Mypinder S Sekhon1, Donald E Griesdale2, Philip N Ainslie3, Peter Gooderham4, Denise Foster5, Marek Czosnyka6, Chiara Robba6, Danilo Cardim7. 1. Division of Critical Care Medicine, Department of Medicine, Vancouver General Hospital, West 12th Avenue, University of British Columbia, Vancouver, BC, V5Z 1M9, Canada. Electronic address: Mypinder.Sekhon2@vch.ca. 2. Division of Critical Care Medicine, Department of Medicine, Vancouver General Hospital, West 12th Avenue, University of British Columbia, Vancouver, BC, V5Z 1M9, Canada; Department of Anaesthesiology, Pharmacology and Therapeutics, Vancouver General Hospital, West 12th Avenue, University of British Columbia, Vancouver, BC, V5Z 1M9, Canada; Centre for Clinical Epidemiology and Evaluation, Vancouver Coastal Health Research Institute, 899 West 12th Avenue, University of British Columbia, Vancouver, BC, V5Z 1M9, Canada. 3. Department of Health and Exercise Sciences, University of British Columbia - Okanagan, Kelowna, BC, Canada. 4. Division of Neurosurgery, Department of Surgery, Vancouver General Hospital, West 12th Avenue, University of British Columbia, Vancouver, BC, V5Z 1M96, Canada. 5. Division of Critical Care Medicine, Department of Medicine, Vancouver General Hospital, West 12th Avenue, University of British Columbia, Vancouver, BC, V5Z 1M9, Canada. 6. Department of Clinical Neurosciences, Division of Neurosurgery, Addenbrookes Hospital, University of Cambridge, Cambridge, United Kingdom. 7. Department of Anaesthesiology, Pharmacology and Therapeutics, Vancouver General Hospital, West 12th Avenue, University of British Columbia, Vancouver, BC, V5Z 1M9, Canada.
Abstract
INTRODUCTION: In hypoxic ischemic brain injury (HIBI), increased intracranial pressure (ICP) can ensue from cerebral edema stemming from cytotoxic and vasogenic mechanisms. Downstream sequelae of restricted cerebral blood flow lead to neurologic braindeath. There is limited data characterizing the temporal trends and patterns of ICP and compliance in human HIBI patients. METHODS: Patients underwent invasive ICP monitoring with a parenchymal probe (Camino) and were managed with a tier-based management algorithm for elevated ICP. Data pertaining to mean arterial pressure (MAP), ICP, brain tissue oxygenation (PbtO2), end tidal carbon dioxide (ETCO2), core body temperature and RAP (moving correlation coefficient between mean ICP and its mean pulse amplitude) as a measure of intracranial compliance were recorded in the ICM + software. Data pertaining to ICP lowering interventions was also collected. RESULTS: Ten patients were included with a median age of 47 (range 20-71) and seven were male (7/10). The mean ICP was 14 mmHg (SD 11) and time of ICP> 20 mmHg was 22% (range 0-100). The mean MAP, ETCO2 and temperature were 89 mmHg (SD 13), 31 mmHg (SD 7), 35.7 °C (SD 0.9), respectively. The mean RAP was 0.58 (SD 0.34) and time of RAP > 0.4 was 78% (range 57-97). There were no significant relationships between ETCO2 and temperature with ICP. CONCLUSIONS: In our cohort, HIBI was characterized by normal ICP but with limited intracranial compliance. However, significant in between patient heterogeneity exists with respect to temporal patterns of intracranial pressure - volume relationships in HIBI. TRIAL REGISTRATION: clinicaltrials.gov (NCT03609333). Crown
INTRODUCTION: In hypoxic ischemic brain injury (HIBI), increased intracranial pressure (ICP) can ensue from cerebral edema stemming from cytotoxic and vasogenic mechanisms. Downstream sequelae of restricted cerebral blood flow lead to neurologic braindeath. There is limited data characterizing the temporal trends and patterns of ICP and compliance in human HIBI patients. METHODS:Patients underwent invasive ICP monitoring with a parenchymal probe (Camino) and were managed with a tier-based management algorithm for elevated ICP. Data pertaining to mean arterial pressure (MAP), ICP, brain tissue oxygenation (PbtO2), end tidal carbon dioxide (ETCO2), core body temperature and RAP (moving correlation coefficient between mean ICP and its mean pulse amplitude) as a measure of intracranial compliance were recorded in the ICM + software. Data pertaining to ICP lowering interventions was also collected. RESULTS: Ten patients were included with a median age of 47 (range 20-71) and seven were male (7/10). The mean ICP was 14 mmHg (SD 11) and time of ICP> 20 mmHg was 22% (range 0-100). The mean MAP, ETCO2 and temperature were 89 mmHg (SD 13), 31 mmHg (SD 7), 35.7 °C (SD 0.9), respectively. The mean RAP was 0.58 (SD 0.34) and time of RAP > 0.4 was 78% (range 57-97). There were no significant relationships between ETCO2 and temperature with ICP. CONCLUSIONS: In our cohort, HIBI was characterized by normal ICP but with limited intracranial compliance. However, significant in between patient heterogeneity exists with respect to temporal patterns of intracranial pressure - volume relationships in HIBI. TRIAL REGISTRATION: clinicaltrials.gov (NCT03609333). Crown
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