Approach To Jaundice History and Examination

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The most important information in the diagnostic evaluation usually comes from the history. In patients presenting with jaundice, the history should be thorough and should include questions focused on identifying the common causes of jaundice. Specific information should include when the jaundice commenced and whether it is of acute or gradual onset. The presence of gastrointestinal symptoms, such as abdominal pain, nausea, vomiting, diarrhea, or changes in stool color can be significant. Itching is common in jaundice and this symptom may. in fact, precede the onset of the yellow color.

Associated symptoms, such as unintended weight loss or the development of adenopathy may lead to the consideration of certain diagnoses, including malignancies. Bruising or bleeding disorders may suggest severe hepatic dysfunction that is interfering with the production of clotting factors. Increasing abdominal girth may be caused by ascites and peripheral edema by obstruction of venous return from the lower extremities or hypoalbuminemia.

A complete review of the past medical history is necessary. Any medications, whether prescription, nonprescription, or herbal supplements, should be reviewed. Acetaminophen is a widely used over-the-counter agent that, in toxic amounts, can cause hepatocellular damage. Numerous herbal agents have been associated with liver damage as well.

The social history is of critical importance in a patient with jaundice. The abuse of alcohol is the most common cause of cirrhosis. IV drug use or unsafe sexual practices can lead to infection with hepatitis B or C. Hepatitis is also associated with getting tattoos if unsterili/.ed equipment is used. Travel history, especially the location and timing of any international travel, can lead to the consideration of hepatitis A.

A comprehensive physical examination is also important in the work-up of someone with jaundice. Along with a general physical examination, certain areas should be emphasized. Jaundice may first be noticed as a yellowing of the sclera, especially in persons with darker skin types. Yellow discoloration can also commonly be seen under the tongue.

Examination of the skin should document the jaundice and also look for clues to its cause. The stigmata of alcohol abuse (e.g.. caput medusa, spider veins)

or IV drug use (needle track marks) should be noted. Large hematomas, by themselves, could be a cause of jaundice as the blood resorbs. Signs of bruising or bleeding should also be documented.

Abdominal examination must include, among other things, evaluation of the general contour of the abdomen, the presence of any ascites, the presence of organomegaly, and any tenderness. Hepatomegaly may or may not occur as a part of liver disease. Right upper quadrant tenderness can be associated with acute hepatitis but also with gallstone disease. Splenomegaly could suggest portal hypertension from cirrhosis or could be caused by malignancy.

Laboratory Testing

The most important initial laboratory evaluation of jaundice is the bilirubin level, which is usually reported as both a total bilirubin and direct bilirubin. The reported direct bilirubin is a measurement of the conjugated bilirubin level. Unconjugated bilirubin can be determined by subtracting the directed bilirubin from the total bilirubin.

The relative relationship of conjugated and unconjugated bilirubin in a jaundiced person can be indirectly evaluated by performing a urinalysis. Conjugated bilirubin is excreted in the urine, whereas unconjugated bilirubin is not. A urinalysis on a jaundice patient who has a high level of bilirubin suggests that the patient has a conjugated hyperbilirubinemia: absence of bilirubin on the urinalysis suggests that it is an unconjugated hyperbilirubinemia.

Unconjugated Hyperbilirubinemia

A mild unconjugated hyperbilirubinemia, usually identified as an incidental finding when liver enzymes are tested for some other reason, is often caused by Gilbert syndrome. Gilbert syndrome is a congenital reduction of conjugation of bilirubin in the liver. It occurs in approximately 5% of the population and is of no health significance. Occasionally, the bilirubin level will increase during times of illness and then recover to its baseline, slightly elevated level, after the illness resolves. In a patient with mildly elevated unconjugated biliru-binemia. otherwise normal liver enzymes and complete blood count (CBC), and who is otherwise well, no further work-up is indicated.

Hemolysis can cause an unconjugated hyperbilirubinemia in proportion to the amount of hemolysis that occurs. It is most often diagnosed by identification of anemia along with the presence of red cell fragments or abnormalities (spherocytosis, thalassemias. Sickle cell disease). The management is to treat the cause of the hemolysis.

Conjugated Hyperbilirubinemia

Hepatitis A is a viral infection of the liver primarily transmitted via fecal-oral contamination. Contaminated food and water are the primary sources of infection. although risks also include drug use (both injection and noninjection)

and male-male sexual contact. Hepatitis A infection is widespread in Africa. Asia, and Central and South America. Travelers to these areas are at risk for infection.

Hepatitis A causes a self-limited illness characterized by jaundice, fever, malaise, and abdominal discomfort. The incubation period is 2-8 weeks, with an average of 4 weeks. While the symptoms can be mild, even asymptomatic in younger patients, there is an approximately 2% fatality rate in those older than age 50 years. The illness tends to last for 4-6 weeks, although some people have an illness that will last up to 6 months. There is no specific treatment for hepatitis A. Supportive care and symptomatic treatments are indicated.

Hepatitis A is diagnosed based on the presence of a conjugated hyperbilirubinemia, elevated hepatic transaminases, and serology. An acute infection causes an elevation of antihepatitis A virus (HAV) IgM. An elevated anti-HAV IgG but negative IgM indicates a history of a previous hepatitis A infection but not acute illness.

Hepatitis A vaccination is available and recommended for those at high risk, including travelers to endemic areas, persons with chronic liver disease, men who have sex with men or children who live in areas with high rates of the illness. Household or sexual contacts of persons infected with hepatitis A can be offered prophylaxis with injections of immunoglobulin.

