Acute viral hepatitis is a systemic infection predominantly affecting the liver. Clinically characterized by malaise, nausea, vomiting, diarrhea, and low-grade fever followed by dark urine, jaundice, and tender hepatomegaly; may be subclinical and detected on the basis of elevated aspartate and alanine aminotransferase (AST and ALT) levels. Hepatitis B may be associated with immune-complex phenomena, including arthritis, serum sickness-like illness, glomerulonephritis, and a polyarteritis nodosa-like vasculitis. Hepatitis-like illnesses may be caused not only by hepatotropic viruses (A, B, C, D, E) but also by other viruses (Epstein-Barr, CMV, coxsackievirus, etc.), alcohol, drugs, hypotension and ischemia, and biliary tract disease (Table 155-1 Clinical and Epidemiologic Features of Viral Hepatitis).
27-nm picornavirus (hepatovirus) with single-stranded RNA genome.
Recovery within 6-12 months, usually with no clinical sequelae; a small proportion will have one or two apparent clinical and serologic relapses; in some cases, pronounced cholestasis suggesting biliary obstruction may occur; rare fatalities (fulminant hepatitis), no chronic carrier state.
Fecal-oral transmission; endemic in underdeveloped countries; food-borne and waterborne epidemics; outbreaks in day-care centers, residential institutions.
After exposure:immune globulin 0.02 mL/kg IM within 2 weeks to household, sexual, and institutional contacts (not casual contacts at work). Before exposure: inactivated HAV vaccine 1 mL IM (unit dose depends on formulation); half dose to children; repeat at 6-12 months; target travelers, military recruits, animal handlers, day-care personnel, laboratory workers, and pts with chronic liver disease (especially hepatitis C).
42-nm hepadnavirus with outer surface coat (HBsAg), inner nucleocapsid core (HBcAg), DNA polymerase, and partially double-stranded DNA genome of 3200 nucleotides. Circulating form of HBcAg is HBeAg, a marker of viral replication and infectivity. Multiple serotypes and genetic heterogeneity.
Recovery >90%, fulminant hepatitis (<1%), chronic hepatitis or carrier state (only 1-2% of immunocompetent adults; higher in neonates, elderly, immunocompromised), cirrhosis, and hepatocellular carcinoma (especially following chronic infection beginning in infancy or early childhood) (Chap. 157 Cirrhosis and Alcoholic Liver Disease). Reactivation of HBV has been observed with immunosuppression, particularly with rituximab.
HBsAg in serum (acute or chronic infection); IgM anti-HBc (early anti-HBc indicative of acute or recent infection). Most sensitive test is detection of HBV DNA in serum; not generally required for routine diagnosis.
Percutaneous (needle stick), sexual, or perinatal transmission. Endemic in sub-Saharan Africa and Southeast Asia, where up to 20% of population acquire infection, usually early in life.
After exposure in unvaccinated persons:hepatitis B immune globulin (HBIG) 0.06 mL/kg IM immediately after needle stick to within 14 days of sexual exposure in combination with vaccine series. For perinatal exposure (HbsAg+ mother) HBIG 0.5 mL in the thigh immediately after birth with the vaccine series started within the first 12 h of life. Before exposure: recombinant hepatitis B vaccine IM (dose depends on formulation as well as adult or pediatric and hemodialysis); at 0, 1, and 6 months; deltoid, not gluteal injection. Has been targeted to high-risk groups (e.g., health workers, persons with multiple sexual partners, IV drug users, hemodialysis pts, hemophiliacs, household and sexual contacts of HBsAg carriers, persons traveling in endemic areas, unvaccinated children <18). Universal vaccination of all children is now recommended in the United States.
Caused by flavi-like virus in the genus Hepacivirus with RNA genome of 9600 nucleotides; genetic heterogeneity. Incubation period 7-8 weeks.
Often clinically mild and marked by fluctuating elevations of serum aminotransferase levels; >50% likelihood of chronicity, leading to cirrhosis in >20%.
Anti-HCV in serum. Current third-generation immunoassay incorporates proteins from the core, NS3, and NS5 regions. The most sensitive indicator of HCV infection is HCV RNA (Fig. 155-3. Scheme of Typical Laboratory Features During Acute Hepatitis C Progressing to Chronicity).
HCV accounts for >90% of transfusion-associated hepatitis cases. IV drug use accounts >50% of reported cases of hepatitis C. Little evidence for frequent sexual or perinatal transmission.
Hepatitis D (Hdv, Delta Agent) 
Defective 37-nm RNA virus that requires HBV for its replication; either co-infects with HBV or superinfects a chronic HBV carrier. Enhances severity of HBV infection (acceleration of chronic hepatitis to cirrhosis, occasionally fulminant acute hepatitis).
Anti-HDV in serum (acute hepatitis D-often in low titer, is transient; chronic hepatitis D-in higher titer, is sustained).
Endemic among HBV carriers in Mediterranean Basin, where it is spread predominantly by nonpercutaneous means. In nonendemic areas (e.g., northern Europe, United States) HDV is spread percutaneously among HBSAg+ IV drug users or by transfusion in hemophiliacs.
Caused by 29- to 32-nm agent resembling caliciviruses but considered within its own genus, Hepevirus. Enterically transmitted and responsible for waterborne epidemics of hepatitis in India, parts of Asia and Africa, and Central America. Self-limited illness with high (10-20%) mortality rate in pregnant women.
| TREATMENT | ||
Viral HepatitisActivity as tolerated, high-calorie diet (often tolerated best in morning), IV hydration for severe vomiting, cholestyramine up to 4 g PO four times daily for severe pruritus, avoid hepatically metabolized drugs; no role for glucocorticoids. Liver transplantation for fulminant hepatic failure. In rare instances of severe acute HBV, treatment with a nucleoside analogue has been used successfully. Most authorities would recommend antiviral therapy for severe acute HBV (Chap. 156 Chronic Hepatitis). For acute HCV, delay in treatment initiation for up to 6 months with counseling and monitoring of HCV RNA levels are recommended. Health workers who sustain HCV-contaminated needle sticks and injection-drug users are the two main settings where acute HCV can be identified and are candidates for treatment (Chap. 156 Chronic Hepatitis). |