PE19.1-17 | Neonatology — Practice Quiz

Score is 7: colour = 1 (blue extremities), HR = 2 (>100), reflex = 1 (grimace), tone = 1 (some flexion), respiration = 2 (cry). Total = 7.

APGAR has 5 parameters (Appearance/colour, Pulse/HR, Grimace/reflex, Activity/tone, Respiration), each 0–2, scored at 1 and 5 minutes. Do not confuse with Ballard score (gestational age) or Silverman-Anderson score (respiratory distress).

Score each APGAR parameter separately: colour (acrocyanosis=1), HR >100=2, grimace=1, some flexion=1, weak cry=2. Sum = 7. APGAR is scored at 1 and 5 minutes.

Ground-glass opacity with air bronchograms in a 32-week preterm is Respiratory Distress Syndrome (RDS) due to surfactant deficiency. Exogenous surfactant (beractant or poractant alfa) is the cornerstone of RDS management, alongside CPAP or mechanical ventilation.

RDS occurs in preterm neonates due to surfactant deficiency; CXR shows bilateral ground-glass opacity with air bronchograms. Treatment: exogenous surfactant + respiratory support. Antenatal corticosteroids (betamethasone) to the mother before 34 weeks reduce severity.

The X-ray picture of bilateral ground-glass with air bronchograms in a preterm neonate is classic for RDS/HMD (hyaline membrane disease) due to surfactant deficiency. Surfactant replacement is the primary treatment; antenatal corticosteroids given to the mother reduce incidence.

O-positive mother and A-positive baby with a positive direct Coombs test is the hallmark of ABO incompatibility — the most common cause of haemolytic jaundice in the newborn. It can occur in the first pregnancy and at 2 days of life.

Jaundice in the first 24 hours is always pathological. ABO incompatibility (mother O, baby A or B) is the commonest cause; positive direct Coombs test confirms immune haemolysis. Manage per AAP/NNF hour-specific nomogram; exchange transfusion if bilirubin approaches dangerous levels.

Jaundice in the first 24 hours is always pathological. ABO incompatibility (mother O, baby A or B) with positive direct Coombs test is haemolytic disease of the newborn. It appears early (day 1–2) and requires phototherapy or exchange transfusion based on the AAP/NNF nomogram.

Jitteriness, hypotonia, seizures with APGAR 5 at 5 min — features of moderate HIE, Sarnat grade II. The evidence-based window for therapeutic hypothermia (33–34°C, whole-body cooling for 72 hours) is within 6 hours of birth for term neonates ≥36 weeks.

HIE is staged by Sarnat criteria (Grades I–III). Therapeutic hypothermia (33–34°C for 72 hours) is the standard of care for moderate-severe HIE in term neonates ≥36 weeks, but MUST begin within 6 hours of birth. Seizures in HIE are managed with phenobarbitone as first-line.

Sarnat staging: Grade I = mild (hyperalert, sympathetic, no seizures); Grade II = moderate (lethargic, seizures, EEG abnormal); Grade III = severe (coma, no spontaneous activity, refractory seizures). Therapeutic hypothermia is effective only if started within 6 hours.

Classic early VKDB (formerly haemorrhagic disease of the newborn): day 2–7 of life, no vitamin K prophylaxis, bleeding from multiple sites, prolonged PT/APTT with normal platelets. Treatment: vitamin K 1 mg IM; severe bleeding may require FFP for immediate correction.

Vitamin K prophylaxis 1 mg IM at birth prevents VKDB. Early VKDB occurs at days 2–7; late VKDB at 2–12 weeks (associated with exclusive breastfeeding and fat malabsorption). Test: prolonged PT/APTT, normal platelet count. Always give vitamin K at birth per NRP.

VKDB (Vitamin K Deficiency Bleeding) is caused by inadequate vitamin K stores and immature vitamin-K-dependent factor synthesis. Without prophylactic vitamin K at birth, factors II, VII, IX, X are deficient → prolonged PT/APTT but normal platelets. Prevention: vitamin K 1 mg IM at birth per NRP protocol.

Kangaroo Mother Care (KMC) — skin-to-skin with mother — is the WHO-recommended standard for stable LBW/preterm neonates. It maintains temperature, promotes breastfeeding, and reduces mortality. Exclusive expressed breast milk feeding reduces sepsis risk.

