The initial laboratory evaluation of the jaundiced patient should include determinations of the serum bilirubin level (both total and the direct-reacting fraction), the serum liver aminotransferase levels, and the serum alkaline phosphatase level; urinalysis for bilirubin and urobilinogen; a complete blood count; and any other pertinent tests suggested by the physical examination and history (e.g., determinations of serum amylase or lipase levels, and prothrombin time). The serum bilirubin level is measured by the van den Bergh reaction using two techniques to measure both total bilirubin and conjugated bilirubin (the direct fraction). The indirect fraction can then be calculated by subtracting the direct fraction from the total.
If the patient has unconjugated hyperbilirubinemia, the bilirubin is usually only mildly elevated and consists predominately (more than 85 percent) of the indirect fraction. Since unconjugated bilirubin is tightly bound to albumin, it does not appear in the urine. Liver aminotransferase levels will be normal, and the blood count and smear may show evidence of anemia or hemolysis. A Coombs test and hemoglobin electrophoresis may be helpful if no history of hemolytic anemia or hemoglobinopathy is known. Gilbert's syndrome is the most common cause of mild unconjugated hyperbilirubinemia. This is an inherited deficiency in bilirubin conjugation that produces no symptoms other than variable elevations of bilirubin and no adverse effects. Factors that can cause bilirubin to rise include fever, heavy physical exertion, fasting, surgery, and heavy alcohol consumption.
A direct-reacting fraction of at least 30 percent (and usually much higher) is present with conjugated hyperbilirubinemia. Conjugated bilirubin is water soluble and appears in the urine at very low serum concentrations. Urobilinogen will be absent from the urine if significant cholestasis is present. If liver enzyme levels are normal, the jaundice is caused by sepsis or recent systemic infection, in-born errors of bilirubin metabolism (such as Rotor syndrome or Dubin-Johnson syndrome), or pregnancy rather than by primary hepatic disease. If liver enzyme levels are abnormal, which is much more common, the pattern of abnormality suggests the cause. Predominance of aminotransferase elevation is more suggestive of hepatocellular disease, such as viral or toxic hepatitis or cirrhosis, while marked elevations of alkaline phosphatase (two to three times normal) and g-glutamyl transpeptidase suggest intra- or extrahepatic obstruction, such as malignancy or gallstones.
Further laboratory testing and imaging studies should be undertaken next, directed by which type of jaundice is present. If the initial laboratory studies suggest hepatocellular disease and the clinical examination suggests viral hepatitis, then serologic studies for viral hepatitis should be done. If the clinical picture points to alcoholic liver disease or other toxins, then prothrombin time, platelet count, and serum albumin levels should be determined to help estimate the degree of liver injury. If results of the serologic studies are negative, there is no improvement with withdrawal of the suspected toxic agent, or there is no other obvious etiology, liver biopsy should be considered.2
If the clinical examination and initial laboratory findings suggest intrahepatic cholestasis or extrahepatic biliary obstruction, ultrasound studies should be performed to look for gallstones, dilated extrahepatic biliary ducts, or masses in the liver, pancreas, or portal area. Computed tomography can also be used but is usually more costly, involves radiation exposure, and is less sensitive than is ultrasound at detecting stones in the gallbladder.
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