Paeds SAQs · fetal-neonatal-and-perinatal
Respiratory distress syndrome of prematurity — formative SAQs
Two formative SAQs on respiratory distress syndrome of prematurity: the surfactant-deficiency mechanism and management ladder, and oxygen targeting with surfactant dosing.
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Target exams
SAQ 1 — Mechanism and the management ladder (10 marks)
A 27-week gestation infant is born to a mother who received antenatal corticosteroids 48 hours before delivery. By two hours of age the infant is on nasal CPAP at 6 cm of water with an inspired oxygen of 0.35, grunting and retracting. [1] [2]
Questions
- Outline the pathophysiological cascade by which surfactant deficiency produces hypoxaemia and acidosis, and explain the clinical sign of expiratory grunting. (5 marks) [1]
- Describe the stepwise management from this point, including the indication and technique for surfactant and the role of caffeine. (5 marks) [1] [8]
Model answer
Pathophysiology (5). Surfactant deficiency raises alveolar surface tension, so alveoli collapse at end-expiration, functional residual capacity and compliance fall, and the lung becomes stiff and under-aerated. Collapsed alveoli are perfused but not ventilated, producing right-to-left intrapulmonary shunting and hypoxaemia that does not correct with oxygen alone, while hypoventilation raises carbon dioxide. The combined respiratory and metabolic acidosis further inhibits residual surfactant function and constricts the pulmonary arterioles, risking persistent pulmonary hypertension. Expiratory grunting is the infant exhaling against a partially closed glottis to generate auto-positive end-expiratory pressure and splint alveoli open against collapse. [1]
Management ladder (5). The infant has met the 2022 guideline surfactant threshold of FiO2 over 0.30 on CPAP. Continue CPAP at 5 to 7 cm of water and give surfactant — poractant alfa 200 mg per kilogram intratracheally — preferring a LISA or MIST technique that delivers surfactant via a thin catheter while the infant stays on CPAP, to reduce mechanical ventilation and bronchopulmonary dysplasia. If the infant cannot be managed on CPAP, intubate, give surfactant down the tube, confirm placement with carbon dioxide detection, and wean the ventilator promptly as compliance improves. Start caffeine citrate, loaded at 20 mg per kilogram then 5 to 10 mg per kilogram daily, to reduce apnoea and aid extubation. Target pre-ductal saturations at 91 to 95 percent, maintain the temperature at 36.5 to 37.5 degrees, and treat with empirical antibiotics while sepsis is excluded. [1] [2] [8]
You have read the opening of this SAQ. The complete unit — every section and its primary-source references — is part of the Paediatrics Fellowship fellowship atlas.
References4Show ledgerHide ledger
- [1]Sweet DG European Consensus Guidelines on the Management of Respiratory Distress Syndrome: 2022 Update. Neonatology, 2023.PMID 36863329
- [2]Polin RA Surfactant replacement therapy for preterm and term neonates with respiratory distress. Pediatrics, 2014.PMID 24379227
- [5]Askie LM Association Between Oxygen Saturation Targeting and Death or Disability in Extremely Preterm Infants in the Neonatal Oxygenation Prospective Meta-analysis Collaboration. JAMA, 2018.PMID 29872859
- [8]Schmidt B Long-term effects of caffeine therapy for apnea of prematurity. N Engl J Med, 2007.PMID 17989382