|Year : 2017 | Volume
| Issue : 3 | Page : 343-346
Survival in a case of aluminum phosphide poisoning with severe myocardial toxicity
Priya Bansal1, Subhash Giri2, Rohit Bansal3, Laxmikant Ramkumarsingh Tomar4
1 Department of Medicine, Lady Hardinge Medical College, New Delhi, India
2 Department of Medicine, UCMS and GTB Hospital, New Delhi, India
3 Department of Medicine, Dr. RML Hospital and PGIMER, New Delhi, India
4 Department of Neurology, GB Pant Hospital, New Delhi, India
|Date of Web Publication||5-Sep-2017|
Department of Medicine, Lady Hardinge Medical College, New Delhi
Source of Support: None, Conflict of Interest: None
Aluminum phosphide (AlP) is a commonly used pesticide (insecticide) in developing countries like India. It is also one of the most common and deadly causes of suicidal poisoning in rural areas, with a lethal dose of 150–500 mg (unexposed tablet) in adults. Death is due to the rapid release of phosphine gas which causes cellular and mitochondrial toxicity leading to cardiovascular collapse and multiorgan failure. Here, we describe a case of AlP poisoning in a young male who developed severe myocarditis and metabolic acidosis after consumption of 3 g of AlP. In spite of a poor predicted outcome, the patient survived due to prompt and aggressive resuscitative measures.
Keywords: Cardiac, celphos, poisoning
|How to cite this article:|
Bansal P, Giri S, Bansal R, Tomar LR. Survival in a case of aluminum phosphide poisoning with severe myocardial toxicity. Indian J Health Sci Biomed Res 2017;10:343-6
|How to cite this URL:|
Bansal P, Giri S, Bansal R, Tomar LR. Survival in a case of aluminum phosphide poisoning with severe myocardial toxicity. Indian J Health Sci Biomed Res [serial online] 2017 [cited 2022 Jul 6];10:343-6. Available from: https://www.ijournalhs.org/text.asp?2017/10/3/343/213994
| Introduction|| |
Aluminum phosphide (AlP) is widely used in rural areas as a fumigant to protect stored grain from pests and rodents. In India, it is marketed as a 3-g tablet under various brand names such as celphos, alphos, and quickphos. If ingested, it is acutely toxic with a high mortality. The fatal dose of an unexposed tablet may be as low as quarter of a tablet. The mortality rate of AlP poisoning is 77%–100%., Although all organs can be involved, the release of the cytotoxic phosphine gas on ingestion primarily affects the heart, lungs, gastrointestinal tract, and kidneys. The dominant clinical feature is severe and refractory hypotension. Complications include fatal dysrhythmias, congestive cardiac failure, gastrointestinal hemorrhage, and acute respiratory distress. We describe a rare case of AlP poisoning in an adult male who survived despite severe myocardial toxicity and metabolic acidosis.
| Case Report|| |
A 34-year-old male presented to the emergency with complaints of epigastric discomfort, nausea, vomiting, restlessness, and profuse diaphoresis for the last 2 h. He gave a history of consumption of an unexposed 3-g tablet of AlP 1 h before the development of these symptoms. He consumed this tablet due to some dispute with his wife. On examination, he had a garlicky odor in his breath; pulse rate (PR) was 126/min and blood pressure (BP) was 110/90 mmHg. Systemic examination was unremarkable.
Hematological parameters such as hemogram, liver function test, and urine examination were normal. There was slightly derangement of blood urea 49 mg/dl and serum creatinine 1.7 mg/dl. Electrocardiogram (ECG) at the time of presentation showed sinus tachycardia and ventricular ectopics. Baseline arterial blood gas (ABG) analysis, blood investigations, and cardiac enzymes were within normal limits. Gastric lavage done with potassium permanganate (1:10,000) and supportive management with intravenous (IV) fluids was given.
Over the next 1 h, he became hemodynamically unstable. His PR and respiratory rate increased. BP fell to 70/50 mmHg and he became agitated, with intractable nausea and vomiting. Repeat ECG [Figure 1] showed ST-T wave changes in the form of ST segment elevation in inferolateral leads and ST depression with T-wave inversion in anteroseptal leads. Cardiac enzymes creatine phosphokinase-MB (CPK-MB) and troponin T (Trop-T) were found to be elevated. ABG showed hypoxia and mild metabolic acidosis. His APACHE II score was calculated to be 15. The patient was given high-flow oxygen, IV fluids, and inotropic support with dopamine, and a central line was also secured. He was also administered IV magnesium sulfate. Metabolic acidosis was corrected by repeated bicarbonate infusions. As the BP dropped further, dopamine infusion was increased, noradrenaline drip was started, and both were titrated according to BP. He was continued on the above treatment for 24 h.
