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  • Jaundice is most often caused by decompensation of preexisting chronic liver disease, alcoholic hepatitis, and gallstone disease.

  • Careful history, physical examination, and routine laboratory tests lead to accurate diagnosis in 85% of patients with jaundice.

  • Cirrhosis can be diagnosed on the basis of two physical findings (asterixis, ascites) and two laboratory findings (decreased serum albumin [<2.8 g/dL], prolonged prothrombin time [INR >1.6]).

  • Dilated intrahepatic bile ducts indicate obstruction from extrahepatic causes (stone, structure, tumor).

  • Absence of dilated ducts in jaundiced patients with serum bilirubin >10 mg/dL suggests intrahepatic cholestasis.

  • Sepsis, drugs, sickle cell disease, and chronic hepatitis are the most common causes of intrahepatic cholestasis.


Jaundice refers to the yellowish discoloration of tissue resulting from the deposition of bilirubin in tissues; this indicates that the serum bilirubin is likely 3 mg/dL or higher. Jaundice most often is the result of acute or chronic liver disease, or biliary tract disease, and less commonly the result of hemolytic disorders. The differential diagnosis of jaundice has changed significantly in the past decade due largely to a sharp decline in the incidence of viral hepatitis types A and B as a result of immunization. The most common causes of jaundice in the adult population now are decompensation of preexisting chronic liver disease, alcoholic hepatitis, sepsis and abnormal hemodynamic conditions, and gallstone disease.


Jaundice can occur as a result of acute or chronic parenchymal liver disease, extrahepatic biliary tract obstruction (due to stone, stricture, or tumor), intrahepatic cholestasis (having several causes, as detailed in the following text), and hemolytic anemia. Serum bilirubin derives from the degradation of senescent red cells in the reticuloendothelial system. Each day a normal individual destroys 50 mL of red blood cells, which gives rise to 7.5 g of hemoglobin. Each gram of hemoglobin that is degraded results in production of 35 mg of bilirubin. Unconjugated bilirubin is liquid soluble, water insoluble, and hence circulates bound to albumin. The hepatic processing of bilirubin involves uptake of unconjugated bilirubin, conjugation with uridine diphosphate glucuronyl transferase, transfer to the bile canaliculus, and excretion into the intrahepatic biliary tree (Figure 38–1). Bilirubin is excreted in the bile primarily as bilirubin diglucuronide (80%), bilirubin monoglucuronide (20%), and unconjugated bilirubin (<1%). Any disease process that results in an increased load of unconjugated bilirubin presented to the liver, impaired conjugation, or impaired excretion of conjugated bilirubin, either intrahepatic or extrahepatic, can lead to accumulation of bilirubin in the blood, resulting in jaundice.

Figure 38–1.

Anatomy of the intrahepatic biliary system. (Reproduced, with permission, from Sherlock S, Dooley J. Diseases of the Liver and Biliary System. 10th ed. London, UK: Blackwell Science, 1997.) (See also Table 37–4 for causes of intrahepatic cholestasis.)



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