Current options for the management of aneurysmal subarachnoid hemorrhage-induced cerebral vasospasm: a comprehensive review of the literature

Abstract

Objectives: Cerebral vasospasm is one of the leading causes of morbi-mortality following aneurysmal subarachnoid hemorrhage. The aim of this article is to discuss the current status of vasospasm therapy with emphasis on endovascular treatment.

Methods: A comprehensive review of the literature obtained by a PubMed search. The most relevant articles related to medical, endovascular and alternative therapies were selected for discussion.

Results: Current accepted medical options include the oral nimodipine and 'triple-H' therapy (hypertension, hypervolemia and hemodilution). Nimodipine remains the only modality proven to reduce the incidence of infarction. Although widely used, 'triple-H' therapy has not been demonstrated to significantly change overall outcome after cerebral vasospasm. Indeed, both induced hypervolemia and hemodilution may have deleterious effects, and more recent physiologic data favor normovolemia with induced hypertension or optimization of cardiac output. Endovascular options include percutaneous transluminal balloon angioplasty (PTA) and intra-arterial (IA) infusion of vasodilators. Multiple case reports and case series have been encountered in the literature using different drug regimens with diverse mechanisms of action. Compared with PTA, IA drug infusion has the advantages of distal penetration and a better safety profile. Its main disadvantages are the more frequent need for repeat treatments and its systemic hemodynamic repercussions. Alternative options using intraventricular/cisternal drug therapy and flow augmentation strategies have also shown possible benefits; however, their use is not yet as well established.

Conclusion: Blood pressure or cardiac output optimization should be the mainstay of hyperdynamic therapy. Endovascular treatment appears to have a positive impact on neurological outcome compared with the natural history of the disease. The role of intraventricular therapy and flow augmentation strategies in association with medical and endovascular treatment may, in the future, play a growing role in the management of patients with severe refractory vasospasm.

Keywords: Angioplasty; Delayed cerebral ischemia; Endovascular treatment; Intra-arterial drug infusion; Subarachnoid hemorrhage; Vasospasm.

Figures

Fig. 1

Angiograms of a 53-year-old gentleman who developed acute neurological symptoms (mental status changes and right hemiparesis) on post-SAH day 6 after a left posterior communicating artery aneurysm rupture. a A left internal carotid artery angiogram was performed, demonstrating severe proximal and distal vasospasm in the middle cerebral, anterior cerebral and posterior communicating arteries (arrows). IA nicardipine infusion was started and 15 mg of nicardipine were administered through the guide catheter. However, the patient developed refractory hypotension and the nicardipine was stopped; 5 mg of milrinone was then infused intra-arterially to complete the treatment. b Posttreatment image demonstrating near-complete reversal of the angiographic vasospasm (arrows).

Fig. 2

A 48-year-old lady who presented with Fisher grade III SAH (a). A CT angiogram was also performed, showing the baseline right middle cerebral artery (MCA) caliber (b). The patient developed a very subtle left pronator drift associated with an increase in TCD velocities in the right MCA on post-SAH day 4. A cerebral angiogram was performed, demonstrating severe vasospasm (c). She was treated with IA infusion of 15 mg of nicardipine through the right internal carotid artery, resulting in near-complete reversal of the vasospasm (d). The following day the patient was neurologically intact, but the TCD value was again markedly elevated in the right MCA territory. A CT angiogram and CT perfusion were performed, demonstrating a significant recurrent vasospasm in the right MCA with an increased mean transit time in its territory (e, f). The patient underwent a new angiogram, confirming severe vasospasm (g). She was successfully retreated with nicardipine and milrinone (h). The patient remained asymptomatic in the following days and was discharged with intact neurological and cognitive functions.