Aluminum phosphide poisoning

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Aluminum phosphide (AlP) poisoning is one of the most lethal forms of self-poisoning worldwide. Upon contact with moisture or gastric acid, AlP liberates phosphine gas (PH₃), which inhibits mitochondrial cytochrome C oxidase, causing profound cellular hypoxia, refractory cardiovascular collapse, and multiorgan failure.[1] There is no specific antidote; mortality ranges from 37-100%.[2]

Background

  • Aluminum phosphide is sold as tablets or pellets (3 g each, containing approximately 56% AlP) under trade names including Celphos, Quickphos, Phostoxin, and Fumitoxin
  • Known colloquially as "rice tablet" in parts of India and Iran
  • Used worldwide as a grain fumigant and rodenticide, especially in developing countries
  • AlP is unstable — releases phosphine gas rapidly on contact with moisture, making it more acutely lethal than zinc phosphide[3]
  • Lethal dose: 150-500 mg (as little as one-tenth of a standard 3 g tablet can be fatal)[1]
  • Deaths from cardiovascular toxicity typically occur within the first 12-24 hours[4]
  • Most poisoning cases are intentional (self-harm) in young adults in agricultural regions of South Asia, the Middle East, and Africa[5]

Mechanism of toxicity

  • AlP + gastric HCl/moisture → phosphine gas (PH₃)
  • Phosphine inhibits cytochrome C oxidase (complex IV of mitochondrial electron transport chain) → blocks oxidative phosphorylation → cellular energy crisis[1]
  • Generates highly reactive hydroxyl radicals → lipid peroxidation, glutathione depletion → oxidative cellular injury
  • Myocardium is the primary target — cell membrane dysfunction, impaired glucose utilization, oxidative stress → cardiogenic shock (most common cause of death)[6]
  • Also targets lungs, liver, kidneys, adrenals, and GI tract
  • Phosphine may also be exhaled by the patient and released from vomitus — posing a risk to healthcare workers

Healthcare worker safety

  • Phosphine gas is hazardous to staff — vomitus, gastric aspirate, and exhaled air may contain phosphine
  • Treat in a well-ventilated area or negative-pressure room
  • PPE including respiratory protection is recommended
  • Exposure at 1400 mg/m³ for 30 minutes can be fatal[4]
  • Handle gastric lavage effluent as hazardous material

Clinical features

  • Onset is rapid (minutes to hours), in contrast to the more delayed presentation of zinc phosphide[3]
  • The cardinal feature is profound, refractory hypotension (present in 50-100% of severe cases)[1]

Gastrointestinal

  • Nausea, vomiting (most common presenting symptom; 74% of cases)[5]
  • Severe epigastric and abdominal pain
  • Diarrhea
  • Hematemesis (from erosive gastropathy)
  • Garlic or decaying fish odor from breath/vomitus (classic but not always present)

Cardiovascular (primary cause of mortality)

  • Refractory hypotension and cardiogenic shock
  • Myocarditis, pericarditis, subendocardial infarction
  • ECG abnormalities: ST-segment elevation/depression, T-wave inversion, QTc prolongation, conduction blocks, ventricular tachycardia, atrial fibrillation[1]
  • Cardiac arrest (often within 12-24 hours of ingestion)
  • Elevated troponin

Respiratory

Metabolic

  • Severe metabolic acidosis (high anion gap; elevated lactate) — most sensitive marker of severity and strongest predictor of mortality[1]
  • Hyperkalemia (from cellular injury and acidosis)
  • Hypomagnesemia (associated with increased mortality)
  • Hypoglycemia (poor prognostic sign)

Hepatic

  • Hepatocellular injury (elevated AST, ALT)
  • Hepatic failure with coagulopathy

Renal

Neurologic

  • Agitation, restlessness, anxiety
  • Altered mental status, delirium, coma
  • Seizures

