Patent ductus arteriosus is a congenital heart defect, most common in premature neonates, in which the fetal ductus arteriosus fails to close after birth, resulting in a persistent left-to-right shunt between the aorta and pulmonary artery.

Patent Ductus Arteriosus (PDA) in Paediatrics

Category	Risk Factor	Mechanism
Genetic	2–4% sibling recurrence risk	Polygenic inheritance
Genetic	Char syndrome (TFAP2B mutation)	Transcription factor defect impairing ductal smooth muscle remodelling
Perinatal	Prematurity	Immature ductal smooth muscle; persistent prostaglandin sensitivity; reduced oxygen-sensing mechanisms
Perinatal	Maternal rubella (1st trimester)	Direct viral damage to ductal wall elastic tissue → impaired constriction
Perinatal	Birth at high altitude	Lower ambient PaO₂ → reduced stimulus for ductal constriction
Maternal drugs	Warfarin exposure	Associated with PDA (5% of fetal warfarin syndrome)
Maternal drugs	Fetal alcohol syndrome	VSD, ASD, TOF, PDA
Chromosomal	Trisomy 21 (less specific)	General association with CHD
Other	Perinatal asphyxia	Prolonged hypoxia maintains ductal patency

^[1]^[2]^[4]

Anatomy and Function of the Ductus Arteriosus

Aetiology (with Hong Kong Focus) and Pathophysiology

Pathophysiology: The Haemodynamic Consequences of PDA

This is the crux of understanding PDA clinically. Follow the logic step by step:

Classification

PDA can be classified by several schemes:

Type	Description
Preterm PDA	Due to ductal immaturity; functional/pharmacological closure possible
Term PDA	Structural defect; pharmacological closure ineffective

This is the most clinically relevant classification ^[1]^[2]:

Size	Qp:Qs	Haemodynamic Impact
Small PDA	< 1.5:1	Minimal; no volume overload
Moderate PDA	1.5–2.2:1	Mild-moderate LV volume overload; may cause symptoms in adolescence/adulthood
Large PDA	> 2.2:1	Significant LV volume overload; HF in infancy

Qp:Qs = ratio of pulmonary blood flow to systemic blood flow. Normal is 1:1. A Qp:Qs of 2:1 means twice as much blood flows through the lungs as through the systemic circulation — the excess is the shunt volume.

Type	Description
A	Conical, well-defined aortic ampulla, narrow at PA end (most common, ~65%)
B	Short, "window-like"
C	Tubular, no constriction
D	Multiple constrictions
E	Elongated, constricted at aortic end

Some severe CHDs require the DA to remain open for survival. In these cases, the DA is life-saving and is kept open with PGE₁ (prostaglandin E₁ / alprostadil) infusion:

Duct-dependent condition	Why the duct is needed
Duct-dependent pulmonary circulation (e.g., critical PS, pulmonary atresia, severe TOF)	DA provides the only source of pulmonary blood flow (aorta → PA)
Duct-dependent systemic circulation (e.g., critical CoA, interrupted aortic arch, HLHS)	DA provides the only source of descending aortic blood flow (PA → aorta)
Duct-dependent mixing (e.g., TGA without VSD)	DA allows mixing between parallel circulations

^[1]^[4]^[5]

Exam Pearl: PGE₁ to Keep the Duct Open

Students often confuse closing and opening the duct:

To CLOSE the duct (preterm PDA): Use COX inhibitors (indomethacin, ibuprofen) or paracetamol → block PGE₂ synthesis
To KEEP the duct OPEN (duct-dependent CHD): Use PGE₁ (alprostadil) infusion
Side effects of PGE₁: apnoea (15–20%), fever, hypotension, seizures → always have intubation equipment ready

Clinical Features

Clinical features are entirely determined by the degree of L-to-R shunting (i.e., PDA size and PVR) ^[1]^[2].

A. Symptoms (with Pathophysiological Basis)

Symptom	Pathophysiological Basis
Heart failure symptoms at 1–2 months of age (term infants) / within days (preterm)	As PVR drops postnatally → increasing L-to-R shunt → LV volume overload → CHF. Earlier in preterms due to lower cardiac reserve and faster PVR drop
Tachypnoea / respiratory distress	Pulmonary overcirculation → pulmonary congestion/oedema → ↓lung compliance → ↑work of breathing
Poor feeding / failure to thrive (FTT)	1) ↑metabolic demand from HF 2) Tachypnoea interferes with feeding 3) Reduced gut perfusion from diastolic run-off
Recurrent chest infections	Pulmonary congestion impairs mucociliary clearance and creates favourable environment for bacterial growth
Excessive sweating (especially during feeds)	Sympathetic activation in response to reduced cardiac output
Irritability / lethargy	Reduced systemic perfusion; low cardiac output state

Symptom	Pathophysiological Basis
↓Exercise tolerance	Mild LV volume overload limits cardiac output augmentation during exercise
HF symptoms in adolescence or adulthood	Chronic volume overload eventually decompensates over years
May be asymptomatic in childhood	Compensatory LV eccentric hypertrophy maintains output

Symptom	Pathophysiological Basis
Asymptomatic	Shunt volume too small to cause significant haemodynamic effects
Incidental murmur	Detected on routine examination
Infective endocarditis (uncommon)	Turbulent jet across PDA damages endothelium → nidus for vegetation. Risk is lifelong even with small PDA ^[1]^[2]

Symptom	Pathophysiological Basis
Differential cyanosis (blue toes, pink fingers)	R-to-L shunt via PDA delivers deoxygenated blood to descending aorta only
Exertional dyspnoea	Fixed high PVR limits pulmonary blood flow
Haemoptysis	Pulmonary arteriolar fragility from severe pHTN
Syncope	Fixed cardiac output; exercise-induced drop in SVR with inability to augment pulmonary flow

B. Signs (with Pathophysiological Basis)

Sign	Pathophysiological Basis
Tachypnoea, intercostal/subcostal recession	Pulmonary congestion → ↓compliance → ↑respiratory effort
FTT / growth faltering	Chronic HF → ↑metabolic demands + ↓caloric intake
Differential cyanosis/clubbing (Eisenmenger only)	R-to-L shunt via PDA to descending aorta → desaturation of lower limbs only

Sign	Pathophysiological Basis
Collapsing (bounding/water-hammer) pulse	Diastolic run-off through PDA → low diastolic BP → wide pulse pressure → brisk upstroke and rapid collapse. Identical mechanism to aortic regurgitation
Increased pulse pressure	Systolic BP may be slightly elevated (hyperdynamic LV); diastolic BP is low (run-off)
Tachycardia	Sympathetic compensation for reduced effective systemic output

The collapsing pulse and wide pulse pressure are hallmark signs of a haemodynamically significant PDA — they indicate substantial diastolic aortic run-off ^[1]^[2].

Sign	Pathophysiological Basis
Displaced, thrusting (hyperdynamic) apex beat	LV volume overload → LV dilatation and eccentric hypertrophy → apex displaced laterally and inferiorly; increased force due to increased stroke volume
Parasternal heave (if pHTN develops)	RV pressure overload from elevated pulmonary pressures

This is one of the most classic and high-yield murmurs in paediatric cardiology:

Feature	Detail	Pathophysiological Basis
Character	Continuous "machinery" murmur (Gibson's murmur)	Pressure gradient between aorta and PA exists throughout BOTH systole and diastole → continuous flow through PDA → continuous murmur. Loudest in late systole, spilling into diastole
Location	Left infraclavicular area / left upper sternal border (LUSB)	Anatomical location of the PDA — beneath the left clavicle
Radiation	May radiate to the back	Along the course of the descending aorta
Grading	Large PDA: 4/6; Moderate: 2–3/6; Small: < 3/6	Louder murmur with larger shunt volume (though not always proportional)
Timing variation	In neonatal period: murmur may be confined to SYSTOLE ONLY	Because PVR is still high in the first few weeks → diastolic gradient is small → diastolic component absent. As PVR drops, the classic continuous murmur develops ^[1]^[2]
In Eisenmenger	Murmur disappears or becomes very soft	When PVR equals or exceeds SVR, there is no pressure gradient → no flow → no murmur. May hear loud P2 instead

Exam Pearl: Why Is the PDA Murmur Continuous?

Most shunt murmurs are NOT continuous. VSD produces a pansystolic murmur because the pressure gradient (LV > RV) exists only in systole. ASD doesn't produce a murmur from the shunt at all (low-velocity flow).

PDA is unique because:

Aortic pressure > PA pressure in both systole AND diastole
Therefore, flow through the PDA is continuous
The murmur peaks in late systole (when the pressure gradient is maximal) and extends through diastole

The ONLY other continuous murmur you need to know is a venous hum (benign, disappears on lying down/turning head).

Finding	When	Pathophysiological Basis
Loud P2 or single S2	If pHTN present	Elevated PA pressure → forceful closure of pulmonary valve
Apical mid-diastolic flow murmur	Large PDA	Increased flow across the mitral valve (functional mitral stenosis) due to high pulmonary venous return
S3 gallop	HF	Rapid ventricular filling into a dilated, volume-overloaded LV

In premature neonates, the clinical signs differ somewhat:

Sign	Detail
Bounding peripheral pulses	Prominent in premature infants due to thin subcutaneous tissue + wide pulse pressure
Hyperactive precordium	Easily visible/palpable LV impulse through thin chest wall
Systolic murmur only (initially)	PVR still relatively high in first days; continuous murmur develops later
Worsening ventilatory requirements	Increasing FiO₂ or ventilator settings needed due to pulmonary oedema
Metabolic acidosis	Reduced systemic perfusion → tissue hypoxia → lactic acidosis
Oliguria	Renal hypoperfusion from diastolic steal
Abdominal distension / feed intolerance	Gut hypoperfusion → risk of NEC

Feature	Small PDA	Moderate PDA	Large PDA
Symptoms	Asymptomatic; IE risk	↓Exercise tolerance; late HF	HF at 1–2mo (days in preterm); FTT; recurrent infections
Pulse	Normal	Bounding	Collapsing; wide pulse pressure
Apex	Normal	Mildly displaced	Displaced, thrusting
Murmur	Continuous, < G3/6, LUSB/L infraclavicular	Continuous, G2–3/6	Continuous, G4/6; ± mid-diastolic rumble
P2	Normal	May be loud	Loud; ± single S2
CXR	Normal	Mild cardiomegaly	Cardiomegaly; pulmonary plethora
ECG	Normal	LVH	LVH, LAE; ± RVH if pHTN

^[1]^[2]

