Initial Serum Ammonia as a Predictor of Neurologic Complications in Patients with Acute Glufosinate Poisoning
2
조회
0
다운로드
8
인용
0
참고문헌
키워드
초록
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.
Abstract
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.
참고문헌 (14)
- Watanabe T, "Neurological effects of glufosinate poisoning with a brief review", Hum Exp Toxicol, 17, pp.35~39 (1998)
- Hoerlein G, "Glufosinate (phosphinothricin), a natural amino acid with unexpected herbicidal properties", Rev Environ Contam Toxicol, 138, pp.73~145 (1994)
- Koyama K, "Delayed and severe toxicities of a herbicide containing glufosinate and a surfactant", Vet Hum Toxicol, 36, pp.17~18 (1994)
- Ebert E, "Summary of safety evaluation toxicity studies of glufosinate ammonium", Food Chem Toxicol, 28, pp.339~349 (1990)
- Hack R, "Glufosinate ammonium--some aspects of its mode of action in mammals", Food Chem Toxicol, 32, pp.461~470 (1994)
- Inoue Y, "Factors associated with severe effects following acute glufosinate poisoning", Clin Toxicol (Phila), 51, pp.846~849 (2013)
- Mao YC, "Hyperammonemia following glufosinate-containing herbicide poisoning: a potential marker of severe neurotoxicity", Clin Toxicol (Phila), 49, pp.48~52 (2011)
- Yang PY, "Acute ingestion poisoning with insecticide formulations containing the pyrethroid permethrin, xylene, and surfactant: a review of 48 cases", Toxicol Clin Toxicol, 40, pp.107~113 (2002)
- Lluís M, "Severe acute poisoning due to a glufosinate containing preparation without mitochondrial involvement", Hum Exp Toxicol, 27, pp.519~524 (2008)
- Bosoi CR, "Identifying the direct effects of ammonia on the brain", Metab Brain Dis, 24, pp.95~102 (2009)
- Ohtake T, "Decreased plasma and cerebrospinal fluid glutamine concentrations in a patient with bialaphos poisoning", Hum Exp Toxicol, 20, pp.429~434 (2001)
- Mao YC, "Acute human glufosinate-containing herbicide poisoning", Clin Toxicol (Phila), 50, pp.396~402 (2012)
- Koyama K, "Cardiovascular effects of a herbicide containing glufosinate and a surfactant: in vitro and in vivo analyses in rats", Toxicol Appl Pharmacol, 145, pp.409~414 (1997)
- Hori Y, "Toxicokinetics of DLglufosinate enantiomer in human BASTA poisoning", Biol Pharm Bull, 26, pp.540~543 (2003)