Patterns of Head Injury in Non Accidental TraumaPatterns of Head Injury in Non Accidental TraumaLawrence 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

IntroductionIntroduction

Scope of the problem

It is estimated that more than 2000 children in the United States die each year as a result of childabuse [1]. Many think that the number is actually higher because many child fatalities, that areactually 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 themajority occurring during the first year of life [2]. Inflicted head injury is the most common cause oftraumatic death in infancy [2, 3]. With inflicted head injury an accurate history is rarely provided atpresentation. 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, thediagnosis and detection of nonaccidental head injury (NAHI) usually comes to rest on radiologicimaging. If radiographic indicators of abuse or neglect are missed, it portends grave consequences forthe child who will invariably be returned to a high risk environment. It is therefore crucial forradiologists to be familiar with the imaging findings of NAHI.

Educational Goals:

1. Review the common radiological features of NAHI.

2. Highlight the subtle and les s apparent indicators of NAHI.

Biomechanics and TerminologyBiomechanics and TerminologyThe various terminologies applied to inflicted head injury in children reflect the evolution in ourunderstanding of the underlying mechanisms necessary to cause some of the inj uries seen. The term“whiplash shaken baby syndrome” was originally coined by Caffey to explain the constellation offindings of subdural and subarachnoid hemorrhages, traction type metaphyseal fractures and retinalhemorrhages in children [5]. Since then terms like shaken baby syndrome, shaken impact syndromeand shaken infant syndrome have all been used in an attempt to explain underlying mechanisms ofinflicted head injury infants. Regardless of terminology it is well accepted that most inflicted headinjuries in children are of the dynamic type. Dynamic injuries may occur in either direct contact traumaor indirect injury. Contact phenomena result in localized distortion or a fracture of the skull, a focalcortical injury, epidural hematoma or subdural hematoma. In contrast to di rect trauma, indirect injuriesare independent of skull deformation and entail inertial loading which occurs with sudden accelerationor deceleration of the head [6]. Although a contact may occur with this mechanism, significant lifethreatening injuries may occur without an impact. Head acceleration or decelerations results in avari ety of strain deformations of the skull and its contents. Shear strain deformation, which producesdisruption 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 otherpathophysiologic alterations or secondary injury (e.g. edema, swelling, hypoxic ischemia, herniation)and produce additional imaging findi ngs.

Scalp Injury (Fig 1)Scalp injuries are usually the result of di rect impact but may not be apparent in inflicted head injuries.When present, these may manifest as abrasion, bruising, laceration, or a burn; subcutaneoushemorrhage or edema (caput succedaneum); subgaleal hemorrhage or a subperiosteal hemorrhage(cephalhematoma). Although C T is well suited to the evaluation of these fluid collections , MR imagingwith its superior soft tissue resol ution 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 radiographicappearances of skull fractures may be classified into simple and complex categories. CT scan mayshow a linear defect on axial sections with bone algorithim (fig 2a) however if the fracture is in theplane of the scan it can easily be overlooked. 3D reconstructions are helpful but may obscure thefracture line due to a smoothing effect (fig 2c). Maximum intensity projection images (MIP) areespecially 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 orsubarachnoid. Epidural hematomas (EDH) are infrequently encountered in infancy and areparticularl y uncommon in cases of abuse. They are usually the result of direct impact injuries andare often associated with skull fractures [8]. In contrast, nonaccidental subdural hemorrhage ismuch more common, usually caused by high energy, angular or rotational accelerationdec elerati on forces delivered during shaking or shaking impact assaults. Shear strain forces resultin disruption of delicate cortical bridging veins as they leave the cortical surfaces to enter the duralvenous sinuses. The injury most frequently involves the cortical venous structures draining intothe superior sagittal sinus. Consequently, the smal lest and earliest collections are encountered inthe interhemispheric regions over the cerebral cortices. Because the underl ying mechanisms aresimilar there is a high association of retinal hemorrhages in nonaccidental trauma with SDH. Acutesubdural collections are hyperdense on CT. However, subacute or chronic subdural hematomastend 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 thedisruption of cortical veins occurring with angular accelerations or decelerations of the head. Incontrast to its high sensitivity for detecting SDH, MRI is relatively insensitive to the presence ofhyperacute or acute SAH. Fluid attenuated Inversion Recovery (FLA IR) imaging is, however, quitesensitive and has resulted in improved detection of SAH (fig 4).

