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Paeds Topicsfetal-neonatal-and-perinatal

Paeds · fetal-neonatal-and-perinatal

Patent ductus arteriosus in preterm infants

Also known as Patent ductus arteriosus · Haemodynamically significant PDA · hsPDA · Preterm ductus arteriosus

Fellowship guide to patent ductus arteriosus in preterm infants: why the preterm ductus fails to close, what makes it haemodynamically significant, the bedside and echocardiographic assessment, the modern expectant-first management ladder with ibuprofen, indomethacin and paracetamol, the ligation causality-or-bias debate, and the evidence behind treating the infant rather than the echo.

high14 referencesUpdated 12 July 202625 min readVerification in progress

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Target exams

RACP General PaediatricsRACP DWERACP DCEMRCPCH TheoryMRCPCH ClinicalABP General PediatricsRCPSC Pediatrics

Red flags

  • A preterm infant needing progressively more ventilation with a falling diastolic pressure and bounding pulses
  • Widened pulse pressure with oliguria and rising creatinine after the first week of life
  • Pulmonary haemorrhage in a ventilated preterm infant
  • Feed intolerance or abdominal distension with bloody stools in an infant with a large left-to-right ductal shunt
  • A preterm infant who deteriorates each time the duct reopens or the shunt increases

Life stages

fetalneonateinfant

Care settings

delivery-roomnicupicuretrieval

Clinical exam formats

written-onlyracp-dce-long-caseracp-dce-short-casemrcpch-communication

Board mappings

  • Fetal and neonatal cardiovascular physiology and ductal closure
  • Recognition of the preterm infant with a significant ductal shunt
  • Neonatal haemodynamics and end-organ perfusion
  • Patent ductus arteriosus: haemodynamic significance and echocardiographic assessment
  • Pharmacological closure: ibuprofen, indomethacin and paracetamol
  • The expectant-first paradigm and the causality-or-bias debate
  • Applied neonatal cardiovascular physiology of ductal closure
  • Prostaglandin-mediated tone and the pharmacology of COX inhibitors
  • Interpreting haemodynamic significance and end-organ effects
  • Short case: the ventilated preterm with a widened pulse pressure
  • Communication: counselling parents about expectant management versus treatment
  • Neonatology: cardiovascular adaptation and the preterm ductus
  • Patient investigation: echocardiographic assessment of ductal significance
  • Patient management: the stepwise treatment ladder
  • Neonatal cardiovascular pathophysiology: failure of ductal closure
  • Pharmacology: prostaglandins, COX inhibitors and paracetamol
  • Evidence-based management of the haemodynamically significant PDA
  • Neonatal haemodynamics scenario station
  • Communication: counselling on treatment versus watchful waiting
  • Neonatology: patent ductus arteriosus in preterm infants
  • Cardiovascular adaptation of the newborn and ductal shunting
  • Pharmacology of cyclo-oxygenase inhibitors and paracetamol
  • Patient Care: management of the haemodynamically significant PDA
  • Medical Knowledge: ductal closure physiology and left-to-right shunt consequences
  • Systems-Based Practice: multidisciplinary neonatal-cardiology decision-making
  • Medical Expert: patent ductus arteriosus in preterm infants
  • Collaborator: neonatology and cardiology shared assessment
  • Health Advocate: judicious use of pharmacotherapy and avoiding harm
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Practise this topic

  • Short-answer question1
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Target exams

RACP General PaediatricsRACP DWERACP DCEMRCPCH TheoryMRCPCH ClinicalABP General PediatricsRCPSC Pediatrics

Red flags

  • A preterm infant needing progressively more ventilation with a falling diastolic pressure and bounding pulses
  • Widened pulse pressure with oliguria and rising creatinine after the first week of life
  • Pulmonary haemorrhage in a ventilated preterm infant
  • Feed intolerance or abdominal distension with bloody stools in an infant with a large left-to-right ductal shunt
  • A preterm infant who deteriorates each time the duct reopens or the shunt increases

