesions are commonly noted in the cerebral
hemispheres at the gray-white matter junctions (fig 7), the corpus callosum, the dorsolateral aspect of
the upper brainstem, the upper pons and the basal ganglia. Because of the superior conspicuity
provided, T2* gradient echo and FLAIR imaging are the preferred MRI techniques for demonstrating
DAI. However, DAI is particularly uncommon in infants.

Atrophy (Fig 8)


Subdural Hematoma
Fig 3. 5 month old male child
with nonreactive pupils and
sus-pected NAHI. Coronal T1
SPGR image demonstrates a
left interhemispheric SDH
(fig 3a). A right SDH (arrows)
which is less apparent on the
TIWI is seen to better advantage on the more sensitive
gradient echo image (fig 3b).

Fig 4. 9 month old male
presenting with suspected
nonaccidental trauma and
retinal hemorrhages. Sagittal
T1-weighted image shows a
right SDH (fig 4a). Axial fluid
attenuated inversion recovery
image demonstrates SAH
(arrows) in the right parietal
region (fig 4b).

Fig 5. 5 month old female
who presented with altered
mental status and retinal
T1weighted (fig 5a.) and gradient
intraparenchymal hematoma.



Fig 3.


Fig 8.


Fig 4.




Fig 8.
2 month old female
infant presenting with seizures
and apnea (same patient as
fig 7.) Initial midline sagittal
preservation of parenchymal
volume. Follow-up MR image
9 days later shows significant
loss of volume and the
relatively rapid progression of
severe diffuse brain injury to


Fig 9.






Fig 5.






Fig 9. 2 year old female who
initially presented with seizure.
Axial T1-weighted image
(fig 9a) shows a small right
SDH (arrows). Axial flair image
(fig 9b) shows a small amount
of SAH (arrows). DWI was
normal. Child injury survey(not
shown) at the time was also
normal. A month later the child
returned with a history of a fall
which resulted in a right
tibia/fibula fracture. A repeat
MR exam shows multiple areas
of subacute infarction on T1,
flair and DWI (fig 9d, e & f).

Atrophy is often the result of primary and secondary traumatic brain injury. When serial imaging
demonstrates an evolution from widespread cerebral edema to cerebral atrophy it is likely that hypoxic
ischemia has played a major role in the cerebral injury. The time course for the development of
cerebral atrophy is variable but the imaging findings may develop rapidly when the initial insult is
severe (fig 8). These findings correspond with the development of cerebral spasticity and a vegetative

Biochemical Alterations
Despite the major advances made in recognizing indicators of NAHI, in some instances there may be
no apparent morphological findings despite significant underlying brain injury. In these instances MR
spectroscopy can be useful and is becoming an important part of the diagnostic armamentarium in
helping to unmask biochemical alterations which may predate any morphological changes.
Additionally MR spectroscopy has been shown to have prognostic implications in NAHI [12].

Discussion & Conclusions
Inflicted head injury is the most common cause of traumatic death in infancy, however history is often
unreliable and physical exam may be unrevealing. Diagnostic imaging therefore plays a crucial role in
identifying potential patterns of abuse. Although no single imaging finding is specific for abuse, no other
medical condition fully mimics all the features of non-accidental injury in infants and children. As
radiologists we have a vital role to play in identifying those imaging findings that can suggest abuse. Our
index of suspicion should be high since failure to identify potential patterns of abuse portends grave
consequences for the child who will invariably be returned to a high risk environment (fig 9). In this
presentation we have attempted to demonstrate the common and some less common patterns of
nonaccidental head injury which have been significantly enhanced since the introduction of MR imaging.
Despite all the technological advances, however, imaging of nonaccidental injury continues to be a
challenge. Some forms of injury like intermittent suffocation and asphyxiation may present with little or
no morphological changes on imaging. MR spectroscopy, however, holds promise for the future by
aiding in the identification of biochemical changes that may predate and morphological findings. This
may help identify children who are subject to subclinical forms of repetitive abuse before a fatality

National Clearing house on Child Abuse and Neglect Information. (No date) Child fatalities fact sheet [online] Available:[2000,February 22]
2. Centers for Disease Control. Childhood injuries in the United States. Am J Dis Child 1990; 627-46.
3. Billmire ME, Myers PA. Serious head injury in infants; accident or abuse? Pediatrics 1985; 75: 340-2
4. 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; 66:409-15
5. Caffey J. The whiplash shaken infant syndrome; manual shaking by the extremities with whiplash-induced intracranial and intraocular bleedings,
linked with residual permanent brain damage and mental retardation. Pediatrics 1974; 54: 396-403
6. Kleinman, Paul K. Diagnostic imaging of child abuse-2nd edition; pg 286-287.
7. James HE, Shut L: The neurosurgeon and the battered child, Surg Neurol 2:415-418, 1974
8. Merten DF, Osborne DRS: Craniocerebral trauma in the child abuse syndrome: radiological observations, Pediatr Radiol 14: 272-277, 1984
9. Kleinman, Paul K. Diagnostic imaging of child abuse-2nd edition; pg 296-297.
10. Cohen RA, KaufmanRA, Myers PA, Towbin RB: Cranial computed tomography in the abused child with head injury, AJR 146:97-102, 1986
11. Bird CR, Drayer BP, Gilles FH: Pathophysiology of "reverse" edema in global cerebral ischemia, AJNR 10: 95-98, 1989
12. Hasler LJ, Arcinue E, Danielsen ER, Bluml S, Ross BD. Evidence from proton magnetic resonance spectroscopy for a metabolic cascade of
neuronal damage in shaken baby syndrome.

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