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Key Clinical Questions

  • image What causes jaundice?

  • image How are biliary obstruction and cholangitis diagnosed?

  • image What are the best imaging modalities?

  • image What treatment strategies should be employed in patients with biliary obstruction or cholangitis?

  • image When should procedure or surgical intervention be considered in patients with cholangitis?

This chapter describes clinical conditions manifested as a result of acute or subacute biliary disease. Particular attention is paid to those conditions that frequently present to the inpatient setting, including jaundice, obstruction, and acute cholangitis.


Jaundice, from the French jaune, refers to the yellowish discoloration of the skin, sclera, and mucus membranes that reflects deposition of bilirubin in tissues. While jaundice is often used interchangeably with hyperbilirubinemia, this discoloration is only apparent when the serum bilirubin level exceeds at least two times the upper limit of normal (0.5-1.0 mg/dL), or over 2 mg/dL. Jaundice is typically recognized earliest in the oral mucus membranes (under the tongue and hard palate) and in the sclera, the latter of which has a high elastin content and a strong binding affinity for bilirubin.


Jaundice results from a pathologic process that interferes with the normal metabolism and excretion of bilirubin (Figure 158-1). ­Physiologically, bilirubin is the product of hemoglobin breakdown formed during the elimination of senescent red blood cells. Macrophages, a component of the reticuloendothelial system, separate hemoglobin molecules into proteins (globulin) and heme. Splitting of the four pyrrole ring of heme produces biliverdin, which is then reduced to bilirubin. This type of bilirubin is unconjugated, and insoluble in water. As a result, it must be attached to albumin for transport to the liver for excretion.

Figure 158-1

Cycling of bilirubin and its products through the liver, intestines, portal and systemic circulations, and kidneys. (B, bilirubin; G, glucuronide; UroB, urobilinogen).

Once in the liver, the bilirubin is rendered more water soluble by conjugation to glucuronic acid. Conjugated bilirubin is excreted into bile and subsequently enters the small intestine and colon. Exposure to oxidizing enzymes in the gut leads to the greenish color of bile. A portion of the bilirubin is deconjugated and reabsorbed into the circulation. The remaining segment is broken down by bacteria into urobilinogen, a fraction of which is converted into stercobilinogen and excreted in the stool, and the rest of which is excreted in the urine. Obstruction of the biliary system can hinder excretion of bilirubin into the gut and simultaneously exceed the processing ability of the kidneys, leading to pale stools and dark urine.

The amount of bilirubin in the serum is determined through measurement of light absorbance of the specimen following chemical treatment. Prior to examination, these specimens must be shielded from light to prevent excessive breakdown and falsely low results. The quantification ...

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