Since the first available report of Alu-Phosphide toxicity in the early 1978 from India, it is now one of the very common causes of toxicity among agricultural pesticides, and it is very lethal toxicity.

Mechanism of Toxicity:

Human toxicity occurs either due to the ingestion of Alu-Phosphide (commonest mode) after exposure or even after absorption through the skin. After ingestion, Alu-Phosphide releases phosphine gas in the presence of hydrochloric acid in the stomach.1

Alu-Phosphide + H2O → Al OH3 + Phosphine

Alu-Phosphide + Hydrochloric Acid → Al Cl3 + Phosphine

The mechanism of toxicity includes failure of cellular respiration due to the effect of phosphine. On Mitochondria, respiratory chain inhibition of cytochrome C oxidase and formation of highly reactive hydroxyl radicals, and hence lead to cell necrosis and death. There is a decrease in the measurement of catalase and increase in the activity of superoxide dismutase in patients of Alu-Phosphide toxicity.

Clinical Feature

The signs and symptoms are non-significant, instantaneous and depend on the dose, mode of entry, and time taken since exposure to toxicity. After inhalation exposure, patients commonly have airway respiratory symptom and breathlessness, chest tightness.2

In mild toxicity, nausea, repeated vomiting, diarrhea, headache, abdominal discomfort or pain. In modest to higher ingestional toxicity, the clinical feature 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.2

The toxicity of Alu-Phosphide particularly affects the cardiac and vascular tissues, which manifest as cardiac manifestations – hypotension. That is not correctable with any amount fluid and adrenergic drug congestive cardiac failure. Electrocardiogram show various abnormalities, myocarditis, subendocardial infarction, or pericarditis.

Diagnosis

• The diagnosis of Al-P commonly based on the clinical doubt or history given by relative or patient him Self.
• Chemical analysis: The most appropriate and important test and it can be utilized for analysis of airtight samples laboratory assessment is mainly done to assess the prognosis.
• Leukopenia indicates higher toxicity.
• Elevated SGOT or SGPT and metabolic acidosis indicate modest to higher ingestional toxicity.
• Electrolyte analysis shows declining magnesium.
• Potassium may be elevated or declining.
• Estimation of plasma renin is significant. As its measurement in blood show a direct association with mortality and is increase in direct proportion to the dose of pesticide.
• The serum measurement of cortisol is commonly found to be declining in higher toxicity.

Treatment Guideline:

Treatment Guideline should be started as soon as sign and symptom support Alu-Phosphide toxicity, and should not be deferred for the laboratory diagnosis.3

Early arrival, resuscitation, diagnosis, in depth supervise, and ancillary therapy may result in good outcome.

Traditionally we are using normal saline or water for stomach wash, but as we have seen in mechanism of phosphine release require water so we should not use normal saline or water. We must use coconut oil for stomach wash with sodium bicarbonate solution (40 mL). It will neutralize hydrochloric acid in stomach. Coconut oil makes a protective layer in stomach and decreases absorption of phosphine. Coconut oil also hampered mixing of tablet of Alu-Phosphide. So, to decrease phosphine gas release as it decreases ATP system generation by effecting mitochondrial cytochrome system. So we have to conserve energy by decrease energy utilization. To achieve this target we must use sedative to decrease activity of patient. If require early mechanical ventilation is preferred. Early mechanical ventilation helps in three ways:4

• First we make respiratory rate fast so as to make gaseous expulsion fast.
• Second we conserve energy by paralyzing respiratory muscle.
• Thirdly by intubating patient we prevent aspiration lipid pneumonia as we using coconut oil for stomach wash

We should not use atropine as much as possible as it increases heart rate and increases energy consumption. We can use iv fluid as much required to maintain hydration and to prevent hypotension. Low dose dopamine can also use for hypotension. Check for pulse and establish intravenous access, preferably central venous, to start normal saline and vasopressor therapy as appropriate. Closely Monitor vital like blood pressure respiration oxygen saturation should be performed.

Decrease the Exposure of Toxicity:

The patient, after occupational or accidental exposure to phosphine gas, should immediately be removed to fresh air. As phosphine is absorbed through the skin mode, decontamination of skin and eyes must be done thoroughly with normal saline as early as possible. After ingestion, stomach lavage with coconut oil to reduce the absorption of unabsorbed toxicity is primarily dependent on the duration of exposure of toxicity and is useful if it is done within 1–2 hours. The role of coconut oil in managing acute Alu- Phosphide toxicity is concluded in a case report even 6 hours post ingestion.5

Hemodynamic Support:

All patients of higher Alu-Phosphide toxicity require continuous invasive hemodynamic supervise and early resuscitation with fluid and vasoactive agents. Between 2–3 liters of normal saline are administered within the first 8–12 hours as guided by central venous pressure. All sympathomimetic drug like Dopamine, Dubutamine, and Noradrenaline can also be used. Hydrocortisone 200–400 mg every 4–6 hours is given intravenously to combat shock; reduce the dose of dopamine, check capillary leakage in lungs (ARDS) and to potentiate the responsiveness of the body to oxygen given for hypoxia. ARDS requires in-depth care supervisee and mechanical ventilation.6

Endogenous and Exogenous Catecholamine Treatment guideline for ventricular arrhythmias is same as in other arrhythmia as DC SHOCk can be given all type of ventricular arrhythmias. Bicarbonate measurement less than 15 meq/L requires sodium bicarbonate solution in a dose of 50–100 meq intravenously every 8 hour till the bicarbonate measurement rises to 18–20 meq/L. Sufferer may require up to 300–500 ml of sodium bicarbonate.7,8

Other Ancillary Therapy:

The role of magnesium sulfate as a potential therapy in Alu-Phosphide toxicity to decrease the likelihood of a fatal outcome has been described in many studies the dosages for magnesium sulfate were different in different studies. The dosages for magnesium sulfate were different in different studies: sugar level high at admission has been found to be a significant bad prognostic factor. Therefore, there is a possible role of medication of hyperglycemia throughout treatment guideline of the toxicity, which may improve the outcome.9,10

Medication Algorithm for Celphos Toxicity:

This toxicity has a bad prognosis if victim consumed more than two tablets, if tablet is fresh mean or if tablet is stored in place openly then is not so powerful, but if freshly taken from wrapper then it is more lethal. The blood phosphine measurement of greater than 1.6 mg/Dl correlates with mortality. Most of the victim expired within the first 24 hours after taken mainly due to ventricular rhythms abnormality and after 24 ours due to intractable shock. In a large study of Alu-Phosphide toxicity, arterial PH, serum bicarbonate measurement and ECG abnormalities were significantly poor prognostic factors.11,12

• Do not use water for Celphos toxicity as a stomach wash.
• Try to sedate patient with sedative so least energy utilization by patient so to conserve ATP.
• If mechanical ventilation required keep maximum respiratory rate so expulse gas very fast.
• Do not use atropine to increase heart rate, keep heart rate between 60–100.
• Whenever required earliest mechanical ventilation is safer

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2. Chopra JS, Kalra OP, Malik VS, et al. Aluminum phosphide poisoning: a prospective study of 16 cases in one year. Postgrad Med J. 1986;62(734):1113-5.
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