Aluminium phosphide poisoning
Encyclopedia
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, is highly toxic 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. It has been reported to be the most common cause of suicidal death in North India
.
The mortality rates from AAlPP published in the literature vary from 40–80%. However, the actual numbers of cases affected are much larger, as less than 5% of those with AAlPP eventually reach a tertiary care centre. Since 1992, when aluminium phosphide became freely available in the market, it has, reportedly, overtaken all other forms of deliberate poisoning, such as organophosphorus and barbiturate poisoning in North India. In a 25 year study on 5,933 unnatural case fatalities in north-west India, AAlPP was concluded to be the major cause of death among all poisonings.
Despite these large numbers, there has been little progress in our understanding of the characteristics of the poison and limited Indian data is available on the predictors of mortality in these patients. One retrospectively study looked at the profile of patients presenting with AAlPP to identify the factors at admission that might be useful in predicting mortality.
for combination with water molecules is:
Phosphine a nucleophile, acts as a strong reducing agent capable of inhibiting cellular enzymes involved in several metabolic processes. Early studies on phosphine demonstrated specific inhibitory effects on mitochondrial cytochrome c
oxidase
. Experimental and observational studies have subsequently demonstrated that the inhibition of cytochrome c oxidase and other enzymes leads to the generation superoxide radicals and cellular peroxides. Cellular injury subsequently occurs through lipid peroxidation and other oxidant mechanisms.
The major lethal consequence of aluminium phosphide ingestion i.e., profound circulatory collapse, is reportedly secondary to these toxins generated, which lead to direct effects on cardiac myocytes, fluid loss, and adrenal gland damage. In addition, phosphine also has corrosive effects on tissues.
. Other features may include dizziness, easy fatigability, tightness in the chest, headache, nausea
, vomiting, diarrhoea, ataxia
, numbness, paraesthesia, tremor, muscle weakness, diplopia
and jaundice
. In severe inhalation toxicity, the patient may develop acute respiratory distress syndrome (ARDS), cardiac failure, cardiac arrhythmias, convulsion and coma, and late manifestation of hepatotoxicity and nephrotoxicity may also occur.
After ingestion, toxic features usually develop within few minutes. In mild poisoning nausea, repeated vomiting, diarrhoea, headache, abdominal discomfort or pain and tachycardia are common clinical features, and these patients usually show recovery. On the other hand, in moderate to severe ingestional poisoning, the signs and symptoms of the gastrointestinal, cardiovascular, respiratory and nervous systems appear initially and, later on, features of hepatic and renal failure and disseminated intravascular coagulation may also occur.
The diagnosis of AlP 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 differentiate from other types of rice tablet that are made up of herbal products.
Silver nitrate
test on gastric aspirate, diluted gastric content is heated in a flask up to 50 °C for 15–20 minutes, keeping silver nitrate paper on the mouth of the flask. If phosphine
is present then the paper will turn black due to silver phosphate. As hydrogen sulfide
also changes the colour, its presence could be differentiated using lead acetate paper, i.e. both papers will turn black in the presence of hydrogen sulfide. Further confirmation of phosphine can be done by putting a drop of ammonium molybdate solution on the black-turned filter paper, and the colour of the paper will change to blue.
as a potential therapy in AlP poisoning to decrease the likelihood of a fatal outcome has been described in many studies.
After ingestion, effectiveness of gut decontamination to reduce the absorption of unabsorbed poison is primarily dependent on the duration of exposure of poison and is useful if it is done within 1–2 h. Gut decontamination should not be performed if the patient has an unprotected airway without endotracheal intubation. Potassium permanganate (1:10,000) is used for gastric lavage through a nasogastric tube as it oxidises phosphine to non-toxic phosphate. This can be followed by approximately 100 g of activated charcoal to reduce absorption if the patient arrives within 1 h after ingestion of a large amount of poison. There are insufficient data to support the routine use of activated charcoal in AlP poisoning as phosphine gas is rapidly absorbed through the gut. Also, position paper on activated charcoal recommends that it should not be administered routinely in the management of poisoned patients.
Myocardial injury and hemodynamic instability is one of the most important features, and most of the deaths in ALP poisoning have been reported to be due to cardiovascular failure. All patients of severe AlP poisoning require continuous invasive hemodynamic monitoring and early resuscitation with fluid and vasoactive agents. Phosphine virtually affects all the organs in body and, therefore, early identification of impending organ failure and appropriate supportive therapy is extremely important till the toxin is excreted from the body. Requirement of endotracheal intubation and mechanical ventilation usually depends on the severity of the acute lung injury and, sometimes, due to poor mental status. Hemodialysis is probably not very effective in removing phosphine but is helpful when renal failure, severe metabolic acidosis or fluid overload is present.
