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Patent Ductus Arteriosus (PDA) Clinical Presentation

  • Author: Luke K Kim, MD; Chief Editor: Stuart Berger, MD  more...
 
Updated: Sep 16, 2015
 

History

As discussed in Pathophysiology, the ductus arteriosus is always patent in the fetus if the cardiovascular system is otherwise normal. Normally, the ductus arteriosus closes functionally in the first 10-18 hours of life. Prematurity, perinatal distress, and hypoxia delay closure of the ductus arteriosus; however, most children who are found to have a ductus arteriosus have no history of precedent risk factors.

Depending on the size of the patent ductus arteriosus (PDA), the gestational age of the neonate, and the pulmonary vascular resistance (PVR), a premature neonate may develop life-threatening pulmonary overcirculation in the first few days of life. Conversely, an adult with a small patent ductus arteriosus (PDA) may present with a newly discovered murmur well after adolescence.

Symptoms

Patients can present at any age. The typical child with a patent ductus arteriosus (PDA) is asymptomatic. At times, the patient may report decreased exercise tolerance or pulmonary congestion in conjunction with a murmur.

Three-week to 6-week-old infants can present with tachypnea, diaphoresis, inability or difficulty with feeding, and weight loss or no weight gain.

A ductus arteriosus with a moderate-to-large left-to-right shunt may be associated with a hoarse cry, cough, lower respiratory tract infections, atelectasis, or pneumonia. With large defects, the patient may have a history of feeding difficulties and poor growth during infancy, described as failure to thrive (FTT). However, frank symptoms of congestive heart failure (CHF) are rare.

Adults whose patent ductus arteriosus (PDA) has gone undiagnosed may present with signs and symptoms of heart failure, atrial arrhythmia, or even differential cyanosis limited to the lower extremities, indicating shunting of unoxygenated blood from the pulmonary to systemic circulation.

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Physical Examination

A patent ductus arteriosus (PDA) is variable in its presentation. It may vary in size from small to large and may not be picked up based on physical examination at birth.

Patients usually appear well and have normal respirations and heart rates. A widened pulse pressure may be noted when the blood pressure is obtained. Suprasternal or carotid pulsations may be prominent.

As many as one third of children with patent ductus arteriosus (PDA) is small for their age. In the presence of significant pulmonary overcirculation, tachypnea, tachycardia, and a widened pulse pressure may be found.

Cardiac assessment

In neonates, a heart murmur is discovered within the first few days or weeks of life. The murmur is usually recognized as systolic rather than continuous in the first weeks of life and can mimic a benign systolic murmur.

Findings upon cardiac examination include the following:

  • If the left-to-right shunt is large, precordial activity is increased, with the magnitude of increased activity related to the magnitude of left-to-right shunt
  • The apical impulse is laterally displaced; a thrill may be present in the suprasternal notch or in the left infraclavicular region
  • The first heart sound (S 1) is typically normal, and the second heart sound (S 2) is often obscured by the murmur; phonocardiographic data from the past suggested the occurrence of paradoxical splitting of S 2 related to premature closure of the pulmonary valve and a prolonged ejection period across the aortic valve
  • The murmur may be only a systolic ejection murmur, or it may be a crescendo/decrescendo systolic murmur that extends into diastole
  • Occasionally, auscultation of the patent ductus arteriosus (PDA) reveals numerous clicks or noises resembling shaking dice or a bag of rocks

In 1898, Gibson described the classic murmur. Subsequently, the hallmark physical finding of patent ductus arteriosus (PDA) has been referred to as a machinery murmur, which is continuous. The murmur may be accentuated in systole. Typically, the murmur is loudest at the left upper chest. If the pulmonary-to-systemic blood ratio approaches or exceeds 2:1, an apical flow rumble, caused by high flow into the left ventricle, is frequently present. Also, because flow through the left ventricle into the aorta is increased, an aortic ejection murmur may be present. If the patent ductus arteriosus (PDA) is small, the amplitude of the murmur may increase with inspiration as pulmonary impedance drops.

The peripheral pulses are often referred to as bounding. This is related to the high left ventricular stroke volume, which may cause systolic hypertension. The phenomenon of bounding pulses also is caused by the low diastolic pressure in the systemic circulation as blood runs off from the aorta into the pulmonary circulation.

Low birth weight premature infant

In the low birth weight premature infant, diagnosing a patent ductus arteriosus (PDA) on auscultation may be difficult. Babies that have a more severe clinical course of hyaline membrane disease (HMD) may have a higher prevalence of patent ductus arteriosus (PDA). The exact reason for this is unclear.

In the low birth weight premature infant, the classic signs of a patent ductus arteriosus (PDA) are usually absent. The classic continuous murmur is rarely heard. A rough systolic murmur may be present along the left sternal border, but a small baby with a large patent ductus arteriosus (PDA) and significant pulmonary overcirculation may have no murmur. In that case, typically, precordial activity is increased and peripheral pulses are bounding. The increased precordial activity is caused by the large left ventricular stroke volume. Bounding pulses are caused by the relatively low systemic arterial blood pressure due to the continuous runoff of blood from the aorta into the pulmonary artery.

