Cerebral vasospasm is the prolonged, intense vasoconstriction of the larger conducting arteries in the subarachnoid space which is initially surrounded by a clot.
[2] Infarction occurs in about half of the symptomatic patients and is significantly associated with factors such as advanced age, a history of hypertension, or diabetes mellitus.
The loss of nitric oxide leads to unopposed contraction of smooth muscle cells in the vessel wall, resulting in acute vasoconstriction.
[5] Elevated levels of endothelin, a potent vasoconstrictor, are consistently observed in patients with vasospasm, contributing to prolonged and sustained narrowing of the arteries.
In chronic vasospasm, alterations in calcium-handling mechanisms in vascular smooth muscle cells may contribute to persistent vasoconstriction that does not respond to traditional vasodilatory signals.
[2] Additional factors that increase the risk include: It is critical to rule out other potential causes of delayed neurological deterioration such as hyponatremia, hypoxemia, infection, cerebral edema, or rebleeding of aneurysms.
The modified Fischer scale, which uses parameters such as clot volume and distribution on CT scans, helps predict the risk and prognosis of vasospasm.
An example is IV magnesium sulfate, which was initially considered for its neuroprotective properties, but was not found to be effective in reducing the risk of vasospasm or infarction in the large multicenter IMASH and IMASH-2 trials [10][11] Current clinical treatments include: While fluid therapy is beneficial for patients with poor neurological status, prophylactic hypervolemia or hypertension is not recommended due to the risk of complications, as outlined by the American Heart Association guidelines.