The neck was supple with bilateral extensor plantar response and a flapping tremor was present.

A diagnosis of septic or metabolic encephalopathy was made as the patient's relatives gave an undocumented history of fever in the initial stage of presentation. The patient was put on 5% dextrose with Ryle’s tube and catheterisation in a propped-up position with frequent monitoring of vitals and CBG. Injection PPI, ondansetron, ceftriaxone 2g iv bd APST were added with rifaximin 550 mg bd and syrup lactulose 15 ml thrice daily with a target of 2-3 semi-formed stools per day.

ABG revealed mild hypokalaemia with alkalosis without hypoxemia or hypercarbia and SPO2 was 92% with 2l/min oxygen therapy.

Blood was sent for CBC, peripheral blood smear, RBS, urea, creatinine, LFT, electrolytes, Procalcitonin, Hepatitis A and E virus IgM antibody, HbsAg, anti-HCV antibody, HIV 1 and 2 ab, EBVNA and IgM anti-VCA ab, HSV 1 and 2 DNA PCR, CRP, serum ammonia, IgM and IgG CMV ab, MP slide and dual antigen, IgM and IgG Dengue ab, typhi Dot M, Covid 19 RTPCR, blood for CS aerobic single hand, serum ceruloplasmin.

Urine RE and CS, Stool for RE and CS, Chest X-ray AP supine view, USG whole abdomen, ECG,2D echocardiography with colour doppler, CT brain plain, EEG and CSF study were done after ruling out papilledema.24-hour urinary copper was also sent.

CBC revealed mild anaemia with TLC of 12,000/mm3 without any toxic granules or thrombocytopenia. Urea was mildly elevated at 60 mg/dl with normal creatinine and there was mild hyponatremia and hypokalaemia. LFT revealed conjugated hyperbilirubinemia with conjugated bilirubin 20 mg/dl and unconjugated bilirubin 14 mg/dl. AST was elevated at 130 U/L and ALT was 198 U/L with an ALP of 280 U/L with a rise of GGT level of 72 U/L.There was mild hypoalbuminemia. Ceruloplasmin and urinary copper levels were normal. USG abdomen revealed gall bladder wall thickening and GB sludge and MRCP done did not reveal any additional abnormality IgM CMV ab was elevated at>0.9 S/Co(>0.8 positive)with normal CMV IgG levels. All other tests of fever profile were unremarkable including Scrub typhus IgM ab and Leptospira and brucella IgM ab. Chest x-ray revealed mild bilateral pleural effusion with normal echocardiography and CT brain.

[3]. The disease presents with less than a 5-fold rise of AST and ALT with a rise of ALP and bilirubin. CMV-induced acute liver failure is extremely rare. [4,5]In immunocompetent hosts infections may range from self-limiting asymptomatic stage to hepatitis. It is transmitted by vertical transmission, via breast milk, blood transfusion, sexual route, and organ transplant [6,7,8,9]

CMV IgM can also be positive in secondary CMV infection, so CMV IgG test in 2 samples taken one month apart is used to diagnose primary CMV infection with the first sample being IgG negative and the second sample IgG positive proving recent infection as per CDC guidelines for CMV diagnosis.

The patient was diagnosed as per CDC (Centres for Disease Control and Prevention). As the patient improved and was non-immune compromised no anti-viral treatment was given. Intravenous corticosteroids in high doses can also be the most important risk factor in CMV liver failure.[10]