Abstract

SESSION TITLE: What's New in Critical Care?SESSION TYPE: Original Investigation PostersPRESENTED ON: 10/18/2022 01:30 pm - 02:30 pmPURPOSE: Cerebral edema is a leading cause of morbidity and mortality in patients with acute liver failure (ALF) that may require invasive intracranial pressure (ICP) monitoring to guide management. The prevalence and management of cerebral edema in the acute on chronic liver failure (ACLF) patient is less understood. There is limited knowledge on the impact each pathological state can have on cerebral hemodynamics, such as cerebral autoregulation. We report our novel experience of dynamic, invasive cerebral autoregulation (CA) monitoring in advanced grade liver failure patients.METHODS: Baseline demographics, clinical information, and multimodality neurologic monitoring data was collected in patients with advanced grade liver failure and grade 4 hepatic encephalopathy (HE). Invasive ICP monitor was placed when non-invasive neuromonitoring, neurological examination and brain imaging were concerning for cerebral edema and intracranial hypertension. Continuous physiologic data was recorded and retrospectively analyzed using ICM+ software (Cambridge, UK). Pressure Reactivity Index (PRx), a model-based index of dynamic CA, was calculated for the duration for the recording. Optimal Cerebral Perfusion Pressure (CPPopt) was calculated by plotting CPP versus PRx with the minimum CPP value of the U-shaped curve as optimal CPP. Data was analyzed by R studio and presented as mean ± standard deviation.RESULTS: Advanced liver failure patients with ALF (2/8) and ACLF (6/8) were admitted to a tertiary referral center intensive care unit. All had a 3T Glascow coma scale and met criteria for Grade 4 HE at the time of ICP monitor placement. On the day of monitoring, ACLF and ALF had similar trends in sodium (146.8±6.9 vs 142.5±0.71 mmol/L, p=0.22), arterial ammonia (168±101.4 vs 91±12.7 umol/L, p=0.17), and MELD-Na scores (27.8±5.8 vs 29.5±7.7 umol/L, p=0.37). There were no significant differences found in ICP (6.04mmHg vs 6.47mmHg, p=0.46), CPP (68.7mmHg vs 69.1mmHg, p=0.48), and PRx (0.473 vs 0.442, p=0.39) between ACLF and ALF respectively. Each patient spent at least 60% of time monitored within impaired CA (range 63% -92%). Given the degree of impaired CA, CPPopt was unable to be calculated. Only 2 of the 8 advanced liver failure patients survived to liver recovery. There were no observed differences in cerebral hemodynamics in survivors compared to the deceased [(ICP 6.03mmHg vs 6.42mmHg, p=0.47; CPP 69.05mmHg vs 68.3mmHg, p=0.38; PRx 0.55 vs 0.43, p=0.23)].CONCLUSIONS: Despite normal ICP and CPP values, a high prevalence of impaired CA was observed in liver failure patients with high grade HE.CLINICAL IMPLICATIONS: In comparison to ALF, these disturbances in CA during ACLF are likely under-recognized by clinicians. These results warrant future prospective studies on the potential clinical significance of these findings and to determine CA prognostic thresholds for the liver failure population.DISCLOSURES: No relevant relationships by Gianina FloccoNo relevant relationships by joao gomesNo relevant relationships by Catherine HassettNo relevant relationships by Aanchal KapoorAuthor relationship with Merck & Co; Merck Manuals Please note: 2020-present Added 04/14/2022 by Christina Lindenmeyer, value=Honoraria SESSION TITLE: What's New in Critical Care? SESSION TYPE: Original Investigation Posters PRESENTED ON: 10/18/2022 01:30 pm - 02:30 pm PURPOSE: Cerebral edema is a leading cause of morbidity and mortality in patients with acute liver failure (ALF) that may require invasive intracranial pressure (ICP) monitoring to guide management. The prevalence and management of cerebral edema in the acute on chronic liver failure (ACLF) patient is less understood. There is limited knowledge on the impact each pathological state can have on cerebral hemodynamics, such as cerebral autoregulation. We report our novel experience of dynamic, invasive cerebral autoregulation (CA) monitoring in advanced grade liver failure patients. METHODS: Baseline demographics, clinical information, and multimodality neurologic monitoring data was collected in patients with advanced grade liver failure and grade 4 hepatic encephalopathy (HE). Invasive ICP monitor was placed when non-invasive neuromonitoring, neurological examination and brain imaging were concerning for cerebral edema and intracranial hypertension. Continuous physiologic data was recorded and retrospectively analyzed using ICM+ software (Cambridge, UK). Pressure Reactivity Index (PRx), a model-based index of dynamic CA, was calculated for the duration for the recording. Optimal Cerebral Perfusion Pressure (CPPopt) was calculated by plotting CPP versus PRx with the minimum CPP value of the U-shaped curve as optimal CPP. Data was analyzed by R studio and presented as mean ± standard deviation. RESULTS: Advanced liver failure patients with ALF (2/8) and ACLF (6/8) were admitted to a tertiary referral center intensive care unit. All had a 3T Glascow coma scale and met criteria for Grade 4 HE at the time of ICP monitor placement. On the day of monitoring, ACLF and ALF had similar trends in sodium (146.8±6.9 vs 142.5±0.71 mmol/L, p=0.22), arterial ammonia (168±101.4 vs 91±12.7 umol/L, p=0.17), and MELD-Na scores (27.8±5.8 vs 29.5±7.7 umol/L, p=0.37). There were no significant differences found in ICP (6.04mmHg vs 6.47mmHg, p=0.46), CPP (68.7mmHg vs 69.1mmHg, p=0.48), and PRx (0.473 vs 0.442, p=0.39) between ACLF and ALF respectively. Each patient spent at least 60% of time monitored within impaired CA (range 63% -92%). Given the degree of impaired CA, CPPopt was unable to be calculated. Only 2 of the 8 advanced liver failure patients survived to liver recovery. There were no observed differences in cerebral hemodynamics in survivors compared to the deceased [(ICP 6.03mmHg vs 6.42mmHg, p=0.47; CPP 69.05mmHg vs 68.3mmHg, p=0.38; PRx 0.55 vs 0.43, p=0.23)]. CONCLUSIONS: Despite normal ICP and CPP values, a high prevalence of impaired CA was observed in liver failure patients with high grade HE. CLINICAL IMPLICATIONS: In comparison to ALF, these disturbances in CA during ACLF are likely under-recognized by clinicians. These results warrant future prospective studies on the potential clinical significance of these findings and to determine CA prognostic thresholds for the liver failure population. DISCLOSURES: No relevant relationships by Gianina Flocco No relevant relationships by joao gomes No relevant relationships by Catherine Hassett No relevant relationships by Aanchal Kapoor Author relationship with Merck & Co; Merck Manuals Please note: 2020-present Added 04/14/2022 by Christina Lindenmeyer, value=Honoraria

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