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J Emerg Trauma Shock. 2011 Jul-Sep; 4(3): 378–384.
PMCID: PMC3162709
Copyright : © Journal of Emergencies, Trauma, and Shock
Managing aluminum phosphide poisonings
Mohan Gurjar, Arvind K Baronia, Afzal Azim, and Kalpana Sharma
Department of Critical Care Medicine, Sanjay Gandhi Postgraduate Institute of Medical Sciences (SGPGIMS), Lucknow, UP, India
Address for correspondence: Dr.Mohan Gurjar, E-mail: m.gurjar/at/rediffmail.com
Received August 31, 2009; Accepted September 2, 2010.
This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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Abstract
Aluminum phosphide (AlP) is a cheap, effective and commonly used pesticide. However, unfortunately, it is now one of the most common causes of poisoning among agricultural pesticides. It liberates lethal phosphine gas when it comes in contact either with atmospheric moisture or with hydrochloric acid in the stomach. The mechanism of toxicity includes cellular hypoxia due to the effect on mitochondria, inhibition of cytochrome C oxidase and formation of highly reactive hydroxyl radicals. The signs and symptoms are nonspecific and instantaneous. The toxicity of AlP particularly affects the cardiac and vascular tissues, which manifest as profound and refractory hypotension, congestive heart failure and electrocardiographic abnormalities. The diagnosis of AlP usually depends on clinical suspicion or history, but can be made easily by the simple silver nitrate test on gastric content or on breath. Due to no known specific antidote, management remains primarily supportive care. Early arrival, resuscitation, diagnosis, decrease the exposure of poison (by gastric lavage with KMnO4, coconut oil), intensive monitoring and supportive therapy may result in good outcome. Prompt and adequate cardiovascular support is important and core in the management to attain adequate tissue perfusion, oxygenation and physiologic metabolic milieu compatible with life until the tissue poison levels are reduced and spontaneous circulation is restored. In most of the studies, poor prognostic factors were presence of acidosis and shock. The overall outcome improved in the last decade due to better and advanced intensive care management.
Keywords: Aluminum phosphide, poisoning, emergency management, critical care
Pesticide poisoning, whether due to self, accidental, occupational or for homicidal purpose, is a global public health problem, and self-poisoning accounts for one-third of the world's suicide rate.[1] In fact, in some parts of developing countries, pesticide poisoning causes more deaths than infection.[2] Each year around 300,000 deaths occur worldwide due to pesticides.[3] The organophosphate, organochlorines and aluminum phosphide (AlP) compounds are commonly used pesticides. AlP is being used as a common outdoor and indoor pesticide in developing countries as it is cheap, effective, free from toxic residue and does not affect seed viability.[4]
Since the first available report of AlP poisoning in the early 1980s from India, it is now one of the most common causes of poisoning among agricultural pesticides.[5–8] Most of the case series are reported from India, while some others are reported from Iran, Sri Lanka and Morocco, with case reports from many developed countries. The demographic profile of most of the case series of AlP poisoning were of the young adult population from rural areas. In a recent scenario, AlP also poses as a threat for chemical terrorism due to the immediate release of lethal phosphine gas.[9]
AlP is a solid fumigant and can be formulated in the form of tablets, pellets, granules or as a dust. Commercially, it is available as dark grey tablets of 3.0 g each, consisting of AlP (56%) and carbamate (44%), in the names of Celphos, Alphos, Quickphos, Phosfume, Phostoxin, Talunex, Degesch, Synfume, Chemfume, Phostek or Delicia.[7,10] AlP is the active component of the mixture as it liberates highly toxic phosphine gas when it comes in contact either with atmospheric moisture or with hydrochloric acid in the stomach.[10–12] Thus, tablets or pellets gradually lose their potency on exposure to atmosphere as they release phosphine gas and leave behind a nontoxic residue in the form of aluminum hydroxide.
