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PE19.1-17 | Neonatology — Graded Quiz
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A term neonate born after prolonged labour is assessed using the Silverman-Anderson score and scores 5 at 30 minutes of life. The score includes grade 2 upper-chest retraction, grade 1 lower-chest retraction, grade 1 xiphoid retraction, grade 0 nasal flaring, and grade 1 expiratory grunt. What does this score indicate?
Silverman-Anderson score 0 = no distress; 1–3 = mild; 4–6 = moderate; 7–10 = severe. Score 5 indicates moderate respiratory distress and warrants supplemental oxygen and close monitoring. Intubation is indicated for severe distress (score ≥7) or failure to improve.
Silverman-Anderson score: 5 parameters of chest-wall mechanics (0–2 each), total 0–10; 0=no distress, 1–3=mild, 4–6=moderate, 7–10=severe. Do NOT confuse with APGAR (post-birth assessment) or Ballard (gestational age).
The Silverman-Anderson Respiratory Distress Score assesses 5 parameters (upper-chest retraction, lower-chest retraction, xiphoid retraction, nasal flaring, expiratory grunt), each 0–2. It is applicable to any neonate and is specifically designed to quantify respiratory distress — NOT gestational age (Ballard) or post-birth condition (APGAR).
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A 2800 g neonate born at 36 weeks has poor perfusion, tachycardia, and a bulging anterior fontanelle at 18 hours of life. MRI brain shows bilateral parieto-occipital haemorrhage. The mother had no antenatal care and the baby received no prophylactic medications at birth. Which investigation is most critical to confirm the underlying coagulopathy?
Intracranial haemorrhage in a neonate without vitamin K prophylaxis (late VKDB) presents with PT and APTT prolongation with normal or near-normal platelet count. The critical coagulation screen is PT, APTT, and fibrinogen to differentiate VKDB (PT/APTT prolonged, platelets normal) from DIC (PT/APTT prolonged, platelets low, fibrinogen low).
Late VKDB (2–12 weeks) can cause catastrophic intracranial haemorrhage. Risk factors: exclusive breastfeeding, no vitamin K prophylaxis, fat malabsorption. Diagnosis: prolonged PT/APTT, normal platelets. Treatment: vitamin K 1 mg IM immediately + FFP 10–15 mL/kg for acute haemostasis.
Late VKDB can present with intracranial haemorrhage at 2–12 weeks, often in exclusively breastfed babies without vitamin K prophylaxis. The coagulation screen (PT/APTT) is critical — PT/APTT prolonged with normal platelets = VKDB. Treat with vitamin K 1 mg IM immediately and FFP for acute correction of severe bleeding.
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A HIV-positive mother (viral load undetectable on HAART) delivers a term neonate. Which ONE statement about perinatal HIV management in this neonate is correct?
NACO/PMTCT guidelines: neonate born to HIV-positive mother receives nevirapine (NVP) syrup for 6 weeks as chemoprophylaxis. Co-trimoxazole (CTX) prophylaxis begins at 6 weeks and continues until HIV status is confirmed negative. HIV DNA PCR (virological test) is done at 6 weeks, not birth, as the first definitive test.
PMTCT protocol (India/NACO): 6-week NVP syrup + CTX from 6 weeks for all HIV-exposed neonates; HIV DNA PCR at 6 weeks as first virological test; breastfeeding with HAART is recommended. Maternal viral suppression on HAART is the most important prevention strategy.
Perinatal HIV management per NACO (India): 6-week NVP prophylaxis for all exposed neonates; CTX from 6 weeks; HIV DNA PCR at 6 weeks (not birth antibody test — maternal antibodies persist 12–18 months); breastfeeding with HAART is currently recommended in India due to nutritional benefits.
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A 30-week neonate (birth weight 1350 g) is being considered for ROP screening. Which of the following is correct regarding ROP screening criteria in India per IAP guidelines?
IAP (2022) ROP screening criteria: all neonates ≤34 weeks GA or birth weight ≤2000 g, plus any neonate >34 weeks with risk factors (oxygen therapy, sepsis, PDA). First exam: 4 weeks postnatal OR 31 weeks corrected gestational age, whichever is LATER (to avoid missing early aggressive posterior ROP). Type 1 (threshold) ROP requires treatment within 72 hours.
