Sylvia Bele1, Martin A Proescholdt2, Andreas Hochreiter3, Gerhard Schuierer4, Judith Scheitzach5, Christina Wendl6, Martin Kieninger7, Andre Schneiker8, Elisabeth Bründl9, Petra Schödel10, Karl-Michael Schebesch11, Alexander Brawanski12. 1. Department of Neurosurgery, University Medical Center Regensburg, Franz Josef Strauß Allee 11, 93053, Regensburg, Germany. sylvia.bele@ukr.de. 2. Department of Neurosurgery, University Medical Center Regensburg, Franz Josef Strauß Allee 11, 93053, Regensburg, Germany. martin.proescholdt@ukr.de. 3. Department of Neurosurgery, University Medical Center Regensburg, Franz Josef Strauß Allee 11, 93053, Regensburg, Germany. andreas.hochreiter@ukr.de. 4. Department of Neuroradiology, University Medical Center Regensburg, Franz Josef Strauß Allee 11, 93053, Regensburg, Germany. institut-nro-r@medbo.de. 5. Department of Neurosurgery, University Medical Center Regensburg, Franz Josef Strauß Allee 11, 93053, Regensburg, Germany. judith.scheitzach@ukr.de. 6. Department of Neuroradiology, University Medical Center Regensburg, Franz Josef Strauß Allee 11, 93053, Regensburg, Germany. christina.wendl@ukr.de. 7. Department of Anesthesiology, University Medical Center Regensburg, Franz Josef Strauß Allee 11, 93053, Regensburg, Germany. martin.kieninger@ukr.de. 8. Department of Anesthesiology, University Medical Center Regensburg, Franz Josef Strauß Allee 11, 93053, Regensburg, Germany. andre.schneiker@ukr.de. 9. Department of Neurosurgery, University Medical Center Regensburg, Franz Josef Strauß Allee 11, 93053, Regensburg, Germany. elisabeth.bruendl@ukr.de. 10. Department of Neurosurgery, University Medical Center Regensburg, Franz Josef Strauß Allee 11, 93053, Regensburg, Germany. petra.schoedel@ukr.de. 11. Department of Neurosurgery, University Medical Center Regensburg, Franz Josef Strauß Allee 11, 93053, Regensburg, Germany. karl-michael.schebesch@ukr.de. 12. Department of Neurosurgery, University Medical Center Regensburg, Franz Josef Strauß Allee 11, 93053, Regensburg, Germany. alexander.brawanski@ukr.de.
Abstract
BACKGROUND: Severe cerebral vasospasm is a major cause of death and disability in patients with aneurysmal subarachnoid hemorrhage. No causative treatment is yet available and hypertensive hypervolemic therapy (HHT) is often insufficient to avoid delayed cerebral ischemia and neurological deficits. We compared patients receiving continuous intra-arterial infusion of the calcium-antagonist nimodipine with a historical group treated with HHT and oral nimodipine alone. METHODS: Between 0.5 and 1.2 mg/h of nimodipine were continuously administered by intra-arterial infusion via microcatheters either into the internal carotid or vertebral artery or both, depending on the areas of vasospasm. The effect was controlled via multimodal neuromonitoring and transcranial Doppler sonography. Outcome was determined by means of the Glasgow Outcome Scale at discharge and 6 months after the hemorrhage and compared to a historical control group. RESULTS: Twenty-one patients received 28 intra-arterial nimodipine infusions. Six months after discharge, the occurrence of cerebral infarctions was significantly lower (42.6 %) in the nimodipine group than in the control group (75.0 %). This result was reflected by a significantly higher proportion (76.0 %) of patients with good outcome in the nimodipine-treated group, when compared to 10.0 % good outcome in the control group. Median GOS was 4 in the nimodipine group and 2 in the control group (p = 0.001). CONCLUSIONS: Continuous intra-arterial nimodipine infusion is an effective treatment for patients with severe cerebral vasospasm who fail to respond to HHT and oral nimodipine alone. Key to the effective administration of continuous intra-arterial nimodipine is multimodal neuromonitoring and the individual adaptation of dosage and time of infusion for each patient.
BACKGROUND: Severe cerebral vasospasm is a major cause of death and disability in patients with aneurysmal subarachnoid hemorrhage. No causative treatment is yet available and hypertensive hypervolemic therapy (HHT) is often insufficient to avoid delayed cerebral ischemia and neurological deficits. We compared patients receiving continuous intra-arterial infusion of the calcium-antagonist nimodipine with a historical group treated with HHT and oral nimodipine alone. METHODS: Between 0.5 and 1.2 mg/h of nimodipine were continuously administered by intra-arterial infusion via microcatheters either into the internal carotid or vertebral artery or both, depending on the areas of vasospasm. The effect was controlled via multimodal neuromonitoring and transcranial Doppler sonography. Outcome was determined by means of the Glasgow Outcome Scale at discharge and 6 months after the hemorrhage and compared to a historical control group. RESULTS: Twenty-one patients received 28 intra-arterial nimodipine infusions. Six months after discharge, the occurrence of cerebral infarctions was significantly lower (42.6 %) in the nimodipine group than in the control group (75.0 %). This result was reflected by a significantly higher proportion (76.0 %) of patients with good outcome in the nimodipine-treated group, when compared to 10.0 % good outcome in the control group. Median GOS was 4 in the nimodipine group and 2 in the control group (p = 0.001). CONCLUSIONS: Continuous intra-arterial nimodipine infusion is an effective treatment for patients with severe cerebral vasospasm who fail to respond to HHT and oral nimodipine alone. Key to the effective administration of continuous intra-arterial nimodipine is multimodal neuromonitoring and the individual adaptation of dosage and time of infusion for each patient.
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