Artigo Acesso aberto Revisado por pares

The effect of nimodipine on cerebral oxygenation in patients with poor-grade subarachnoid hemorrhage

2004; American Association of Neurological Surgeons; Volume: 101; Issue: 4 Linguagem: Inglês

10.3171/jns.2004.101.4.0594

ISSN

1933-0693

Autores

Michael Stiefel, Gregory G. Heuer, John M. Abrahams, Stephanie Bloom, Michelle J. Smith, Eileen Maloney‐Wilensky, M. Sean Grady, Peter D. LeRoux,

Tópico(s)

Neurosurgical Procedures and Complications

Resumo

Object. Nimodipine has been shown to improve neurological outcome after subarachnoid hemorrhage (SAH); the mechanism of this improvement, however, is uncertain. In addition, adverse systemic effects such as hypotension have been described. The authors investigated the effect of nimodipine on brain tissue PO 2 . Methods. Patients in whom Hunt and Hess Grade IV or V SAH had occurred who underwent aneurysm occlusion and had stable blood pressure were prospectively evaluated using continuous brain tissue PO 2 monitoring. Nimodipine (60 mg) was delivered through a nasogastric or Dobhoff tube every 4 hours. Data were obtained from 11 patients and measurements of brain tissue PO 2 , intracranial pressure (ICP), mean arterial blood pressure (MABP), and cerebral perfusion pressure (CPP) were recorded every 15 minutes. Nimodipine resulted in a significant reduction in brain tissue PO 2 in seven (64%) of 11 patients. The baseline PO 2 before nimodipine administration was 38.4 ± 10.9 mm Hg. The baseline MABP and CPP were 90 ± 20 and 84 ± 19 mm Hg, respectively. The greatest reduction in brain tissue PO 2 occurred 15 minutes after administration, when the mean pressure was 26.9 ± 7.7 mm Hg (p < 0.05). The PO 2 remained suppressed at 30 minutes (27.5 ± 7.7 mm Hg [p < 0.05]) and at 60 minutes (29.7 ± 11.1 mm Hg [p < 0.05]) after nimodipine administration but returned to baseline levels 2 hours later. In the seven patients in whom brain tissue PO 2 decreased, other physiological variables such as arterial saturation, end-tidal CO 2 , heart rate, MABP, ICP, and CPP did not demonstrate any association with the nimodipine-induced reduction in PO 2 . In four patients PO 2 remained stable and none of these patients had a significant increase in brain tissue PO 2 . Conclusions. Although nimodipine use is associated with improved outcome following SAH, in some patients it can temporarily reduce brain tissue PO 2 .

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