The silent dragon—hepatitis C - Home Study Program

AORN Journal, June, 2003 by Beverly Walker, Linda Howard

At the cellular level, necrotic hepatocytes infiltrate portal tracts, leading to inflammatory changes in the liver bed. Inflammatory cells also can collect throughout the parenchyma in small clusters. As the disease progresses, necrosis and liver cell death may lead to fibrosis. When mild, the fibrosis is confined to portal tracts and immediately adjacent parenchymal tissue. Subsequent resistance to portal blood flow and formation of dense connective tissue causes further damage that can lead to diffuse fibrosis. In this more severe state, fibrosis bridges portal tracts and extends to hepatic veins. (20) Progression to cirrhosis occurs in at least 20% of patients (21) in whom fibrous septae divide clusters of liver cells into nodules and these, along with fatty infiltrates, replace mildly fibrotic tissue. The nodules do not have the plate-like structure of normal liver tissue and are less functional. The extent of fibrosis is the determining factor in staging the disease and is assessed with a liver biopsy. (22) Cirrhosis and end-stage liver disease can occur rapidly in some patients, but from most reports it takes 20 years of histological changes for cirrhosis to develop. Another 10 years usually pass before hepatocellular carcinoma develops. (23) When the liver becomes cirrhotic, complications, such as jaundice, ascites, variceal hemorrhage, or encephalopathy, can develop. This transition marks the progression from compensated to decompensated cirrhosis, an indicator of liver failure. (24)

The risk of progressing from chronic disease to liver failure or cancer increases with even moderate alcohol consumption. Other factors, including large viral loads, such as those received with blood transfusions, and the age of the patient at the time of infection, seem to impact the rate of disease progression. (25) One study in Germany followed 458 children who underwent heart surgery before 1991 when the country began screening their blood supply for HCV. (26) Fifteen percent acquired HCV during their procedures. Twenty years later, nearly one-half of the HCV-infected children in the study had cleared their viremia without therapeutic intervention. In the children with persistent infection, few had gone on to develop liver disease.

INCIDENCE AND TRANSMISSION

It is estimated that 1.8% of the general population in the United States is infected with HCV. (27) The disease is more common among ethnic and minority groups, and new studies report that veterans appear to be at higher risk of carrying the virus than the population at large. (28) Prevalence of infection in the United States also varies according to risk factors within population groups. (29) Tables 1, 2, and 3 illustrate the incidence, population groups at risk, and modes of transmission.

Most HCV transmission comes from direct percutaneous exposure to blood. Although it generally is thought that HBV infection occurs more easily than HCV, experts from the CDC found evidence to suggest otherwise when investigating a hepatitis outbreak in Karachi, Pakistan. They traced the infectious outbreak to syringe reuse at a local clinic. Multiple patients were injected with medications from syringes that were shared between patients. Forty-four percent of the patients who contracted hepatitis from this incident carded HCV, and 29% were infected with HBV. Based on this data, investigators concluded that HCV is transmitted more easily than HBV. (30)