Hemispheric encephalitis secondary to HAV
DOI:
https://doi.org/10.37018/cmer2954Keywords:
Encephalitis, HAV, ChildAbstract
A 2-year male child, presented to National Institute of Child Health (NICH), with acute onset high grade fever and focal left sided seizures for 1 day, followed by left hemiparesis and encephalopathy. Developmental and family history was unremarkable. On physical examination, patient’s body temperature rose up to 38.7 °C. Though he had pallor along with hepatomegaly, there were no signs of jaundice or ascites. Central nervous system examination showed encephalopathy as well as positive neck stiffness. Motor system examination revealed generalized decrease in bulk of upper and lower limbs, but rest of the findings were localized to left side of the body, showing hypertonia, decreased power, brisk muscle stretch reflex, and positive ankle clonus and left Babinski sign.
Blood investigations showed anemia (hemoglobin 9.1g/dl), leukocytosis (white blood cells 22.1 cells/μL) and raised aspartate aminotransferase (AST) levels (826 IU/L). Total bilirubin and direct bilirubin levels were normal (0.3 mg/dL and 0.1 mg/dL, respectively). Serum ammonia (64 μg/dL) and lactic acid (1.6 μg/dL) levels were also within normal ranges. The cerebrospinal fluid (CSF) was also clear, with 0 leukocytes/μL, protein levels of 25 mg/dL, and normal glucose levels (82 mg/dL), no organism was seen on gram stain. Hepatitis A Ig M antibody came out to be reactive.
Brain computed tomography showed large hypo density along with effacement of sylvian fissure, sulci, gyri on right side involving frontal, parietal, and temporal and occipital lobe on ipsilateral side. On post contrast, there was remarkable meningeal enhancement on right side. MRI brain revealed cortical and subcortical large area of abnormal signal intensity seen in fronto-parietal and occipital cortex on the right side along with laminar necrosis.
Seizures were controlled by given intravenous injection phenytoin and leviteracetam in bolus and then maintenance doses. Intravenous acyclovir was started
due to clinical suspicion of herpes encephalitis but was stopped after observing clinical improvement and identification of Ig M antibody of HAV. Patient conscious level improved after 2 weeks. AST levels also decreased to 20 IU/L and he was discharged with advice to follow up after 14 days
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