Shaken Baby Syndrome. a Case Report

8/2/2019 Shaken Baby Syndrome. a Case Report

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uncontrolled movements of the upper and lower limbs. Physicalexamination was unremarkable. The fontanel was normal. Therewas no fever. Hematologic laboratory data and blood chemicalvalues were normal. No skin lesions or occult bone fractures werefound. Both parents denied a history of craniocerebral trauma.Shortly after admission, the boys clinical condition deterioratedrapidly. He developed repetitive generalized tonic-clonic seizuresand severe respiratory depression, requiring urgent intubation. Thechild was ventilated, and given phenytoin.

A noncontrast CT scan of the brain (Fig. 1) showed multipleareas of decreased attenuation in both cerebral hemispheres. Therewere thin, hypodense subdural collections over both frontal lobes.The low-density appearance of these collections could point to

subacute or chronic subdural hematomas, or acute traumatic hy-gromas. The diagnosis of shaken-baby syndrome was suspected.Fundoscopic examination revealed widespread bilateral retinalhemorrhages, but no papillary edema. Plain radiographs of thechest, axial skeleton, and extremities showed no abnormalities.Emergency MRI of the brain was performed on the same day(Fig. 2) using the following pulse sequences: axial turbo fluid-attenuated inversion recovery (FLAIR) images, axial inversionrecovery T1-weighted images, axial echo-planar DW-MRI scans

with b values of 0, 500, and 1,000 mm2

/s (trace images and ADCmaps), coronal HASTE T2-weighted scans, and MR angiography(MRA) with 3D time-of-flight technique and maximum intensityprojection reconstructions. The MRI examination confirmedbilateral subdural hematomas, extending into the interhemisphericfissure (Fig. 2a, b). The DW-MRI scans revealed gyriform areas ofrestricted diffusion involving the edematous cortical gray matter ofboth hemispheres (Fig. 2c, d). These areas were hypointense on thecorresponding ADC maps. This indicates cytotoxic edema, pre-sumably due to widespread cortical hypoxic-ischemic brain dam-age. The parenchymal abnormalities were not well seen on theFLAIR images, though it must be remembered that FLAIR imagesin infants are relatively insensitive in comparison with those ofolder children and adults. MRA showed normal intracranialarteries. There was no evidence of venous sinus occlusion.

When confronted with the imaging findings, the father admitted

to vigorous shaking of the baby. The subdural hematomas wereremoved neurosurgically, and a ventricular catheter was placed.During the first postoperative day, rapid increase in intracranialpressure was observed. Despite maximal antiedematous and anti-convulsive treatment, including administration of pentobarbital,the elevation of intracranial pressure persisted. Follow-up CT scanson days 2 and 6 after admission demonstrated a dramatic increaseof the cerebral parenchymal ischemic areas and the appearance ofintracerebral hemorrhage (Fig. 3). Over the next few days, thepatients clinical condition gradually improved. The boy wasextubated on day 9 and discharged from the ICU to a pediatricward in hemodynamically and respiratory stable condition, butwith no evidence of higher cortical functions.

The child survived and was last seen at the age of 9 months.There was eye contact and motor development was scored atapproximately 4 months. Clinical examination revealed acquired

microcephaly, a convergent squint, and spastic quadriplegia.

Discussion

The diagnosis of SBS remains a formidable clinicalchallenge. The consequences of this diagnosis are grave,

Fig. 1 Axial noncontrast CT scan obtained on the day ofadmission from a 2-month-old baby boy with suspected shakenbaby syndrome (SBS). Thin, hypodense extra-axial effusions areseen over both frontal lobes. Multiple hypodense areas areobserved in the frontal, temporal, and occipital lobes

Fig. 2 MRI examination, obtained 2 h after admission. a, b Axialturbo FLAIR images reveal bilateral subdural hematomas,extending into the interhemispheric fissure. c, d Axial diffusion-weighted MR images (DW-MRI), obtained with a b value of1,000 mm2/s, show confluent hyperintensities involving the corticalgray matter and subcortical white matter in the frontal andtemporal and occipital lobes. The lesions were hypointense on theapparent diffusion-coefficient (ADC) maps, indicating areas ofrestricted diffusion. This finding is consistent with diffuse hypoxic-ischemic brain injury

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both for the baby and his/her parents or caregivers.Missing the diagnosis of SBS in an acutely ill infant canlead to permanent neurological damage or even death[14]. On the other hand, when a false-positive diagnosisof SBS is made, parents or caregivers may be falselyaccused of assault.

By clinical examination one cannot differentiate withcertainty between accidental and inflicted injury, espe-cially in the absence of external signs of violence [12, 15].Retinal hemorrhages in an infant are a cardinal featureof SBS. Traditionally, retinal hemorrhages were believed

to be caused by an abrupt rise of intracranial pressure(shaking plus strangulation or suffocation mechanism);however, recent evidence suggests that the retinal hem-orrhages could be the result of mechanical shaking for-ces [11]. Whatever the etiology, the finding of retinalhemorrhages is not specific, nor does their absence ruleout the possibility of nonaccidental trauma.

