51: Sudden and Acute Deterioration Post-VA ECMO Decannulation in Celphos Poisoning: A Case of Refractory Cardiogenic Shock and Neurological Injury

Introduction: Aluminum phosphide (celphos) poisoning causes severe cardiogenic shock, myocardial toxicity, and multi-organ failure, often requiring veno-arterial extracorporeal membrane oxygenation (VA-ECMO) for circulatory support. Delayed deterioration post-decannulation, along with the unpredictable toxic effects of celphos, complicates patient management. Case Presentation: A 25-year-old male presented with severe cardiogenic shock and ventricular tachycardia (VT) following celphos poisoning. Despite vasopressors and antiarrhythmics, he required VA-ECMO due to hemodynamic instability. After 24 hours on ECMO, he was decannulated with improved hemodynamics, though cardiac function remained compromised on 2D echocardiography. Hours post-decannulation, the patient deteriorated acutely, developing profound hypotension, recurrent VT, and acute kidney injury (AKI) with anuria, alongside reduced GCS. Despite escalation of inotropes, vasopressors, and antiarrhythmic drugs, conventional therapies failed to stabilize him. A delayed toxic effect of celphos was suspected. Re-institution of VA-ECMO was delayed by 18 hours due to logistical issues, during which the patient developed hypoxic brain injury. Once VA-ECMO was re-initiated, his hemodynamics stabilized, but neurological recovery was poor. He was discharged with a tracheostomy to a long-term care facility with significant neurological deficits. Conclusions: This case illustrates the acute deterioration that can occur after VA-ECMO decannulation in celphos poisoning, likely due to delayed toxic effects. The 18-hour delay in VA-ECMO re-initiation contributed to prolonged hypotension and severe neurological damage. Early recognition of deterioration and prompt ECMO access are critical for optimizing outcomes in such high-risk patients. VA-ECMO is crucial for managing cardiogenic shock in celphos poisoning, but delayed re-institution in cases of acute deterioration can result in poor neurological outcomes. Timely re-initiation of ECMO is essential to prevent irreversible damage.