الفهرس 
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Abstract
Neonatal hyperbilirubinemia is a very common clinical problem encountered during the neonatal period. It occurs due to excessive formation of unconjugated (indirect) bilirubin and limited ability of the neonatal liver to rapidly clear it from the blood. Infants, especially preterms, have higher rates of bilirubin production than adults because they have red cells with a higher turnover and a shorter life span. Neonatal hyperbilirubinemia, by definition, is a rise in levels of total serum bilirubin greater than 5 mg/dL or 86 μmol/liter per day.
High serum bilirubin levels can be toxic, as bilirubin inhibits mitochondrial enzymes and can interfere with DNA synthesis, induce DNA-strand breakage, and inhibit protein synthesis and phosphorylation. Bilirubin has an affinity for membrane phospholipids and inhibits the uptake of tyrosine, a marker of synaptic transmission. It also inhibits the function of N-methyl-D-aspartate–receptor ion channels. This suggests that bilirubin can interfere with neuro-excitatory signals and impair nerve conduction (particularly in the auditory nerve). Bilirubin can inhibit ion exchange and water transport in renal cells, which may explain the neuronal swelling that occurs in the bilirubin encephalopathy associated with kernicterus.
Untreated severe hyperbilirubinemia is an important health problem, as it may cause acute bilirubin encephalopathy, kernicterus, cerebral palsy, behavioral and neurological impairment and mental retardation even in term newborns.
The treatment options for jaundice include: phototherapy, further subdivided into conventional & intensive, exchange transfusion, and