Hepatitis: A Pandemic Predicament NUR/426 April 26, 2011 Hepatitis: A Pandemic Predicament Viral hepatitis could be considered a disease of “antiquity” when Hippocrates described his infectious icterus findings 2400 years ago (Schmid, 2001). It is unclear what type of liver disease infiltrated the population at the time. However, by many historical accounts, the Middle Ages were inflicted by outbreaks commonly referred to as “campaign or epidemic jaundice” and were related to wars, famines, and natural disasters (Schmid, 2001, p. 718).

The historic timeline of hepatitis worldwide is hazily documented. During the Napoleonic campaigns in Russia and Egypt, jaundice was well known to inflict soldiers and civilian populations. Officials in the American Civil War noted approximately 70,000 soldiers were affected by viral hepatitis. In fact, the common areas of care for such patients at the time were referred to as “camp jaundice” (Dooley, 2005, p. 71). During World War II, military researchers began a concentrated investigation of the pandemic predicament, its origin, method of transmission, and best treatments.

Their search for answers would lead to many more questions, taking doctors and researchers on a circuitous mind quest toward finding a remedy to a virus that has shrouded itself in mystery for generations. “Viral hepatitis is a systemic, viral infection in which necrosis and inflammation of liver cells produce a characteristic cluster of clinical, biochemical, and cellular changes” (Smeltzer & Bare, 2004, p. 1093). Hepatitis with its known five classifications (A, B, C, D, & E) has become a public health concern in modern time due to the increase of infections.

The virus merits worldwide attention because of the ease of transmission and high morbidity. Researchers have estimated that 60% to 90% of cases of hepatitis are unreported due to mild symptoms and misdiagnosis (Smeltzer & Bare, 2004). Hepatitis A (HAV) was once referred to as infectious hepatitis. The disease is caused by an RNA virus of the Enterovirus family. Transmission of this virus is exposure to infected feces and is often transmitted by consuming contaminated food or water (Smeltzer & Bare, 2004). Hepatitis A often manifests in patients without jaundice or symptoms.

If a patient experiences symptoms, it can often be mistaken for a mild flu-like illness with perhaps an upper- respiratory infection and low grade fever (Smeltzer & Bare, 2004). The majority of the patients recover fully. This form of hepatitis rarely causes cirrhosis of the liver or death. While assessing a patient with hepatitis A, the liver and spleen may be enlarged as well as the hallmark sign of jaundice. Beyond these findings, there are few physical signs that point to hepatitis A (Smeltzer & Bare, 2004). Hepatitis A antigens may be found in the stool and serum when symptoms are presented (Smeltzer & Bare, 2004).

A vaccine is available to prevent Hepatitis A. For those not vaccinated an intramuscular injection of globulin during the incubation period or within two weeks of exposure will assist in suppressing symptoms and promoting active immunity (Smeltzer & Bare, 2004). Hepatitis B (HBV) is referred to as serum hepatitis and can be transmitted through intimate contact. The disease may be spread through sexual activity or blood exposure. The hepatitis B virus has been found in blood, saliva, semen, and vaginal secretions (Smeltzer & Bare, 2004).

Hepatitis B is a virus of concern for healthcare workers because of their increased potential exposure to infected patients. For that, healthcare workers are encouraged and sometimes required to receive the vaccine. Greater than 90% of people infected with hepatitis B will develop antibodies and recover within six months. The treatments for HBV are two antiviral medications, lamivudine (Epvir) and adefovir (Hepseral). Bed rest is also recommended for patients until hepatic enlargement subsides and elevated serum bilirubin and liver enzymes return to normal (Smeltzer & Bare, 2004).

The mortality rate for hepatitis B is 10%. Statistically, 10% of the people infected with the virus may progress to a carrier status or develop chronic hepatitis (Smeltzer & Bare, 2004). Hepatitis C (HCV) was commonly referred to as non-A and non-B hepatitis. HCV is primarily classified when hepatitis A, B, and D are ruled out as the viral infection. Blood transfusion and sexual contact make up for the majority of cases of hepatitis C in the United States. However, there is an increase of infections related to sharing of needles by IV drug users and unintentional needle sticks among healthcare workers.

In fact, there are approximately 35,000 new cases reported each year in the United States. It is projected that there will be a “fourfold” increase of HCV infections from 1990 to 2015 (Smeltzer & Bare, 2004, p. 1099). Symptoms of HCV mirror that of HBV with mild flu-like symptoms and hepatic enlargement with an incubation period from 15 to 160 days. People who experience chronic episodes are at risk of severe liver disease that includes cirrhosis and liver cancer (Smeltzer & Bare, 2004). Studies have also indicated that consumption of alcohol on a regular basis may accelerate the progression of the disease.

Therefore, caution must be taken for those who drink alcoholic beverages as well as take various medications daily. Researchers have indicated that, “there is no benefit from rest, diet, or vitamin supplements” regarding the treatment of HCV (Smeltzer & Bare, 2004, p. 1099). The disease has been treated with a combination of interferon (Intron-A) and ribavirin (Rebetol). These drugs have been effective in the improvement of patient’s condition when suffering from relapses and at times promoting remissions.

