Subject:

Ch03: Neonatology — Preterm, Asphyxia, Jaundice

Preparatory Mindset

Neonatology covers the preterm infant, birth asphyxia (APGAR), and neonatal jaundice — three of the most examinable topics in paediatrics (18CM exam tested). The mindset:

The OSCE pattern: "is this jaundice physiological or pathological?", "does this newborn need phototherapy?" (bilirubin-for-age thresholds), and APGAR + neonatal resuscitation steps.


Core Concepts

1. The preterm infant

Definitions:

TermCriteria
Preterm<37 weeks completed gestation
Moderately preterm33-36 weeks
Very preterm<32 weeks
Extremely preterm<28 weeks
Low birth weight (LBW)<2500 g
Very low birth weight (VLBW)<1500 g
Extremely low birth weight (ELBW)<1000 g
SGABirth weight <10th percentile for GA

Risk factors: preterm labour, PPROM, multiple gestation, preeclampsia/placental insufficiency (SGA), cervical shortening, infection, previous preterm birth, maternal age, smoking.

Survival: improves with gestational age; extremely preterm (<28 wk) — high mortality and neurodisability even with NICU (survival by GA: ~50% at 24 wk, >90% by 30 wk in high-income settings).

Physical features: thin translucent skin, lanugo, decreased subcutaneous fat, soft ear cartilage, immature genitalia, sole creases (fewer with earlier GA), flexed vs extended posture.

Clinical hazards — the "systems at risk" (must know):

SystemComplication
RespiratoryRDS (surfactant deficiency), apnoea of prematurity, BPD (bronchopulmonary dysplasia), pneumothorax
GINEC (necrotising enterocolitis) — feed intolerance, bloody stool, pneumatosis intestinalis; feeding difficulties
NeurologicalIVH (intraventricular haemorrhage), PVL (periventricular leukomalacia), apnoea, poor temperature regulation
OcularROP (retinopathy of prematurity) — screening schedule by GA/weight; risk: oxygen, prematurity
MetabolicHypoglycaemia, hypocalcaemia, hypothermia (large surface area:weight), jaundice (immature liver)
ImmuneInfection/sepsis (immature immunity, invasive lines) — leading cause of death
HaematologicalAnaemia of prematurity, jaundice

Management principles:

  1. Thermal care — warm environment, skin-to-skin, incubator (avoid hypothermia).
  2. Respiratory support — antenatal corticosteroids (betamethasone) before preterm delivery reduce RDS; surfactant replacement; CPAP/ventilation as needed; oxygen targets (avoid hyperoxia → ROP).
  3. Feeding — early trophic feeds, breast milk (reduces NEC), fortification; total parenteral nutrition (TPN) if unable.
  4. Infection prevention — hand hygiene, antibiotics early if suspected.
  5. Screening — ROP, hearing, head USS (IVH), developmental follow-up.
  6. Kangaroo care, family-centred care.

2. Birth asphyxia and APGAR

APGAR score (at 1, 5, 10 min) — 0-2 each, total 10:

Sign012
Appearance (colour)Blue/paleBody pink, extremities blueCompletely pink
Pulse (HR)Absent<100>100
Grimace (response)No responseGrimaceCry/cough/sneeze
Activity (tone)FlaccidSome flexionActive
RespirationAbsentSlow, irregularStrong cry

Neonatal resuscitation (the NRP sequence): dry & warm → position → airway (suction) → breathing (PPV with bag-mask; oxygen per protocol) → circulation (chest compressions if HR <60 despite ventilation) → drugs (epinephrine) — the "ABC" ladder.

Hypoxic-ischaemic encephalopathy (HIE) staging (Sarnat):

StageFeatures
Mild (I)Hyperalert, normal tone, over-reactive; resolves in 24-48 h
Moderate (II)Lethargic, hypotonia, weak suck, seizures; needs treatment
Severe (III)Comatose, flaccid, absent reflexes, seizures; poor prognosis

Treatment: therapeutic hypothermia (cooling 33.5 °C × 72 h) for moderate-severe HIE (start within 6 h) — reduces death and disability; supportive (glucose, electrolytes, anticonvulsants for seizures, ventilation).

Sequelae: cerebral palsy, intellectual disability, epilepsy, sensorineural deafness — worse with severe HIE.

3. Neonatal jaundice

Definition: bilirubin >85 μmol/L (5 mg/dL) visible clinically. Physiological jaundice appears day 2-3, peaks day 4-5 (term), resolves by 2 weeks; unconjugated; mild.

Pathological jaundice (red flags):

Causes:

CategoryExamples
Increased productionHaemolysis (ABO/Rh incompatibility, G6PD deficiency, spherocytosis), bruising/cephalohematoma, polycythaemia
Decreased conjugationPhysiological (immature UGT), prematurity, breast milk jaundice (late, benign)
Decreased excretion (conjugated)Biliary atresia (urgent — Kasai), neonatal hepatitis, metabolic (galactosaemia)
SepsisAny newborn jaundice + ill → sepsis workup

The danger — kernicterus (bilirubin encephalopathy):

Investigations: total + direct bilirubin, FBC + blood film (haemolysis), blood group + DAT (Coombs), G6PD (Chinese/Mediterranean boys), reticulocyte count, sepsis screen if ill, urine reducing substances (galactosaemia), stool colour (biliary atresia).

