💡 Key clinical clue: A continuous “machinery” murmur maximal at the left infraclavicular area is classic for a Patent Ductus Arteriosus (PDA).
This congenital shunt connects the aorta and pulmonary artery and fails to close after birth.
🩸 Causes left-to-right shunt, pulmonary overcirculation, and later → Eisenmenger’s reversal (right-to-left shunt with cyanosis of toes but not fingers).
⚠️ Carries a significant risk of infective endocarditis.
🧠 About
- Common congenital lesion, particularly in premature infants and females (2:1).
- In fetal life, the ductus arteriosus (DA) shunts blood from the pulmonary artery → descending aorta, bypassing the lungs.
- After birth, increased oxygen tension and reduced prostaglandin levels should trigger closure within hours–days.
- PGE₂ (Prostaglandin E₂) keeps the duct open; NSAIDs (Indomethacin/Ibuprofen) help close it.
🌍 Risk Factors
- Premature birth (commonest cause).
- Female sex and high-altitude birth.
- Maternal rubella infection in 1st trimester.
- Fetal alcohol exposure or chromosomal abnormalities (e.g. Down, Edwards).
⚙️ Pathophysiology
- Persistence of the ductus → continuous flow from aorta (high pressure) → pulmonary artery (low pressure).
- Results in pulmonary overcirculation, left atrial and left ventricular volume overload, and eventually heart failure.
- Chronically increased pulmonary vascular resistance can cause shunt reversal → Eisenmenger’s syndrome with cyanosis confined to the lower limbs.
🧪 Dynamic Response to Drugs
- ↑ Oxygen & NSAIDs → close the ductus arteriosus.
- ↑ Prostaglandin E₂ → keeps ductus open (useful in duct-dependent lesions like TGA, CoA, ToF).
🩺 Clinical Features
- 💧 Infants: Poor feeding, failure to thrive, sweating, tachypnoea.
- 🔊 Murmur: Continuous “machinery” murmur below left clavicle, with thrill.
- ❤️ Cardiac signs: Bounding (“water-hammer”) pulse, wide pulse pressure, displaced apex beat.
- 🫁 Respiratory: Recurrent chest infections due to pulmonary congestion.
- 🔵 Eisenmenger’s physiology: Cyanosis of toes but not fingers (“differential cyanosis”).
🧫 Investigations
- Bloods: FBC, U&E, CRP, BNP (may be elevated if cardiac strain).
- ECG: May show LV hypertrophy or biventricular strain.
- CXR: Cardiomegaly + pulmonary plethora (overcirculation).
- Echocardiogram: Diagnostic — parasternal short-axis or suprasternal view shows continuous flow between aorta & pulmonary artery.
- Cardiac catheterisation: Defines size/anatomy pre-intervention.
🩹 Management
- 👶 Premature infants: May close spontaneously; trial of NSAIDs (Indomethacin or Ibuprofen) within first 10–14 days of life to inhibit prostaglandin synthesis.
- 💊 Medical therapy: Treat heart failure — diuretics, digoxin if needed.
- 🩺 Transcatheter closure: Amplatzer duct occluder device via catheter (first-line in children & adults if PDA remains open).
- 🔪 Surgical ligation: If duct large or unsuitable for catheter closure.
- 🦠 Infective endocarditis prophylaxis: Important in unrepaired PDA or early post-repair period.
📈 Prognosis
- Excellent if diagnosed and treated early — most children live normal lives post-closure.
- If untreated → progressive pulmonary hypertension, Eisenmenger’s syndrome, heart failure, and endocarditis risk.
💡 Teaching Tip
- PDA highlights how foetal circulation physiology continues postnatally — the duct that was essential in utero becomes pathological after birth.
- Mnemonic: “PGE keeps PDA open” — prostaglandins prolong ductal patency, NSAIDs close it.
- Compare and contrast with other left-to-right shunts (ASD, VSD) — continuous murmur is unique to PDA.
📚 References
- BNF: NSAIDs for ductal closure
- NICE NG204 (2021): Specialist neonatal management guidance
- Ohlsson A & Walia R. Indomethacin and ibuprofen for PDA in preterm infants. Cochrane Database Syst Rev, 2020.
- Gatzoulis MA et al., Congenital Heart Disease in Adults, 4th Ed. Elsevier 2021.