ROP is caused by oxygen toxicity and abnormal retinal vasculogenesis in preterm neonates. Screen all neonates ≤34 weeks GA or ≤2000 g (India). Maintain SpO₂ 91–95% in preterm neonates to reduce risk. Type 1 (threshold) ROP: treat within 72 hours with laser or intravitreal bevacizumab.
ROP screening: ≤34 weeks or BW ≤2000 g in India (broader than US AAO criteria). Timing: 4 weeks postnatal or 31 weeks CGA (whichever later). Oxygen toxicity (hyperoxia) is the primary risk factor but not the only criterion for screening. Threshold/Type 1 ROP requires urgent laser/intravitreal anti-VEGF within 72 hours.
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A term neonate develops seizures at 12 hours of life. Blood glucose is 90 mg/dL, serum calcium is 6.8 mg/dL (ionised calcium 0.95 mmol/L), serum sodium 138 mEq/L. The mother had gestational diabetes (IDM). What is the most likely cause of seizures?
Serum calcium 6.8 mg/dL (normal term neonate >8.0 mg/dL) = hypocalcaemia. IDM neonates are at high risk of early hypocalcaemia (first 3 days) due to relative hypoparathyroidism and magnesium depletion. Blood glucose 90 mg/dL excludes hypoglycaemia; sodium is normal.
Neonatal hypocalcaemia (Ca <8.0 mg/dL term, <7.5 mg/dL preterm): early type associated with IDM, prematurity, asphyxia; late type (day 5–7) with phosphate-loaded formula. Treat: 10% calcium gluconate 2 mL/kg IV over 10–15 min with cardiac monitoring (risk of bradycardia).
Neonatal hypocalcaemia: total serum Ca <8.0 mg/dL (or ionised Ca <1.1 mmol/L) in term neonates, <7.5 mg/dL in preterm. Early-onset (day 1–3) is associated with IDM, birth asphyxia, and prematurity. Symptoms: jitteriness, seizures, apnoea, tetany. Treat with IV 10% calcium gluconate 2 mL/kg slow IV bolus.
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A 38-week neonate delivered via LSCS (indication: previous LSCS) develops tachypnoea (rate 72/min), subcostal recession, and mild cyanosis at 2 hours of life. CXR shows bilateral streaky opacities with fluid in the fissures. Blood glucose and sepsis screen are normal. What is the most likely diagnosis?
TTN is the most common cause of respiratory distress in term/near-term neonates born by elective LSCS. Mechanism: delayed resorption of lung fluid due to absence of vaginal squeeze. CXR: bilateral streaky opacities with fluid in horizontal fissure. Self-resolving in 24–72 hours with supplemental oxygen.
TTN is the most common neonatal respiratory distress; resolves in 24–72 hours with supportive O₂. Risk factors: elective LSCS without labour, male sex, macrosomia, maternal asthma. Treatment: supplemental O₂, CPAP rarely needed; antibiotics if infection cannot be excluded.
TTN (Transient Tachypnoea of the Newborn) classically follows elective LSCS without labour — amniotic fluid is not adequately squeezed from the lung. Bilateral streaky opacities and fissure fluid on CXR are characteristic. RDS shows bilateral ground-glass with air bronchograms in premature neonates. MAS requires meconium-stained amniotic fluid.
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A 3-day-old neonate develops generalised tonic seizures with focal clonic movements. Anterior fontanelle is tense. CSF shows xanthochromia with 200 RBCs, protein 150 mg/dL, and glucose 30 mg/dL (blood glucose 75 mg/dL). What is the first-line antiseizure medication and the most important investigation to guide further management?
Phenobarbitone 20 mg/kg IV is the first-line antiseizure drug for neonatal seizures per WHO/IAP guidelines. MRI brain is the most sensitive imaging to identify the aetiology (HIE, haemorrhage, malformation). The CSF picture (xanthochromia, elevated protein, reduced glucose) suggests subarachnoid haemorrhage or meningitis — MRI defines the extent.
