Zinc phosphide poisoning

Background

  • Zinc phosphide (Zn₃P₂) poisoning is a potentially lethal toxicity caused by ingestion of a widely available rodenticide.
  • Upon contact with gastric acid, zinc phosphide is hydrolyzed into phosphine gas (PH₃), which inhibits mitochondrial cytochrome C oxidase and causes multiorgan cellular hypoxia and death.[1] There is no specific antidote; mortality ranges from 37-100% in severe cases.[2]
  • Zinc phosphide is a dark gray/black crystalline powder used as a rodenticide against mice, rats, gophers, and squirrels
  • Registered for pesticide use in the United States since 1947; widely available in developing countries[3]
  • Most cases of significant poisoning are intentional (self-harm) in adults, particularly in the Indian subcontinent, Iran, Thailand, and Mexico[4]
  • Accidental ingestion occurs in children (attracted to bait formulations) and through contaminated food
  • Toxic dose: symptoms may occur with >40 mg/dose; lethal dose estimated at 4-5 g in adults (approximately 40-80 mg/kg)[5]

Mechanism of toxicity

  • Zinc phosphide reacts with gastric HCl → liberates phosphine gas (PH₃)
    • Gastric acid and recent food intake accelerate phosphine release
    • An empty stomach may delay symptom onset up to 12 hours[3]
  • Phosphine is absorbed through the GI tract and lungs → distributed to liver, kidneys, heart, brain, and adrenals
  • Phosphine inhibits cytochrome C oxidase (complex IV of mitochondrial electron transport chain) → disrupts oxidative phosphorylation → cellular anoxia[1]
  • Additionally causes direct oxidative stress with lipid peroxidation, glutathione depletion, and free radical formation
  • Primary target organs: heart (most common cause of early death), lungs, liver, kidneys
  • Zinc phosphide is radiopaque on abdominal radiography due to its zinc component[6]

Healthcare worker safety

  • Phosphine gas may be released from the patient's vomitus and gastric contents — this is hazardous to healthcare workers[3]
  • Treat in a well-ventilated area or negative-pressure room
  • Use appropriate personal protective equipment
  • Gastric lavage effluent should be handled as hazardous material

Clinical features

  • Onset of systemic symptoms is typically delayed compared to aluminum phosphide (hours to >12 hours post-ingestion)[4]
  • Patients may be initially asymptomatic and then deteriorate suddenly — including sudden cardiac arrest in asymptomatic patients[7]

Gastrointestinal (earliest)

  • Nausea, vomiting (may have garlic/fishy odor), retching
  • Epigastric and abdominal pain
  • Diarrhea (may be bloody)
  • Hematemesis

Cardiovascular (most common cause of death)

Respiratory

  • Dyspnea, tachypnea, cyanosis
  • Acute pulmonary edema (cardiogenic and non-cardiogenic)
  • ARDS
  • Respiratory failure

Metabolic

  • Severe metabolic acidosis (high anion gap; elevated lactate) — correlates with severity[4]
  • Hyperkalemia, hyponatremia, hypocalcemia, hypomagnesemia
  • Hypoglycemia (poor prognostic indicator)

Hepatic

  • Hepatocellular injury (elevated AST, ALT)
  • Acute hepatic failure — may progress over the first week[8]
  • Coagulopathy

Renal

Neurologic

  • Headache, dizziness, agitation, restlessness
  • Altered mental status, delirium
  • Seizures, coma

Hematologic

  • Methemoglobinemia (less common than in aluminum phosphide poisoning)
  • Intravascular hemolysis (rare)
  • DIC