AlP + 3H2O → Al (OH)3 + PH3
AlP + 3HCl → AlCl3 + PH3
Phosphine gas is colorless and odorless in the pure form but, due to the presence of substituted phosphines and diphosphines, it has a foul odor resembling decaying fish or garlic.[4] Normally, phosphine is undetectable in air or water. It is inflammable and may spontaneously ignite in air at ambient temperature at concentrations above the threshold limit range of 1.9% (v/v).[13,14] It is soluble in water as well as in organic solvents, while in air it reacts with OH radicals and is removed by this mechanism.
The ammonium carbamate component is present in commercially available tablets to prevent phosphine from combusting by decomposing to ammonia and carbon dioxide.[15] Other by-products of commercial tablets are aluminum oxide and diphosphine gas. The amount of diphosphine gas, which is spontaneously inflammable in the air, depends on the excess amount of phosphorous compared with aluminum in the tablets.[16]
Human toxicity occurs either due to the ingestion of AlP (commonest mode) after exposure and injury from phosphine inhalation (uncommon) or even after absorption through the skin (rare). After ingestion, AlP releases phosphine gas in the presence of HCl in the stomach, which is rapidly absorbed throughout the gastrointestinal tract, leading to systemic toxic effects involving the heart, lung, kidney, liver with manifestation of serious cardiac arrhythmias, intractable shock, acidosis and pulmonary edema. After absorption, phosphine is oxidised to oxyacids. Phosphine is excreted in the urine as hypophosphite and also through the lung in the unchanged form.
In addition to the corrosive action of phosphine, the mechanism of toxicity includes failure of cellular respiration due to the effect on mitochondria, inhibition of cytochrome C oxidase and formation of highly reactive hydroxyl radicals.[17,18] Cellular injury due to lipid peroxidation is also suggested.[19] There is a decrease in the level of catalase and increase in the activity of superoxide dismutase in patients of AlP poisoning.[20] The reduction of glutathione concentration in different tissues in AlP poisoning also explains the cellular injury as glutathione is a protecting factor against oxidation by catalysing the reduction of the oxygen peroxide in O2 and H2O.[21] Indicators of oxidative stress (reduced glutathione, malonyldialdehyed) reach peak levels within 48 h of exposure of poison, approaching normalisation by day 5.[19,22]
Phosphine, either during inhalation or exhalation after ingestion, directly produces injury to the alveolar capillary membrane in addition to oxidative injury leading to acute lung injury. The exact underlying mechanism of cardiotoxicity and acute circulatory failure caused by phosphine is not well defined.
Histopathological findings of vital organs were found to be suggestive of cellular hypoxia.[23–27] Myocardial muscles in nonsurvivors showed myocyte vacuolation, areas of myocytolysis and degeneration.[28] Histological changes on human brain showed disorganisation of the different layers, paucity of glial cells, degeneration of neurons and appearance of necrotic patches. In other organs like in lung, diffuse vessel injury with edema and atelectasis; in liver, centrilobular necrosis; and in kidney, tubular degeneration findings may be present.
