NEONATAL JAUNDICENEONATAL JAUNDICENEONATAL JAUNDICENEONATAL 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?Why is Neonatal Jaundice important?Why is Neonatal Jaundice important?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 bilirubinMetabolism of bilirubinMetabolism of bilirubinMetabolism of bilirubinBreakdown of RBCs

Unconjugated bilirubin

Bound to albumin (excess bilirubin gets freeCNS)

Conjugation (glucuryonyl transferase)

Enterohepaticcirculation

Excretion as urobilinogen & stercobilinogen

Deconjugation (glucuronidase)

Gut

• What’s the commonest cause of neonatal jaundice?

• What’s the most important cause of neonatal

jaundice?

Physiologic jaundicePhysiologic jaundice

M.Khashaba,MD professor of Pediatrics,Mansoura

Physiologic JaundicePhysiologic JaundicePhysiologic JaundicePhysiologic 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 JaundiceFactors Leading to Physiologic JaundiceFactors Leading to Physiologic JaundiceFactors Leading to Physiologic Jaundice

• Increase bili. Load:Increase bili. Load:

– Short life span of RBC.

– Large red cell mass.

– Deconjugation in the intestine.

• Decreased hepatic conjugation:Decreased hepatic conjugation:

– Relative lmmaturity of enzymes.

– Dehydration & hypocaloric intake.

M.Khashaba,MD professor of Pediatrics,Mansoura

Factors Exaggerating Physiologic JaundiceFactors 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 JaundiceCauses of Neonatal JaundiceCauses of Neonatal JaundiceCauses of Neonatal Jaundice

ed hemolysis

• Deficient conjugution (unconjugated hyperbili-

rubinemia).

excretion (conjugated hyperbilirubinemia).

M.Khashaba,MD professor of Pediatrics,Mansoura

Pathological HyperbilirubinemiaPathological HyperbilirubinemiaPathological HyperbilirubinemiaPathological Hyperbilirubinemia

Unconjugated Conjugated

Hemolysis:* Rh. incompatibility* ABO incompatibility* Heriditary hemolytic anemia* Infections* Extravasated blood* Polycythemia

conjugation:* Criggler Najjar syndrome* Inhibited enzyme:-Hypoxia-Acidosis-Hypothyroidism-Breast milk jaundice

M.Khashaba,MD professor of Pediatrics,Mansoura

Pathological HyperbilirubinemiaPathological HyperbilirubinemiaPathological HyperbilirubinemiaPathological HyperbilirubinemiaSuggestive criteria: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 ContinuePathological Hyperbilirubinemia Continue

Mg/dl

15

Seru

m b

ilirub

in

Day of life

2 4 6 8 10 12 14

Conjugated + prolonged jaundice

Physiological jaundice

Hemolysis

M.Khashaba,MD professor of Pediatrics,Mansoura

Persisting Prolonged JaundicePersisting Prolonged Jaundice• Unconjugated:

– Hypothyroidism.

– Pyloric stenosis.

– Breast milk jaundice.

– Griggler-Najjar syndrome.

• Conjugated

M.Khashaba,MD professor of Pediatrics,Mansoura

Conjugated hyperbilirubinemea Conjugated hyperbilirubinemea

• Pathological.

• Prompt diagnosis and referral to a specialized

center is needed.

M.Khashaba,MD professor of Pediatrics,Mansoura

Important causes for Conjugated Important causes for Conjugated HyperbilirubinemiaHyperbilirubinemia

1. Biliary atresia.

2. Neonatal hepatitis.

3. α1 Antitrypsin deficiency.

4. Inspissated bile syndrome

M.Khashaba,MD professor of Pediatrics,Mansoura

Breast Milk Jaundice Breast Milk Jaundice (Prolonged unconjugated hyperbilirubinemia)(Prolonged unconjugated hyperbilirubinemia)

Breast Milk Jaundice Breast Milk Jaundice (Prolonged unconjugated hyperbilirubinemia)(Prolonged unconjugated hyperbilirubinemia)

Theory:Theory:

• Breast milk contains substances which interfere with conjugation (Non esterified LCFA).

Value: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 jaundiceBreast 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 Prolonged unconjugated hyper bilirubinemia 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 Baseline Tests for Early Onset

Significant Jaundice 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 IncompatibilityRhesus IncompatibilityRhesus IncompatibilityRhesus 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. IncompatibilityManagement of Rh. IncompatibilityAntenatal ManagementAntenatal Management

Management of Rh. IncompatibilityManagement of Rh. IncompatibilityAntenatal ManagementAntenatal 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. IncompatibilityPostnatal Management

Management of Rh. IncompatibilityPostnatal Management

• Exchange transfusiona- 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 Differential Diagnosis of Neonatal Jaundice According to Time of AppearanceAccording to Time of Appearance

Differential Diagnosis of Neonatal Jaundice Differential Diagnosis of Neonatal Jaundice According to Time of AppearanceAccording 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 mother Group O women pass anti A or B Abs to her

fetus (A or B)

First baby usually not affected First baby may be affected

Increase severity of disease with successive

pregnancy

No relation between severity & birth order

Significant pallor Pallor is not usually present

Liver & spleen usually palpable Liver & spleen not usually palpable

Diagnosis:

* evidence of hemolytic anemia

* +ve Coomb’s test

* Mother Rh –ve, baby +ve

* Hb is usually normal

* Coomb’s test may be negative

* Mother group O, baby A or B

* Prevention anti D given to the mother.

* Blood for exchange Rh –ve blood, same

ABO group of baby

* No preventive measures

* O-blood same 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

KernicterusKernicterusKernicterusKernicterus

• 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 Cellular mechanisms of bilirubin neurotoxicityneurotoxicity

Injurious effect on:

1. Glucose utilization.

2. Oxidative phosphorylation .

3. 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-KernicterusPost-KernicterusPost-KernicterusPost-Kernicterus

• Mental retardation.

• C.P.

• Deafness.

M.Khashaba,MD professor of Pediatrics,Mansoura

Treatment of Unconjugated Treatment of Unconjugated Hyperbilirubinemia Hyperbilirubinemia

Treatment of Unconjugated Treatment of Unconjugated Hyperbilirubinemia 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