Hepatitis C, Jaundice, Current Information On Hepatitis C & treatments for the medical professional and patient. | Hepatitis Central

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A yellowing of the skin, sclerae, and other tissues due to excess circulating bilirubin. Mild jaundice, best seen by examining the sclerae in natural light, is usually detectable when serum bilirubin reaches 2 to 2.5 mg/dL.


The differential diagnosis of jaundice involves asking specific questions to narrow the possibilities. The first question should be whether the jaundice is due to hemolysis or an isolated disorder of bilirubin metabolism (uncommon), hepatocellular dysfunction (common), or biliary obstruction (intermediate). If hepatobiliary disease is present, other important questions follow: Is the condition acute or chronic? Is it due to primary liver disease or to a systemic disorder involving the liver? Are viral infection, alcohol, or other drugs responsible? Is cholestasis of intra- or extrahepatic origin? Will surgical therapy be needed? Are complications present? These questions are approached by clinical, functional, and morphologic assessment. Diagnostic errors usually result from an inadequate history and physical examination with undue reliance on laboratory data.


Mild hyperbilirubinemia with normal transaminase and alkaline phosphatase levels usually reflects hemolysis or Gilbert’s syndrome rather than liver disease; bilirubin fractionation usually settles the issue. By contrast, the depth of jaundice and the fractionation of bilirubin do not help to differentiate hepatocellular from cholestatic jaundice. Striking transaminase elevations (> 500 u.) suggest a hepatitis or an acute hypoxic episode, and disproportionate increases of alkaline phosphatase a cholestatic or infiltrative disorder. In the latter, bilirubin is typically normal or only slightly increased. Bilirubin levels > 25 to 30 mg/dL are usually due to renal dysfunction and/or hemolysis superimposed on severe hepatobiliary disease, as the latter alone rarely causes such deep jaundice. Low albumin and high globulin levels indicate chronic rather than acute liver disease. Improvement of an elevated prothrombin time after giving vitamin K (5 to 10 mg IM for 2 to 3 days) favors a cholestatic over a hepatocellular process, but this has limited diagnostic value since patients with hepatocellular disease may also improve when given vitamin K.

Radiologic procedures are of greatest value in the diagnosis of infiltrative and cholestatic disorders. Abdominal ultrasound (US) and CT scans often detect metastatic and other focal liver lesions and have largely replaced radionuclide scans for this purpose. MRI, also valuable, is confined to a few centers. These procedures are less helpful in diffuse hepatocellular disorders (eg, cirrhosis), since findings are usually nonspecific. The crucial role of radiology to investigate cholestatic jaundice is discussed below.


Percutaneous liver biopsy has great diagnostic value but is not usually required in jaundice. Peritoneoscopy (laparoscopy) permits direct inspection of the liver and gallbladder without the trauma of a full laparotomy and is useful in selected patients. Rarely, diagnostic laparotomy may be needed in some patients with cholestatic jaundice or unexplained hepatosplenomegaly.


The Merck Manual