Accumulation of the bilirubin in the bloodstream causes yellow pigmentation of the plasma, leading to the discoloration of the heavily perfused tissues. Serum bilirubin level accumulates when its production from heme exceeds its metabolism and excretion. Imbalance between production and clearance may result either from the excess release of bilirubin precursors into the bloodstream or from physiologic processes that impair the hepatic uptake, metabolism or excretion of this metabolite.
Clinically, hyperbilirubinemia appears as jaundice or icterus, yellow pigmentation of the skin and sclera. Jaundice can usually be detected when the serum bilirubin level excels 34 to 43 μmol/L (2.0 to 2.5 mg/dL); meanwhile the normal serum bilirubin concentrations range from 5 to 17μmol/L (0.3 to 1.0 mg/dL). A similar sign of hyperbilirubinemia is darkened urine, which results from renal excretion of bilirubin in the form of bilirubin glucutonide. Bilirubin is present in body fluids (cerebrospinal fluid, joint effusions, ascites, pleural effusion and cysts, etc.) in proportion to their albumin content and is absent from true secretions such as tears, saliva, and pancreatic juice.
In most cases, hyperbilirubinemia itself has little pathophysiologic effect. Unlike circulating bile salts, whose levels are same elevated in cholestasis and biliary obstruction, bilirubin does not become deposited in cutaneous tissues and does not produce pruritus. In conditions such as neonatal jaundice or type I or II Crigler-Najjar syndrome, extremely high concentrations (>340μmol/L or >20 m4g/dL) of unconjugated bilirubin can accumulate, and the resulting diffusion of bilirubin into the central nervous system can cause encephalopathy (Kernicterus) and permanent impairment of nervous system.
The risk of kernicterus is increased by conditions that favors elevated circulating levels of unbound, unconjugated bilirubin, such as hemolysis, hypoalbuminemia, acidosis and increased levels of compounds that compete for albumin being such as free fatty acids and drugs. Exposure to blue light causes conformational changes in unconjugated bilirubin, rendering it more polar and water soluble. These ‘‘photoisomers’’ are taken up and excreted by the liver and kidney, without need for normal conjugation. Intense treatment with blue light can provide sufficient isomerization of unconjugated bilirubin circulating through the skin to reduce the risk of kernicterus in patients with neonatal jaundice.
The urine normally contains no detectable bilirubin by usual clinical assays, although traces may be detectable by sensitive spectrophotometric procedures. The presence of bilirubin in the urine is evidence of conjugated hyperbilirubinemia and can be a useful differentiating point early in the evaluation of bile. Qualitative determination of the bilirubin in urine may be accomplished by specific reaction with Ictotest tablets or dipstick. The foam test also is a simple, valid, qualitative test.
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