Diabetes mellitus increases risk of vasospasm following aneurysmal subarachnoid hemorrhage independent of glycemic control.

Objective: Symptomatic cerebral vasospasm (SCV) is a morbid sequela of subarachnoid hemorrhage (SAH). Its etiology is multifactorial and predicting onset can be challenging. Diabetes mellitus (DM) is known to affect vasoactive properties of vessels, but it has not been definitively correlated with SCV. We report that pre-existing DM is independently and strongly correlated with SCV, despite intensive glycemic control.

Methods: This is a retrospective chart review of all patients with aneurysmal subarachnoid hemorrhage (aSAH) admitted to a single academic medical center between January 2002 and January 2008 (n = 145). Patients presenting greater than 14 days after ictus, as well as those not surviving the first 3 days post-ictus were excluded from analysis. Remaining patients (n = 113) were assessed for study parameters including pre-existing DM, mean daily blood glucose, and additional known correlates to SCV. Multivariate analysis was performed to assess risk factors for SCV development. The primary outcome measure was SCV, defined as neurological change in conjunction with evidence of vessel spasm by either angiography or transcranial ultrasound.

Results: Of 113 patients included in the study, 42 (37%) had SCV. Patients with DM (80% incidence of SCV) had an increased risk of subsequently developing SCV (OR 9.90, P = 0.031). Elevated blood glucose was not associated with increased risk of vasospasm and no difference in glycemic control was noted between patients with or without DM. SCV resulted in worsened mortality and Glasgow Outcome Score for survivors (P < 0.005).

Conclusion: In this group of patients with SAH, diabetes mellitus is identified as a risk factor for development of SCV. Blood glucose management during hospitalization was similar in diabetics and non-diabetics, suggesting that the longstanding effects of microvascular disease may be more relevant in the development of SCV then acute glycemic control in these patients.