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Neonatal Jaundice (NNJ) : Approach

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Jaundice refers to accumulation of bilirubin in the epidermal tissues of the body, resulting in a yellowish tinge to the skin, sclera, and mucosa. Atleast 5 mg/dl of bilirubin level is required for clinically recognizing hyperbilirubinemia.

A) Physiological Neonatal Jaundice:

General consideration:

Causes:

  1. Bilirubin overproduction: Relative to adults, they have –
    • relative polycythemia at birth
    • relatively shorter life span of fetal red blood cells (~ 90 days)
  2. Slower excretion of bilirubin:
    • conjugation mechanism is not fully functional at birth (decreased UDPG-T activity)
    • increased enterohepatic recirculation (decreased stool output in the first few days of life and lack of normal gut flora in the neonatal intestines)
    • decreased uptake (lower levels of lignadins and decreased binding of ligandin) and decreased excretion by liver

B) Pathological Jaundice:

General consideration:

Causes:

  1. Bilirubin overproduction:
    • Hemolysis:
      • ABO incompatibility, Rh incompatibility
      • Congenital hemolytic disease: G6PD deficiency (more common in persons of Asian, African, or Mediterranean descent), RBC membrane defects such as spherocytosis
      • Acquired hemolysis: Sepsis, Vitamin K deficiency, Nitrofurantoin, Sulfonamides, Antimalarials, Penicillins
    • Extravasated blood: Petechiae, Cephalhematoma, Pulmonary/Cerebral/Occult hemorrhage
    • Polycythemia: Infant born to diabetic mothers, LGA, SGA, Delayed cord clamping
    • Increased enterohepatic circulation: Pyloric stenosis, Hirschprung disease, Meconium ileus, Intestinal atresia
  2. Bilirubin undersecretion:
    • Conjugation defect or delay: Criggler-Najar syndrome, Gilbert syndrome, Hypothyroidism, Prematurity, UDGP-T variant
    • Increased enterohepatic circulation: Inadequate breastfeeding (Breast feeding jaundice), Intestinal obstruction
    • Cholestatic jaundice: Biliary atresia, Dubin-Johnson and Rotor syndrome, Choledochal cyst, Cystic fibrosis, Alpha-1 antitrypsin deficiency

HISTORY FOR NEONATAL JAUNDICE

Mnemonics: DEFGhI

  1. Delivery complications:
    • Assisted delivery (forceps/vaccum)
    • Delayed cord clamping
  2. Ethnicity: African, Asian or Mediterranean
  3. Family history:
    • Anemia and jaundice: Spherocytosis, G6PD deficiency
    • Liver disease: Galactosemia, Gilbert disease
    • Sibling: Rh incompatibility
    • Blood group of mother and child
  4. Gestational history:
    • IUGR
    • Gestational Diabetes
    • TORCH infection
    • Maternal use of drugs like sulfonamides (displace bilirubin from albumin and also cause G6PD deficiency hemolysis)
  5. Input/Output:
    • Input: Poor feeding, Exclusive breast feeding
    • Output: Poor voiding/stooling ouptut, Color of urine and stool (dark urine and acholic stools in cholestatic jaundice)

Prolonged jaundice: If the jaundice persists beyond 2 weeks in term neonate and beyond 3 weeks in preterm neonate, the cause may be –

  1. Hypothyroidism
  2. Biliary atresia
  3. Hemolytic diseases
  4. Urinary tract infection

Difference between breast milk and breastfeeding jaundice:

  Breast milk jaundice Breast feeding jaundice
Onset and Duration Late onset and Prolonged (>3 wks) Early onset and resolve by 3 weeks
Incidence 2-4 % 12-13 %
Course By day 4, instead of usual fall in total serum bilirubin, it may continue to rise and may reach 20-30 mg/dl by 14 days of life. It falls rapidly in 48 hours if breast feeding is stopped. If breast feeding is continued, it stays elevated and slowly falls returning to normal by 4 to 12 weeks. It appears between 24-72 hours, peaks by 1-2 weeks and disappears by 3rd week.
Mechanism Unidentified factors in milk that inhibit bilirubin metabolism

 

