NEONATAL JAUNDICE

Professor
Mohamed Khashaba
Professor of Pediatrics

Mansoura Faculty of Medicine

 Objectives
1. Understand why neonatal jaundice is
important.
2. Understand the etiology of physiologic
jaundice.
3. Identify the causes of pathologic jaundice.
4. Know the treatment of neonatal jaundice.

M.Khashaba,MD professor of Pediatrics,Mansoura

Why is Neonatal Jaundice important?

• It may indicate underlying disease.

• Neurotoxicity of unconjugated bilirubin.

M.Khashaba,MD professor of Pediatrics,Mansoura

M.Khashaba,MD professor of Pediatrics,Mansoura
 Metabolism of bilirubin
Breakdown of RBCs

Unconjugated bilirubin

Bound to albumin (excess bilirubin gets free→CNS)

↓
Conjugation
(glucuryonyl transferase)

Enterohepatic
Gut circulation

Excretion as Deconjugation
urobilinogen & (glucuronidase)
stercobilinogen
• What’s the commonest cause of neonatal jaundice?

• What’s the most important cause of neonatal

jaundice?

Physiologic jaundice

M.Khashaba,MD professor of Pediatrics,Mansoura

 Physiologic Jaundice

• Occurs in 60% of full terms & 80% of pre terms.

• Bilirubin has an antioxidant properties (may be

beneficial).

M.Khashaba,MD professor of Pediatrics,Mansoura

 Factors Leading to Physiologic Jaundice

• Increase bili. Load:

– Short life span of RBC.
– Large red cell mass.
– Deconjugation in the intestine.
• Decreased hepatic conjugation:
– Relative lmmaturity of enzymes.
– Dehydration & hypocaloric intake.
M.Khashaba,MD professor of Pediatrics,Mansoura
Factors Exaggerating Physiologic Jaundice
• Prematurity.
• Breast feeding.
• Deficient intake.
• Polycythemia.
• Enclosed Hge.
• Oriental race.

M.Khashaba,MD professor of Pediatrics,Mansoura

M.Khashaba,MD professor of Pediatrics,Mansoura
 Causes of Neonatal Jaundice

∀ ↑ ed hemolysis
• Deficient conjugution (unconjugated hyperbili-
rubinemia).
∀ ↓excretion (conjugated hyperbilirubinemia).

M.Khashaba,MD professor of Pediatrics,Mansoura

 Pathological Hyperbilirubinemia

Unconjugated Conjugated

↑ Hemolysis: ↓ conjugation:
* Rh. incompatibility
* Criggler Najjar syndrome
* ABO incompatibility
* Inhibited enzyme:
* Heriditary hemolytic anemia -Hypoxia
* Infections -Acidosis
* Extravasated blood -Hypothyroidism
* Polycythemia -Breast milk jaundice

M.Khashaba,MD professor of Pediatrics,Mansoura

 Pathological Hyperbilirubinemia
Suggestive criteria:
• Family history.
• Onset: <2nd day or > 7th day.
• Duration: > 2 weeks.
• Peak bilirubin > 15 mg/dl.
• Rate of bilirubin increase > 5mg / 24 hrs.
• Conjugated bilirubin > 2 mg/dl.
• Pallor, hepatomegaly, splenomegaly….
• Light stool or dark urine.
M.Khashaba,MD professor of Pediatrics,Mansoura
Pathological Hyperbilirubinemia Continue

Mg/dl Hemolysis
Serum bilirubin

Conjugated + prolonged jaundice

15

Physiological jaundice

2 4 6 8 10 12 14
Day of life
M.Khashaba,MD professor of Pediatrics,Mansoura
 Persisting Prolonged Jaundice
• Unconjugated:
– Hypothyroidism.
– Pyloric stenosis.
– Breast milk jaundice.
– Griggler-Najjar syndrome.
• Conjugated

M.Khashaba,MD professor of Pediatrics,Mansoura

 Conjugated hyperbilirubinemea

• Pathological.
• Prompt diagnosis and referral to a specialized
center is needed.

