Management of life threatening multiorgan dysfunction due to glufosinate ammonium poisoning- A rare case report

Glufosinate ammonium is an herbicide that is considered one of the most hazardous substances and is prohibited in 29 countries worldwide. The mechanism involves inhibition of the enzyme glutamine synthase, leading to an increase in blood ammonia levels and subsequent damage to various organs, particularly the nervous system. Hyperammonaemia is considered one of the main mechanisms of glufosinate ammonia toxicity in humans. Commercial preparations also contain surfactants ranging from 30% to 70%, which can contribute to cardiovascular depression. The most striking feature is late-onset amnesia; this is due to the toxin-induced damage to the hippocampus. This case of a 31-year-old female who consumed 500 ml of a glufosinate ammonium-based herbicide highlights the entire clinical management. She presented to us after 48 hours with a GCS of 8. She was intubated and ventilated for 5 days, during which she developed seizures, arrhythmias, myocarditis, and pulmonary oedema. She was started on vasopressors and antiarrhythmic, and we used colchicine for myocarditis, as it inhibits the activity of NLRP3 (NOD-, LRR-, and pyrin domain-containing protein 3), mediating its anti-inflammatory properties. We have also used Intralipid emulsion therapy, as lipid emulsions can isolate the lipophilic toxins, reducing their bioavailability and toxicity. The timely use of amiodarone infusion, colchicine and the intralipid emulsion therapy reflected in the clinical outcome of the patient. She was extubated after 4 days and discharged in a stable hemodynamic state after two more days of general ward observation.