Causes of neonatal jaundice

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"neonatal jaundice" causes

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Causes of Neonatal Jaundice

Neonatal jaundice (hyperbilirubinemia) is the yellow discoloration of skin and sclera caused by elevated bilirubin. It becomes clinically visible when total bilirubin exceeds ~5 mg/dL. Nearly every newborn develops some degree of unconjugated hyperbilirubinemia in the first week of life due to three physiologic factors: (1) increased bilirubin production, (2) decreased hepatic clearance/conjugation, and (3) increased enterohepatic resorption.

The first and most important distinction is unconjugated vs. conjugated hyperbilirubinemia. Conjugated hyperbilirubinemia in a neonate is always pathologic.

Unconjugated (Indirect) Hyperbilirubinemia

1. Physiologic / Benign

Cause	Key Features
Physiologic jaundice of the newborn	~50% of normal newborns; appears days 2-3, peaks days 4-5, resolves by 2 weeks; rarely rises >5 mg/dL/day
Breast milk jaundice	2nd most common cause; peaks later than physiologic jaundice; may persist weeks to months; mechanism uncertain - possibly hormonally mediated or increased enterohepatic circulation of bilirubin

2. Hemolysis

Cause	Notes
ABO incompatibility	Most common isoimmune cause; presents <24 hours
Rh (D) incompatibility	Can be severe; presents <24 hours
G6PD deficiency	X-linked; important cause especially in certain ethnic groups
Hereditary spherocytosis / elliptocytosis	Red cell membrane defects
Sickle cell anemia / thalassemia	Hemoglobinopathies
Pyruvate kinase deficiency	Red cell enzyme defect
Birth trauma hematomas	Cephalhematoma, intracranial/intraventricular hemorrhage - physiologic breakdown of extra blood load
Polycythemia	Increased red cell mass → increased bilirubin load

3. Infection

Sepsis (bacterial)
Urinary tract infection
TORCH infections (Toxoplasmosis, Rubella, CMV, Herpes, Syphilis) - can cause both conjugated and unconjugated

4. Obstruction (increased enterohepatic circulation)

Hirschsprung disease
Meconium ileus
Duodenal atresia
Pyloric stenosis (presents >1 week)

5. Metabolic / Genetic

Cause	Mechanism
Crigler-Najjar syndrome	Congenital absence or deficiency of glucuronyl transferase (UGT1A1)
Gilbert syndrome	Mild reduction in UGT1A1; benign
Galactosemia	Also causes conjugated jaundice
Congenital hypothyroidism	Prolonged jaundice; always screen

Conjugated (Direct) Hyperbilirubinemia

Always pathologic. Causes include:

Biliary / Structural

Biliary atresia - progressive jaundice with dark urine and acholic (pale) stools; age-sensitive - Kasai procedure must be done early
Choledochal cyst
Alagille syndrome (bile duct paucity)
Bile duct strictures / inspissated bile syndrome
Byler disease (progressive familial intrahepatic cholestasis)
Congenital hepatic fibrosis

Infectious

Neonatal hepatitis (idiopathic or viral)
TORCH infections (CMV, rubella, toxoplasmosis, syphilis, HSV)
Gram-negative sepsis / listeriosis / tuberculosis
Hepatitis B, HIV, echovirus, coxsackievirus

Metabolic / Genetic (conjugated predominant)

Condition	Note
α1-Antitrypsin deficiency	Common genetic cause of neonatal liver disease
Galactosemia	Galactose-1-phosphate accumulation
Tyrosinemia	Liver dysfunction
Glycogen storage disease type IV
Niemann-Pick / Gaucher / Wolman disease	Lysosomal storage disorders
Cystic fibrosis	Inspissated secretions
Zellweger syndrome	Peroxisomal disorder
Dubin-Johnson / Rotor syndrome	Defects in bilirubin transport
Neonatal hypopituitarism

Other

Parenteral nutrition (TPN) - prolonged use causes cholestasis
Drugs/toxins

Timing as a Diagnostic Clue

Onset	Likely Cause
<24 hours	Hemolysis (ABO/Rh incompatibility), TORCH infections, birth trauma hematoma, sepsis
Days 2-3	Physiologic jaundice
Days 3-7	Infection (sepsis, UTI), Crigler-Najjar/Gilbert syndrome, TORCH
>1 week	Breast milk jaundice, biliary atresia, hepatitis, hypothyroidism, metabolic disorders (galactosemia), red cell enzyme/membrane defects, pyloric stenosis

Key Complications

Kernicterus: unconjugated bilirubin crosses the blood-brain barrier at levels >20-25 mg/dL, causing bilirubin-induced neurologic dysfunction (BIND). Chronic irreversible damage = kernicterus. Most common causes of severe hyperbilirubinemia are hemolytic disease of the fetus/newborn (HDFN) and sepsis.

Sources: Rosen's Emergency Medicine, 9th Ed., p. 3225-3226; Tintinalli's Emergency Medicine, Table 116-7; Quick Compendium of Clinical Pathology, 5th Ed., Table 1.5

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Summary of All Answers

Section 1:

Q1 (10 marks): Both options answered - RDS (causes of respiratory distress + etiology/pathophysiology/management of RDS in preterm) AND Neonatal Jaundice (causes + pathophysiology of physiological jaundice + treatment modalities including phototherapy, exchange transfusion, pharmacological)
Q2 (6 marks each): Rickets X-ray features & treatment | Hepatitis A diagnosis/investigations/management | WHO xerophthalmia staging + NPCB Vitamin A schedule
Q3 (6 marks each): Neonatal hypoglycemia | Breastfeeding counselling (antenatal + postnatal) | Adolescence & health problems | Tanner staging in females
Q4 (2 marks each): Microcephaly | Moro reflex | Red flags in development | Rotavirus vaccine | Age-independent anthropometric parameters | High anion gap acidosis causes

Section 2:

Q5 (10 marks): Developmental principles + detailed milestone table (gross motor, fine motor, language, social up to 2 years) | SAM definition + PEM classification + WHO 10-step management + prevention
Q6 (6 marks each): Severe dehydration classification + WHO Plan C fluid management | Fever+splenomegaly differentials + Malaria investigations/treatment | Catch-up immunization at 9 months + AEFI classification
Q7 (6 marks each): Measles clinical features + complications | Dengue phases + warning signs + DSS management | Toddler behavioural problems + PICA | Childhood TB clinical features + diagnostic approach
Q8 (2 marks each): Zinc deficiency | Caput vs Cephalohematoma | JSSK entitlements | Hyperkalemia ECG changes | BMI | Neonatal Mortality Rate

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