Jaundice is the yellow coloration of the sclera due to excess bilirubin. It may also affect the skin. If there is yellowness of the skin and not of the sclera it is not jaundice. This is most likely to be meconium aspiration or due to carotenaemia.
Bilirubin is produced by the destruction of effete red blood cells in the reticular-endo the legal system and from other haem proteins in the liver and bone marrow. Both sources produce unconjugated bilirubin
which is bound to albumin and transported to the liver. Here it undergoes conjugation mediated by the glucosyl transferase enzyme. The conjugated bilirubin is excreted with bile into the intestine where it is passed out as stercobilin. It is also passed out through urine as urobilinogen. It is important to note that conjugated bilirubin can be re-converted to unconjugated bilirubin in the gastrointestinal tract by the action of B-glucosidase especially if there is GIT stasis or delay.
Unconjugated bilirubin is water-insoluble but fat-soluble and it is toxic to the brain. It can be excreted in the urine. There are two types of jaundice. These are physiological jaundice and pathological jaundice.
Physiologic jaundice is not present at birth as the mother clears bilirubin before birth. At birth, however, the bilirubin level gradually builds up but does not appear before one to two days. They usually clear untreated, and does not. There are permissible levels and duration of clearance of bilirubin in both make a baby sick. term baby and preterm baby.
Permissible levels Duration of clearance Pre-term baby It does not mean that these values are safe. If the duration of clearance exceeds the above-given values it is no longer physiologic jaundice. This is so because the glucuronidase enzyme in the liver by now should have been fully developed. Pathologic jaundice is due to inherent problems in the baby.
The causes are as follows:
1. Glucose – 6-phosphate dehydrogenase deficiency:- The deficiency of this enzyme in the baby account for about 50-70% of neonatal jaundice. The enzyme deficiency when exposed to oxidants such as 8 – amino quinolones; sulphonamides, camphor products, and infection causes jaundice
2. Infection:- This is the second commonest cause of jaundice. The organisms are usually gram-negative and hemolytic organisms.
3. Low birth weight:- Pre-term (premature) babies are more likely to have jaundice as there is a greater deficiency of glucosyltransferase.
4. Feto-maternal blood incompatibility:- ABO and rhesus are implicated.
5. Idiopathic (unknown cause).
6. Close hemorrhage (rare)
7. Delayed clamping of cord (rare)
Criteria for pathological jaundice:
(a) Clinical jaundice in the first 24 hours of life.
(b) Total serum bilirubin level increasing by more than 5 mg % per day.
(c) Today serum bilirubin level. Full-term baby more than 12.9 mg %
(ii) Pre-term baby more than 15mg%
(d) Conjugated serum bilirubin more than 1.5-2mg%