eMedicine Specialties > Pediatrics: Cardiac Disease and Critical Care Medicine > Cardiology

Patent Ductus Arteriosus

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

Updated: Jul 23, 2009

Introduction

Background

Patent ductus arteriosus (PDA) is one of the more common congenital heart defects. The presentation widely varies. Depending on the size of the patent ductus arteriosus, the gestational age of the neonate, and the pulmonary vascular resistance, 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 may present with a newly discovered murmur well after adolescence.

During fetal life, the ductus arteriosus is a normal structure that allows most of the blood leaving the right ventricle to bypass the pulmonary circulation and pass into the descending aorta. Typically, only about 10% of the right ventricular output passes through the pulmonary vascular bed.

The ductus arteriosus is a remnant of the distal sixth aortic arch and connects the pulmonary artery at the junction of the main pulmonary artery and the origin of the left pulmonary artery to the proximal descending aorta just after the origin of the left subclavian artery. Most typically, it is a left aortic remnant. A right-sided patent ductus arteriosus can occur, or the ductus arteriosus can be present on both the right and the left. Although a left ductus arteriosus is a normal structure during normal fetal development, the presence of a right ductus arteriosus is usually associated with other congenital abnormalities of the cardiovascular system, most typically involving the aortic arch or conotruncal development.

Pathophysiology

A patent ductus arteriosus produces a left-to-right shunt. In other words, it allows blood to go from the systemic circulation to the pulmonary circulation. Therefore, pulmonary blood flow is excessive.

Schematic diagram of left-to-right shunt of blood flow from descending aorta via patent ductus arteriosus (PDA) to main pulmonary artery

If the systemic vascular resistance is high and/or the pulmonary vascular resistance is low, the flow through the ductus arteriosus is potentially large. Beginning at the ductus arteriosus, the course of blood flow in a typical patent ductus arteriosus with pulmonary overcirculation is as follows: patent ductus arteriosus, pulmonary arteries, pulmonary capillaries, pulmonary veins, left atrium, left ventricle, aorta, patent ductus arteriosus. Therefore, a large left-to-right shunt through a patent ductus arteriosus results in left atrial and left ventricular enlargement. Additionally, the pulmonary veins and the ascending aorta can be dilated with a sufficiently large patent ductus arteriosus. Also, if little or no restriction is present at the level of the patent ductus arteriosus, pulmonary hypertension results.

The ductus arteriosus is normally patent during fetal life. This patency is promoted by continual production of prostaglandin E₂ (PGE2) by the ductus. Prostaglandin antagonism, such as maternal use of nonsteroidal anti-inflammatory medications, can cause fetal closure of the ductus arteriosus. This can be associated with severe fetal cardiovascular compromise.

Normally, functional closure of the ductus arteriosus occurs by about 15 hours of life in healthy infants born at term. This occurs by abrupt contraction of the muscular wall of the ductus arteriosus, which is associated with increases in the partial pressure of oxygen (PO₂) coincident with the first breath. This was first demonstrated by multiple experiments in the 1940s and has been subsequently confirmed. Although the neonatal ductus appears to be highly sensitive to changes in arterial oxygen tension, the actual reasons for closure or persistent patency are complex and involve manipulation by the autonomic nervous system, chemical mediators, and the ductal musculature.

Although functional closure usually occurs in the first few hours of life, true anatomic closure, in which the ductus loses the ability to reopen, may take several weeks. Cassels et al defined true persistence of the ductus arteriosus as a patent ductus arteriosus present in infants older than 3 months.¹

Frequency

United States

The estimated incidence in children born at term is between 0.02% and 0.006% of live births. This incidence is increased in children who are born prematurely, children with a history of perinatal asphyxia, and, possibly, children born at high altitude. Perinatal asphyxia usually only delays the closure of the ductus, and, over time, the ductus typically closes without specific therapy.

