Hepatitis (Viral)

– A diffuse inflammation of the cells of the liver that produces liver enlargement and jaundice.

Causes and Incidence

The cause is a variety of hepatotropic viruses. To date, five viral types that cause primary hepatitis have been positively identified; these viruses are known as hepatitis A (HAV), hepatitis B (HBV), hepatitis C (HCV), hepatitis D (HDV), and hepatitis E (HEV). Viruses F and G have been discovered and may also cause primary hepatitis. Other viruses tentatively labeled as GB-A, GB-B, and GB-C are being tested to see if they differ from F and G and if they also cause hepatitis. HAV is transmitted by con-taminated food and water and by the fecal-oral route; HBV and HDV are transmitted by contact with bodily fluids, HCV by percutaneous exposure to blood, and HEV by con-taminated water and the fecal-oral route. Note: Hepatitis may also occur as a secondary infection and is associated with viruses from other primary diseases, including cytomegalovirus, Epstein-Barr, herpes simplex, varicella-zoster, coxsackie B, and rubella viruses.

Primary viral hepatitis occurs worldwide. More than 70,000 cases are reported annually in the United States, and the incidence is rising. Hepatitis A is seen most often in children and young adults, but the incidence is rising in those who are HIV positive. Hepatitis B affects all age groups; about 10% of all transfusion-related hepatitis is this type. Hepatitis C accounts for about 20% of all cases and for most transfusion-related cases. It is seen across all age groups. Hepatitis D is seen in individuals who are susceptible to HBV or may be HBV carriers, such as hemophiliacs and IV drug users. The disease manifestation is severe in children. Hepatitis E is seen primarily among young adults in developing countries in Africa, Asia, or Central America. It is most severe in pregnant women.

Disease Process

The etiologic agent, mode of transmission, and clinical course vary according to the hepatitis type. However, the pathophysiology is the same. The causative agent invades the mononuclear cells in the liver, replicates, and sets up an inflammatory process in the parenchyma and portal ducts, causing hepatic cell necrosis, cellular collapse, and accumulation of necrotic tissue in the lobules and portal ducts. This results in interference with bilirubin excretion. Cellular regeneration and mitosis occur simultaneously with cellular necrosis, and the liver regenerates within 2 to 3 months. Continuation of the inflammatory response sets up a chronic disease process.

Symptoms

Incubation
HAV: 15 to 50 days; HBV: 45 to 180 days; HCV: 14 to 182 days; HDV: 14 to 70 days; HEV: 15 to 64 days

Communicability
HAV: last half of incubation until 1 week after onset of jaundice; HBV: during incubation and entire clinical course (carrier state may persist for years); HCV: 1 week before clinical onset to indefinite period of time as carrier; HDV: throughout clinical disease; HEV: unknown

Preicteric phase
Malaise, headache, nausea and vomiting, anorexia, myalgia, chills, fever, upper quadrant abdominal pain; HBV, HDV: hives, itching, erythema, arthritis

Icteric phase
Appetite returns; malaise continues; jaundice with or without itching; dark urine; claycolored stools

Potential Complications

Complications include development of chronic hepatitis, spontaneous relapse, and cirrhosis. Severe fulminant hepatitis with rapid cellular destruction, no regeneration, and accompanying encephalopathy occur in 1% of cases and are usually fatal.

Diagnostic Tests

Serum enzymes (aspartate aminotransferase [serum glutamic oxaloacetic transaminase], alanine aminotransferase [serum glutamic pyruvic transaminase]) 8 to 20 times normal values during the prodromal and clinical phases, lactate dehydrogenase is 1 to 3 times normal. These elevations are the hallmark of the disease. The differential diagnosis is based on the clinical history and various laboratory tests. In HAV, the stool is positive for the virus 2 to 4 weeks after exposure, and the enzyme-linked immunosorbent assay (ELISA) shows a rise in HAV antibodies. In HBV, serum antigen tests detect HBAg, and serum antibody tests detect a rise in anti-HBe. A serum test for HCV is now available.

Treatments

Surgery
None.

Drugs
Immune globulin for prophylaxis in those exposed to HAV and HBV; vaccine for prophylaxis in individuals exposed to or at high risk of contracting HBV; antiemetics (chlorpromazine is contraindicated in hepatic disease) for nausea; analgesics for pain (acetaminophen is preferred).

General
Bed rest; diet as tolerated, with frequent, small, lowfat, high-carbohydrate meals; adequate fluid intake; appropriate infection precautions, dictated by transmission routes; monitoring by liver function tests until normal value is achieved.