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Neonatal Jaundice: Notes, PPT and PYQs for MBBS

Neonatal jaundice is yellow discolouration of a newborn's skin and eyes caused by raised serum bilirubin. It is very common and usually physiological, but pathological jaundice can lead to bilirubin encephalopathy and kernicterus if missed. It is a core Final Year Paediatrics topic, with links to Physiology, Biochemistry and Obstetrics.

SME-reviewed. Updated 2026.
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Quick Summary: What You Need to Know for University Exams

  • Jaundice becomes visible in newborns at a serum bilirubin of about 5 mg/dL.
  • Physiological jaundice appears after 24 hours, peaks around days 3 to 5 in term babies and settles within about 2 weeks.
  • Jaundice within the first 24 hours is always pathological.
  • Important causes: Rh and ABO haemolytic disease, G6PD deficiency, sepsis, and conjugated causes such as biliary atresia.
  • Phototherapy is the main treatment; exchange transfusion is used for severe or rapidly rising bilirubin.
  • Untreated severe unconjugated hyperbilirubinaemia can cause kernicterus.
  • Pale stools with dark urine point to conjugated jaundice and need urgent evaluation for biliary atresia.

Neonatal Jaundice Across MBBS Subjects

MBBS Year

1st Year

What Is Usually Asked

Bilirubin metabolism, conjugation, Crigler-Najjar and Gilbert syndromes

MBBS Year

1st Year

Subject

Physiology

What Is Usually Asked

Fetal and neonatal red cells

MBBS Year

2nd Year

Subject

Pathology

What Is Usually Asked

Haemolytic disease of the newborn

MBBS Year

Final Year

What Is Usually Asked

Physiological versus pathological jaundice, evaluation, phototherapy, exchange transfusion

Definition and Classification

Definition: Neonatal jaundice is yellowish discolouration of the skin and sclera in a newborn due to raised serum bilirubin (hyperbilirubinaemia).

Physiological Versus Pathological Jaundice

Feature

Onset

Physiological

After 24 hours

Pathological

Within the first 24 hours, or any time with worrying features

Feature

Peak (term baby)

Physiological

Around days 3 to 5

Pathological

Variable

Feature

Duration

Physiological

Resolves within about 2 weeks in term babies (longer in preterm babies)

Pathological

Persists beyond 2 weeks in term or 3 weeks in preterm babies

Feature

Rate of rise

Physiological

Slow

Pathological

Rapid (more than about 5 mg/dL per day)

Feature

Bilirubin level

Physiological

Below phototherapy thresholds

Pathological

Above age-specific phototherapy thresholds

Feature

Conjugated bilirubin

Physiological

Not raised

Pathological

May be raised (any significant rise is pathological)

Feature

Baby's condition

Physiological

Well

Pathological

May be unwell, lethargic or feeding poorly

Aetiology (Causes)

Unconjugated Hyperbilirubinaemia

Category

Physiological

Causes

Normal newborn adaptation

Category

Haemolytic

Causes

Rh isoimmunisation, ABO incompatibility (typically mother group O, baby group A or B), G6PD deficiency, hereditary spherocytosis

Category

Increased red cell breakdown

Causes

Cephalhaematoma, bruising, polycythaemia

Category

Infection

Causes

Neonatal sepsis

Category

Feeding-related

Causes

Breastfeeding (suboptimal intake) jaundice in the first week; breast milk jaundice later, peaking in the second or third week

Category

Endocrine and genetic

Causes

Hypothyroidism (prolonged jaundice), Crigler-Najjar syndrome, Gilbert syndrome

Category

Others

Causes

Intestinal obstruction, maternal diabetes, prematurity

Conjugated Hyperbilirubinaemia (Always Pathological)

  • Biliary atresia
  • Neonatal hepatitis
  • Congenital infections (TORCH)
  • Choledochal cyst
  • Metabolic disorders such as galactosaemia
  • Sepsis and prolonged parenteral nutrition

