ACUTE VIRAL HEPATITIS

Viruses can affect the liver, either primarily, e.g. hepatitis

A, B, C, E or as part of a systemic involvement, e.g.
cytomegalo-virus (CMV), Epstein-Barr virus (EBV), herpes
simplex virus (HSV). In Indian children, hepatitis A is the
commonest cause (40-60%) of acute viral hepatitis,
followed by hepatitis E (10-20%) and hepatitis B (7-17%).
Nearly 8-20% patients have coinfection with more than
one virus, HA V and HEV being the commonest. Hepatitis
A and E are transmitted by feco-oral route whereas HBV
and HCV are transmitted by parenteral or vertical (mother
to baby) route (Table 11.24) (see also Chapter 10).
Clin ical Features
Following exposure, patients show a prodrome characterized
by low grade fever, malaise, anorexia and
vomiting, followed by appearance of jaundice. Examination
shows icterus, hepatomegaly and splenomegaly
(small, soft in 15-20%). Mild ascites may be present in
10-15% cases, which resolves completely on followup.
Over the next few weeks, the appetite improves, jaundice
resolves and the child gets better. In young children
asymptomatic and anicteric presentation of hepatitis A
infection can occur.
Diseases of Gastrointestinal System and Liver
Table 11.24: Epidemiological profile of different hepatitis viruses
Virus A B C E
Type of virus RNA DNA RNA RNA
Incubation period, days 15-40 50-150 30-150 15-45
Route of infection
Feco-oral + +
Parenteral or others Rare Usually perinatal, Usually perinatal,
by sexual contact by sexual contact
Chronic liver disease + +
Vaccine Available Available No No (being developed)
Diagnostic test IgM; anti-HA V HBsAg; IgM anti-HBc Anti-HCV antibody; IgM anti-HEV
Differential Diagnosis
The conditions, which mimic the clinical features of viral
hepatitis include enteric fever, falciparum malaria,
leptospirosis and viral hemorrhagic fever. Other
conditions that need to be differentiated include drug
induced hepatitis, acute presentation of autoimmune liver
disease or Wilson disease.
Investigations
Direct hyperbilirubinemia with markedly elevated ALT/
AST and normal albumin and prothrombin time are usual.
Mild leukopenia with relative lymphocytosis is seen.
Ultrasound is not routinely required, but shows mildly
enlarged liver with increased echogenicity and edema of
gallbladder wall. Viral serologies help determine the
etiology of acute viral hepatitis, as shown in Table 11.24.
Complications
These include:
1. Acute liver failure. The appearance of irritability, altered
sleep pattern, persistent anorexia and uncorrectable
coagulopathy (despite administration of vitamin K)
suggests the development of acute liver failure.
ii. Aplastic anemia
iii. Pancreatitis
iv. Serum sickness, vasculitis-like reaction may be seen
in hepatitis B infection
v. Hemolysis (cola-colored urine) with renal failure in
subjects with glucose-6-phosphate dehydrogenase
deficiency
vi. Chronic liver disease: In patients with viral hepatitis due
to HBV, repeat testing for hepatitis B surface antigen
should be done after 6 months to document clearance
or persistence of infection. A majority (95%) clear
hepatitis B infection after acute icteric infection.
Management
Maintaining adequate oral intake is essential intravenous
fluids are given if persistent vomiting and dehydration
are present. There is no advantage of enforced bed rest,
but vigorous activity should be avoided. No specific
HCVRNA
dietary modification is recommended. The child should
be monitored for appearance of complications like
encephalopathy.
Prevention
Public health measures like sanitation, safe drinking water
supply, hand washing and proper food hygiene are of
utmost importance, especially in epidemics of hepatitis A
or E. Proper screening of blood and blood products and
safe injection practices are essential. Universal immunization
against hepatitis B is the most effective way of
preventing hepatitis B related disease