Acute aluminium phosphide poisoning (AAlPP) is a large, though under-reported, problem in the Indian subcontinent. Aluminium phosphide (AlP), which is readily available as a fumigant for stored cereal grains, sold under various brand names such as QuickPhos and Celphos, is highly toxic, especially when consumed from a freshly opened container. Death results from profound shock, myocarditis and multi-organ failure. Aluminium phosphide has a fatal dose of between 0.15 and 0.5 grams (0.0053 and 0.0176Â oz). It has been reported to be the most common cause of suicidal death in North India. Several incidents of death in travelers in Thailand and other parts of Southeast Asia may have been caused by aluminum phosphide or chlorpyrifos, an organophosphate insecticide, used in an attempt to kill bedbugs in hotels.
Mortality rates
The mortality rates from AAlPP vary from 40 to 80 percent. The actual numbers of cases may be much larger, as less than five percent of those with AAlPP eventually reach a tertiary care center. Since 1992, when aluminium phosphide became freely available in the market, it had, reportedly, overtaken all other forms of deliberate poisoning, such as organophosphorus and barbiturate poisoning, in North India. In a 25-year-long study on 5,933 unnatural deaths in northwest India, aluminium phosphide poisoning was found to be the major cause of death among all cases of poisonings.
Mechanism of toxicity
The toxicity of aluminium phosphide is attributed to the liberation of phosphine gas, a cytotoxic compound that causes free radical mediated injury, inhibits vital cellular enzymes and is directly corrosive to tissues. The following reaction releases phosphine when AlP reacts with water in the body:
- AlP + 3 H2O â†' Al(OH)3 + PH3, and
- AlP + 3 HCl â†' AlCl3 + PH3 (stomach)
Signs, symptoms, and diagnosis
After ingestion, toxic features usually develop within a few minutes. The major lethal consequence of aluminium phosphide ingestion is profound circulatory collapse, is reportedly secondary to these toxins generated, which lead due to direct effects on cardiomyocytes, fluid loss, and adrenal gland damage. The signs and symptoms are non-specific, dose dependent and evolve with time passing. The dominant clinical feature is severe hypotension refractory to dopamine therapy. Other features may include dizziness, fatigue, tightness in the chest, headache, nausea, vomiting, diarrhoea, ataxia, numbness, paraesthesia, tremor, muscle weakness, diplopia and jaundice. If severe inhalation occurs, the patient may develop acute respiratory distress syndrome (ARDS), heart failure, arrhythmias, convulsion and coma. Late manifestation include liver and kidney toxicities.
The diagnosis of AAlP usually depends on the clinical suspicion or history (self-report or by attendants). At some places, tablets of AlP are also referred to as “rice tablets†and, if there is a history of rice tablet ingestion, then it should be treated differently from other types of rice tablets that are made up of herbal products. For a silver nitrate test on gastric aspirate, diluted gastric content can be positive.
Management and outcome
The management of AAlPP remains purely supportive because no specific antidote exists. Mortality rates approach 60%. The role of magnesium sulfate as a potential therapy in AlP poisoning may decrease the likelihood of a fatal outcome, and has been described in many studies. After ingestion, removal of unabsorbed poison from the gut ("gut decontamination"), especially if administered within 1â€"2 hours, can be effective. Potassium permanganate (1:10,000) gastric lavage can decompose the toxin. All patients of severe AlP poisoning require continuous invasive hemodynamic monitoring and early resuscitation with fluid and vasoactive agents.
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