Severe hypoglycemia as a presenting feature of aluminum phophide poisoning

To the Editor: Aluminium phosphide (AlP) is a highly effective insecticide. It is known as a suicide poison because of high mortality and easy over-the-counter availability. It has no specific antidote. Fatal dose for an average-sized individual is 150 to 500 mg. The mortality rate is very high varying from 60% to 80%.¹ Death occurs due to toxic myocarditis, multi-organ failure, and profound shock. Its toxicity is due to the release of phosphine (PH³), which occurs when it comes in contact with moisture or gastric juice. PH³ is a mitochondrial toxin. Hyperglycemia following AIP ingestion has been described as poor prognostic factor.² Mild hypoglycemia has already been reported, but severe hypoglycemia as presenting feature of AlP poisoning is extremely rare.³

We report a case of a 19 year-old male who came to our emergency in deep coma and profound shock, about 7-and-a-half hours after ingestion of 1 (3 g) tablet of AlP. On investigation, he had severe metabolic acidosis with pH 6.86, blood sugar of 15 mg/dL, oxygen saturation of 70%, and serum lactate of 13 mmol/L. The electrocardiogram revealed T-wave inversion in leads II, III, and aVF with ST elevation in VI with sinus tachycardia. His Troponin I level was 0.36 μg/L.

The patient was immediately intubated for mechanical ventilation and was treated with 2 boluses of 50% dextrose (50 mL each) intravenously, followed by 10% dextrose as a continuous infusion. His repeat blood sugar level was 110 mg/dL and continued to remain normal thereafter. Despite normalization of blood glucose, there was no change in neurological status of the patient. After initial stabilization, the patient received gastric lavage with aliquot of 50 mL sodium bicarbonate and 50 mL coconut oil through nasogastric tube. He was also given 4 g magnesium sulphate intravenously as a bolus followed by 2 g magnesium sulphate intravenously at every every 6 hours, adequate fluid boluses and 100 mL of 8.4% sodium bicarbonate along with double inotropic support. The patient also received N-acetylcysteine. Despite extensive supportive care, patient died after 30 hours of ED presentation.

PH₃ poisoning following AlP ingestion develops rapidly, and the majority (95%) of deaths occur within 12 to 24 hours because of cardiovascular dysfunction, intractable hypotension, and multi-organ dysfunction. Changes in blood glucose levels are well known following AIP ingestion. It has been previously observed that elevation, reduction, and lack of effect on blood glucose level can occur in AlP poisoning. ⁴ Mild hypoglycemia is common in AlP poisoning; however, severe hypoglycemia is extremely rare. A probable relation exists between AlP and severe hypoglycemia based on Naranjo Scale. Several mechanisms have been suggested for hypoglycemia in AlP poisoning. Inhibition of hepatic gluconeogenesis and glycogenolysis, damage to adrenal cortex along with decreased cortisol, and glucagon and epinephrine production may precipitate hypoglycemia. Release of insulin-like growth factor in response to severe shock also contributes to hypoglycemia.⁵ Studies have shown that non-survivors in AlP poisoning had significantly higher blood glucose level than survivors, and these studies concluded that hyperglycemia prognosticates higher mortality. AlP causes rapid onset of shock, severe metabolic acidosis, cardiac dysrhythmias, and ARDS. Various studies have concluded that hyperglycemia, high SAPS II and high APACHE II score, hypotension, acidosis, leukocytosis, hyperuricemia, ECG abnormalities, low Glasgow coma scale, acute renal failure, low prothrombin time, methemoglobinemia, use of vasoactive drugs, lack of vomiting after ingestion, and use of mechanical ventilation are markers of poor prognosis. However, instead of hyperglycemia, which is a poor prognostic factor, severe hypoglycemia was present in our case, which could be one of the poor prognostic factors.

To conclude severe hypoglycemia is extremely rare following acute AIP poisoning. Similar to hyperglycemia, hypoglycemia could also be a predictor of mortality and should be included in the poor prognostic marker in AIP poisoning.