Aluminium phosphide poisoning - all true except
inhibits cytochrome a oxidase Aluminium phosphide produces phosphine gas on coming in contact with moisture which inhibits cytochrome c oxidase (and not cytochrome a oxidase). Sub-endocardial infarction and esophageal strictures both have been described with ALP poisoning (Ref: various journals on web) Aluminium phosphide poisoning It is one of the most common causes of acute poisoning in India. Acute aluminium phosphide (Celphos) poisoning is an extremely lethal poisoning. The absence of a specific antidote results in very high moality and the key to treatment lies in rapid decontamination and institution of resuscitative measures. Aluminium phosphide (A1P) is one of the most commonly used grain fumigants because of its propeies which are considered to be near ideal; it is toxic to all stages of insects, highly potent, does not affect seed bility, is free from toxic residues. After ingestion of aluminium phosphide, phosphine gas is released in the stomach which after absorption into the circulation results in early signs and symptoms. AlP causes widespread organ damage due to cellular hypoxia as a consequence of non-competitive inhibition of the enzyme cytochrome oxidase of the mitochondria. Organs with the greatest oxygen requirements appear to be especially sensitive to phosphine, including the brain, kidneys, hea, and liver. The initial symptoms after ingestion are retrosternal burning, epigastric pain and vomiting which are soon followed by development of hypotension which is the cardinal feature. Other common features are restlessness, tachypnoea, oliguria or anuria, jaundice, impaired sensorium and cardiac arrhythmias. Several EKG abnormalities have been described. These have been attributed to focal myocardial necrosis and changes in action membrane potential as result of alteration in permeability of Na+, Mg++ and Ca+ ions Diagnosis A positive history of ingestion is the basis of diagnosis in most cases. The presence of typical clinical features, garlicky (or decaying fish) odour from the mouth and highly variable arrhythmias in a young patient with shock and no previous history of cardiac disease points towards aluminium phosphide poisoning. Confirmation can be done by the Silver Nitrate Test. In this test, 5 ml of gastric aspirate and 15 ml of water are put in a flask and the mouth of the flask is covered by filter paper impregnated with 0.1N silver nitrate. The flask is heated at 50 o C for 15 to 20 min. If phosphine is present the filter paper turns black. However the most specific and sensitive method for detecting the presence of P1-13 in blood/air is gas chromatography. (Vies Jansen A, Thrane KE. Gas chromatographic determination of PH3 in ambient air. Analysis 1978;103:1195-8.) Management The management continues to be unsatisfactory as there is no specific antidote and remains suppoive only. The most impoant factor for success is resuscitation of shock and institution of suppoive measures as soon as possible. To reduce the absorption of phosphine, gastric lavage with potassium permanganate (1:10,000) is done. Permanganate is used as it oxidizes PH3 to form non-toxic phosphate. This is followed by a slurry of activated charcoal (approximately 100 gin) given through a nasogastric tube. A cathaic (liquid paraffin) is given to accelerate the excretion of aluminium phosphide and phosphine. Antacids and proton pump blockers are added for symptomatic relief.
subendocardial infarction
produces phosphine gas
oesophageal stricture
inhibits cytochrome a oxidase