Pathophysiology

Why Newborns Develop Jaundice (Physiological Mechanisms)

  1. Increased bilirubin production: Newborns have a high red cell mass, and fetal red cells have a shorter lifespan
  2. Reduced uptake: Lower levels of the liver binding protein (ligandin)
  3. Reduced conjugation: Immature activity of the liver enzyme UDP-glucuronyl transferase
  4. Increased enterohepatic circulation: Gut enzymes deconjugate bilirubin, which is then reabsorbed

Bilirubin Encephalopathy

  1. Very high unconjugated bilirubin exceeds the binding capacity of albumin
  2. Free unconjugated bilirubin, which is lipid-soluble, crosses the blood-brain barrier
  3. It deposits in the basal ganglia (especially the globus pallidus), hippocampus, brainstem nuclei and cerebellum
  4. This causes neuronal injury (bilirubin encephalopathy) and, if permanent, kernicterus

Risk factors for brain injury: prematurity, haemolysis, sepsis, acidosis, hypoalbuminaemia and drugs that displace bilirubin from albumin.

(Examiner may ask you to draw the bilirubin metabolism pathway.)


Clinical Features

  • Yellow skin and sclera, progressing from the head downwards (cephalocaudal progression)
  • Dark urine and pale stools in conjugated jaundice
  • Pallor, hepatosplenomegaly or hydrops in haemolytic disease
  • Lethargy, poor feeding or temperature instability in sepsis

Kramer's Rule (Clinical Estimate)

Zone

1

Area

Head and neck

Approximate Bilirubin (mg/dL)

About 4 to 8

Zone

2

Area

Upper trunk to umbilicus

Approximate Bilirubin (mg/dL)

About 5 to 12

Zone

3

Area

Lower trunk and thighs

Approximate Bilirubin (mg/dL)

About 8 to 16

Zone

4

Area

Arms and legs below knees

Approximate Bilirubin (mg/dL)

About 11 to 18

Zone

5

Area

Palms and soles

Approximate Bilirubin (mg/dL)

Above 15

Kramer's rule is only a rough guide. Always confirm with transcutaneous or serum bilirubin measurement.

Acute Bilirubin Encephalopathy

Phase

Early

Features

Lethargy, hypotonia, poor suck

Phase

Intermediate

Features

Irritability, high-pitched cry, hypertonia, arching of the neck (retrocollis) and back (opisthotonus), fever

Phase

Advanced

Features

Deep stupor or coma, seizures, apnoea

Kernicterus (Chronic Bilirubin Encephalopathy)

  • Choreoathetoid cerebral palsy
  • Sensorineural hearing loss
  • Upward gaze palsy
  • Dental enamel defects
  • Intellectual disability in some children

Diagnosis

Investigation

Total serum bilirubin with direct (conjugated) fraction

Purpose

Confirms level and type

Investigation

Transcutaneous bilirubin

Purpose

Non-invasive screening

Investigation

Maternal and baby blood group and Rh type

Purpose

Suspected Rh or ABO incompatibility

Investigation

Direct Coombs test

Purpose

Immune haemolysis

Investigation

Haemoglobin, haematocrit, reticulocyte count, peripheral smear

Purpose

Haemolysis, spherocytes, polycythaemia

Investigation

G6PD assay

Purpose

G6PD deficiency

Investigation

Sepsis screen

Purpose

Suspected infection

Investigation

Thyroid function

Purpose

Prolonged jaundice

Investigation

Liver function tests, ultrasound, hepatobiliary scan

Purpose

Conjugated jaundice, suspected biliary atresia

Hour-specific bilirubin nomograms (such as the Bhutani nomogram and current American Academy of Pediatrics thresholds) are used to decide the need for phototherapy based on the baby's age in hours, gestational age and risk factors.


