Metronidazole-Induced Encephalopathy in Alcoholic Liver Disease: A Diagnostic and Therapeutic Challenge.
Autor: | Sonthalia N; Department of Gastroenterology, Topiwala National Medical College and BYL Ch Hospital, Mumbai, Maharashtra, India., Pawar SV; Department of Gastroenterology, Topiwala National Medical College and BYL Ch Hospital, Mumbai, Maharashtra, India., Mohite AR; Department of Gastroenterology, Topiwala National Medical College and BYL Ch Hospital, Mumbai, Maharashtra, India., Jain SS; Department of Gastroenterology, Topiwala National Medical College and BYL Ch Hospital, Mumbai, Maharashtra, India., Surude RG; Department of Gastroenterology, Topiwala National Medical College and BYL Ch Hospital, Mumbai, Maharashtra, India., Rathi PM; Department of Gastroenterology, Topiwala National Medical College and BYL Ch Hospital, Mumbai, Maharashtra, India., Contractor Q; Department of Gastroenterology, Topiwala National Medical College and BYL Ch Hospital, Mumbai, Maharashtra, India. |
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Jazyk: | angličtina |
Zdroj: | The Journal of emergency medicine [J Emerg Med] 2016 Oct; Vol. 51 (4), pp. e79-e83. Date of Electronic Publication: 2016 Jul 25. |
DOI: | 10.1016/j.jemermed.2016.05.038 |
Abstrakt: | Background: Acute encephalopathy in a patient with alcoholic liver disease (ALD) is a commonly encountered emergency situation occurring most frequently due to liver failure precipitated by varying etiologies. Acute reversible cerebellar ataxia with confusion secondary to prolonged metronidazole use has been reported rarely as a cause of encephalopathy in patients with ALD. Case Report: We describe a decompensated ALD patient with recurrent pyogenic cholangitis associated with hepatolithiasis who presented to the emergency department with sudden-onset cerebellar ataxia with dysarthria and mental confusion after prolonged use of metronidazole. Magnetic resonance imaging (MRI) of the brain was suggestive of bilateral dentate nuclei hyper intensities on T2 and fluid-attenuated inversion recovery sections seen classically in metronidazole-induced encephalopathy (MIE). Decompensated liver cirrhosis resulted in decreased hepatic clearance and increased cerebrospinal fluid concentration of metronidazole leading to toxicity at a relatively low total cumulative dose of 22 g. Both the clinical symptoms and MRI brain changes were reversed at 7 days and 6 weeks, respectively, after discontinuation of metronidazole. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: A patient with ALD presenting with encephalopathy creates a diagnostic dilemma for the emergency physician regarding whether to continue metronidazole and treat for hepatic encephalopathy or to suspect for MIE and withhold the drug. Failure to timely discontinue metronidazole may worsen the associated hepatic encephalopathy in these patients. Liver cirrhosis patients have higher mean concentration of metronidazole and its metabolite in the blood, making it necessary to keep the cumulative dose of metronidazole to < 20 g in them. (Copyright © 2016 Elsevier Inc. All rights reserved.) |
Databáze: | MEDLINE |
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