What is the treatment for aluminum phosphide poisoning?

Treatment of Aluminum Phosphide Poisoning

Insulin-euglycemia therapy combined with aggressive supportive care is the most effective treatment for aluminum phosphide poisoning, significantly reducing mortality from >90% to approximately 35% compared to vasopressor-only supportive care. 1

Immediate Management Priority: Insulin-Euglycemia Therapy

The cornerstone of treatment is high-dose insulin with dextrose to maintain euglycemia, which has transformed outcomes in this previously near-universally fatal poisoning:

• Administer regular insulin as a continuous infusion starting with a bolus followed by maintenance dosing, while simultaneously giving hypertonic dextrose (typically 10-50% dextrose solutions) to maintain blood glucose between 100-200 mg/dL 1, 2
• This therapy directly counteracts the cardiotoxic effects by improving myocardial contractility and hemodynamics, independent of its glucose-lowering effects 3, 1
• Insulin-euglycemia reduces vasopressor requirements (median 7 mg vs 26 mg norepinephrine), decreases intubation rates (61% vs 82%), and improves blood pressure parameters within 6 hours 1
• The most recent and highest-quality randomized trial (2023) demonstrated mortality reduction from 96.3% with standard care alone to 64.8% with insulin-euglycemia therapy 1

Critical monitoring requirement: Check blood glucose every 30-60 minutes initially and adjust dextrose infusion rates accordingly to prevent hypoglycemia, which is the main manageable adverse effect 3, 1, 2

Supportive Cardiovascular Management

While insulin-euglycemia is primary therapy, additional cardiovascular support is essential:

• Vasopressor support with norepinephrine for refractory hypotension, though insulin therapy substantially reduces vasopressor requirements 1
• Calcium gluconate (100-200 mg/kg/dose) via slow IV infusion with continuous ECG monitoring for life-threatening arrhythmias, particularly those associated with hyperkalemia 4
• Avoid administering sodium bicarbonate and calcium through the same IV line to prevent precipitation 4
• Continuous cardiac monitoring is mandatory as cardiotoxicity manifests as arrhythmias, ST-segment changes, and elevated troponin levels 5

Metabolic Correction

• Sodium bicarbonate (1-2 mEq/kg IV push) for severe metabolic acidosis, which develops rapidly and contributes to cardiovascular collapse 4
• Monitor and treat hyperkalemia aggressively, as it contributes to fatal arrhythmias 4
• Insulin-euglycemia therapy itself improves bicarbonate and lactate levels more effectively than supportive care alone 1

Respiratory Support

• Consider CPAP ventilation for patients with adequate consciousness and no contraindications 4
• Mechanical ventilation may be required, though insulin-euglycemia therapy reduces this need significantly 1
• Ensure proper ventilation of treatment areas as phosphine gas is highly toxic to healthcare providers 4

Adjunctive Therapies with Emerging Evidence

Recent research suggests potential benefit from combination therapy, though evidence is less robust than for insulin-euglycemia:

• Trimetazidine with N-acetyl cysteine and vitamin C showed cardioprotective and antioxidant effects in animal models, improving survival and hemodynamic parameters 6
• Magnesium sulfate may reduce cardiac arrhythmias, though no standardized dosing protocol exists 5

Management of Aluminum Toxicity Component

If serum aluminum levels are measured and elevated (relevant primarily in patients with renal impairment or on dialysis):

• For aluminum levels 60-200 μg/L: Administer deferoxamine (DFO) at 5 mg/kg with high-flux dialysis membranes for effective clearance of aluminum-DFO complexes 4
• For aluminum levels >200 μg/L: Do NOT administer DFO due to high risk of acute aluminum neurotoxicity; instead perform intensive daily dialysis with high-flux membranes for 4-6 weeks 4
• Avoid intravenous iron administration if DFO is given to limit feroxamine formation 4
• DFO therapy carries 91% mortality risk from mucormycosis in dialysis patients; use reduced dosing (5 mg/kg) with expanded intervals 4

Critical Pitfalls to Avoid

• Never rely on vasopressor-only therapy: This approach results in >96% mortality 1
• Do not delay insulin-euglycemia therapy: Early initiation is critical as ingestion of as little as 150-500 mg can be fatal 4
• All exposures require ICU-level care regardless of initial presentation 4
• Do not use aluminum hydroxide as a phosphate binder for more than 1-2 days to avoid cumulative aluminum toxicity 4
• Hyperbaric oxygen therapy has no role in aluminum phosphide poisoning and would dangerously delay appropriate treatment 7

Monitoring for Multi-Organ Failure

• Watch for rhabdomyolysis by monitoring creatinine kinase and potassium; treat with aggressive hydration and urine alkalinization if myoglobinuria develops 4
• Monitor liver function tests as hepatotoxicity commonly occurs 6
• Assess renal function as acute kidney injury frequently complicates the clinical course 4