Let's consolidate the "why" behind the key features:

Clinical Feature	Why?
Continuous murmur	Aorta > PA pressure in both systole and diastole → continuous flow
Left infraclavicular location	Anatomical site of PDA
Wide pulse pressure / collapsing pulse	Diastolic run-off from aorta → PA via PDA drops diastolic pressure
Displaced thrusting apex	LV volume overload → eccentric LV dilatation
Loud P2	Pulmonary hypertension → forceful pulmonary valve closure
Differential cyanosis	Eisenmenger: R-to-L shunt enters aorta below L SCA → lower body deoxygenated
HF at 1–2 months	PVR drops over weeks → shunt increases → LV overloaded
HF in days (preterm)	Immature myocardium + faster PVR drop + lower cardiac reserve
NEC risk in preterm	Diastolic run-off → mesenteric hypoperfusion
IVH risk in preterm	Fluctuating cerebral blood flow from run-off + hyperdynamic circulation

High Yield Summary

Patent Ductus Arteriosus (PDA) — Key Points for Exams:

PDA = persistent patency of the ductus arteriosus connecting the aorta (distal to L SCA) to the PA (at junction of MPA and LPA)
Fetal DA kept open by: low PaO₂ + high PGE₂. Closes at birth due to: ↑PaO₂ + ↓PGE₂
Functional closure: 10–15 hours. Anatomical closure: 2–3 weeks
Epidemiology: 1/2500–5000 live births, F > M = 2:1, much more common in preterms
Risk factors: prematurity (most important), maternal rubella, high altitude, Char syndrome
L-to-R shunt (aorta → PA) → pulmonary overcirculation + LV volume overload + diastolic run-off
Hallmark signs: Continuous "machinery" (Gibson's) murmur at L infraclavicular/LUSB + collapsing pulse + wide pulse pressure
Murmur may be systolic only in neonatal period (before PVR drops)
Large PDA: HF at 1–2mo (term) or days (preterm); Moderate: ↓exercise tolerance; Small: asymptomatic
Eisenmenger syndrome → differential cyanosis (blue legs, pink hands) — irreversible, contraindicates closure
Preterm PDA: close with COX inhibitors (indomethacin/ibuprofen) or paracetamol
Duct-dependent CHD: keep open with PGE₁ (alprostadil) infusion
CXR large PDA: cardiomegaly + pulmonary plethora. ECG: LVH, LAE, ± RVH
Echo is diagnostic and assesses size, shunt ratio, and PA pressure

Active Recall - Patent Ductus Arteriosus

Differential Diagnosis of Patent Ductus Arteriosus (PDA) in Paediatrics

When a child presents with features suggestive of PDA — a continuous murmur at the left infraclavicular area, bounding pulses, wide pulse pressure, signs of heart failure in infancy, or an incidental echocardiographic finding — you need to think systematically about what else could produce these findings. The differential diagnosis is best approached by asking: "What else can mimic the key features of PDA?"

The three cardinal features that drive the DDx are:

Continuous murmur (heard in systole AND diastole)
Wide pulse pressure / collapsing pulse (suggesting diastolic run-off)
Left heart volume overload with pulmonary overcirculation (suggesting a significant L-to-R shunt)

We will also consider the DDx of heart failure presenting at 1–2 months of age (the typical presentation of a large PDA in term infants) and the DDx in preterm neonates with a haemodynamically significant duct.

A continuous murmur means the sound extends from systole into diastole without interruption. This requires a pressure gradient that persists throughout the entire cardiac cycle between two communicating structures. The ductus arteriosus achieves this because aortic pressure exceeds pulmonary artery pressure in both systole and diastole. But other conditions can do the same:

Condition	Mechanism of Continuous Murmur	Key Distinguishing Features
Patent ductus arteriosus	Aorta-to-PA flow throughout the cardiac cycle	Left infraclavicular/LUSB location; machinery quality; collapsing pulse; wide pulse pressure ^[1]^[2]
Venous hum (benign)	Turbulent flow in internal jugular veins due to gravity in upright position	Disappears on lying supine or turning head; heard over right supraclavicular area; very common in children aged 3–8 years. NO haemodynamic compromise. This is the most common cause of a continuous murmur in children ^[1]
Aortopulmonary window (AP window)	Direct communication between ascending aorta and main PA → continuous flow	Murmur at upper sternal border, often louder and lower than PDA; early heart failure (large defect); no diastolic run-off to same degree as PDA because the window is typically large and non-restrictive (pressure may equalise) → murmur may become purely systolic
Coronary arteriovenous fistula	Abnormal communication between a coronary artery and a cardiac chamber (usually RA/RV) or PA → continuous flow	Continuous murmur lower on precordium than PDA (mid-sternal or towards apex); may cause steal from myocardium → ischaemia signs
Ruptured sinus of Valsalva aneurysm	Aortic sinus ruptures into RA or RV → continuous aorta-to-right heart flow	Rare in children; sudden onset continuous murmur with acute HF; murmur at right or left sternal border
Surgical systemic-to-pulmonary shunt (e.g., Blalock-Taussig shunt)	Surgically created aortic-to-PA communication (subclavian artery to PA) — identical physiology to PDA	History of prior cardiac surgery for cyanotic CHD; murmur location corresponds to shunt site (usually infraclavicular)
Aortopulmonary collaterals (MAPCAs)	Systemic arterial collaterals to pulmonary arteries → continuous flow from high-pressure systemic to lower-pressure pulmonary circulation	Seen in pulmonary atresia with VSD ^[3]; multiple murmurs over the back; uneven pulmonary vascularity on CXR
Peripheral pulmonary artery stenosis	Turbulent flow across stenotic branch PAs producing a systolic murmur that extends into diastole	Common in neonates (physiological — resolves by 6 months); heard over both lung fields and back; no diastolic run-off
Coarctation of the aorta with collaterals	Intercostal collateral arteries develop to bypass the coarctation → continuous flow through tortuous collaterals	Continuous murmur over the back; weak/absent femoral pulses with radio-femoral delay; upper limb hypertension; rib notching on CXR (older children) ^[4]
Arteriovenous malformation (systemic)	High-flow AV communication anywhere in the body (cranial, hepatic, pulmonary) → continuous bruit	Bruit at the site of the AVM (e.g., cranium in vein of Galen malformation → high-output HF in neonates); not at typical PDA location

Exam Trap: Venous Hum vs PDA

The venous hum is the most common continuous murmur heard in children — it is entirely benign. If they describe a continuous murmur that disappears on lying down or with neck compression/head turning, it is a venous hum, NOT a PDA. PDA murmur does not change with posture.

Wide pulse pressure means the gap between systolic and diastolic BP is large (typically > 40 mmHg in children, though this is age-dependent). The mechanism is always diastolic run-off — blood escaping from the aorta during diastole through some abnormal pathway. PDA causes this because blood flows from the aorta into the PA during diastole. Other causes include:

Condition	Mechanism	Key Distinguishing Features
PDA	Diastolic run-off via ductus to PA	Continuous murmur at L infraclavicular area
Aortic regurgitation (AR)	Diastolic backflow from aorta to LV	Early diastolic decrescendo murmur at left sternal border (NOT continuous); displaced apex; may have Austin Flint murmur
Aortopulmonary window	Diastolic run-off via AP communication	Murmur at LUSB; early HF
Systemic AV fistula (e.g., hepatic haemangioma, vein of Galen malformation)	High-flow arteriovenous communication → reduced SVR → high output state	Continuous bruit at site of AVM; high-output HF in neonates; hepatomegaly (hepatic AVM)
Truncus arteriosus	Single great artery overriding both ventricles → unrestricted pulmonary flow → diastolic run-off via large PAs	Single S2; ejection click; systolic murmur; cyanosis with HF (common mixing lesion) ^[1]
Thyrotoxicosis / severe anaemia / sepsis	Non-cardiac: high output state → low SVR → wide pulse pressure	Tachycardia, warm peripheries, other systemic features

Acyanotic CHD with L-to-R shunts characteristically present with heart failure at approximately 2–3 months of age, as pulmonary vascular resistance (PVR) drops and shunt volume increases ^[1]^[5]. The key L-to-R shunt lesions that must be differentiated from PDA are:

Condition	Shunt Level	Key Distinguishing Features
Ventricular septal defect (VSD)	Ventricular level (LV → RV)	Most common CHD (~30%) ^[1]; pansystolic murmur at lower left sternal border (NOT continuous); thrill may be palpable; NO collapsing pulse (no diastolic run-off); murmur loudness inversely proportional to defect size in small VSDs
Patent ductus arteriosus (PDA)	Great artery level (Aorta → PA)	Continuous murmur at L infraclavicular area; collapsing pulse; wide pulse pressure
Atrial septal defect (ASD)	Atrial level (LA → RA)	Usually asymptomatic in childhood (low-pressure shunt, compensated for years); fixed widely split S2 with ejection systolic murmur at LUSB (increased flow across pulmonary valve, NOT across the defect itself); no collapsing pulse; HF rare before adulthood unless very large ^[1]
Atrioventricular septal defect (AVSD)	AV junction (combined atrial + ventricular level + abnormal AV valves)	Strongly associated with Down syndrome (trisomy 21) ^[1]; features of both ASD and VSD; AV valve regurgitation murmur; superior axis on ECG (pathognomonic); HF at 1–2 months
Aortopulmonary window	Great artery level (ascending aorta → main PA)	Rare; continuous or systolic murmur at upper sternal border; early severe HF
Truncus arteriosus	Single outflow trunk overriding both ventricles → unrestricted pulmonary flow	Cyanotic + HF (common mixing); single S2; ejection click; may have truncal valve regurgitation

In the NICU setting, the question is often: "Is this baby's clinical deterioration due to a haemodynamically significant PDA (hsPDA) or something else?" ^[6]

Condition Mimicking hsPDA	Key Distinguishing Features
Sepsis / necrotising enterocolitis (NEC)	Abdominal distension, bloody stools, pneumatosis on AXR; fever/hypothermia; raised CRP/procalcitonin. NEC can coexist with PDA (PDA increases NEC risk via diastolic steal)
Worsening respiratory distress syndrome (RDS)	Worsening ventilation needs without new murmur or bounding pulses; CXR shows ground-glass opacification rather than pulmonary plethora
Pneumonia	New infiltrates on CXR; signs of infection; purulent tracheal aspirates
Intraventricular haemorrhage (IVH)	Sudden deterioration with full fontanelle, apnoea, seizures; confirmed on cranial ultrasound
Heart failure from other structural CHD	Echocardiography is essential — may reveal VSD, AVSD, coarctation, or other lesion rather than isolated PDA

Key Point: Echo Is Essential

In both term and preterm infants, echocardiography is the gold standard to confirm PDA and exclude other structural heart disease. Never rely on murmur alone — a preterm PDA may have no murmur initially, and a murmur may be caused by a different lesion entirely. Always get an echo before initiating pharmacological closure in a preterm neonate.

