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Latest revision as of 22:57, 29 July 2020

Neonatal jaundice Microchapters

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ahmed Elsaiey, MBBCH [2]

Overview

If left untreated, neonatal jaundice may lead to brain damage. Common complications of neonatal jaundice include acute bilirubin encephalopathy and kernicterus. Prognosis of neonatal jaundice is excellent with the proper treatment.

Natural history, complications and prognosis

Natural history

  • If left untreated, neonatal jaundice may develop bilirubin related brain damage.

Complications

  • Common complications of neonatal jaundice include the following:
    • Acute bilirubin encephalopathy:[1][2][3]
      • Bilirubin is toxic to the brain and high levels may cause acute bilirubin encephalopathy.
      • In the beginning, it may be asymptomatic or the infant is sleepy and hypotonic.
      • If the encephalopathy not diagnosed early, more complications will develop as lethargy, seizures, inability to feed, and apnea in severe cases.
      • It is better to diagnose it early in order not to develop severe cases of encephalopathy.
    • Kernicterus:[4][5]
      • Kernicterus is the chronic neurologic dysfunction that results from high levels of bilirubin.
      • Kernicterus occurs due to damage of the basal ganglia with the precipitating bilirubin.
      • Kernicterus can present with the following features:
        • Hearing impairement
        • Gaze abnormality
        • Cerebral palsy like features
      • The neurological manifestations of Kernicterus are reversible with exchange transfusion and decreasing the high bilirubin levels.

Prognosis

  • Prognosis of neonatal jaundice is excellent with receiving the proper treatment.

References

  1. Chuniaud L, Dessante M, Chantoux F, Blondeau JP, Francon J, Trivin F (1996). "Cytotoxicity of bilirubin for human fibroblasts and rat astrocytes in culture. Effect of the ratio of bilirubin to serum albumin". Clin Chim Acta. 256 (2): 103–14. PMID 9027422.
  2. Bratlid D (1990). "How bilirubin gets into the brain". Clin Perinatol. 17 (2): 449–65. PMID 2196140.
  3. Hoffman DJ, Zanelli SA, Kubin J, Mishra OP, Delivoria-Papadopoulos M (1996). "The in vivo effect of bilirubin on the N-methyl-D-aspartate receptor/ion channel complex in the brains of newborn piglets". Pediatr Res. 40 (6): 804–8. doi:10.1203/00006450-199612000-00005. PMID 8947954.
  4. van Toorn R, Brink P, Smith J, Ackermann C, Solomons R (2016). "Bilirubin-Induced Neurological Dysfunction: A Clinico-Radiological-Neurophysiological Correlation in 30 Consecutive Children". J Child Neurol. 31 (14): 1579–1583. doi:10.1177/0883073816666473. PMID 27591005.
  5. Wickremasinghe AC, Risley RJ, Kuzniewicz MW, Wu YW, Walsh EM, Wi S; et al. (2015). "Risk of Sensorineural Hearing Loss and Bilirubin Exchange Transfusion Thresholds". Pediatrics. 136 (3): 505–12. doi:10.1542/peds.2014-3357. PMID 26283777.

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