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Pseudotumor Cerebri in Childhood Hepatitis E Virus Infection

We report a 7-year-old boy with acute Hepatitis E virus (HEV) infection who developed pseudotumor cerebri (PC), manifested by symptoms and signs of increased intracranial pressure in the presence of normal cerebrospinal fluid (CSF) examination and cranial magnetic resonance (MR) scan. To our knowledge, this is the first report to describe PC in relation to acute HEV infection in the English literature. A 7-year-old, otherwise healthy boy was initially seen following 7 days of low-grade fever, malaise and dark yellow urine. Mild pallor, icterus and 2.5 cm hepatomegaly were noted on physical examination. The full blood count was normal.The liver function tests showed the following values: total serum bilirubin 6.8 mg/dL (conjugated fraction 3.9), alanine aminotransferase 654 IU/L, aspartate aminotransferase 578 IU/L, prothrombin time 15 seconds (normal: <12 seconds). The serum IgM and IgG anti-HEV antibodies were positive while serological tests were negative for hepatitis A, B, and C viruses, Epstein-Barr virus, Cytomegalovirus, Toxoplasma gondii, Dengue virus,Leptospira,Rubella virus,Parvovirus B19, and HIV. The blood and urine cultures remained sterile. Serum ammonia, lactate and ceruloplasmin values were within the reference range.Abdominal ultrasonography confirmed the hepatomegaly with increased hepatic echogenicity. Forty-eight hours later he complained of generalized headache, double vision, and developed recurrent bouts of vomiting without nausea. There was no impairment in his consciousness.The vitals, including the blood pressure, were normal. His neurological examination revealed impaired abduction in the right eye, suggestive of right 6th cranial nerve palsy. The pupils were bilaterally symmetrical with normal reaction to light and accommodation. The examination of the optic fundi revealed papilledema stage 2 (early papilledema as per Frisen scale). The remainder of the neurological examination was normal. His lumbar puncture showed an increased opening pressure (260 mm of water). The CSF was clear with normal cell count, protein, and glucose content. His cranial MR scan and MR venography were normal. He was managed with supportive therapy for both his conditions. The abducens palsy subsided in 3 days with return of satisfactory vision. The serum bilirubin and liver enzymes returned to normal in 5 weeks. Hepatitis E virus is an enterically transmitted RNA virus endemic in parts of the developing world and associated with poor water sanitation. It manifests itself as a brief icteric illness, similar to hepatitis A, and most often affects young adults. Sporadic reports of neurological manifestations occurring in association with HEV infection are documented that include transverse myelitis, Guillain-Barre syndrome (additionally with left infranuclear facial palsy), and meningoencephalitic seizures. HEV implicated isolated cranial neuropathies consist of a single report each of oculomotor palsy and Bell’s palsy. The temporal course of events and the exclusion of other common etiologies of PC in children, especially infections and drugs, strongly implicate HEV in the causation of the symptoms. In conclusion, acute HEV infection should be included in the list of etiologies responsible for causing PC in children. Supportive management of such children may result in swift and satisfactory outcome.