Neonatology questions that can be asked for my interview as pediatric SR

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High-Yield Neonatology Q&A — Pediatric SR Interview

1. NEONATAL RESPIRATORY DISTRESS SYNDROME (RDS / HMD)

Q1. What is the pathophysiology of neonatal RDS?

A: RDS (Hyaline Membrane Disease) results from a deficiency of surfactant in premature lungs. Surfactant (mainly dipalmitoyl phosphatidylcholine + surfactant proteins SP-A, SP-B, SP-C, SP-D) normally reduces alveolar surface tension. Its deficiency leads to:

Alveolar collapse (atelectasis) at end-expiration
Protein-rich fluid transudation forming hyaline membranes
Hypoxia → pulmonary vasoconstriction → right-to-left shunting → worsening hypoxia

Surfactant production begins ~24 weeks, matures by ~34–36 weeks. — Robbins Basic Pathology; Murray & Nadel's Respiratory Medicine

Q2. What are the risk factors for RDS?

Prematurity (most important — <34 weeks)
Male sex
Maternal diabetes (insulin inhibits surfactant synthesis)
Caesarean section without labour (labour stimulates surfactant release)
Second twin
Perinatal asphyxia
Protective factors: Prolonged ROM, maternal hypertension, antenatal corticosteroids, female sex, African-American race

Q3. How does antenatal corticosteroid therapy work in RDS?

A: Betamethasone (12 mg IM × 2 doses, 24 hours apart) or Dexamethasone given to the mother at 24–34 weeks gestation:

Accelerates surfactant synthesis by inducing type II pneumocyte maturation
Reduces RDS incidence by ~50%
Also reduces IVH, NEC, and overall neonatal mortality
Optimal benefit when given >24h and <7 days before delivery

Q4. What are the criteria for surfactant therapy? Name the types.

Prophylactic surfactant: Given in delivery room to infants <27 weeks (before first breath/within 15 min)
Rescue/therapeutic surfactant: FiO₂ >0.30–0.40 on CPAP, or requiring mechanical ventilation

Types:

Type	Example
Natural/animal-derived	Poractant alfa (Curosurf), Beractant (Survanta), Calfactant (Infasurf)
Synthetic	Lucinactant (contains SP-B analogue)

Preferred: Natural surfactants (faster response, lower dose needed) Route: Intratracheal instillation (INSURE technique — Intubate–Surfactant–Extubate to CPAP)

Q5. What are the X-ray findings in RDS?

Ground-glass (reticulogranular) opacity — diffuse, bilateral
Air bronchograms (air-filled bronchi visible against opaque lung)
Low lung volumes
In severe cases: whiteout lung

2. NEONATAL JAUNDICE & HYPERBILIRUBINEMIA

Q6. What is physiologic jaundice? How does it differ from pathological jaundice?

Feature	Physiologic	Pathological
Onset	>24 hours	<24 hours
Duration	Resolves by day 7 (term), day 14 (preterm)	Persists >2 weeks (term)
TSB rise	<5 mg/dL/day	>5 mg/dL/day
Conjugated bilirubin	<20% of total	May be elevated
Cause	Hemolysis + immature UGT enzyme	Hemolysis, sepsis, metabolic, biliary atresia

Mechanism of physiologic jaundice: accelerated hemolysis of fetal Hb + immature hepatic bilirubin glucuronosyltransferase (B-UGT) + reduced UDP-glucuronate synthesis — Harper's Illustrated Biochemistry; Sleisenger & Fordtran's GI & Liver Disease

Q7. What is kernicterus? What bilirubin level is dangerous?

A: Kernicterus is bilirubin-induced neurologic dysfunction (BIND) caused by unconjugated bilirubin crossing the blood-brain barrier and depositing in basal ganglia, hippocampus, and brainstem nuclei.

Clinical features:

Acute: Hypotonia → hypertonia, high-pitched cry, opisthotonus, seizures, sunset sign
Chronic: Choreoathetosis, hearing loss (sensorineural), dental enamel hypoplasia, upward gaze palsy, intellectual disability

Risk threshold: Generally >20–25 mg/dL in term infants; lower in preterm, sick, or hypoalbuminemic infants (bilirubin/albumin ratio matters)

— Goldman-Cecil Medicine; Medical Physiology (Boron & Boulpaep)

Q8. How does phototherapy work?

