급성 엔도설판 중독의 임상적 고찰
Clinical Analysis of Acute Endosulfan Poisoning: Single Center Experience
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Purpose: Acute endosulfan poisoning is rare but causes significant morbidity and mortality. The aim of our study is to describe complications and features of seizure and determine factors associated with mortality in acute endosulfan poisoning. Methods: Twenty-eight adult patients with acute endosulfan poisoning admitted to our emergency department during a 15-year period were studied retrospectively. The clinical features of seizure, use of antiepileptic drugs during seizure, and hospital courses were evaluated. Clinical factors between survived group and non-survived group were compared for identification of factors associated with mortality. Results: Of the 28 patients with endosulfan poisoning, 4 patients (14.3%) died and 15 (53.6%) patients developed generalized tonic-clonic seizure. Thirteen patients (46.4%) and 5 patients (17.9%) progressed to status epilepticus (SE) and refractory status epilepticus (RSE), respectively. SE and RSE were associated with mortality. Almost all significant complications including shock, acute renal failure, hepatic toxicity, rhabdomyolysis, and cardiac injury developed in SE and RSE patients. Conclusion: SE and RSE were important contributors to death in endosulfan poisoning. Emergency physicians treating endosulfan poisoning should make an effort not to progress seizure following endosulfan poisoning to SE and RSE using a rapid and aggressive antiepileptic drug.
Abstract
Purpose: Acute endosulfan poisoning is rare but causes significant morbidity and mortality. The aim of our study is to describe complications and features of seizure and determine factors associated with mortality in acute endosulfan poisoning. Methods: Twenty-eight adult patients with acute endosulfan poisoning admitted to our emergency department during a 15-year period were studied retrospectively. The clinical features of seizure, use of antiepileptic drugs during seizure, and hospital courses were evaluated. Clinical factors between survived group and non-survived group were compared for identification of factors associated with mortality. Results: Of the 28 patients with endosulfan poisoning, 4 patients (14.3%) died and 15 (53.6%) patients developed generalized tonic-clonic seizure. Thirteen patients (46.4%) and 5 patients (17.9%) progressed to status epilepticus (SE) and refractory status epilepticus (RSE), respectively. SE and RSE were associated with mortality. Almost all significant complications including shock, acute renal failure, hepatic toxicity, rhabdomyolysis, and cardiac injury developed in SE and RSE patients. Conclusion: SE and RSE were important contributors to death in endosulfan poisoning. Emergency physicians treating endosulfan poisoning should make an effort not to progress seizure following endosulfan poisoning to SE and RSE using a rapid and aggressive antiepileptic drug.
참고문헌 (23)
- Nelson LS, "Goldfrank’s toxicologic emergencies", pp.1477~1493 (2011), McGraw-Hill
- Han BG, "Effect of Seizure on Prognosis in Acute Endosulfan Intoxication", J Korean Soc Clin Toxicol, 7, pp.77~82 (2009)
- Moon JM, "Acute endosulfan poisoning : a retrospective study", Hum Exp Toxicol, 28, pp.309~316 (2009)
- Moses V, "Acute intentional toxicity : endosulfan and other organochlorines", Clin Toxicol(Phila), 48, pp.539~544 (2010)
- Kim SI, "Measurement of Volume of a Swallow for Liquid Swallowing in Healthy Young Adults", J Korean Soc Clin Toxicol, 11, pp.114~118 (2013)
- Brophy GM, "Guidelines for the evaluation and management of status epilepticus", Neurocrit Care, 17, pp.3~23 (2012)
- Vale C, "The organochlorine pesticides gammahexachlorocyclohexane (lindane), alpha-endosulfan and dieldrin differentially interact with GABA (A) and glycine-gated chloride channels in primary cultures of cerebellar granule cells", Neuroscience, 117, pp.397~403 (2003)
- Eyer F, "Acute endosulfan poisoning with cerebral edema and cardiac failure", J Toxicol Clin Toxicol, 42, pp.927~932 (2004)
- Towne AR, "Determinants of mortality in status epilepticus", Epilepsia, 35, pp.27~34 (1994)
- Novy J, "Refractory status epilepticus : a prospective observational study", Epilepsia, 51, pp.251~256 (2010)
- Walton NY, "Systemic effects of generalized convulsive status epilepticus", Epilepsia, 34(Suppl 1), pp.S54~S58 (1993)
- Fountain NB, "Status epilepticus: risk factors and complications", Epilepsia, 41(Suppl 2), pp.S23~S30 (2000)
- Fujikawa DG, "Status epilepticus-induced neuronal loss in humans without systemic complications or epilepsy", Epilepsia, 41, pp.981~991 (2000)
- Bassin S, "Clinical review : status epilepticus", Crit Care, 6, pp.137~142 (2002)
- Chen JW, "Status epilepticus : pathophysiology and management in adults", Lancet Neurol, 5, pp.246~256 (2006)
- Naylor DE, "Trafficking of GABA(A) receptors, loss of inhibition, and a mechanism for pharmacoresistance in status epilepticus", J Neurosci, 25, pp.7724~7733 (2005)
- Kalender S, "Endosulfan-induced cardiotoxicity and free radical metabolism in rats : the protective effect of vitamin E", Toxicology, 202, pp.227~235 (2004)
- Blanco-Coronado JL, "Acute intoxication by endosulfan", J Toxicol Clin Toxicol, 30, pp.575~583 (1992)
- Ozmen O, "Pathological and immunohistochemical examinations of the pancreas in subacute endosulfan toxicity in rabbits", Pancreas, 39, pp.367~370 (2010)
- Lee SJ, "Two cases of acute intoxication of endosulfan", J Korean Soc Clin Toxicol, 1, pp.47~50 (2003)
- Boereboom FT, "Nonaccidental endosulfan intoxication : a case report with toxicokinetic calculations and tissue concentrations", J Toxicol Clin Toxicol, 36, pp.345~352 (1998)
- Moon HJ, "Availability of intravenous lipid emulsion therapy on endosulfan-induced cardiovascular collapse", Am J Emerg Med, 31, pp.886.e1~886.e2 (2013)
