Gunnar Bentsen1, Audun Stubhaug, Per K Eide. 1. Faculty of Medicine, Division of Anesthesiology and Intensive Care Medicine, Rikshospitalet University Hospital, University of Oslo, Oslo, Norway. gunnar.bentsen@rikshospitalet.no
Abstract
OBJECTIVE: A bolus infusion of 7.2% saline in 6% hydroxyethyl starch 200/0.5 (HS) attenuates static intracranial pressure (mean ICP) in subarachnoid hemorrhage patients. This study addressed how HS affects intracranial pulsatility, which is more indicative of intracranial compliance than static ICP. DESIGN: Retrospective analysis of prospectively collected data. SETTING: Intensive care unit in a university hospital. PATIENTS: Sedated and mechanically ventilated patients suffering from spontaneous subarachnoid hemorrhage. INTERVENTIONS: Twenty patients received an infusion of HS, mean 1.5 mL/kg. Static ICP was characterized by mean ICP and intracranial pulsatility by mean ICP wave amplitude, both parameters determined simultaneously during consecutive 6-sec time windows. We compared average values of these parameters during 15-min periods just before the infusion and after maximum effect was reached. MEASUREMENTS AND MAIN RESULTS: Mean ICP wave amplitude decreased 3.4 mm Hg from a baseline of 9.8 mm Hg, p < 0.0001. However, even though a target level of <15 mm Hg was reached for mean ICP in 65% of interventions, the target of <5 mm Hg for mean ICP wave amplitude was reached in only 30% of interventions. We found no correlation between changes in mean ICP wave amplitude and mean systemic arterial blood pressure wave amplitude, p = 0.27. CONCLUSIONS: The results confirm that osmotherapy attenuates both static ICP (mean ICP) and pulsatile ICP (mean ICP wave amplitude). Most importantly, however, during the majority of HS infusions, the target value of mean ICP wave amplitude was not reached even though the targets for mean ICP and mean cerebral perfusion pressure were reached. This suggests that the intracranial compliance state was still unfavorable even though mean ICP and mean cerebral perfusion pressure had reached normal ranges. The reduction in intracranial pulsatility could not be explained by attenuation in arterial pulsatility because there was no correlation between ICP and arterial blood pressure wave amplitudes.
OBJECTIVE: A bolus infusion of 7.2% saline in 6% hydroxyethyl starch 200/0.5 (HS) attenuates static intracranial pressure (mean ICP) in subarachnoid hemorrhagepatients. This study addressed how HS affects intracranial pulsatility, which is more indicative of intracranial compliance than static ICP. DESIGN: Retrospective analysis of prospectively collected data. SETTING: Intensive care unit in a university hospital. PATIENTS: Sedated and mechanically ventilated patients suffering from spontaneous subarachnoid hemorrhage. INTERVENTIONS: Twenty patients received an infusion of HS, mean 1.5 mL/kg. Static ICP was characterized by mean ICP and intracranial pulsatility by mean ICP wave amplitude, both parameters determined simultaneously during consecutive 6-sec time windows. We compared average values of these parameters during 15-min periods just before the infusion and after maximum effect was reached. MEASUREMENTS AND MAIN RESULTS: Mean ICP wave amplitude decreased 3.4 mm Hg from a baseline of 9.8 mm Hg, p < 0.0001. However, even though a target level of <15 mm Hg was reached for mean ICP in 65% of interventions, the target of <5 mm Hg for mean ICP wave amplitude was reached in only 30% of interventions. We found no correlation between changes in mean ICP wave amplitude and mean systemic arterial blood pressure wave amplitude, p = 0.27. CONCLUSIONS: The results confirm that osmotherapy attenuates both static ICP (mean ICP) and pulsatile ICP (mean ICP wave amplitude). Most importantly, however, during the majority of HS infusions, the target value of mean ICP wave amplitude was not reached even though the targets for mean ICP and mean cerebral perfusion pressure were reached. This suggests that the intracranial compliance state was still unfavorable even though mean ICP and mean cerebral perfusion pressure had reached normal ranges. The reduction in intracranial pulsatility could not be explained by attenuation in arterial pulsatility because there was no correlation between ICP and arterial blood pressure wave amplitudes.
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