Management of Zinc Phosphide Poisoning
Zinc phosphide poisoning requires aggressive supportive care with immediate decontamination, airway protection, and cardiovascular support—there is no antidote, and treatment success depends entirely on early recognition and intensive supportive measures. 1, 2, 3
Immediate Priorities and Decontamination
Contact poison control immediately (1-800-222-1222 in the US) while initiating treatment, as expert toxicological guidance is critical for managing this rare but lethal poisoning 4
Healthcare workers must use full personal protective equipment (PPE) including gloves, gowns, and respiratory protection when handling the patient or contaminated materials, as zinc phosphide reacts with gastric acid to produce highly toxic phosphine gas that can cause secondary exposure 4, 2
Remove all contaminated clothing immediately and perform thorough dermal decontamination with copious soap and water to prevent continued absorption 4, 5
Perform gastric lavage and administer activated charcoal if the patient presents within 1-2 hours of ingestion and the airway can be protected—approximately 70% of patients in the Thai cohort underwent gastrointestinal decontamination 6
Do NOT induce vomiting, as this increases the risk of aspiration of phosphine gas and worsens outcomes 4, 5
Airway and Respiratory Management
Perform early endotracheal intubation for any patient with respiratory distress, altered mental status, or hemodynamic instability, as pulmonary edema is a major cause of immediate death from phosphine gas toxicity 1, 2, 3
Avoid neuromuscular blockers metabolized by cholinesterase (succinylcholine and mivacurium) if intubation is required, though this is primarily a concern in organophosphate poisoning 7, 5
Provide mechanical ventilation with lung-protective strategies for patients who develop non-cardiogenic or cardiogenic pulmonary edema 3
In the Thai study, 31 patients (6.8%) required intubation and ventilator support, highlighting the severity of respiratory complications 6
Cardiovascular Support
Aggressive fluid resuscitation and early vasopressor support are critical, as profound circulatory collapse from direct myocardial toxicity and fluid loss is the primary mechanism of death 1, 3
Treat hypotension and dysrhythmias according to standard ACLS protocols, with inotropic drugs required in 4.2% of patients in the Thai cohort 4, 6
Monitor continuously for cardiac dysrhythmias, as delayed cardiotoxicity can occur even after initial stabilization due to direct effects on cardiac myocytes 1, 3
Four moribund patients in the Thai study received hyperinsulinemia-euglycemia therapy and intravenous hydrocortisone, though all died—suggesting these interventions may be considered in extremis but have limited efficacy 6
Metabolic and Laboratory Monitoring
Monitor serial electrolytes closely, particularly potassium and sodium, as hyperkalemia and hypernatremia are associated with mortality 6, 3
Check serial blood glucose, as in-hospital hypoglycemia is associated with poor outcomes 6
Monitor for metabolic acidosis (or mixed metabolic acidosis and respiratory alkalosis), which is frequent and indicates severe cellular hypoxia from mitochondrial toxicity 3
Assess renal function serially, as acute kidney injury develops in many patients and is associated with mortality 6, 3
Obtain baseline and serial liver function tests, as hepatic necrosis can occur from phosphine-induced cellular damage 3
Check coagulation studies, as disseminated intravascular coagulation has been reported 3
Seizure and Neurological Management
Administer benzodiazepines (diazepam or midazolam) for seizures or severe agitation if they occur 4, 5
Monitor for changes in mental status, which are common presenting symptoms and indicate severe toxicity 1
Observation and Disposition
All patients must be observed in the hospital for a minimum of 48-72 hours, even if initially asymptomatic, due to the risk of delayed cardiovascular and respiratory complications 5, 6
The median hospital stay in the Thai cohort was 2 days, with a 7% mortality rate 6
Patients presenting with abnormal vital signs (tachycardia, hypotension, tachypnea), acidosis, electrolyte abnormalities, or delayed presentation (>2 hours from ingestion) require ICU admission and aggressive monitoring, as these factors are significantly associated with mortality 6
Pathophysiology and Clinical Presentation
Zinc phosphide reacts with gastric hydrochloric acid to produce phosphine gas, which causes cellular hypoxia via mitochondrial toxicity by perturbing mitochondrial morphology, inhibiting oxidative respiration by 70%, and causing severe drops in mitochondrial membrane potential 2, 3
The most common clinical presentations are gastrointestinal (68.8%), cardiovascular (22.0%), and respiratory (13.8%) symptoms 6
Immediate deaths result from pulmonary edema, while delayed deaths (hours to days) are related to direct cardiotoxicity, hepatic necrosis, and renal failure 1, 3
Critical Pitfalls to Avoid
Never delay supportive treatment while waiting for laboratory confirmation or toxicology analysis—treat based on history of exposure and clinical presentation 4, 5
Do not underestimate the risk of secondary exposure to healthcare workers from phosphine gas released from gastric contents during lavage or emesis—full PPE is mandatory 4, 2
Do not discharge patients early or observe them in non-monitored settings, as delayed cardiovascular collapse can occur even in initially stable patients 5, 6
Recognize that there is no antidote—all treatment is supportive, and survival depends on the intensity and timeliness of supportive care 1, 2, 8, 3