ArticleClinical medicine insights. Case reports2026
Reversible Atrial Fibrillation and Cardiogenic Shock Following Acute Aluminum Phosphide Poisoning: A Case Report and Literature Review.
Article in Clinical medicine insights. Case reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Successful rescue of a patient with extensive lethal-dose aluminum phosphide poisoning complicated by multiple organ dysfunction syndrome.The Journal of international medical research · 2026Article
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6 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Background: Aluminum phosphide (ALP) is a highly toxic pesticide widely used as a grain fumigant, especially in low- and middle-income countries. Ingestion of ALP releases phosphine gas, causing cellular oxidative damage and profound mitochondrial dysfunction. The cardiovascular system is particularly affected, typically resulting in refractory hypotension and dysrhythmias. There is no specific antidote, so management is entirely supportive. We report a case of intentional ALP ingestion leading to new-onset atrial fibrillation with rapid ventricular response and mild left ventricular dysfunction. Case Presentation: A 32-year-old Black African man presented 4 hours after ingesting 4 ALP tablets. He developed hypotension, tachycardia, and metabolic acidosis. Six hours into intensive care unit (ICU) care, he acutely developed atrial fibrillation with rapid ventricular response (heart rate ~140/minute) and persistent hypotension. Laboratory troponin remained normal, but echocardiography showed mild global left ventricular systolic dysfunction. Management and Outcome: The patient received aggressive supportive care, including intravenous fluids, vasopressors, corticosteroids, and repeated magnesium sulfate and electrolyte repletion. Amiodarone infusion was used for rate control (to avoid negative inotropic effects). No invasive therapies were needed. The atrial fibrillation reverted to sinus rhythm within 18 hours. Hemodynamics normalized over 24 to 48 hours, and the patient fully recovered without neurologic sequelae. On follow-up, cardiac function and electrocardiogram (ECG) were normal. Conclusion: This case highlights that surviving ALP-induced cardiotoxicity is possible with prompt aggressive supportive therapy. Key learning points include recognition of ALP ingestion in shock, vigilance for life-threatening arrhythmias, and tailored management (eg, use of amiodarone and careful fluid and pressor support). The patient's full recovery underscores that even severe ALP cardiotoxicity can be reversible with appropriate care.
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