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Previous Volume 344:581-590 February 22, 2001 Number 8 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

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Icterus neonatorum, or neonatal jaundice, has long been recognized.¹ The term "kernicterus" was introduced in the early 1900s to refer to the yellow staining of the basal ganglia observed in infants who died with severe jaundice.² From the 1950s through the 1970s, because of a high incidence of Rh hemolytic disease and kernicterus, pediatricians were aggressive in treating jaundice.³ However, several factors have changed the management of jaundice. Studies in the 1980s and 1990s suggested that kernicterus from jaundice was rare and that too many infants were being treated unnecessarily.^4,5,6,7 Also, newborn infants were being discharged from the hospital sooner . . . [Full Text of this Article]

Pathophysiology

Causes

Cellular Toxic Effects of Bilirubin

Factors That Influence the Neurotoxic Effects of Bilirubin

Clinical Features of Kernicterus

Prediction of the Risk of Severe Hyperbilirubinemia

Transcutaneous Measurement of Bilirubin

Measurement of Carbon Monoxide to Evaluate Bilirubin Production

Prevention

Reduction of Bilirubin in the Enterohepatic Circulation

Inhibition of Bilirubin Production

Treatment

Phototherapy

Exchange Transfusion

Pharmacologic Therapies

Prevention of Bilirubin Encephalopathy

Approach to Jaundice

Conclusions

Source Information

From the Department of Neonatology, Stanford University School of Medicine, Stanford, Calif. (P.A.D., D.K.S.); and Bikur Cholim Hospital and Hebrew University and Haddassah Medical School, Jerusalem, Israel (D.S.S.).

Address reprint requests to Dr. Dennery at the Department of Pediatrics, Stanford University Medical Center, Stanford, CA 94305, or at dennery@leland.stanford.edu.

References

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