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Rudolph's Pediatrics, 22e

Chapter 48. Infant of a Diabetic Mother

Hyperbilirubinemia and Polycythemia

Hyperbilirubinemia occurs more frequently in the IDM than in the general population. The pathogenesis remains uncertain because red blood cell life
span, osmotic fragility, and deformability are not different between the 2 groups. Some research points to increased hemoglobin turnover.21
However, other information points to delayed clearance of bilirubin by the liver.22 Other risk factors for hyperbilirubinemia are macrosomia, which
increases the risk for birth trauma, bruising and cephalohematoma, and polycythemia. Because of an increased hemoglobin load, bilirubin levels rise
more rapidly and peak later in IDMs than in neonates of nondiabetic women.

Chronic fetal hyperglycemia and hyperinsulinemia increase the fetal metabolic rate and increase oxygen consumption. Given that the fetus develops in
a relatively hypoxic environment and oxygen extraction from maternal blood is at a maximal rate, the fetus increases its oxygen­carrying capacity by
increasing erythropoiesis. Increased red cell production puts the infant at risk for polycythemia (hematocrit > 65). Up to 20% of IDMs have
polycythemia. The associated hyperviscosity and vascular sludging that can occur puts this group of infants at risk for stroke, seizures, necrotizing
enterocolitis, renal vein or sinus venous thrombosis, and persistent pulmonary hypertension of the newborn. Symptomatic polycythemic infants
should be treated with a partial exchange transfusion (see Chapter 53).

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