From week 6 of fetal life until birth, the ductus is responsible for most of the right ventricular outflow. Normally, functional closure of the ductus arteriosus occurs by about 15 hours of life in healthy, full-term infants.
- In full-term infants PDA accounts for 5%-10% of all congenital heart disease1
- In preterm infants the incidence of PDA can be up to 60%1
- Among neonates with a birth weight ≤ 2.6 lb, 80% have PDA1
- Among preterm infants presenting with respiratory distress syndrome, about 80% have PDA1
- A PDA that fails to close by 2-3 days after birth may result in infant morbidity and mortality of up to 30%1
- Left untreated, a PDA carries mortality rates of:2
by age 20
by age 60
Patients with a moderate left-to-right shunt may remain asymptomatic for years. However, historical series have shown that chronic volume overload may ultimately lead to severe complications:3
- Congestive heart failure
- Atrial arrhythmias
- Irreversible hypertensive pulmonary vascular disease
- In rare cases: ductus aneurysm or acute aortic dissection
Data reveal that 57.6% of patients with PDA had 1 or more associated cardiac malformations. The most common concomitant cardiac lesions were:4
Atrial septal defect (ASD)
The Krichenko classification of PDA, based on angiography, includes 6 types:
The PDA can range from a small hemodynamically insignificant lesion that is not heard on auscultation to one that without intervention is large enough to cause congestive heart failure and pulmonary hypertension.6,7
If PDA is left untreated, the mortality rate is 20% by age 20 years, 42% by age 45, and 60% by age 60.7
Complications from an untreated PDA may include heart failure, renal dysfunction, necrotizing enterocolitis, intraventricular hemorrhage, diminished nutrition and growth, and potentially chronic lung disease.
Patients with a large PDA, when untreated, are at risk of developing Eisenmenger Syndrome, in which the usual left-to-right shunting reverses to a right-to-left shunt. At this point the PDA is irreversible, PDA closure is contraindicated, and lung transplantation may be the only option for long-term survival.
Neonatal Presentation at Physical Exam
Assessment can reveal:
- Wide pulse pressure
- Bounding peripheral pulses
- Apnea (in neonates)
- Unexplained metabolic acidosis
- Hypotension and systemic hypoperfusion
Though not often observed in preterm infants, a murmur often obscures the S2. The murmur may be noticeable only during systole, or it may be a crescendo-decrescendo systolic murmur that extends into diastole.
Depending on the system affected by hypoperfusion, patients can also present with:
- Respiratory failure
- Cardiac hypertrophy
- Renal dysfunction
- Inability to tolerate feeding
- Necrotizing enterocolitis
Adult Presentation at Physical Exam
Among adults, closure is indicated for patients with:
- Left atrial and/or LV enlargement
- Pulmonary arterial hypertension
- Left-to-right shunt
- Prior endarteritis
Echocardiography and/or angiography can differentiate between PDA and coronary arteriovenous fistulas, which can have a similar presentation.
The American College of Cardiology noted that many PDAs are now closed in infancy or childhood with catheter-based or surgical approaches. For those whose ductus remains patent in adulthood, catheter- based or surgical intervention consideration depends on the symptoms and physiological expression of the lesion.5
Yet in clinical practice there are inconsistencies in therapy strategies, especially for small and hemodynamically insigniﬁcant PDA. Some clinicians support closure to eliminate the lifelong risk of infective endarteritis, and others maintain that it is unnecessary.3
When an infant is asymptomatic or well controlled on medical therapy, closure treatment may be delayed until transcatheter therapy can be offered.
Adults with PDA are better suited for percutaneous closure due to high rates of success and low rates of complications.
Even when patients present with a small asymptomatic PDA, transcatheter device closure is a reasonable therapeutic approach.8
The information provided is not intended for medical diagnosis or treatment as a substitute for professional advice. Consult with a physician or qualified healthcare provider for appropriate medical advices.
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- Dice JE, et al. Patent ductus arteriosus: an overview. Pediatr Pharmacol Ther. 2007;12:138-146.
- Kim LK. Patent ductus arteriosus. Medscape. https://emedicine.medscape.com/article/891096-overview.
- Baruteau AE, et al. Transcatheter closure of patent ductus arteriosus: past, present and future. Arch Cardiovasc Dis. 2014;107:122-132.
- Tripathi A, et al. Prevalence and management of patent ductus arteriosus in a pediatric Medicaid cohort. Clin Cardiol. 2013;36:502-506. doi: 10.1002/clc.22150
- Stout KK, et al. 2018 AHA/ACC Guideline for the Management of Adults with Congenital Heart Disease: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Circulation. 2018;000:e000-e000. doi: 10.1161/CIR.0000000000000603.
- Philip, Ranjit, B. Rush Waller III, Vijaykumar Agrawal, Dena Wright, Alejandro Arevalo, David Zurakowski, and Shyam Sathanandam. "Morphologic characterization of the patent ductus arteriosus in the premature infant and the choice of transcatheter occlusion device." Catheterization and Cardiovascular Interventions 87, no. 2 (2016): 310-317.
- Kim LK. Patent ductus arteriosus. Medscape. emedicine.medscape.com/article/891096-overview. Updated December 31, 2017.
- Warnes CA, et al. ACC/AHA 2008 Guidelines for the Management of Adults with Congenital Heart Disease. J Am Coll Cardiol. 2008;52:e143–e263.