Mortality/Morbidity

Low birthweight premature infants

As many as 20% of neonates with respiratory distress syndrome have a patent ductus arteriosus. In babies who are less than 1500 g at birth, many studies show the incidence of a patent ductus arteriosus to exceed 30%. The increased patency in these groups is thought to be due to both hypoxia in babies with respiratory distress and immature ductal closure mechanisms in premature babies. Premature babies, particularly low birthweight neonates, are more likely to have problems related to patent ductus arteriosus. Spontaneous closure of the patent ductus arteriosus in premature neonates is common, but respiratory distress and impaired systemic oxygen delivery (congestive heart failure) often drive the need for therapy to effect ductal closure in this group. Low birthweight neonates with a patent ductus arteriosus are more likely to develop chronic lung disease.

Otherwise healthy infants, children, adolescents, and adults
 
In the preantibiotic era, Campbell et al estimated the natural history mortality rates for untreated patent ductus arteriosus to be 0.42% per year from age 2-19 years, 1-1.5% per year in the third decade, 2-2.5% per year in the fourth decade, and 4% per year in persons older than 40 years.² Currently, with the availability of antibiotics to treat endocarditis and low-risk surgery and catheter techniques to obliterate the patent ductus arteriosus, the mortality rate appears to be quite low except in the extremely premature infant.

Sex

The female-to-male ratio is 2:1 if not associated with other risk factors. In patients in whom the patent ductus arteriosus is associated with a specific teratogenic exposure, such as congenital rubella, the incidence is equal between the sexes.

Age

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.

Clinical

History

The typical child with a patent ductus arteriosus (PDA) is asymptomatic.

• A history of premature birth, perinatal distress, or perinatal hypoxia may be present.
• Some series have suggested that children born at extreme altitude have an increased incidence of a persistent patent ductus arteriosus.
• Occasionally, a history of feeding difficulties and poor growth during infancy, described as failure to thrive, is found. However, frank symptoms of congestive heart failure are rare.
• In the low birthweight premature infant, diagnosing a patent ductus arteriosus on auscultation may be difficult. Babies that have a more severe clinical course of hyaline membrane disease may have a higher prevalence of patent ductus arteriosus. The exact reason for this is unclear.

Physical

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

• 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 (S₁) is typically normal. The second heart sound (S₂) is often obscured by the murmur. Phonocardiographic data from the past suggested the occurrence of paradoxical splitting of S₂ related to premature closure of the pulmonary valve and a prolonged ejection period across the aortic valve.
  • In 1898, Gibson described the classic murmur. Subsequently, the classic patent ductus arteriosus murmur 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 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.
• In the low birthweight premature infant, the classic signs of a patent ductus arteriosus 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 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.

Causes

• Familial cases of patent ductus arteriosus have been recorded, but a genetic cause has not been determined. In infants born at term who have a persistent patent ductus arteriosus, the recurrence rate among siblings is 5%. Some early evidence suggests that as many as one third of cases are caused by a recessive trait labeled PDA1, located on chromosome 12, at least in some populations. 
• Several chromosomal abnormalities are associated with persistent patency of the ductus arteriosus. Implicated teratogens include congenital rubella (associated with patent ductus arteriosus and pulmonary artery branch stenosis), fetal alcohol syndrome, maternal amphetamine use, and maternal phenytoin use.

Differential Diagnoses

Aortopulmonary Septal Defect
Coronary Artery Fistula
Sinus of Valsalva Aneurysm
Tetralogy of Fallot With Absent Pulmonary Valve

Other Problems to Be Considered

Venous hum
Atrioventricular malformation

Workup

Imaging Studies

The following studies are indicated in patent ductus arteriosus (PDA):