The permissible exposure limit of phosphine is <0.3 ppm in the working environment and levels greater than 50 ppm are dangerous to life, while at 400–600 ppm it is lethal within half an hour.[29,30] Individuals working in the manufacturing facility of AlP or methamphetamine (phosphine is a by-product), engaged in placing AlP tablets on the stacks of grains and in the vicinity of application are at risk for unintentional exposure of phosphine gas, with few reported fatalities.[31–34]
The signs and symptoms are nonspecific, instantaneous and depend on the dose, route of entry and time lapse since exposure to poison. After inhalation exposure, patients commonly have airway irritation and breathlessness.[4] Other features may include dizziness, easy fatigability, tightness in the chest, headache, nausea, vomiting, diarrhea, ataxia, numbness, paraesthesia, tremor, muscle weakness, diplopia and jaundice.[7,29,35] 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.[7,25,29,36]
After ingestion, toxic features usually develop within few minutes. In mild poisoning nausea, repeated vomiting, diarrhea, headache, abdominal discomfort or pain and tachycardia are common clinical features, and these patients usually show recovery.[7] 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.[7,37]
The toxicity of AlP particularly affects the cardiac and vascular tissues, which manifests as profound and refractory hypotension, congestive heart failure, electrocardiographic (ECG) abnormalities, myocarditis, subendocardial infarction or pericarditis. ECG abnormalities include rhythm disturbances, ST-T changes and conduction defects. Temporal correlation in ECG changes showed that during the initial 3–6 h, sinus tachycardia is predominant, in the 6–12 h period ST-T changes and conduction disturbances appear, while in the later period, arrhythmias occurred.[38] In a study by Siwach et al., the incidence of various arrhythmias on holter monitoring in patients of AlP poisoning showed ventricular tachycardia in 40%, ventricular fibrillation in 23.3%, supraventricular tachycardia in 46.7% and atrial flutter/fibrillation in 20% of the cases.[39] The frequency of hypotension varies from 76% to 100%.[40,41] The exact mechanism of refractory shock is not clear; it may be due to several factors like myocardial damage, peripheral vasodilatation and fluid loss. In few cases of AlP poisoning, there was follow-up of cardiac function by echocardiography, revealing dysfunction of the left ventricle that was reversible over few days.[42–44]
Respiratory features may include cough, dyspnoea, cyanosis, pulmonary edema, respiratory failure and ARDS. Metabolic acidosis may be present probably due to the accumulation of lactic acid caused by blockage of oxidative phosphorylation and poor tissue perfusion. Patients may remain conscious till the late stage but can have manifestations like headache, dizziness, altered sensorium, convulsion and coma.[7,35]
Both hypo- and hypermagnesemia following AlP poisoning have been described in the literature, although their pathogenesis is not clear.[40,45,46] Other uncommon findings in AlP poisoning are intravascular hemolysis, acute adrenocortical insufficiency, hepatitis, acute tubular necrosis, pancreatitis, hypo- or hyperglycemia, methhemoglobinemia, microangiopathic hemolytic anemia and disseminated intravascular coagulation.[37,47–53] In follow-up among survivors, one-third of the patients had dysphagia due to esophageal complications, including esophageal stricture or tracheo-esophageal fistula.[54]
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.[55] It is important to differentiate as management of these two types of rice tablet poisonings are different. In case of doubt, diagnosis can be made easily by simple silver nitrate-impregnated paper test on gastric content or on breath.[7,56,57] Chemical analysis for phosphine in blood or urine is not recommended as phosphine is rapidly oxidised to phosphite and hypophosphite.[16]
For the silver nitrate test on gastric aspirate, diluted gastric content is heated in a flask up to 50°C for 15-20 mins, 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 color, its presence could be differentiate by 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 color of the paper will change to blue.[58]
However, gas chromatography with a nitrogen–phosphorous detector is the most specific and sensitive test and it can be used for analysis of airtight samples (viscera and gastric content) collected during autopsy.[59]
MANAGEMENT
Management should be started as soon as history and clinical examination support AlP poisoning, and should not be delayed for the confirmatory diagnosis [Figure 1]. Unfortunately, due to no known specific antidote, management remains primarily supportive care. As each poison has a definite elimination time, so also is the case with AlP. Early arrival, resuscitation, diagnosis, intensive monitoring and supportive therapy may result in good outcome. Care of patients with severe poisoning can be enhanced by consultation with a medical toxicologist or a regional poison center.
