Holding on by a Breath: Carbamazepine Overdose and Neurologic Dysfunction

Abstract

SESSION TITLE: Critical Care 1 SESSION TYPE: Affiliate Case Report Slide PRESENTED ON: Sunday, October 29, 2017 at 10:45 AM - 12:00 PM INTRODUCTION: Carbamazepine overdose is known to cause coma, however continuous electroencephalogram (cEEG) findings of a burst suppression pattern are rare. We report a case of carbamazepine overdose with cranial nerve (CN) areflexia, cEEG burst suppression pattern, and brain death mimicry with complete neurologic recovery. CASE PRESENTATION: A 54-year-old woman with a history of bipolar disorder was found unresponsive by her husband. An empty bottle of carbamazepine was identified by medical personnel. She was intubated for respiratory depression, and a neurological assessment revealed an absence of CN reflexes. Her initial carbamazepine level was 15ug/mL and peaked at 57ug/mL. There was concern for severe anoxic brain injury due to periods of apnea on the ventilator and complete CN areflexia. A cEEG revealed a burst suppression pattern. A computed tomography scan showed diffuse cerebral edema. Intermittent dialysis was initiated for treatment of severe carbamazepine toxicity. Five days following initial presentation, she regained all her CN reflexes. On day seven, she was extubated with complete neurological recovery and no evidence of neurological sequela. DISCUSSION: Carbamazepine is a frequently prescribed medication with well-known side effects. Carbamazepine toxicity producing CN areflexia with EEG burst suppression pattern has not been well described. A review of the literature revealed one case report of a patient presenting with burst suppression pattern, abundant epileptiform activity, and generalized seizures which resolved within 24 hours. Unfortunately, the patient expired and clinical correlation based on cEEG improvement could not be ascertained. In contrast, our patient had a prolonged course of CN areflexia and burst suppression, with complete neurological recovery. Typically, prolonged areflexia and an EEG burst suppression pattern are predictors of poor outcome in hypoxic-ischemic brain injuries. However, these predictors have not been well studied in patients with carbamazepine toxicity. CONCLUSIONS: Our case illustrates that CN areflexia and an EEG burst suppression pattern in carbamazepine toxicity may not be predictive of neurological outcome. Clinicians must be aware of the potentially reversible neurological sequelae following carbamazepine toxicity and refrain from early prognostication in this group of patients. Reference #1: De Rubeis DA, et al. Continuous EEG Monitoring in a Patient With Massive Carbamazepine Overdose, Journal of Clinical Neurophysiology 18(02):166-168 DISCLOSURE: The following authors have nothing to disclose: Susannah Kurtz, Adiac Espinosa Hernandez, Ismini Kourouni, Karishma Parekh, James Salonia No Product/Research Disclosure Information