Management of Aluminum Phosphide (Celphos) Poisoning
Aluminum phosphide poisoning requires immediate aggressive supportive care with no specific antidote available; survival depends on early gastric decontamination, hemodynamic support, and intensive monitoring, with emerging evidence supporting adjunctive therapies like magnesium sulfate and membrane stabilizers.
Immediate Decontamination and Safety Measures
Healthcare providers must use appropriate personal protective equipment when managing aluminum phosphide exposure to prevent secondary contamination. 1
Perform extensive gastric lavage immediately with a mixture of coconut oil and sodium bicarbonate solution to prevent further phosphine gas liberation and facilitate removal of unabsorbed tablets. 2, 3
Remove all contaminated clothing and perform copious irrigation with soap and water for any dermal exposure. 1
Critical Pathophysiology to Understand
Aluminum phosphide releases highly toxic phosphine gas upon contact with moisture in the gastrointestinal tract, which inhibits cytochrome oxidase and the electron transport chain, causing profound cellular hypoxia and myocardial suppression. 4, 5, 3
The mortality rate ranges from 70-100% with ingestion of as little as 150-500 mg, making this one of the most lethal poisonings encountered. 4
Spontaneous ignition can occur as a rare complication due to phosphine gas release. 6
Cardiovascular Management (Primary Cause of Death)
Establish invasive hemodynamic monitoring immediately as cardiovascular collapse is the predominant clinical presentation (58% of cases) and leading cause of death. 2, 4
Administer intravenous magnesium sulfate as a membrane stabilizer to counteract myocardial suppression and arrhythmias. 4, 3
Use vasopressors aggressively for refractory shock, as hypotension from direct myocardial toxicity is the primary mechanism of death. 3
Monitor continuously for cardiac arrhythmias ranging from ST-T changes to supraventricular tachycardia and fatal ventricular tachycardia. 4, 5
Consider advanced interventions like intra-aortic balloon pump or extracorporeal membrane oxygenation (ECMO) for severe refractory cardiogenic shock. 4
Adjunctive Pharmacotherapy (Emerging Evidence)
Administer trimetazidine as a cardioprotective agent to preserve myocardial function against phosphine-induced mitochondrial toxicity. 4
Give N-acetylcysteine, thiamine, vitamin C, and hydrocortisone as potential membrane stabilizers and antioxidants to decrease likelihood of fatal outcome. 4
These agents lack high-quality evidence but have shown promise in case reports and should be considered given the absence of specific antidotes and extremely high mortality. 4
Metabolic and Organ Support
Aggressively correct severe metabolic acidosis with sodium bicarbonate, as acidosis compounds cardiovascular collapse. 4, 3
Monitor closely for acute renal failure and provide renal replacement therapy if indicated. 4
Watch for hepatobiliary impairment as part of multi-organ dysfunction. 4
Monitoring and Duration of Care
Maintain intensive monitoring for at least 48-72 hours minimum, as delayed complications can occur even in initially stable patients. 7, 8
The mean ICU stay is approximately 5-6 days for survivors. 2
Serial assessment of cardiovascular status, renal function, acid-base balance, and cardiac rhythm is essential throughout hospitalization. 2, 3
Contact Expert Resources
- In the United States, immediately contact poison control at 1-800-222-1222 for expert guidance on case-specific management decisions. 8
Critical Pitfalls to Avoid
Do not delay gastric decontamination - early lavage with coconut oil and sodium bicarbonate mixture is one of the few interventions that may improve survival. 2, 3
Do not underestimate the lethality - even small ingestions (2 tablets = 6g) can be fatal despite aggressive management. 4
Do not rely on standard resuscitation protocols alone - aluminum phosphide requires specific adjunctive therapies beyond typical supportive care. 4, 3
Be prepared for spontaneous ignition during gastric lavage or autopsy due to phosphine gas release. 6