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Patent Ductus Arteriosus (PDA)
- 1. DR. SAYEEDUR RAHMANKHAN RUMI [email protected] MD (CARDIOLOGY) FINAL PART STUDENT NHFH&RI PATENT DUCTUS ARTERIOSUS
- 2. Definition • Patent ductusarteriosus, the most common type of extracardiac shunt, represents persistent patency of the vessel that normally connects the pulmonary arterial system and the aorta in a fetus.
- 3. Incidence • PDA occursin approximately 1 of 2,000 live births, but it is relatively uncommon among the adult population. • In infants, it accounts for 10% to 12% of all congenital heart disease • PDAs are twice as common in female infants as in male infants • In rubella syndrome male female are affected equally
- 4. Risk factors • Maternalrubella infection • Birth at high altitude • Premature birth • Female sex, and • Genetic factors • In infants born at < 28 weeks of gestation, there is a 60% incidence of PDA
- 5. Embryology • The ductusarteriosus is a normal and essential component of cardiovascular development that originates from the distal sixth left aortic arch. • A PDA is most commonly funnel shaped with the larger aortic end (ampulla) distal to the left subclavian artery, then narrowing toward the pulmonary end, with insertion at the junction of the main and left pulmonary arteries
- 6. Fetal circulation • Thepresence of the ductus arteriosus in the fetal circulation is essential to allow right-to-left shunting of nutrient-rich, oxygenated blood from the placenta to the fetal systemic circulation, thereby bypassing the fetal pulmonary circuit • In the fetus, the ductus arteriosus is kept open by Low arterial oxygen content and Placental prostaglandin E2 (PGE2)
- 7. Birth • Several changesoccur at birth to initiate normal functional closure of the ductus arteriosus within the first 15 to 18 hours of life. • Spontaneous respirations result in increased blood oxygen content. • Prostaglandin levels decrease because of placental ligation and increased metabolism of prostaglandins within the pulmonary circulation by prostaglandin dehydrogenase. • Generally, the ductus arteriosus is hemodynamically insignificant within 15 hours and completely closed by 2 to 3 weeks
- 8. Classification Isolated PDAs, areoften categorized according to the degree of left-to-right shunting, which is determined by both the size and length of the duct and the difference between systemic and pulmonary vascular resistance, as follows: • Silent: tiny PDA detected only by nonclinical means (usually echocardiography) • Small: continuous murmur common; Qp/Qs <1.5 • Moderate: continuous murmur common; Qp/Qs 1.5 to 2.2 • Large: continuous murmur present; Qp/Qs >2.2 • Eisenmenger: continuous murmur absent; substantial pulmonary hypertension, differential hypoxemia, and differential cyanosis (pink fingers, blue toes)
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- 10. Natural History • UnlikePDA in premature infants, spontaneous closure of a PDA is rare in full-term infants and children. • This is because the PDA in term infants results from a structural abnormality of the ductal smooth muscle rather than a decreased responsiveness of the ductal smooth muscle to oxygen. • CHF or recurrent pneumonia develops if the shunt is large. • Pulmonary vascular obstructive disease may develop if a large PDA with pulmonary hypertension is left untreated. • Although rare, an aneurysm of PDA may develop and possibly rupture in adult life.
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- 12. History • The historyof the mother’s pregnancy and of perinatal events may provide clues associated with a high incidence of PDA, such as exposure to rubella in the first trimester in a non immunized mother. • PDA is also more common in premature infants, especially those with birth asphyxia or respiratory distress
- 13. Symptoms • Severity ofsymptoms depends on the degree of left-to- right shunting; and it is determined by the size of the PDA, ductal resistance, cardiac output, as well as the systemic and pulmonary vascular resistances. • Patients with small PDA are asymptomatic. • With larger PDAs, symptoms may develop. • The most common symptom is exercise intolerance followed by dyspnea, peripheral edema, and palpitations.
- 14. Signs • Tachycardia andtachypnea may be present in infants with CHF. • Bounding peripheral pulses • Wide pulse pressure • Hyperactive precordium: With a large shunt • Systolic thrill: may be present at the upper left sternal border. • The P2 is usually normal, but its intensity may be accentuated if pulmonary hypertension is present.
- 15. • A grade1 to 4 of 6 continuous (“machinery”) murmur is best audible at the left infraclavicular area or upper left sternal border. • An apical diastolic rumble may be heard when the PDA shunt is large. • Patients with small ductus do not have the above findings.
- 16. • The durationof the diastolic murmur reflects pulmonary artery pressures; elevated pulmonary artery pressures lead to a decreased gradient for left-to-right flow through the PDA during diastole, which results in a shorter diastolic murmur. • As pulmonary pressure increases, the systolic component of the murmur shortens. • Right-to-left flow may not generate a systolic murmur. • Differential cyanosis: If pulmonary vascular obstructive disease develops, a right-to-left ductal shunt results in cyanosis only in the lower half of the body.
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- 18. ECG • With asmall shunt the ECG is normal. • Left ventricular hypertrophy of the volume overload type, with deep Q waves and increased R- wave voltage in the left precordial leads, is noted with increasing shunt size with left ventricular volume overload. • Right ventricular hypertrophy is seen with pulmonary hypertension.
- 19. CXR • Chest radiographsmay be normal with a small-shunt PDA. • Cardiomegaly of varying degrees occurs in moderate- to large-shunt PDA with enlargement of the LA, LV, and ascending aorta. • Pulmonary vascular markings are increased. • With pulmonary vascular obstructive disease, the heart size becomes normal, with a marked prominence of the PA segment and hilar vessels.
- 20. CXR P/A viewof a 2-day-old infant demonstrating the ductus bump (arrow).