A: Phototherapy converts unconjugated (fat-soluble) bilirubin into:

Photoisomers (configurational & structural isomers — lumirubin) — water-soluble, excreted in bile and urine without conjugation
Optimal wavelength: 460–490 nm (blue-green light)
Factors increasing efficacy: Irradiance ≥30 µW/cm²/nm, surface area exposure, distance from light source

Q9. Indications for exchange transfusion?

TSB rising despite intensive phototherapy
TSB at exchange threshold per AAP nomogram (based on gestational age + risk factors)
Signs of acute bilirubin encephalopathy at any TSB
Hydrops fetalis with severe hemolytic disease
Double volume exchange transfusion (160 mL/kg) via umbilical vein — removes ~85% of sensitized RBCs and ~50% of bilirubin

Q10. Causes of conjugated hyperbilirubinemia (direct > 2 mg/dL or >20% of total)?

Biliary atresia (most important surgical cause — presents at 2–6 weeks)
Neonatal hepatitis (idiopathic, CMV, rubella, toxoplasma, HBV)
Choledochal cyst
Alagille syndrome
Alpha-1 antitrypsin deficiency
Galactosemia, tyrosinemia
CF, parenteral nutrition cholestasis
Sepsis

Key investigation: Abdominal USS, HIDA scan (no hepatic uptake in biliary atresia), liver biopsy Management of biliary atresia: Kasai portoenterostomy (before 60 days — best outcomes)

3. BIRTH ASPHYXIA & HIE

Q11. Define perinatal asphyxia and HIE. What is the Sarnat grading?

A: Perinatal asphyxia: failure of gas exchange at birth → hypoxia + hypercapnia + metabolic acidosis (pH <7.0, base deficit >12 mmol/L, Apgar <5 at 5 min, need for resuscitation)

Hypoxic Ischemic Encephalopathy (HIE) — Sarnat Grading:

Grade	Clinical Features	EEG	Outcome
I (Mild)	Hyperalertness, jitteriness, poor feeding, no seizures	Normal	Good
II (Moderate)	Lethargy, hypotonia, seizures (24–48h), MAS	Low voltage, periodic	Variable (20–40% disability)
III (Severe)	Coma, flaccid, absent reflexes, refractory seizures	Burst suppression/isoelectric	Poor (>50% death/severe disability)

Q12. What is therapeutic hypothermia? Criteria and mechanism?

A: Whole-body cooling to 33–34°C for 72 hours, initiated within 6 hours of birth.

Criteria (all must be met):

≥36 weeks gestation
≥35 weeks in some centres
Evidence of asphyxia (Apgar ≤5 at 10 min, resuscitation needed, pH <7.0 or BE ≤-16, or abnormal neurologic exam)
No major congenital anomalies

Mechanism: Reduces secondary energy failure (delayed neuronal death) by:

↓ Cerebral metabolic rate
↓ Excitotoxic amino acid release (glutamate)
↓ Free radical production
↓ Apoptosis cascade

Reduces death + disability by ~30% in moderate-severe HIE.

4. NECROTIZING ENTEROCOLITIS (NEC)

Q13. What is NEC? What are the Bell's staging criteria?

A: NEC is an acute inflammatory bowel necrosis primarily affecting premature infants. Pathogenesis involves gut immaturity, bacterial colonization (dysbiosis), and an exaggerated inflammatory response.

Bell's Staging:

Stage	Clinical	Radiological	Treatment
IA/IB	Suspected — temperature instability, gastric residuals, abdominal distension	Normal or mild ileus	NBM, observe
IIA/IIB	Confirmed — absent bowel sounds, abdominal tenderness, +/- metabolic acidosis	Pneumatosis intestinalis	NBM, TPN, IV antibiotics (10–14 days)
IIIA/IIIB	Advanced — peritonitis, shock, DIC	Portal venous gas, pneumoperitoneum	Surgery (peritoneal drain or laparotomy)

Pneumatosis intestinalis (gas in bowel wall) = pathognomonic radiological sign.

Q14. Risk factors for NEC and how to prevent it?

