When to administer magnesium sulphate (MgSO4) in a patient with aluminium phosphide poisoning and signs of cardiac instability, such as arrhythmias or hypotension?

Magnesium Sulphate in Aluminium Phosphide Poisoning: When to Administer

Magnesium sulphate should be administered when patients with aluminium phosphide poisoning develop cardiac arrhythmias, particularly torsades de pointes, polymorphic ventricular tachycardia with QT prolongation, or other ventricular arrhythmias, despite the lack of proven mortality benefit.

Primary Indication: Cardiac Arrhythmias

The American Heart Association guidelines support magnesium sulphate specifically for torsades de pointes and polymorphic VT with prolonged QT interval in aluminium phosphide poisoning 1. This recommendation extends from the broader guideline that intravenous magnesium sulfate is recommended for patients with QT prolongation due to medication or acquired factors who develop recurrent torsades de pointes 2.

Specific Arrhythmia Scenarios:

• Torsades de pointes with acquired QT prolongation: Administer IV magnesium sulfate as first-line antiarrhythmic therapy 2
• Recurrent polymorphic VT: Use magnesium when associated with QT prolongation 1
• Ventricular arrhythmias in general: Magnesium is often administered when VAs are present in toxic exposures 2

Critical Context: Limited Efficacy in Aluminium Phosphide

Despite widespread use, magnesium sulphate has NOT been proven to reduce mortality in aluminium phosphide poisoning. A randomized study of 105 patients found no significant difference in mortality rates between those treated with and without magnesium sulphate 3. Another study of 50 patients confirmed that magnesium sulphate therapy did not improve survival, with deaths primarily due to intractable shock, shock coupled with arrhythmias, and ARDS 4.

Key Mechanistic Considerations:

• Hypomagnesemia is NOT a feature of aluminium phosphide poisoning: Serum and RBC magnesium levels remain within normal range throughout the first 24 hours 4
• Tissue magnesium is actually elevated: Non-survivors show significantly higher tissue magnesium content in brain, stomach, kidneys, liver, lungs, and heart compared to controls 4
• Different mechanism than organophosphates: Aluminium phosphide releases phosphine gas causing direct cellular toxicity and intractable shock, NOT cholinergic crisis 5

Dosing Protocol (When Arrhythmias Present)

Based on the studied regimen 3:

• Initial bolus: 1.0 g (8.1 mEq or 4.05 mmol) magnesium sulphate in 100 mL of 5% dextrose IV over bolus
• Loading phase: 1.0 g every hour for 3 successive hours
• Maintenance: 1.0 g every 6 hours for 24 hours (total 30 mmol over 24 hours initially, then 16 mmol daily for up to 5 days)

Electrolyte repletion targets per AHA guidelines: Maintain potassium ≥4.0 mmol/L and magnesium ≥2.0 mmol/L 2.

Critical Safety Monitoring

Patients with renal failure can develop magnesium toxicity at lower doses 5, 1. Cardiac effects of magnesium toxicity include:

• AV block
• Bradycardia
• Hypotension
• Cardiac arrest 5

Have calcium gluconate or calcium chloride immediately available for reversal of magnesium toxicity 5. Monitor for adverse effects including flushing, sweating, hypotension, depressed reflexes, flaccid paralysis, hypothermia, circulatory collapse, and respiratory paralysis 6.

When Magnesium Fails

If recurrent torsades de pointes cannot be suppressed with IV magnesium, increase heart rate with atrial or ventricular pacing or isoproterenol 2.

For refractory cardiogenic shock or cardiac arrest despite maximal medical therapy including magnesium, VA-ECMO is reasonable 2. Case reports demonstrate successful outcomes with ECMO in aluminium phosphide poisoning with severe cardiotoxicity 7, 8.

Common Pitfalls to Avoid

• Do not rely on magnesium as primary therapy: The immediate causes of death (intractable shock, arrhythmias, ARDS) require aggressive supportive management, continuous cardiac monitoring, and appropriate antiarrhythmic agents 4
• Do not assume hypomagnesemia: Unlike other toxidromes, magnesium levels are normal or elevated in aluminium phosphide poisoning 4
• Do not confuse with organophosphate poisoning: Atropine and pralidoxime are NOT indicated 5
• Monitor magnesium levels closely: Particularly in renal impairment to prevent iatrogenic toxicity 1

Practical Algorithm

1. Confirm aluminium phosphide poisoning with history and clinical presentation (shock, metabolic acidosis, arrhythmias)
2. Initiate aggressive supportive care as primary management
3. Monitor continuous ECG for arrhythmias and QT prolongation
4. If torsades de pointes or polymorphic VT develops: Administer IV magnesium sulphate per protocol above 2, 1
5. If arrhythmias persist: Consider pacing or isoproterenol 2
6. If refractory shock/arrest: Consider VA-ECMO 2
7. Throughout: Monitor for magnesium toxicity with calcium reversal agent ready 5, 6