What is the emergency management of calcium phosphide (Celphos) poisoning?

Emergency Management of Calcium Phosphide (Celphos) Poisoning

Celphos poisoning requires immediate aggressive supportive care with no specific antidote available; survival depends on rapid gastrointestinal decontamination, hemodynamic stabilization, and intensive monitoring, with mortality remaining extremely high despite maximal intervention.

Immediate Priorities and Safety Measures

Healthcare Worker Protection

• Ensure all staff wear full-face gas masks and butyl rubber gloves before patient contact, as phosphine gas exposure has caused severe illness requiring ICU admission in healthcare workers. 1
• Treat patients in well-ventilated areas; phosphine vapor in poorly ventilated spaces has required healthcare workers to receive atropine, pralidoxime, and intubation. 1
• Remove all contaminated clothing immediately to prevent secondary exposure. 2

Initial Stabilization

• Secure airway, breathing, and circulation as the absolute priority. 3
• Contact poison control center immediately while initiating treatment for specialized toxicology guidance. 2
• Establish large-bore intravenous access and begin aggressive crystalloid resuscitation (10-20 mL/kg boluses) for hypotension and volume depletion. 2

Gastrointestinal Decontamination

Perform extensive gastric lavage with a mixture of coconut oil and sodium bicarbonate solution immediately upon presentation. 4

• Coconut oil may prevent phosphine absorption and has shown positive clinical significance in survivors who ingested lethal doses. 5
• Administer activated charcoal (1 g/kg) via nasogastric tube only if advised by poison control, though evidence for benefit is limited. 2, 1
• Never induce vomiting, as this provides no benefit and increases aspiration risk. 2

Cardiovascular Management

Hemodynamic Support

• Administer vasopressors (norepinephrine preferred) for hypotension refractory to fluid resuscitation. 2, 1
• Monitor continuously for profound circulatory collapse, which is the major lethal consequence of phosphide poisoning. 6
• For life-threatening arrhythmias, administer calcium gluconate (100-200 mg/kg/dose) via slow IV infusion with continuous ECG monitoring. 1

Arrhythmia Management

• Ventricular tachycardia associated with aluminum phosphide poisoning may be unresponsive to standard therapy including magnesium sulfate, amiodarone, and electrocardioversion. 7
• Toxic myocarditis with elevated troponin levels commonly develops within 10 hours of ingestion. 7
• Consider VA-ECMO for refractory cardiogenic shock at centers where available, though outcomes remain poor. 2

Metabolic and Acid-Base Management

• Administer sodium bicarbonate (1-2 mEq/kg IV push) for severe metabolic acidosis. 1, 5
• Do not administer sodium bicarbonate and calcium through the same IV line. 1
• Monitor serum lactate and base deficit to assess tissue perfusion and shock severity. 2

Respiratory Management

• Provide supplemental oxygen to maintain adequate tissue oxygenation. 2
• Intubate early for respiratory failure, obtunded mental status, or airway protection needs. 2
• Consider CPAP ventilation for patients with adequate consciousness and no contraindications. 1
• Monitor for pulmonary edema, which may be cardiogenic or non-cardiogenic. 6

Renal Support

• Initiate continuous veno-venous hemofiltration for refractory acidemia, hypotension, or acute renal failure. 7
• Monitor serum creatinine and urine output closely, as acute renal failure is frequent. 6

Aluminum Toxicity Considerations

If serum aluminum levels are measured and exceed 200 μg/L, do NOT administer deferoxamine due to high risk of acute neurotoxicity; instead, perform intensive high-flux hemodialysis daily for 4-6 weeks. 1

• For aluminum levels between 60-200 μg/L, deferoxamine may be given at 5 mg/kg with careful monitoring and high-flux dialysis. 1
• Deferoxamine therapy carries a 91% mortality risk from mucormycosis in dialysis patients. 1

Additional Supportive Measures

• Administer magnesium sulfate intravenously for documented hypomagnesemia or refractory arrhythmias, though evidence on magnesium disturbances is conflicting. 6, 5
• Monitor for and treat complications including disseminated intravascular coagulation, hepatic necrosis, and rhabdomyolysis. 1, 6
• Serial monitoring of hemoglobin/hematocrit, liver function tests, and coagulation parameters is essential. 2

Critical Pitfalls to Avoid

• Ingestion of as little as 150-500 mg can be fatal; all exposures require ICU-level care regardless of initial presentation. 1
• Do not delay supportive care while awaiting toxicology confirmation, as clinical deterioration is rapid and phosphine assays are rarely available. 2
• Avoid succinylcholine for intubation if cholinesterase inhibition is suspected. 1
• Do not use aluminum hydroxide as a phosphate binder for more than 1-2 days to avoid cumulative aluminum toxicity. 1

Prognosis and Monitoring

• Mortality remains extremely high (58% in one series) despite aggressive intervention, with no known antidote available. 4, 8, 6
• Mean ICU stay for survivors is approximately 6 days. 4
• Continuous cardiac monitoring should continue for at least 6 hours after symptom resolution. 3
• Postmortem findings typically show contraction band necrosis, coagulation necrosis, edema, and hemorrhage in cardiac myocytes. 7