Risk factors: Prematurity (<32 weeks, <1500g), formula feeding, polycythemia, PDA, congenital heart disease, IUGR
Prevention:
- Breast milk (reduces NEC risk by 6–10x)
- Antenatal steroids
- Slow enteral feeding advancement
- Probiotics (Lactobacillus, Bifidobacterium — evidence growing)
- Avoiding unnecessary antibiotics

5. NEONATAL SEPSIS

Q15. Early-onset vs late-onset neonatal sepsis — differences?

Feature	Early-Onset Sepsis (EOS)	Late-Onset Sepsis (LOS)
Age	0–72 hours (some: <7 days)	>72 hours (>7 days)
Source	Vertical (maternal)	Nosocomial or community
Organisms	GBS, E. coli, Listeria, Klebsiella	CoNS (S. epidermidis), S. aureus, Klebsiella, Pseudomonas, Candida
Presentation	Respiratory distress, shock	Fever/hypothermia, poor feeding, apnea, bulging fontanelle (meningitis)
Empirical antibiotics	Ampicillin + Gentamicin	Vancomycin + Aminoglycoside (or add antifungal if Candida risk)

Q16. What are the clinical features and diagnosis of neonatal sepsis?

A: Clinical (SNAPPE-II score factors):

Temperature instability (hypothermia more common than fever)
Respiratory distress, apnea
Poor feeding, vomiting, abdominal distension
Jitteriness, seizures, hypotonia
Jaundice, hepatomegaly, petechiae

Investigations:

Blood culture (gold standard) — 1 mL minimum
CBC: neutropenia (<1500), neutrophilia, toxic granules, I:T ratio >0.2
CRP (rises after 12–24h), Procalcitonin (rises earlier, more specific)
Blood glucose, serum electrolytes, LFTs
CSF if meningitis suspected (pleocytosis >25 WBC/mm³ in term neonate)

6. PREMATURITY & COMPLICATIONS

Q17. What are the complications of prematurity? (Systematic approach)

System	Complication
Respiratory	RDS, BPD (Bronchopulmonary Dysplasia), apnea of prematurity
Neurological	IVH (Intraventricular Hemorrhage), periventricular leukomalacia (PVL), hearing loss
GI	NEC, feeding difficulties, cholestasis
CVS	PDA (Patent Ductus Arteriosus), hypotension
Ophthalmological	Retinopathy of Prematurity (ROP)
Metabolic	Hypoglycemia, hypocalcemia, osteopenia of prematurity
Haematological	Anemia of prematurity, IVH coagulopathy
Immune	Infection susceptibility

Q18. Classify and manage IVH (Intraventricular Hemorrhage)?

A: Papile Grading (Cranial USS):

Grade	Description
I	Germinal matrix hemorrhage only
II	IVH without ventricular dilatation
III	IVH with ventricular dilatation
IV	IVH + periventricular hemorrhagic infarction

Germinal matrix (subependymal region) most vulnerable in <32 weeks
Peak incidence: 24–72 hours of life
Prevention: Antenatal steroids, Indomethacin (prophylactic), avoid rapid volume expansion, gentle ventilation, maintain stable BP
Management: Supportive; Grade III/IV — serial USS, neurosurgical consult if progressive hydrocephalus (reservoir/shunt)

Q19. What is BPD? How is it defined and managed?

A: Bronchopulmonary Dysplasia = chronic lung disease of prematurity (Jobe & Bancalari definition, 2001):

Oxygen requirement at 36 weeks PMA (postmenstrual age) for >28 days
Mild: Room air at 36 weeks
Moderate: FiO₂ <30% at 36 weeks
Severe: FiO₂ ≥30% or PPV/CPAP at 36 weeks

Pathogenesis: Arrested alveolarization + vascular development from O₂ toxicity, volutrauma, infection

Management:

Optimal nutrition (120–150 kcal/kg/day)
Fluid restriction
Diuretics (furosemide, hydrochlorothiazide + spironolactone)
Bronchodilators (salbutamol pRN)
Systemic steroids (Dexamethasone) — only for ventilator-dependent BPD; risks: CP, growth delay
Inhaled steroids (budesonide — less systemic effects)
Pulmonary vasodilators if PH develops (Sildenafil, iNO)

7. PATENT DUCTUS ARTERIOSUS (PDA)

Q20. How does PDA present and how do you manage it in a premature infant?