Other

Differential diagnosis

Evaluation

Workup

  • Silver nitrate test: simple bedside diagnostic test[1]
    • Expose filter paper impregnated with silver nitrate solution to the patient's gastric aspirate, vomitus, or exhaled breath
    • Positive test: paper turns black (silver phosphide formation) — confirms phosphine exposure
  • ABG/VBG: metabolic acidosis with elevated lactate — severity correlates directly with mortality
  • ECG: continuous monitoring; look for ST changes, QTc prolongation, arrhythmias, conduction blocks
  • CBC, BMP, hepatic function panel, coagulation studies (PT/INR)
  • Cardiac biomarkers: troponin (serial), BNP
  • Serum magnesium, calcium, phosphorus
  • Blood glucose (monitor frequently; hypoglycemia is a poor prognostic indicator)
  • Chest radiograph: pulmonary edema, ARDS
  • Echocardiography: assess myocardial function; may show global hypokinesis in severe myocarditis
  • Abdominal radiograph: AlP tablets are not reliably radiopaque (unlike zinc phosphide)
  • Methemoglobin level if cyanosis present
  • Salicylate, acetaminophen, ethanol levels if intentional co-ingestion suspected

Diagnosis

  • Primarily clinical: history of ingestion of fumigant/rodenticide tablet + garlic odor + rapid-onset refractory shock + metabolic acidosis
  • Silver nitrate test on gastric aspirate or breath is the most accessible confirmatory test
  • Phosphine gas levels are not routinely available
  • Poor prognostic indicators:[1][5]
    • Shock or hypotension at presentation
    • Severe metabolic acidosis (pH <7.2) or elevated lactate
    • Cardiac arrhythmias
    • Hyperkalemia
    • Hypoglycemia
    • Need for vasopressors or mechanical ventilation
    • Amount ingested >1.5 g

Management

No specific antidote exists. Management is aggressive supportive care and GI decontamination.[1]

GI decontamination

  • Gastric lavage with potassium permanganate (KMnO₄ 1:10,000) — oxidizes phosphine to non-toxic phosphate[1]
  • Coconut oil (100-200 mL via NG tube) — forms a protective mucosal barrier and may reduce phosphine liberation; reported to decrease absorption even up to 6 hours after ingestion[7]
  • Sodium bicarbonate (NaHCO₃ 7.5%) added to lavage fluid — neutralizes gastric acid to reduce phosphide-to-phosphine conversion[8]
  • Do NOT use plain water for lavage — promotes phosphine gas formation
  • Activated charcoal: limited evidence of benefit (phosphine is a gas and poorly adsorbed); may be given if co-ingestant suspected
  • Do NOT induce emesis — re-exposure risk and aspiration hazard

Cardiovascular support (core of management)

  • Aggressive IV fluid resuscitation
  • Vasopressors: norepinephrine or dopamine for refractory hypotension; high doses frequently required[1]
  • Intra-aortic balloon pump (IABP): case reports of use as rescue therapy for refractory cardiogenic shock[9]
  • Hyperinsulinemia-euglycemia therapy (HIE): emerging evidence suggests benefit by shifting myocardial metabolism from beta-oxidation to glycolysis, improving contractility[6]
    • Insulin 1 IU/kg/h with dextrose infusion to maintain euglycemia
  • ECMO (extracorporeal membrane oxygenation): may be considered as bridge therapy in refractory cardiogenic shock in centers with capability
  • Continuous cardiac monitoring — arrhythmias are common and frequently fatal
  • For ventricular tachycardia or Torsades de pointes: magnesium sulfate, lidocaine, defibrillation
    • Avoid class IA (procainamide, quinidine), IC, and III antiarrhythmics — risk of further QTc prolongation

Magnesium sulfate

  • IV magnesium sulfate — membrane stabilizer, antioxidant (restores glutathione), cardioprotective[1]
  • Multiple dosing regimens described; one protocol: 1 g IV q1h for 3 hours, then 6 g/day infusion for 3-5 days[8]
  • Studies suggest improved survival, particularly in patients with hypomagnesemia[1]
  • Monitor for magnesium toxicity (loss of DTRs, respiratory depression)

Sodium bicarbonate

  • IV sodium bicarbonate for correction of metabolic acidosis
  • Also used in gastric lavage (see above)
  • May help stabilize myocardial membranes

