What is the treatment for zinc phosphide poisoning?

Treatment of Zinc Phosphide Poisoning

There is no specific antidote for zinc phosphide poisoning; treatment is aggressive supportive care with immediate airway management, gastrointestinal decontamination, and intensive monitoring for multiorgan failure, as the mortality rate is approximately 7% and deaths occur from refractory hypotension, arrhythmias, and respiratory failure. 1, 2, 3

Immediate Management and Decontamination

Airway and Breathing

• Secure the airway early with endotracheal intubation if the patient shows respiratory distress, altered mental status, or signs of impending respiratory failure, as phosphine gas causes pulmonary edema and respiratory toxicity 2, 3
• Provide 100% oxygen and mechanical ventilation support as needed for patients with respiratory compromise 1, 3
• Approximately 7% of patients require intubation and ventilator support 3

Gastrointestinal Decontamination

• Perform gastric lavage immediately upon presentation to remove unabsorbed zinc phosphide before it reacts with gastric acid to form phosphine gas 3
• Administer a single dose of activated charcoal after gastric lavage 3
• Approximately 70% of patients undergo gastrointestinal decontamination 3
• Do not induce vomiting, as this may worsen the clinical condition 4

Personal Protection

• Use appropriate personal protective equipment when handling the patient, as phosphine gas can be exhaled and poses a risk to healthcare workers 2, 5

Supportive Care and Monitoring

Cardiovascular Support

• Monitor for tachycardia, hypotension, and arrhythmias, which indicate severe poisoning and predict mortality 3
• Administer inotropic drugs (required in 4.2% of patients) for refractory hypotension 3
• Deaths within the first 12-24 hours are primarily due to refractory hypotension and arrhythmias 6

Metabolic and Electrolyte Management

• Monitor and aggressively correct electrolyte abnormalities, particularly hypokalemia, hypocalcemia, hypernatremia, and hyperkalemia, as these predict worse outcomes 1, 3
• Monitor blood glucose closely and treat hypoglycemia, as in-hospital hypoglycemia is associated with mortality 3
• Correct metabolic acidosis with supportive measures 1, 3

Renal Function

• Monitor for acute kidney injury, which commonly develops and may require hemodialysis 1, 6
• Initiate renal replacement therapy promptly if acute kidney injury develops, as this can be life-saving 6
• Zinc phosphide causes acute tubular necrosis and tubulointerstitial nephritis 6

Hepatic Protection

• Monitor liver enzymes, as hepatotoxicity develops from phosphine-induced mitochondrial toxicity 1, 2, 6
• Consider alpha-lipoic acid (ALA) administration for hepatoprotection, as one case report demonstrated sixfold improvement in pseudocholinesterase levels with ALA use, though this is not yet standard practice 1
• N-acetylcysteine may be administered alongside ALA for additional hepatoprotection 1

Respiratory Monitoring

• Obtain chest X-ray to evaluate for pulmonary edema and atelectasis 1, 2
• Monitor for development of bacterial pneumonia secondary to atelectasis, which is a dangerous complication 1
• Late deaths (beyond 24 hours) are commonly due to adult respiratory distress syndrome 6

Hospital Observation and Follow-up

• Admit all patients for a minimum of 2 days of observation, regardless of initial presentation, as delayed toxicity can occur 3
• The median hospital stay is 2 days for uncomplicated cases 3
• Monitor continuously for cardiovascular symptoms, respiratory symptoms, electrolyte imbalances, kidney function, and blood glucose 3

Prognostic Indicators

Poor Prognostic Factors

• Delayed presentation (longer duration from ingestion to hospital arrival) 3, 6
• Abnormal vital signs at presentation: tachycardia, hypotension, tachypnea 3
• Metabolic acidosis 3
• Electrolyte abnormalities: hypernatremia, hyperkalemia 3
• Development of coagulopathy 6
• Hyperglycemia 6
• Multiorgan failure with elevated liver enzymes 6
• Requirement for endotracheal intubation or inotropic support 3

Pathophysiology Context

Zinc phosphide reacts with gastric hydrochloric acid to produce phosphine gas, which causes cellular hypoxia through inhibition of cytochrome C oxidase in mitochondria 5, 6. This results in multiorgan dysfunction affecting the liver, heart, kidneys, and lungs 2, 5, 6. The immediate toxicity manifests as gastrointestinal symptoms (68.8% of patients), cardiovascular symptoms (22%), and respiratory symptoms (13.8%) 3.

Common Pitfalls

• Do not delay treatment while waiting for laboratory confirmation; treat based on history and clinical presentation 3
• Do not underestimate patients with initially normal vital signs, as delayed deterioration can occur 3
• Ensure adequate monitoring duration, as complications can develop beyond the initial presentation 3, 6
• Do not use neuromuscular blockers metabolized by cholinesterase (this is specific to organophosphate poisoning, not zinc phosphide) 7