Differential cyanosis (blue lower limbs, pink upper limbs) is nearly pathognomonic for Eisenmenger PDA, but consider:

Condition	Pattern	Mechanism
Eisenmenger PDA	Pink upper body, blue lower body	R-to-L shunt via PDA inserts distal to L SCA → desaturated blood to descending aorta only ^[1]^[2]
Interrupted aortic arch with PDA	Pink RUL, blue lower body; ± blue LUL depending on type	Descending aortic flow depends on R-to-L PDA; in type B, left subclavian arises distal to interruption ^[4]
Critical coarctation with PDA	Pink upper body, blue lower body	Similar to interrupted arch — lower body perfused by R-to-L duct flow
Reverse differential cyanosis (blue upper body, pink lower body)	Seen in TGA with coarctation or pHTN	PA (oxygenated blood from LV) supplies descending aorta via PDA while aorta (deoxygenated from RV) supplies upper body ^[3]

This is clinically critical — a PDA may be the only thing keeping a child alive in duct-dependent circulation:

Duct-Dependent Condition	Consequence of Ductal Closure
Critical coarctation of aorta	Collapse and shock on day 2 of life as lower body loses perfusion ^[4]^[5]
Interrupted aortic arch	Cardiovascular collapse — descending aorta entirely duct-dependent ^[4]
Critical pulmonary stenosis / pulmonary atresia (with intact ventricular septum or VSD)	Severe cyanosis — pulmonary blood flow depends on PDA ^[3]
Transposition of great arteries (TGA) with intact ventricular septum	Severe cyanosis and death — PDA provides critical intercirculatory mixing ^[3]
Hypoplastic left heart syndrome (HLHS)	Systemic collapse — systemic circulation entirely duct-dependent

Always consider: "Is this PDA the disease, or is it keeping this child alive?" In any neonate presenting with cyanosis or shock whose condition worsens as the duct closes, think of duct-dependent CHD and commence PGE₁ infusion immediately to reopen/maintain the duct while arranging urgent echocardiography ^[3]^[4]^[5].

Presenting Feature	Top Differential Diagnoses
Continuous murmur	PDA, venous hum, AP window, coronary AV fistula, surgical BT shunt, MAPCAs, CoA with collaterals
Wide pulse pressure / collapsing pulse	PDA, aortic regurgitation, AP window, systemic AV fistula, truncus arteriosus, high-output states
L-to-R shunt with HF at 1–2 months	VSD, PDA, AVSD, large ASD, AP window
Differential cyanosis	Eisenmenger PDA, interrupted aortic arch, critical CoA
Preterm neonate with worsening haemodynamics	hsPDA, sepsis, NEC, worsening RDS, IVH, other structural CHD

High Yield Summary

Differential Diagnosis of PDA — Key Points for Exams:

The most common cause of a continuous murmur in children is a venous hum (benign) — it disappears on lying supine
PDA is the most common PATHOLOGICAL cause of a continuous murmur — machinery quality, L infraclavicular, with collapsing pulse
Other continuous murmur causes: AP window, coronary AV fistula, MAPCAs, surgical shunts, CoA with collaterals
Wide pulse pressure DDx: PDA, aortic regurgitation, AP window, systemic AV fistula, truncus arteriosus
L-to-R shunt lesions presenting with HF at 1–2 months: VSD (pansystolic murmur, LLSB), PDA (continuous murmur, L infraclavicular), AVSD (Down syndrome, superior axis), ASD (usually asymptomatic in childhood)
Differential cyanosis (pink arms, blue legs) = Eisenmenger PDA, interrupted aortic arch, or critical CoA — all involve R-to-L flow via a duct to descending aorta
Always ask: "Is this PDA the disease, or is it keeping the child alive?" — duct-dependent CHD requires PGE₁, not closure
Echo is essential — never treat based on murmur alone; exclude other structural CHD

Active Recall - Differential Diagnosis of PDA

References

^[1] Senior notes: Adrian Lui Pediatrics.pdf (p190, p202) ^[2] Senior notes: Ryan Ho Cardiology.pdf (p189) ^[3] Senior notes: Adrian Lui Pediatrics.pdf (p215, p219 — Pulmonary atresia with VSD; TGA) ^[4] Senior notes: Adrian Lui Pediatrics.pdf (p212 — Interrupted aortic arch) ^[5] Lecture slides: GC 147. Heart failure and cyanosis in children acyanotic and cyanotic congenital heart disease - Part 1.pdf ^[6] Senior notes: Adrian Lui Pediatrics.pdf (p36 — Problems related to prematurity)

Diagnostic Criteria, Diagnostic Algorithm, and Investigation Modalities for Patent Ductus Arteriosus (PDA) in Paediatrics

Diagnostic Criteria

PDA does not have a single universally agreed "diagnostic criteria" set in the way that, say, rheumatic fever (Jones criteria) or Kawasaki disease do. The diagnosis is established by echocardiography demonstrating a patent communication between the descending aorta and the pulmonary artery. However, the clinical question is not just "Is there a PDA?" but rather "Is this PDA haemodynamically significant?" — because management hinges entirely on this distinction.

This is particularly important in preterm neonates, where the decision to treat pharmacologically or surgically depends on whether the PDA is causing clinically relevant haemodynamic compromise. There is no single universally adopted scoring system, but the following echocardiographic and clinical markers are used:

Echocardiographic markers of haemodynamically significant PDA (hsPDA):

Parameter	Significant	Explanation
Ductal diameter	> 1.5 mm (or > 1.5 mm/kg in preterms)	Larger duct → greater shunt volume
LA:Ao ratio	> 1.4:1 (normal ~1:1)	LA dilates from increased pulmonary venous return (volume overload from L-to-R shunt)
LV dimensions	Dilated LV (LVIDd > 2 SD for age)	LV volume overload from the shunt
Ductal flow pattern	Pulsatile, unrestricted ("growing" pattern with low-velocity flow indicating no pressure gradient)	Restrictive flow (high velocity, small jet) = small, non-significant PDA. Unrestrictive flow = near-equalisation of aortic and PA pressures = large shunt
Diastolic flow in descending aorta	Absent or retrograde diastolic flow	Diastolic "steal" — blood runs backwards from the aorta into the PA via the PDA during diastole, robbing the systemic circulation
Diastolic flow in coeliac/mesenteric/cerebral arteries	Absent or reversed end-diastolic flow	Systemic hypoperfusion from diastolic run-off — correlates with risk of NEC, IVH, renal impairment
Qp:Qs ratio	> 1.5:1 (moderate), > 2.2:1 (large)	Calculated from echo measurements of flow across pulmonary and aortic valves; directly quantifies the shunt ^[1]^[2]

Clinical markers of haemodynamic significance:

Marker	Significance
Bounding/collapsing pulses	Diastolic run-off
Widening pulse pressure	> 25 mmHg in preterms is suggestive
Hyperdynamic precordium	LV volume overload
Worsening ventilatory requirements	Pulmonary oedema from overcirculation
Metabolic acidosis	Systemic hypoperfusion
Oliguria ( < 1 mL/kg/hr)	Renal hypoperfusion
Feed intolerance / abdominal distension	Mesenteric steal

Term PDA vs Preterm PDA: Different Diagnostic Paradigms

Term infant PDA: Diagnosis is usually clinical (continuous murmur + collapsing pulse) confirmed by echo. The question is "How big is the shunt?" to guide intervention timing.
Preterm PDA: Diagnosis is often echocardiographic first (echo screening in at-risk preterms < 28 weeks), because clinical signs may be subtle, absent, or non-specific. The question is "Is this PDA haemodynamically significant enough to warrant treatment?"

Investigation Modalities

CXR is a first-line, readily available investigation that provides indirect evidence of the haemodynamic consequences of PDA. It does NOT directly visualise the duct.

Findings by PDA size:

PDA Size	CXR Findings	Pathophysiological Explanation
Small PDA	Normal CXR	Shunt volume too small to cause cardiac chamber enlargement or pulmonary overcirculation ^[1]^[2]
Large PDA	Cardiomegaly (LV dilatation)	LV volume overload → LV dilates → increased cardiothoracic ratio ( > 0.6 in neonates, > 0.55 in infants, > 0.5 in children)
Large PDA	Pulmonary plethora (increased pulmonary vascular markings)	Excessive pulmonary blood flow from L-to-R shunt → engorged pulmonary vessels visible on CXR ^[1]^[2]
Large PDA + pHTN	Prominent main PA segment	Dilated main pulmonary artery from chronically elevated PA pressure
Eisenmenger PDA	Peripheral pruning of pulmonary vessels with prominent central PA	Pulmonary arteriolar obliteration → reduced peripheral flow but dilated proximal PAs

Specific CXR features to look for:

Heart size: Cardiothoracic ratio — remember age-specific normal values
Pulmonary vascularity: Compare with size of the descending branch of the right PA (should be ≤ width of the trachea). Plethoric = too many, too large vessels
Lung fields: Pulmonary oedema (perihilar haziness, Kerley B lines) in decompensated HF
Thymus: Should be present in neonates — absence suggests DiGeorge syndrome (associated with conotruncal anomalies, but useful to note when doing a systematic CHD workup) ^[4]

CXR Interpretation Pearl

A normal CXR does NOT exclude PDA. Small PDA has no CXR abnormalities. Even moderate PDA may have only subtle changes. CXR tells you about consequences (volume overload, pulmonary congestion), not the anatomy. Echo is always needed.

ECG provides indirect evidence of chamber enlargement and pressure/volume overload resulting from PDA. Like CXR, it does not directly diagnose PDA.