Antioxidant therapy

  • N-acetylcysteine (NAC): hepatoprotective, replenishes glutathione; loading dose 140 mg/kg, maintenance 70 mg/kg for 17 additional doses[6]
  • Vitamin C: 1 g IV q8h (antioxidant; limited evidence)
  • Vitamin E: 100 IU q12h (antioxidant; limited evidence)

Additional supportive measures

  • Hydrocortisone: IV stress-dose steroids for refractory shock (relative adrenal insufficiency may contribute)[5]
  • Calcium gluconate: for hypocalcemia
  • Hemodialysis: not effective at removing phosphine (protein-bound), but essential for supportive management of AKI, hyperkalemia, and refractory acidosis[4]
  • Blood products: as needed for coagulopathy/DIC
  • Intubation and mechanical ventilation for respiratory failure

Disposition

  • All patients with confirmed or suspected AlP ingestion must be admitted to the ICU — even if initially stable[1]
  • Continuous cardiac monitoring for a minimum of 72 hours — most deaths occur within 12-24 hours, but delayed deterioration can occur
  • Serial ABGs, ECGs, cardiac biomarkers, LFTs, renal function, electrolytes, and blood glucose every 4-6 hours during the first 48 hours
  • Death typically occurs from refractory cardiogenic shock within 24 hours in severe cases[4]
  • Survivors of the acute phase generally recover fully if organ failure is supported
  • All intentional ingestions: psychiatric evaluation mandatory prior to discharge
  • Contact Poison control (1-800-222-1222 in the US) for all cases
  • Key differences from zinc phosphide poisoning:
Feature Aluminum phosphide Zinc phosphide
Onset of systemic toxicity Rapid (minutes to hours) Delayed (hours to >12 hours)
Stability of compound Unstable; rapid phosphine release Relatively stable
Radiopaque on X-ray No (not reliably) Yes (zinc component)
Mortality rate Higher (37-100%) Lower (~7-37%)
Primary cause of death Cardiogenic shock Cardiogenic shock/hepatic failure
Hepatic failure Less prominent More prominent (delayed)

See Also

External Links

References

  1. ↑ 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 1.11 1.12 1.13 Gurjar M, et al. Managing aluminum phosphide poisonings. J Emerg Trauma Shock. 2011;4(3):378-384. doi:10.4103/0974-2700.83868
  2. ↑ Wahab A, Zaheer MS, Wahab S, Khan RA. Acute aluminium phosphide poisoning: an update. Hong Kong J Emerg Med. 2008;15:152-155.
  3. ↑ 3.0 3.1 Trakulsrichai S, et al. Clinical characteristics of zinc phosphide poisoning in Thailand. Ther Clin Risk Manag. 2017;13:335-340.
  4. ↑ 4.0 4.1 4.2 4.3 Turkmen YH, et al. Successful Management of Aluminium Phosphide Poisoning Resulting in Cardiac Arrest. Turk J Anaesthesiol Reanim. 2016;44(3):155-157. doi:10.5152/TJAR.2016.96168
  5. ↑ 5.0 5.1 5.2 5.3 Teshome Z, et al. Clinical Profile and Treatment Outcome of Aluminum Phosphide Poisoning in Felege Hiwot Referral Hospital, Northwest Ethiopia. Open Access Emerg Med. 2021;13:223-230. doi:10.2147/OAEM.S313181
  6. ↑ 6.0 6.1 6.2 Aluminum phosphide poisoning and its clinical management. Nature Research Intelligence. 2025.
  7. ↑ Shadnia S, et al. Successful treatment of acute aluminium phosphide poisoning: possible benefit of coconut oil. Hum Exp Toxicol. 2005;24(4):215-218.
  8. ↑ 8.0 8.1 Agrawal VK, et al. Aluminum phosphide poisoning: possible role of supportive measures in the absence of specific antidote. Indian J Crit Care Med. 2015;19(2):113-115. doi:10.4103/0972-5229.151019
  9. ↑ Siddaiah L, et al. Intra-aortic balloon pump in toxic myocarditis due to aluminium phosphide poisoning. J Med Toxicol. 2009;5(2):80-83.
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