Hemolytic anemia is noted to be a common side-effect of this treatment and if severe enough may require the discontinuation of the drugs (Smeltzer & Bare, 2004). The article on viral hepatitis in Harrison’s principles of Internal Medicine states: “The typical morphologic lesions of all types of viral hepatitis are similar” (Dienstag & Isselbacher, 2005, p. 1828, pp. 8). Lesions present microscopically with panlobular infiltration of mononuclear cells, hepatocyte necrosis, hyperplastic Kupffer cells, and cholestasis.

Hepatic regeneration occurs early in the disease process, and it is manifested by numerous mitotic figures, multinucleated cells, and pseudoacinar formations. The mononuclear infiltration is presented by lymphocytes, plasma cells and eosinophils. Hepatic cell damage is evidenced by cell degeneration and necrosis, dropout cells, ballooning of cells, and acidophilic degeneration forming Councilman Bodies. Lesions in hepatitis C are marked by a relative paucity of inflammation, evident in activation of sinusoidal lining cells, lymphoid aggregates, fat droplets, and disorderly clustering of biliary epithelial cells.

Bridging hepatic necrosis is present in some patients. Bridging occurs between lobules, and it is caused by massive cell dropout and disruption of the reticulin framework. A bridge consists of inflammatory debris, degenerating hepatocytes, and condensation of the reticulin framework. The bridge crosses adjacent portal areas, portal to central veins, or central vein to central vein. HBsAg is localized to the cytoplasm and the plasma membrane, whereas HBcAg is predominantly located in the nuclei. These antigens are detected by immunohystochemical and electron-microscopic studies.

HCV antigens are found in the cytoplasm. On an organ level, the liver is usually enlarged, tender, and jaundiced. Other systems may be affected during an event of acute hepatitis. Arthralgia and arthritis occur when the joints are involved. Confusion, decreased level of consciousness, and memory loss are evident with hepatic encephalopathy. Hematuria and proteinuria indicate kidney damage. A potentially fatal complication of viral hepatitis is fulminant hepatitis. Massive liver necrosis occurs in a relatively short amount of time, and is rarely associated with hepatitis C.

Clinical manifestations of hepatitis can vary from flu-like symptoms to fatal liver failure and depends on the vitality of the immune system and on various virus-host factors. It typically progresses in several phases. The first phase occurs after a prodromal period that depends on the infective agent and for hepatitis C it is from 15 – 160 days. The prodromal phase, which is the onset of disease, begins suddenly with anorexia, malaise, nausea, vomiting, urticarial eruption, arthralgia, myalgia, photophobia, pharyngitis, cough, low grade fever, and coryza.

Clay-colored stools, dark urine, and weight loss may be noted before the onset of the icteric phase. Clinical jaundice is present and prodromal symptoms usually subside. Right upper quadrant pain is associated with enlargement of the liver and stretching of the visceral peritoneum. Cholestatic symptoms are due to extrahepatic biliary obstruction. Splenomegaly and cervical adenopathy may be present during this phase. The recovery phase or post-icteric phase ranges from two to 12 weeks. It may be longer with hepatitis C.

While symptoms may diminish during the recovery phase, liver enlargement and abnormal liver function tests will still be evident. Full clinical and biochemical recovery can take up to three months with hepatitis C infection. Some infected patients never develop clinical jaundice. “Globally, an estimated 180 million people are infected with the hepatitis C virus” (Merck Pharmaceuticals, 2011). Hepatitis C has a variety of different risk factors associated with it and health care workers are certainly within one of the top risk groups.

When assessing a patient, it is prudent to assess for all of the probable risk factors to determine if testing is appropriate. If a patient has engaged in any risky behaviors, such as illicit drug use, tattoos, body piercings, or has a history of multiple sex partners (more than 10 in a lifetime), it follows that they should be tested for the virus. Other risk factors outside of behaviors should also be considered. If a patient has a history of long-term hemodialysis therapy, receiving a blood transfusion prior to 1992, or receiving clotting factor concentrates prior to 1987, they may also be at risk (Mayo Clinic. om, 2011). Because hepatitis C is a blood borne pathogen, all forms of blood to blood transmission should be considered. Approximately one in 20 babies born to hepatitis positive mothers are afflicted with the disease as well (Pub Med Health. com, 2010). When considering all of the risk factors, there is a clear and observable correlation with hepatitis C risk and that of other patient populations. Because HIV transmission shares all the same risk factors, this entire patient population should also be considered an “at risk” group. The same must be considered for another group as well.

One in 10 of the nation’s Veterans are infected with the hepatitis C virus, which is five times greater than the 1. 8% infection rate of the general American population. A study that was performed in 1999 by the Veterans Health Administration (VHA) concluded that one in 10 of all Veterans in the system tested positive for the virus with 62. 7% noted to be from the Vietnam era. The reasons thought to have contributed to these heightened numbers among Vietnam Vets, was due to the promiscuous nature of their sexual activity with the locals in an area endemic for the virus.