|Figure 1: Electrocardiogram suggestive of ST-T wave changes in the form of ST segment elevation in inferolateral leads and ST depression with T-wave inversion in anteroseptal leads|
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After 2 days of hemodynamic instability, there was an improvement in orientation, PR, and BP. His inotropes were slowly tapered. The ST-T changes on ECG were reverted [Figure 2]. Repeat cardiac enzymes and ABG were normal. He was discharged with appropriate psychiatric counseling after 7 days.
| Discussion|| |
AlP is a pesticide commonly used for storage of cereal grains by farmers and villagers. In India, it is also one of the most common and deadly causes of suicidal poisoning, with a mortality rate of 77%–100%.,,,
Unexposed tablets of AlP are more lethal than exposed tablets. The lethal dose is approximately 150–500 mg/70 kg. Ingestion of AlP release phosphine gas that rapidly absorbed from the lungs and gastrointestinal tract and causes inhibition of cytochrome C oxidase in mitochondria, failure of cellular respiration, and formation of highly reactive hydroxyl radicals causing cell death.,
The clinical presentation is nonspecific, and toxic features may be seen within a few minutes after ingestion [Table 1]., It particularly affects the cardiovascular system and presents as profound hypotension, heart failure, myocarditis, subendocardial infarction, and ECG abnormalities such as ST-T changes, conduction defects, and rhythm disturbances in the form of supraventricular tachycardia, ventricular ectopics, ventricular tachycardia, and ventricular fibrillation. The frequency of hypotension varies from 76% to 100%. The refractory shock is due to myocardial injury, peripheral vasodilatation, and dehydration. Our patient remained in a hemodynamically unstable for 2 days and required continuous inotropic support. The patient had features of myocarditis; ECG showed ventricular ectopics, ST segment elevation in inferolateral leads, and ST depression with T-wave inversion in anteroseptal leads; Cardiac enzymes, CPK-MB and Trop-T, were elevated. Other features of toxicity include acute respiratory distress syndrome (ARDS) and neurological manifestations such as convulsions and coma.
Metabolic acidosis is caused by the accumulation of lactic acid due to the blockage of oxidative phosphorylation and poor tissue perfusion. IV sodium bicarbonate could be considered for mild to moderate metabolic acidosis and use of IV sodium bicarbonate for the “aggressive correction of acidosis” protocol resulted in significant improvement in patient outcome.
Factors found to be associated with an increased risk of mortality were serum creatinine concentration >1.0 mg % (P = 0.01), pH <7.2 (P = 0.014), serum bicarbonate value <15 mmol/L (P = 0.048), need for mechanical ventilation (P = 0.045), need for vasoactive drugs such as dobutamine (P = 0.027) and noradrenaline (P = 0.048), and a low APACHE II score at admission (P = 0.019).”
The diagnosis is based on clinical history and suspicion in a case of rapidly deteriorating clinical state following unknown substance ingestion. Phosphine gas resembles garlic-like smell due to the presence of substituted compound. Laboratory diagnosis can be made by the silver nitrate test done on breath or gastric content. “Gas chromatography with nitrogen–phosphorous detector” is the most specific and sensitive test for the detection of AlP in autopsy samples (viscera and gastric contents).
There is no known specific antidote for AlP poisoning. Gastric lavage must be done within 1–2 h of presentation with potassium permanganate (1:10,000) as it oxidizes phosphine to nontoxic phosphate. Hemodialysis is helpful when severe metabolic acidosis, renal failure, or fluid overload is present as required in selected patients. Both hypo- and hyper-magnesemia have been seen in AlP poisoning. Although the pathophysiology of magnesium imbalance is not clear, therapeutically, it acts as a cell membrane stabilizer in the myocardium and combats free radical stress due to phosphine.
A few authors have reported survival following AlP ingestion using various interventions, summarized in [Table 2].
|Table 2: Cases of patient survival following aluminum phosphide poisoning|
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Our patient had profound shock, severe metabolic acidosis, low APACHE II score, and serious myocardial toxicity as demonstrated by ECG and raised cardiac biomarkers, predicting poor survival and high mortality. Magnesium sulfate was successfully used for treatment, with reversibility of the cardiotoxicity demonstrated by ECG.
| Conclusion|| |
- Knowledge of this usual presentation though nonspecific, clinical experience is essential to make a sound judgment
- Survival in AlP poisoning is rare if a patient has consumed more than 150–500 mg of an unexposed tablet, and most of the deaths are consequent to cardiovascular failure, ARDS, and multiorgan dysfunction
- In this patient, survival was attributed to persistence of vomiting, early availability of resuscitative care including optimal IV fluids, timely use of inotropes, prompt correction of metabolic acidosis, and use of magnesium sulfate
- In spite of the high mortality (77%–100%) associated with acute AlP poisoning, survival may be possible in patients who are identified and managed promptly.
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Conflicts of interest
There are no conflicts of interest.
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[Figure 1], [Figure 2]
[Table 1], [Table 2]