What is the management of vasospasm post intracranial aneurysm (cerebral aneurysm) coiling procedure?

From the Guidelines

Vasospasm monitoring after intracranial aneurysm coiling is crucial, and management includes prophylactic nimodipine (60mg orally every 4 hours for 21 days) to reduce poor outcomes related to vasospasm, as recommended by the American Heart Association 1.

Key Considerations

• The highest risk period for vasospasm is days 3-14 post-procedure, and monitoring typically occurs for 14-21 days.
• Daily neurological examinations and transcranial Doppler ultrasonography are recommended to detect early vasospasm.
• If vasospasm is detected or suspected, immediate intervention includes induced hypertension (systolic blood pressure 160-180 mmHg) using vasopressors like norepinephrine or phenylephrine, maintenance of euvolemia, and consideration of endovascular therapy for refractory cases.

Endovascular Options

• Intra-arterial vasodilators (verapamil 2.5-10mg, nicardipine 2.5-5mg, or milrinone 5-15mg) or balloon angioplasty for accessible vessels larger than 2mm may be considered.
• The use of cerebral angioplasty and/or selective intra-arterial vasodilator therapy is reasonable in patients with symptomatic cerebral vasospasm, particularly those who are not rapidly responding to hypertensive therapy 1.

Importance of Early Detection and Intervention

• Cerebral vasospasm can lead to delayed cerebral ischemia, which significantly increases morbidity and mortality following aneurysmal subarachnoid hemorrhage.
• Early detection and prompt intervention are essential to prevent permanent neurological deficits.
• Maintenance of euvolemia and normal circulating blood volume is recommended to prevent delayed cerebral ischemia (DCI), and induction of hypertension is recommended for patients with DCI unless blood pressure is elevated at baseline or cardiac status precludes it 1.

From the FDA Drug Label

Although the clinical studies described below demonstrate a favorable effect of nimodipine on the severity of neurological deficits caused by cerebral vasospasm following SAH, there is no arteriographic evidence that the drug either prevents or relieves the spasm of these arteries Nimodipine has been shown, in 4 randomized, double-blind, placebo-controlled trials, to reduce the severity of neurological deficits resulting from vasospasm in patients who have had a recent subarachnoid hemorrhage (SAH).

Vasospasm post intracranial aneurysm coiling period can be managed with nimodipine, as it has been shown to reduce the severity of neurological deficits resulting from vasospasm in patients with subarachnoid hemorrhage (SAH) 2 3.

• The mechanism of action of nimodipine is as a calcium channel blocker, which inhibits contractions of vascular smooth muscle.
• Clinical trials have demonstrated a favorable effect of nimodipine on the severity of neurological deficits caused by cerebral vasospasm following SAH. However, there is no arteriographic evidence that the drug either prevents or relieves the spasm of these arteries.

From the Research

Vasospasm Post Intracranial Aneurysm Coiling Period

• Vasospasm is a common cause of mortality and morbidity following rupture of intracranial aneurysm 4.
• Hemodynamic therapy, angioplasty, and intra-arterial infusion of vasodilators are used to treat vasospasm, but no case control studies exist proving the superiority of one method over the others 4.
• Intra-arterial nimodipine (IAN) has been shown to cause immediate angiographic reversal of vasospasm in majority of patients, but this does not necessarily translate into a long lasting clinical response 4, 5.
• The final outcome in patients who received hemodynamic therapy is comparable to those who received additional IAN 4.
• IAN does not appear to provide a major added advantage over the conventional hemodynamic therapy 4.
• Long-term, continuous intra-arterial nimodipine treatment can be applied as a rescue therapy with relative safety for more than 2 weeks to prevent secondary cerebral ischemia in well-selected patients with prolonged severe macrovasospasm 6.
• Aggressive endovascular treatment of patients with unsecured ruptured cerebral aneurysm and associated vasospasm is safe and effective, and can improve outcome in each patient 7.

Treatment Options

• Intra-arterial nimodipine (IAN) is a treatment option for vasospasm, but its effectiveness is still being studied 4, 5, 6.
• Hemodynamic therapy is a conventional treatment option for vasospasm, and its outcome is comparable to IAN 4.
• Angioplasty is another treatment option for vasospasm, and can be performed alone or in combination with IAN and aneurysm embolization 8, 7.
• Aneurysm embolization is a treatment option for unsecured ruptured cerebral aneurysm, and can be performed in combination with angioplasty and IAN 7.

Outcome

• The outcome of patients with vasospasm can be improved with aggressive endovascular treatment, including angioplasty, IAN, and aneurysm embolization 7.
• Long-term, continuous intra-arterial nimodipine treatment can improve outcome in well-selected patients with prolonged severe macrovasospasm 6.
• The final outcome in patients who received hemodynamic therapy is comparable to those who received additional IAN 4.
• A good clinical recovery was seen in almost half of the patients after 6 months of treatment with IAN 5.