Persistent electrical storm following strong acid descaling agent ingestion successfully rescued with venoarterial extracorporeal membrane oxygenation: a case report.

backgroundIngestion of industrial strong acids is typically associated with corrosive injury to the gastrointestinal tract and severe metabolic disturbances. While cardiac complications are uncommon, the occurrence of a persistent electrical storm following strong acid ingestion is rarely documented. This case highlights a life-threatening manifestation of non-hydrofluoric acid poisoning, characterized by refractory ventricular arrhythmias and cardiogenic shock, which necessitated advanced extracorporeal life support. CASE PRESENTATION: A 62-year-old man accidentally ingested approximately 100 mL of a commercial descaling agent containing hydrochloric and sulfuric acids. He presented with hematemesis, profound metabolic acidosis, and severe ionized hypocalcemia. Approximately two hours after admission, the patient experienced a sudden loss of consciousness due to recurrent ventricular fibrillation. Despite repeated defibrillation, cardiopulmonary resuscitation (CPR), and administration of epinephrine, he experienced a persistent electrical storm and rapidly progressed to refractory cardiogenic shock. Venoarterial extracorporeal membrane oxygenation (VA-ECMO) was initiated as a physiological bridge for circulatory stabilization, alongside continuous renal replacement therapy (CRRT) to proactively manage metabolic triggers. Following the initiation of VA-ECMO, hemodynamic status improved promptly and ventricular arrhythmias ceased. Myocardial function gradually recovered, allowing for successful weaning from extracorporeal support after nine days. Subsequent endoscopy revealed severe corrosive gastritis and pyloric stenosis, managed via laparoscopic jejunostomy. The patient recovered without recurrent arrhythmia and was discharged in improved condition.

conclusionsIn our experience, strong acid ingestion can precipitate malignant ventricular arrhythmias and cardiogenic shock, likely mediated by profound metabolic acidosis and refractory hypocalcemia. This case suggests that caustic acid exposure carries a significant arrhythmogenic risk even in the absence of fluoride toxicity. Our findings indicate that timely escalation to VA-ECMO, combined with aggressive correction of metabolic disturbances, can be lifesaving when conventional therapies fail, providing a critical bridge to recovery for reversible toxin-induced myocardial instability.