Neonatal seizures: phenobarbitone 20 mg/kg IV is first-line; second-line: phenytoin or midazolam. Causes include HIE (most common), metabolic (hypoglycaemia, hypocalcaemia, hyponatraemia), infection, and structural. MRI brain is the preferred imaging modality.
Phenobarbitone 20 mg/kg IV is the first-line drug for neonatal seizures, followed by a second dose (10 mg/kg) if needed. MRI brain (not CT) is preferred for delineating cortical injury. EEG is complementary (especially for subclinical seizures) but not the primary investigation to guide acute management.
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A baby born at 28 weeks is now 4 weeks old and is screened for retinopathy of prematurity. Fundoscopy shows a demarcation line (ridge) separating vascularised and avascular retina, with new vessel growth crossing into the vitreous. This finding in zone II is classified as:
Stage 3 ROP: extraretinal fibrovascular proliferation (new vessels crossing into vitreous). Stage 1 = demarcation line; Stage 2 = ridge; Stage 3 = ridge + extraretinal neovascularisation. Stage 3 in zone II with plus disease = Type 1 ROP, requiring treatment within 72 hours (laser or intravitreal anti-VEGF).
ROP staging: 1=demarcation line, 2=ridge, 3=extraretinal neovascularisation, 4=partial detachment, 5=total detachment. Zones I (posterior), II (mid-periphery), III (anterior). Plus disease (dilated tortuous vessels) indicates active progression. Type 1 ROP (threshold) in zone I/II requires treatment within 72 hours.
ROP staging: Stage 1 = flat demarcation line; Stage 2 = elevated ridge; Stage 3 = ridge + extraretinal neovascularisation into vitreous; Stage 4 = partial retinal detachment; Stage 5 = total retinal detachment. New vessels crossing into vitreous = Stage 3.
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A newborn is noted to have a cleft palate and cleft lip at birth. The parents ask about feeding challenges and the timing of surgical repair. Which statement is CORRECT?
Cleft lip and palate feeding: use specialised feeders (Haberman/Pigeon teat) and upright positioning. Timing: Rule of 10 for cleft lip repair (10 weeks, 10 pounds, Hb 10 g/dL) = approximately 3–6 months; palate repair at 9–18 months (before speech development) to minimise velopharyngeal insufficiency.
Cleft lip/palate: specialised feeding with Haberman/Pigeon teat. Rule of 10 for cleft lip repair (~3 months). Palate repair 9–18 months before speech development. Associated with Pierre Robin sequence (micrognathia, glossoptosis, cleft palate). Check for other congenital anomalies.
Feeding with cleft lip/palate is possible with specialised teats and positioning; NG tube is used only if adequate oral intake cannot be achieved. Surgical timing follows the 'rule of 10' for lip (3–6 months) and palate repair at 9–18 months to preserve speech development.
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A 30-week preterm neonate develops abdominal distension, bloody stools, and bilious aspirates on day 10. X-ray shows pneumatosis intestinalis. Temperature is unstable. Which of the following best describes the diagnosis and initial management priority?
Necrotising enterocolitis (NEC): preterm neonate, day 10 (NEC peaks at 2–3 weeks in VLBW), triad of abdominal distension + bloody stools + bilious aspirates, with pneumatosis intestinalis on X-ray (pathognomonic). Management: NPO/bowel rest, NG decompression, IV fluids, broad-spectrum antibiotics (ampicillin + gentamicin ± metronidazole), surgical review for Bell stage IIB/III.
NEC: primarily affects VLBW preterm neonates, peaks days 10–20. Bell staging: I=suspected (bloody stools, feeding intolerance), II=definite (pneumatosis intestinalis on X-ray), III=advanced (perforation). Treatment: bowel rest, NG suction, IV antibiotics. Prevention: breast milk feeding, probiotic supplementation (evidence-based).
NEC is the most common surgical emergency in preterm neonates. Pneumatosis intestinalis (intramural gas on X-ray) is pathognomonic of NEC (Bell stage II). Stage III (perforation) = pneumoperitoneum → emergency surgery. Management: bowel rest for at least 10–14 days, antibiotics, and close surgical monitoring.
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