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I. DEFINITION

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When the rate of bilirubin production exceeds the rate of elimination, the end result is an increase in the total serum bilirubin (TSB), a clinical condition called hyperbilirubinemia. The accumulation of bilirubin (yellow-orange pigment) in the skin, sclera, and mucosa is called jaundice.

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II. INCIDENCE

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Neonatal hyperbilirubinemia is a common problem. Approximately 60–70% of term and ∼80% of preterm infants develop jaundice in the first week of life. Incidence is higher in populations living at higher altitudes. Incidence also varies with ethnicity. It is lower in African Americans and higher in East Asians, Greeks, and Native Americans.

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III. PATHOPHYSIOLOGY

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  1. Physiologic jaundice. In newborns, a progressive elevation of serum unconjugated bilirubin is almost universal during the first week of life. Although most of these infants are healthy and will not need therapy, they need to be monitored closely because severe unconjugated hyperbilirubinemia can be potentially toxic to the neurons. Physiologic ranges of TSB remain controversial because levels are affected by several factors, such as gestational age, birthweight, disease state, degree of hydration, nutritional status, and ethnic background. Data from recent studies suggest that the upper limits of TSB levels (95th percentile) found in diverse populations of normal newborn infants may be as high as 17–18 mg/dL. Studies published for predominantly term breast-fed infants suggest that a typical peak for TSB is ∼8–9 mg/dL. Preterm infants have no established “physiologic” bilirubin guidelines.

    1. Exclusion criteria for diagnosis of physiologic jaundice

      1. Jaundice appearing within the first 24 hours of life.

      2. TSB level >95th percentile for age in hours based on a nomogram for hour-specific serum bilirubin concentration (Figure 100–1).

      3. Bilirubin level increasing at a rate >0.2 mg/dL/h or >5 mg/dL/d.

      4. Direct serum bilirubin level >1.5–2.0 mg/dL or >20% of the TSB.

      5. Jaundice persisting for >2 weeks in full-term infants.

    2. Pathophysiologic mechanisms that predispose newborn infants to hyperbilirubinemia

      1. Increased bilirubin synthesis. Increased synthesis due to larger red blood cell (RBC) mass, increased hemoglobin breakdown up to 2–3 times the adult rate (due to shorter life span of neonatal RBCs), and increased rate of RBC degradation in the bone marrow before release to the circulation.

      2. Decreased binding and transport. Decreased hepatic uptake of bilirubin from plasma due to decreased plasma albumin and liver transfer protein, ligandin.

      3. Impaired conjugation and excretion. Relatively reduced transferase (uridine diphosphate glucuronyl transferase [UDPGT]) activity in the newborn liver resulting in decreased mono- and diglucuronide bilirubin conjugates that can be excreted in the bile.

      4. Enhanced enterohepatic circulation. Conjugated bilirubin is unstable and can be hydrolyzed by the intestinal enzyme β-glucuronidase to its unconjugated form. Once hydrolyzed and unconjugated, bilirubin is readily absorbed through the intestinal mucosa. Sterility of intestinal mucosa prevents further formation of the more excretable products, urobilin and stercobilin.

  2. Breast-feeding and jaundice. Most studies indicate that breast-feeding is a significant risk factor for hyperbilirubinemia. Jaundice associated with breast-feeding is divided into 2 types based on ...

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