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Neonatal Hyperbilirubinemia

  1. Physiological Jaundice:
    1. Appears after 30 hrs of life(30-72 hrs) Q
    2. Term- Peak 3-4 days (12mg) - (N) 7-10 days Q
    3. Preterm - Peak 5-7 days (15mg) - (N) 10-14 da Q ys
  2. Pathological jaundice;
    1. Appearing in 1st 24 hrs of life
    2. >0.2 mg/dl/hr of Serum Bilirubin
    3. Direct bilirubin > 2.0 mg% or >15% of total serum bilirubin (TSB)
    4. Jaundice persisting for >14 days in preterm & >8 days in term.
    5. Hyperbilirubinemia in the phototherapy range.
Unconjugated hyperbilirubinemia Conjugated hyperbilirubinemia

i. Immaturity
ii. Hemolytic diseases
iii. (Rh ,ABO, G6PD Def)

​iv. Breast milk jaundice
v. Hypothyroidism
vi. Pyloric stenosis
vii. Crigler-Najjar syndrome
viii. Gilbert syndrome
ix. Sepsis
x. Concealed hemorrhage
xi. Drugs (NovoBiocin taken by mother)

i. Idiopathic neonatal hepatitis
ii. Hepatitis

iii. Biliary Atresia
iv. Bile duct malformations

v. Intrauterine infections
vi. Hypothyroidism

vii. Galactosemia
viii. Alpba-I -antitrypsin deficiency

ix. Cystic Fibrosis
x. TPN



Neonantal hepatitis-: MC form of cholestatic jaundice



Neonatal Hepatitis



Most common: Idiopathic

Multiple etiologies like Intrauterine infections, Viral infections, Sepsis, Storage disorders

Congenital Malformation


Often SGA, Growth retarded & have increased association with infections & genetic abnormalities

Often Full term, AGA, Look apparently healthy except for jaundice


Variable color

Always Acholic / Pale / Clay / Chalky


Variable color

Always dark color urine staining nappies

UBG in urine




Poor uptake, normal secretion of dye into gut

No secretion of dye into Gut

Liver Biopsy

Alteration of lobular architecture, Focal hepato-cellular necrosis, Giant cells frequent with ballooning of their cytoplasm

Ductular proliferation & fibrosis, Giant cells infrequent


Underlying causes

Kasai’s porto-enterostomy usually before 60 days (2 months) of life to reestablish the biliary flow into gut

  1. Pathological
    • Hemolytic diseases
    • Hypothyroid disease
    • Septicemia
    • Crigler Najjar Syndrome
    • Gilbert syndrome
    • Pyloric stenosis
    • Drugs (eg Novobiocin taken by mother)

Breast Feeding Jaundice


Early onset, due to inadequate feeding leads to increased enterohepatic circulation and thus increased bilirubin levels


Breast-milk jaundice:

  • Those who are exclusively breast fed.
  1. It is late onset. Occur in term infants, in 2-4% cases.
  2. Present by D4. Instead of fall, bilirulin continues to rise and may reach 20-30 mg% by 14 days of age. Then it falls. If breast feeding is stopped bilirubin level falls rapidly.
  3. Recurrence late is 70% in future pregnancy.
  1. Mechanism: Not known. But it may be due to:
    1. Unidentified factors (3-α, 20-beta pregnandiol and free FA) in breast milk interfering with bilirubin metabolism, is thought to be causative agent.
    2. Increased enterohepatic circulation in breast fed infants. Because they ingest β- glucoronidase (this enzyme convert conjugated Bilirubin to unconjugated bilirubin) present in breast milk.
    3. Colonization of gut is also delayed.
    4. Intestinal bacteria can prevent enterohepatic circulation of bilirubin by converting Conjugated Bilirubin to urobilinoids, which are not substrates for β-glucoronidase.

Causes of Jaundice in first 24 hours: Q

  1. F- Feto maternal blood group incompatibility (Rh. ABO) (Most common cause)
  2. I- Intrauterine infection
  3. R- RBC enzyme defect
  4. S- Spherocytosis
  5. T- α- Thalassemia
  6. Crigler- Najjar syndrome
  7. Lucey Driscoll syndrome

Management of hyperbilirubinemia in the healthy term newborn Q

  1. Now based on hour Specific bilirubin charts Q
  2. Prepared by Dr. V. K. Bhutani Q

Management of hyperbilirubinemia in the pre term new born

  1. Drugs Phenobarbitone, Agar , Tin metalloporphyrin
  2. Phototherapy
  3. Exchange transfusion

Photo –Therapy :


Mechanism of action


  1. Structured Isomerization : Bilirubin Lumirubin; Irreversible reaction; most important mechanism for bilirubin clearance in phototherapy.
  2. Photoisomerization
  3. Photo-oxidation Q
  4. Special blue lamp with 425-475 nm wavelength Q
  5. Dose: 6-12 μ ïw/cm2 /nm Q

Side Effects of Photo Rx Q

  1. Bronze body syndrome
  2. Hypolekemia
  3. Retinal damage
  4. Watery diarroheav. Transsible water loss

Pharmacotherapy Q

  1. Phenobarbitone
  2. Agar
  3. Metalloprotoporphyrins- Tin and Zinc (act by inhibiting heme oxygenase)

Exchange Transfusion


Double volume (160 ml / kg) Q



87% of infants blood is replaced


Complications of DVET

  1. Hyperkalemia
  2. Acid base imbalance – citrate is metabolized to alkali – metab alkalosis
  3. Infections – hiv, hbv, hcv and bacterial sepsis, nec
  4. Bleeding –d/t thrombocytopenia and deficient clotting factors
  5. Cardiovascular complications e.g. –umbilical vein or portal vein perforation, thrombosis, embolism, arrhythmias etc.
  6. Graft vs host disease
  7. Hypothermia/hyperthermia/nec

Rh Incompatibility

  1. Mother is Rh negative and fetus Rh positive
  2. The anti D antibodies - IgG type are formed
  3. Which cross over to the fetus and destroy Rh positive fetal blood cells.
  4. Concomitants fetomaternal ABO incompatibility-some protection
  5. First baby is usually not affected

Abo Hemolytic Disease Of The Newborn.


Type A or B infants


Type O mothers


Mother make anti A or anti B antibodies of the IgG class


Type A or B mother  antibodies of the IgM class which do not cross placenta.

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