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.
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:
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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
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The apical impulse is laterally displaced; a thrill may be present in the suprasternal notch or in the left infraclavicular region
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The first heart sound (S1) is typically normal, and 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
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The murmur may be only a systolic ejection murmur, or it may be a crescendo/decrescendo systolic murmur that extends into diastole
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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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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.
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Diagram illustrating the patent ductus arteriosus.
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Diagram illustrating ligation of the patent ductus arteriosus.
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Diagram illustrating division and oversewing of the patent ductus arteriosus.
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Diagram illustrating patch closure of the patent ductus arteriosus.
