Viral hepatitis can be caused by any one of the Hepatitis A, Hepatitis B, Hepatitis C, Hepatitis E and Delta viru, Epstein-Barr virus, cytomegalovirus, herpes simplex virus, rubella virus and virus of yellow fever.
Hepatitis A Virus
This is a RNA virus transmitted by fecoral route. Incubation period is 2-6 weeks. It leads to acute hepatitis and does not lead to chronic disease or carrier state. Jaundice does not occur in half of the patients.
Hepatitis B Virus
This is a DNA virus transmitted parenterally or sexual intercourse. Workers dealing with blood products are at a higher risk.. The incubation period is 2-25 weeks. About 10 percent patients develop chronic disease or a carrier state.
Hepatitis C Virus
This is a single standard RNA virus transmitted parenterally. The incubation period varies from 2-25 weeks. About 20-30 percent develop chronic hepatitis, 50 percent of which is chronic active hepatitis which would ultimately lead to cirrhosis of liver.
This is caused by RNA virus. It resembles Hepatitis A, it is transmitted by feco-oral route and is found to occur in endemic areas like India, Asia, Africa and Central America. It is seen to occur in individuals who are immune to Hepatitis A Virus infection.
This is a small RNA virus which is infectious only in presence of Hepatitis B surface antigen. It is thus a “superinfection” to hepatitis B infection with a rise in liver function tests. It usually has a chronic severe clinical course.
Epstein-Barr virus, cytomegalovirus, herpes simplex virus, rubella virus and virus of yellow fever may all cause hepatitis.
- Mononuclear cell infiltration
- Cellular ballooning and necrosis
- Condensed cytoplasm with pyknotic nuclei also called acidophilic bodies.
Clinical Features of Viral Hepatitis
- Influenza-like syndrome is common in hepatitis a with malaise, anorexia and fatigue
- Arthritis and urticaria is common with hepatitis B and is probably due to circulating immune complexes
- Jaundice with dark urine and light stool occur in 50 percent of patients
- Tender hepatomegaly is common and splenomegaly occurs in 20 percent of cases
Lab Studies in Viral Hepatitis
- Elevated SGOT, SGPT, LDH, Bilirubin and alkaline phosphatase
- Specific viral marker tests
Complication of Acute Viral Hepatitis
- Fulminant hepatic failure
- Relapsing hepatitis
- Cholestatic hepatitis
- Post-hepatitis syndrome
- Chronic hepatitis
- Cirrhosis of liver
- Hepatocellular carcinoma
- Aplastic anemia
- Henoch Schonlein purura
- Renal failure
- Connective tissue disease
- Papular acrodermatitis
Treatment of Viral Hepatitis
- High calorie diet
- Avoid fatty foods
- No hepatotoxic drug or alcohol to be taken
- Continuous monitoring by clinical and labortary parameters
Variants of Acute Viral Hepatitis
Hepatitis can assume varied forms depending on type & severity of infection and individual immunity.It can be of following forms
There is rapid onset of liver failure due to rapid liver cell necrosis which occurs due to modification of host response to viral infection, allowing rapid viral replication Hepatitis B and C and superinfection with delta agent accounts for majority of the cases.
Mortality in 3 weeks is 30 percent and 90-100 percent above age 60 die.
Clinically there is progressive jaundice, hepatic encephalopathy and hepatorenal syndrome prothrombin time is elevated.
There are features of obstructive jaundice with alkaline phosphatase elevated more than SGPT, during the course of viral hepatitis.
It is to be differentiated from biliary obstruction. The prognosis is excellent, recovery occurs over few months.
This occurs several weeks or months after apparent recovery. Sometimes it may be a second bout of hepatitis with a different virus.
Viral hepatitis with autoimmune features
It occurs in 5 percent of patients with hepatitis B due to circulating immune complexes. Anorexia, malaise, fatigue, urticaria, angioedema migrating arthralgia and non-deforming arthritis of knee, ankle and wrist may occur along with vasculitis and glomerulonephritis. Prognosis is excellent as these rarely persist beyond 2 weeks.
