<unk>  is defined as irreversible brain damage due to chronic high levels of unconjugated bilirubin in the baby's blood. It will develop if the high levels of unconjugated bilirrubin are not treated early. Hyperbilirubinemia frequently occurs in newborns, but it is mostly benign. Severe cases can progress to<unk>  and developmental abnormalities. The risk of bilirubin-induced neurologic damage and<unk>  is higher in preterm than term neonates and the former suffer adverse effects at lower total bilirubin levels with worse long-term outcomes. Liver metabolizes and excretes bilirubin. During pregnancy, the mother's liver metabolizes it for the baby. After birth, some newborns may have liver enzymes that are still immature, specially if they are preterm. Due to that, bilirubin level rises in the baby's blood and accumulates in the skin and sclera of eyes, causing jaundice. The tissues protecting the brain (the blood-brain barrier) are immature in newborns, therefore, they are vulnerable to increased levels of unconjugated bilirubin. Bilirubin penetrates the brain and is deposited in the basal ganglia, hippocampus, geniculate bodies and cranial nerve nuclei causing irreversible damage. Depending on the level of exposure, the effects range from unnoticeable to severe brain damage. Many conditions may cause jaundice, but when it occurs within (24 hours) of life it is always pathological. If it happens after 24 hours of life, it can be physiologic. Some of the several underlying pathologic processes responsible for hyperbilirubinemia are G6PD deficiency, Crigler-Najjar syndrome, Gilbert syndrome, hemolytic disorders, and decreased ability to conjugate bilirubin in neonates and infants. Newborn babies are often polycythemic, meaning they have too many red blood cells. When red cells are destroyed, one of the byproducts is bilirubin, which circulates in the blood and causes jaundice. When hyperbilirubinemia occurs in adult and older children, it is frequently due to liver abnormalities. 
Some medications, such as the antibiotic trimethoprim/sulfamethoxazole may induce this disorder in the newborn, either when taken by the mother or given directly to the patient, due to displacement of bilirubin from binding sites on serum albumin. The bilirubin is then free to pass into the central nervous system. In the (first 48 hrs of life), A baby should be checked for jaundice and if it is discharged before 72 hrs, the baby should be seen after 2 days. The treatment is phototherapy and exchange transfusion.
Kernicterus
Clubbing
Dot hemorrhage
Vulvar pruritus
Haemobilia
Vaginal bleeding
Hematochezia
Varicose veins