KMC is skin-to-skin care between a stable LBW neonate and mother, ideally continuous. Benefits: thermal regulation, breastfeeding support, reduced infection, lower mortality. Weight criteria for LBW: <2500 g; very LBW <1500 g; extremely LBW <1000 g.

KMC (skin-to-skin between stable LBW baby and mother) is proven to reduce mortality, hypothermia, and infection. It should be initiated as soon as the neonate is stable. Expressed breast milk is the preferred feed for preterm neonates, delivered via nasogastric tube if sucking reflex is absent.

Neonatal hypoglycaemia is defined as blood glucose <45 mg/dL in symptomatic neonates. The correct treatment is 10% dextrose 2 mL/kg IV bolus, followed by a continuous infusion at a glucose infusion rate (GIR) of 6–8 mg/kg/min. This gives 200 mg/kg of glucose without the risk of rebound hypoglycaemia or vein damage from hypertonic solutions.

Neonatal hypoglycaemia is blood glucose <45 mg/dL. High-risk groups: IDM (infant of diabetic mother), LBW/preterm, macrosomic, asphyxiated, and polycythaemic neonates. Treatment: 10% dextrose 2 mL/kg IV bolus, then continuous infusion; monitor blood glucose every 30–60 min until stable.

Symptomatic neonatal hypoglycaemia (blood glucose <45 mg/dL) requires 10% dextrose 2 mL/kg IV bolus. Do not use 25% dextrose (too hypertonic, risks sclerosis); do not use oral glucose for a symptomatic neonate with poor feeding.

Per NRP/HBB: if HR <100 bpm after initial steps (dry, stimulate, position), begin PPV (bag-mask ventilation) immediately. PPV is the single most effective intervention in neonatal resuscitation. Chest compressions are indicated only if HR <60 bpm despite effective PPV (ratio 3:1).

The 'golden minute' in NRP: complete initial steps (dry, stimulate, suction if needed) and begin PPV within 1 minute for apnoeic neonates or HR <100 bpm. Compressions (3:1) start at HR <60 bpm despite PPV. Epinephrine (IV/IO) is the last resort.

NRP algorithm: initial steps (dry, stimulate) → PPV if HR <100 or apnoea → chest compressions only if HR <60 despite PPV (3:1 ratio) → epinephrine if HR <60 despite compressions. PPV precedes compressions; compressions precede epinephrine.

Late-onset neonatal sepsis (LOS, >72 hours) in hospitalised preterm neonates is dominated by Gram-positive organisms (coagulase-negative Staphylococcus, S. aureus) and Gram-negative bacilli (Klebsiella, E. coli, Pseudomonas). CoNS is the most common LOS organism in NICU settings due to central lines.

Neonatal sepsis: EOS <72 h (GBS, Listeria — maternally acquired); LOS >72 h (CoNS, Klebsiella, E. coli — hospital/community acquired). Empirical antibiotics for LOS in NICU: vancomycin (for CoNS/MRSA) + broad Gram-negative cover (aminoglycoside or 3rd-generation cephalosporin per local antibiogram).

Early-onset sepsis (EOS, <72 h) is caused by GBS and Listeria (maternally acquired). Late-onset sepsis (LOS, >72 h) is caused by hospital-acquired organisms: CoNS, S. aureus, Klebsiella, E. coli, Acinetobacter — especially in VLBW neonates with IV lines.

Breast milk jaundice peaks at 10–14 days and can persist 3–12 weeks in exclusively breastfed, otherwise well neonates. It is caused by glucuronidase and lipase in breast milk that increase enterohepatic circulation of bilirubin. Coombs negative, no haemolysis, conjugated bilirubin normal.

Breast milk jaundice is unconjugated hyperbilirubinaemia peaking at 2–3 weeks in well breastfed neonates. Investigate to exclude pathological causes. Most cases can be managed by continuing breastfeeding with monitoring; phototherapy is used if bilirubin approaches dangerous levels per the NNF nomogram.

Breastfeeding jaundice (early) is due to insufficient intake in days 2–5; breast milk jaundice (late) peaks at 2–3 weeks due to breast-milk constituents. Both have normal conjugated bilirubin (unconjugated hyperbilirubinaemia). Cholestasis would show elevated direct/conjugated bilirubin.