M.Khashaba,MD professor of Pediatrics,Mansoura

 Important causes for Conjugated
Hyperbilirubinemia

1. Biliary atresia.
2. Neonatal hepatitis.
3. α1 Antitrypsin deficiency.
4. Inspissated bile syndrome

M.Khashaba,MD professor of Pediatrics,Mansoura

 Breast Milk Jaundice
(Prolonged unconjugated hyperbilirubinemia)

Theory:
• Breast milk contains substances which interfere with
conjugation (Non esterified LCFA).
Value:
• D.D of prolonged jaundice.
• Non harmful to the baby.
Stoppage of breast feeding is not recommended.

M.Khashaba,MD professor of Pediatrics,Mansoura

 Breast milk jaundice

• A well and thriving ,breast fed baby who

has unconjugated hyperbilirubinemia.

• Diagnosis is by exclusion.

M.Khashaba,MD professor of Pediatrics,Mansoura

 Prolonged unconjugated hyper
bilirubinemia

 The following tests may be required:

1. Thyroid function.
2. Hemoglobin and BBCS morphology.
3. Urine culture.
4. Liver function.

M.Khashaba,MD professor of Pediatrics,Mansoura

• EARLY ONSET HYPERBILIRUBINEMIA

– Hemolytic until proved otherwise

M.Khashaba,MD professor of Pediatrics,Mansoura

 Baseline Tests for Early Onset
Significant Jaundice

1. Serum bilirubin.
2. Blood group.
3. Coomb’s test.
4. Blood picture , including Retic. count.

M.Khashaba,MD professor of Pediatrics,Mansoura

 Rhesus Incompatibility
• Mother Rh-ve and baby Rh+ve.
• First baby is not affected & severity of disease
increase with subsequent pregnancy.
• Jaundice during 1st 24 hrs.
• Significant pallor.
• Liver & spleen usually palpable.
• Hydrops foetalis in severe cases.

M.Khashaba,MD professor of Pediatrics,Mansoura

 Management of Rh. Incompatibility
Antenatal Management
• Serial anti D.
• Evaluation of fetal well-being:
– Repeat fetal U/S.
– Amniocentesis.
• Interference:
– Premature labor.
– Intrauterine packed O -ve cells transfusion.

M.Khashaba,MD professor of Pediatrics,Mansoura

Management of Rh. Incompatibility
Postnatal Management
• Exchange transfusion
a- Immediately after delivery:
• Cord Hb <11mg/dl.
• Cord bili >5mg/dl.
• Reticulocytic count >15%.
• Previous history of severe disease.
b- At any time:
• Rise of bili >0.5mg/hr.
• Serum bilirubin >20mg/dl.
• Phototherapy:
– Before and after exchange.
M.Khashaba,MD professor of Pediatrics,Mansoura
 Differential Diagnosis of Neonatal Jaundice
According to Time of Appearance

Jaundice in the first day:

• Hemolytic jaundice is likely:
– Rh. Incompatibility.
– ABO incompatibility.

• Intrauterine infection.

M.Khashaba,MD professor of Pediatrics,Mansoura

 Rhesus incompatibility ABO incompatibility

Immune response by Rh –ve mothe r Group O wome n pass anti A or B Abs to he r

fe tus (A or B)

First baby usually not affe cte d First baby may be affe cte d

Incre ase severity of dise ase with successive No re lation be twee n seve rity & birth orde r

pre gnancy

Significant pallor Pallor is not us ually prese nt

Live r & spleen usually palpable Live r & spleen not us ually palpable

Diagnosis:

* evide nce of he molytic ane mia * Hb is usually normal

* +ve Coomb’s test * Coomb’s test may be ne gative

* Mothe r Rh –ve, baby +ve * Mothe r group O, baby A or B

* Pre ve ntion anti D give n to the mothe r. * No pre ve ntive me asure s

* Blood for e xchange Rh –ve blood, same

ABO group of baby * O-blood s ame Rh group of baby

M.Khashaba,MD professor of Pediatrics,Mansoura

Differential Diagnosis of Neonatal Jaundice According to Time of Apparance
Continue

Jaundice in the 2nd - 3rd day:

• Physiologic jaundice.

