JAUNDICE in the NEWBORN Causes And Treatment

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Jaundice in the Newborn

Jaundice in the Newborn

Jaundice in the Newborn“Hyperbilirubinemia”: is an increase in unconjugated bilirubin caused by either overproduction of bilirubin or deficiency in its conjugation. Hyperbilirubinemia in the newborn is an accumulation of serum bilirubin above normal levels.

It carries the risk of kernicterus, a serious condition causing serious neurological impairment.

Early diagnosis and appropriate treatment can virtually eliminate this risk.


Occurs in 50% of term infants, 80% of preterm.

Predisposing factors:

1. Blood group incompatibility with mother.

2. Prematurity.

3. Infection.

4. Birth trauma.

5. Polycythemia.

6. Maternal or neonatal metabolic or endocrine disorders.

7. Malfunction of the gastrointestinal tract.

Altered physiology :

Hemoglobin in the RBCs is broken down in the presence of the enzyme called heme oxygenase into :

1. Globin is reduced to amino acids.

2. Iron is broken off and storied.

3. Porphyrin moiety is broken into biliverdin, which is reduced to bilirubin.

Bilirubin is released into the circulation where it combines with albumin ( unconjugated or indirect bilirubin ). The liver selectively removes this albumin-bound bilirubin from the blood.

Once the unconjugated bilirubin is in the liver, it is converted into direct or conjugated water-soluble bilirubin with the aid of enzyme , one of which is glucuronosyl transferase . from the liver,  conjugated bilirubin is excreted via the bile into the intestine and is excreted in the stool or is hydrolyzed to unconjugated bilirubin in the intestine and reabsorbed across the intestinal mucosa into the circulation ( enterohepatic circulation ) .

Bacterial action forms urobilinogen. Which is either excreted in the stool or reabsorbed by the liver or kidney an excreted in the urine.

Common Causes:

Overproduction of bilirubin.

1. physical jaundice ( normal).

– Increased RBCs.

– The decreased life span of RBCs.

– Increased enterohepatic circulation.

– Defective uptake.

– Defective conjugation.

2. Erythrocyte destruction (Hemolytic Anaemia).

–  Erythroblastosis ( isoimmunization due to Rh or ABO incompatibility )

– Glucose-6posphate dehydrogenase deficiency ( G6PD).

– Infection.

– Sequestered blood.

3. Gastrointestinal obstruction.

4. Polycythemia.

Clinical manifestations:

– The onset of clinical jaundice seen when serum bilirubin levels are less than 5-7 mg/ dl.

– Physiological jaundice occurs 3-5 days after birth.

– Increase in unconjugated levels, levels must not exceed 5mg/dl per day.

– Peak bilirubin levels not to exceed 12mg/dl in full-term infant and 15 mg/dl in the premature infant.

– Erythroblastosis may occur within 24 hours after birth.

Signs and symptoms may include :
1. Sclera appearing yellow before skin.

2. Skin appearing light to bright yellow.

3. Lethargy.

4. Poor feeding.

5. Dark stool.

6. Dark amber concentrated urine.


– Phototherapy.

– Exchange transfusion.

– Enzyme induction agent.


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