Differential diagnosis


Toxic gas exposure

Evaluation

Workup

  • Abdominal radiograph — zinc phosphide is radiopaque; positive X-ray is an indication for aggressive GI decontamination and portends worse prognosis[6]
    • Serial abdominal X-rays to confirm complete decontamination
  • ABG/VBG — metabolic acidosis with elevated lactate is the earliest and most sensitive marker of systemic toxicity; severity correlates with prognosis[4]
  • CBC, BMP, hepatic function panel, coagulation studies (PT/INR), lipase
  • Cardiac biomarkers (troponin, BNP) — myocardial injury monitoring
  • ECG — continuous monitoring for dysrhythmias; sinus tachycardia is common; may progress to fatal rhythm
  • Blood glucose — hypoglycemia is a poor prognostic indicator
  • Serum magnesium, calcium, phosphorus
  • Methemoglobin level (co-oximetry)
  • CK — for rhabdomyolysis
  • Chest radiograph — for pulmonary edema, ARDS
  • Salicylate, acetaminophen, ethanol levels — if intentional ingestion
  • Phosphine levels are not routinely available or clinically useful in acute management
  • Echocardiography — to assess myocardial function if hemodynamically unstable

Diagnosis

  • Clinical: history of rodenticide ingestion + GI symptoms + metabolic acidosis + cardiovascular collapse
  • Radiopaque material on abdominal X-ray in the setting of rodenticide ingestion is highly suggestive
  • Garlic or decaying fish odor to breath/vomitus is a classic but unreliable finding
  • Patients with positive abdominal X-ray are at higher risk for sudden deterioration even if asymptomatic[6]

Management

No specific antidote exists. Treatment is supportive with GI decontamination and organ support.[1]

GI decontamination

  • Gastric lavage with coconut oil (200 mL) + sodium bicarbonate (NaHCO₃ 7.5%, 50 mL):[1]
    • Coconut oil forms a protective mucosal layer and may reduce phosphine liberation
    • Bicarbonate decreases gastric acid–driven conversion of phosphide to phosphine
    • Do NOT use water for lavage — water promotes phosphine gas formation
    • Alternative lavage solutions: potassium permanganate (1:10,000), liquid paraffin, or olive oil
  • Activated charcoal (50 g) — may reduce absorption; administer after lavage[4]
  • Whole-bowel irrigation with polyethylene glycol (PEG) — if radiopaque material visible beyond the stomach on X-ray
    • Some authors caution that PEG's water base could promote phosphine release; castor oil is an alternative for bowel evacuation[9]
  • Repeat abdominal X-rays to confirm clearance of all radiopaque material

Cardiovascular support

  • Aggressive IV fluid resuscitation
  • Vasopressors (norepinephrine, dopamine) for refractory hypotension
  • Continuous cardiac monitoring (sudden cardiac arrest may occur in asymptomatic patients)[7]
  • Hyperinsulinemia-euglycemia therapy (HIE): case reports suggest benefit in refractory cardiogenic shock[1]
    • Insulin loading dose 1 IU/kg/h, maintenance 1-7 IU/kg/h; dextrose infusion to maintain euglycemia
  • Intravenous lipid emulsion (ILE) — case reports of use for refractory shock; mechanism unclear[1]

Magnesium sulfate

  • IV magnesium sulfate — membrane stabilizer and antioxidant; case-control studies suggest mortality reduction >50%[1]
  • Multiple regimens described; one common protocol: 1 g/hour for 24 hours, then 1 g every 6 hours for 5-7 days
  • Monitor serum magnesium; avoid toxicity (loss of deep tendon reflexes, respiratory depression)

Antioxidant therapy

  • N-acetylcysteine (NAC): loading dose 140 mg/kg, maintenance 70 mg/kg for 17 doses — hepatoprotective, replenishes glutathione[1]
  • Vitamin C: 1 g IV q8h for the first 24 hours (antioxidant; limited evidence)
  • Vitamin E: 100 IU q12h for 72 hours (antioxidant; limited evidence)
  • Alpha-lipoic acid: iron chelation and antioxidant properties; case report of use in combination therapy[10]

Metabolic acidosis

  • Correct with IV sodium bicarbonate as needed
  • Refractory acidosis is a poor prognostic sign
  • Treat underlying cause (tissue hypoperfusion)