Life stages

fetalneonateinfant

Care settings

delivery-roomnicupicuretrieval

Clinical exam formats

written-onlyracp-dce-long-caseracp-dce-short-casemrcpch-communication

Board mappings

  • Fetal and neonatal cardiovascular physiology and ductal closure
  • Recognition of the preterm infant with a significant ductal shunt
  • Neonatal haemodynamics and end-organ perfusion
  • Patent ductus arteriosus: haemodynamic significance and echocardiographic assessment
  • Pharmacological closure: ibuprofen, indomethacin and paracetamol
  • The expectant-first paradigm and the causality-or-bias debate
  • Applied neonatal cardiovascular physiology of ductal closure
  • Prostaglandin-mediated tone and the pharmacology of COX inhibitors
  • Interpreting haemodynamic significance and end-organ effects
  • Short case: the ventilated preterm with a widened pulse pressure
  • Communication: counselling parents about expectant management versus treatment
  • Neonatology: cardiovascular adaptation and the preterm ductus
  • Patient investigation: echocardiographic assessment of ductal significance
  • Patient management: the stepwise treatment ladder
  • Neonatal cardiovascular pathophysiology: failure of ductal closure
  • Pharmacology: prostaglandins, COX inhibitors and paracetamol
  • Evidence-based management of the haemodynamically significant PDA
  • Neonatal haemodynamics scenario station
  • Communication: counselling on treatment versus watchful waiting
  • Neonatology: patent ductus arteriosus in preterm infants
  • Cardiovascular adaptation of the newborn and ductal shunting
  • Pharmacology of cyclo-oxygenase inhibitors and paracetamol
  • Patient Care: management of the haemodynamically significant PDA
  • Medical Knowledge: ductal closure physiology and left-to-right shunt consequences
  • Systems-Based Practice: multidisciplinary neonatal-cardiology decision-making
  • Medical Expert: patent ductus arteriosus in preterm infants
  • Collaborator: neonatology and cardiology shared assessment
  • Health Advocate: judicious use of pharmacotherapy and avoiding harm
The fellowship answer

A patent ductus arteriosus (PDA) in a preterm infant is persistent postnatal patency of the ductus arteriosus, the fetal vessel that shunts blood from the pulmonary artery to the descending aorta, beyond the expected functional closure window of the first few days of life. The preterm ductus fails to close because its immature smooth muscle contracts weakly to oxygen and remains exquisitely sensitive to the relaxing prostaglandins that fall only slowly after birth. It becomes haemodynamically significant when the falling pulmonary vascular resistance converts the shunt to a substantial left-to-right flow, producing pulmonary over-circulation (rising ventilator and oxygen need, pulmonary oedema) and systemic diastolic steal (low diastolic pressure, oliguria, renal dysfunction, gut ischaemia). The bedside triad is bounding pulses, a hyperdynamic precordium and a widened pulse pressure. Echocardiography defines significance: a duct diameter above 1.5 mm, a left atrial-to-aortic root ratio above 1.5, and diastolic flow reversal in the descending aorta. The modern answer is expectant management first and treat the infant, not the echo — most preterm ducts close spontaneously, and the BeNeDuct and PDA-TOLERATE trials showed no benefit of routine early closure. When a truly haemodynamically significant duct causes end-organ compromise, pharmacological closure with ibuprofen, indomethacin or paracetamol is the next step, with surgical or transcatheter ligation reserved for failure or contraindication.

[13][7]
Treat the infant, not the echo — and never close a duct-dependent circulation

A large duct on echocardiography in an infant who is weaning, passing urine and feeding is not an indication for treatment. Conversely, a falling diastolic pressure with oliguria, rising creatinine, pulmonary haemorrhage or escalating ventilation in an infant with a substantial left-to-right shunt is a haemodynamically significant PDA demanding action. Before any cyclo-oxygenase inhibitor, exclude duct-dependent congenital heart disease (e.g. hypoplastic left heart, coarctation, pulmonary atresia) — closing that duct is catastrophic. Always confirm a normal cardiac structure on echocardiography first. [7] [13]

The diastolic steal is the silent killer

The danger of a significant PDA is not the systolic murmur but the diastolic steal — blood is sucked from the systemic circulation into the lungs during diastole, gutturally underperfusing the kidneys, gut and brain. Oliguria, a rising creatinine, metabolic acidosis, feed intolerance and intraventricular haemorrhage are the clinical fingerprints of the steal, often before the murmur is loud. A widening pulse pressure with a falling diastolic pressure is the bedside signature that the shunt has become haemodynamically important. [13] [10]

Overview & Definition

A 26-week infant, three days old, ventilated for respiratory distress syndrome, is weaning nicely. Over the next 48 hours the team notice bounding pulses, a widened pulse pressure, and a creeping oxygen and ventilator requirement. The echocardiogram shows a 2 mm duct with left-to-right flow and diastolic flow reversal in the descending aorta. This is the classic presentation of a patent ductus arteriosus (PDA) becoming haemodynamically significant, and the decisions made here are some of the most contested in modern neonatology. [13] [7]