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Fig 8. 2 month old femaleinfant presenting with seizuresand apnea (same patient as fig7.) Initial midline sagittal T1WIshows relative preservation ofparenchymal volume. Follow-up MR i mage 9 days latershows significant loss ofvolume and the rel atively rapidprogression of severe diffusebrain injury to atrophy.

Scalp Swelling

Fracture Shear Injury

Atrophy

Infarction

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Fig 5. 5 month old femalewho presented with alteredmental status and retinal hemo-rrhages on physical examin-ation. Sagittal T1-weighted (fig5a.) and gradient echo (fig 5b)images demonstrate an intra-parenchymal hematoma.

Fig 4. 9 month old malepresenting with suspectednonaccidental trauma andretinal hemorrhages. SagittalT1-weighted image shows aright SDH (fig 4a). Axial fluidattenuated inversion recoveryimage demonstrates SAH(arrows) in the right parietalregion (fig 4b).

Fig 3. 5 month old male childwith nonreactive pupils andsus-pected NAHI. Coronal T1SPGR image demonstrates aleft interhemispheric SDH(fig 3a). A right SDH (arrows)which is less apparent on theTIWI is seen to better ad-vantage on the more sensitivegradient echo image (fig 3b).

Subdural Hematoma

SubarachnoidHemorrhage

IntraparenchymalHematoma

Fig 7. 14 day old male infantwith new onset focal seizures,fever and swelling on the rightforehead. Axial CT shows afocus of hemorrhage over theleft temporal tip (arrow)(fig 7a). Axial T1 and T2-weighted images confirm thepresence of hemorrhage atthe right temporal tip (fig 7b &c). Diffusion weighted imageshows two punctuate foci ofrestricted diffusion (arrows) inthe left parietal l obe mos tconsistent with axonal injury(fig 7d). ADC values (notshown) were diminished.

Fig 2 8 month old male withsuspected NAHI (same patientas fig 1). Axial nonenhancedCT exam with bone algorithimshows a linear defect (arrow)in the ri ght pari etal regi on(fig 2a) consistent with frac-ture. A second fracture in theleft parietal region (arrow) isless apparent. 3D recon-structed images (fig 2b) depictthe right parietal fractureclearly (arrows) however, theleft parietal fracture (arrows) isless apparent due to asmoothing effect (fig 2c). MIPimages (fig 2d) shows the leftparietal fracture to bestadv antage.

Fig 9. 2 year old female whoinitially presented with seizure.Axial T1-weighted i mage(fig 9a) shows a small rightSDH (arrows). Axial flair image(fig 9b) shows a small amountof SAH (arrows). DWI wasnormal. Child injury survey(notshown) at the time was alsonormal. A month later the childreturned with a history of a fallwhich resulted in a righttibia/fibula fracture. A repeatMR exam shows multiple areasof subacute infarction on T1,flair and DWI (fig 9d, e & f).

Fig 6. 2 month old femaleinfant presenting withseizures and apnea. Non-enhanced CT (NECT) showsthe reversal sign with diffuseand extensive hypodensity ofthe cerebral cortices andrelative sparing of the basalganglia and cerebellum.

Hypoxic Ischemic Injury

Fig 1. Scout image from aCT exam in an 8 month oldmale with suspected NAHIhead injury shows biparietalsoft tissue swelling (fig 1a.).Coronal T1 gradient echoimages (fig 1b) show thebiparietal subgaleal hemato-mas to better advantage.

Fig 1.

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Fig 4.

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Fig 9.

Fig 8.

Fig 7.