A: Presentation:

Hyperdynamic precordium, bounding pulses, wide pulse pressure
Continuous machinery murmur (or systolic only in very premature)
Respiratory deterioration, increased FiO₂ requirement
Confirmed by echocardiography (left-to-right shunt, LA:Ao ratio >1.4)

Management:

Fluid restriction, positive pressure (CPAP/ventilation)
Medical closure: Indomethacin (0.1–0.2 mg/kg IV q12h × 3 doses) or Ibuprofen (preferred — less renal side effects) or Paracetamol (IV, newer agent with good safety profile)
Surgical ligation: If medical therapy fails or contraindicated (NEC, renal failure, thrombocytopenia)
Conservative management is increasingly favored for hemodynamically insignificant PDA in stable premature infants

8. APGAR SCORE & NEONATAL RESUSCITATION

Q21. What is the Apgar score? What does each component assess?

Sign	0	1	2
Appearance (color)	Blue/pale all over	Peripheral cyanosis	Pink all over
Pulse (HR)	Absent	<100 bpm	≥100 bpm
Grimace (reflex irritability)	None	Grimace	Cry/cough/sneeze
Activity (tone)	Limp	Some flexion	Active motion
Respiration	Absent	Slow/irregular	Good cry

Assessed at 1 and 5 minutes; if <7 at 5 min, continue every 5 min up to 20 min
Score 7–10: Normal; 4–6: Moderate depression; <4: Severe depression

Q22. What are the steps of neonatal resuscitation (NRP 2020)?

Initial steps (30 sec): Warm, dry, stimulate, position, clear airway (bulb suction only if meconium-stained AND non-vigorous)
Evaluate: HR, breathing, color/SpO₂
PPV (positive pressure ventilation) if: HR <100, apnea/gasping; rate 40–60/min; use 21% O₂ in term, 21–30% in preterm
Chest compressions if HR <60 after 30 sec of effective PPV; ratio 3:1 (compressions:breaths), rate 120 events/min
Epinephrine (1:10,000) if HR <60 after 60 sec of chest compressions: 0.1–0.3 mL/kg IV (or 0.5–1 mL/kg ETT — less preferred)
Consider: Volume expansion (NS 10 mL/kg) if hypovolemia

9. NEONATAL HYPOGLYCEMIA

Q23. Define neonatal hypoglycemia and its management?

Definition: Blood glucose <47 mg/dL (2.6 mmol/L) — operational threshold (AAP, WHO)
Some use <40 mg/dL in first few hours; <45 mg/dL beyond that

At-risk groups: IDM (infant of diabetic mother), IUGR/SGA, LGA, prematurity, perinatal stress/asphyxia, polycythemia

Clinical features: Jitteriness, poor feeding, apnea, hypotonia, seizures, temperature instability (many are asymptomatic)

Management:

Asymptomatic, >36 weeks, glucose 30–47: Early oral feed; recheck in 30–60 min
If fails or symptomatic: IV 10% Dextrose 2 mL/kg bolus (200 mg/kg) → maintenance GIR 6–8 mg/kg/min
Refractory hypoglycemia: consider glucagon (0.02 mg/kg IM), hydrocortisone (1 mg/kg q6h), diazoxide (hyperinsulinism)

10. MECONIUM ASPIRATION SYNDROME (MAS)

Q24. What is MAS and how do you manage it?

A: Meconium aspiration syndrome: Aspiration of meconium-stained amniotic fluid causing:

Mechanical obstruction (ball-valve → air trapping, air leak)
Chemical pneumonitis
Surfactant inactivation
Persistent pulmonary hypertension (PPHN) in 20–30%

Obstetric management: Routine suctioning at birth NO LONGER recommended for meconium-stained fluid (NRP 2015)

Only intubate and suction if non-vigorous infant with meconium present

Neonatal management:

Respiratory support: CPAP → mechanical ventilation (high frequency if needed)
Surfactant therapy (reduces severity)
iNO (inhaled Nitric Oxide) for PPHN
ECMO if refractory (oxygenation index >40)
Broad-spectrum antibiotics (pneumonitis → risk of super-infection)

11. RETINOPATHY OF PREMATURITY (ROP)

Q25. Classify ROP and when to screen?