• Chest radiography
  • If significant left-to-right shunt through the patent ductus arteriosus is present, the pulmonary arteries, pulmonary veins, left atrium, and left ventricle are enlarged. Also, the ascending aorta may be prominent.
  • Usually, chest radiographic findings are normal until the magnitude of the ratio of pulmonary to systemic circulation (QP/QS) exceeds 2:1. With marked pulmonary overcirculation, pulmonary edema may occur. In elderly individuals, the patent ductus arteriosus may calcify and may be visible on a standard radiograph.
• Doppler echocardiography
  • The echocardiographic findings are typically diagnostic. Relying on alternative imaging techniques to make the diagnosis of patent ductus arteriosus is unusual. By 2-dimensional echocardiography, the patent ductus arteriosus can be seen most easily in the parasternal short axis view and from the suprasternal notch. The classic patent ductus arteriosus connects the junction of the main pulmonary artery and the left pulmonary artery with the aorta just below and opposite the left subclavian artery.
  • If no other abnormalities are present, Doppler echocardiography reveals continuous flow from the aorta into the main pulmonary artery. If the magnitude of the left-to-right shunt is large, continued flow around the aortic arch into the ductus arteriosus in diastole and flow reversal in the descending aorta are evident. Also, variable levels of continuous flow in the branch pulmonary arteries related to the magnitude of shunt are observed. As the shunt magnitude increases, increased flow in the pulmonary veins is evident and the left atrium enlarges. With a small or moderate-sized patent ductus arteriosus, the left ventricular size is often normal, but as shunt magnitude increases, the left ventricular diastolic size also increases.

Other Tests

• With a small patent ductus arteriosus, the ECG findings are typically normal. Left ventricular hypertrophy may be present with a larger patent ductus arteriosus. This is typically seen as tall R waves in the lateral precordial leads (V₆).
• In the neonate, especially the premature neonate with a large patent ductus arteriosus, T-wave inversion and ST segment depression may be present, suggesting ischemia or a supply-demand mismatch. This is thought to be related to increased myocardial work due to the left-to-right shunt and pulmonary overcirculation in the face of low aortic and coronary diastolic blood pressure due to the runoff of blood from the aorta into the pulmonary arteries.

Treatment

Medical Care

The premature neonate with a significant patent ductus arteriosus (PDA) is usually treated with intravenous indomethacin or ibuprofen.³ This has been quite successful in most patients. Whether results with intravenous indomethacin are superior to those with surgical closure of the patent ductus arteriosus, even in the premature neonate in whom the safety of the surgery is a concern, is unclear.⁴

Intravenous indomethacin was the standard drug treatment until the last few years. A few years ago, intravenous ibuprofen was approved by the US Food and Drug Association (FDA). Ibuprofen and indomethacin are equally effective; however, other differences are noted. Indomethacin appears to decrease the incidence of intraventricular hemorrhage. Ibuprofen has less renal toxicity.

Although diuretics and fluid restriction have been recommended for the treatment of symptomatic neonates, no rigorously collected data support this approach. In fact, a systematic review of furosemide use in preterm neonates with respiratory distress syndrome showed no long-term benefits and an increased risk of symptomatic patent ductus arteriosus.⁵

Spontaneous closure is common. If significant respiratory distress or impaired systemic oxygen delivery is present, therapy is usually prudent. Intravenous indomethacin (or the new preparation of intravenous ibuprofen) is frequently effective in closing a patent ductus arteriosus if it is administered in the first 10-14 days of life. Another option is surgical ligation, discussed in Surgical Care.

After the first birthday, the most common treatment for a patent ductus arteriosus is occlusion at cardiac catheterization. In fact, as catheterization techniques advance, the ability to close defects in smaller infants has also been reported with high levels of success. Over the last 4 decades, many techniques and devices have been used for patent ductus arteriosus occlusion. For many years, the most common device used for patent ductus arteriosus occlusion has been a Gianturco spring occluding coil. In experienced hands with proper patient selection, this has become a procedure associated with high success and low morbidity. Coil occlusion is best suited to close a patent ductus arteriosus with a minimal internal diameter of less than 2.5 mm. Success is usual with a patent ductus arteriosus diameter of 2.5-3 mm, but a larger patent ductus arteriosus is probably best served by alternate techniques.

More recently, the Amplatzer patent ductus arteriosus device has expanded the ability to close patent ductus arteriosus at cardiac catheterization. This device is more reliable and easier to implant in a large patent ductus arteriosus than spring occluding coils. Other occlusion devices remain under investigation. Most patients with an isolated patent ductus arteriosus can have successful treatment by catheterization after the first few months of life.