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Contributor Information and Disclosures
Author

Luke K Kim, MD Assistant Professor of Medicine, Department of Internal Medicine, Division of Cardiology, New York Presbyterian Hospital, Weill Cornell Medical Center

Disclosure: Nothing to disclose.

Coauthor(s)

Jeffrey C Milliken, MD Chief, Division of Cardiothoracic Surgery, University of California at Irvine Medical Center; Clinical Professor, Department of Surgery, University of California, Irvine, School of Medicine

Jeffrey C Milliken, MD is a member of the following medical societies: Alpha Omega Alpha, American Association for Thoracic Surgery, American College of Cardiology, American College of Chest Physicians, American College of Surgeons, American Heart Association, American Society for Artificial Internal Organs, California Medical Association, International Society for Heart and Lung Transplantation, Phi Beta Kappa, Society of Thoracic Surgeons, SWOG, Western Surgical Association

Disclosure: Nothing to disclose.

Chief Editor

Stuart Berger, MD Medical Director of The Heart Center, Children's Hospital of Wisconsin; Associate Professor, Department of Pediatrics, Section of Pediatric Cardiology, Medical College of Wisconsin

Stuart Berger, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American College of Chest Physicians, American Heart Association, Society for Cardiovascular Angiography and Interventions

Disclosure: Nothing to disclose.

Acknowledgements

Hugh D Allen, MD Professor, Department of Pediatrics, Division of Pediatric Cardiology and Department of Internal Medicine, Ohio State University College of Medicine

Hugh D Allen, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Heart Association, American Pediatric Society, American Society of Echocardiography, Society for Pediatric Research, Society of Pediatric Echocardiography, and Western Society for Pediatric Research

Disclosure: Nothing to disclose.

David FM Brown, MD Associate Professor, Division of Emergency Medicine, Harvard Medical School; Vice Chair, Department of Emergency Medicine, Massachusetts General Hospital

David FM Brown, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Steven J Compton, MD, FACC, FACP Director of Cardiac Electrophysiology, Alaska Heart Institute, Providence and Alaska Regional Hospitals

Steven J Compton, MD, FACC, FACP is a member of the following medical societies: Alaska State Medical Association, American College of Cardiology, American College of Physicians, American Heart Association, American Medical Association, and Heart Rhythm Society

Disclosure: Nothing to disclose.

Christopher I Doty, MD, FACEP, FAAEM Assistant Professor of Emergency Medicine, Residency Program Director, Department of Emergency Medicine, Kings County Hospital Center, State University of New York Downstate Medical Center

Christopher I Doty, MD, FACEP, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, Council of Emergency Medicine Residency Directors, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Gehaan D'Souza, MD University of California-Irvine School of Medicine

Disclosure: Nothing to disclose.

Justin Galovich, MD Resident Physician, Department of Surgery, University of California, Irvine, School of Medicine

Justin Galovich, MD is a member of the following medical societies: American College of Surgeons

Disclosure: Nothing to disclose.

Christopher Johnsrude, MD, MS Chief, Division of Pediatric Cardiology, University of Louisville School of Medicine; Director, Congenital Heart Center, Kosair Children's Hospital

Christopher Johnsrude, MD, MS is a member of the following medical societies: American Academy of Pediatrics and American College of Cardiology

Disclosure: St Jude Medical Honoraria Speaking and teaching

Steven R Neish, MD, SM Director of Pediatric Cardiology Fellowship Program, Associate Professor, Department of Pediatrics, Baylor College of Medicine

Steven R Neish, MD, SM is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, and American Heart Association

Disclosure: Nothing to disclose.

Girish Sethuraman, MD, MPH Assistant Professor, University of Maryland School of Medicine

Girish Sethuraman, MD, MPH is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, American Public Health Association, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Gary Setnik, MD Chair, Department of Emergency Medicine, Mount Auburn Hospital; Assistant Professor, Division of Emergency Medicine, Harvard Medical School

Gary Setnik, MD is a member of the following medical societies: American College of Emergency Physicians, National Association of EMS Physicians, and Society for Academic Emergency Medicine

Disclosure: SironaHealth Salary Management position; South Middlesex EMS Consortium Salary Management position; ProceduresConsult.com Royalty Other

Mark S Slabinski, MD, FACEP, FAAEM Vice President, EMP Medical Group

Mark S Slabinski, MD, FACEP, FAAEM is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, and Ohio State Medical Association

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Reference Salary Employment

Park W Willis IV, MD Sarah Graham Distinguished Professor of Medicine and Pediatrics, University of North Carolina at Chapel Hill School of Medicine

Park W Willis IV, MD is a member of the following medical societies: American Society of Echocardiography

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

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Schematic diagram of a left-to-right shunt of blood flow from the descending aorta via the patent ductus arteriosus (PDA) to the main pulmonary artery.
Diagram illustrating the patent ductus arteriosus.
Diagram illustrating ligation of the patent ductus arteriosus.
Diagram illustrating division and oversewing of the patent ductus arteriosus.
Diagram illustrating patch closure of the patent ductus arteriosus.
 
 
 
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