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■ Hyponatremia from SIADH or cerebral salt-wasting syndrome
■ Heparin-induced thrombocytopenia
■ Cardiac arrhythmias and myocardial damage
■ Acute hydrocephalus: managed by external ventricular drainage or lumbar
drainage
■ Pneumonia, DVT, pulmonary embolus, and respiratory failure
■ Neurogenic cardiac stunning (reduction of function of heart contraction)
and pulmonary edema
Management of Cerebral Vasospasm and Delayed
Cerebral Ischemia After aSAH
■ Oral nimodipine should be administered to all patients with aSAH. (This
agent has been shown to improve neurological outcomes but not cerebral
vasospasm. The value of other calcium antagonists, oral or IV, remains
uncertain.)
■ Maintenance of euvolemia and normal circulating blood volume is recom-
mended to prevent delayed cerebral ischemia.
■ Prophylactic hypervolemia or balloon angioplasty before the development
of angiographic spasm is not recommended.
■ TCD is reasonable to monitor for the development of arterial vasospasm.
■ Perfusion imaging with CT or MRI can be useful to identify regions of
potential brain ischemia.
■ Induction of HTN is recommended for patients with delayed cerebral
ischemia unless BP is elevated at baseline or cardiac status precludes it.
Cerebral angioplasty or selective intra-arterial vasodilator therapy is reason-
able in patients with symptomatic cerebral vasospasm, particularly those
who are not rapidly responding to hypertensive therapy.
Cerebral Vascular Accident (CVA):
Ischemic Stroke
CVA is a sudden disruption of blood flow to a part of the brain resulting in brain
tissue damage and neurological deficits. CVA is also called brain attack or
stroke.
Pathophysiology
■ Causes of CVA include thrombosis, embolism, systemic hypoperfusion.
Cocaine use doubles the risk of CVA.

NEURO