Typically, complete occlusion is achieved at catheterization. Occasionally, a tiny residual left-to-right shunt remains at the end of the procedure, which closes by thrombus formation over the following days or weeks. Left-to-right shunt rarely persists through a partially occluded patent ductus arteriosus. Usually, the magnitude of the shunt is significantly smaller than prior to occlusion. Due to concerns about the long-term risk of endocarditis, this residual defect should be closed. Often, this can be accomplished with a second catheter procedure. Rare reports describe association of a persistently patent ductus after occlusion attempts with hemolysis or endocarditis.

Procedural risks of patent ductus arteriosus occlusion by catheter are few and largely influenced by the experience of the physician performing the procedure. These risks include embolization of the device being used to occlude the patent ductus arteriosus, blood vessel injury, and stroke. In the case of device embolization, the device can usually be retrieved by transcatheter techniques, and a second device can be successfully placed in the patent ductus arteriosus.

Surgical Care

Surgical ligation or surgical ligation and division remain the standard treatment of large patent ductus arteriosus that require treatment in infancy. This is a particularly successful procedure in the hands of an experienced pediatric cardiovascular surgeon. The techniques are reviewed in Patent Ductus Arterious: Surgical Perspective.

When performed by an experienced pediatric cardiac surgeon, patent ductus arteriosus ligation is a low-risk procedure with excellent results. This is true even in the smallest premature babies. The risks include hemorrhage, vessel damage, ligation of the wrong vessel (left pulmonary artery or aorta), recurrent laryngeal nerve or phrenic nerve damage, or infection.

While indomethacin therapy is preferred in most intensive care nurseries as the first-line approach to effect patent ductus arteriosus closure, the benefits of this approach over surgical ligation are not obvious. In most studies that attempt to evaluate differences in the outcomes for indomethacin therapy and surgical closure, results are similar. A Cochrane Database Systematic Review failed to demonstrate that the net harm-to-benefit ratio favored either surgical ligation or medical therapy.³   Observational studies suggest that surgical ligation is associated with higher likelihood of chronic lung disease, retinopathy of prematurity, and neurosensory impairment. These data may be questionable because surgical ligation is not available in every nursery, whereas medical therapy is widely available. 

Consultations

Consultation with a pediatric cardiologist and pediatric cardiovascular surgeon may be indicated.

Medication

In the presence of symptoms of pulmonary overcirculation or pulmonary hypertension related to a patent ductus arteriosus (PDA), closing the patent ductus arteriosus is usually most prudent; therefore, anticongestive therapy is not discussed. Intravenous indomethacin or intravenous ibuprofen is used to treat patent ductus arteriosus in the neonate. 

In a prospective, randomized, controlled trial, Attridge et al studied whether measuring b-type natriuretic peptide (BNP) concentrations can be used to reduce the number of indomethacin doses for patent ductus arteriosus and, thus, reduce nephrotoxicity.⁶ Results showed that patients in the BNP-guided group received fewer primary indomethacin doses compared with the group that was not guided by BNP concentrations. Renal toxicity is associated with indomethacin, and dose reduction guided by BNP may reduce this risk.

Prostaglandin inhibitors

In the neonate, ductal patency appears to be related to continued production of prostaglandin. This is particularly true in the premature infant; therefore, prostaglandin inhibition can affect ductal closure.

Indomethacin (Indocin)

This is the only medication indicated for PDA closure available in the United States. Prostaglandins, especially E-type prostaglandins, maintain the patency of the ductus. Thus, inhibition of prostaglandin synthesis by indomethacin results in constriction of the ductus arteriosus.

Dosing

Adult

Not indicated

Pediatric

Many dosage regimens are noted, and the dose depends on postnatal age (PNA) at time of first dose; one example is as follows:
PNA <48 hours: 0.1 mg/kg IV q12h for 3 doses
PNA 2-7 days: 0.2 mg/kg IV q12h for 3 doses
PNA >7 days: 0.25 mg/kg IV q12h for 3 doses

Interactions

Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effects of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently

Contraindications

Documented hypersensitivity; GI bleeding; anuria

Precautions

Pregnancy

Precautions

Caution with intraventricular hemorrhage (particularly if active hemorrhage), renal failure, thrombocytopenia, and severe hyperbilirubinemia; increases risk of acute renal failure in patients with preexisting renal disease or compromised renal perfusion; reversible leukopenia may occur (discontinue if persistent leukopenia, granulocytopenia, or thrombocytopenia); adjust dosage interval with renal insufficiency

Ibuprofen lysine injection (NeoProfen)

The mechanism of action that results in PDA closure in neonates is not known; however, ibuprofen is an inhibitor of prostaglandin synthesis. Indicated to close a clinically significant PDA in premature infants who weigh between 500-1500 g at <32 wk GA when usual medical management (eg, fluid restriction, diuretics, respiratory support) is ineffective.

