Patent Ductus Arteriosus

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CHAPTER 43 Patent Ductus Arteriosus

Patent ductus arteriosus (PDA) is defined as incomplete closure and patency of the ductus arteriosus beyond functional closure after birth. The ductus arteriosus is a vessel that extends from the anterolateral aspect of the descending thoracic aorta to the superior aspect of the main pulmonary artery, close to the origin of the left pulmonary artery. Embryologically, it is a remnant of the distal left sixth aortic arch. A normal and vital structure in the fetus, it is necessary for diverting blood flow from the main pulmonary artery to the aorta, thereby bypassing the high-resistance pulmonary circulation.1 This diversion is crucial to normal development of the right ventricle and results in passage of only 10% of the right ventricular cardiac output through the lungs. Premature closure of the ductus arteriosus in the fetus, as seen with maternal use of nonsteroidal anti-inflammatory drugs (NSAIDs), leads to right ventricular failure and fetal hydrops (Fig. 43-1).2

The duct functionally closes in the first 18 hours of life in full-term healthy infants. However, it fully closes several weeks later, after which it is unable to regain its patency. In premature infants, patency can be seen up to 10 days after birth.3,4 Some consider the patency abnormal only after 3 months of age. The patency causes a left to right shunt that increases pulmonary blood flow at the expense of systemic flow.5 If untreated, based on the size of the PDA, pulmonary hypertension and Eisenmenger syndrome develop in children and adults (Fig. 43-2).1


PDA can be isolate or part of a complex cardiac malformation.7 The overall incidence in children born at term is 0.02% to 0.08%, which accounts for approximately 10% of all congenital heart disease. Most cases are sporadic. It is more common in premature and term infants with maternal rubella infection in the first trimester of pregnancy. Maternal use of amphetamine and phenytoin and fetal alcohol syndrome are also associated with PDA.8 PDA is more frequent in certain genetic syndromes such as trisomy 21, trisomy 18, 4p− syndrome, Holt-Oram syndrome, Carpenter syndrome, and Char syndrome.1,9

The cause of isolated cases is unknown. The underlying cause of PDA in the setting of maternal rubella and genetic syndromes is structural abnormality of the ductus hindering normal closure after birth. The mechanism of PDA in infants born prematurely or infants who have experienced perinatal hypoxia is most likely physiologic factors impeding the normal constriction of the ductus arteriosus.

PDA is twice as common in females when it is isolated and sporadic; however, if associated with prematurity or prenatal infection, the frequency is equal between the genders.9 A study by Mangones and colleagues,10 which compared the prevalence of various congenital cardiovascular malformations by race and ethnicity, showed no racial preference for isolated PDA and an overall less frequency of congenital cardiac malformations in Hispanics. However, a previous study by Chavez and associates11 described an increased prevalence of isolate PDA in African Americans.


The magnitude of left to right shunting depends on the flow resistance of the ductus arteriosus and the pressure gradient between the aorta and pulmonary artery. The flow resistance depends mainly on the diameter and length of the narrowest portion of the ductus arteriosus. The pressure gradient between the two ends of the PDA depends on the pulmonary and systemic vascular resistance and the cardiac output. The larger the diameter of the narrowest portion of the ductus, the greater the impact of changes in the systemic and pulmonary resistance on the pressure gradient and, therefore, on the magnitude of shunting. If the narrow portion is small in caliber, thereby a restrictive shunt, then the length of the narrow portion is important. A longer length of the ductus is associated with a smaller magnitude of shunting.1,6,8

The left to right shunt causes overcirculation and fluid overload of the pulmonary bed, which lead to decreased lung compliance and increased work of breathing. The shunting also causes left heart volume overload and, if the ductus is moderate to large in size, the increased left atrial and left ventricular end-diastolic pressures can eventually lead to hypertrophy of the left ventricle. The wall tension of the hypertrophied left ventricle causes catecholamine release, which results in tachycardia and therefore a shorter diastolic time. On the other hand, the diastolic blood pressure of the aorta decreases because of blood passage through the ductus during diastole. This decreased diastolic pressure and shorter diastolic time causes decreased coronary perfusion and, when combined with increased myocardial tension and oxygen demand, may result in subendocardial ischemia, which can be detected by elevated troponin levels.12

When the pulmonary arteries are subjected to long-standing increased flow and high pressure, microvascular injury develops, which leads to intimal proliferation and arteriolar medial hypertrophy. This eventually causes fibrosis and obliteration of the pulmonary arterioles and capillaries, and pulmonary arterial hypertension ensues. As the pulmonary vascular resistance gradually increases and approaches or exceeds the systemic vascular resistance, ductal shunting reverses and becomes right to left. This is called Eisenmenger syndrome.1,6,8

Clinical Features

Age of clinical presentation and presence of and type of symptoms at the time of presentation depend on the size of the PDA and pulmonary vascular resistance. The clinical presentation can vary from no symptoms, where the shunt is diagnosed incidentally, to congestive heart failure and Eisenmenger syndrome. Many patients have exercise intolerance or the diagnosis of reactive airway disease.1,8,13 Most patients compensate well, even with a moderate left to right shunt and remain asymptomatic during childhood. A well-tolerated PDA can become clinically significant when combined with effects of acquired conditions such as ischemic heart disease or calcific aortic stenosis. The hallmark physical finding is a machinery murmur, which is a continuous murmur detected at the left upper sternal border. If the shunt is moderate or large, the left ventricular impulse will be prominent and laterally displaced and the pulse pressure will be increased, resulting in a bounding peripheral pulse.

Eisenmenger syndrome presents with cyanosis and clubbing that may spare the fingers because the right to left shunting is distal to the subclavian arteries. This cyanosis may be more profound when systemic vascular resistance is decreased, such as after exercise or hot weather. On auscultation, there may be no murmur, a high-frequency diastolic decrescendo murmur of pulmonary regurgitation, and/or a holosystolic murmur from tricuspid valve regurgitation. Peripheral edema is a late manifestation caused by right ventricular dysfunction.14,15


Clinical Presentation

Imaging Technique and Findings

Computed Tomography

Computed tomography angiography (CTA) is useful for demonstrating the PDA, especially when it is not detectable on echocardiography, but is suspected. CTA also helps in characterizing the morphology of PDA and determining whether it is calcified, both important factors in treatment planning. Other associated vascular anomalies, such as a vascular ring or the presence of other associated congenital heart disease, can be detected by CTA. Multidetector CT (MDCT) involves faster imaging with a smaller contrast bolus, allowing increased use of this modality in the assessment of mediastinal vascular anomalies and acquired disease. The quick scanning results in fewer motion artifacts and the ability to evaluate children and older patients. The higher spatial resolution and presence of multiple rows of detectors along the longitudinal axis of the patient allow better multiplanar-reformatted and surface-shaded three-dimensional images to be created. These are most useful for quickly displaying the anatomy of the vascular abnormality and its relationship with adjacent structures. The ease of use of MDCT and its excellent depiction of anatomy has rendered CTA a common first means of evaluating for vascular anomalies in the thorax. The disadvantage of CTA is the use of intravenous iodinated contrast, contraindicated for patients with renal failure and for those who are allergic to intravenous contrast (Fig. 43-5).1719