Figure 1
Figure 1
Emergency management of aluminum phosphide/phosphine poisoning
Immediate primary survey should be performed by any trained health care provider to support or to restore effective oxygenation, ventilation and circulation. The health care provider must take personal protection measures, including full face mask and rubber gloves during decontamination.[57] “Spontaneous ignition” is a rare but possible finding in case of AlP poisoning.[16,60]
Confirm airway patency and, if required, protect the airways with endotracheal tube to prevent aspiration pneumonitis, start supplementary oxygen, check for pulse and establish intravenous access, preferably central venous, to start normal saline and vasopressor therapy as appropriate. Monitoring of vitals should be performed very closely. Initial investigation should include ECG, chest X-ray, blood glucose, arterial blood gas, electrolytes including magnesium, routine hemogram, liver function test and renal function test. Repeated or continuous ECG and echocardiography can reveal cardiac dysfunction early.
The victim, after occupational or accidental exposure to phosphine gas, should immediately be removed to fresh air. As phosphine is absorbed through the cutaneous route, decontamination of skin and eyes must be carried out thoroughly with plain water as early as possible.[7]
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 nontoxic phosphate. This can be followed by approximatly 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.[61] Sorbitol solution at a dose of 1–2 ml/kg may be used as cathartic. In vitro experimental findings suggest that fat and oil, mainly vegetable oils and liquid paraffin, inhibit phosphine release from the ingested AlP.[62] The possible role of coconut oil in managing acute AlP poisoning is concluded in a case report even 6 h post ingestion.[63] Phosphine excretion can be increased by maintaining adequate renal perfusion and urine output.
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. This is important to attain adequate tissue perfusion and oxygenation and physiologic metabolic milieu compatible with life until the tissue poison levels are reduced and spontaneous circulation is restored.
All patients of severe AlP poisoning require continuous invasive hemodynamic monitoring and early resuscitation with fluid and vasoactive agents. Fluid therapy could be guided by central venous pressure (CVP) or pulmonary artery wedge pressure (PAWP) monitoring. For refractory hypotension, norepinephrine or phenylephrine could be used. Readiness of anti-arrhythmic agents, DC cardioversion and temporary pacemaker should be available at the bedside. Vasoactive agents with more β-receptor agonist action like dopamine and dobutamine should be used cautiously as they are prone to inducing arrhythmias. The reversibility of myocardial injury over few days was objectively assessed by repeated echocardiography.[42–44] Gupta et al. showed normalisation of the echocardiographic findings in patients who survived AlP poisoning on day 5.[42]
The role of advanced measures like use of intra-aortic balloon pump (IABP) to mechanically support the heart has been demonstrated in toxic myocarditis with refractory shock due to AlP poisoning.[64,65] The possibility of a beneficial effect of extracorporeal life support (ECLS) as a supportive measure for intractable circulatory collapse is not evaluated in this poisoning as it was successfully used in many other drug-induced cardiotoxicities.[66] This may prove as a useful treatment modality in the future as this device can maintain adequate tissue perfusion to prevent multiorgan failure and give time to recovery of myocardial tissue from phosphine-induced injury.
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.
Patients who develop cyanosis and are not responding to oxygen therapy, then methemoglobinemia should be ruled out by multiple wave length cooximetry or plasma level of methemoglobin.[52] Symptomatic methemoglobinemia requires antidote therapy with intravenous methylene blue (1% solution) 2 mg/kg of body weight over 5 mins, which and can be repeated if the cyanosis is not resolved.
Intravenous sodium bicarbonate could be considered for mild to moderate metabolic acidosis or as a rescue therapy in severe acidosis before dialysis could be commenced. In a recent study, using intravenous sodium bicarbonate for the “aggressive correction of acidosis” protocol resulted in significant improvement in patient outcome (30% vs. 55%).[67] Hemodialysis is probably not very effective in removing phosphine but is helpful when renal failure, severe metabolic acidosis or fluid overload is present.
