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• W4387248538 abstract "SESSION TITLE: Critical Care Case Report Posters 29 SESSION TYPE: Case Report Posters PRESENTED ON: 10/09/2023 02:10 pm - 02:55 pm INTRODUCTION: Laryngospasm is a rare side effect of ketamine and can precipitate negative pressure pulmonary edema due to patient inspiration against a closed airway. Here, we present a case of negative pressure pulmonary edema after ketamine-induced laryngospasm. CASE PRESENTATION: A 22-year-old with recently diagnosed hypertension presented to the emergency department after a witnessed seizure. Upon arrival, he was hypertensive to the 190s and afebrile. During the postictal period, he became described as violently agitated requiring mechanical and chemical restraints including lorazepam, midazolam, haloperidol, and diphenhydramine. As he remained combative, intravenous ketamine was given in 3 separate doses totaling 100mg over a 2 hour period. After the last dose, he was noted to have high pitched sonorous breathing with desaturations. During intubation he had notable laryngospasm and pulmonary edema radiographically and clinically with pink frothy secretions in his endotracheal tube With mechanical ventilatory support and a single dose of furosemide, his oxygen requirements dramatically improved within the first 4 hours and was extubated 36 hours after intubation. He had dramatic radiographic improvement as well. Of note, MRI brain showed signal abnormalities consistent with posterior reversible encephalopathy syndrome (PRES) likely related to his hypertension, and he was initiated on antihypertensive therapy. DISCUSSION: Laryngospasm is a reported serious side effect of most anesthetic agents, including ketamine. It occurs due to prolonged vocal cord adduction and treatment involves continuous positive pressure ventilation and succinylcholine administration.1 Delayed treatment of laryngospasm can rarely lead to negative pressure pulmonary edema (NPPE) due to vigorous inspiratory effort against an obstructed upper airway, resulting in generation of high negative intrathoracic pressures, increasing venous return and hydrostatic pressure.2 This capillary leak within the pulmonary circulation generates pink, frothy sputum characteristic of NPPE. Ketamine is also independently associated with inducing pulmonary edema by inhibiting alveolar sodium transport channels.3 Management involves positive pressure ventilation, and NPPE typically resolves within 12-48 hours with prompt intervention. Unlike cardiogenic pulmonary edema, diuretics are not indicated in NPPE and actually have been shown to worsen hypovolemia and hypoperfusion. CONCLUSIONS: Ketamine use is increasing today with its new applications in agitation and pain management ,and this case highlights the necessity of prompt recognition of its side effects, including laryngospasm. REFERENCE #1: Ead, Heather. Review of laryngospasm and noncardiogenic pulmonary edema. Dynamics (Pembroke, Ont.) 14, no. 3 (2003): 9-12. REFERENCE #2: 2. Lemyze, Malcolm, and Jihad Mallat. Understanding negative pressure pulmonary edema. Intensive care medicine 40 (2014): 1140-1143. REFERENCE #3: Cui, Yong, Hongguang Nie, Hong Ma, Lei Chen, Lin Zhang, Junke Wang, and Honglong Ji. Ketamine inhibits lung fluid clearance through reducing alveolar sodium transport. Journal of Biomedicine and Biotechnology 2011 (2011). DISCLOSURES: No relevant relationships by Ella Ishaaya No relevant relationships by Janine Vintch" @default.
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• W4387248538 date "2023-10-01" @default.
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• W4387248538 title "NEGATIVE PRESSURE PULMONARY EDEMA AFTER KETAMINE-INDUCED LARYNGOSPASM" @default.
• W4387248538 doi "https://doi.org/10.1016/j.chest.2023.07.1854" @default.
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