A: Screening: All infants <32 weeks OR <1500g; or 1500–2000g with unstable clinical course

First screen at 4 weeks chronological age OR 31 weeks PMA (whichever is later)

ICROP3 Classification:

Zone (I, II, III — from optic disc outward)
Stage (1: demarcation line; 2: ridge; 3: extraretinal fibrovascular proliferation; 4: partial retinal detachment; 5: total retinal detachment)
Plus disease: Tortuous, dilated posterior vessels (adverse sign)
AP-ROP (aggressive posterior ROP): rapidly progressing, zone I/posterior zone II, plus disease

Treatment:

Laser photocoagulation (gold standard for Type 1 ROP)
Anti-VEGF (Bevacizumab/Ranibizumab intravitreal) — especially for Zone I, AP-ROP
Surgery (vitreoretinal) for Stage 4–5

12. COMMON VIVA EXTRAS

Q26. What is the significance of Group B Streptococcus (GBS) in neonates? Prophylaxis?

GBS (S. agalactiae) = leading cause of early-onset neonatal sepsis and meningitis
IAP (Intrapartum Antibiotic Prophylaxis): Penicillin G (or Ampicillin if unavailable) in labor for:
- GBS vaginal/rectal culture positive at 35–37 weeks
- Previous infant with invasive GBS disease
- GBS bacteriuria in current pregnancy
- Preterm labor <37 weeks (unknown status)
- ROM >18 hours (unknown status)
- Intrapartum fever ≥38°C

Q27. What is TTN (Transient Tachypnea of the Newborn)?

A: TTN results from delayed clearance of fetal lung fluid (most common cause of neonatal respiratory distress in term/near-term infants)

Common after elective C-section (no labour-driven catecholamine surge, no vaginal squeeze)
Presents within 2–6 hours; tachypnea (RR >60), mild grunting, mild cyanosis
CXR: Hyperinflation, central streaking (fluid in fissures), fluid in horizontal fissure ("wet silhouette")
Self-resolving within 24–72 hours
Management: Supplemental O₂; if O₂ demand high → rule out RDS/infection

Q28. Congenital Hypothyroidism — Neonatal Screening?

Most common preventable cause of intellectual disability
Detected by newborn screening (TSH heel-prick) at 48–72 hours
TSH >20 mU/L requires repeat; TSH >40 mU/L with low T4 = diagnostic
Clinical features (often absent at birth): prolonged jaundice, constipation, hypotonia, large anterior fontanelle, macroglossia, umbilical hernia, dry skin, hoarse cry
Treatment: Levothyroxine 10–15 mcg/kg/day — start within 2 weeks; goal T4 in upper half of normal range

Q29. What is NAS (Neonatal Abstinence Syndrome)?

A: Withdrawal syndrome in neonates born to mothers using opioids (heroin, methadone, buprenorphine), benzodiazepines, alcohol, SSRIs

Finegan scoring (modified Finnegan Scale): Score ≥8 on 3 occasions → pharmacological treatment

Morphine (first-line opioid replacement, 0.04 mg/kg q4h then wean)
Clonidine, Phenobarbital (adjuncts for non-opioid NAS)
Non-pharmacological: Quiet, dark environment, swaddling, breastfeeding (if mother on methadone/buprenorphine and no HIV/drug use), SSC (skin-to-skin)

Q30. Fluid requirements and nutritional targets in premature neonates?

Age	Fluids (mL/kg/day)
Day 1	60–80 (VLBW: 80–100 due to insensible losses)
Day 2–3	80–120
Day 4–7	120–150
After 1 week	150–180

Nutritional targets (VLBW <1500g):

Calories: 110–130 kcal/kg/day (up to 150 in BPD)
Protein: 3.5–4 g/kg/day (start parenteral protein from Day 1)
Lipids: Start 1 g/kg/day, advance to 3–3.5 g/kg/day
Enteral feeds: Preferably expressed breast milk; start minimal enteral nutrition (MEN) early (10–20 mL/kg/day) even on TPN

Quick viva tips:

Always know definitions with numbers (e.g., gestational age cutoffs, Apgar intervals, bilirubin thresholds)

For any complication of prematurity, link to pathophysiology + prevention + management

Know indications AND contraindications for major interventions (surfactant, hypothermia, iNO, exchange transfusion)

Be ready to discuss recent changes: INSURE vs LISA/MIST for surfactant; conservative PDA management; anti-VEGF in ROP

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