PATENT DUCTUS ARTERIOSUS (PDA)

The patent ductus arteriosus (PDA) is a congenital heart disease caused by the failure of the ductus arteriosus to close after birth, resulting in the passage of blood from the descending aorta to the pulmonary artery.

During fetal life, the ductus arteriosus is an essential vascular structure that connects the pulmonary artery to the aortic arch, just distal to the origin of the left subclavian artery.
This communication allows blood to bypass the pulmonary circulation, which is still immature and characterized by high vascular resistance.
In the fetus, blood flow through the ductus arteriosus is right-to-left, meaning from the pulmonary artery to the aorta, due to high pulmonary pressure and low systemic vascular resistance. The duct remains open due to high levels of prostaglandins (PGE2 and PGI2) produced by the placenta and the vascular wall itself.

After birth, with the first breath, significant hemodynamic changes occur:

• Reduction of pulmonary resistance: leads to a decrease in pressure in the pulmonary artery.
• Increase in partial oxygen pressure (PaO₂): stimulates the contraction of smooth muscle cells in the duct wall.
• Removal of the placenta: causes a decrease in prostaglandin (PGE2) levels, accelerating duct closure.

These factors induce a functional closure of the ductus arteriosus within the first 24-48 hours of life. Over the following days or weeks, the duct undergoes progressive remodeling, with endothelial cell proliferation and fibrotic tissue deposition, leading to its permanent anatomical closure.

The patent ductus arteriosus (PDA) occurs when the duct fails to close spontaneously, allowing continuous blood flow between the aorta and pulmonary artery. This creates a left-to-right shunt (from the aorta to the pulmonary artery), the clinical impact of which depends on the duct's size and the volume of shunted blood.

The persistence of this connection between the aorta and the pulmonary artery leads to dysfunctional conditions responsible for the clinical picture:

• Increased pulmonary venous return: leading to overload of the left heart chambers (left atrium and ventricle).
• Excessive pulmonary blood flow: causes an increase in pulmonary arterial pressure.
• Progressive dilation of the cardiac chambers, predisposing to congestive heart failure.

In severe cases, pulmonary hypertension may progress to irreversible pulmonary vascular disease (Eisenmenger syndrome). In this condition, the pressure gradient reverses, causing desaturated blood to flow from the pulmonary artery to the aorta, leading to systemic cyanosis.

Clinical presentation

The symptoms of PDA vary greatly depending on the duct size.

• Small PDA (minimal shunt): generally asymptomatic, sometimes associated with a continuous murmur (Gibson murmur) in the left infraclavicular area.
• Moderate PDA (significant shunt): may cause exertional dyspnea, fatigue, growth difficulties in neonates, and signs of cardiac overload.
• Large PDA (high-volume shunt): can lead to congestive heart failure, with tachypnea, feeding difficulties, hepatomegaly, and peripheral edema.

When severe pulmonary hypertension develops, the pressure gradient reverses, and desaturated blood from the pulmonary artery enters the systemic circulation, causing cyanosis and chronic hypoxemia.

Physical examination

On auscultation, a characteristic continuous murmur (systolic-diastolic) "machinery murmur" in the left infraclavicular area is typically heard. In cases of advanced pulmonary hypertension, the second heart sound is accentuated with a marked pulmonary component.
From a hemodynamic perspective, the patient may present with bounding peripheral pulses due to increased pulse pressure and the presence of continuous arterial runoff into the pulmonary circulation, along with tachypnea, polypnea, and intercostal retractions.

Diagnosis

Diagnosis is primarily based on echocardiography with Doppler, which confirms the presence of a shunt and assesses its severity while measuring pulmonary pressures. Chest X-ray may reveal cardiomegaly and increased pulmonary vascular markings in cases of excessive pulmonary blood flow. Electrocardiography may show signs of left-sided volume overload in significant PDA cases.

Treatment

The treatment of patent ductus arteriosus varies based on the neonate's characteristics and the severity of the congenital defect. There are three main therapeutic options:

• Pharmacological closure (preterm infants): In preterm neonates, PDA closure can be achieved with prostaglandin synthesis inhibitors, such as ibuprofen, which is preferred due to its better safety profile, or indomethacin, which is also effective but with more side effects. Paracetamol is an alternative in some cases. This therapy is ineffective in term neonates and older children.
• Percutaneous closure: If PDA persists beyond the first months of life and is hemodynamically significant, the preferred treatment is percutaneous closure using a transcatheter device (e.g., Amplatzer duct occluder), performed in interventional cardiology as a minimally invasive procedure.
• Surgical correction: Indicated in neonates with a very large duct not amenable to percutaneous treatment, in patients with complications (such as infective endocarditis on the patent ductus), or in cases of developing Eisenmenger syndrome where closure is still feasible.

If treated early, PDA has an excellent prognosis, and the patient can lead a normal life.
When left untreated, possible complications include heart failure, irreversible pulmonary hypertension, infective endocarditis, and Eisenmenger syndrome, which renders the duct inoperable.

References
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