Acute methemoglobinemia caused by suicidal ingestion of liquid fertilizer

To the Editor:

We report a case of acute methemoglobinemia caused by suicidal ingestion of a nitrate-containing liquid fertilizer.

A 62-year-old woman with a history of gastrectomy for the treatment of gastric cancer attempted to commit suicide by ingesting alcohol, diazepam, and approximately 200 mL of liquid fertilizer (Hyponex^®; Hyponex Japan, Tokyo, Japan; the ingredients were nitrogen compounds 6%, including 1.05% nitrate; phosphoric acid 10%; potassium 5%). There was no family history of glucose-6-phospate dehydrogenase deficiency. She was transported to our hospital approximately one hour after ingestion. She was comatose and had a Glasgow Coma Scale score of 6 (E1V1M4) presumably due to the ingested alcohol and diazepam. Her heart rate was 87 beats/min, blood pressure was 80/47 mm Hg, and respiratory rate was 20 breaths/min; pulse oximetry indicated 98% saturation without supplemental oxygen. At this time, her methemoglobin level was within normal limits (1.2%). Gastric lavage was performed and activated charcoal was administered via a nasogastric tube. The initial test results revealed hyperkalemia (7.5 mEq/L). With the administration of bicarbonate and glucose–insulin therapy, hyperkalemia was alleviated. Five hours after the ingestion, she developed cyanosis (89% saturation). The methemoglobin level was elevated to 20.2%, and it increased to 22.0% at seven hours after the ingestion. Eventually it returned to normal 17 hours after the ingestion without specific therapy. She was conscious approximately 18 hours after the ingestion and was extubated. She was discharged on the fourth hospital day.

Liquid fertilizers are widely used for growing agricultural crops and generally consist of nitrogen, phosphoric acid, and potassium. It is known that containing potassium can cause hyperkalemia, however, acute toxic effects of nitrogen (nitrate) in fertilizer is unlikely in adults. Previous reports of the use of nitrate for medicinal purposes indicate that a single oral dose less than 7000–8000 mg is non-toxic in the short-term,¹ suggesting that our case of methemoglobinemia with ingestion of approximately 2.1 g of nitrate is an isolated incident.

Unlike nitrate, nitrite oxidizes the Fe²⁺ in hemoglobin to Fe³⁺, thus causing the conversion of hemoglobin to methemoglobin. Chronic exposure of newborns and infants to nitrogen compounds may cause methemoglobinemia as a result of the conversion of nitrate to nitrite.²

Many gastrointestinal bacteria can reduce nitrate to nitrite under certain (neutral pH) circumstances.³ When gastrointestinal conditions remain acidic (with sufficient acid secretion), bacterial multiplication is inhibited,⁴ and the nitrate reduction response is not activated. Newborns and infants have higher pH levels in the stomach which may affect the occurrence of methemoglobinemia. Post-gastrectomy patients and patients with gastrointestinal diseases reportedly experience hypoacidity or even anacidic conditions in the stomach.⁵ Therefore, our case of methemoglobinemia may have been caused by increased levels of bacteria in the gastrointestinal tract resulting from abnormal acidity levels.

In patients with liquid fertilizer poisoning, nitrate can be reduced to nitrite under specific conditions, such as gastrointestinal disorders, and this may cause acute methemoglobinemia.

Declaration of interest

The authors report no declarations of interest. The authors alone are responsible for the content and writing of the paper.