Phosphoridine (Pralidoxime) Should NOT Be Used for Aluminum Phosphide Poisoning
Phosphoridine (pralidoxime) has no role in treating aluminum phosphide poisoning and should never be administered. Aluminum phosphide is not an organophosphate compound, and pralidoxime is specifically designed to reactivate acetylcholinesterase inhibited by organophosphates—a mechanism completely unrelated to aluminum phosphide toxicity. 1, 2, 3
Critical Distinction: Different Toxins, Different Mechanisms
Why This Confusion Exists
The similar names can be misleading:
- Aluminum phosphide releases phosphine gas, which causes cellular hypoxia by inhibiting cytochrome c oxidase and disrupting mitochondrial function 4, 5
- Organophosphates inhibit acetylcholinesterase at cholinergic synapses, causing cholinergic crisis 3
These are completely different poisoning syndromes requiring entirely different management approaches.
Pralidoxime's Mechanism Is Irrelevant to Aluminum Phosphide
Pralidoxime works by reactivating acetylcholinesterase that has been covalently bound by organophosphate molecules at nicotinic receptors. 3 This mechanism has zero applicability to aluminum phosphide poisoning, where the primary pathology is mitochondrial dysfunction and cellular hypoxia from phosphine gas. 4, 5
What Actually Works for Aluminum Phosphide Poisoning
There is no specific antidote for aluminum phosphide poisoning. 2, 4, 6 Management is entirely supportive with aggressive early intervention:
Immediate Supportive Care (First 30 Minutes)
- Aggressive fluid resuscitation: 30 mL/kg isotonic crystalloid bolus within the first hour 2
- Sodium bicarbonate for severe acidosis: 1-2 mEq/kg IV push when pH <7.1 or bicarbonate <10 mEq/L 1, 2
- Continuous cardiac monitoring with calcium gluconate (100-200 mg/kg) ready for life-threatening arrhythmias 1, 2
- Early endotracheal intubation for altered mental status, severe acidosis, or hemodynamic instability 2
Gastrointestinal Decontamination
- Gastric lavage with diluted potassium permanganate or coconut oil if presenting within 1-2 hours 5, 7, 8
- Activated charcoal may be considered if presenting ≤1 hour after ingestion, though efficacy for phosphine gas adsorption is uncertain 2
Adjunctive Therapies Without Strong Evidence
Emerging case reports suggest potential benefit from:
- Magnesium sulfate IV for membrane stabilization 6, 7, 8
- Trimetazidine for cardioprotection 6, 8
- N-acetylcysteine, thiamine, vitamin C, hydrocortisone as supportive measures 6
However, these remain experimental with no high-quality evidence demonstrating mortality benefit.
The Deferoxamine Question: Also Not Indicated
Deferoxamine (DFO) is NOT indicated for acute aluminum phosphide poisoning. 2 This is another common source of confusion:
- DFO is used only for chronic aluminum overload in dialysis patients, not acute aluminum phosphide ingestion 9, 1, 2
- For serum aluminum levels >200 μg/L, DFO is contraindicated due to risk of acute neurotoxicity; intensive dialysis is recommended instead 1, 2
- For levels 60-200 μg/L, DFO at 5 mg/kg may be given with high-flux dialysis, but this applies to chronic aluminum toxicity, not acute phosphide poisoning 1
- DFO carries a 91% mortality risk from mucormycosis in dialysis patients 1
Critical Pitfalls to Avoid
- Do not treat aluminum phosphide poisoning as organophosphate poisoning: Atropine and pralidoxime have no role and will not help 2, 3
- Do not delay basic supportive care while pursuing experimental therapies; fluid resuscitation and vasopressors are the cornerstone 2, 5
- Ensure adequate ventilation of treatment areas: Phosphine gas can cause secondary exposure to healthcare workers requiring atropine, pralidoxime, and intubation—but this is for organophosphate exposure from the gas, not treatment of the aluminum phosphide-poisoned patient 1, 3
- All exposures require ICU-level care for 48-72 hours minimum: Ingestion of as little as 150-500 mg can be fatal, with mortality rates of 70-100% 2, 6, 8
Prognosis and Monitoring
The mortality rate for aluminum phosphide poisoning exceeds 70% despite aggressive supportive care. 4, 8 Poor prognostic factors include:
- Presence of severe metabolic acidosis 5, 8
- Refractory shock requiring high-dose vasopressors 5, 8
- Development of multi-organ failure 4, 5
Monitor for: cardiac arrhythmias, refractory hypotension, acute renal failure, hepatobiliary impairment, rhabdomyolysis (creatine kinase and potassium), and severe metabolic acidosis. 1, 6, 5