eMedicine Specialties > Pediatrics: Cardiac Disease and Critical Care Medicine > Cardiothoracic Surgery

Patent Ductus Arteriosus, Surgical Treatment

Author: Mary C Mancini, MD, PhD, Professor and Chief, Cardiothoracic Surgery, Department of Surgery, Louisiana State University Health Sciences Center-Shreveport
Contributor Information and Disclosures

Updated: Oct 28, 2009

Introduction

The ductus arteriosus connects the main pulmonary trunk to the descending aorta distal to the origin of the left subclavian artery. In most individuals, the ductus arteriosus is located on the left side; however, if a right aortic arch is present, the ductus arteriosus may be located on the right or left side. The ductus arteriosus is very rarely bilateral. The structure varies in length and diameter. Histologically, the media of the ductus is composed of smooth muscle, and the intima is much thicker than the aorta. Contraction of this muscular media after birth causes shortening of the ductus and its functional closure. Folding of the endothelium and proliferation of the subintimal layers cause permanent closure, which usually occurs during the first 2-3 weeks of life. Persistence of a patent ductus occurs in several conditions.

Diagram illustrates the patent ductus arteriosus.

Diagram illustrates the patent ductus arteriosus.

Diagram illustrates the patent ductus arteriosus.

Diagram illustrates the patent ductus arteriosus.


History of the Procedure

Munro initially described surgical ligation of the patent ductus arteriosus in 1907. Gross performed the first successful operation in 1939.1 Catheter-based closure of the structure was first performed in 1971.

Problem

In normal fetal circulation, the unexpanded lungs receive only 5-8% of the blood entering the pulmonary artery. The ductus arteriosus serves as the predominant route of circulation passing through the right ventricle and pulmonary artery. Approximately 55-60% of the systemic circulation passes from right to left through the ductus.

In the fetus, the oxygen tension is relatively low because the pulmonary system is nonfunctional. This, coupled with high levels of circulating prostaglandins, acts to keep the ductus open. The high levels of prostaglandins result from the little amount of pulmonary circulation and the high levels of production in the placenta.

At birth, the placenta is removed, eliminating a major source of prostaglandin production, and the lungs expand, activating the organ in which most prostaglandins are metabolized. In addition, with the onset of normal respiration, oxygen tension in the blood markedly increases. Pulmonary vascular resistance decreases with this activity. These events result in contraction of the smooth muscle within the wall of the ductus, which results in its closure. A preferential shift of blood flow occurs; the blood moves away from the ductus and directly from the right ventricle into the lungs. Until functional closure is complete and pulmonary vascular resistance is lower than systemic vascular resistance, some residual left-to-right flow occurs from the aorta through the ductus and into the pulmonary arteries.

Alterations in any one of the aforementioned steps results in persistent ductal patency, left-to-right flow through the structure, and increased pulmonary blood flow.

Frequency

A persistent ductus arteriosus has been estimated to occur in 1 in 2500-5000 live births. As an isolated lesion, it represents 9-12% of all congenital heart lesions. The female-to-male ratio is 2:1.

Etiology

The factors responsible for continued patency of the ductus arteriosus are unknown, and even the conditions that have an effect on patency are not well understood.

Prematurity or immaturity of the infant at the time of delivery contributes to the patency of the ductus. Several factors are involved, including immaturity of the smooth muscle within the structure or the inability of the immature lungs to clear the circulating prostaglandins that remain from gestation. These mechanisms are not fully understood. Conditions that contribute to low oxygen tension in the blood, such as immature lungs, coexisting congenital heart defects, and high altitude, are associated with persistent patency of the ductus.

The incidence of rubella infection in the first trimester of pregnancy, particularly through 4 weeks' gestation, associated with patent ductus arteriosus is very high (£ 85%).

Incidence of patent ductus arteriosus is as much as 2-4% in siblings of patients with the condition. A socioeconomic association without a racial factor has also been observed with patency; an increased incidence of patients with patent ductus arteriosus appears to arise from lower socioeconomic origins.

Pathophysiology

With patency of the ductus and a decrease in pulmonary vascular resistance to below the level of systemic vascular resistance, blood flows from the aorta into the pulmonary artery through the ductus, resulting in a left-to-right shunt. The flow occurs through systole and diastole. This combination of blood passes through the lungs, into the left atrium, into the left ventricle, and back into the aorta. The result is an increased volume load on the left atrium and left ventricle. The increase in left ventricular stroke volume is proportional to the size of the ductus.

The increased left ventricular stroke volume and the central runoff from the aorta into the pulmonary artery results in a widened pulse pressure.

An absolute increase occurs in the total circulating volume of the patient, which is proportional to the amount through the left-to-right shunt. Pulmonary engorgement results with decreased pulmonary compliance. The reaction of the pulmonary vasculature to the increased blood flow is unpredictable.

