Respiratory distress syndrome of prematurity — formative SAQs

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

1. Outline the pathophysiological cascade by which surfactant deficiency produces hypoxaemia and acidosis, and explain the clinical sign of expiratory grunting. (5 marks) [1]
2. 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]

SAQ 2 — Oxygen targeting and surfactant dosing (10 marks)

A 26-week gestation infant is being managed for severe RDS. The team is debating the oxygen saturation target and the surfactant preparation and dose. [1] [5]

Questions

1. Justify the recommended oxygen saturation target for this infant, citing the evidence and the harms of both lower and higher targets. (5 marks) [5]
2. State the surfactant preparation, initial dose and dosing interval you would use, and outline the LISA approach and its rationale. (5 marks) [1] [2]

Model answer

Oxygen targeting (5). The recommended pre-ductal target is 91 to 95 percent beyond the first minutes. The evidence is the NeOProM prospective meta-analysis of the SUPPORT, BOOST II and COT trials, which compared a lower target of 85 to 89 percent with a higher target of 91 to 95 percent in extremely preterm infants. The higher target reduced mortality; the lower target reduced severe retinopathy of prematurity but increased death. The synthesis is to target 91 to 95 percent, because both sustained hypoxia (death and hypoxic injury) and sustained hyperoxia (retinopathy and oxidative lung injury) are harmful, and the first minutes after birth are allowed to run lower before climbing toward target. [5]

Surfactant dosing (5). Poractant alfa is given at an initial dose of 200 mg per kilogram, which is 2.5 mL per kilogram of the 80 mg per mL preparation, with up to two further doses of 100 mg per kilogram if the FiO2 remains elevated. The LISA approach — less invasive surfactant administration — delivers the dose through a thin catheter placed through the vocal cords while the infant remains spontaneously breathing on nasal CPAP, avoiding intubation and mechanical ventilation. Its rationale is that it provides the surfactant the lung needs while sparing the infant the volutrauma, inflammation and bronchopulmonary-dysplasia risk of intubation, with the COIN and SUPPORT trials supporting the early-CPAP philosophy that LISA extends. [1] [2]