Pediatric emergency medicine trisk 0885 0885
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excreted in feces, while 10% is reabsorbed into the liver via enterohepatic
circulation.
Newborn infants inherently possess multiple factors which contribute to the
development of physiologic hyperbilirubinemia: increased red blood cell (RBC)
volume, decreased RBC life span, immature hepatic uptake and conjugation, and
increased enterohepatic circulation. Hyperbilirubinemia is considered pathologic
when it is present in the first day of life, when the level exceeds the age-specific
95th percentile or has a concerning rate of rise (greater than 0.2 mg/dL/hr), when
the conjugated fraction is high, or in the presence of concerning physical
examination or laboratory findings.
DIFFERENTIAL DIAGNOSIS
The causes of unconjugated hyperbilirubinemia may be classified into three
groups, based on mechanism of accumulation: excess bilirubin production,
decreased bilirubin conjugation, impaired bilirubin excretion ( Table 45.1 ).
Excess Bilirubin Production
The numerous causes of hemolysis may be categorized as intravascular or
extravascular. Intravascular hemolysis may be further divided into intrinsic and
extrinsic RBC defects. Inherited RBC enzyme deficiencies include glucose-6phosphate dehydrogenase (G6PD) deficiency and pyruvate kinase deficiency.
G6PD is common in children of African, Asian, and Mediterranean descent;
patients with this disorder who are exposed to oxidant stress (e.g., fava beans,
sulfa drugs) may present with acute rapid hemolysis (see Chapter 93 Hematologic
Emergencies ). Children with hemoglobinopathies, such as sickle cell disease and
thalassemias, are prone to hemolysis. Congenital defects in the RBC membrane
found in hereditary spherocytosis and hereditary elliptocytosis increase the
fragility of the corpuscles, which predisposes patients to hemolytic episodes.
Maternal–fetal blood group incompatibility is critical to recognize early. When
maternal antibodies are produced against fetal RBC antigens, the neonate can
develop a Coombs positive isoimmune hemolytic anemia. ABO incompatibility
generally occurs in infants with A or B blood groups whose mothers have type O
blood group; maternal anti-A and anti-B antibodies are produced and can result in
hemolysis with a positive direct Coombs test. Rh-negative mothers may become
sensitized to an Rh-positive fetus during pregnancy and mount an antibody
response during a subsequent pregnancy leading to Rh disease of the newborn.
Administration of Rho (D) immune globulin (RhoGAM) to Rh-negative mothers
who have not yet developed anti-Rh antibodies can prevent Rh isoimmunization.
Infections such as sepsis, urinary tract infection (UTI), and malaria are also
