Metronidazole-Induced Encephalopathy Mimicking Hepatic Encephalopathy in a Patient With Residual Liver Abscess: A Case Report

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Dr Urja Pujara
Dr Mehul Marwadi
Dr Parth Patel
Dr Ritesh Patel

Abstract

Background
Metronidazole is commonly used for anaerobic and protozoal infections, including liver abscess. Though it's a relatively safe drug, it can rarely cause neurotoxicity leading to metronidazole-induced encephalopathy (MIE). This entity is clinically important because it may present with acute or subacute altered sensorium and may closely mimic hepatic encephalopathy, This is particularly more
likely to occur in patients with underlying liver disease or in cases with intra-abdominal infection.
Case Report
We report a 45 years old man with a recent liver abscess which was managed with percutaneous drainage and prolonged metronidazole therapy. Patient developed progressive anorexia followed by confusion and irritability without focal neurological deficits. Given the clinical context, hepatic encephalopathy, central nervous system infection, metabolic causes and drug-induced toxicity were considered as differential diagnosis and a work-up was initiated. Magnetic Resonance Imaging (MRI) demonstrated a characteristic bilateral symmetric pattern involving cerebral white matter and the corpus callosum with additional symmetric signal changes in the cerebellar dentate nuclei and brainstem-related structures. These imaging findings were consistent with toxic encephalopathy highly suggestive of MIE. Metronidazole was promptly discontinued and supportive care was provided. concurrent measures for possible hepatic encephalopathy were continued during the acute phase. The patient improved steadily after withdrawal of metronidazole and was discharged with complete clinical recovery.
Conclusion
This case underscores the need for heightened awareness of MIE in patients receiving prolonged metronidazole particularly when co-existing hepatic comorbidity creates diagnostic ambiguity. Recognition of the typical symmetric MRI pattern and early cessation of the offending agent are key to preventing unnecessary investigations and achieving favorable neurological outcomes.

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