Electroconvulsive Therapy Induced Neurogenic Pulmonary Edema in a Survivor of Carbon Monoxide Poisoning: A Case Report.
Source: PubMed, NCBI / U.S. National Library of Medicine
Neurogenic pulmonary edema (NPE) is a life-threatening complication of severe central nervous system (CNS) injury. Carbon monoxide (CO) poisoning causes significant CNS insults, including direct neurotoxicity and autonomic dysfunction, creating a high-risk neurological state. Electroconvulsive therapy (ECT), while an effective treatment for severe depression, induces profound physiological stress that can exacerbate underlying neuropathology, thereby increasing the risk of NPE. We present the case of a 62-year-old male with severe depression who was hospitalized after a suicide attempt through CO poisoning, who developed NPE after undergoing his first ECT session. Shortly after the first ECT treatment, the patient became hypertensive, agitated and developed respiratory distress. NPE was diagnosed based on clinical findings and radiographic evidence of prominent pulmonary vasculature. Despite medical management, the patient required emergent intubation and intensive care unit (ICU) management. The patient's condition improved with supportive care, and he was successfully extubated the following day. ECT was discontinued. This case highlights a rare but severe complication of ECT in a patient with pre-existing CNS vulnerability from CO poisoning. The physiological stress from ECT likely precipitated the sympathetic surge leading to NPE. This report underscores the potential dangers of performing ECT after recent CO poisoning and, when considered with the related research discus
Abstract
Neurogenic pulmonary edema (NPE) is a life-threatening complication of severe central nervous system (CNS) injury. Carbon monoxide (CO) poisoning causes significant CNS insults, including direct neurotoxicity and autonomic dysfunction, creating a high-risk neurological state. Electroconvulsive therapy (ECT), while an effective treatment for severe depression, induces profound physiological stress that can exacerbate underlying neuropathology, thereby increasing the risk of NPE. We present the case of a 62-year-old male with severe depression who was hospitalized after a suicide attempt through CO poisoning, who developed NPE after undergoing his first ECT session. Shortly after the first ECT treatment, the patient became hypertensive, agitated and developed respiratory distress. NPE was diagnosed based on clinical findings and radiographic evidence of prominent pulmonary vasculature. Despite medical management, the patient required emergent intubation and intensive care unit (ICU) management. The patient's condition improved with supportive care, and he was successfully extubated the following day. ECT was discontinued. This case highlights a rare but severe complication of ECT in a patient with pre-existing CNS vulnerability from CO poisoning. The physiological stress from ECT likely precipitated the sympathetic surge leading to NPE. This report underscores the potential dangers of performing ECT after recent CO poisoning and, when considered with the related research discussed herein, suggests that recent CO poisoning should be considered a relative contraindication for ECT. Clinicians must be vigilant about this complication and be prepared for its management.