bubble_chart Overview

Patent ductus arteriosus (PDA) is one of the most common congenital heart diseases in children. The ductus arteriosus is the main physiological blood flow channel in the fetal circulation. Normally, it functionally closes shortly after birth, followed by anatomical closure. However, under certain pathological conditions, the ductus arteriosus remains open, resulting in patent ductus arteriosus. Since the aortic pressure is higher than the pulmonary artery pressure, blood continuously shunts from the aorta to the pulmonary artery through the patent ductus during both systole and diastole. This leads to excessive volume load on the left ventricle and a significant increase in pulmonary blood flow, causing pulmonary artery hypertension and increased load on the right ventricle. Initially, pulmonary artery hypertension is dynamic but gradually progresses to become resistive, eventually resulting in right-to-left shunting.

bubble_chart Diagnosis

(1) Symptoms Individuals with small ducts and minimal shunting may experience no subjective symptoms. Those with moderate to large ducts may exhibit dyspnea during exercise, general fatigue, recurrent respiratory infections, or may present with heart failure. In cases complicated by bacterial endocarditis, systemic infection symptoms such as fever, chest pain, and peripheral vascular embolism may occur.

(2) Signs Patients with significant shunting may display growth retardation. Commonly observed peripheral vascular signs include widened pulse pressure, decreased diastolic pressure, water-hammer pulse, capillary pulsation, and pistol-shot sounds. The heart may be grade II enlarged, predominantly in the left ventricle. A systolic tremor may be palpated at the left sternal border between the 1st and 2nd intercostal spaces, sometimes extending into diastole, accompanied by a continuous machinery-like bruit. In cases of large shunting, a diastolic flow murmur may be heard at the apex. Patients with pulmonary hypertension may only exhibit a systolic murmur, and severe cases may present with cyanosis, often with faint or absent murmurs.

(3) X-ray Examination Small ducts may show normal lung fields or grade I increased pulmonary vascular markings, or only grade I left ventricular enlargement. Larger ducts typically present with prominent pulmonary vascular markings, cardiac enlargement predominantly in the left ventricle and left atrium, a bulging pulmonary artery segment, and a widened main pulmonary artery. Funnel-shaped signs may also be observed. In pulmonary hypertension, the right ventricle may be significantly enlarged, and fluoroscopy may reveal the "hilar dance" phenomenon.

(4) Electrocardiogram Small ducts may yield normal results, while larger ducts may show left axis deviation, left ventricular hypertrophy, and broad P waves in lead II, suggesting left atrial enlargement. Pulmonary hypertension may result in biventricular hypertrophy, with severe cases predominantly affecting the right ventricle and showing right axis deviation.

(5) Echocardiography Two-dimensional imaging in the short-axis view of the main pulmonary artery may reveal communication between the main pulmonary artery and the descending aorta, though false positives are common. Left atrial and left ventricular enlargement may be observed. Pulsed Doppler sampling within the main pulmonary artery may detect a diastolic turbulent flow spectrum. In pulmonary hypertension, turbulent flow may only appear in early diastole, serving as strong corroborative evidence. Color Doppler may reveal a multicolored shunt flow from the descending aorta into the main pulmonary artery.

(6) Cardiac Catheterization and Angiography Small to moderate ducts can often be diagnosed non-invasively. For challenging cases, retrograde ascending aortography may be performed, revealing dilation of the ascending aorta and aortic arch, simultaneous opacification of the pulmonary artery and aorta, and occasionally the presence of a patent ductus arteriosus.

bubble_chart Treatment Measures

﹝Treatment﹞

(1) Surgical treatment is highly effective. Once diagnosed, surgical intervention is necessary, with a surgical mortality rate of less than 1%. Without surgery, there is a risk of combined infective endocarditis. The optimal age for elective surgery is between 1 to 6 years old. Postoperatively, the continuous murmur in most children disappears immediately, and the cardiac shadow significantly shrinks within 3 to 6 months after surgery, gradually returning to normal completely. Recanalization after duct ligation rarely occurs, but if it does, reoperation with cutting and suturing is required.

(2) In recent years, there have been reports both domestically and internationally on the use of interventional methods to occlude the duct. The method involves first inserting a steel wire from the stirred pulse end, passing it through the stirred pulse duct via the right heart, and then pulling it out from the venous end to form a circular path in the body. A prepared plastic plug is then pushed through the circulatory path to the stirred pulse duct to create an occlusion. This method is less likely to succeed in preschool children due to their narrow blood vessels.

(3) In premature infants, the stirred pulse duct often closes naturally after birth upon reaching maturity. Therefore, asymptomatic cases may not require treatment. For symptomatic cases, prostaglandin synthetase inhibitors such as indomethacin can be tried, at a dose of 0.2 mg/kg per administration, orally, rectally, or intravenously. If ineffective, the dose can be repeated once or twice at 8-hour intervals, with a total dose not exceeding 0.6 mg/kg. Contraindications include renal dysfunction, serum creatinine >132.6 µmol/L (1.5 mg/dl), urea nitrogen >7.1 mmol/L (20 mg/dl), bleeding tendency, platelet < 50×10⁹/L, or suspected necrotizing small intestine colitis. For cases where indomethacin treatment is ineffective or contraindicated, timely surgical treatment should be provided.