Dosing

Adult

Not indicated

Pediatric

Premature infants with birth weight 500-1500 g and <32 wk GA: 10 mg/kg IV for first dose, then 5 mg/kg IV for second and third doses after 24 and 48 h, respectively
Infuse each dose over 15 min

Interactions

None reported

Contraindications

Proven or suspected infection that is untreated; congenital heart disease in whom patency of the PDA is necessary for satisfactory pulmonary or systemic blood flow (eg, pulmonary atresia, severe tetralogy of Fallot, severe coarctation of the aorta); active bleeding, especially intracranial hemorrhage or GI bleeding; thrombocytopenia, coagulation defects, necrotizing enterocolitis, significant renal impairment

Precautions

Pregnancy

Precautions

May decrease urinary output, if anuria or marked oliguria (urinary output <0.6 mL/kg/h) occurs at scheduled time of second or third doses, do not administer these doses until lab confirms normal renal function; if ductus arteriosus closes or size is significantly reduced after first dose, no further doses are necessary; dilute prior to administration; do not infuse via same IV port as TPN; use extravasation precautions (drug irritating to tissues); may alter usual signs of infection; may inhibit platelet aggregation

Follow-up

Further Inpatient Care

• Typically, hospitalization following treatment for patent ductus arteriosus (PDA) is minimal. Patients who have catheter closure of patent ductus arteriosus are usually sent home on the day of the procedure. Even patients who have standard surgery with a thoracotomy rarely are hospitalized for longer than 2 or 3 days.
• The appropriate care and length of hospitalization of premature neonates with a patent ductus arteriosus are primarily determined based on abnormalities of other organ systems. However, babies who have effective closure of patent ductus arteriosus appear to have shorter hospital stays than babies whose patent ductus arteriosus remains a problem.

Further Outpatient Care

• Once the patent ductus arteriosus is closed, no special limitations or care is necessary.
• Most physicians recommend antibiotic prophylaxis at times of risk of bacteremia for 6-12 months following closure, whether by catheter or surgery.

Complications

• Endocarditis
• Congestive heart failure
• Pulmonary vascular obstructive disease
• Aortic rupture

Prognosis

• Typically, following patent ductus arteriosus closure, patients experience no further symptoms and have no further cardiac sequelae.
• Premature infants who had a significant patent ductus arteriosus are more likely to develop bronchopulmonary dysplasia.

Miscellaneous

Special Concerns

• Some canine breeds, such as certain strains of poodle, have a large prevalence of patent ductus arteriosus.

Multimedia

Media file 1: Schematic diagram of left-to-right shunt of blood flow from descending aorta via patent ductus arteriosus (PDA) to main pulmonary artery

References

1. Cassels DE, Bharati S, Lev M. The natural history of the ductus arteriosus in association with other congenital heart defects. Perspect Biol Med. Summer 1975;18(4):541-72. [Medline].

2. Campbell DC, Hood RH Jr, Dooley BN. Patent ductus arteriosus. Review of literature and experience with surgical corrections. J Lancet. Oct 1967;87(10):415-8. [Medline].

3. [Best Evidence] Ohlsson A, Walia R, Shah S. Ibuprofen for the treatment of patent ductus arteriosus in preterm and/or low birth weight infants. Cochrane Database Syst Rev. Jan 23 2008;CD003481. [Medline].

4. Sekar KC, Corff KE. Treatment of patent ductus arteriosus: indomethacin or ibuprofen?. J Perinatol. May 2008;28 Suppl 1:S60-2. [Medline].