Key paediatric ECG considerations:

Normal neonatal ECG shows right ventricular dominance (right axis, tall R in V1, deep S in V6) because the RV is thicker in utero to support the systemic circulation via the ductus ^[3]
By 1 month, QRS axis shifts leftward (~90°); by 1 year, adult-like LV dominance (~60°) ^[3]
Must interpret all ECG findings in context of age-specific normal values (crucial in paediatrics)

Findings by PDA size:

PDA Size	ECG Findings	Pathophysiological Explanation
Small PDA	Normal ECG	No significant volume or pressure overload ^[1]^[2]
Large PDA	LVH (left axis deviation, tall R in V6, deep S in V1)	LV volume overload → LV eccentric hypertrophy ^[1]^[2]^[3]
Large PDA	LAE (P wave duration ≥ 0.10 s, notched/biphasic P wave)	LA dilatation from increased pulmonary venous return ^[1]^[2]^[3]
Large PDA + pHTN	± RVH (right axis deviation, tall R in V1, deep S in V6)	RV pressure overload from elevated pulmonary artery pressure ^[1]^[2]
Large PDA + pHTN	± RAE (tall, peaked P waves ≥ 3 mm)	RA pressure rises with RV pressure overload → RA dilatation ^[1]^[2]
Eisenmenger PDA	Dominant RVH pattern	Suprasystemic PVR → RV pressure overload dominates

Specific ECG patterns to recognise:

ECG Pattern	Criteria (Paediatric)	Seen in PDA when...
LVH	Left axis deviation + tall R in V6 + deep S in V1	Significant L-to-R shunt with LV volume overload
LV strain	Inverted T wave in V6 or lead I	Severe, longstanding LV volume overload ^[3]
LAE	P wave duration ≥ 0.10 s; notched ("P mitrale") or biphasic in V1	Large pulmonary venous return → LA dilatation ^[3]
RVH	Right axis deviation + tall R in V1 + deep S in V6; upright T in V1 between 3 days and 6 years suggests RVH	pHTN developing ^[3]
BiVH (Katz-Wachtel phenomenon)	LVH + RVH criteria met; large equiphasic QRS complexes in V2–V5	Large PDA with both LV volume overload AND RV pressure overload from pHTN ^[3]

ECG Trap: Normal Neonatal RV Dominance vs Pathological RVH

In a neonate, right axis deviation and tall R in V1 are normal. Do NOT over-diagnose RVH in a newborn. However, if RV dominance persists or increases beyond the expected age (e.g., right axis with tall R in V1 in a 6-month-old), this is abnormal and suggests RV pressure overload (from pHTN or an obstructive right heart lesion).

Conversely, finding LVH in a neonate (when RV dominance should be normal) IS significant — it suggests significant left heart volume overload.

Echocardiography is the definitive diagnostic investigation for PDA ^[1]^[2]. It provides direct anatomical visualisation and comprehensive haemodynamic assessment.

Modalities used:

Echo Modality	What It Shows in PDA
2D imaging	Direct visualisation of the ductus arteriosus connecting the descending aorta to the PA; duct morphology (conical, tubular, window-type); measurements of ductal diameter
Colour-flow Doppler	Demonstrates the direction and pattern of flow through the PDA — typically red (towards transducer) in the PA during L-to-R shunt, showing continuous flow. Bidirectional or R-to-L flow indicates elevated PVR
Pulsed-wave / Continuous-wave Doppler	Measures velocity of flow across the PDA; estimates pressure gradient (using modified Bernoulli equation: ΔP = 4v²); determines PA systolic pressure
M-mode	Measures LA and Ao root dimensions → LA:Ao ratio; measures LV dimensions (LVIDd, LVIDs)

Key echocardiographic parameters and their interpretation:

Parameter	Normal	Haemodynamically Significant PDA	Why It Matters
Ductal diameter	Closed or tiny (< 1.5 mm)	> 1.5 mm or > 1.5 mm/kg	Larger duct = less resistance to flow = greater shunt volume
LA:Ao ratio	~1.0:1	> 1.4:1	LA enlarges because of increased pulmonary venous return from pulmonary overcirculation. This is one of the most practical bedside echo markers of hsPDA
LV internal diameter (LVIDd)	Normal for age/weight	> 2 SD above mean for age	LV dilates from chronic volume overload
Ductal flow pattern	No flow (closed duct)	Continuous L-to-R flow; unrestricted = low velocity, pulsatile; restrictive = high velocity, continuous	Unrestricted flow means PA pressure is close to aortic pressure (large shunt). Restrictive flow means a significant gradient exists (small/moderate duct with lower pressure transmission)
Diastolic flow in descending aorta	Continuous forward flow	Absent or retrograde diastolic flow	"Diastolic steal" — blood flows backwards from the aorta into the PDA during diastole instead of perfusing the body. Correlates with end-organ hypoperfusion (gut, kidneys, brain)
PA systolic pressure	< 25 mmHg (estimated from TR jet or PDA gradient)	> 50% systemic → moderate pHTN; suprasystemic → Eisenmenger	Determines whether closure is safe or contraindicated
Qp:Qs	1:1	> 1.5:1 (moderate), > 2.2:1 (large)	Directly quantifies shunt magnitude. Calculated from echo Doppler measurements of flow across the pulmonary and aortic valves ^[1]^[2]

Echo also excludes other structural CHD:

Always perform a complete structural survey — look for VSD, ASD, coarctation, aortic arch anomalies, TGA
Must exclude duct-dependent lesions — if you find a large PDA in a cyanotic neonate, do NOT close it before ruling out duct-dependent pulmonary or systemic circulation

Echo in preterm PDA — staged assessment protocol:

Many NICUs employ a structured echocardiographic assessment for preterm infants at risk of hsPDA ^[7]:

Timing	Purpose
Day 1–3 of life	Baseline: Is a PDA present? Initial size and flow pattern
Day 3–7	Has the PDA closed spontaneously? If not, is it becoming haemodynamically significant?
Post-treatment	Has pharmacological closure been successful? Is there residual flow?
Pre-discharge	Confirm closure or plan outpatient follow-up

Cardiac catheterisation is rarely needed for diagnosis of isolated PDA in the modern era, as echocardiography provides all necessary information. However, it has specific roles ^[1]^[2]:

Indication	What It Provides
Pre-intervention haemodynamic assessment (when echo is equivocal)	Direct measurement of PA pressure, PVR (in Wood units), Qp:Qs via oximetry
Assessment of PVR operability (large PDA with suspected pHTN)	PVR > 12 WU or PAP suprasystemic = closure contraindicated; PVR 8–12 WU = caution, increased perioperative risk ^[1]
Pulmonary vasodilator testing	If pHTN is borderline, test reactivity with inhaled NO or oxygen to determine reversibility
Therapeutic: transcatheter device closure	Simultaneous diagnostic and therapeutic procedure — see Management section

Catheterisation findings in PDA:

Finding	Explanation
Step-up in oxygen saturation at PA level	Oxygenated blood from the aorta enters the PA via PDA → oxygen saturation in PA is higher than in RV (the "step-up" confirms the L-to-R shunt at PA level)
Elevated PA pressure	Direct manometry confirms degree of pHTN
Calculation of Qp:Qs	Using the Fick principle with oxygen saturations: Qp:Qs = (SaO₂ − SvO₂) / (SpvO₂ − SpaO₂)
PVR calculation	PVR = (mean PAP − LA pressure) / Qp. Measured in Wood units (WU). Critical for determining operability
Angiography	Injection of contrast into the aortic arch delineates the duct anatomy (Krichenko classification for device selection)

Investigation	Role in PDA	Findings
Pulse oximetry (pre- and post-ductal)	Screening in neonates; detection of differential cyanosis	Pre-ductal (right hand) SpO₂ > post-ductal (either foot) SpO₂ by > 3% suggests R-to-L ductal shunt (seen in duct-dependent CHD or Eisenmenger PDA). Note: L-to-R PDA will NOT show a pre-/post-ductal difference (both are well-oxygenated)
BNP / NT-proBNP	Biomarker of volume overload and ventricular wall stress; adjunct in preterm PDA assessment	Elevated in hsPDA; can help guide treatment decisions and monitor response to therapy. Cut-offs are not firmly established in neonates but NT-proBNP > 10,000 pg/mL in first week correlates with hsPDA
Blood gas (arterial/capillary)	Assess for metabolic acidosis in preterm with suspected hsPDA	Metabolic acidosis (low pH, elevated lactate) suggests systemic hypoperfusion from diastolic steal
Renal function (urea, creatinine)	Monitor for renal impoperfusion; baseline before NSAID therapy	Elevated creatinine suggests renal hypoperfusion; also needed to assess safety of indomethacin/ibuprofen (nephrotoxic)
CT angiography / MRI	Rarely used for isolated PDA; reserved for complex anatomy	Delineation of complex aortic arch anatomy, unusual PDA morphology, or MAPCAs ^[1]

Investigation	Small PDA	Moderate PDA	Large PDA	Eisenmenger PDA
CXR	Normal	Mild cardiomegaly	Cardiomegaly + pulmonary plethora	Prominent central PA, peripheral pruning
ECG	Normal	LVH	LVH, LAE, ± RVH	Dominant RVH, RAE
Echo	Small duct, restrictive flow; normal LA:Ao and LV	Moderate duct; LA:Ao 1.2–1.4; mild LV dilatation	Large duct; LA:Ao > 1.4; LV dilatation; reversed diastolic flow in descending aorta	R-to-L flow; suprasystemic PA pressure
Catheterisation	Not needed	Rarely needed	May be needed for PVR assessment	Essential for PVR quantification

^[1]^[2]^[3]

Pre-ductal saturation is measured from the right hand (supplied by the brachiocephalic trunk, which arises proximal to the ductus). Post-ductal saturation is measured from either foot (supplied by the descending aorta, distal to the ductus insertion).

Scenario	Pre-ductal (RH)	Post-ductal (foot)	Interpretation
Normal / L-to-R PDA	95–100%	95–100%	Oxygenated blood from aorta flows INTO PA (not into descending aorta from PA), so both saturations are high
R-to-L PDA (Eisenmenger or duct-dependent)	95–100%	< 90% (> 3% lower than pre-ductal)	Deoxygenated blood from PA enters descending aorta → lower limb desaturation
TGA with PDA	Low	Higher than pre-ductal ("reverse differential")	Mixing at ductal level; LV (connected to PA in TGA) sends oxygenated blood to descending aorta via PDA

Newborn pulse oximetry screening (performed at 24–48 hours) can detect critical CHD including duct-dependent lesions. A post-ductal SpO₂ < 95% or a pre-/post-ductal difference > 3% warrants urgent echocardiography ^[5].

Why Does a Normal L-to-R PDA NOT Show a Pre-/Post-Ductal SpO₂ Difference?

Because in L-to-R PDA, oxygenated blood flows FROM the aorta INTO the PA. The descending aorta still receives fully oxygenated blood from the LV — the shunt goes the other way. Only when the shunt reverses (R-to-L, i.e., Eisenmenger or duct-dependent physiology) does deoxygenated blood enter the descending aorta, causing lower post-ductal saturations.

