Toxicology

Aluminum phosphide (AlP) reacts with moisture (including atmospheric humidity and gastric juices) to release phosphine gas (PH3), which is highly toxic. Phosphine disrupts mitochondrial oxidative phosphorylation, leading to cellular hypoxia and energy depletion. Additionally, phosphine induces the formation of highly reactive hydroxyl radicals, contributing to cellular damage and multiple organ failure.

Clinical Presentation

Symptoms of aluminum phosphide poisoning can range from mild to severe and are often acute, manifesting within minutes to hours after exposure:

• Gastrointestinal Symptoms: Nausea, vomiting, abdominal pain, and diarrhea. Vomiting may include the characteristic smell of garlic or fish due to the released phosphine gas.
• Cardiovascular Symptoms: Hypotension, tachycardia, chest pain, and in severe cases, acute myocardial depression and congestive heart failure.
• Respiratory Symptoms: Dyspnea, cough, and pulmonary edema.
• Neurological Symptoms: Dizziness, headache, lethargy, seizures, and coma.
• Metabolic Changes: Metabolic acidosis is common due to increased lactic acid production from cellular hypoxia.

Diagnosis

Diagnosis is primarily based on the history of exposure and clinical presentation. Specific tests include:

• Blood Tests: To check for metabolic acidosis and electrolyte imbalances.
• Electrocardiogram (ECG): May show signs of myocardial injury or other cardiac effects.
• Chest X-ray or CT Scan: To detect pulmonary edema or other respiratory complications.
• Measurement of Phosphine Levels: Not routinely available and rarely performed in clinical settings.

Management

Management of aluminum phosphide poisoning focuses on immediate supportive care and specific treatments:

• Decontamination: If ingestion is suspected, gastric lavage may be performed with a slurry of activated charcoal, although its efficacy is controversial because phosphine is rapidly absorbed.
• Supportive Care: Includes fluid resuscitation, electrolyte balance, and management of hypotension using vasopressors if necessary.
• Cardiovascular Support: Echocardiography to assess myocardial function and appropriate cardiac support including inotropes if indicated.
• Respiratory Support: Oxygen supplementation or mechanical ventilation for patients experiencing respiratory distress or failure.
• Correction of Metabolic Acidosis: Administration of intravenous sodium bicarbonate.
• Antidotes: There is no specific antidote for phosphine toxicity. Some reports suggest the use of magnesium sulfate as a potential treatment to reduce the severity of cardiac toxicity, but evidence is limited.
• Prevention of Absorption: Attempts to limit further absorption of the toxin using agents like activated charcoal can be considered, although their benefit in aluminum phosphide poisoning is not well-established.

Prognosis

The prognosis of aluminum phosphide poisoning is generally poor, especially in cases with significant cardiovascular compromise. Early and aggressive treatment improves survival chances, but mortality remains high due to profound shock and myocardial damage.

Prevention

Preventive measures are crucial in environments where aluminum phosphide is used:

• Proper Storage and Handling: Strict guidelines to prevent accidental exposure.
• Education and Training: For workers handling these compounds to ensure they understand the risks and safety measures.
• Use of Personal Protective Equipment (PPE): Including masks and gloves to minimize exposure risks.