Organ failure management

  • Hepatic failure: supportive; vitamin K, FFP for coagulopathy; liver transplant if fulminant[8]
  • Acute kidney injury: hemodialysis for standard indications (uremia, hyperkalemia, volume overload, refractory acidosis)
    • Hemodialysis does not effectively remove phosphine
  • Methemoglobinemia: Methylene blue 1-2 mg/kg IV if symptomatic
  • Intubation and mechanical ventilation for respiratory failure/pulmonary edema

Disposition

  • All patients with confirmed or suspected zinc phosphide ingestion must be admitted — even if initially asymptomatic[7]
  • ICU admission for all significant ingestions — continuous cardiac monitoring is mandatory
  • Monitoring period: minimum 72 hours; risk of cardiovascular collapse greatest in first 24-48 hours but delayed hepatic failure may occur through the first week[8]
  • Serial ABGs, LFTs, coagulation studies, renal function, and ECGs every 6-12 hours
  • Serial abdominal X-rays until all radiopaque material has cleared
  • Prognosis is worse with:[4]
    • Large ingested volume
    • Delayed presentation to hospital
    • Metabolic acidosis or elevated lactate at presentation
    • Hypotension, tachycardia, or tachypnea on arrival
    • Hyperkalemia, hypoglycemia
    • Acute kidney injury, need for vasopressors or intubation
  • All intentional ingestions: psychiatric evaluation mandatory prior to discharge
  • Contact Poison control (1-800-222-1222 in the US) for all cases

Medication Dosing

N-Acetylcysteine 140mg/kg PO loading dose, then 70mg/kg q4hr x 17 doses PO Magnesium sulfate 1g/hr IV x 24hr, then 1g q6hr x 5-7 days IV

See Also

External Links

References

  1. ↑ 1.0 1.1 1.2 1.3 1.4 1.5 1.6 1.7 Arroyo-Arcos CR, et al. Zinc Phosphide Poisoning: From A to Z. Toxics. 2023;11(7):555. doi:10.3390/toxics11070555
  2. ↑ Dogan E, Güzel A, Ciftçi T, et al. Zinc Phosphide Poisoning. Case Rep Crit Care. 2014;2014:589712. doi:10.1155/2014/589712
  3. ↑ 3.0 3.1 3.2 Zinc Phosphide Technical Fact Sheet. National Pesticide Information Center (NPIC). Oregon State University.
  4. ↑ 4.0 4.1 4.2 4.3 4.4 4.5 Trakulsrichai S, et al. Clinical characteristics of zinc phosphide poisoning in Thailand. Ther Clin Risk Manag. 2017;13:335-340. doi:10.2147/TCRM.S129610
  5. ↑ Proudfoot AT. Aluminium and zinc phosphide poisoning. Clin Toxicol (Phila). 2009;47(2):89-100. doi:10.1080/15563650802016425
  6. ↑ 6.0 6.1 6.2 Hassanian-Moghaddam H, Shahnazi M, Zamani N, Bahrami-Motlagh H. Abdominal imaging in zinc phosphide poisoning. Emerg Radiol. 2014;21(3):329-331. doi:10.1007/s10140-014-1195-3
  7. ↑ 7.0 7.1 7.2 Parhizgar P, et al. Sudden Cardiac Arrest in an Asymptomatic Zinc Phosphide-Poisoned Patient: A Case Report. Cardiovasc Toxicol. 2020;20(5):525-530. doi:10.1007/s12012-020-09578-2
  8. ↑ 8.0 8.1 8.2 Saraf V, et al. Acute liver failure due to zinc phosphide containing rodenticide poisoning: clinical features and prognostic indicators of need for liver transplantation. Indian J Gastroenterol. 2015;34(4):325-329. doi:10.1007/s12664-015-0583-2
  9. ↑ Shakoori V, et al. Successful management of zinc phosphide poisoning. Indian J Crit Care Med. 2016;20(6):368-370. doi:10.4103/0972-5229.183907
  10. ↑ Takacs A, et al. Successful management of zinc phosphide poisoning — a Hungarian case. Int J Emerg Med. 2020;13:51. doi:10.1186/s12245-020-00307-8
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