继发于甲肝病毒的半球脑炎

Aijaz Ahmed, M. Ashfaq, Bader u Nisa, H. Waseem
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摘要

一名2岁男童,提交给国家儿童健康研究所(NICH),急性高热和局灶性左侧癫痫发作1天,随后出现左偏瘫和脑病。发育和家族史无显著差异。体检时,患者体温高达38.7℃。虽然他面色苍白,肝肿大,但没有黄疸或腹水的迹象。中枢神经系统检查显示脑病和阳性颈部僵硬。运动系统检查显示上肢和下肢体积全身性减小,但其余发现局限于身体左侧,表现为强直,力量减弱,肌肉伸展反射活跃,踝关节阵挛阳性,左巴宾斯基征。血液检查显示贫血(血红蛋白9.1g/dl),白细胞增多(白细胞22.1个细胞/μL),谷草转氨酶(AST)升高(826 IU/L)。总胆红素和直接胆红素水平正常(分别为0.3 mg/dL和0.1 mg/dL)。血清氨(64 μg/dL)、乳酸(1.6 μg/dL)均在正常范围内。脑脊液(CSF)也很清楚,0个白细胞/μL,蛋白水平25 mg/dL,葡萄糖水平正常(82 mg/dL),革兰氏染色未见生物。结果显示,甲型肝炎igg抗体具有反应性。脑部电脑断层显示大量低密度伴右侧脑沟、脑沟、脑回消失,累及同侧额叶、顶叶、颞叶和枕叶。造影后,右侧脑膜明显增强。脑MRI示右侧额顶叶和枕叶皮层皮层下可见大面积异常信号,伴椎板坏死。癫痫发作通过静脉注射苯妥英和左iteracetam控制。因临床怀疑为疱疹性脑炎开始静脉注射阿昔洛韦,观察临床好转并检出HAV Ig M抗体后停止静脉注射。2周后患者意识水平有所改善。AST水平也降至20 IU/L, 14天后出院,建议随访
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Hemispheric encephalitis secondary to HAV
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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