High Yield Summary

Diagnosis of PDA — Key Points for Exams:

Echocardiography is the gold standard — confirms PDA, measures ductal diameter, assesses LA:Ao ratio, Qp:Qs, LV dimensions, diastolic flow patterns, and PA pressure
LA:Ao ratio > 1.4 indicates haemodynamically significant PDA in preterm infants
Reversed/absent diastolic flow in descending aorta = diastolic steal = systemic hypoperfusion = hsPDA
CXR: Large PDA → cardiomegaly + pulmonary plethora; Small PDA → normal
ECG: Large PDA → LVH + LAE ± RVH (if pHTN); Small PDA → normal
Remember age-specific ECG normals — RV dominance is normal in neonates; LVH in a neonate IS significant
Cardiac catheterisation is reserved for PVR assessment in borderline pHTN cases and for transcatheter closure
PVR > 12 WU or suprasystemic PAP = closure contraindicated (Eisenmenger)
Pre-/post-ductal SpO₂ difference > 3% suggests R-to-L ductal shunt (Eisenmenger or duct-dependent CHD) — a normal L-to-R PDA shows NO difference
Newborn pulse oximetry screening at 24–48 hours can detect critical CHD

Active Recall - PDA Diagnosis and Investigations

References

^[1] Senior notes: Adrian Lui Pediatrics.pdf (p199, p202) ^[2] Senior notes: Ryan Ho Cardiology.pdf (p189) ^[3] Senior notes: Adrian Lui Pediatrics.pdf (p199 — ECG in paediatrics, chamber enlargement criteria) ^[4] Senior notes: Adrian Lui Pediatrics.pdf (p212 — Interrupted aortic arch; DiGeorge thymus absence) ^[5] Lecture slides: GC 147. Heart failure and cyanosis in children acyanotic and cyanotic congenital heart disease - Part 1.pdf ^[7] Senior notes: Ryan Ho Fundamentals.pdf (p39 — Heart murmurs reference)

Management of Patent Ductus Arteriosus (PDA) in Paediatrics

Management of PDA is fundamentally determined by three factors: (1) the age group (preterm vs term), (2) the haemodynamic significance of the PDA, and (3) the presence of complications such as heart failure or pulmonary hypertension. The overarching principle is that a PDA that is causing harm should be closed, but how it is closed differs dramatically between preterm and term infants.

Management depends on size, symptoms, shunt ratio (Qp:Qs) and pulmonary pressure ^[1]^[2].

Before discussing specific treatments, let's establish the framework:

Clinical Scenario	Management Approach
Silent/tiny PDA (incidental echo finding, no murmur)	Observation; no intervention needed
Small PDA (audible murmur, Qp:Qs < 1.5:1, normal chambers)	Historically observed with IE prophylaxis counselling; current 2024 AHA guidelines support transcatheter closure for all audible PDAs due to lifetime IE risk
Moderate PDA (Qp:Qs 1.5–2.2:1, mild LV dilatation)	Elective closure (transcatheter preferred)
Large PDA (Qp:Qs > 2.2:1, HF symptoms)	Medical stabilisation of HF → definitive closure (transcatheter or surgical)
Preterm hsPDA	Conservative supportive care → pharmacological closure → surgical/transcatheter closure if refractory
Eisenmenger PDA (PVR suprasystemic)	Closure CONTRAINDICATED — palliative care, pulmonary vasodilator therapy, consider heart-lung transplant ^[1]^[2]

Treatment Modalities

This is the first-line approach for preterm PDA, based on growing evidence that many preterm PDAs close spontaneously and that aggressive early treatment may not improve long-term outcomes.

Rationale: The preterm duct has the potential for delayed spontaneous closure. Up to 34% of hsPDAs in extremely preterm infants close without pharmacological intervention by discharge. Conservative management avoids drug side effects while supporting the infant through the period of haemodynamic compromise.

Measure	Mechanism / Rationale
Fluid restriction (typically 130–150 mL/kg/day, avoid excessive volumes)	Reduces intravascular volume → reduces preload → reduces LV volume overload and pulmonary congestion. However, overly restrictive fluids impair nutrition, so balance is key
Respiratory support (CPAP, mechanical ventilation with appropriate PEEP)	PEEP increases intrathoracic pressure → reduces pulmonary blood flow → may reduce L-to-R shunt. Also supports gas exchange in the setting of pulmonary oedema
Nutritional optimisation (concentrated feeds, fortified breast milk)	Increased metabolic demands from HF require higher caloric intake; concentrated formulas reduce volume while maintaining calories
Maintain adequate haematocrit (target Hb > 12 g/dL in symptomatic preterm)	Anaemia → reduced oxygen-carrying capacity → compensatory increase in cardiac output → worsens HF. Also, low haematocrit reduces blood viscosity → increases ductal flow
Avoid excessive supplemental oxygen	O₂ caution in large L-to-R shunt: ↑PAO₂ → pulmonary vasodilation → ↓PVR → ↑shunting ^[8]. Only give enough O₂ to maintain target SpO₂ (90–95% in preterms)

The Shifting Paradigm: Conservative vs Early Treatment

Traditional teaching was to treat all hsPDAs aggressively with early pharmacological closure. However, multiple recent RCTs (including the PDA-TOLERATE trial and Baby-OSCAR trial, 2019–2023) have shown that early pharmacological treatment does NOT reduce the composite outcome of death or BPD in extremely preterm infants. Current practice (2024–2026) increasingly favours an initial conservative approach ("expectant management") in many centres, reserving pharmacotherapy for infants with clear haemodynamic compromise refractory to supportive care.

II. Pharmacological Closure (Preterm Neonates Only)

Pharmacological closure is effective in preterm infants only — it does NOT work in term infants because term PDA is a structural defect, not simply persistent prostaglandin sensitivity.

Mechanism: All pharmacological agents work by inhibiting prostaglandin synthesis, thereby removing the PGE₂-mediated vasodilatory signal that keeps the immature duct open. Without PGE₂, the ductal smooth muscle constricts, leading to functional and eventually anatomical closure.

COX enzymes (COX-1 and COX-2) catalyse the conversion of arachidonic acid to prostaglandins, including PGE₂. Inhibiting COX → ↓PGE₂ → ductal constriction.

Agent	Ibuprofen	Indomethacin
Class	Non-selective COX inhibitor	Non-selective COX inhibitor
Route	IV (preferred) or oral/rectal	IV
Dosing	Loading: 10 mg/kg IV, then 5 mg/kg at 24h and 48h (3-dose course)	Loading: 0.2 mg/kg IV, then 0.1–0.25 mg/kg at 12–24h intervals (3-dose course; dose escalates with postnatal age)
Efficacy	~70–80% closure rate when given early (< 7 days)	~70–80% closure rate
Advantages	Less renal side effects than indomethacin (better maintained renal blood flow); does not reduce cerebral or mesenteric blood flow as significantly	Well-established; also reduces IVH risk (reduces cerebral blood flow fluctuation)
Disadvantages	Displaces bilirubin from albumin → avoid in significant hyperbilirubinaemia	More nephrotoxic; reduces cerebral and mesenteric blood flow (risk of NEC); oliguria
Current preference	Ibuprofen is preferred first-line in most centres (including Hong Kong) due to better renal safety profile	Still used; some centres prefer it for its IVH-protective effect

Feature	Detail
Mechanism	Inhibits PGE₂ synthesis via the peroxidase component of COX (different site from NSAIDs — acts on the POX active site of prostaglandin H₂ synthase). This reduces PGE₂ production in a gentler manner than COX inhibitors
Route	IV or oral
Dosing	15 mg/kg every 6 hours for 3–7 days (IV or oral)
Efficacy	~70–80% (comparable to COX inhibitors in recent meta-analyses)
Advantages	Fewer renal side effects than COX inhibitors; does not affect platelet function; safe in the setting of thrombocytopenia, NEC, or renal impairment — can be used when COX inhibitors are contraindicated
Disadvantages	Theoretical hepatotoxicity (though not demonstrated at standard doses in neonates); some concern about long-term neurodevelopmental effects (very preliminary data, not established)
Current status	Increasingly used as first-line alternative or when COX inhibitors are contraindicated. Some centres now use paracetamol as first-line given its safety profile

Contraindication	Reason
Duct-dependent congenital heart disease	Closing the PDA would be fatal — the duct is keeping the child alive (critical CoA, PA with IVS, TGA, HLHS, etc.)
Active NEC or suspected NEC	COX inhibitors reduce mesenteric blood flow → worsen gut ischaemia. Paracetamol may be cautiously used
Significant renal impairment (creatinine > 1.5–1.8 mg/dL, urine output < 0.6 mL/kg/hr)	COX inhibitors are nephrotoxic → worsen renal failure. Paracetamol is preferred if treatment needed
Active bleeding / severe thrombocytopenia (platelets < 50,000/μL)	COX inhibitors impair platelet function → increase bleeding risk. Paracetamol does not affect platelets
Significant hyperbilirubinaemia (especially for ibuprofen)	Ibuprofen displaces bilirubin from albumin binding sites → increases free bilirubin → risk of kernicterus
Term infant PDA	Pharmacological closure is ineffective — the defect is structural, not prostaglandin-dependent

Exam Must-Know: Three Drugs for Preterm PDA Closure

The three pharmacological agents for preterm PDA closure and their key differences:

Indomethacin — most nephrotoxic, reduces IVH risk (reduces cerebral flow fluctuation)
Ibuprofen — preferred in most centres; better renal profile
Paracetamol — safe in renal impairment, thrombocytopenia, NEC; alternative/first-line in some centres

None of these work in term PDA — because term PDA is structural, not prostaglandin-dependent.

When a PDA causes heart failure — whether in a symptomatic term infant or a preterm neonate — medical treatment of HF is needed as a bridge to definitive closure or while assessing suitability for intervention.

