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Aluminium phosphide poisoning – During the last few years great attention of medical fraternity is focused on large scale poisoning by aluminum phosphide carrying with it high degree of mortality.

Aluminium phosphide marketed in the form of Pellets pack of 3 gms (Quickphos, cellphos) is extensively used in India as a grain preservative. It has been described as an ideal pesticide because it is cheap, highly effective and easy to use.

Each 3 gm tablet contains 56% aluminum phosphide, (ALP) and 44% ammonium carbonate. Each 3 gm tablet can break 1 gm of phosphine (PH3) on exposure to moisture in a chemical reaction which is accelerated by the presence of hydrochloric acid in the stomach.

The human toxicity is acute and occurs either due to inhalation of phosphine from the fumigated grains or after ingestion of aluminium phosphide. The lethal dose for human beings is 150-500 mg/70 KBW.

Till recently most acute cases reported in literature were due to inhalatioll of phosphine but in the last few years most of the cases are due to ingestion of the tablets. The ingestion is usually intentional (accidental or suicidal). The residue in fumigated food grains includes phosphide and hypo-phosphite and in general is below the WHO FAO recommended levels of 0.1 mg/kg of PH3 for raw cereals.


The phosphine liberated in the stomach is widely absorbed throughout the gastrointestinal tract leading to organ damage which is wide spread. Phosphine is also excreted unchanged through the lungs.

In experimental animals phosphine is found to cause non-competitive inhibition of electron transport in cytochrome oxidase leading to diffuse cellular hypoxia. There is now an increasing awareness of the ingestional toxicity of aluminium phosphide and because of its high mortality and lethal nature; it is posing a serious challenge to the acumen of physicians in the Indian subcontinent.


Aluminium phosphide poisoning is wide spread in various parts of India where it is extensively used as a grain preservative and because of its easy availability in the household it has become an important means of self poisoning.

Cases have been extensively reported from northern Belt of India like Chandigarh, Madhya Pradesh, Rajasthan, Punjab and Haryana. In fact it is common to come across on average 3-4 cases of aluminium phosphide poisoning in any big hospital of northern India.

Clinical Manifestations

Aluminium phosphide poisoning is a systemic system and it affects various organ systems like the cardiovascular, gastrointestinal, renal respiratory and hepatobiliary system. The presenting clinical features usually pertain to the G.I. tract and patients with moderate to severe toxicity present with epigastric discomfort, nausea, and vomiting and burning sensation in stomach.

The cardiovascular involvement which may take the form of myocarditis, peripheral circulatory failure, arrhythmias or cardiac failure which is found to be of severe nature and is usually the cause of death. Electro-cardiographic abnormalities include ST-T wave changes, supra ventricular tachycardia with conduction defect, atrial fibrillation, wandering pacemaker, bundle branch block, ventricular tachycardia atrioventricular dissociation and sinus arrest.

Rarely pericarditis has been observed. Nervous system involvement occurs in the form of headache, parasthesia, dizziness, ataxia, intention tremors and peripheral muscle injury. Shock is one of the cardinal manifestations and majority of patients come in shock with thready or impalpable pulse, cold extremities, restlessness, palpitation and tachypnoea. Other features include altered sensorium, cough and seizures.

Occasionally cases may come with picture of adult respiratory distress syndrome (ARDS), pulmonary edema, acute renal failure and peripheral circulatory failure often leading to death which is serious complications.


The pathogenesis of shock a cardinal feature of aluminimum phosphide poisoning is difficult to explain. It may be due to toxic effects of its absorbed products responsible for alterations not only in the patho-physiology of various vital organs but also producing a severe degree of cellular damage. However the possibility of electrolyte disturbances as well as cardiac dysarrhythmias as the cause of shock cannot be ruled out.

The pathogenesis of organ damage (heart, liver, kidneys, lungs and brain) and shock in aluminimum phosphide poisoning is not well understood. Phosphide is reported to cause non-competitive inhibition of cytochrome oxidase of mitochondria in experimental animals.