Management

General Measures

  1. Encourage frequent, effective breastfeeding
  2. Identify and treat the underlying cause
  3. Monitor bilirubin and the baby's clinical condition
  4. Check for danger signs of bilirubin encephalopathy

Phototherapy

Aspect

Mechanism

Key Points

Blue-green light (about 460 to 490 nm) converts bilirubin into water-soluble isomers, including lumirubin, which are excreted in bile and urine without conjugation

Aspect

Indication

Key Points

Bilirubin above the age-specific threshold for gestation and risk

Aspect

Care during phototherapy

Key Points

Eye shields, maximum skin exposure, regular turning, temperature and hydration monitoring, continued feeding

Aspect

Side effects

Key Points

Dehydration, loose stools, skin rash, temperature instability, bronze baby syndrome in babies with conjugated hyperbilirubinaemia

Exchange Transfusion

  • Used for very high or rapidly rising bilirubin despite phototherapy, or with signs of bilirubin encephalopathy
  • A double-volume exchange removes bilirubin and antibody-coated red cells and corrects anaemia
  • Complications include infection, electrolyte imbalance, thrombosis and cardiac arrhythmias

Other Treatments

  • Intravenous immunoglobulin in immune haemolytic disease (Rh or ABO) to reduce the need for exchange transfusion
  • Biliary atresia: early Kasai portoenterostomy gives the best results; later cases may need liver transplantation

Complications

  • Acute bilirubin encephalopathy
  • Kernicterus with permanent neurological damage
  • Sensorineural hearing loss
  • Complications of exchange transfusion
  • Liver cirrhosis in untreated biliary atresia

Prevention

  • Anti-D immunoglobulin for Rh-negative mothers, given antenatally and after delivery of an Rh-positive baby, to prevent Rh isoimmunisation
  • Blood grouping in pregnancy
  • Early and frequent breastfeeding
  • Bilirubin screening before discharge and follow-up of babies discharged early
  • Awareness of the "stool colour card" to detect pale stools early

Prognosis

Physiological jaundice resolves without harm. Pathological jaundice has an excellent outcome when detected and treated early. Kernicterus is permanent, so prevention through timely screening and treatment is essential.


Quick Viva Questions

Q: At what serum bilirubin level does jaundice become visible in newborns? A: About 5 mg/dL.

Q: When is neonatal jaundice always pathological? A: When it appears within the first 24 hours of life.

Q: How does phototherapy work? A: It converts bilirubin into water-soluble isomers, such as lumirubin, which are excreted without needing conjugation.

Q: Which part of the brain is most affected in kernicterus? A: The basal ganglia, especially the globus pallidus.

Q: What stool colour suggests biliary atresia? A: Pale or clay-coloured stools, with dark urine.

Q: What is the typical blood group combination in ABO incompatibility? A: Mother group O with baby group A or B.


How Neonatal Jaundice Appears in MBBS University Exams

Typical question styles (not attributed to specific papers or years):

  1. "Differentiate physiological from pathological jaundice. Discuss the approach to a newborn with jaundice." (Long essay, Paediatrics)
  2. "Discuss the causes and management of neonatal hyperbilirubinaemia." (Long essay)
  3. "Write a short note on phototherapy." (Short note)
  4. "Write a short note on kernicterus." (Short note)
  5. "Write a short note on Rh isoimmunisation and its prevention." (Short note, Obstetrics)
  6. "Write a short note on exchange transfusion." (Short note)

Frequently Asked Questions

What is the difference between physiological and pathological neonatal jaundice?

Physiological jaundice appears after 24 hours, peaks around days 3 to 5 in term babies and resolves within about 2 weeks. Pathological jaundice appears in the first 24 hours, rises rapidly, exceeds phototherapy thresholds, persists or involves raised conjugated bilirubin.

What is the difference between breastfeeding jaundice and breast milk jaundice?

Breastfeeding jaundice occurs in the first week because of inadequate milk intake. Breast milk jaundice appears later and peaks in the second or third week in a well, thriving baby.

Can I download the neonatal jaundice PPT for my presentation?

Yes. Use the Download PPT button at the top of this page. The GeckoMed app also gives offline access to the slides and notes.

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