Chapter 33 Hepatitis and Cirrhosis
Clinical Case Problem 1: A 50-Year-Old Man with Ascites
Select the best answer to the following questions
1. Which of the following statements regarding this patient’s condition is false?
2. Which of the following statements regarding alcoholic hepatitis is false?
3. What is the most common cause of cirrhosis in the United States?
4. The ascites associated with cirrhosis generally should be treated by which of the following?
5. Clinical manifestations of cirrhosis include which of the following?
Clinical Case Problem 2: A Nauseated 25-Year-Old Schoolteacher with Icterus and Right Upper Quadrant Pain
8. What is the most likely diagnosis in this patient?
9. Which of the following tests is the most sensitive in confirming the diagnosis suspected in this patient?
10. Initial screening for hepatitis B should include which of the following?
11. Which of the following laboratory test results is (are) usually abnormal in a patient with acute viral hepatitis?
12. Indications for the use of hepatitis B vaccine include which of the following?
13. Which of the following types of viral hepatitis is (are) associated with the development of chronic active hepatitis?
14. Which of the following is (are) a complication(s) of alcoholic cirrhosis?
Clinical Case Management Problem
Describe the relationship between cirrhosis of the liver and right-sided heart failure.
Answers
1. c. This patient has alcoholic hepatitis with cirrhosis of the liver. Alcohol abuse is thought to be related to one in five hospitalizations in the United States. Many cases of cirrhosis of the liver are directly attributable to alcohol abuse, although infectious agents, particularly hepatitis C, are an emerging cause. Cirrhosis is an irreversible inflammatory disease that disrupts liver structure and function. Alcoholic hepatitis is seen in approximately 30% of heavy drinkers. Men with alcoholic hepatitis usually consume at least 70 g of alcohol daily and have done so an average of 10 years. In women, a lower threshold of 20 to 40 g for the same period is average for the development of hepatitis. Cirrhosis is the disorganization of hepatic tissues caused by diffuse fibrosis and nodular regeneration. Nodules of regenerated tissue form between fibrous bands, giving the liver a cobbled appearance.
Symptoms of early alcoholic liver disease include weakness, fatigue, and weight loss. In advanced disease, the patient develops anorexia, nausea and vomiting, swelling of the abdomen and the lower extremities, and central nervous system symptoms related to the cirrhotic liver disease. Other symptoms that may occur include loss of libido in both sexes, gynecomastia in men, and menstrual irregularities in women.
The liver of patients with alcoholic hepatitis and cirrhosis is usually enlarged, palpable, and firm. In advanced cirrhosis, the liver may actually shrink. Dermatologic manifestations include spider nevi, palmar erythema, telangiectases on exposed areas, and occasional evidence of vitamin deficiencies. Although jaundice is rarely an initial sign, it usually develops later. Other later developing signs include ascites, lower extremity edema, pleural effusion, purpuric lesions, asterixis, tremor, delirium, coma, fever, splenomegaly, and superficial venous dilation on the abdomen and thorax. There appears to be a genetic predisposition to the development of these complications. Of patients with advanced cirrhosis, 50% will be dead in a period of 2 years; 65% will be dead in 5 years. Hematemesis, jaundice, and ascites are unfavorable signs.
2. a. The first clinical stage of alcoholic liver disease is termed alcoholic hepatitis. Alcoholic hepatitis is a precursor of cirrhosis that is characterized by inflammation, degeneration, and necrosis of hepatocytes and infiltration of polymorphonuclear leukocytes and lymphocytes.
During the past 10 years in the United States, deaths from alcohol-related liver disease have increased. The incidence is greatest in middle-aged men, and mortality from cirrhosis is higher in blacks than in whites. Although alcoholic cirrhosis is a prevalent type of cirrhosis, only approximately 15% of alcoholics actually develop the disease. There appears to be a genetic predisposition to its development. The amount and duration of alcohol consumption are directly correlated with the extent of damage to the liver.
The symptoms of alcoholic hepatitis include anorexia, nausea, vomiting, weight loss, emesis, fever, and generalized abdominal pain. Hepatomegaly is found in 80% to 90% of these patients. Other signs include jaundice, ascites, splenomegaly, and spider angiomas.
Laboratory abnormalities in alcoholic hepatitis include hyperbilirubinemia and elevated serum transaminase. The ratio of serum AST to ALT is often 2:1 or greater. This can help differentiate alcoholic hepatitis from viral hepatitis. Other laboratory abnormalities include elevated alkaline phosphatase, hypoalbuminemia, and prolonged prothrombin time.
The prognosis of alcoholic hepatitis is variable; many patients develop only a mild illness. However, there is a 10% to 15% mortality rate from the acute event.
The treatment of alcoholic hepatitis involves cessation of alcohol consumption, increased calorie and protein intake, and vitamin supplementation (especially thiamine).
Alcoholic cirrhosis develops in approximately 50% of patients surviving alcoholic hepatitis. In the other 50%, various degrees of hepatic fibrosis develop.
3. c. The most common cause of cirrhosis in the United States is now hepatitis C, surpassing alcohol-induced cirrhosis. Hepatitis C virus (HCV) is also the most common cause of hepatocellular carcinoma. More than 4 million Americans are infected with HCV, and the yearly incidence is 35,000. Worldwide, an estimated 3% of the population is chronically infected. Patients with hepatitis C go on to develop chronic active hepatitis in more than 50% of cases and subsequent cirrhosis in approximately 20% to 40% of cases. HCV is also the leading cause of liver transplantation. Hepatitis A does not progress to chronic active hepatitis. Hepatitis B progresses to chronic active hepatitis and subsequently to cirrhosis in up to 10% to 15% of cases. Cytomegalovirus infection does not produce cirrhosis.
