57 Hepatitis

Overview/pathophysiology

Viral hepatitis may be caused by one of five viruses that are capable of infecting the liver: hepatitis A (HAV), B (HBV), C (HCV), D or delta (HDV), or E (HEV). A sixth virus, hepatitis G (HGV), has been isolated in a few cases of hepatitis caused by other viruses of the five common strains. It is not known what the role of HGV is in liver disease, nor are clinical manifestations, natural history, or pathogenesis known. Although symptomatology is similar among all the hepatitis viruses, immunologic and epidemiologic characteristics are different. When hepatocytes are damaged, necrosis and autolysis can occur, which in turn lead to abnormal liver functioning. Generally these changes are completely reversible after the acute phase. In some cases, however, massive necrosis can lead to acute liver failure and death.

Chronic hepatitis is inflammation of the liver for more than 6 months. Forms of chronic hepatitis are associated with infection from HBV, HCV, and HDV; viral infections such as cytomegalovirus (CMV); excessive alcohol consumption; inflammatory bowel disease; and autoimmunity (chronic active lupoid hepatitis).

Alcoholic hepatitis occurs as a result of tissue necrosis caused by alcohol abuse; it is nonviral and noninfectious. Generally it is a precursor to cirrhosis (see p. 403), but it may occur simultaneous with cirrhosis.

Jaundice is discoloration of body tissues from increased serum levels of bilirubin (total serum bilirubin more than 2.5 mg/dL). Jaundice may be seen in any patient with impaired hepatic function and occurs as bilirubin begins to be excreted through the skin. There is also an increased excretion of urobilinogen and bilirubin by the kidneys, resulting in darker, almost brownish, urine. Jaundice is classified as follows.

Prehepatic (hemolytic):

Caused by increased production of bilirubin following erythrocyte destruction. Prehepatic jaundice is implicated when the indirect (unconjugated) serum bilirubin is more than 0.8 mg/dL.

Hepatic (hepatocellular):

Caused by the dysfunction of the liver cells (hepatocytes), which reduces their ability to remove bilirubin from the blood and form it into bile. Hepatic jaundice is also implicated with indirect serum bilirubin and is associated with acute hepatitis.

Posthepatic (obstructive):

Caused by an obstruction of the flow of bile out of the liver and resulting in backed-up bile through the hepatocytes to the blood. Posthepatic jaundice is implicated when direct serum bilirubin is more than 0.3 mg/dL.

Health care setting

Primary care, with possible brief hospitalization resulting from complications

Assessment

Signs and symptoms:

Nausea, vomiting, malaise, anorexia, epigastric discomfort, aversion to smoking, muscle or joint aches, fatigue, irritability, pruritus, slight to moderate temperature increases, dark urine, clay-colored stools, and jaundice.

Acute hepatic failure:

Nausea, vomiting, and abdominal pain tend to be more severe. Jaundice is likely to appear earlier and deepen more rapidly. Mental status changes (possibly progressing to encephalopathy), coma, seizures, ascites, sharp rise in temperature, significant leukocytosis, coffee-ground emesis, gastrointestinal (GI) hemorrhage, purpura, shock, oliguria, and azotemia all may be present.

Physical assessment:

Presence of jaundice; palpation of lymph nodes and abdomen may reveal lymphadenopathy, hepatomegaly, and splenomegaly. Liver size usually is small with acute hepatic failure.

History of:

Clotting disorders, multiple blood transfusions, excessive alcohol ingestion, parenteral drug use, exposure to hepatotoxic chemicals or medications (including over-the-counter medications or herbal supplements), travel to developing countries.

Diagnostic tests

Immunoglobulins:

Chronic infection markers are present for HBV, HCV, and HDV. They are HBsAg, anti-HBc IgG for hepatitis B; anti-HCV (enzyme-linked immunosorbent assay) and HCV RNA quantitation for hepatitis C; and anti-HDV IgG for hepatitis D.

Serum enzymes:

Aspartate aminotransferase (AST) and alanine aminotransferase (ALT) are initially elevated and then drop. Gamma-glutamyl transpeptidase (GGT) is elevated early in liver disease and persists as long as cellular damage continues.

Other hematologic tests:

Total bilirubin may be elevated, and prothrombin time (PT) may be prolonged. Differential white blood cell (WBC) count reveals leukocytosis, monocytosis, and atypical lymphocytes.

Urine tests:

Reveal elevation of urobilinogen, mild proteinuria, and mild bilirubinuria.

Liver biopsy:

Although this procedure is performed to obtain a definitive diagnosis of hepatitis, clinically it is not always advisable because of the high risk of bleeding. When performed, a biopsy is obtained percutaneously or via laparoscopy to collect a specimen for histologic examination to confirm differential diagnosis.

Nursing diagnosis:

Fatigue

related to decreased metabolic energy production occurring with faulty absorption, metabolism, and storage of nutrients

Desired Outcome: By at least 24 hr before hospital discharge, patient relates decreasing fatigue and increasing energy.

ASSESSMENT/INTERVENTIONS	RATIONALES
Take a diet history to determine food preferences. Consult dietitian regarding increased intake of carbohydrates or other high-energy food sources within prescribed dietary limitations. Encourage significant other to bring in desirable foods if permitted. Monitor and record intake.	In general, dietary management consists of giving palatable meals as tolerated without overfeeding. If oral intake is substantially decreased, parenteral or enteral nutrition may be initiated. Sodium restrictions may be indicated in the presence of fluid retention. Protein is moderately restricted, or eliminated, depending on the degree of mental status changes (i.e., encephalopathy). If no mental status changes are noted, normal amounts of high biologic value protein are indicated to facilitate tissue healing, promote energy, and decrease fatigue. All alcoholic beverages are strictly forbidden. When appetite and food selection are poor, vitamins may be given to supplement dietary intake.
Encourage small, frequent feedings, and provide emotional support during meals.	Smaller and more frequent meals are usually better tolerated in patients who are fatigued, nauseated, and anorexic.
Provide rest periods of at least 90 min before and after activities and treatments.	Rest facilitates recovery after the body has experienced stress and may be indicated when symptoms are severe, with a gradual return to normal activity as symptoms subside.
Avoid activity immediately after meals.	Exercise after meals increases potential for nausea and vomiting, which could cause loss of nutrients and exacerbate fatigue.
Keep frequently used objects within easy reach.	This will help conserve patient’s energy.
Decrease environmental stimuli; provide back massage and relaxation tapes; and speak with patient in short, simple terms.	These measures promote rest and sleep.
Administer acid suppression therapy, antiemetics, antidiarrheal medications, and cathartics as prescribed.	These agents minimize gastric distress and promote absorption of nutrients, which will help provide energy and reverse feelings of fatigue.

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