Type:
Educational Exhibit
Keywords:
Diagnostic procedure, CT, Neuroradiology brain, Haemorrhage
Authors:
P. Dewachter, T. Vanderhasselt, K. De Smet, J. de Mey; Brussels/BE
DOI:
10.1594/ecr2012/C-1270
Background
Traumatic brain injury can result in hemorrhage in midbrain and pons at the time of impact (primary) or in a later stage (secondary).
Secondary brainstem hemorrhage is called Duret hemorrhage.
Duret hemorrhage is caused by downward (transtentorial) cerebral herniation due to raised intracranial pressure from a rapidly expanding supratentorial mass lesion.
Duret hemorrhage has a high incidence of death and persistent vegetative outcome.
There are few case reports describing good outcome.
Arterial damage or venous congestion caused by sudden downward movement of the brainstem against a fixed basilar artery leads to disruption of the perforating arteries.
Animal models showing raised ICP induced by inflation of intracranial balloons support this theory. Stretching and disruption of paramedian pontine perforating arteries may directly lead to hemorrhaging.
Venous congestion due to venous thrombosis and venous infarction can also evolve to hemorrhage.
Surgical decompression may promote Duret hemorrhage as part of a reperfusion injury.
The reported incidence is higher in neuropathological (30-60%) than in radiological (5-10%) studies.
This discrepancy can be explained by the fact that 20% of the damage is microscopically and by the fact that bleeding often occurs after the initial computed tomography (CT).
Differential diagnosis includes primary traumatic brainstem hemorraghes,
hypertensive bleeds and ruptured arteriovenous malformations.
Duret hemorrhage represents 5-13% of traumatic brainstem injuries.