4. d. The treatment of ascites and the edema associated with ascites includes the following: (1) sodium restriction to 800 mg of Na+/day (or 2 g of NaCl); (2) spironolactone (Aldactone), 25 to 100 mg four times per day (effective in 40% to 75% of cases); (3) paracentesis; (4) combination diuretic therapy with furosemide in those patients who do not respond, with either spironolactone plus hydrochlorothiazide or spironolactone plus furosemide; and (5) paracentesis with albumin (or dextran) infusion in refractory cases. There must be complete abstention from alcohol. Fluid restriction is unnecessary unless serum sodium concentration is less than 120 to 125 mEq/L.
The 1-year survival rate of patients with cirrhosis with ascites is 50%, compared with 90% in patients with uncomplicated cirrhosis. Formation of ascites results from a combination of portal hypertension, hypoalbuminemia, lymphatic leakage, and sodium retention. The management of ascites in patients with cirrhosis is complicated. Diagnostic paracentesis should be performed in any patient with cirrhosis who undergoes clinical deterioration. Defined indications for the treatment of ascites include significant patient discomfort, respiratory compromise, large umbilical hernia, and recurrent bacterial peritonitis.
Sodium restriction is considered the cornerstone of therapy for ascites. Patients with cirrhosis require significant curtailment of sodium intake (800 mg/day) to obtain clinical benefit. Approximately 10% to 20% of patients who maintain a strict low-salt diet achieve complete resolution of ascites without additional therapy. However, hyponatremia may accompany sodium restriction, and severe hyponatremia (serum sodium concentration of less than 125 mEq) is a reason to begin fluid restriction as well. The majority of patients will also require diuretics.
Spironolactone (Aldactone), an aldosterone antagonist, is the first-line diuretic of choice in the treatment of cirrhotic ascites. It is effective in controlling up to 50% of patients with cirrhosis. Other potassium-sparing diuretics may be substituted for spironolactone, including triamterene and amiloride. The addition of loop diuretics (e.g., furosemide) is sometimes needed to achieve maximum benefit. Alternatives to furosemide include bumetanide and torsemide. Watch for hypokalemia with diuretics. Up to 90% of patients with cirrhosis and ascites will respond to diuretics and salt restriction. For those who do not, periodic paracentesis with albumin replacement is an alternative, as are portacaval shunts and transjugular intrahepatic portosystemic shunts, the latter for those requiring frequent large-volume paracentesis.
5. e. The clinical manifestations of cirrhosis were discussed previously. Another common finding in cirrhosis is hypoalbuminemia due to poor hepatic synthetic function.
6. c. Cirrhosis is an irreversible inflammatory condition of disordered and disrupted liver structure and function. Cirrhosis results from the disorganization of hepatic tissues caused by diffuse fibrosis and nodular regeneration. Micronodular and macronodular fibrosis occurs. Nodules of regenerated tissue form between the fibrous bands, giving the liver a cobbled appearance. The liver is initially larger than normal and then usually becomes smaller than normal in the later stages. The changes in the liver result in increased portal vein pressure, which leads to the formation of ascites and to esophageal varices.
7. e. In uncomplicated cirrhosis, treatment includes cessation of alcohol use, maintenance of proper nutrition, and use of beta blockers to reduce portal hypertension. Patients with uncomplicated cirrhosis may have a relatively benign course of illness for many years. Once the patient has an episode of decompensation, such as fluid retention, variceal bleeding, encephalopathy, spontaneous bacterial peritonitis, or hepatorenal syndrome, mortality is high without transplantation.
8. a. This patient most likely has hepatitis A. Hepatitis A occurs either spontaneously or in epidemics. Transmission is through the oral-fecal route. The presenting signs and symptoms of hepatitis A include (1) general malaise and fatigue; (2) general myalgias; (3) arthralgias; (4) abdominal pain; (5) nausea and vomiting; (6) severe anorexia, out of proportion to the degree of illness; and (7) aversion to smoking (if the patient smokes). Hepatitis B and hepatitis C are unlikely in this case because risk factors are absent. Although infectious mononucleosis may involve the liver and present with some of the same signs and symptoms, hepatitis A is much more likely, given the history of travel to an endemic area.
9. b. Acute infection with hepatitis A is confirmed by the demonstration of IgM antibodies to HAV (IgM anti-HAV). These antibodies persist for approximately 12 weeks after appearance. IgG antibodies to HAV follow and simply indicate exposure at some time in the past. HAV core antigen is incorrect because hepatitis A does not possess a recognizable core antigen; the tests using core antigen apply to hepatitis B only, and antibodies to HB core antigen have nothing to do with hepatitis A. Choice e, anti–hepatitis C virus, is incorrect because it does not give any information about hepatitis A infection.
10. d. There are so many antigens and antibodies associated with hepatitis virology that it is difficult to determine what is what. However, it can be simplified considerably. Initial screening for hepatitis B should include HBsAg and anti-HBc (HBcAb, the antibody to the core antigen). These two tests will identify most cases of acute hepatitis B. There is a period between the clearance of HBsAg and the appearance of anti-HBs (HBsAb) that lasts for 4 to 6 weeks. During this time, the only marker for hepatitis B that can detect the infection with any certainty is anti-HBc (HBcAb). If acute hepatitis B is suggested from the initial screening, further laboratory tests should be ordered. These include the following:
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