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Published on: May 29, 2020
Bilirubin Induced Encephalopathy
Parvaneh Karimzadeh1,2, Minoo Fallahi3, Mohammad Kazemian3
1Pediatric Neurology Research Center, Research Institute for Children's Health, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Insights
Neonatal hyperbilirubinemia can cause bilirubin-induced encephalopathy (BIE) if untreated. Early intervention prevents BIE, but chronic forms lack definitive treatment, impacting infant neurological health.
Area of Science:
- Neonatology
- Pediatric Neurology
Background:
- Hyperbilirubinemia is a common neonatal disorder.
- Delayed diagnosis of indirect hyperbilirubinemia can lead to bilirubin-induced encephalopathy (BIE).
- BIE incidence is higher in underdeveloped regions, particularly affecting preterm neonates.
Purpose of the Study:
- To review the pathophysiology, diagnosis, and management of neonatal hyperbilirubinemia and BIE.
- To highlight the neurological sequelae of untreated BIE.
Main Methods:
- Literature review of neonatal hyperbilirubinemia and BIE.
- Discussion of diagnostic imaging, specifically brain MRI.
- Overview of current treatment modalities.
Main Results:
- BIE presents acutely or chronically with distinct neurological deficits.
- Brain MRI is crucial for diagnosing BIE.
- Phototherapy and exchange transfusion can prevent BIE if initiated early.
Conclusions:
- While acute BIE is preventable, chronic bilirubin encephalopathy has no definitive treatment.
- Prompt diagnosis and management of neonatal jaundice are critical to prevent long-term neurological damage.
Abstract:
Hyperbilirubinemia is one of the most common neonatal disorders. Delayed diagnosis and treatment of the pathologic and progressive indirect hyperbilirubinemia lead to neurological deficits, defined as bilirubin induced encephalopathy (BIE) (2). The incidence of this disorder in underdeveloped countries is much more than developed areas. All neonates with the risk factors for increased the blood level of indirect bilirubin are at risk for BIE, especially preterm neonates which are prone to low bilirubin kernicterus . BIE can be transient and acute (with early, intermediate and advanced phases)or be permanent, chronic and lifelong ( with tetrad of symptoms including visual (upward gaze palsy), auditory (sensory neural hearing loss), dental dysplasia abnormalities, and extrapyramidal disturbances (choreoathetosis cerebral palsy).Beside the abnormal neurologic manifestations of the jaundiced neonates ,brain MRI is the best imaging modality for the confirmation of the diagnosis. Although early treatment of extreme hyperbilirubinemia by phototherapy and exchange transfusion can prevent the BIE, unfortunately the chronic bilirubin encephalopathy does not have definitive treatment.
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