• A Raabe, J Beck, J Berkefeld, W Deinsberger, J Meixensberger, P Schmiedek, V Seifert, H Steinmetz, A Unterberg, P Vajkoczy, C Werner, and Deutschen Gesellschaft für Anästhesiologie und Intensivmedizin.
• Klinik und Poliklinik für Neurochirurgie, Klinikum der Johann-Wolfgang-Goethe-Universität Frankfurt am Main, Germany. A.Raabe@em.uni-frankfurt.de
• Zentralbl. Neurochir. 2005 May 1;66(2):79-91.

AbstractAfter SAH, primary and secondary complications are frequent and often require neurosurgical interventions to avoid secondary brain damage. The authors of the present paper have summarized the available data about the treatment modalities often used for patients with SAH. The present recommendations have been developed as a neurosurgical and neuroanestesiological consensus. Evidence from prospective, randomized, double blind, placebo-controlled studies support grade A recommendations (standard) for the prophylaxis and treatment of cerebral vasospasm with oral Nimodipine in good grade patients. For intravenous Nimodipine or for oral nimodipine treatment in poor grade patients, available data only support grade C recommendations (options). Despite the lack of data supporting standards (grade A) or guidelines (grade B), avoidance and rigorous treatment of hypotension and hypovolemia remains the mainstay in the prophylaxis and treatment of a delayed ischemic neurological deficit (DIND). Prophylactic hypervolemia or prophylactic hypertension and hypervolemia was shown to be ineffective in reducing symptomatic vasospasm and improving outcome (grade B). Therapeutic hypertensive hypervolemic hemodilution is recommended as a treatment of symptomatic vasospasm but no prospective studies are available (grade C recommendation). Suggested target values for moderate triple-H-therapy are CPP 80- 120 mmHg (MAP 90-130), CVP > 7 mmHg and Hk 0.25-0.40. Balloon angioplasty should be considered for treatment of DIND cause by focal, proximal cerebral vasospasm. There is no evidence supporting the routine use of antifibrinolyticals, steroids or anticonvulsive prophylaxis. Clinical data indicate that current prophylaxis and treatment of cerebral vasospasm is still insufficient and aggressive triple-H-therapy is associated with an increased incidence of complications.

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