The amount of blood that flows through the ductus is related to the size and shape of the structure and to the differences between the systemic and pulmonary resistances. The wider and shorter the ductus, the greater the blood flow through it. Higher systemic pressures provide a higher driving force behind the blood flowing through the structure. The lower the pulmonary resistance, the less the impediment affects ductal flow. Conversely, higher pulmonary vascular resistance can sometimes reverse the flow through the patent ductus arteriosus.

Presentation

No typical clinical history is observed in patients with patent ductus arteriosus. Most patients are asymptomatic and are found to have a heart murmur on physical examination. At times, the patient may report decreased exercise tolerance or pulmonary congestion in conjunction with a murmur. Patients can present at any age. However, 3-week to 6-week-old infants can present with tachypnea, diaphoresis, inability or difficulty with feeding, and weight loss or no weight gain.

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.

A continuous machinery murmur is the hallmark physical finding of patent ductus arteriosus. The murmur begins shortly after the first heart sound, peaks at approximately the second heart sound, and diminishes through diastole. The murmur may be local or widely radiate, and it may vary in intensity from very soft to grade 6. A thrill may be palpated. Often, a left ventricular heave or lift may be felt on palpation of the chest. The second heart sound is increased in intensity and widely split because of the increased pulmonary blood flow. In patients with a larger ductus, a diastolic rumble may be heard. The peripheral pulses are prominent and bounding in small patients with a large ductus.

Indications

Congestive heart failure is an indication for closure of the patent ductus arteriosus in infancy. If medical therapy is ineffective, urgent intervention to close the structure should be undertaken. All patent ductus arteriosus should be closed because of the risk of bacterial endocarditis associated with the open structure. Over time, the increased pulmonary blood flow precipitates pulmonary vascular obstructive disease, which is ultimately fatal.

Relevant Anatomy

In the normal heart with a left aortic arch, the patent ductus arteriosus forms a connection between the pulmonary artery and the aorta, just distal to the origin of the left subclavian artery. It passes from the anterior aspect of the pulmonary artery to the posterior aspect of the aorta. Typically, the ductus has a conical shape with a large aortic end tapering into the small pulmonary connection. The ductus may take many shapes and forms, from short and tubular to long and tortuous. An anatomic marker of the ductus is the recurrent laryngeal nerve, which encircles the left subclavian artery and can be found adjacent to the ductus.

Contraindications

Relatively few contraindications to closure of the patent ductus arteriosus are recognized. Clearly, attention must be paid to the existence of other congenital heart lesions that impair pulmonary blood flow. In these patients, all attempts should be made to preserve ductal flow until a more permanent palliative shunt can be constructed or definitive repair can be undertaken. Contraindications to catheter-based closure currently involve the size of the patient. Very small premature infants still require surgical closure. Contraindications to surgical closure include concurrent uncontrolled sepsis and an inability of the patient to tolerate general anesthesia.

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References

References

  1. Kaemmerer H, Meisner H, Hess J, Perloff JK. Surgical treatment of patent ductus arteriosus: a new historical perspective. Am J Cardiol. Nov 1 2004;94(9):1153-4. [Medline].

  2. [Best Evidence] Attridge JT, Kaufman DA, Lim DS. B-type natriuretic peptide concentrations to guide treatment of patent ductus arteriosus. Arch Dis Child Fetal Neonatal Ed. May 2009;94(3):F178-82. [Medline].

  3. Lin CC, Hsieh KS, Huang TC, Weng KP. Closure of large patent ductus arteriosus in infants. Am J Cardiol. Mar 15 2009;103(6):857-61. [Medline].

  4. Rapacciuolo A, Losi MA, Borgia F, et al. Transcatheter closure of patent ductus arteriosus reverses left ventricular dysfunction in a septuagenarian. J Cardiovasc Med (Hagerstown). Apr 2009;10(4):344-8. [Medline].

  5. Chen Z, Chen L, Wu L. Transcatheter Amplatzer Occlusion and Surgical Closure of Patent Ductus Arteriosus: Comparison of Effectiveness and Costs in a Low-Income Country. Pediatr Cardiol. Apr 14 2009;[Medline].

  6. Tomita H, Uemura S, Haneda N, et al. Coil occlusion of PDA in patients younger than 1 year: Risk factors for adverse events. J Cardiol. Apr 2009;53(2):208-13. [Medline].

  7. Hoellering AB, Cooke L. The management of patent ductus arteriosus in Australia and New Zealand. J Paediatr Child Health. Apr 2009;45(4):204-9. [Medline].

  8. Burney K, Thayur N, Husain SA, Martin RP, Wilde P. Imaging of implants on chest radiographs: a radiological perspective. Clin Radiol. Mar 2007;62(3):204-12. [Medline].

  9. Castaneda A. Congenital heart disease: a surgical-historical perspective. Ann Thorac Surg. Jun 2005;79(6):S2217-20. [Medline].

  10. Freed MD, Heymann MA, Lewis AB, et al. Prostaglandin E1 infants with ductus arteriosus-dependent congenital heart disease. Circulation. Nov 1981;64(5):899-905. [Medline].

