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A well recognized complication of aneurysmal subarachnoid hemorrhage, with an incidence between 20-40%.
It can lead to major disability or mortality.
The incidence of traumatic subarachnoid hemorrhage leading to vasospasm is underestimated.
Following mild head trauma, cerebral vasospasm is generally asymptomatic.
Post traumatic vasospasm is considered in all patients with diffuse subarachnoid hemorrhage or intraventricular hemorrhage, especially with delayed neurological deterioration.
Significant narrowing of the blood vessels in the brain develops gradually over the first few days after the aneurysmal rupture.
This kind of narrowing usually is maximal in about a week’s time following intracerebral hemorrhage.
Cerebral vasospasm is the prolonged, intense vasoconstriction of the larger
arteries in the subarachnoid space which is initially surrounded by a clot.
Vasospasm is the one of the leading causes of death after the aneurysmal rupture along with the effect of the initial hemorrhage and later bleeding.
The pathophysiology of vasospasm after traumatic subarachnoid hemorrhage is unknown but associated with two theories.
Firstly, chemical therapy where spasmogenic and neuro inflammatory substances produced by subarachnoid blood degradation are associated with decreased nitric oxide availability and with increased sensitivity to endothelin.
Secondly, a mechanical theory where the stretching and pulling forces are applied to cerebral vessels during the trauma and favors vasospasm.
Diagnosis is related to clinical presentation and imaging which includes CT angiography showing irregularity in the caliber of involved blood vessels with narrowing compared to the opposite side, and associated with decreased perfusion in the territory of the blood vessel.
Digital subtraction angiography is the primary standard for the diagnosis of posttraumatic vasospasm.
Management of post traumatic vasospasm is the painted but consideration is given for placement of intra-arterial calcium channel blockers.