5. Brion LP, Soll RF. Diuretics for respiratory distress syndrome in preterm infants. Cochrane Database Syst Rev. Jan 23 2008;CD001454. [Medline].

6. [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].

7. Bose CL, Laughon MM. Patent ductus arteriosus: lack of evidence for common treatments. Arch Dis Child Fetal Neonatal Ed. Nov 2007;92(6):F498-502. [Medline].

8. Cambier PA, Kirby WC, Wortham DC, Moore JW. Percutaneous closure of the small (less than 2.5 mm) patent ductus arteriosus using coil embolization. Am J Cardiol. Mar 15 1992;69(8):815-6. [Medline].

9. Corbet AJ. Medical manipulation of the ductus arteriosus. In: The Science and Practice of Pediatric Cardiology. Lippincott Williams & Wilkins; 1997:2489-514.

10. Dudell GG, Gersony WM. Patent ductus arteriosus in neonates with severe respiratory disease. J Pediatr. Jun 1984;104(6):915-20. [Medline].

11. Gross RE, Hubbard JP. Surgical ligation of a patent ductus arteriosus. JAMA. 1939;112:729-31.

12. Heymann MA, Rudolph AM. Control of the ductus arteriosus. Physiol Rev. Jan 1975;55(1):62-78. [Medline].

13. [Best Evidence] Madan JC, Kendrick D, Hagadorn JI, Frantz ID 3rd. Patent ductus arteriosus therapy: impact on neonatal and 18-month outcome. Pediatrics. Feb 2009;123(2):674-81. [Medline].

14. Mahony L, Carnero V, Brett C, et al. Prophylactic indomethacin therapy for patent ductus arteriosus in very- low-birth-weight infants. N Engl J Med. Mar 4 1982;306(9):506-10. [Medline].

15. [Best Evidence] Malviya M, Ohlsson A, Shah S. Surgical versus medical treatment with cyclooxygenase inhibitors for symptomatic patent ductus arteriosus in preterm infants. Cochrane Database Syst Rev. Jan 23 2008;CD003951. [Medline].

16. Mullins CE, Pagotto L. Patent ductus arteriosus. In: The Science and Practice of Pediatric Cardiology. Lippincott Williams & Wilkins; 1997:1181-98.

17. Ramsay JM, Murphy DJ Jr, Vick GW 3rd, et al. Response of the patent ductus arteriosus to indomethacin treatment. Am J Dis Child. Mar 1987;141(3):294-7. [Medline].

18. Rashkind WJ, Mullins CE, Hellenbrand WE, Tait MA. Nonsurgical closure of patent ductus arteriosus: clinical application of the Rashkind PDA Occluder System. Circulation. Mar 1987;75(3):583-92. [Medline].

19. Reller MD, Colasurdo MA, Rice MJ, McDonald RW. The timing of spontaneous closure of the ductus arteriosus in infants with respiratory distress syndrome. Am J Cardiol. Jul 1 1990;66(1):75-8. [Medline].

20. Van Overmeire B, Smets K, Lecoutere D, et al. A comparison of ibuprofen and indomethacin for closure of patent ductus arteriosus. N Engl J Med. Sep 7 2000;343(10):674-81. [Medline].

Keywords

patent ductus arteriosus, patent arterial duct, PDA, congenital heart defect, aorticopulmonary shunt, aorticopulmonary communication, ductus arteriosus, pulmonary hypertension, respiratory distress syndrome, congestive heart failure, rubella, fetal alcohol syndrome

Contributor Information and Disclosures

Author

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.

Medical Editor

Christopher Johnsrude, MD, Associate Professor of Pediatrics, Director of Electrophysiology, University of Louisville School of Medicine; Consulting Staff, Pediatric Cardiology Associates, PSC
Christopher Johnsrude, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Cardiology
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: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

Managing Editor

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.

CME Editor

Gilbert Z Herzberg, MD, Assistant Professor, Department of Pediatrics, Section of Pediatric Cardiology, New York Medical College; Consulting Staff, Department of Pediatrics, Sound Shore Medical Center
Gilbert Z Herzberg, MD is a member of the following medical societies: American Academy of Pediatrics
Disclosure: Nothing to disclose.

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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