The role of magnesium sulfate as a potential therapy in AlP poisoning to decrease the likelihood of a fatal outcome has been described in many studies (up to 50% reduction in mortality).[22,35,38,45,68,69] It acts as a cell membrane stabilisation factor and, possibly, by this mechanism, reduces the incidence of fatal arrhythmias, but the exact mechanism is still unclear as this is a weak antiarrhythmic. Magnesium sulfate also has an anti-peroxident effect and it combats free radical stress due to phosphine.[22] The dosages for magnesium sulfate were different in different studies: (a) 3 g as infusion over 3 h, followed by 6 g per 24 h for 3–5 days, (b) 1g stat, then 1 g every hour for the next 2 h and then 1–1.5 g every 6 h for 5–7 days, (c) 4 g stat, 2 g after one hour and then 1 g every three-hourly and (d) 3 g bolus followed by 6 g infusion over the next 12 h for 5–7 days.[4,7,68,69]
In a critical evaluation and metaanalysis of the published studies showing usefulness of magnesium sulfate therapy in reducing mortality, Siwach et al. revealed that none of the workers had taken into consideration the dose of AlP while analysing their result.[44,70] In their study, they found that serum and tissue magnesium content was within the normal range and mortality was not significantly different in patients who were not treated with magnesium therapy. At present, the routine use of intravenous magnesium sulfate therapy is questionable with the existing literature as hypermagnesemia has also been described in some cases of AlP poisoning.[40]
Hyperglycemia at admission has been found to be a significant poor prognostic factor.[51] Therefore, there is a possible role of treatment of hyperglycemia throughout management of the poisoning, which may improve the outcome.[71] Steroid administration could be considered as a possibility of management if impaired adrenal function has been found.[48] Many therapeutic agents with antioxidant properties have been tried in experimental animal studies with phosphine toxicity, like n-acetylcysteine, glutathione, melatonin, vitamin C and beta carotene, but there is a need for human trials before their routine use in AlP poisoning.[21,72,73] The possible role of trimetazidine as the treatment of cardiovascular manifestation has been demonstrated, which is an anti-ischemic drug that acts by reducing oxygen consumption.[74]
Before discharge, all the survivors with swallowing difficulty must undergo a barium swallow study and upper gastrointestinal endoscopy for early detection of esophageal complications due to AlP ingestion.[54] Survivors also need psychosocial counselling.
This poisoning has a high mortality (30–100%) and survival is unlikely if more than 1.5 g is ingested.[35,41,75–77] Although the lethal dose is 150–500 mg for an adult, case reports of survival have been reported even after the ingestion of 9.0 g or more.[7,44,63,78] The possible explanations of these survivals are: presence of vomiting, exposure of tablets before ingestion and early availability of supportive care. Ingestion of “unexposed tablets” of AlP is associated with a greater risk and fatal outcome as these tablets retain their potency. The serum phosphine level of more than 1.6 mg/dl correlates with mortality.[79] Most of the patients died within the first 24 h after ingestion mainly due to arrhythmia and after 24 h due to refractory shock, acidosis and ARDS.[78] Sudden fatalities in children due to AlP toxicity were also presented during some physical activity with no preceding clinical sign or symptoms of toxicity.[80]
In a retrospective analysis of one of the largest series (471 patients) of AlP poisoning, arterial pH, serum bicarbonate level and ECG abnormalities were significantly poor prognostic factors.[81] Other poor prognostic factors are shock, altered mental status, high APACHE II score, acute kidney injury, low prothrombin rate, hyperleucocytosis, requirement of mechanical ventilation, lack of vomiting after ingestion, hyperglycemia and time lapsed after exposure.[35,40,41,45,46,51,68,69,76,77,82]
CONCLUSION
The case fatality ratio declined in the last decade due to improved intensive care. Strict implementation of nationwide pesticide regulation, including restricting the availability of poison, being aware of its toxicity and providing improved medical management in consultation with regional or national poison control centers could further reduce the mortality due to AlP toxicity as there is no antidote available presently.
Footnotes
Source of Support: Nil
Conflict of Interest: None declared.
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