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   MeshID        = D007647 |
   MeshID        = D007647 |
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'''Kernicterus''' is damage to the brain centers of infants caused by elevated levels of [[bilirubin]]. This may be due to several underlying pathologic processes. Newborn babies are often [[polycythemic]], meaning they have too many [[red blood cell]]s. When they break down the cells, one of the byproducts is [[bilirubin]], which circulates in the blood, and causes [[Neonatal_jaundice|jaundice]]. Alternately, Rh incompatibility between mother and fetus may cause [[hemolysis]] of fetal red blood cells, thereby releasing unconjugated bilirubin into the fetal blood. Since the fetal [[blood brain barrier]] is not fully formed, some of this released bilirubin enters the brain and interferes with normal neuronal development.
{{Infobox_Disease |
  Name          = {{PAGENAME}} |
  Image          = Bilirubin.svg  |
  Caption        = [[Bilirubin]] |
  DiseasesDB    = 7161 |
  ICD10          = {{ICD10|P|57||p|50}} |
  ICD9          = {{ICD9|773.4}}, {{ICD9|774.7}} |
  ICDO          = |
  OMIM          = |
  MedlinePlus    = 003243 |
  eMedicineSubj  = ped |
  eMedicineTopic = 1247 |
  MeshID        = D007647 |
}}
'''Kernicterus''' is damage to the brain centers of infants caused by increased levels of unconjugated-indirect [[bilirubin]] which is free (not bound to albumin). This may be due to several underlying pathologic processes. Newborn babies are often [[polycythemic]], meaning they have too many [[red blood cell]]s. When they break down the cells, one of the byproducts is [[bilirubin]], which circulates in the blood and causes [[Neonatal_jaundice|jaundice]]. Alternately, Rh incompatibility between mother and fetus may cause [[hemolysis]] of fetal red blood cells, thereby releasing unconjugated bilirubin into the fetal blood. Since the fetal [[blood brain barrier]] is not fully formed, some of this released bilirubin enters the brain and interferes with normal neuronal development.
Kernicterus may also be found in infants as a symptom of [[Crigler-Najjar syndrome]] type I, a hereditary hyperbilirubinemia that is fatal within 18 months of life.


In adults and older children, jaundice is harmless in and of itself. However, the tissues protecting the brain (the [[blood-brain barrier]]) are immature in newborns. Bilirubin penetrates the brain and is deposited in the basal ganglia, causing irreversible damage. Depending on the level of exposure, the effects range from unnoticeable to severe [[brain damage]].
In adults and older children, jaundice is harmless in and of itself. However, the tissues protecting the brain (the [[blood-brain barrier]]) are immature in newborns. Bilirubin penetrates the brain and is deposited in the [[basal ganglia]], causing irreversible damage. Depending on the level of exposure, the effects range from unnoticeable to severe [[brain damage]].


Some medications, such as [[trimethoprim]]/[[sulfamethoxazole]] may induce this disorder to the baby when taken by the mother.
Some medications, such as the antibiotic [[co-trimoxazole]] (a combination of [[trimethoprim]]/[[sulfamethoxazole]]) may induce this disorder in the baby, either when taken by the mother or given directly to the baby, due to displacement of [[bilirubin]] from binding sites on [[serum albumin]]. The [[bilirubin]] is then free to pass into the [[Central Nervous System]], because the baby's [[blood-brain barrier]] is not fully developed.


The word origantes from the [[German language|German]] ''kern'', nucleus, kernel, and the [[Greek language|Greek]] ''ikterus'', jaundice.<ref>{{cite web
|url = http://dissertations.ub.rug.nl/FILES/faculties/medicine/2006/a.m.hafkamp/01_1.pdf
|title = Oral treatment of unconjugated hyperbilirubinemia
|accessdate = 2008-09-06
|author = Anja M. Hafkamp
|year = 2006
|format = PDF
|work = PhD thesis
|publisher = Department of Pediatrics; Center for Liver, Digestive and Metabolic Diseases; University Medical Center [[University of Groningen|Groningen]]
|pages = p. 21}}</ref>
==References==
<references/>
== External links ==
*[http://bilitool.org BiliTool - Hyperbilirubinemia Risk Assessment for Newborns]
*[http://www.cdc.gov/ncbddd/dd/kernichome.htm CDC’s National Center on Birth Defects and Developmental Disabilities]
* [http://www.pickonline.org/ PICK - Parents of Infants and Children with Kernicterus]
{{Certain conditions originating in the perinatal period}}
[[Category:Neurology]]
[[Category:German loanwords]]
[[de:Bilirubinenzephalopathie]]
[[es:Kernicterus]]
[[it:Kernittero]]
[[nl:Kernicterus]]
[[pl:Żółtaczka jąder podkorowych mózgu]]
[[ru:Ядерная желтуха]]
[[tr:Kernikterus]]
== External links ==
== External links ==
*[http://www.cdc.gov/ncbddd/dd/kernichome.htm CDC’s National Center on Birth Defects and Developmental Disabilities]
*[http://www.cdc.gov/ncbddd/dd/kernichome.htm CDC’s National Center on Birth Defects and Developmental Disabilities]

Revision as of 18:23, 9 March 2009

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Kernicterus
Bilirubin
ICD-10 P57
ICD-9 773.4, 774.7
DiseasesDB 7161
MedlinePlus 003243
eMedicine ped/1247 
MeSH D007647
Kernicterus
File:Bilirubin.svg
Bilirubin
ICD-10 P57
ICD-9 773.4, 774.7
DiseasesDB 7161
MedlinePlus 003243
eMedicine ped/1247 
MeSH D007647

Kernicterus is damage to the brain centers of infants caused by increased levels of unconjugated-indirect bilirubin which is free (not bound to albumin). This may be due to several underlying pathologic processes. Newborn babies are often polycythemic, meaning they have too many red blood cells. When they break down the cells, one of the byproducts is bilirubin, which circulates in the blood and causes jaundice. Alternately, Rh incompatibility between mother and fetus may cause hemolysis of fetal red blood cells, thereby releasing unconjugated bilirubin into the fetal blood. Since the fetal blood brain barrier is not fully formed, some of this released bilirubin enters the brain and interferes with normal neuronal development. Kernicterus may also be found in infants as a symptom of Crigler-Najjar syndrome type I, a hereditary hyperbilirubinemia that is fatal within 18 months of life.

In adults and older children, jaundice is harmless in and of itself. However, the tissues protecting the brain (the blood-brain barrier) are immature in newborns. Bilirubin penetrates the brain and is deposited in the basal ganglia, causing irreversible damage. Depending on the level of exposure, the effects range from unnoticeable to severe brain damage.

Some medications, such as the antibiotic co-trimoxazole (a combination of trimethoprim/sulfamethoxazole) may induce this disorder in the baby, either when taken by the mother or given directly to the baby, due to displacement of bilirubin from binding sites on serum albumin. The bilirubin is then free to pass into the Central Nervous System, because the baby's blood-brain barrier is not fully developed.

The word origantes from the German kern, nucleus, kernel, and the Greek ikterus, jaundice.[1]

References

  1. Anja M. Hafkamp (2006). "Oral treatment of unconjugated hyperbilirubinemia" (PDF). PhD thesis. Department of Pediatrics; Center for Liver, Digestive and Metabolic Diseases; University Medical Center Groningen. pp. p. 21. Retrieved 2008-09-06.

External links

Template:Certain conditions originating in the perinatal period

de:Bilirubinenzephalopathie it:Kernittero nl:Kernicterus

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Template:Certain conditions originating in the perinatal period Template:SIB de:Bilirubinenzephalopathie

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