Aluminium phosphide
Aluminium phosphide is an inorganic compound used as a wide band gap semiconductor and a fumigant. This colourless solid is generally sold as a grey-green-yellow powder due to the presence of impurities arising from hydrolysis and oxidation.-Properties:...
(AlP), which is readily available as a fumigant for stored cereal grains, is highly toxic when consumed from a freshly opened container. Death results from profound shock, myocarditis
Myocarditis
Myocarditis is inflammation of heart muscle . It resembles a heart attack but coronary arteries are not blocked.Myocarditis is most often due to infection by common viruses, such as parvovirus B19, less commonly non-viral pathogens such as Borrelia burgdorferi or Trypanosoma cruzi, or as a...
and multi-organ failure. Aluminium phosphide has a fatal dose of between 0.15 and 0.5 grams. It has been reported to be the most common cause of suicidal death in North India
North India
North India, known natively as Uttar Bhārat or Shumālī Hindustān , is a loosely defined region in the northern part of India. The exact meaning of the term varies by usage...
.
The mortality rates from AAlPP published in the literature vary from 40–80%. However, the actual numbers of cases affected are much larger, as less than 5% of those with AAlPP eventually reach a tertiary care centre. Since 1992, when aluminium phosphide became freely available in the market, it has, reportedly, overtaken all other forms of deliberate poisoning, such as organophosphorus and barbiturate poisoning in North India. In a 25 year study on 5,933 unnatural case fatalities in north-west India, AAlPP was concluded to be the major cause of death among all poisonings.
Despite these large numbers, there has been little progress in our understanding of the characteristics of the poison and limited Indian data is available on the predictors of mortality in these patients. One retrospectively study looked at the profile of patients presenting with AAlPP to identify the factors at admission that might be useful in predicting mortality.
Mechanism of intoxication
Aluminium phosphide is an extremely toxic compound and has resulted in a high mortality rate. The toxicity of aluminium phosphide is attributed to the liberation of phosphine gas, which is cytotoxic and causes free radical mediated injury. The chemical formulaChemical formula
A chemical formula or molecular formula is a way of expressing information about the atoms that constitute a particular chemical compound....
for combination with water molecules is:
- AlP + 3 H2O → Al(OH)3 + PH3, and
- AlP + 3 HCl → AlCl3 + PH3 (stomach)
Phosphine a nucleophile, acts as a strong reducing agent capable of inhibiting cellular enzymes involved in several metabolic processes. Early studies on phosphine demonstrated specific inhibitory effects on mitochondrial cytochrome c
Cytochrome c
The Cytochrome complex, or cyt c is a small heme protein found loosely associated with the inner membrane of the mitochondrion. It belongs to the cytochrome c family of proteins. Cytochrome c is a highly soluble protein, unlike other cytochromes, with a solubility of about 100 g/L and is an...
oxidase
Oxidase
An oxidase is any enzyme that catalyzes an oxidation-reduction reaction involving molecular oxygen as the electron acceptor. In these reactions, oxygen is reduced to water or hydrogen peroxide ....
. Experimental and observational studies have subsequently demonstrated that the inhibition of cytochrome c oxidase and other enzymes leads to the generation superoxide radicals and cellular peroxides. Cellular injury subsequently occurs through lipid peroxidation and other oxidant mechanisms.
The major lethal consequence of aluminium phosphide ingestion i.e., profound circulatory collapse, is reportedly secondary to these toxins generated, which lead to direct effects on cardiac myocytes, fluid loss, and adrenal gland damage. In addition, phosphine also has corrosive effects on tissues.
Signs and symptoms
The signs and symptoms are non-specific, instantaneous and depend on the dose, route of entry, and time lapse since exposure to the poison. After inhalation exposure, patients commonly have airway irritation and breathlessness. The dominant clinical feature is severe hypotension refractory to dopamineDopamine
Dopamine is a catecholamine neurotransmitter present in a wide variety of animals, including both vertebrates and invertebrates. In the brain, this substituted phenethylamine functions as a neurotransmitter, activating the five known types of dopamine receptors—D1, D2, D3, D4, and D5—and their...
. Other features may include dizziness, easy fatigability, tightness in the chest, headache, nausea
Nausea
Nausea , is a sensation of unease and discomfort in the upper stomach with an involuntary urge to vomit. It often, but not always, precedes vomiting...
, vomiting, diarrhoea, ataxia
Ataxia
Ataxia is a neurological sign and symptom that consists of gross lack of coordination of muscle movements. Ataxia is a non-specific clinical manifestation implying dysfunction of the parts of the nervous system that coordinate movement, such as the cerebellum...
