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  1. Distinguish laboratory tests that require specific interpretation or extra attention in children than adults.

  2. Recognize pediatric-specific situations which may affect lab results.

  3. Identify laboratory assays which have age-dependent reference intervals.

  4. Discuss the signs and symptoms of lead poisoning, as well as treatment options.

  5. Summarize the causes and associated testing of hyperbilirubinemia in infants.


There are numerous tests routinely ordered in pediatric practice which, while not exclusive to pediatrics, have special significance in young populations. Conversely, other tests, such as prostate specific antigen, which are commonplace in adult practice, are rarely used in pediatrics. This chapter will review the most common tests which are particularly important in pediatric medicine, and special considerations for evaluating laboratory results in this unique population.



Plasma bilirubin circulates primarily in two forms, the water-insoluble unconjugated bilirubin (Bu), which circulates non-covalently bound to albumin, and water-soluble conjugated bilirubin (Bc) in which bilirubin is covalently bound to one or two glucuronide molecules. Bc is sometimes referred to as direct bilirubin because in most common diazo-based methods, the form of bilirubin which reacts directly is mostly Bc. Bu was then referred to as “indirect” bilirubin and was the total bilirubin minus the direct. The term indirect bilirubin is no longer used. A third form of circulating bilirubin, delta bilirubin, is composed of conjugated bilirubin bound covalently to albumin and will not be discussed further here. Total serum bilirubin (TSB) is the sum of all forms of bilirubin in circulation. Bu is a by-product of the catabolism of the heme moiety in hemoglobin and is transported by albumin to the liver where glucuronosyl transferases conjugate glucuronide molecules to Bu, thereby converting it to Bc. Bc is then excreted through the bile duct into the gastrointestinal tract where it is further broken down by intestinal bacteria into urobilinogens and excreted.1

Following birth, there is a rise in oxygen tension in the newborn's circulation, resulting in a downregulation of erythropoietin.2 That, along with the relatively short lifespan of red cells containing fetal hemoglobin results in significant physiological hemolysis and decrease in hematocrit.3 The resulting release of hemoglobin and its breakdown leads to a physiological increase in Bu. The immature neonatal liver lacks sufficient glucuronosyl transferases to match the demand for bilirubin conjugation, thereby restricting conversion to Bc and excretion. Consequently, the newborn has a relatively high normal range for Bu and TSB. Generally, no additional intervention is required for this mild jaundice, termed “neonatal jaundice” (marked primarily by yellowing of the skin), which usually resolves within 3-4 weeks after birth. However, in some newborns, the bilirubin concentration can rise to dangerous concentrations in the first 24-72 hours of life. In these cases, medical intervention such as phototherapy or, much more rarely, exchange transfusion is required ...

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