- 21. Echocardiogram TTE has a42% sensitivity and 100% specificity for the diagnosis of PDA. • On 2-D echo, the left-sided chambers (LA and LV) are dilated due to increased venous return from the pulmonary circulation. • This constitutes left ventricular volume overload. • Due to dilatation of left atrium, the ratio between size of the left atrium and proximal aorta (LA : Ao ratio) exceeds 1.3.
- 22. Parasternal long axisshowing LA and left ventricular enlargement Echocardiogram in parasternal short axis demonstrating a patent ductus arteriosus with color-flow mapping indicating reversed flow
- 23. Continuous wave Doppler echocardiogrampositioned through the PDA, showing retrograde flow throughout the cardiac cycle Pulsed-Doppler echocardiogram shows increased diastolic flow in the branch pulmonary artery
- 24. Cardiac Catheterization Catheter trajectory: •Catheter may easily pass from PA to Ao through the PDA. • It gives a specific appearance “Hair pin” appearance.
- 25. • Oxymetry: Steps upof O2 saturation in PA in comparison to RA. • Pressure study: RV & PA pressure is normal, but elevated in large PDA. PVR is normal in infant & children but elevated in adult. • LV graphy: to see associated VSD • Aortography: to see PDA & associated CoA
- 26. MRI & CT •Magnetic resonance imaging (MRI) and computed tomography may be useful in defining the anatomy in patients with unusual PDA geometry and in patients with associated abnormalities of the aortic arch.
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- 28. Medical Pharmacological closure ofduct: • For premature infants, treatment with indomethacin is usually the first-line therapy (0.2 mg/kg intravenously every 12 hours for up to three doses). • Indomethacin therapy has been associated with an increased bleeding tendency resulting from platelet dysfunction, decreased urine output secondary to renal dysfunction, and necrotizing enterocolitis. • Ibuprofen has achieved closure rates equivalent to those of indomethacin with less renal toxicity. Secondary measures: • Prophylaxis against IE • Treatment of HF
- 29. ACC/AHA 2008 Guidelinesfor the Management of Adults With Congenital Heart Disease Class I Recommendations for Closure of Patent Ducts Arteriosus 1. Closure of a PDA either percutaneously or surgically is indicated for the following: a. Left atrial and/or LV enlargement or if PAH is present, or in the presence of net left-to-right shunting b. Prior endarteritis 2. Consultation with ACHD interventional cardiologists is recommended before surgical closure is selected as the method of repair for patients with a calcified PDA. 3. Surgical repair by a surgeon experienced in CHD surgery is recommended when: a. The PDA is too large for device closure. b. Distorted ductal anatomy precludes device closure (eg, aneurysm or endarteritis).
- 30. Nonsurgical Closure • Sincethe early 1990s, transcatheter techniques have become the first-line therapy for most PDAs. • Complications: Rare. • The most common complication is embolization of the coil or device. • Percutaneous coils were developed in 1992 and are the preferred treatment for older children and adults with PDAs < 3.5 mm in diameter Duct-Occlud coil
- 31. Amplatzer Ductal Occluder •The ADO, a cone-shaped plug occluder made of thrombogenic wire mesh delivered with a 5F to 7F venous system, is the preferred device for percutaneous closure of moderate to large PDAs. • The ADO stents the PDA, and blood is forced to flow through the center of the device, which is lined with thrombogenic wire mesh. • The PDA then essentially clots off. • Advantages include simple implantation, ability to retract the ADO into the sheath and redeploy if needed, and high success rates. • There is an 89% occlusion rate on post procedure day 1 and 97% to 100% complete occlusion after 1month
- 32. Amplatzer ADO IAmplatzer ADO II
- 33. Lateral angiogram showingcoil occlusion of a patent ductus arteriosus (PDA). A. Small PDA allows shunting from descending aorta to pulmonary artery (arrow). B. Shunting is eliminated by an Amplatzer ductal occluder device placed in the ductus arteriosus (arrow).
- 34. Surgical Closure • In1938, the first successful closure of a PDA was performed, which was the first repair of a congenital heart defect. • With continued advances in percutaneous closure devices, surgery has become second-line therapy for most adults with PDAs Procedure: 1. Ligation and division through left posterolateral thoracotomy without cardiopulmonary bypass is the standard procedure. 2. The technique of video-assisted thoracoscopic surgery (VATS) clip ligation has become the standard of care for surgical management of ductus with adequate length (to allow safe ligation), which is performed through three small ports in the fourth intercostal space.
- 35. Mortality: • The surgicalmortality rate is <1% for both techniques. Complications: • Injury to the recurrent laryngeal nerve (hoarseness) • The left phrenic nerve (paralysis of the left hemidiaphragm) • The thoracic duct (chylothorax) is possible. • Recanalization (reopening) of the ductus is possible, although rare, occurring after ligation alone (without division).
- 36. Complications of PDA Themost common complications of PDA include • CHF • Infective endocarditis • Pulmonary hypertension
- 37. Differential diagnosis • VSDassociated with aortic insufficiency • Aortopulmonary window • Pulmonary atresia with systemic collateral vessels • Innocent venous hum • Arteriovenous communications such as • pulmonary arteriovenous fistula • coronary artery fistula • systemic arteriovenous fistula • Ruptured sinus of Valsalva aneurysm
- 38. Reproductive Issues • Pregnancyis well tolerated in women with silent and small PDAs and in patients who were asymptomatic before pregnancy. • In women with a hemodynamically important PDA, pregnancy may precipitate or worsen heart failure. • Pregnancy is contraindicated in those with Eisenmenger syndrome because of the high maternal (≈50%) and fetal (≈60%) mortality.
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