What is the emergency management of aluminum phosphide (wheat‑pill) poisoning?

Emergency Management of Aluminum Phosphide (Wheat-Pill) Poisoning

Aluminum phosphide poisoning requires immediate aggressive supportive care with priority given to airway management, hemodynamic stabilization, and early consideration of hemodialysis, as there is no specific antidote available. 1

Immediate Stabilization and Priorities

Secure airway, breathing, and circulation first—this takes absolute priority over antidote administration or toxin identification. 2, 1 Management follows standard BLS and ACLS protocols, with cardiac arrest due to toxicity managed according to current resuscitation standards. 2

• Contact your regional poison control center immediately (1-800-222-1222 in the US) for specialized toxicological consultation, as aluminum phosphide poisoning requires expert guidance that most clinicians encounter infrequently. 2, 1
• Establish hemodynamic monitoring and maintain systolic blood pressure >80 mm Hg with aggressive fluid resuscitation and vasopressor support. 1, 3
• Treat based on clinical presentation and exposure history without delay—do not wait for confirmatory testing. 1, 3

Critical context: Ingestion of as little as 150-500 mg (one tablet of phostoxin contains 3 grams) can be fatal, and all exposures require ICU-level care. 1, 4 Mortality rates range from 52-90% despite intensive care, with death typically occurring within 24-72 hours due to toxic chemical myocarditis and circulatory collapse. 5, 4, 6

Gastrointestinal Decontamination

• Perform early gastric lavage with diluted potassium permanganate or a combination with coconut oil and sodium bicarbonate. 5, 7
• Activated charcoal can be considered for gastrointestinal decontamination, although its ability to adsorb phosphine gas is uncertain (low-quality evidence). 1
• Do NOT induce vomiting, as this may worsen cardiovascular instability and delay definitive care. 8, 3
• Charcoal should not be administered for ingestions of caustic substances, metals, or hydrocarbons. 2

Cardiovascular Support

The primary lethal consequence is profound circulatory collapse secondary to direct effects on cardiac myocytes, fluid loss, and adrenal gland damage. 9

• Administer intravenous magnesium sulfate (1-2 g MgSO₄ bolus IV push), which appears to reduce mortality from 90% to 52% through membrane-stabilizing action. 7, 6
• For life-threatening arrhythmias, calcium gluconate (100-200 mg/kg/dose) via slow infusion with ECG monitoring can be given for cardiac membrane stabilization. 1
• For bradycardia or heart block, atropine 0.5-1.0 mg IV every 3-5 minutes (up to 3 mg) is recommended. 8
• Consider intra-aortic balloon pump or digoxin for refractory cardiogenic shock. 5
• Trimetazidine may have a useful role as it can stop ventricular ectopic beats and preserve oxidative metabolism. 5

Metabolic Management

Phosphine rapidly perturbs mitochondrial morphology, inhibits oxidative respiration by 70%, and causes severe drops in mitochondrial membrane potential—this failure of cellular respiration is the primary mechanism of toxicity, not simply cytochrome C oxidase inhibition. 9

• Administer sodium bicarbonate (1-2 mEq/kg IV push) for severe metabolic acidosis, which is frequent in aluminum phosphide poisoning. 1, 5
• Address hypocalcemia and other electrolyte derangements that develop during the acute phase. 3
• Do not administer sodium bicarbonate and calcium through the same IV line. 1
• Monitor serum creatinine kinase and potassium to detect rhabdomyolysis. 1
• Treat rhabdomyolysis with adequate hydration and urine alkalinization if myoglobinuria develops. 1

Aluminum Toxicity Management (If Applicable)

• Measure serum aluminum levels if aluminum toxicity is suspected, particularly in dialysis patients. 1
• For serum aluminum levels between 60-200 µg/L: Administer deferoxamine (DFO) at 5 mg/kg intravenously with careful monitoring; use high-flux dialysis membranes to enhance clearance of aluminum-DFO complexes. 1
• For serum aluminum levels >200 µg/L: Deferoxamine should be avoided due to high risk of precipitating acute aluminum neurotoxicity; instead, initiate intensive high-flux hemodialysis daily for 4-6 weeks until levels decline. 1
• Do not administer intravenous iron to limit formation of feroxamine if DFO is administered. 1
• Warning: DFO therapy can precipitate fatal mucormycosis with 91% mortality in dialysis patients; reduced dosing (5 mg/kg) and expanded intervals between treatments minimize this risk. 1

Respiratory Management

• Place on mechanical ventilation if respiratory failure develops. 4
• Consider continuous positive airway pressure (CPAP) ventilation for patients with adequate consciousness and without contraindications. 1
• Avoid succinylcholine or mivacurium for intubation if cholinesterase inhibition is suspected. 1

Neurological Management

• Administer benzodiazepines (diazepam or midazolam) for seizures or severe agitation if they occur. 8, 3
• Do not use neuromuscular blockers without adequate sedation, as they mask seizure activity without treating it. 8, 3

Healthcare Worker Safety

Phosphine gas released from aluminum phosphide is highly toxic and can affect healthcare providers through secondary exposure. 1, 3

• Ensure treatment areas are well-ventilated; in poorly ventilated spaces, healthcare workers have required atropine, pralidoxime, and intubation after exposure to phosphine vapor. 1
• Never initiate patient care without full-face gas masks and butyl rubber gloves; secondary exposure has caused severe illness requiring ICU admission in healthcare workers. 1
• Remove all contaminated clothing and thoroughly wash exposed skin with soap and water. 8, 3

Monitoring and Disposition

• Observe all patients for at least 48-72 hours, even if initially stable, due to risk of delayed cardiac effects. 8, 3
• Monitor for multi-organ failure including hepatic necrosis, acute renal failure, disseminated intravascular coagulation, and pulmonary edema (which may be cardiogenic or non-cardiogenic). 4, 9
• Laboratory findings typically show leukocytosis, prolonged PT, elevated AST/ALT, elevated CPK (rhabdomyolysis), elevated BUN/creatinine, and metabolic acidosis. 4
• ECG changes include inverted T waves and signs of toxic chemical myocarditis. 4, 6

Critical Pitfalls to Avoid

• Do not delay treatment while waiting for confirmatory testing—treat empirically based on exposure history and clinical presentation. 1, 3
• Do not assume stability means safety—cardiac toxicity can be delayed and sudden, with systemic toxicity appearing shortly after ingestion. 8, 9
• Avoid physical restraints without adequate sedation, as this can worsen outcomes. 1
• Do not use aluminum hydroxide as a phosphate binder for more than 1-2 days to avoid cumulative aluminum toxicity. 1