Bilirubin Encephalopathy - Severe Neonatal Jaundice

Bilirubin is the main product of the decomposition of old red blood cells. Bilirubin is filtered from the blood by the liver, and excreted in the bile. As the liver becomes increasingly damaged, total bilirubin increases. Most of total bilirubin metabolized, and this section referred to as the direct bilirubin. When the sections are increased, the cause is usually outside the liver. If direct bilirubin is low while high total bilirubin, this indicates damage to the liver or bile duct in the liver.

Bilirubin contain dyes that give color to the dirt. If the level is very high, the skin and eyes may be yellow , resulting in symptoms of jaundice.

Severe neonatal jaundice and is not administered properly can cause complications bilirubin encephalopathy. This occurs due to the binding of bilirubin acid free with a cell wall lipids neurons in the basal ganglia, brain stem and cerebellum which leads to cell death. In infants with sepsis , hypoxia and asphyxia can cause damage to the blood-brain barrier. With the jaundice, bilirubin bound to plasma albumin get into the extracellular fluid. So far the relationship between elevated levels of serum bilirubin with bilirubin encephalopathy have known. But there has been no study that get specific value of total serum bilirubin in term infants with non- hemolytic hyperbilirubinemia may result in interference with the intelligence or neurological damage it causes.

Factors affecting the toxicity of bilirubin in the newborn brain cells are very complex and not yet fully understood. These factors include: the concentration of serum albumin, albumin binding with bilirubin, albumin penetration into the brain, and brain cells insecurity facing toxic effects of bilirubin. However, this situation is unusual events are found even in premature infants and serum albumin levels that were previously thought to put premature infants at risk for bilirubin encephalopathy.

Infants who survived after experiencing bilirubin encephalopathy will have permanent brain damage in the form of cerebral palsy manifestations, epilepsy and mental retardation or only minor defects such as learning disorders and perceptual disorder motors.

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