Acute hepatitis a virus infection presenting with multiorgan dysfunction: a case report

Introduction Acute hepatitis due to hepatitis a virus is usually a benign self-limiting disease conferring lifelong immunity. However, few cases have been reported in literature with fulminant hepatitis. We report this extremely rare case with multiorgan dysfunction including liver failure, hepatic encephalopathy, renal failure, pleural effusion, pericardial effusion and hematologic dysfunction as a sequale of this infection in an otherwise healthy male at the age of 18. Case presentation An 18 years old Pakistani male presented with two days history of fever, cough, headache and vomiting. His condition gradually deteriorated and on day 7 developed multiorgan dysfunction. Initially Immunoglobulin M anti hepatitis a virus was borderline 1.40 but repeated titers one week later confirmed the diagnosis of acute hepatitis a virus infection. Conclusion This original case report highlights the importance of focusing first uncommon manifestations of common illnesses while diagnosing difficult cases. Moreover this case also adds knowledge to the limited available data regarding complications and predictors of prognosis.


Introduction
Hepatitis A virus has plagued mankind for centuries by causing acute hepatitis associated with significant morbidity and occasional mortality. HAV is a 7.5-kb positivestrand RNA virus of the Picornaviridae family and the only member of the genus Hepatovirus [1]. All four genotypes belong to a single serotype. HAV is spread via the fecal-oral route. The incubation period averages 30 days (range 15 to 49 days). The prevalence of HAV infection varies among countries in Asia [2]. Countries with high endemicity for HAV infection include Pakistan, India, China, Nepal, Bangladesh, Myanmar and the Philippines. Most people in these countries are exposed during childhood. HAV infection usually results in an acute, self-limiting illness and only rarely leads to fulminant hepatic failure [3]. In young children, the disease is often asymptomatic, whereas in older children and adults there might be a range of clinical manifestations from mild, anicteric infection to fulminant hepatic failure. The risk of fulminant hepatitis is high in patients having an underlying chronic liver disease and are aged more than 40 years [4]. This case report describes a young person from a highly HAV endemic area with serologically confirmed acute HAV infection with multiorgan involvement.

Case presentation
An 18 years old Pakistani male presented with about two days history of intermittent fever with chills, nonproductive cough, generalized headache, nausea and nonbilious vomiting. He vomited thrice on day 1 and five times on the next day. Vomitus contained food particles and was devoid of blood. Clinical examination was unremarkable except raised temperature ranging from 37.22°C (310.4 kelvin) to 39.44°C (312.6 kelvin) with relative bradycardia (pulse ranging from 56/minute to 84/minute). Initial investigations revealed raised serum alanine aminotransferase (2043u/l), low normal platelet count (165 × 10 9 /l) and total white cell count (4.2 × 10 9 /l) with normal differential count and morphology. Other investigations including haemoglobin, malarial parasite slides, bilirubin, alkaline phosphatase, aspartate aminotransferase, albumin, urea, creatinine, electrolytes, plasma glucose, widal test, DIC screening, urinalysis and chest radiograph were within normal limits. He was provisionally diagnosed as a case of anicteric hepatitis with differential diagnoses of malaria and enteric fever due to their high prevalence in the area. He was managed with antimalarial (artemether), third generation cephalosporin (Ceftriaxone) and supportive parenteral fluids. Samples for blood cultures, viral (including hepatitis and dengue) screening, typhi dot, serology for brucella, leptospira, rickettsia and toxoplasma were sent to laboratory.
Echocardiography showed minimal amount of pericardial effusion with no evidence of tamponade. He was managed with frusemide and haemodialyzed thrice on day 7,8 and 10 via dual lumen catheter in right subclavian vein.
On day 10, he started showing signs of improvement with better control of blood pressure, urinary output improving to 900 ml/24 hours and significant improvement in the levels of serum urea/creatinine as well as the liver function tests etc. Repeated IgM anti hepatitis A virus was positive, while rest of the investigations including blood cultures, serum cryoglobulins, aldolase, rheumatoid factor, complement levels, autoimmune and vasculitic screening revealed no abnormality. Dual lumen catheter was removed post dialysis on day 10.
On day 16, investigations revealed normal serum albumin, coagulation profile, cardiac enzymes, electrolytes and blood counts while levels of serum urea 11.2 mmol/l, creatinine 246 umol/l, alanine aminotransferase 127 u/l, bilirubin 38 mmol/l, alkaline phosphatase 594 u/l were showing gradual improvement.
Follow up on day 23 revealed completely normal clinical and laboratory parameters including renal, hepatic, cardiac, pleural and hematological functions. Monthly follow up during last five months has not shown any evidence of relapse.

Discussion
HAV infection usually results in an acute, self-limiting illness conferring lifelong immunity and only rarely leads to fulminant hepatic failure. Fulminant hepatic failure occurs more commonly in patients with underlying liver disease; particularly chronic hepatitis B and C infection, advanced age and addiction of intravenous drugs [3][4][5][6]. This case is very unusual as there was no pre-existing hepatic or non hepatic illness or other risk factors.
Few cases of acute renal failure and nephrotic syndrome have been reported in the literature in association with HAV infection [7][8][9][10]. Acute tubular necrosis was the most common form of renal injury in such patients while in others renal biopsy was suggestive of interstitial nephritis, immune complex mesangial glomerulonephritis [7], and IgA dominant glomerulonephritis. Only once IgA dominant glomerulonephritis was accompanied with cutaneous cryoglobulinemic vasculitis. This is a truly rare event in which a young patient at the age of 18, experienced multiorgan dysfunction secondary to hepatitis A virus infection comprising of fulminant liver failure, hepatic encephalopathy, acute renal failure, pleural effusion, pericardial effusion and hematological dysfunction within short span of time and without preexisting underlying liver disease.

Conclusion
This emphasizes the importance of focusing on common illnesses with their uncommon manifestations while searching for solution of various clinical diagnostic mysteries even in the absence of poor prognostic markers.