Hepatitis with aplastic anemia
This is rarely seen with acute viral hepatitis. The mortality rate is high and no treatment has been effective.
Prevention of Viral Hepatitis
Prevention is an important aspect of disease control. For hepatitis prevention a good hygiene and good habits play important role.
The patient should avoid salivary transmission to others by avoiding kissing, spitting, sharing food, cigarettes or utensils and sexual contact.
Infected stools and urine in Hepatitis A and E must be disposed off carefully.
Another method of protection is immunization against the disease.
All immune globulin (Ig) preparations contain anti-HAV. It should be given within 2 weeks of contact in the dose of 0.02 ml/kg. For travelers a dose 0.06 ml/kg should be given every 6 months.
Now vaccination of hepatitis A is also available and even included in national vaccination schedule.
A vaccine for active immunization has been prepared from HBsAg carrier serum as well as by genetic engineering from recombinant yeast. For pre-exposure prophylaxis, Hepatitis Vaccine must be given at 0, 1 and 6 months interval. The dose is 20 mcg for immunocompromised adults and 10 mcg for infants and children under 10 years.
For post-exposure cases, a combination of HBIG (fo rapid achievement of high circulating titre of anti-HBs) and hepatitis B vaccine (for long lasting immunity) is given. For perinatal exposure of infants of HBsAg positive mothers, HBIG 0.5 ml should be given in thigh at birth followed by Hepatitis B vaccine 10 mcg started with a week of birth and repeated at 1 and 6 months.
For percutaneous exposure a single dose of 0.06 ml/kg of HBIG is given followed by three doses of hepatitis B vaccine. Usually patients retain protective levels for 5 years after complete vaccination.
There is no immunoprophylaxis to prevent delta superinfection. Susceptible persons are vaccinated with Hepatitis B vaccine.
Non-A Non-B Hepatitis
IG prophylaxis in this hepatitis is not known to be beneficial and is not recommended.
Chronic persistent hepatitis
CPH is a mild non-progressive inflammation limited to the portal triad (Triaditis) but without hepatic necrosis or fibrosis. It can occur following hepatitis B or hepatitis non-A non-B.
The patient is usually asymptomatic or may have mild discomfort over right quadrant, malaise, fatigue, anorexia and weight loss. Serum bilirubin, SGOT, SGPT and alkaline phosphatase may be elevated but serum albumin and prothrombin time are normal.
Liver biopsy gives the diagnosis. There is no specific treatment.
Chronic active hepatitis
CAH is an aggressive and progressive inflammation of the liver cells with piecemeal necrosis and fibrosis which can lead to cirrhosis.
It occurs following hepatitis B and hepatitis non-A non-B viruses.
Some patients are asymptomatic and detected by abnormal blood tests done on routine check-up. In most of the patients there is severe illness with fever, malaise, pain in the right hypochondriac region, edema or ascites.
Autoimmune features like arthralgia and arthritis, skin eruption and pleurisy may be present. Secondary amenorrhea and infertility may be present in females. Serum bilirubin, SGOT, SGPT prothrombin time and gamma globulins are markedly elevated.
Serum albumin is low. Antinuclear, antithyroid and anti-smooth muscle antibodies are present and LE cell preparations may be positive. Liver biopsy shows severe hepatic necrosis involving the hepatic lobule in an irregular and patchy manner (piecemeal necrosis).
In severe cases, bands of necrosis may join the adjacent portal tracts and central vein (bridging hepatic necrosis). In untreated cases, this may progress to cirrhosis with fibrosis and regenerating nodule.
The course in an untreated case is gradually downhill, with development of cirrhosis and all its complications like encephalopathy, ascites and bleeding esophageal varices.
Prednisolone alone and in combination with azathioprine significantly improve survival even when cirrhosis has developed.