Jaundice at 3nd - 5th day:

• Septicemia.
• Hematoma.
• Polycythemia.
M.Khashaba,MD professor of Pediatrics,Mansoura
Differential Diagnosis of Neonatal Jaundice According to
Time of Apparance

Continue

After the first week:

• Septicemia.
• Cholestasis.

M.Khashaba,MD professor of Pediatrics,Mansoura

 Kernicterus

• Yellow staining of basal ganglia & brain stem.

• Due to escape of free bili. From blood to brain

cells.

M.Khashaba,MD professor of Pediatrics,Mansoura

M.Khashaba,MD professor of Pediatrics,Mansoura
Keructerus Continue

Pathophysiology:
• Serum unconjugated bili. Exceeds carrying
capacity of serum albumin.
• A level of >25 mg/dl of bili. Is critical.
• Factors disturbing BBB increase vulnerability
of brain cells.

M.Khashaba,MD professor of Pediatrics,Mansoura

 Cellular mechanisms of bilirubin
neurotoxicity

Injurious effect on:

2. Glucose utilization.

3. Oxidative phosphorylation .

4. DNA synthesis.

M.Khashaba,MD professor of Pediatrics,Mansoura

4.Protein synthesis.

5.Protein Phosphorylation.

6.Neurotransmittor synthesis.

7. Ion transport.

8.Synaptic transmission.

9.Excitatory amino acid homeostasis.

M.Khashaba,MD professor of Pediatrics,Mansoura

 Factors Related To Brain
Damage
1. Serum concentration of bilirubin.
2. Bilirubin binding by albumin.
3. Status of the blood-brain barrier.
4. Susceptibility of the CNS.

M.Khashaba,MD professor of Pediatrics,Mansoura

Keructerus Continue

Early signs:
• Poor feeding.
• Impaired reflexes.
• Altered consciousness.
• Convulsions & opisthotonus.

M.Khashaba,MD professor of Pediatrics,Mansoura

M.Khashaba,MD professor of Pediatrics,Mansoura
 Post-Kernicterus

• Mental retardation.
• C.P.
• Deafness.

M.Khashaba,MD professor of Pediatrics,Mansoura

 Treatment of Unconjugated
Hyperbilirubinemia
• Specific treatment.
• General measures.
• Phototherapy.

M.Khashaba,MD professor of Pediatrics,Mansoura

Treatment of Unconjugated Hyperbilirubinemia Continue

• Phototherapy.

M.Khashaba,MD professor of Pediatrics,Mansoura

Treatment of Unconjugated Hyperbilirubinemia Continue

• Indications of phototherapy:
– Serum unconjugated bili. 12-25 mg/dl in
healthy full terms.
– Lower levels in:
• Preterm & sick baby.
• Hemolytic jaundice.

M.Khashaba,MD professor of Pediatrics,Mansoura

Treatment of Unconjugated Hyperbilirubinemia Continue

• Exchange transfusion indications:

– S. bili. >25 mg/dl in healthy full term.
– Lower levels in:
• Preterm & sick babies.
• Hemolytic jaundice.

M.Khashaba,MD professor of Pediatrics,Mansoura

Treatment of Unconjugated Hyperbilirubinemia Continue

• Aim of exchange transfusion:

– Remove bili.
– Remove sensitized cells.
– Correct anemia.

M.Khashaba,MD professor of Pediatrics,Mansoura

Treatment of Unconjugated Hyperbilirubinemia Continue
• Technique of exchange transfusion.
– Amount:
• Double blood volume.
– Type:
• Rh. Incomatibilty (Rh. -ve).
• ABO incompatibility (O).
• Other indications (same group of baby).
– Technique:
• UVC pull and push technique.

M.Khashaba,MD professor of Pediatrics,Mansoura

 Objectives
1. Understand why neonatal jaundice is
important.
2. Understand the etiology of physiologic
jaundice.
3. Identify the causes of pathologic jaundice.
4. Know the treatment of neonatal jaundice.

M.Khashaba,MD professor of Pediatrics,Mansoura