Management:

TreatmentIndication/action
PhototherapyBlue-green light converts bilirubin to excretable photoisomers; threshold by bilirubin-for-gestational-age curves (hour-specific); monitor bilirubin q6-12 h; side effects — loose stools, rash, hyperthermia, dehydration
Exchange transfusionSevere/rapidly rising bilirubin above exchange threshold, or signs of bilirubin encephalopathy, or failed phototherapy; replaces sensitised RBCs + removes bilirubin/antibody
IVIGHaemolytic disease (Rh/ABO) with bilirubin approaching exchange level — reduces need for exchange
Treat causeSepsis (antibiotics), biliary atresia (Kasai portoenterostomy <60 days), galactosaemia (milk-free diet)
Breast milk jaundiceBenign late jaundice — continue breastfeeding, reassure

Preterm vs term infant — preterm features (translucent skin, lanugo, immature features) and the hazards of prematurity (RDS, NEC, IVH, ROP).

New Ballard score — assessment of gestational age in newborns by neuromuscular and physical maturity (used to confirm GA when dates unsure).

Neonatal jaundice — physiological (day 2-3, benign) vs pathological (early &lt;24 h, rapidly rising, conjugated, prolonged); phototherapy thresholds are bilirubin-for-age.


High-Yield Points

TopicMust-remember
Preterm<37 weeks; LBW <2500, VLBW <1500, ELBW <1000 g
RDSSurfactant deficiency — antenatal steroids + surfactant
NECFeed intolerance + bloody stool + pneumatosis; breast milk reduces risk
IVHIntraventricular haemorrhage — preterm; head USS screen
ROPRetinopathy of prematurity — oxygen-related; screening
HypothermiaLarge SA:weight — thermal care first
APGAR0-3 severe, 4-6 moderate, 7-10 normal; at 1/5/10 min
HIE treatmentTherapeutic hypothermia (moderate-severe, within 6 h)
HIE sequelaeCP, ID, epilepsy, deafness
Physiological jaundiceDay 2-3, peaks 4-5, resolves by 2 wk; unconjugated
Pathological red flags<24 h onset, rapid rise, too high for age, conjugated, prolonged
Kernicterus chronicAthetoid CP + sensorineural deafness
Biliary atresiaConjugated jaundice + pale stools — Kasai <60 days
PhototherapyBlue light; bilirubin-for-GA thresholds
Exchange transfusionSevere/encephalopathy/failed phototherapy
IVIGHaemolytic disease approaching exchange level
G6PDHaemolysis trigger — Chinese/Mediterranean boys

Topic Summary

Preterm infants (<37 wk) face RDS, NEC, IVH, ROP, hypothermia, hypoglycaemia, infection — managed with thermal care, respiratory support (steroids/surfactant), breast milk feeding, and screening. Birth asphyxia is assessed with APGAR; moderate-severe HIE is treated with therapeutic hypothermia (within 6 h), with long-term neurodevelopmental follow-up. Neonatal jaundice — physiological (day 2-3, benign) vs pathological (<24 h, rapidly rising, conjugated, prolonged); kernicterus (athetoid CP + deafness) is the preventable disaster — treat with phototherapy → exchange transfusion, investigate early jaundice (haemolysis, sepsis, biliary atresia).


LMCHK OSCE Practice — Newborn Jaundice Assessment

Station setup: A term newborn, born 30 hours ago by normal vaginal delivery (O-positive mother, A-positive baby), is noted to be deeply jaundiced. He is feeding poorly and lethargic. Bilirubin (18 h): total 280 μmol/L, direct 12 μmol/L; Hb 140 g/L; reticulocytes 8%; DAT (Coombs) positive.

Candidate tasks (8 min):

  1. Take a focused history (onset of jaundice, feeding, urine/stool colour, family history of G6PD/haemolysis).
  2. Recognise this as pathological early jaundice (<24 h onset, rapidly rising, ill baby) — likely ABO incompatibility haemolytic disease (A baby + O mother + positive DAT).
  3. Order urgent investigations: total + direct bilirubin, FBC + film, blood group + DAT, G6PD, reticulocytes, sepsis screen (ill baby), urine reducing substances.
  4. Plan immediate treatment: phototherapy now (bilirubin-for-age above threshold); IVIG (haemolytic disease approaching exchange level); exchange transfusion if bilirubin continues rising toward exchange threshold or signs of encephalopathy; monitor for kernicterus (lethargy, opisthotonos).
  5. Explain to parents: cause (blood group incompatibility), treatment, kernicterus risk, and follow-up (hearing, development).

Key marking cues: