Nicholas A Morris1, David Robinson2, J Michael Schmidt2, Hans Peter Frey2, Soojin Park2, Sachin Agarwal2, E Sander Connolly3, Jan Claassen4. 1. Department of Neurology, Program in Trauma, University of Maryland Medical Center, Baltimore, MD, United States. 2. Department of Neurology, Columbia University Medical Center, New York, NY, United States. 3. Department of Neurosurgery, Columbia University Medical Center, New York, NY, United States. 4. Department of Neurology, Columbia University Medical Center, New York, NY, United States. Electronic address: jc1439@cumc.columbia.edu.
Abstract
AIMS: The mechanism, effects, and outcomes of cardiac arrest (CA) caused by subarachnoid haemorrhage (SAH) remain unclear. We compared SAH patients presenting with CA to other high-grade SAH patients presenting without CA in order to better understand (1) the cause of CA, (2) cerebral pathophysiology following CA, and (3) outcomes of CA in patients with SAH. METHODS: We performed a retrospective analysis of a prospectively collected observational cohort. 31 Hunt-Hess 5 patients that presented with CA were compared to 146 Hunt-Hess 5 patients that presented without CA. Clinical and imaging findings were predefined and adjudicated. Cerebral physiology measures were available for a subset of patients, matched 1:1 by age. RESULTS: Twenty-two (71%) CA patients had pulseless electrical activity/asystole compared to 2 (6%) with a shockable rhythm. The CA patients were younger (OR 0.96, 95% CI 0.93-0.99, p=0.009), had more SAH on CT (OR 1.07, 95% CI 1.01-1.13, p=0.02), and had higher in-hospital mortality (87% vs. 58%, OR 6.2 (2.1-26.6), p=0.004). There were no differences in aneurysm location, cerebral herniation, or ictal seizures. Despite similar cerebral perfusion pressure, CA patients had pathologically lower brain tissue oxygenation, lower glucose, and higher lactate to pyruvate ratios. CONCLUSIONS: CA in SAH is associated with larger volume bleeds. Despite normal cerebral perfusion pressures, CA patients show compromised cerebral physiology.
AIMS: The mechanism, effects, and outcomes of cardiac arrest (CA) caused by subarachnoid haemorrhage (SAH) remain unclear. We compared SAHpatients presenting with CA to other high-grade SAHpatients presenting without CA in order to better understand (1) the cause of CA, (2) cerebral pathophysiology following CA, and (3) outcomes of CA in patients with SAH. METHODS: We performed a retrospective analysis of a prospectively collected observational cohort. 31 Hunt-Hess 5 patients that presented with CA were compared to 146 Hunt-Hess 5 patients that presented without CA. Clinical and imaging findings were predefined and adjudicated. Cerebral physiology measures were available for a subset of patients, matched 1:1 by age. RESULTS: Twenty-two (71%) CA patients had pulseless electrical activity/asystole compared to 2 (6%) with a shockable rhythm. The CA patients were younger (OR 0.96, 95% CI 0.93-0.99, p=0.009), had more SAH on CT (OR 1.07, 95% CI 1.01-1.13, p=0.02), and had higher in-hospital mortality (87% vs. 58%, OR 6.2 (2.1-26.6), p=0.004). There were no differences in aneurysm location, cerebral herniation, or ictal seizures. Despite similar cerebral perfusion pressure, CA patients had pathologically lower brain tissue oxygenation, lower glucose, and higher lactate to pyruvate ratios. CONCLUSIONS: CA in SAH is associated with larger volume bleeds. Despite normal cerebral perfusion pressures, CA patients show compromised cerebral physiology.
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