  11. Friedman WF, Hirschklau MJ, Printz MP, et al. Pharmacologic closure of patent ductus arteriosus in the premature infant. N Engl J Med. Sep 2 1976;295(10):526-9. [Medline].

  12. Heymann MA, Rudolph AM, Silverman NH. Closure of the ductus arteriosus in premature infants by inhibition of prostaglandin synthesis. N Engl J Med. Sep 2 1976;295(10):530-3. [Medline].

  13. Johnson DH, Rosenthal A, Nadas AS. A forty-year review of bacterial endocarditis in infancy and childhood. Circulation. Apr 1975;51(4):581-8. [Medline].

  14. Jones JC. Twenty-five years experience with the surgery of patent ductus arteriosus. J Thorac Cardiovasc Surg. Aug 1965;50:149-65. [Medline].

  15. Panagopoulos PG, Tatooles CJ, Aberdeen E, et al. Patent ductus arteriosus in infants and children. A review of 936 operations (1946-69). Thorax. Mar 1971;26(2):137-44. [Medline].

  16. Radtke WA. Interventional pediatric cardiology: state of the art and future perspective. Eur J Pediatr. Aug 1994;153(8):542-7. [Medline].

  17. Rao PS, Sideris EB, Haddad J, et al. Transcatheter occlusion of patent ductus arteriosus with adjustable buttoned device. Initial clinical experience. Circulation. Sep 1993;88(3):1119-26. [Medline].

  18. Vida VL, Lago P, Salvatori S, et al. Is there an optimal timing for surgical ligation of patent ductus arteriosus in preterm infants?. Ann Thorac Surg. May 2009;87(5):1509-15; discussion 1515-6. [Medline].

  19. Warren R. Landmark perspective: Patent ductus arteriosus. JAMA. Mar 2 1984;251(9):1203-7. [Medline].

  20. Zupancic JA, Richardson DK, O'Brien BJ, Cronin CG, Schmidt B, Roberts R. Retrospective economic evaluation of a controlled trial of indomethacin prophylaxis for patent ductus arteriosus in premature infants. Early Hum Dev. Feb 2006;82(2):97-103. [Medline].

Further Reading

Keywords

patent ductus arteriosus, PDA, persistent ductus arteriosus, aortopulmonary connection, heart defect, cardiac defect, pediatric cardiac surgery, catheter-based closure of PDA, thoracotomy, PDA closure, treatment, diagnosis

Contributor Information and Disclosures

Author

Mary C Mancini, MD, PhD, Professor and Chief, Cardiothoracic Surgery, Department of Surgery, Louisiana State University Health Sciences Center-Shreveport
Mary C Mancini, MD, PhD is a member of the following medical societies: American Association for Thoracic Surgery, American College of Surgeons, American Surgical Association, Phi Beta Kappa, Society of Thoracic Surgeons, and Southern Surgical Association
Disclosure: Nothing to disclose.

Medical Editor

Jonah Odim, MD, PhD, MBA, Senior Medical Officer, Transplantation Immunology Branch, Division of Allergy, Immunology, and Transplantation, National Institute of Allergy and Infectious Diseases, National Institutes of Health
Jonah Odim, MD, PhD, MBA is a member of the following medical societies: American College of Cardiology, American College of Chest Physicians, American College of Physician Executives, American College of Surgeons, American Heart Association, American Society for Artificial Internal Organs, American Society of Transplant Surgeons, Association for Academic Surgery, Association for Surgical Education, Canadian Cardiovascular Society, International Society for Heart and Lung Transplantation, National Medical Association, New York Academy of Sciences, Royal College of Physicians and Surgeons of Canada, Society of Critical Care Medicine, and Society of Thoracic Surgeons
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

John Myers, MD, Director, Pediatric and Congenital Cardiovascular Surgery, Departments of Surgery and Pediatrics, Professor, Penn State Children's Hospital, Milton S Hershey Medical Center
John Myers, MD is a member of the following medical societies: American Association for Thoracic Surgery, American College of Cardiology, American College of Surgeons, American Heart Association, American Medical Association, Congenital Heart Surgeons Society, Pennsylvania Medical Society, and Society of Thoracic Surgeons
Disclosure: Nothing to disclose.

CME Editor

Daniel Rauch, MD, FAAP, Director, Pediatric Hospitalist Program, Associate Professor, Department of Pediatrics, New York University School of Medicine
Daniel Rauch, MD, FAAP is a member of the following medical societies: Ambulatory Pediatric Association, American Academy of Pediatrics, and Society of Hospital Medicine
Disclosure: Baxter Honoraria Consulting

Chief Editor

Stuart Berger, MD, Professor of Pediatrics, Division of Cardiology, Medical College of Wisconsin; Chief of Pediatric Cardiology, Medical Director of Pediatric Heart Transplant Program, Medical Director of The Heart Center, Children's Hospital 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, and Society for Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.

 
 
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