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Purpose: Glufosinate poisoning can cause neurologic complications that may be difficult to treat due to delayed manifestation. Studies assessing possible predictors of complications are lacking. Although serum ammonia level is a potential predictor of severeneurotoxicity, it has only been assessed via case reports. Therefore, we investigated factors that predict neurologic complicationsin acute glufosinate-poisoned patients. Materials and Methods: We conducted a retrospective review of 45 consecutive glufosinate-poisoning cases that were diagnosed in the emergency department (ED) of Wonju Severance Christian Hospital between May 2007 and July 2014. Patients with a Glasgow Coma Scale (GCS) score of <8, seizure, and/or amnesia were defined to a neurologic complication group. Results: The neurologic complication group (29 patients, 64.4%) comprised patients with GCS<8 (27 patients, 60.0%), seizure (23 patients, 51.1%), and amnesia (5 patients, 11.1%). Non-neurologic complications included respiratory failure (14 patients, 31.1%), intubation and ventilator care (23 patients, 51.1%), shock (2 patients, 4.4%), pneumonia (16 patients, 35.6%), acute kidney injury (10 patients, 22.2%), and death (4 patients, 8.9%). Complications of GCS<8, seizure, respiratory failure, and intubation and ventilatorcare appeared during latent periods within 11 hrs, 34 hrs, 14 hrs, and 48 hrs, respectively. Initial serum ammonia was a predictorof neurologic complications [odds ratio 1.039, 95% confidence interval (1.001–1.078), p=0.046 and area under the curve 0.742]. Conclusion: Neurologic complications developed in 64.4% of patients with acute glufosinate poisoning. The most common complicationwas GCS<8. Initial serum ammonia level, which can be readily assessed in the ED, was a predictor of neurologic complications.

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