Teaching Case

Two-month-old male infant is brought to the emergency room by ambulance. He suffers from rhythmic tonic-clonic seizure on the left side of his body and a flaccid paresis on the right side. Eyes are open, sight deviation to the right. No fever. Normal delivery. Parents state a fall from his bed (height 40 cm) two days ago, otherwise no reported trauma.

• Bilateral thin supratentorial subdural hematomas (SDH) with epitentorial, parafalcine and infratentorial extension.
• Subarachnoidal haemorrhage (SAH) close to the vertex.
• SAH in the quadrigeminal cistern.
• Shearing injury in the frontoparietal white matter.
• Extensive cortical diffusion restriction supratentorial bilateral with sparing of the right MCA territory. Less prominent diffusion restriction of the caudate nuclei and the thalami resp. infratentorial pronounced on the left side.
• Global edematous brain swelling.
• Bilateral retinal hemorrhages.

The immature brain of children < 2 years of age is characterized by relative high water content, prominent subarachnoid spaces, large head-to-body ratio with weak neck muscles and partially myelinated axons. Therefore they are especially susceptible to damage due to acceleration/deceleration and rotational forces by violent movements such as shaking. Typical findings in such incidents include: subdural hematomas, SAH, retinal haemorrhages and hypoxic-ischemic injury. These findings are referred to as abusive head trauma (AHT), or non-accidental trauma. The SDH occurs due to tearing of the bridging veins at the vertex. SAH manifests as a result of tearing of small pial and subarachnoid vessels. Parenchymal damage in AHT include diffuse brain swelling consisting of cytotoxic and vasogenic oedema, shearing injuries and cerebral contusions/hematomas. Cytotoxic oedema is the most common parenchymal damage pattern, but the pathophysiology is uncertain so far and probably multifactorial. Possible explanations include: direct traumatic injury with oxidative stress and excitotoxicity (also due to seizure activity), altered autoregulation of cerebral blood flow, focal diffuse axonal injury at the cervico-medullary junction with resulting apnea, which may be caused by strangulation, arterial dissection or as a secondary injury due to venous congestion because of prominent SDH. The pathophysiological mechanism of excitotoxicity could result from traumatic rupture of the neuronal cell membranes with excessive release of glutamate and secondary entry of sodium and calcium into the cells via AMPA-/NMDA-receptors. Water molecules follow the gradient passively and result in cytotoxic oedema leading to cell death. [1, 3, 4, 7].

The clinical presentation of AHT is nonspecific. It can range from inconsolable crying to vomiting, lethargy, seizures and coma. Often there is discordance between stated history/injury mechanism and degree of injury on imaging. Unprovoked seizures and apnea should raise suspicion for AHT. The discrepancy between reported trauma mechanism and the extent of injury seen on imaging should be communicated. [4, 5].

Imaging recommendations: MRI should be performed 24- 48 h after presentation to define extent of injury. The following sequences should be acquired: DWI, SWI, axial T2w, axial T1w without and with contrast and MRA to detect dissection. In case of suspected fracture also consider performing a head CT. The key findings include: SDH, SAH, retinal haemorrhages, diffuse brain swelling and cytotoxic oedema. Different signal intensities of the intracranial haemorrhage indicate repeated trauma and should raise the suspicion. [1,2,6].

Retinal haemorrhage and hypoxic-ischemic injury are associated with more severe neurological damage and worse clinical outcome. Severity of hypoxic ischemic injury is correlated with severity of seizure activity. The mortality rate ranges from 20 – 25 % and many suffer from long-term neurologic impairment (including delayed development, epilepsy and cognitive impairments). [1, 8, 9].

The most common injury patterns in AHT include: retinal haemorrhages, SDH/SAH due to torn bridging veins and cytotoxic oedema as a correlate of hypoxic-ischemic injury. Hypoxic ischemic injury (HII) is the most common intraparenchymal damage pattern in children suffering from AHT, followed by contusions and diffuse axonal injuries. HII is associated with a more severe outcome. Suspicion should be raised if there’s a discordance between stated injury mechanism and actual extent on imaging.  [6, 8].

All patient data have been completely anonymised throughout the entire manuscript and related files.