, numbness, paraesthesia, tremor, muscle weakness, diplopia
Diplopia
Diplopia, commonly known as double vision, is the simultaneous perception of two images of a single object that may be displaced horizontally, vertically, or diagonally in relation to each other...
and jaundice
Jaundice
Jaundice is a yellowish pigmentation of the skin, the conjunctival membranes over the sclerae , and other mucous membranes caused by hyperbilirubinemia . This hyperbilirubinemia subsequently causes increased levels of bilirubin in the extracellular fluid...
. In severe inhalation toxicity, the patient may develop acute respiratory distress syndrome (ARDS), cardiac failure, cardiac arrhythmias, convulsion and coma, and late manifestation of hepatotoxicity and nephrotoxicity may also occur.
After ingestion, toxic features usually develop within few minutes. In mild poisoning nausea, repeated vomiting, diarrhoea, headache, abdominal discomfort or pain and tachycardia are common clinical features, and these patients usually show recovery. On the other hand, in moderate to severe ingestional poisoning, the signs and symptoms of the gastrointestinal, cardiovascular, respiratory and nervous systems appear initially and, later on, features of hepatic and renal failure and disseminated intravascular coagulation may also occur.
The diagnosis of AlP 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 differentiate from other types of rice tablet that are made up of herbal products.
Silver nitrate
Silver nitrate
Silver nitrate is an inorganic compound with chemical formula . This compound is a versatile precursor to many other silver compounds, such as those used in photography. It is far less sensitive to light than the halides...
test on gastric aspirate, diluted gastric content is heated in a flask up to 50 °C for 15–20 minutes, keeping silver nitrate paper on the mouth of the flask. If phosphine
Phosphine
Phosphine is the compound with the chemical formula PH3. It is a colorless, flammable, toxic gas. Pure phosphine is odourless, but technical grade samples have a highly unpleasant odor like garlic or rotting fish, due to the presence of substituted phosphine and diphosphine...
is present then the paper will turn black due to silver phosphate. As hydrogen sulfide
Hydrogen sulfide
Hydrogen sulfide is the chemical compound with the formula . It is a colorless, very poisonous, flammable gas with the characteristic foul odor of expired eggs perceptible at concentrations as low as 0.00047 parts per million...
also changes the colour, its presence could be differentiated using lead acetate paper, i.e. both papers will turn black in the presence of hydrogen sulfide. Further confirmation of phosphine can be done by putting a drop of ammonium molybdate solution on the black-turned filter paper, and the colour of the paper will change to blue.
Management and outcome
The management of AAlPP remains purely supportive because no specific antidote is known. Aluminium phosphide is an extremely toxic compound with mortality close to 60%. The role of magnesium sulfateMagnesium sulfate
Magnesium sulfate is a chemical compound containing magnesium, sulfur and oxygen, with the formula MgSO4. It is often encountered as the heptahydrate epsomite , commonly called Epsom salt, from the town of Epsom in Surrey, England, where the salt was distilled from the springs that arise where the...
as a potential therapy in AlP poisoning to decrease the likelihood of a fatal outcome has been described in many studies.
After ingestion, effectiveness of gut decontamination to reduce the absorption of unabsorbed poison is primarily dependent on the duration of exposure of poison and is useful if it is done within 1–2 h. Gut decontamination should not be performed if the patient has an unprotected airway without endotracheal intubation. Potassium permanganate (1:10,000) is used for gastric lavage through a nasogastric tube as it oxidises phosphine to non-toxic phosphate. This can be followed by approximately 100 g of activated charcoal to reduce absorption if the patient arrives within 1 h after ingestion of a large amount of poison. There are insufficient data to support the routine use of activated charcoal in AlP poisoning as phosphine gas is rapidly absorbed through the gut. Also, position paper on activated charcoal recommends that it should not be administered routinely in the management of poisoned patients.
Myocardial injury and hemodynamic instability is one of the most important features, and most of the deaths in ALP poisoning have been reported to be due to cardiovascular failure. All patients of severe AlP poisoning require continuous invasive hemodynamic monitoring and early resuscitation with fluid and vasoactive agents. Phosphine virtually affects all the organs in body and, therefore, early identification of impending organ failure and appropriate supportive therapy is extremely important till the toxin is excreted from the body. Requirement of endotracheal intubation and mechanical ventilation usually depends on the severity of the acute lung injury and, sometimes, due to poor mental status. Hemodialysis is probably not very effective in removing phosphine but is helpful when renal failure, severe metabolic acidosis or fluid overload is present.