Cerebral Vasospasm

Recognize DCI at the bedside - New focal deficit, falling level of consciousness, headache, or confusion in the 3-to-14-day window. Deficits map to territory: MCA gives hemiparesis and aphasia in the dominant hemisphere, ACA gives leg weakness, drowsiness, and abulia, vertebrobasilar gives generalized depression of consciousness. Rule out raised ICP, hydrocephalus, rebleed, hypoxemia, and hyponatremia before calling it vasospasm.

Confirm it - Digital subtraction angiography is the gold standard. CT angiography with CT perfusion mean transit time is the common workhorse. Transcranial Doppler is the noninvasive bedside screen — mean flow velocities above 200 cm/second indicate severe proximal vasospasm, though TCD misses distal vessels. EEG can flag DCI 24-72 hours early by a falling alpha/delta ratio, which is most useful when the exam is already poor.

Nimodipine - Oral nimodipine for every SAH patient. It reduces DCI and improves neurologic outcomes.

Hyperdynamic therapy, not triple-H - Current management is fluid resuscitation to euvolemia plus induced hypertension once the aneurysm is secured, with systolic targets of 180-220 mm Hg or CPP above 80 mm Hg. Triple-H therapy (hypervolemia, hypertension, hemodilution) is no longer supported — it reversed spasm but bought pulmonary edema and other complications.

Do not anesthetize the pressure away - Induction agents and volatiles drop blood pressure, and this is the one patient where a "normal" MAP is a hypoperfusion event. Keep the pressor and inotrope infusions running and target the preoperative pressure through induction, positioning, and emergence.

Intra-arterial vasodilators spill over - Verapamil, nicardipine, papaverine, and nitroprusside given intra-arterially reach the systemic circulation. Have vasopressor boluses drawn and be ready to turn the infusion up. Verapamil and other cardiac depressants are best avoided when the heart is already stunned.

Airway - Most of these patients arrive intubated. General endotracheal anesthesia is the usual choice for endovascular treatment, for airway protection and because a confused, moving patient is not workable during angioplasty.

Oxygen delivery - Keep hemoglobin above 9 g/dL, avoid hypoxia, and optimize ICP. This is a supply-demand problem in a vessel that cannot dilate.

Volume targets - Normovolemia, with CVP 8-10 mm Hg or PCWP 14-16 mm Hg as the yardstick. Judicious fluid management limits volume overload, pulmonary edema, and worsening cardiac failure.

Stress-induced cardiomyopathy - Takotsubo or neurogenic stunned myocardium is common after SAH and undercuts your ability to deliver induced hypertension. Support with inotropes rather than escalating vasoconstriction into a failing ventricle.

Escalation - Balloon angioplasty or intra-arterial vasodilators are used for vasospasm refractory to hyperdynamic therapy, and are first line at some centers.

Cerebral vasospasm is a delayed, reversible narrowing of the cerebral arteries and arterioles, mostly the large proximal vessels of the circle of Willis. It classically appears 3 to 14 days after aneurysmal subarachnoid hemorrhage, but also follows AVM rupture, non-aneurysmal SAH, traumatic brain injury, and inflammatory conditions.

Hemoglobin breakdown products drive it: they release oxidative radicals and vasoconstrictors such as endothelin-1, scavenge nitric oxide, and trigger calcium release in vascular smooth muscle, all on top of inflammatory remodeling that narrows the arterial wall. Angiographic vasospasm appears in 60-90% of SAH patients but only about 30% become symptomatic. What matters clinically is delayed cerebral ischemia (DCI) — the infarction and mortality that follow. Perioperatively, a narrowed vessel plus a drop in perfusion pressure equals a stroke.