• Miriam M Treggiari, Bernhard Walder, Peter M Suter, and Jacques-André Romand.
• Division of Surgical Intensive Care, Department of Anesthesia, Pharmacology, and Surgical Intensive Care, University Hospitals, Geneva, Switzerland. treggmm@u.washington.edu
• J. Neurosurg. 2003 May 1; 98 (5): 978-84.

ObjectThere is uncertainty about the efficacy of hypertension, hypervolemia, and hemodilution (triple-H) therapy in reducing the occurrence of delayed ischemic neurological deficits (DINDs) and death after subarachnoid hemorrhage. The authors therefore conducted a systematic review to evaluate the efficacy of triple-H prevention in decreasing the rate of clinical vasospasm, DINDs, and death.MethodsThe authors systematically reviewed studies identified based on a MEDLINE, EMBASE, and COCHRANE Register search of articles published between 1966 and 2001, and reference lists of identified articles. An independent assessment of each study's methodological quality, population, intervention, and outcomes (rates of symptomatic vasospasm, DINDs, and death) was performed. Summary relative risk estimates were calculated for the main outcomes using fixed- or random-effect models, as appropriate. Only four prospective, comparative studies with a total of 488 patients were identified. The median internal validity score was 0.5 (range 0-2); the median external validity score was 3 (range 2-6). Compared with no prevention, triple-H therapy was associated with a reduced risk of symptomatic vasospasm (relative risk [RR] 0.45, 95% confidence interval [CI] 0.32-0.65), but not DIND (RR 0.54, 95% CI 0.2-1.49). The risk of death was higher (RR 0.68, 95% CI 0.53-0.87). Sensitivity analyses including only randomized, controlled trials showed no evidence of statistically significant results for these major end points.ConclusionsThe paucity of information and important limitations in the design of the studies analyzed preclude evaluation of the efficacy of triple-H prevention and formulation of any recommendations regarding its use for the prevention of cerebral vasospasm.

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