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Hepatitis is defined as acute inflammation of hepatic parenchyma. In the United States the most common types of hepatitis are secondary to viral etiologies and are labeled as hepatitis A, B, and C. Table 38-3 outlines the various serologic markers for viral hepatitis. Viral hepatitis is less frequently attributed to Epstein-Barr virus, toxoplasmosis, and cytomegalovirus. Additional causes of hepatitis include bacterial and fungal sources, autoimmune and metabolic disorders, toxic poisoning, and various hepatotoxic medications (e.g., isoniazid, acetaminophen) and alternative supplements. Acetaminophen overdose should be considered in acute nonviral hepatitis and treated immediately with n-ace-tylcysteine to avoid permanent hepatic damage and death. Patients presenting with acute hepatitis often exhibit low-grade fever, fatigue, lethargy, anorexia, RUQ pain, nausea, vomiting, diarrhea, arthralgias and myalgias, and in severe cases, dark urine and jaundice.

Serum bilirubin, transaminases, and ALP levels can be greatly elevated in all forms of acute hepatitis, but the specific values have poor prognostic value. Alarm symptoms of severe hepatic parenchymal destruction include mental status changes (hepatic encephalopathy), asterixis, ascites, and prolongation of prothrombin time (PT). These patients may require hospitalization, with attention toward improving nutritional status and specialist referral for liver transplantation evaluation. Most cases of acute hepatitis resolve without complications, so most patients can be managed as an outpatient, although they must take proper contact isolation precautions and allow for a slow return to usual activity. A patient's symptomatic improvement usually precedes the resolution of liver function serologies.

Viral Hepatitis

Hepatitis A is endemic worldwide, with 10% of U.S. children seropositive and up to 100% of preschool children seropositive in areas where sanitation and socioeconomic status is

Figure 38-12 Endoscopic retrograde cholangiopancreatography (ERCP) with stent placement to identify and treat gallstones (arrows). (CourtesyDr. PerryPernicano.)

poor in less developed countries (Marsano, 2003). The virus has received sporadic national attention in the United States from outbreaks in restaurants from undercooked meat and vegetable sources. Spread through the fecal-oral route, severe hepatitis can be seen after an incubation period of 2 to 6 weeks, but the vast majority of patients recover completely within this time frame and without permanent hepatic damage. Once a patient contracts hepatitis A, immunity follows with the appearance of anti-HAV IgG antibodies, and there is no chronic carrier state. If exposed to hepatitis A during a known incubation period, the patient should be passively immunized with immune globulin. Vaccination is recommended in high-risk populations and before travel to endemic areas (CDC, 1999).

Despite the availability of a highly effective vaccine against hepatitis B, approximately 2 billion people worldwide are infected, 350 million with chronic active infection accounting for 600,000 attributable deaths annually worldwide (WHO, 2009). Hepatitis B is spread via blood and body fluid contact through heterosexual and homosexual relations, by sharing of needles by infected drug abusers, and by accidental needle sticks in the medical setting. In areas of high disease prevalence (e.g., Southeast Asia, China), transmission is primarily from mother to child during childbirth or in early childhood. The vaccination for hepatitis B uses recombinant DNA, requires 3 doses on a set schedule, and confers immunity in the majority of recipients. In a child born to a mother positive for hepatitis B surface antigen

Table 38-3 Viral Hepatitis Serologic Tests and definitions

(HBsAg), in addition to the vaccine, hepatitis B hyperimmune globulin should be administered during the first 12 hours of life. Patients with chronic infection can develop cirrhosis and end-stage liver disease. Antiviral treatments for hepatitis B are indicated for patients with moderate to severe disease activity diagnosed on liver biopsy. Current therapies include interferon and more recently, lamivudine and adefovir (Marsano, 2003).

Hepatitis C affects more than 300 million people worldwide and 4 million people in the United States. At least six genotypes and 100 subtypes have been identified (Bukh, 2000). The diagnosis is established with serum testing for HCV RNA antibodies; although an antibody is induced, it is not protective against disease contraction and progression. Transmission occurs via blood or body fluid contamination through IV and intranasal drug use, blood transfusions, and in health care workers (e.g., needle stick or skin disruption with contaminated instrument). Data on sexual transmission and though tattooing have been inconsistent. Co-infection with human immunodeficiency virus (HIV) increases the risk of transmission sexually, as well as vertically mother to child. In patients with chronic hepatitis C, alcohol use rapidly accelerates liver damage and cirrhosis. Many experts believe lifelong abstinence from alcohol and IV and intranasal drugs should be immediate on diagnosis and enforced before initiating antiviral therapies.

Therapy with pegylated interferon and ribavirin has been shown to achieve sustained viral eradication in almost 50% of patients with hepatitis C (Shehab, 2004). Patients should be monitored for side effects of antiviral treatment, which may require dose adjustments or discontinuation of therapy. Duration and success of therapy depend on viral genotype and possible downward adjustments in therapeutic doses. Sustained virologic response ranges from 42% in genotype1 to 80% in genotypes 2 and 3 (Marsano, 2003).

Hepatitis D virus (delta hepatitis) is usually only seen in IV drug users and in former carriers of hepatitis B as a co-infection. Hepatitis E is an enteric virus only rarely identified in the United States, characterized by an acute self-limited illness without a chronic carrier state.

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