The management framework for paediatric heart failure (as per lecture slides ^[5]):

1. Identification of the cause and precipitating factors 2. Tackling of precipitating factors 3. General supportive management 4. Medical therapy of heart failure (diuretics, digoxin, ACEI, carvedilol) 5. Treatment of underlying cause, if possible, by surgical or catheter intervention 6. Mechanical circulatory support and heart transplantation

Specific medications for PDA-related HF:

Drug	Class	Mechanism in PDA Context	Paediatric Dosing
Furosemide (frusemide)	Loop diuretic	Reduces preload by promoting salt and water excretion → relieves pulmonary congestion and oedema	1–2 mg/kg/dose IV/oral, 1–3 times daily
Spironolactone	MRA (mineralocorticoid receptor antagonist)	Potassium-sparing diuretic; anti-fibrotic effects; counteracts RAAS activation	1–3 mg/kg/day oral in 1–2 divided doses
Captopril / Enalapril	ACE inhibitor	Reduces afterload (↓SVR) → improves forward cardiac output; also ↓ RAAS-mediated fluid retention. Caution: reducing SVR may increase the L-to-R shunt if the PDA is still open, but the net effect is beneficial because improved LV function and reduced congestion outweigh this	Captopril: 0.1–0.5 mg/kg/dose TDS; Enalapril: 0.05–0.1 mg/kg/dose BD (start low, titrate up)
Digoxin	Cardiac glycoside	Positive inotrope (inhibits Na⁺/K⁺-ATPase → increases intracellular Ca²⁺ → increased contractility); also slows AV conduction. Seldom used due to narrow therapeutic index ^[8]	Loading: 20–30 μg/kg (term), 15–20 μg/kg (preterm); Maintenance: 5–10 μg/kg/day
Carvedilol	Non-selective β-blocker + α1-blocker	Neurohormonal modulation (reduces sympathetic overdrive); anti-remodelling. Used in chronic HF, not acute decompensation	0.05–0.1 mg/kg/dose BD, titrate slowly

General supportive measures ^[8]:

Bed rest with elevation of bed head → improves lung function by reducing hydrostatic pulmonary oedema
High caloric diet → increased metabolic demands from HF require caloric supplementation (up to 120–150 kcal/kg/day in infants)
Fluid restriction → reduces volume overload
Oxygen with caution → in large L-to-R shunt, excessive O₂ causes pulmonary vasodilation → ↓PVR → ↑shunting ^[8]
Treat precipitating factors → infection, anaemia, arrhythmia, electrolyte disturbance

HF Stage	Medical Therapy
Stage A (at risk, no symptoms)	No specific treatment
Stage B (structural, asymptomatic)	ACEI/ARB + beta-blocker (e.g., carvedilol)
Stage C (structural, symptomatic)	ACEI/ARB + beta-blocker + MRA ± diuretics
Stage D (refractory)	Above + IV inotropes (e.g., dobutamine, milrinone), diuretics, ± mechanical support ^[8]

Transcatheter device closure is now the preferred method for PDA closure in term infants and older children — it is minimally invasive, avoids thoracotomy, and has excellent success rates.

Feature	Detail
Procedure	Catheter inserted via femoral artery or vein → device deployed across the PDA under fluoroscopic and echocardiographic guidance
Devices	Amplatzer Duct Occluder (ADO) I or II; Amplatzer Vascular Plug; coils (for small PDAs); Piccolo™ Occluder (for small preterms ≥ 700g)
Success rate	> 95% immediate closure; > 98% at 1 year
Advantages	No thoracotomy; shorter hospital stay (usually 1–2 days); lower morbidity; cosmetically superior; avoids cardiopulmonary bypass
Minimum weight	ADO I: typically > 5–6 kg; Piccolo™: ≥ 700 g (FDA-approved for preterm ≥ 700 g)
Timing	Elective: usually after 6–12 months of age in term infants; earlier if symptomatic and weight allows

Indications for transcatheter closure:

Indication	Rationale
All audible PDAs (moderate or small with murmur) in term infants	Lifetime risk of IE; LV volume overload in moderate PDAs; current guidelines support closure [2024 AHA/ACC]
Haemodynamically significant PDA with Qp:Qs > 1.5:1	Volume overload; HF risk
PDA with LV dilatation	Evidence of haemodynamic consequence
History of infective endocarditis	Definitive prevention of recurrence

Contraindications:

Contraindication	Reason
PVR > 12 WU or PAP suprasystemic (Eisenmenger)	Risk of precipitating acute RV heart failure + ↓LV output — closing the PDA removes the "pop-off valve" for the RV → acute RV decompensation ^[1]^[2]
PVR 8–12 WU or PAP 75–100% systemic	↑Risk of perioperative complications — exercise extreme caution; may attempt trial occlusion with catheter to assess haemodynamic response before definitive closure ^[1]^[2]
Duct-dependent circulation	The PDA is life-sustaining
Infant too small for device (< 700 g for Piccolo™)	Technical limitation; surgical ligation preferred
Unfavourable anatomy (very short/window-type duct)	Device may embolise or obstruct LPA or aorta

Surgical closure was historically the only option and remains important in specific situations.

Feature	Detail
Procedure	Left posterolateral thoracotomy (through 3rd or 4th intercostal space) → PDA identified → ligation (suture tie) or division (cut between ligatures) or clip application
No cardiopulmonary bypass needed	The PDA is an extracardiac structure — surgery is performed through the chest without stopping the heart
Success rate	> 99%
Mortality	< 1% (extremely low in isolated PDA)

Indications for surgical closure:

Indication	Rationale
Preterm PDA refractory to pharmacological closure	COX inhibitors and paracetamol have failed or are contraindicated
Preterm PDA where pharmacological closure is contraindicated	Active NEC, severe renal failure, thrombocytopenia — and conservative measures insufficient
Term infant too small or with anatomy unsuitable for transcatheter device	Weight < 5 kg (for conventional devices); unfavourable duct morphology
Large PDA with heart failure refractory to medical management	Definitive closure needed urgently
Associated cardiac anomaly requiring surgical repair	PDA ligated at the time of open-heart surgery for the other lesion

Complications of surgical ligation:

Complication	Mechanism
Recurrent laryngeal nerve palsy	The left recurrent laryngeal nerve loops around the aortic arch at the level of the ligamentum arteriosum/PDA — surgical manipulation can damage it → hoarse cry, feeding difficulties
Phrenic nerve palsy	Left phrenic nerve runs near the operative field → diaphragmatic paralysis → respiratory compromise
Chylothorax	Thoracic duct injury during dissection → lymphatic fluid leakage into pleural space
Pneumothorax	From thoracotomy
Incomplete closure / recanalisation	Rare; more common with ligation alone than with division
Post-ligation cardiac syndrome (preterm)	Acute LV dysfunction after PDA ligation → hypotension, low cardiac output. Mechanism: sudden increase in LV afterload (SVR rises when diastolic run-off ceases) in a myocardium adapted to low afterload. Occurs in ~30% of preterm surgical ligations → managed with milrinone (inodilator)

VI. Special Situations

In duct-dependent CHD, the PDA must be kept OPEN with PGE₁ (alprostadil) infusion — closing it would be fatal.

Feature	Detail
Drug	Prostaglandin E₁ (PGE₁, alprostadil)
Route	Continuous IV infusion
Starting dose	0.01–0.05 μg/kg/min (lower dose for maintenance after duct has reopened)
Higher dose	Up to 0.1 μg/kg/min to reopen a closing duct
Mechanism	PGE₁ binds EP4 receptors on ductal smooth muscle → activates adenylate cyclase → ↑cAMP → smooth muscle relaxation → ductal dilation
Side effects	Apnoea (15–20% — most important; always have intubation equipment ready), fever, hypotension, flushing, diarrhoea, seizures (rare), cortical hyperostosis (with prolonged use)

Scenario	Management
Silent PDA (tiny, incidental)	Observation
Small PDA (audible, no LV dilatation)	Transcatheter closure (elective) — prevents lifetime IE risk
Moderate PDA (LV dilatation, Qp:Qs 1.5–2.2)	Transcatheter closure (elective)
Large PDA with HF (Qp:Qs > 2.2)	Medical Mx of HF (diuretics, ACEI, digoxin, nutrition) → definitive closure (transcatheter or surgical)
Preterm hsPDA	Conservative → Pharmacological (ibuprofen/indomethacin/paracetamol) → Surgical ligation if refractory
PDA with pHTN (PVR < 8 WU)	Closure safe
PDA with pHTN (PVR 8–12 WU)	Caution — ↑periop risk; trial occlusion at catheterisation ^[1]^[2]
Eisenmenger PDA (PVR > 12 WU)	Closure CONTRAINDICATED; pulmonary vasodilators; transplant ^[1]^[2]
Duct-dependent CHD	PGE₁ infusion to maintain duct patency

High Yield Summary

Management of PDA — Key Exam Points:

Management depends on size, symptoms, Qp:Qs, and pulmonary pressure ^[1]^[2]
Preterm PDA: Conservative first → Pharmacological closure (ibuprofen preferred, indomethacin or paracetamol alternatives) → Surgical ligation if refractory
Term PDA: Pharmacological closure does NOT work. Transcatheter device closure is first-line; surgical ligation if too small or unsuitable anatomy
Three drugs for preterm PDA closure: Indomethacin (most nephrotoxic, reduces IVH), Ibuprofen (preferred, less nephrotoxic), Paracetamol (safe in renal failure/thrombocytopenia/NEC)
Medical HF management (per lecture slides): Identification of cause → tackle precipitants → supportive measures → medical therapy (diuretics, digoxin, ACEI, carvedilol) → surgical/catheter intervention → mechanical support/transplant ^[5]
Avoid excessive O₂ in large L-to-R shunt → pulmonary vasodilation → ↓PVR → ↑shunting ^[8]
Closure contraindicated if PVR > 12 WU or PAP suprasystemic (Eisenmenger) → risk of acute RV failure ^[1]^[2]
PVR 8–12 WU: caution, ↑periop risk ^[1]^[2]
Duct-dependent CHD: PGE₁ (alprostadil) 0.01–0.05 μg/kg/min → keep duct open; SE: apnoea (have intubation ready)
Post-ligation cardiac syndrome in preterms: acute LV dysfunction from sudden afterload increase; treat with milrinone
Surgical complications: recurrent laryngeal nerve palsy (hoarse cry), phrenic nerve palsy, chylothorax

Active Recall - PDA Management

References

^[1] Senior notes: Adrian Lui Pediatrics.pdf (p200, p202) ^[2] Senior notes: Ryan Ho Cardiology.pdf (p189, p191, p194) ^[5] Lecture slides: GC 147. Heart failure and cyanosis in children acyanotic and cyanotic congenital heart disease - Part 1.pdf (p36) ^[8] Senior notes: Adrian Lui Pediatrics.pdf (p200 — Management of paediatric HF, O₂ caution)

Complications of Patent Ductus Arteriosus (PDA) in Paediatrics

The complications of PDA arise from two fundamental haemodynamic derangements: (1) pulmonary overcirculation from the L-to-R shunt, and (2) systemic hypoperfusion from diastolic run-off ("steal"). The severity and type of complications differ between preterm and term infants, and between treated and untreated PDA. We will also cover complications of the treatments themselves.

