Discuss the clinical features, investigations and management of aluminium phosphide poisoning.

Introduction

Aluminium phosphide (ALP, "rice tablet", "wheat pill", celphos, quickphos) is a solid fumigant pesticide used to protect stored grain. It is a major cause of fatal self-poisoning in North India, particularly in agricultural regions. Mortality is extremely high — commonly quoted at 50–90% — because there is no antidote and death occurs from refractory circulatory failure.

A single fresh 3 g tablet is potentially lethal. Tablets exposed to air lose potency, which explains occasional survival after large ingestions.

Mechanism

On contact with moisture and gastric acid, ALP liberates phosphine gas (PH3):

AlP + 3H2O → Al(OH)3 + PH3↑

Phosphine is a potent mitochondrial poison:

• Inhibits cytochrome c oxidase, blocking oxidative phosphorylation and halting cellular ATP production.
• Generates reactive oxygen species with lipid peroxidation, and inhibits catalase and superoxide dismutase.
• Causes direct myocardial injury with profound depression of contractility, and widespread endothelial damage with capillary leak.

The result is cellular hypoxia despite adequate oxygenation, with the heart most severely affected.

Clinical Features

• Early (minutes to hours): vomiting, epigastric pain, retrosternal burning, nausea, and a characteristic garlic or decaying-fish odour of the breath and vomitus — a valuable diagnostic clue.
• Cardiovascular — dominant and fatal: profound refractory hypotension and shock, myocarditis, arrhythmias of every kind (sinus tachycardia, ventricular ectopics, VT, VF, conduction block), and cardiogenic pulmonary oedema. Shock typically appears within 6 hours and is remarkably resistant to fluids and inotropes.
• Respiratory: dyspnoea, ARDS, pulmonary oedema.
• Metabolic: severe high anion gap metabolic acidosis from lactate accumulation, hypoglycaemia (or hyperglycaemia), hypomagnesaemia and hypokalaemia.
• Hepatic and renal: transaminitis, jaundice, acute kidney injury.
• Neurological: restlessness, agitation, confusion, coma; seizures are less common.
• Late survivors may develop hepatic dysfunction and, rarely, oesophageal stricture.

Investigations

• ECG and continuous cardiac monitoring — ST-T changes, arrhythmias, conduction defects.
• Arterial blood gas — severe metabolic acidosis with raised lactate; this is a major prognostic marker.
• Electrolytes with magnesium, blood glucose, renal and liver function, cardiac troponin, and coagulation profile.
• Echocardiography — reduced ejection fraction and global hypokinesia, guiding inotrope choice.
• Silver nitrate paper test on gastric aspirate or breath — paper impregnated with silver nitrate blackens in the presence of phosphine, a simple confirmatory bedside test.
• Chest X-ray for pulmonary oedema and ARDS.

Management — Supportive, as There Is No Antidote

1. Resuscitation

• Airway, breathing, circulation; high-flow oxygen; secure large-bore access; intubate and ventilate for respiratory failure or coma.
• Staff protection: phosphine gas is released from the patient's vomitus and gastric contents; manage in a well-ventilated area and avoid mouth-to-mouth resuscitation.

2. Gastric decontamination

• Gastric lavage with potassium permanganate solution — oxidises phosphine to non-toxic phosphate. Traditionally recommended and still widely practised in India.
• Coconut oil has been used to retard phosphine release, and sodium bicarbonate lavage to reduce acid-driven hydrolysis.
• Activated charcoal may be given.
• Decontamination is most useful very early and must never delay resuscitation.

3. Circulatory support — the central challenge

• Cautious fluid resuscitation guided by central venous pressure or echocardiography; excessive fluid worsens pulmonary oedema in a failing myocardium.
• Vasopressors and inotropes — noradrenaline, dopamine, dobutamine — usually in high doses, often with disappointing response.
• Intravenous magnesium sulphate — widely used in India for its antiarrhythmic and membrane-stabilising effect and its correction of the hypomagnesaemia that accompanies poisoning. Evidence is observational rather than definitive.
• Correct acidosis with bicarbonate in severe acidaemia; correct hypoglycaemia, hypokalaemia and hypomagnesaemia.
• Reported adjuncts with limited evidence: N-acetylcysteine (antioxidant), intravenous lipid emulsion, glucose-insulin-potassium infusion, and extracorporeal membrane oxygenation (ECMO) in centres where available, which offers the best reported outcomes in refractory cardiogenic shock.

4. Monitoring and aftercare

Continuous ECG, invasive blood pressure where possible, urine output, serial ABG and lactate. Lactate clearance and shock reversal in the first 24 hours are the strongest prognostic indicators. Psychiatric evaluation for all survivors of deliberate ingestion.