Hepatitis B virus infection is transmitted via contact with contaminated blood or body fluids. Sexual contact and needle sharing are common mechanisms of infection. Hepatitis B may also be vertically transmitted from mother to baby. The incubation period from exposure to clinical symptoms is 6 weeks to 6 months. Only 50% of infections with hepatitis B are symptomatic. Approximately 1% of infections result in hepatic failure and death. Along with the acute symptoms, which are similar to hepatitis A, hepatitis B can cause a chronic infection. Chronic hepatitis B is highly related to the age of the patient—90% of infected infants and 60% of children younger than age 5 years develop chronic hepatitis B, which can lead to cirrhosis and hepatocellular carcinoma.

Serologic studies, using several markers, are necessary to determine the presence and type of hepatitis B infection that is present. Hepatitis B surface antigen (HBsAg) is present in both acute and chronic infections. Its presence is associated with contagiousness to others. Patients with the e antigen (HBeAg) are 100 limes more infectious than those lacking the HBeAg. Antibody to the surface antigen (anti-HBs) is seen in resolved infections and is the serologic marker produced after hepatitis B vaccination. An IgM antibody to the hepatitis B core antigen (anti-HBcAg IgM) is diagnostic of an acute infection. A measurable level of HBsAg with a negative anti-HBcAg IgM is diagnostic of chronic hepatitis B. Figures 46-1 and 46-2 show the serologic studies associated with acute hepatitis B infection and chronic hepatitis B infection.

Acute hepatitis B infection is treated supportively. Persons with chronic hepatitis B may be candidates for antiviral therapy. They should be referred to

Acute hepatitis B with recovery

Acute hepatitis B with recovery

Hep Igg And Igm

Weeks after exposure

Figure 46-1. Acute hepatitis B with recovery. {Reproduced with permission from Briscoe. DB. Lange Q&A: USMLE Step 3. 4th ed. New York: McGraw-Hill. 2005:48. )

a specialist both to evaluate the appropriateness of therapy and to monitor for the development of hepatocellular carcinoma or cirrhosis.

Hepatitis B vaccination is universally recommended for children. Vaccination is also recommended for adults at high risk of disease, including healthcare and public safety workers, IV drug users, persons with chronic liver disease, and dialysis patients.

Chronic hepatitis B infection

Chronic hepatitis B infection

Physical Exam Hepatitis

Weeks after exposure

Figure 46-2. Chronic hepatitis B infection. (Reproduced with permission from Briscoe. DB. Lange Q&A: USMLE Step 3. 4tlt ed. New York: McGraw-Hill. 2005:48.)

Hepatitis C, formerly known as non-A. non-B hepatilis, is the most common cause of chronic liver disease in the United States, with more than 4 million infected persons. Transmission occurs via exposure to infected blood or body fluids via sexual contact, needle sharing, or accidental exposure of healthcare workers, and by vertical transmission. Blood or blood-product transfusion was a common source of exposure prior to 1992.

The virus can be detected in the blood within 1-3 weeks of exposure, with liver cell injury detectable in 4—12 weeks. Most infections are asymptomatic, but hepatitis C can cause an acute illness with jaundice, malaise, and anorexia. Of those infected with hepatitis C, 60-85% will develop a chronic infection, with measurable levels of hepatitis C virus RNA (HCV RNA) for more than 6 months.

Chronic hepatitis C can lead to cirrhosis and hepatocellular carcinoma. Disease activity can be monitored by serial measurements of HCV RNA along with transaminases levels. Chronic hepatitis C can be treated with antiviral therapy, using ribavirin and/or interferon, but results are variable and there is no cure. There is currently no vaccination available for hepatitis C.

Alcohol abuse can cause an acute, severe hepatitis, or chronic fatty liver, hepatitis, and cirrhosis. Alcohol leads to a conjugated hyperbilirubinemia by impairing bile acid secretion and uptake. Transaminase levels from alcohol abuse typically show the aspartate aminotransferase (AST) being elevated out of proportion to the alanine aminotransferase (ALT); viral hepatitis usually causes greater elevations of the ALT (see Case 41 for a more thorough discussion of alcohol abuse).

Physical obstructions of bile drainage can also cause conjugated hyperbilirubinemia. Common etiologies include gallstones that become impacted in the bile ducts, postoperative biliary strictures or extrinsic compression of the bile ducts by tumors, such as pancreatic cancer. Imaging of the bile system with ultrasound, computed tomography (CT) scan, or magnetic resonance imaging (MR1) is usually diagnostic. Endoscopic retrograde cholangiopancreatography (ERCP) can be diagnostic and, in some cases, therapeutic.

Comprehension Questions

|46.1] A 32-year-old male with no significant medical history comes in for evaluation of an elevated bilirubin level that was detected on blood work required for a preemploymcnt physical. The bilirubin level was 1.5 mg/dL (normal up to 1.0 mg/dL) with an elevated unconjugated component. He feels fine, takes no medications, occasionally drinks a beer, and is married and monogamous. His liver enzymes, chemistries, and complete blood count (CBC) are normal. What is the next step in his evaluation?

A. Reassurance

B. Counsel on alcohol reduction

C. Abdominal ultrasound

D. Hepatitis serologies

|46.2] Six months after diagnosis with an acute infection with hepatitis B. a patient has the following serologic studies: HBsAg negative; anti-HBsAg positive; HBeAg negative; anti-HBcAg positive. What is your interpretation of these results?

A. Chronic active hepatitis B

B. Resolved acute infection

C. Resolved acute infection but contagious to sexual contacts

D. Resolved infection but at risk for reinfection in the future

[46.3] Which of the following is most likely to cause an unconjugated hyperbilirubinemia?

A. Hepatitis A

B. Gallstone in the common bile duct

C. Chronic alcohol use

D. Spherocytosis

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