The ductus arteriosus is the fetal vessel connecting the main pulmonary artery to the descending aorta. In utero it shunts the right ventricular output away from the high-resistance lungs and toward the placenta. After birth it is meant to close — first functionally, by smooth muscle contraction within hours, then anatomically, by intimal proliferation over two to three weeks, leaving the ligamentum arteriosum. A PDA in the preterm context is persistent patency beyond this expected window. It is not a congenital malformation in the usual sense; it is the predictable consequence of an immature ductal wall meeting the postnatal circulation. [7] [14]

The distinction that governs all management is between a PDA that is merely present and one that is haemodynamically significant — a substantial left-to-right shunt producing measurable pulmonary over-circulation and systemic hypoperfusion. Most preterm ducts stay open for a while and most close on their own; only a minority cause the end-organ compromise that justifies treatment. Holding the question "is this duct significant?" at the centre of every assessment is the single most important habit for this topic, because the evidence base of the last decade has remorselessly dismantled the older reflex of closing every duct. [1] [11]

~55–65%PDA in infants under 28 weekspatent at 4–7 days
over 50%Spontaneous closureeven in ELBW with expectant care
under 1%Term infants affectedtrue congenital PDA is a different entity

The modern story of the preterm PDA is a story of restraint winning over intervention. Three decades of trials — from prophylactic indomethacin to early ibuprofen to the BeNeDuct trial of expectant management — have shown that routine closure does not improve survival without bronchopulmonary dysplasia, does not improve long-term neurodevelopment, and carries real harms. The fellowship candidate who can articulate why practice shifted, and name the trials, will answer this topic well. [1] [6] [11]

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References14ShowHide
  1. [1]Hundscheid T, Onland W, Kooi EMW, et al Expectant Management or Early Ibuprofen for Patent Ductus Arteriosus. N Engl J Med, 2023.PMID 36477458
  2. [2]Mitra S, Florez ID, Tamayo ME, et al Association of Placebo, Indomethacin, Ibuprofen, and Acetaminophen With Closure of Hemodynamically Significant Patent Ductus Arteriosus in Preterm Infants: A Systematic Review and Meta-analysis. JAMA, 2018.PMID 29584842
  3. [3]Ohlsson A, Walia R, Shah SS Ibuprofen for the treatment of patent ductus arteriosus in preterm or low birth weight (or both) infants. Cochrane Database Syst Rev, 2020.PMID 32045960
  4. [4]Jasani B, Mitra S, Shah PS Paracetamol (acetaminophen) for patent ductus arteriosus in preterm or low birth weight infants. Cochrane Database Syst Rev, 2022.PMID 36519620
  5. [5]Fowlie PW, Davis PG, McGuire W Prophylactic intravenous indomethacin for preventing mortality and morbidity in preterm infants. Cochrane Database Syst Rev, 2010.PMID 20614421
  6. [6]Clyman RI, Liebowitz M, Kaempf J, et al PDA-TOLERATE Trial: An Exploratory Randomized Controlled Trial of Treatment of Moderate-to-Large Patent Ductus Arteriosus at 1 Week of Age. J Pediatr, 2019.PMID 30340932
  7. [7]Benitz WE Patent Ductus Arteriosus in Preterm Infants. Pediatrics, 2016.PMID 26672023
  8. [8]Liebowitz M, Kaempf J, Erdeve O, et al Comparative effectiveness of drugs used to constrict the patent ductus arteriosus: a secondary analysis of the PDA-TOLERATE trial. J Perinatol, 2019.PMID 30850756
  9. [9]Liebowitz M, Katheria A, Sauberan J, et al Lack of Equipoise in the PDA-TOLERATE Trial: A Comparison of Eligible Infants Enrolled in the Trial and Those Treated Outside the Trial. J Pediatr, 2019.PMID 31255386
  10. [10]Weisz DE, McNamara PJ Patent ductus arteriosus ligation and adverse outcomes: causality or bias? J Clin Neonatol, 2014.PMID 25024972
  11. [11]Mitra S, Scrivens A, Fiander M, et al Early treatment versus expectant management of hemodynamically significant patent ductus arteriosus for preterm infants. Cochrane Database Syst Rev, 2025.PMID 40548426
  12. [12]Mitra S, de Boode WP, Weisz DE, et al Interventions for patent ductus arteriosus (PDA) in preterm infants: an overview of Cochrane Systematic Reviews. Cochrane Database Syst Rev, 2023.PMID 37039501
  13. [13]Mitra S, Weisz D, Jain A, et al Management of the patent ductus arteriosus in preterm infants. Paediatr Child Health, 2022.PMID 35273674
  14. [14]Chorne N, Jegatheesan P, Lin E, et al Risk factors for persistent ductus arteriosus patency during indomethacin treatment. J Pediatr, 2007.PMID 18035143

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