A. Complications of the Untreated PDA Itself

This is the most common complication of a haemodynamically significant PDA and represents the clinical endpoint of chronic LV volume overload.

Feature	Detail
Mechanism	L-to-R shunt → pulmonary overcirculation → ↑pulmonary venous return → LA and LV volume overload → LV dilatation → when compensatory mechanisms (Frank-Starling, sympathetic activation, RAAS) are exhausted → CHF ^[1]^[2]
Timing	Term infants: HF symptoms at 1–2 months (as PVR drops and shunt volume increases) ^[1]^[2]. Preterm infants: within days (faster PVR drop + lower myocardial reserve + immature contractile machinery) ^[1]^[2]
Clinical features	Tachypnoea, tachycardia, hepatomegaly, poor feeding, FTT, sweating (especially during feeds), recurrent chest infections
Why 1–2 months?	At birth, PVR is still high → limits L-to-R shunting. Over 6–8 weeks, PVR drops physiologically as pulmonary vasculature remodels → shunt volume increases progressively → LV cannot cope → HF

Why Does the LV Fail and Not the RV?

In PDA with L-to-R shunt, it is the LV that is volume-overloaded (receiving increased pulmonary venous return), NOT the RV. The RV is only affected later if pulmonary hypertension develops (pressure overload). This is different from ASD, where the RV is volume-overloaded.

Feature	Detail
Mechanism	Three converging factors: (1) ↑metabolic demand — the heart is working harder (hyperdynamic circulation, increased myocardial oxygen consumption), increasing total energy expenditure by 20–30%; (2) ↓caloric intake — tachypnoea interferes with feeding (the infant cannot coordinate suck-swallow-breathe), leading to poor feeding and early fatigue; (3) ↓gut perfusion — diastolic run-off reduces mesenteric blood flow → impaired nutrient absorption
Clinical importance	FTT is a major indication for definitive PDA closure. If an infant with PDA is not growing despite optimised nutrition, the PDA needs to be closed ^[1]
Assessment	Serial plotting on growth charts (weight, length, head circumference) — expect weight to falter first, then length, then head circumference if severe

Feature	Detail
Mechanism	Pulmonary overcirculation → chronic pulmonary congestion → oedematous, fluid-logged airways → impaired mucociliary clearance → favourable environment for bacterial colonisation → recurrent pneumonia and bronchiolitis
Clinical relevance	Recurrent chest infections in an infant should always prompt consideration of an underlying L-to-R shunt (VSD, PDA, AVSD) ^[1]
Organisms	RSV bronchiolitis (PDA infants have worse outcomes), bacterial pneumonia (S. pneumoniae, H. influenzae)

Feature	Detail
Mechanism	Chronic excessive pulmonary blood flow → shear stress on pulmonary arteriolar endothelium → endothelial dysfunction → release of vasoconstrictors (endothelin-1) + reduced vasodilators (NO, prostacyclin) → pulmonary arteriolar remodelling (medial hypertrophy → intimal fibrosis → plexiform lesions) → progressive, eventually fixed elevation of PVR
Definition	PA pressure > 50% systemic pressure = moderate pHTN. PAP suprasystemic = severe / Eisenmenger ^[1]
Timeline	Risk increases with size of PDA and duration of exposure. In a large PDA, irreversible changes can begin within the first 1–2 years of life. This is why early closure (before 6–12 months) is recommended for large PDAs
Clinical signs	Loud P2, single S2, RV heave, loss of the continuous murmur (pressure gradient equalises → flow ceases → murmur disappears)

The most feared long-term complication of an untreated large PDA. Once established, it is irreversible and carries a poor prognosis ^[2]^[9].

Feature	Detail
Definition	Triad of: (1) congenital L-to-R shunt, (2) pulmonary arterial disease, (3) cyanosis ^[9]
Incidence	Up to 80% in large, unrepaired VSD and PDA in infancy/early childhood ^[9]
Mechanism	Chronic pulmonary overcirculation → irreversible pulmonary vascular disease with ↑PVR → eventual equalisation or suprasystemic PA pressure → reversal of shunt to R-to-L → systemic hypoxia (cyanosis) ^[1]^[2]^[9]
Clinical features	Differential cyanosis and clubbing (toes blue, fingers pink) — because the PDA inserts distal to L SCA → deoxygenated blood enters descending aorta only ^[1]^[2]
	Exertional dyspnoea, fatigue — fixed PVR limits pulmonary blood flow
	Reactive erythrocytosis (polycythaemia) — chronic hypoxia stimulates EPO → ↑red cell mass → hyperviscosity → fatigue, headache, stroke risk ^[9]
	Haemoptysis — rupture of fragile pulmonary vessels under high pressure ^[9]
	Stunted growth — chronic hypoxia impairs growth ^[9]
	Loss of the continuous murmur — pressure equalisation eliminates the gradient → no flow → no murmur. May hear loud P2 and new PR/TR murmur instead ^[9]
Complications of Eisenmenger syndrome	Cardiac: progressive right HF, arrhythmia, IE (rare) ^[9]
	Pulmonary: pulmonary artery thrombosis, massive haemoptysis ^[9]
	Systemic: stunted growth, polycythaemia, cerebral embolism/abscess (paradoxical embolism through R-to-L shunt → emboli bypass pulmonary filter → reach systemic/cerebral circulation) ^[9]
Management	Closure CONTRAINDICATED. Avoid ↓afterload (strenuous exercise, vasodilators, anaesthesia). Pregnancy absolutely contraindicated (maternal mortality 30–50%) ^[9]
	Pulmonary vasodilators: endothelin receptor antagonist (bosentan), prostacyclin analogues (epoprostenol, iloprost), PDE5 inhibitors (sildenafil) ^[9]
	Curative: heart-lung transplantation or lung transplantation + intracardiac repair ^[9]
Prognosis	30–40% 10-year mortality with mean age of death at 37 years if transplant not done ^[9]

Why Is Closure Contraindicated in Eisenmenger Syndrome?

When PVR is suprasystemic, the R-to-L PDA shunt acts as a "pop-off valve" for the RV — it decompresses the right heart by allowing some blood to bypass the lungs. If you close the PDA:

RV suddenly faces the full brunt of suprasystemic PVR with no escape route → acute RV failure
LV is underfilled (because RV cannot push blood through the lungs adequately) → ↓LV output → cardiogenic shock
The fixed, irreversible pulmonary vascular disease means PVR will NOT decrease after closure This is why PAP suprasystemic or PVR > 12 WU is an absolute contraindication to closure ^[1]^[2]

Feature	Detail
Mechanism	Turbulent high-velocity jet from the aorta through the PDA into the PA damages the endothelial surface of the PA at the jet impact site → endothelial denudation → platelet-fibrin deposition → nidus for bacterial colonisation → vegetation formation
Location of vegetations	Typically on the pulmonary artery side of the ductus (at the jet impact site), or on the pulmonary valve
Risk	Even small PDAs carry a lifetime IE risk — the smaller the PDA, the higher the jet velocity, the more endothelial damage. This is paradoxical but important. Lifetime IE risk estimated at ~0.5% per year ^[2]
Organisms	Viridans streptococci (most common), Staphylococcus aureus, HACEK group
Prevention	2024 AHA/ACC guidelines support closure of all audible PDAs partly to eliminate lifetime IE risk. Antibiotic prophylaxis for dental procedures is recommended for the first 6 months after device/surgical closure, and lifelong if a residual shunt remains
Clinical features	Fever, malaise, new/changing murmur, splenomegaly, petechiae, splinter haemorrhages, Janeway lesions, Osler nodes. In children, often presents more insidiously than in adults

B. Complications Specific to Preterm PDA

Preterm infants with hsPDA are vulnerable to end-organ hypoperfusion from diastolic run-off ("steal") in addition to the pulmonary overcirculation seen in term infants. These complications are unique to or much more common in the preterm population ^[6]:

Feature	Detail
Mechanism	Diastolic run-off through the PDA → blood "stolen" from the descending aorta during diastole → mesenteric hypoperfusion → intestinal ischaemia → mucosal barrier breakdown → bacterial translocation → NEC
Evidence	hsPDA is an independent risk factor for NEC in VLBW infants. The combination of reversed diastolic flow in the superior mesenteric artery (on echo) and PDA strongly predicts NEC
Clinical features	Abdominal distension, bilious aspirates, bloody stools, pneumatosis intestinalis on AXR
Practical implication	Active or suspected NEC is a contraindication to COX inhibitor therapy (further reduces mesenteric flow). Paracetamol may be cautiously used as an alternative

Feature	Detail
Mechanism	Two pathways: (1) Diastolic steal → fluctuating cerebral blood flow (alternating hyperperfusion during systole and hypoperfusion during diastole) → fragile germinal matrix vessels in preterm brain rupture; (2) Hyperdynamic circulation → increased cerebral systolic flow → increased transmural pressure across immature capillaries
Risk period	First 72 hours of life (when the germinal matrix is most fragile); hsPDA increases risk
Grades	Grade I (subependymal), Grade II (into ventricle without dilatation), Grade III (with ventricular dilatation), Grade IV (parenchymal involvement)
Protective effect of indomethacin	Indomethacin reduces cerebral blood flow variability → may reduce IVH incidence. This was the basis for prophylactic indomethacin trials (though current practice has moved away from routine prophylaxis)

Feature	Detail
Mechanism	Diastolic run-off → reduced renal perfusion pressure → pre-renal AKI → oliguria ( < 1 mL/kg/hr), rising creatinine
Clinical significance	Oliguria is a clinical marker of hsPDA. Also important to check renal function before starting COX inhibitors (which are themselves nephrotoxic)

Feature	Detail
Mechanism	Pulmonary overcirculation from PDA → pulmonary oedema → need for prolonged mechanical ventilation and supplemental oxygen → ventilator-induced and oxygen-induced lung injury → arrest of alveolar development → BPD ^[6]
Controversy	The causal relationship between PDA and BPD is debated. PDA may be a marker of extreme prematurity rather than a direct cause of BPD. Recent trials suggest that aggressive early PDA treatment does not significantly reduce BPD rates
Definition	Need for supplemental oxygen or respiratory support at 36 weeks' corrected gestational age

Feature	Detail
Mechanism	Diastolic steal → cerebral hypoperfusion → ischaemic injury to watershed areas (periventricular white matter) in the premature brain
Long-term consequence	Cerebral palsy (especially diplegic CP), developmental delay ^[6]

