A Systematic Review of Aluminium Phosphide Poisoning

Abstract

Every year, about 300,000 people die because of pesticide poisoning worldwide. The most common pesticide agents are organophosphates and phosphides, aluminium phosphide (AlP) in particular. AlP is known as a suicide poison that can easily be bought and has no effective antidote. Its toxicity results from the release of phosphine gas as the tablet gets into contact with moisture. Phosphine gas primarily affects the heart, lungs, gastrointestinal tract, and kidneys. Poisoning signs and symptoms include nausea, vomiting, restlessness, abdominal pain, palpitation, refractory shock, cardiac arrhythmias, pulmonary oedema, dyspnoea, cyanosis, and sensory alterations. Diagnosis is based on clinical suspicion, positive silver nitrate paper test to phosphine, and gastric aspirate and viscera biochemistry. Treatment includes early gastric lavage with potassium permanganate or a combination with coconut oil and sodium bicarbonate, administration of charcoal, and palliative care. Specifi c therapy includes intravenous magnesium sulphate and oral coconut oil. Moreover, acidosis can be treated with early intravenous administration of sodium bicarbonate, cardiogenic shock with fl uid, vasopresor, and refractory cardiogenic shock with intra-aortic baloon pump or digoxin. Trimetazidine may also have a useful role in the treatment, because it can stop ventricular ectopic beats and bigeminy and preserve oxidative metabolism. This article reviews the epidemiological, toxicological, and clinical/pathological aspects of AlP poisoning and its management.

Use of continuous renal replacement therapy in acute aluminum phosphide poisoning: a novel therapy

“…3 The cardiac manifestations are common in severe poisoning which include profound hypotension, dry pericarditis, myocarditis, acute congestive heart failure and ECG abnormalities like dysrhythmias, ST-T wave changes and conduction defects. 3,4 Other clinical features are respiratory distress, headache, dizziness, convulsion, encephalopathy and coma. 3 The rare clinical features include disseminated intravascular coagulation, hepatic necrosis and renal failure.…”

“…There are various mechanisms postulated that includes inhibition of cytochrome C oxidase, oxidative stress and extra-mitochondrial release of free oxygen radicals that causes ineffective adenosine triphosphate (ATP) production, lipid peroxidation and protein denaturation of the cell membrane in various organs. [2][3][4] The organs predominantly affected are heart, lungs, kidneys and gastrointestinal tract. 4 The most common clinical features include nausea, vomiting, abdominal pain.…”

“…[2][3][4] The organs predominantly affected are heart, lungs, kidneys and gastrointestinal tract. 4 The most common clinical features include nausea, vomiting, abdominal pain. 3 The cardiac manifestations are common in severe poisoning which include profound hypotension, dry pericarditis, myocarditis, acute congestive heart failure and ECG abnormalities like dysrhythmias, ST-T wave changes and conduction defects.…”

“…3 The rare clinical features include disseminated intravascular coagulation, hepatic necrosis and renal failure. 2,4 The diagnosis is clinical with positive history of ingestion, typical clinical features, garlicky odor, arrhythmias and profound shock. [2][3][4] The mortality rate of AP poisoning is 31% even in tertiary care centers with fatal dose between 0.15 and 0.5 grams.…”

“…2,4 The diagnosis is clinical with positive history of ingestion, typical clinical features, garlicky odor, arrhythmias and profound shock. [2][3][4] The mortality rate of AP poisoning is 31% even in tertiary care centers with fatal dose between 0.15 and 0.5 grams. 5 The most common cause of mortality is cardiogenic shock in these patients.…”