Many of the Veterans received tattoos during their service from dirty tattoo needles and illicit drug use was prevalent as well. There was also potential for infection from the jet “air gun” injections used to inoculate the men before deployment. Within the VHA, simply the status of “Vietnam era service” is considered adequate justification for hepatitis testing (HCVets, 2010). After assessment of the aforementioned risk factors, the physician may determine testing is necessary. A medical provider may order liver function tests to check for liver damage.

These tests can be performed by collecting a small blood sample; if it comes back with elevated results the physician may order a hepatitis C antibody test. There are two antibody tests to choose from, the HCV EIA and the HCV RIBA (Franciscus, 2006). These tests will identify antibodies made when the patient was first exposed. Once someone is exposed to hepatitis C, they will carry the HCV antibody with them for life (Franciscus, 2006). If the patient should possess antibodies in their blood, then the HCV RNA viral load test is ordered.

These tests will confirm whether or not the patient is currently infected with the hepatitis C virus, and whether or not treatment will be effective. The two types of viral load tests are qualitative and quantitative. Qualitative informs physicians of the virus’ presence and quantitative explains the amount of the virus present in the blood. Viral load results can be low, less than 800,000 IU/mL or high, greater than 800,000 IU/mL (Franciscus, 2006). If the test results are elevated and hepatitis C is confirmed, genotype testing may be the next step, as this test will determine which treatment is the most beneficial.

A liver biopsy is also helpful in establishing to what extent the liver has been damaged and if scar tissue is present (WebMD, 2009). Health promotion strategies must begin with patient education. The public must be made aware that vaccines are available for hepatitis A and hepatitis B and that there is currently no vaccine to protect against hepatitis C. To avoid spreading hepatitis C, infected persons should not share personal hygiene items like toothbrushes, razors, or nail grooming supplies. It is also highly recommended that they use a condom while having intercourse (Arizona Department of Health Services, 2011).

Other prevention strategies carriers should take would be to keep all cuts and open sores covered, avoid reusing needles, and avoid donating blood, plasma, tissues, and other organs (Arizona Department of Health Services, 2011). If not infected, practice safe sex and when receiving a piercing or tattoo, be sure the facility uses sterile equipment, and practices good hygiene techniques. Healthcare workers should always practice universal precautions with every patient because everyone is a potential carrier of hepatitis C and other blood borne diseases.

Many resources are available to the public that serve as a venue for information on all forms of hepatitis. Online websites are accessible to all ages and diverse societal groups. First, www. helppreventhepatitis. com is a site packed with information about the disease and also focuses on ways of prevention. Second, www. kidshealth. org relates to adolescents through age-appropriate education and advice on developing healthy habits and making good choices. Last, www. cdc. gov/hepatitis is the gold standard for informing the public on updated information on hepatitis, trends, treatments, and revention. As discussed within these websites and throughout this paper, hepatitis infection can be a devastating health event. However with prevention of the many risk factors, it can be avoided and if infected, in many instances it is quite treatable. References Arizona Department of Health Services. (2011, March). Hepatitis C Basics. Retrieved from http://www. azdhs. gov/phs/oids/hepc/hecq. htm Dooley, D. P. (2005). History of U. S. Military contributions to the Study of Viral Hepatitis. Military Medicine, 170(4), 71-76. Franciscus, A. (2006, February). Hepatitis C Diagnostic Tests.

Retrieved from http://hcvadvocate. org/hepatitis/factsheets_pdf/diagnostic_FS. pdf HCVets. com. (2010, April). Welcome page. Retrieved from http://www. hcvets. com/ Kasper, D. , & Fauci, A. , & Longo, D. , & Braunvald, E. , & Hauser, S. , & Jameson, J. (Eds) (2005) Harrison’s Principles of Internal Medicine (16th ed. ). The McGraw-Hill Companies, Inc. Mayo Clinic. com. (2011). Hepatitis C Risk Factors. Retrieved from http://www. mayoclinic. com/health/hepatitis-c/DS00097/DSECTION=risk-factors Merck Pharmaceuticals. (2011). Chronic Hepatitis Continuing to Pursue Answers for a Growing Epidemic.

Retrieved from http://www. allabouthepc. com/hepc/allabouthepc/hcp/article-1. jsp Pub Med Health. com. (2010, November). Hepatitis C. Retrieved from http://www. ncbi. nlm. nih. gov/pubmedhealth/PMH0001329/ Schmid, R. (2001). History of viral hepatitis: A tale of dogmas and misinterpretations. Journal of Gastroenterology and Hepatology, 1(16), 718-722. Smeltzer, S. C. , & Bare, B. (2004). Medical Surgical Nursing (10th ed. ). Philadelphia, PA: Lippincott William & Wilkins. WebMD. (2009, July). Hepatitis C Guide. Retrieved from http://www. webmd. com/hepatitis/hepc-guide/hepatitis-c-exams-and-tests