Ingestion of Beta-glucuronidase of milk and increased enterohepatic circulation

 Decreased intake of milk leading to decreased gut motility and increased enterohepatic circulation

PHYSICAL EXAMINATION FOR NEONATAL JAUNDICE

  1. Small or large for gestational age (SGA, LGA)
  2. Preterm
  3. Excessive weight loss since birth
  4. Ruddiness
  5. Bruising or cephalohematomas
  6. Hepatosplenomegaly (as a sign of infection, hemolysis, or liver disease)
  7. Abdominal distention (as a sign of obstruction)
  8. Vital sign abnormalities (as a sign of infection)
  9. Omphalitis
  10. Chorioretinitis (TORCH infection)
  11. Signs of hypothyroidism

Bilirubin toxicity

2.5 mg of bilirubin will bind tightly with 1 gm of Albumin. Hence, the causes may be –

  1. Decreased binding of bilirubin to albumin: Prematurity, Free fatty acids, Drugs
  2. Blood brain barrier disruption: Hyperosmolarity, Anoxia, Hypercarbia, Prematurity

Levels of bilirubin toxicity:

1. Acute Bilirubin Encephalopathy:

a. Early phase: Hypotonia, Lethargy, High-pitched cry, Poor sucking

b. Intermediate phase: Hypertonia of extensor muscles (opisthotonus, rigidity, oculogyric crisis, retrocollis), Irritability, Fever, Seizures

c. Advance phase: Pronounced opisthotonus, shrill cry, apnea, seizures, coma and death

2. Chronic Bilirubin Encephalopathy (Kernicterus):

APPROACH TO MANAGEMENT OF NEONATAL JAUNDICE

 

A. Investigations:

1. Total serum bilirubin (TSB):

Indications are:

2. If bilirubin is > 12 mg/dl and infant is < 24 hours or Mother belongs to Rh-ve blood group:

3. Direct bilirubin level:

4. Hematocrit:

5. Investigations for cholestatic jaundice:

B. Treatment of Unconjugated Neonatal Jaundice:

1. General measures:

2. Infants with hemolytic disease (including Rh incompatibility):

3. Healthy late-preterm and term infants:

Perform visual assessment of jaundice every 12 hourly during initial 3 to 5 days supplemented by Transcutaneous bilirubinometer (TcB) if available. In infants more than 35 weeks gestation, this level should be plotted on an age-specific nomogram to determine the risk level.

Step 1: Does the baby have serious jaundice ?

Step 2: If any of the above is present:

Step 3: If none of the above is present, continue observation every 12 hours

4. Premature infants: Start phototherapy and exchange transfusion at following levels

Weight Phototherapy Exchange transfusion
<1000 gm Within 24 hours 10-12 mg/dl
1000-1500 gm 7-9 mg/dl 13-15 mg/dl
1500-2000 gm 10-12 mg/dl 15-18 mg/dl
2000-2500 gm 13-15 mg/dl 18-20 mg/dl

C. Treatment of Conjugated Neonatal Jaundice:

The stepwise approach to the diagnosis of biliary atresia entails a percutaneous liver biopsy and surgical intervention. If the liver histology is consistent with the diagnosis of biliary atresia, then the surgeon will perform an intraoperative cholangiogram. Intraoperative cholangiogram is considered the gold standard in the diagnosis of biliary atresia, and if the diagnosis is confirmed, the surgeon will proceed with the Kasai portoenterostomy.

PHOTOTHERAPY

1. Mechanism of Action:

2. Indications:

3. Contraindications:

4. Technique:

5. Adverse effects of phototherapy:

  1. Insensible water loss
  2. Watery diarrhea and increased fetal water loss
  3. Hypocalcemia
  4. Tanning
  5. Bronze baby syndrome
  6. Upsets maternal-infant interactions

EXCHANGE TRANSFUSIONS

1. Mechanism of Action: Removes partially hemolyzed and Antibody-coated RBCs as well as unattached Antibodies and replaces with donor RBCs without sensitizing antigen. With half hour, bilirubin levels return to 60% of pre-exchange level.

2. Indications:

3. Blood:

4. Technique:

4. Complications:

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