Basilar thrombosis with hemorrhagic transformation

Case contributed by Frank Gaillard
Diagnosis certain

Presentation

Sudden onset loss of conciousness.

Patient Data

Age: 50 years
Gender: Male

CT brain on admission

ct

There is a hyperdense basilar tip. Subtle hypodensity is noted at the left anterior pons, which may be artefactual. Hypodensity at the left internal capsule posterior limb is consistent with prior lacunar nfarct. No intracranial hemorrhage or collections. No evidence of mass effect. Normal grey-white matter differentiation. Ventricles and sulci are age-appropriate. Hypoplastic frontal sinuses. Imaged calvarium and paranasal sinuses are otherwise clear.

CTA at same time

ct

There is poor opacification of the distal basilar artery/basilar tip likely reflecting CTA quality than a real finding. Both proximal P1 are poorly opacified by contrast, although distal P1 and the remainder of both PCA appear normal.

The patient immediately proceeded to a cerebral DSA and successful clot retrieval.

CT brain next day

ct

There are bilateral PCA territory hemorrhagic infarcts, with hyperdensity of the sulci consistent with laminar necrosis. Low density is also seen within the thalamus bilaterally, with hemorrhage seen within the left thalamus consistent with thalomo-perforator distribution infarcts (hemorrhagic on the left). There is an infarct also seen within the right cerebellum and middle cerebellar peduncle uncle. Likely further infarct seen within the left cerebellum. No obstruction/compression to the 4th ventricle. The high density within the basilar artery has resolved. When compared to the previous imaging there is diffuse cerebral edema. No hydrocephalus identified.

MRI Brain Day 2

mri

Very extensive infarction is demonstrated in the posterior circulation-bland infarcts with restricted diffusion shown in the posterior inferior cerebellar artery territory bilaterally, anterior inferior cerebellar artery territory, and the right superior cerebellar artery territory. Hemorrhagic change is demonstrated within the infarcts in both posterior cerebral artery territories within the occipital lobes, and in the left thalamus. Bland infarction shown on the right thalamus and bilateral midbrain. There are punctate areas of infarction seen in other vascular distributions, in particular to areas within the right middle cerebral artery, and peripherally in the left middle cerebral artery territory.

Case Discussion

The patient passed away a few days later.

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