C. Complications of PDA Treatment

Drug	Complications	Mechanism
Indomethacin	Nephrotoxicity (oliguria, ↑creatinine)	COX inhibition → ↓renal prostaglandin-mediated afferent arteriolar vasodilation → ↓GFR
	Reduced mesenteric blood flow → NEC risk	COX inhibition → ↓gut prostaglandin-mediated vasodilation
	Reduced cerebral blood flow	Vasoconstriction of cerebral vessels
	Platelet dysfunction → bleeding	COX-1 inhibition → ↓thromboxane A₂ → impaired platelet aggregation
	GI perforation (rare, <2%)	Direct mucosal injury + ischaemia
Ibuprofen	Similar to indomethacin but less nephrotoxic	Better preservation of renal prostaglandin function
	Displaces bilirubin from albumin → risk of kernicterus	Competes for albumin binding sites → ↑free unconjugated bilirubin
Paracetamol	Hepatotoxicity (theoretical at standard doses)	NAPQI accumulation if glutathione depleted; rarely clinically significant in neonates at therapeutic doses
	Possible transient ↑liver enzymes	Direct hepatocellular effect
All agents	Failure to close (20–30%)	Drug may not achieve sufficient PGE₂ suppression; structural component to ductal patency
All agents	Reopening after initial closure (up to 20–30%)	Especially in extremely preterm infants; immature duct may reconstrict but not achieve anatomical closure

Complication	Mechanism	Incidence
Recurrent laryngeal nerve palsy	Left recurrent laryngeal nerve loops around the aortic arch / ligamentum arteriosum at the PDA site → surgical manipulation damages it	5–9%
Presentation: hoarse cry, weak voice, feeding difficulty (aspiration risk)	Unilateral vocal cord paralysis → incomplete glottic closure
Phrenic nerve palsy	Left phrenic nerve runs near the surgical field → injury → diaphragmatic paralysis	1–5%
Presentation: raised hemidiaphragm, respiratory compromise	Loss of diaphragmatic excursion on affected side
Chylothorax	Thoracic duct injury during dissection → lymphatic fluid accumulates in pleural space	1–4%
Post-ligation cardiac syndrome	Acute LV dysfunction after PDA ligation. Mechanism: LV was adapted to a low-afterload state (diastolic run-off through PDA reduced effective SVR). Sudden removal of run-off → acute ↑afterload → immature preterm LV cannot cope → hypotension, low cardiac output	~30% of preterm ligations
Management: milrinone (inodilator — improves contractility + reduces afterload)	Phosphodiesterase-3 inhibitor → ↑cAMP → inotropy + vasodilation
Pneumothorax	Complication of thoracotomy	Variable
Incomplete closure / recanalisation	More common with ligation alone (vs division); the ligature may loosen over time	Rare (< 1% with modern surgical technique)
Scoliosis (long-term)	Thoracotomy in a growing infant → asymmetric chest wall growth	Reported but uncommon

Complication	Mechanism	Incidence
Device embolisation	Undersized device or unfavourable anatomy → device dislodges into PA or aorta	< 1–2%
Residual shunt	Incomplete seal around device	5–10% immediately; most close spontaneously with endothelialisation
LPA stenosis	Device protrudes into LPA lumen → partial obstruction	More common in small infants with short ducts; Piccolo™ device designed to minimise this
Aortic obstruction	Device protrudes into aortic isthmus → coarctation-like physiology	Rare; more common in small infants
Haemolysis	High-velocity residual jet through/around device → mechanical shearing of red blood cells	Rare; usually self-limiting
Vascular access complications	Femoral artery/vein injury (thrombosis, pseudoaneurysm, haematoma) in small infants	More common in younger/smaller patients
IE on device	Theoretical risk during endothelialisation period	Very rare; antibiotic prophylaxis recommended for 6 months post-procedure

Timeline	Complications
Acute (preterm NICU)	HF, NEC, IVH, renal impairment, PVL
Subacute (infancy)	HF, FTT, recurrent chest infections
Chronic (childhood if untreated)	Pulmonary hypertension → Eisenmenger syndrome
Lifelong (even small PDA)	Infective endocarditis
Post-treatment	Drug side effects (nephrotoxicity, GI perforation, kernicterus); surgical complications (RLN palsy, post-ligation cardiac syndrome); device complications (embolisation, LPA stenosis)

Scenario	Outcome
Small PDA, closed electively	Excellent; normal life expectancy; IE risk eliminated
Moderate/large PDA, closed before pHTN	Excellent; HF resolves, LV remodels, normal life expectancy
Large PDA, closed late but before Eisenmenger	Good, but may have residual LV dilatation and mild pHTN
Eisenmenger PDA	30–40% 10-year mortality; mean age of death 37 years without transplant ^[9]
Preterm hsPDA, successfully closed	Prognosis determined primarily by degree of prematurity and associated morbidities (BPD, IVH, NEC) rather than PDA itself
pHTN and Eisenmenger in PDA	Develops in approximately 5% of all PDA cases ^[2]

High Yield Summary

Complications of PDA — Key Exam Points:

CHF at 1–2 months (term) or within days (preterm) — from LV volume overload as PVR drops
FTT — ↑metabolic demand + ↓caloric intake + ↓gut perfusion
Recurrent chest infections — pulmonary congestion impairs mucociliary clearance
Pulmonary hypertension → Eisenmenger syndrome — the most feared long-term complication; irreversible; closure contraindicated; 30–40% 10-year mortality ^[9]
Eisenmenger triad: (1) congenital L-to-R shunt, (2) pulmonary arterial disease, (3) cyanosis ^[9]
Eisenmenger PDA → differential cyanosis (blue toes, pink fingers) + loss of murmur + polycythaemia + risk of cerebral embolism/abscess ^[9]
Infective endocarditis — even small PDAs carry lifetime IE risk; turbulent jet damages PA endothelium
Preterm-specific complications: NEC, IVH, renal impairment, PVL, BPD — all from diastolic steal + pulmonary overcirculation
Drug complications: Indomethacin (nephrotoxic, ↓mesenteric flow); Ibuprofen (less nephrotoxic, displaces bilirubin); Paracetamol (safest, theoretical hepatotoxicity)
Surgical complications: Recurrent laryngeal nerve palsy (hoarse cry), post-ligation cardiac syndrome (30%, treat with milrinone), chylothorax, phrenic nerve palsy
Device complications: Embolisation, LPA stenosis, aortic obstruction, residual shunt

Active Recall - PDA Complications

References

^[1] Senior notes: Adrian Lui Pediatrics.pdf (p193, p202) ^[2] Senior notes: Ryan Ho Cardiology.pdf (p189) ^[6] Senior notes: Adrian Lui Pediatrics.pdf (p36 — Problems related to prematurity) ^[9] Senior notes: Ryan Ho Cardiology.pdf (p186 — Eisenmenger syndrome); Senior notes: Adrian Lui Pediatrics.pdf (p193 — Eisenmenger complications and prognosis)

Patent Ductus Arteriosus

Definition

Epidemiology

Risk Factors

Anatomy and Function of the Ductus Arteriosus

Fetal Anatomy

Fetal Function

Why Does the DA Stay Open In Utero?

Normal Postnatal Closure

Aetiology (with Hong Kong Focus) and Pathophysiology

Aetiology

Pathophysiology: The Haemodynamic Consequences of PDA

Step 1: Direction of Shunt

Step 2: Volume Overload to Pulmonary Circulation

Step 3: Left Heart Volume Overload

Step 4: Hyperdynamic Circulation and "Run-off"

Step 5: Consequences of the Shunt

Step 6: Eisenmenger Syndrome (End-stage, Irreversible)

Classification

A. By Gestational Age Context

B. By Haemodynamic Significance (Shunt Ratio, Qp:Qs)

C. By Anatomical Morphology (Krichenko Classification — for interventional planning)

D. Duct-Dependent Circulation (Special Category)

Clinical Features

A. Symptoms (with Pathophysiological Basis)

Large PDA (Qp:Qs > 2.2:1)

Moderate PDA (Qp:Qs = 1.5–2.2:1)

Small PDA (Qp:Qs < 1.5:1)

Eisenmenger Syndrome (Late / Untreated Large PDA)

B. Signs (with Pathophysiological Basis)

General Inspection

Pulse and Blood Pressure

Precordium

Auscultation — The Murmur of PDA

Additional Auscultatory Findings

Signs Specific to Preterm PDA

Summary Table of Clinical Features by PDA Size

Key Concepts — Connecting Clinical Features to Pathophysiology

Active Recall - Patent Ductus Arteriosus

References

A. Differential Diagnosis of a Continuous Murmur in a Child

B. Differential Diagnosis of Wide Pulse Pressure / Collapsing Pulse in a Child

C. Differential Diagnosis of Acyanotic CHD Presenting with Heart Failure at 1–2 Months (L-to-R Shunt Lesions)

D. Differential Diagnosis in the Preterm Neonate with Suspected PDA

E. Differential Diagnosis of Differential Cyanosis

F. Conditions Where PDA Coexists with (and May Mask) Other CHD

Summary: Systematic DDx Approach by Presenting Feature

Active Recall - Differential Diagnosis of PDA

Diagnostic Criteria

A. Confirming the Diagnosis of PDA

B. Defining Haemodynamic Significance (hsPDA)

Diagnostic Algorithm

Investigation Modalities

1. Chest X-Ray (CXR)

2. Electrocardiogram (ECG)

3. Echocardiography (Echo)

4. Cardiac Catheterisation

5. Additional Investigations

Summary Table: Investigations by PDA Size

Pre- and Post-Ductal Saturations — A Special Note

Active Recall - PDA Diagnosis and Investigations

General Principles of PDA Management

Management Algorithm

Treatment Modalities

I. Conservative / Supportive Management (Preterm Neonates)

II. Pharmacological Closure (Preterm Neonates Only)

A. COX Inhibitors (Cyclooxygenase Inhibitors)

B. Paracetamol (Acetaminophen)

Contraindications to Pharmacological Closure

III. Medical Management of Heart Failure (Term and Preterm)

IV. Definitive Closure — Transcatheter Device Closure (First-Line for Term PDA)

V. Definitive Closure — Surgical Ligation / Division

VI. Special Situations

A. Duct-Dependent Congenital Heart Disease

B. Eisenmenger PDA

C. The "Silent" / Very Small PDA

Summary Table: Management by Clinical Scenario

Active Recall - PDA Management

A. Complications of the Untreated PDA Itself

1. Congestive Heart Failure (CHF)