The ductus arteriosus is a vascular fetal structure that usually closes in the first 48 hours after birth; a patent ductus arteriosus (PDA) occurs when it fails to close.
Persistence of the ductus arteriosus can result in heart failure, increased pulmonary pressures, and endarteritis.
The incidence and sequelae of a PDA are more significant in premature infants than infants born at full-term.
Clinical history and presentation can vary significantly depending on age of the child and the size of the ductus. Patients may be entirely asymptomatic or have signs and symptoms of heart failure and hemodynamic instability.
Treatment options vary depending on the age of the patient and the size of the ductus. Practice may vary significantly between institutions.
Patent ductus arteriosus (PDA) describes the persistence of a fetal vascular structure, known as the ductus arteriosus, after birth. The ductus arteriosus connects the main pulmonary artery to the aorta, allowing blood to bypass the lungs in utero. It usually closes in the first 48 hours of life.
History and exam
Key diagnostic factors
- presentation in infancy
Other diagnostic factors
- tachypnea/shortness of breath (SOB)
- failure to thrive
- exercise intolerance
- widened pulse pressure
- machine-like continuous murmur/Gibson murmur in children born at full-term
- low diastolic blood pressure (BP)
- increased respiratory symptoms with upper respiratory infection
- murmur heard only during systole
- hyperdynamic precordium
- systolic thrill
- third heart sound heard at apex
- mid-diastolic rumble heard at apex
- bounding peripheral pulses
- pulmonary rales
- maternal rubella
- female sex
- respiratory distress syndrome (RDS)
- high altitude
- family history
- black race
1st investigations to order
- chest x-ray
Investigations to consider
- cardiac catheterization and angiography
premature very low birth weight infants: prophylactic therapy
premature infants (<32 weeks)
term infants and children: small-to-moderate-sized ducts
term infants and children: large ducts and/or symptomatic infants too small for device closure
Joyce T. Johnson, MD, MS
Assistant Professor, Pediatric Cardiology
Ann & Robert H. Lurie Children's Hospital of Chicago
Northwestern University Feinberg School of Medicine
JTJ declares that she has no competing interests.
Nelangi M. Pinto, MD
Associate Professor, Pediatrics
University of Utah
Salt Lake City
NMP declares that she has no competing interests.
Dr Joyce T. Johnson and Dr Nelangi M. Pinto would like to gratefully acknowledge Dr Anji T. Yetman, a previous contributor to this topic.
ATY declares that she has no competing interests.
Michael Cheung, BSc (Hons), MB ChB, MRCP, FRACP
Department of Cardiology
Royal Children's Hospital
MC declares that he has no competing interests.
Rajat Bhatt, MD
Texas Tech University Health Sciences Center (TTUHSC)
RB declares that he has no competing interests.
Henry M. Sondheimer, MD
Professor of Pediatrics
The Children's Hospital
HMS declares that he has no competing interests.
- Venous hum
- Coronary artery fistula
- Left-sided shunts (ventricular septal defect, atrioventricular septal defect)
- 2020 ESC guidelines for the management of adult congenital heart disease (previously grown-up congenital heart disease)
- 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
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