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      Case report: Invasive neuromonitoring in status epilepticus induced hypoxic ischemic brain injury

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          Abstract

          Objectives

          Literature on invasive neuromonitoring and bilateral decompressive craniectomies (BDC) in patients with refractory status epilepticus (RSE)-mediated hypoxic-ischemic brain injury (HIBI) is limited. Neuromonitoring can guide decision making and treatment escalation.

          Methods and results

          We report a case of a 17 years-old male who was admitted to our hospital’s intensive care unit for RSE. HIBI was detected on neuroimaging on this patient’s second day of admission after he developed central diabetes insipidus (DI). Invasive neuromonitoring revealed raised intracranial pressure (ICP) and brain hypoxia as measured by reduced brain tissue oxygen tension (PbtO 2). Treatments were escalated in a tiered fashion, including administration of hyperosmolar agents, analgesics, sedatives, and a neuromuscular blocking drug. Eventually, BDC was performed as a salvage therapy as a means of controlling refractory ICP crisis in the setting of diffuse cerebral edema (DCE) following HIBI.

          Discussion

          SE-mediated HIBI can result in refractory ICP crisis. Neuromonitoring can help identify secondary brain injury (SBI), guide treatment strategies, including surgical interventions, and may lead to better outcomes.

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          Most cited references27

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          Guidelines for the evaluation and management of status epilepticus.

          Status epilepticus (SE) treatment strategies vary substantially from one institution to another due to the lack of data to support one treatment over another. To provide guidance for the acute treatment of SE in critically ill patients, the Neurocritical Care Society organized a writing committee to evaluate the literature and develop an evidence-based and expert consensus practice guideline. Literature searches were conducted using PubMed and studies meeting the criteria established by the writing committee were evaluated. Recommendations were developed based on the literature using standardized assessment methods from the American Heart Association and Grading of Recommendations Assessment, Development, and Evaluation systems, as well as expert opinion when sufficient data were lacking.
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            Nonconvulsive electrographic seizures after traumatic brain injury result in a delayed, prolonged increase in intracranial pressure and metabolic crisis.

            To determine whether nonconvulsive electrographic post-traumatic seizures result in increases in intracranial pressure and microdialysis lactate/pyruvate ratio. Prospective monitoring with retrospective data analysis. Single center academic neurologic intensive care unit. Twenty moderate to severe traumatic brain injury patients (Glasgow Coma Score 3-13). Continuous electroencephalography and cerebral microdialysis were performed for 7 days after injury. Ten patients had seizures and were compared with a matched cohort of traumatic brain injury patients without seizures. The seizures were repetitive and constituted status epilepticus in seven of ten patients. Using a within-subject design, post-traumatic seizures resulted in episodic increases in intracranial pressure (22.4 +/- 7 vs. 12.8 +/- 4.3 mm Hg; p < .001) and an episodic increase in lactate/pyruvate ratio (49.4 +/- 16 vs. 23.8 +/- 7.6; p < .001) in the seizure group. Using a between-subjects comparison, the seizure group demonstrated a higher mean intracranial pressure (17.6 +/- 6.5 vs. 12.2 +/- 4.2 mm Hg; p < .001), a higher mean lactate/pyruvate ratio (38.6 +/- 18 vs. 27 +/- 9; p < .001) compared with nonseizure patients. The intracranial pressure and lactate/pyruvate ratio remained elevated beyond postinjury hour 100 in the seizure group but not the nonseizure group (p < .02). Post-traumatic seizures result in episodic as well as long-lasting increases in intracranial pressure and microdialysis lactate/pyruvate ratio. These data suggest that post-traumatic seizures represent a therapeutic target for patients with traumatic brain injury.
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              Ketamine to treat super-refractory status epilepticus

              To test ketamine infusion efficacy in the treatment of super-refractory status epilepticus (SRSE), we studied retrospectively SRSE patients who were treated with ketamine. Additionally, we studied the effect of high doses of ketamine on brain physiology as reflected by invasive multimodality monitoring (MMM). We studied a consecutive series of 68 SRSE patients who were admitted between 2009 and 2018, were treated with ketamine and monitored with scalp EEG. Eleven of these patients underwent MMM at the time of ketamine administration. We compared patients who had seizure cessation after ketamine initiation to those who did not. Mean age was 53+/-18 years old, 46% of patients were female. Seizure burden decreased by at least 50% within 24 hours of starting ketamine in 55 (81%) patients, with complete cessation in 43 (63%). Average dose of ketamine infusion was 2.2+/-1.8 mg/kg/h, with median duration of 2 (1; 4) days. Average dose of midazolam was 1.0+/-0.8 mg/kg/h at the time of ketamine initiation and was started at a median of 0.4 (0.1; 1.0) days before ketamine. Using a generalized linear mixed effect model, ketamine was associated with stable mean arterial pressure (OR 1.39, 95% CI 1.38-1.40), and with decreased in vasopressor requirements over time. We found no effect on intracranial pressure, cerebral blood flow, and cerebral perfusion pressure. Ketamine treatment was associated with a decrease in seizure burden in patients with SRSE. Our data support the notion that high dose ketamine infusions are associated with decreased vasopressor requirements without increased intracranial pressure. This study provides Class IV evidence that ketamine decreases seizures in patients with SRSE.
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                Author and article information

                Contributors
                URI : https://loop.frontiersin.org/people/2416125/overviewRole: Role:
                Role: Role:
                Journal
                Front Neurol
                Front Neurol
                Front. Neurol.
                Frontiers in Neurology
                Frontiers Media S.A.
                1664-2295
                30 November 2023
                2023
                : 14
                : 1284098
                Affiliations
                Neurological Institute, Cooper University Hospital , Camden, NJ, United States
                Author notes

                Edited by: Sean Ruland, Loyola University Medical Center, United States

                Reviewed by: Lauren Koffman, Temple University Hospital, United States; Rick Gill, Loyola University Chicago, United States; Sanam Baghshomali, Temple University Hospital, United States; Xin Zhou, Temple University Health System, Inc, United States

                *Correspondence: Karandeep Singh Bhatti, karandeepsinghbhatti22@ 123456gmail.com
                Article
                10.3389/fneur.2023.1284098
                10720614
                38099068
                f1b8f73f-6f67-4990-8d63-c5f9c4e044af
                Copyright © 2023 Bhatti and Rajagopalan.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                : 27 August 2023
                : 08 November 2023
                Page count
                Figures: 4, Tables: 0, Equations: 0, References: 27, Pages: 7, Words: 4506
                Funding
                The author(s) declare that no financial support was received for the research, authorship, and/or publication of this article.
                Categories
                Neurology
                Case Report
                Custom metadata
                Neurocritical and Neurohospitalist Care

                Neurology
                invasive neuromonitoring,diffuse cerebral edema,continuous eeg monitoring,bilateral decompressive craniectomy,refractory intracranial hypertension,icp monitoring,refractory status epilepctius,brain tissue oxygen monitoring

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