Increasingly, therefore, the diagnosis of SBS relies onradiologic evidence of intracranial damage. CT hasrevolutionized the assessment and management of sus-pected SBS, and remains the principal imaging modalityin the acute setting [2, 10]. CT scans of the brain nearlyalways demonstrate subdural hematomas, which are the

most common manifestations of SBS. Subdural hema-tomas of varying ages, or located in the interhemisphericfissure are considered to be highly suggestive of shakinginjury [1]. It is believed that the acceleration/decelerationforces which occur during violent shaking are sufficientto cause rupture of the vulnerable bridging veins, which,in young babies, can easily be torn [2]. Infants tend tohave relatively large volumes of cerebrospinal fluidaround the brain, which allows for greater movementwithin the cranial vault [11]. Moreover, the neck muscles

of babies are not strong enough to support the range ofmotion of their relatively large heads. The presence ofsubdural hemorrhages can also be explained by a com-bination of severe hypoxia, brain swelling, and raisedcentral venous pressure, which causes blood to leak fromintracranial veins into the subdural space [16]. It must beremembered, however, that not all subdural hematomas

are due to child abuse.MRI has increased the sensitivity for diagnosing SBS

in detecting and characterizing small extra-axial hem-orrhages in infants with equivocal CT findings [2, 10].On CT, subdural collections are often of a nonspecificcharacter (e.g., subacute or chronic sudural hematomasthat are of low density or isodense), as shown in ourpatient. MRI has a 50% greater rate of detection ofsubdural hematomas than CT [17]. Moreover, MRI ismore accurate in dating subdural hematomas and allowsdifferentiation of a recent subdural hemorrhage fromone superimposed on a pre-existing one [18]. Even moreimportantly, MRI reveals the presence of nonhemor-

rhagic parenchymal brain damage not shown or under-estimated on the acutely performed cerebral CT scan,such as diffuse axonal trauma or hypoxic-ischemicencephalopathy [2, 3, 15, 19]. DW-MRI is a techniquethat is sensitive to restricted diffusion, reflecting cyto-toxic edema, which occurs in acute hypoxic-ischemicbrain damage. In our patient, we found widespread,gyriform regions of decreased diffusion in the corticalgray matter. This pattern suggests that the neurophys-iopathology of the severe encephalopathy in SBS ishypoxic-ischemic brain damage, and NOT diffuse trau-matic axonal injury. Neuropathological studies byGeddes et al. have confirmed that global severe hypoxic

damage is by far the most common histological findingin inflicted head injury in children, and that widespreadaxonal damage is much less frequent [20, 21]. The dif-fusion abnormalities observed in our patient were pre-dominantly found in cortical gray matter, whichappeared thickened and edematous. Other investigatorshave shown diffusion abnormalities in the subcorticalbrain tissue, consistent with watershed infarctions,especially in the posterior brain regions [15]. Magneticresonance spectroscopy findings confirm that the path-ophysiology of nonaccidental head trauma is due tohypoxic-ischemic injury, by showing the metabolicchanges occurring in the infant brain after a shakinginjury [22]. Hypoxic injury to the brain results in loss ofN-acetyl aspartate and accumulation of lactate, al-though the mechanism in SBS appears to be somewhatdifferent from hypoxic injury alone [22].

In summary, in our patient with SBS, DW-MRIshowed a dramatically greater lesion extent than wasseen on conventional MR images or on CT scans. DW-MRI may represent the most sensitive and specifictechnique in the evaluation of cerebral damage in shakenbabies. The use of DW-MRI may help to guide clinical

Fig. 3 Follow-up noncontrast CT scan (day 6 after admission)shows a dramatic increase of the cerebral parenchymal abnormal-ities, which are seen as hypodense regions (suggestive of edema)and hyperdense areas (indicating intraparenchymal hemorrhage).The density in the left frontal horn is a shunt catheter. There is asmall amount of blood in the occipital horn on the right

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management of these patients, to identify children athigh risk for poor outcome, and to provide an estimateregarding the timing of the alleged assault. Thus, thetime-dependent signal intensity changes on DW-MRImay be of great importance in forensic medicine. Theareas of restricted diffusion indicate cytotoxic edemaand confirm the neuropathological observations that the

parenchymal brain damage in SBS is predominantly dueto diffuse hypoxic-ischemic encephalopathy, and not todiffuse axonal injury [21].

Acknowledgements We are grateful to V. De Groot, MD, forproviding fundoscopic evidence of retinal hemorrhages. We alsothank G. Van Hoorde for photographic assistance.

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Shaken Baby Syndrome. a Case Report