Neonatal jaundice is the discoloration of body tissue and fluid by bile pigment. In normal circumstances, bile pigments from haemolysed senile red blood cells are carried to the liver where they are conjugated and excreted via the urine and stools. Accumulation of the bile pigment will occur if there is;
A. excessive destruction of the red blood cells
B. abnormality in the transportation of bile
C. abnormality in conjugation of bile
Jaundice of immaturity
Destruction of red blood cells occurs after birth. If the liver is immature and cannot cope with its normal functions, conjugation and excretion of the bile pigments are inadequate and jaundice ensued.
This type of jaundice occurs in 50% of full term and about 70-80% of premature babies. It is usually not present within the first 24hrs of life, rather it is usually detected on the second or third day of life.
The jaundice should begin to disappear by the end of the first week, and generally it is not noticeable within a fortnight.
This type jaundice is not accompanied by other symptoms except in severe cases, when the baby may become lethargic and sluggish with its feeds.
Haemolytic jaundice is usually associated with destruction haemolysis of red blood cells. Conditions which predispose to haemolysis are Rhesus and ABO blood group incompatibility.
In these conditions, large numbers of red blood cells are destroyed, and there is an exexcessive and rapid production of bile pigments which normal liver cannot conjugate.
The bile pigment (bilirubin) accumulate in the tissues, causing clinical jaundice within 12-24hrs of birth.
The jaundice may be associated with anaemia which can run a rapidly progressive course. In severe cases, the baby is drowsy, has rapid respiration and may develop heart failure, kernicterus and die.
Glucose-6-phosphate dehydrogenase (G-6-PD) deficiency; Glucose- 6-phosphate dehydrogenase is n essential enzyme in the red blood cells.
The absence of this enzyme result in easy destruction of the red cells. The haemolysis could be precipitated by drugs such as salicylates or infection.
Neonatal jaundice of the haemolytic type may be caused by excessive administration of vitamin k and sulphonamides.
An infection, which may be bacterial, viral, or protozoa, is a common cause of neonatal jaundice, especially in babies born outside the hospital.
The organism usually enters the body through the umbilical cord and may attack the liver cells.
There is usually a great deal of constitutional disturbance and septicaemia may set in. It usually develop within seven days of birth and the prognosis is poor.
It is due to congenital obligation or absence of the bile duct. Therefore, there is an accumulation of bile in the liver and jaundice appears.
In type, the urine is dark in colour and the stool is pale. Neonatal jaundice associated with pale stools, dark urine and persisting beyond the second week of life is suggestive of obstructive jaundice.
The digestion of fat and the child’s appetite are always impaired in this type of jaundice. In few cases, operative measures may relieve the obstruction.
Effects of jaundice in the neonate
Kenicterus: A yellow staining of the brain cells in the basal ganglia. It occurs in the presence of excessive unconjugated bilirubin in the blood.
Brain damage occurs and may lead to cerebral palsy or death of the baby. Clinically baby with kenicterus refuses feeds, is lethargic there is rigidity of the body with complete opisthotonos and may have convulsions.
Usually, babies with kenicterus die and those who survive develop permanent physical and mental handicap.
Liver cirrhosis may occur, especially in obstructive jaundice, because the accumulation of bile destroys the liver cells readily.
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