Patent ductus arteriosus in preterm infants — formative SAQs

SAQ 1 — A weaning preterm who stops weaning (10 marks)

A 26-week gestation, 780 g infant is day 5 of life, ventilated for respiratory distress syndrome and weaning on volume-targeted ventilation. Over 36 hours the oxygen requirement has risen from 28% to 42%, the team note bounding pulses and a hyperdynamic precordium, the blood pressure is 52/24 (mean 34), the urine output has fallen to 0.8 mL/kg/h, and there is a soft systolic murmur at the upper left sternal border. The functional echocardiogram shows a 2.1 mm duct with left-to-right flow, a left atrial-to-aortic root ratio of 1.7, and diastolic flow reversal in the descending aorta. ^[13]

a) What makes this ductus arteriosus haemodynamically significant? Give the bedside and echocardiographic evidence. (3 marks) ^[13]

This is a haemodynamically significant PDA. The bedside evidence is the large left-to-right shunt signature — bounding pulses, a hyperdynamic precordium and a widened pulse pressure with a characteristically low diastolic (52/24) — combined with end-organ compromise in the form of oliguria (0.8 mL/kg/h) and a rising oxygen requirement. The echocardiographic evidence is the constellation of a duct diameter above 1.5 mm (2.1 mm), a left atrial-to-aortic root ratio above 1.5 (1.7), and diastolic flow reversal in the descending aorta, which is the direct fingerprint of the systemic steal. ^[13]

b) Explain in mechanistic terms why the preterm ductus fails to close and why the shunt becomes left-to-right. (3 marks) ^[13]

The preterm ductus fails for three reasons: its smooth muscle is immature (a thinner medial layer with a weak contractile response to oxygen), it is abnormally sensitive to the relaxing prostaglandins that fall only slowly after birth because clearance is poor, and its intimal cushions are underdeveloped, so the substrate for anatomic closure is deficient. The shunt becomes left-to-right because the pulmonary vascular resistance falls over the first week of life, reversing the pressure gradient across the duct so blood flows from the aorta into the pulmonary circulation in systole and diastole. ^[13]

c) Outline your immediate management, including the conservative measures you would institute before reaching for a drug. (2 marks) ^[13]

The immediate management begins with expectant, supportive care: correct hypoxia and acidosis (both relax the ductal smooth muscle), treat anaemia to preserve oxygen delivery, review the ventilation toward lung-protective settings with permissive hypercapnia, and avoid fluid overload while modestly restricting intake. Support the circulation with a vasoconstrictor if hypotension persists (volume boluses rarely help the steal-driven hypotension and may worsen the shunt), and reduce or pause feeds to protect the gut. The end-organ signs are charted serially, because the decision to escalate is made on trajectory. ^[13]

d) State the two landmark trials that anchor the expectant-first paradigm and what they showed, and the first-line drug with its dose if escalation is needed. (2 marks) ^[1]

The BeNeDuct trial (NEJM 2023) showed that early ibuprofen did not improve death or bronchopulmonary dysplasia compared with expectant management, and the PDA-TOLERATE trial showed that treating a moderate-to-large duct at one week did not reduce death or bronchopulmonary dysplasia either. If this infant's end-organ compromise progresses despite supportive care, the first-line drug is ibuprofen 10 mg/kg then 5 mg/kg at 24 and 48 hours. ^{[1] [6]}