K S Olsen1, N Juul, G E Cold. 1. Department of Anesthesia and Intensive Care, Glostrup Hospital, University of Copenhagen, Denmark. kask@glostruphosp.kbhamt.dk
Abstract
BACKGROUND: The effect of alfentanil on intracranial pressure (ICP) in patients with supratentorial cerebral tumors has only been sparsely examined and with somewhat contradictory results. METHODS: Thirty-one patients were anesthetized with propofol and fentanyl. After removal of the bone flap a bolus-dose of alfentanil 10 (group 1), 20 (group 2), or 30 microg kg(-1) (group 3) was administered followed by an infusion of 10, 20, or 30 microg.kg(-1).h(-1) to patients in groups 1, 2, and 3, respectively. A control group received no alfentanil. Subdural ICP, mean arterial blood pressure (MAP), and cerebral perfusion pressure (CPP) were monitored and arterial and jugular bulb blood were sampled before and every minute for 5 min after the bolus administration of alfentanil and again after 5 min of hyperventilation to be able to calculate cerebral arterio-venous oxygen content difference (AVDO2) and carbon dioxide reactivity (CO2-reactivity). RESULTS: No changes in subdural ICP or AVDO2 from alfentanil in the study period were observed within the groups. However, alfentanil decreased MAP and CPP. The maximum CPP decrease (mean value of each group) was 4 mmHg, 8 mmHg, and 18 mmHg in groups 1, 2, and 3, respectively. There was no difference between groups as regards the CO2-reactivity. CONCLUSION: We conclude that administration of alfentanil to propofol-fentanyl anesthetized patients with supratentorial cerebral tumors decreases MAP and CPP in a dose-related way, but does not influence subdural ICP, AVDO2 or the CO2-reactivity.
RCT Entities:
BACKGROUND: The effect of alfentanil on intracranial pressure (ICP) in patients with supratentorial cerebral tumors has only been sparsely examined and with somewhat contradictory results. METHODS: Thirty-one patients were anesthetized with propofol and fentanyl. After removal of the bone flap a bolus-dose of alfentanil 10 (group 1), 20 (group 2), or 30 microg kg(-1) (group 3) was administered followed by an infusion of 10, 20, or 30 microg.kg(-1).h(-1) to patients in groups 1, 2, and 3, respectively. A control group received no alfentanil. Subdural ICP, mean arterial blood pressure (MAP), and cerebral perfusion pressure (CPP) were monitored and arterial and jugular bulb blood were sampled before and every minute for 5 min after the bolus administration of alfentanil and again after 5 min of hyperventilation to be able to calculate cerebral arterio-venous oxygen content difference (AVDO2) and carbon dioxide reactivity (CO2-reactivity). RESULTS: No changes in subdural ICP or AVDO2 from alfentanil in the study period were observed within the groups. However, alfentanil decreased MAP and CPP. The maximum CPP decrease (mean value of each group) was 4 mmHg, 8 mmHg, and 18 mmHg in groups 1, 2, and 3, respectively. There was no difference between groups as regards the CO2-reactivity. CONCLUSION: We conclude that administration of alfentanil to propofol-fentanyl anesthetized patients with supratentorial cerebral tumors decreases MAP and CPP in a dose-related way, but does not influence subdural ICP, AVDO2 or the CO2-reactivity.