A marked increase in plasma rennin activity in shock due to aluminimum phosphide is also seen. Hypokalemia and hypo-magnesaemia are thought to play a role in the pathogenesis of cardiac arrhythmias.

Major organs show some degree of damage. Marked congestion, patchy necrosis and mono nuclear infiltration of heart, lungs, stomach, liver kidney and brain has been seen. Lungs show not only septal congestion and hemorrhage, inflammatory infiltration, but also alveolar edema and patchy atelectasis. Vascular congestion and edema is the hallmark of damage in the vital organs.

Various theories ranging from injuries to these vital organs by free radicals or hypoxia due to inhibition of cytochrome oxidase have been postulated.


The diagnosis is based on reliable history and / or the production of remaining tablets / empty container by the attendants of the patient for identification. Patient’s breath has garlic like smell.

Further confirmation can be made by subjecting the gastric lavage fluid to silver nitrate test. This test is based on the property of PH3 to reduce silver nitrate to metallic silver which appears black to the naked eye. A filter paper impregnated with silver nitrate is treated with gastric lavage fluid or placed before the mouth of the patient since significant amounts of Phosphine (PH3) are liberated unchanged through the lungs.

A positive test is given by the color change to black. The color change may take a few hours and in order to avoid false positive results due to the presence of hydrogen sulphide in the atmosphere air, a control should be used. Investigations include ECG, blood urea, serum bilirubin, blood gas analysis and urine examination.


There is no known antidote to aluminium phosphide and management of the patient is mainly supportive in order to sustain life till phosphine is excreted from the body by lungs and kidneys. Gastric lavage with potassium permanganate (1 in 10,000) is to be done in all cases. Patients in shock are managed by intravenous fluids (4-6 liters of normal saline) dopamine and steroids.

There is controversy about the use of magnesium sulphate but then magnesium sulfate is used because of its membrane stabilizing effect as well as for its anti-arrhythmic action. Intravenous magnesium sulphate (a loading dose of 4 gm over 4 hours followed by 1 gm I/V 6 hourly) and calcium gluconate IG I/V 6 hourly are employed. Calcium gluconate is beneficial because of its cardio protective action.

Since plasma rennin activity is high in such patients. ACE inhibitors have been employed by some to combat shock. Since commonest abnormality in all such patients is severe hypoxemia with metabolic acidosis, in addition to above measures to combat acidosis intravenous sodium bicarbonate is employed. Patients vital functions including urinary output, blood pressure control and cardiac arrhythmias are monitored round the clock.


Aluminium phosphide poisoning carries a high degree of mortality. Most of the deaths occur in first twenty four hours. Severe metabolic acidosis, shock, peripheral circulatory failure and acute renal failure are poor prognostic indicators. Development of various life threatening cardiac arrhythmias also pertains to the serious mature of disease.

Patients who recover, in such people recovery is complete and no long term squeal are seen in the survivors. A large dose of it is associated with higher mortality but it is difficult to identify the minimum lethal dose as the most important factor affecting mortality is whether the tablets were pre-exposed or not. Tablets pre-exposed to atmosphere with consequent loss of phosphine are less harmful than tablets in sealed containers.

To summaries, aluminimum phosphide poisoning due to ingestion is a life threatening emergency with very high mortality and in the absence of a specific antidote poses a serious problem and challenge to the acumen of physicians.

Aluminium phosphide poisoning Summary

• Aluminium phosphide – grain preservative – poisoning – suicidal/accidental.

• Each 3 gm tablet contains 56% aluminium phosphide (ALP) and 44% aluminium carbonate.

• Toxicity either by inhalation or by ingestion.

• Systemic contamination affects various organs.

• Toxicity – nausea, vomiting, peripheral circulatory failure, cardiac arrhythmias. shock. ARDS Acute renal failure, death.

• No known antidote. Gastric lavage with potassium permagnate (1 in 10,000 dilutions).

• Intravenous magnesium sulphate (loading dose of 4 gm over 6 hrs followed by IG I/V 6 hrly) + calcium gluconate IG I/V 6 hrly.



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