Metolachlor Poisoning with Lactic Acidosis Improved by Thiamine Administration: A Case Report.

BACKGROUND Metolachlor is a chloroacetamide herbicide that is extensively used worldwide. Ingestion of metolachlor causes acute toxicity via the generation of methemoglobin. Elevated levels of methemoglobin inhibit the transport of oxygen to tissue, causing hypoxia and lactic acidosis. A common treatment approach has been to reduce methemoglobin by administration of methylene blue. Herein, we present a case of metolachlor poisoning causing lactic acidosis that was treatable by thiamine administration, in which the methemoglobin level was not elevated. CASE REPORT A 61-year-old man was admitted to the emergency room with seizures and impaired consciousness after the ingestion of metolachlor (250 mL, 83%) with the intent to commit suicide. The patient's methemoglobin and lactate levels on admission were 0.9% and 11.8 mmol/L, respectively. After admission, the levels of lactate decreased gradually; however, they increased 13 h after admission. There was no evidence of heavy alcohol consumption, hyponutrition, or chronic thiamine deficiency. We initially administered a thiamine bolus (100 mg), which immediately improved his consciousness, followed by continuous administration of the same substance (1500 mg/day). The patient's consciousness improved, and was discharged from the intensive care unit on day 4. CONCLUSIONS Metolachlor can cause metabolic dysfunction and lactic acidosis without an increase in methemoglobin. Moreover, thiamine administration may be beneficial for patients with metolachlor intoxication exhibiting symptoms of elevated lactate levels, impaired consciousness, and lack of elevated methemoglobin levels.