Fig 6. Intracranial Injury (continued)

< Intra-axial

Most intra-axial lesions in contrast to extra-axial lesions are nonhemorrhagic although hemorrhagiclesions can occur (fig 5). Nonhemorrhagic intra-axial lesions which are more difficult to identify early inthei r 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, diffusecerebral edema or hypoxic ischemic injury. More focal manifestations include focal infarcts or axonalinjury.

< Diffuse Cerebral Edema

Brain edema is the most profound pathologic alteration encountered with inflicted brain injury, yet themost poorly understood. Brain edema a consequence of increased brain water (cytotoxic andvasogenic) may occur as a reponse to direct focal injury such as cerebral contusion or diffuse primaryinjury such as diffuse axonal injury (DAI). Furthermore, vascular occlusion due to cerebral brain stemherniation as well as pressure necrosis may lead to cerebral edema. CT images obtained immedi atelyafter the traumatic event often show no evidence of swelling or edema. Swelling or edema maybec ome manifest on CT within a few hours with extens ive loss of gray-white differenti ation and diffusehypodensity. These findings carry a poor clinical outcome regardless of the c linical grade.

< Hypoxic Ischemic Injury (Fig 6)

There is a tendency for profoundly injured infants to develop CT manifestations of brain edema thatprimarily involves the cerebral cortex and subcortical white matter but apparently spares the basalganglia, thalami brainstem and cerebellum. This finding is often associated with subdural hematomaand can be unilateral or bi lateral . Cohen and colleagues [10] coined the term reversal sign to descri bethis phenomenon (fig 6). The pathogenesis of the reversal sign is not entirely understood butexperimental studies appear to indicate that cerebral cortical gray matter is particularly sensitive tohypoxic ischemic injury. Bird and associates suggest that the peripheral low density with relativecentral high density is related to the passive congestion and distension of deep medullary veinsbec ause of parti al 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 angularacceleration during shaking or blunt impact trauma. Histologically the lesion is characterized by axonalswelling or the so called retraction balls. Lesions are commonly noted in the cerebral hemispheres atthe gray-white matter junctions (fig 7), the corpus callosum, the dorsolateral aspect of the upperbrainstem, 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 parti cularly uncommon in infants.

< Atrophy (Fig 8)

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

< Biochemical Alterations

Despite the major advances made in recognizing indicators of NAHI, in some instances there may beno apparent morphological findings despite significant underlying brain injury. In these instances MRspectroscopy can be useful and is becoming an important part of the diagnostic armamentarium inhel ping to unmask biochemical alterati ons which may predate any morphological changes . AdditionallyMR spectroscopy has been shown to have prognostic implications in NAHI [12].

Discussion & ConclusionsDiscussion & ConclusionsInflicted head injury is the most common cause of traumatic death in infancy, however history is oftenunreliable and physical exam may be unrevealing. Diagnostic imaging therefore plays a crucial role inidentifying potential patterns of abuse. Although no single imaging finding is specific for abuse, no othermedical condition fully mimics all the features of non-accidental injury in infants and children. Asradiologists we have a vital role to play in identifying those imaging findings that can suggest abuse. Ourindex of suspicion should be high since failure to identify potential patterns of abuse portends graveconsequences for the child who will invariably be returned to a high risk environment (fig 9). In thispresentation we have attempted to demonstrate the common and some less common patterns ofnonaccidental 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 achallenge. Some forms of injury like intermittent suffocation and asphyxiation may present with little or nomorphological changes on imaging. MR spectroscopy, however, holds promise for the future by aiding inthe identification of biochemical changes that may predate and morphological findings. This may helpidentify children who are subject to subclinical forms of repetitive abuse before a fatality occurs.

References: 1. National Clearing house on Child Abuse and Neglect Information. (No date) Child fatalities fact sheet [online] Available:

www.calib.com/nccanch/pubs/factsheet/fatality.html[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 andbiomechanical 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 ofneuronal damage in shaken baby syndrome.

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Fig 2.