Introduction Aneurysmal subarachnoid hemorrhage (SAH) is associated with high morbidity and mortality primarily attributed to the delayed onset of cerebral vasospasm. Patient outcomes after aneurysmal SAH have considerably improved largely due to early intervention, aggressive treatment and advances in endovascular and surgical techniques. The understanding of cerebral vasospasm and SAH has significantly improved; however, an effective solution remains elusive and the condition continues to cause devastation.

Materials and methods We retrospectively analyzed 180 vasospasm cases at our institution from October 2001 through May 2008. The ruptured aneurysms were treated via endovascular coiling and open surgical clipping. Our current treatment archetype is to perform diagnostic cerebral angiography as early as possible on patients with symptomatic or severe vasospasm indicated by transcranial Doppler or CT angiography, mitigated by the use of intravenous vasopressors. All patients receive oral nimodipine and intravenous magnesium supplementation as tolerated, and often received intravenous nicardipine for blood pressure control. Our drug of choice for intra-arterial injection is nicardipine delivered via selective guide catheter placement, unless hyperselective microcatheter injection is more prudent. We frequently add intra-arterial milrinone; however, we feel its duration of action is significantly shorter than nicardipine. After two endovascular treatments we discontinue heparin and often substitute intravenous argatroban for prevention or treatment of heparin induced thrombocytopenia II.

Results A total of 33 patients (Hunt and Hess scores (HH) 1–2, six; HH 3, 12; HH 4–5, 15) were treated with balloon angioplasty. Two (6.06%) were discharged with modified Rankin Scale (mRS) 0–2, 21 (63.64%) were mRS 3–5 and 10 (30.3%) died.

Including the full range of HH classifications, 49.4% of the patients experienced a stroke before vasospasm treatment was initiated; only 11.7% presented with infarct.

The distributions of clinical grades are HH 1–2, 29.5% and HH 3, 30.0%. Of note, 40.5% of our total cases in this retrospective review were HH 4–5 on admission; most experienced an unfavorable outcome.

Our data suggest that HH 3 patients demonstrate an increased risk for unfavorable outcome. Of the patients in this cohort who did poorly, approximately 53.7% suffered from a cerebral ischemic event before vasospasm treatment. While this cohort presented with mild clinical deficits, our data suggest delay in treatment of cerebral vasospasm adversely affects outcome.

Conclusion The most tenable conclusion from our data is the need for earlier detection and treatment of cerebral vasospasm. Our results may indicate that the HH 3 population would demonstrate the most improvement from intervention; however, a larger prospective, randomized study is needed to validate this assumption. The cohort of patients who demonstrated the worst outcomes was those who underwent balloon angioplasty, regardless of concomitant intra-arterial vasodilator therapy or other concomitant therapies. Use of balloon angioplasty is variable among physicians but is generally reserved for patients who do not respond to intra-arterial nicardipine and/or milrinone. Due to the non-randomized, retrospective nature of these data, no conclusions can be drawn from the treatment course; however, cerebral vasospasm is a complex multifactorial problem and its prevention and successful treatment will most likely require a combination of approaches.