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Patent
ductus arteriosus (PDA) is a persistence of the fetal connection
(ductus arteriosus) between the aorta and pulmonary artery after birth,
resulting in a left-to-right shunt. Symptoms may include failure
to thrive, poor feeding, tachycardia, and tachypnea. A continuous
machine-like murmur in the upper left sternal border is common.
Diagnosis is by echocardiography. Administration of indomethacin
with or without fluid restriction may be tried in premature infants
with a significant shunt but not in term infants with PDA. If the
connection persists, surgical or catheter-based correction is indicated.
Endocarditis prophylaxis is recommended before and for 6 to 12 mo
after correction.
Patent ductus arteriosus (PDA) accounts for 5 to 10% of congenital heart anomalies; the male:female ratio is 1:3. PDA is very common among premature infants (in 45% with birth weight < 1750 g; in about 80% with birth weight < 1200 g). Significant PDA causes heart failure (HF) in 15% of premature infants with birth weight < 1750 g and in 40 to 50% of those with birth weight < 1500 g.
The ductus arteriosus is a normal connection between the pulmonary artery and aorta; it is necessary for proper fetal circulation. At birth, the rise in Pao2 and decline in prostaglandin concentration cause closure of the ductus arteriosus, typically within the 1st 10 to 15 h of life. If this normal process does not occur, PDA results (see
Fig. 5: Congenital Cardiovascular Anomalies: In patent ductus arteriosus, pulmonary blood flow, LA and LV volumes, and ascending AO volume are increased. ).
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Fig. 5
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In patent ductus arteriosus, pulmonary blood flow, LA and LV volumes, and ascending AO volume are increased.
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AO = aorta; LA = left atrium; LV = left ventricle; PA = pulmonary artery.
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Physiologic consequences depend on ductal size. A small ductus rarely produces symptoms. A large (and short) ductus causes a large left-to-right shunt. Over time, a large shunt results in pulmonary artery hypertension and elevated pulmonary vascular resistance, ultimately leading to Eisenmenger's syndrome (see Congenital Cardiovascular Anomalies: Eisenmenger's Syndrome).
Symptoms and Signs
Clinical presentation depends on PDA size and gestational age at delivery. Infants and children with a small PDA are generally asymptomatic; infants with a large PDA present with signs of HF (eg, failure to thrive, poor feeding, tachypnea, dyspnea with feeding, tachycardia). Premature infants may present with respiratory distress, apnea, or other serious complications (eg, necrotizing enterocolitis). Signs of HF occur earlier in premature infants than in full-term infants and may be more severe.
Most children with a small PDA have normal heart sounds and peripheral pulses. A grade 1 to 3/6 continuous machinery murmur is heard best in the upper left sternal border.
Full-term infants with significant PDA shunt have full or bounding peripheral pulses with a wide pulse pressure. A grade 1 to 3/6 continuous machinery murmur is characteristic. A gallop rhythm may be audible if HF develops.
Premature infants with significant shunt have bounding pulses and a hyperdynamic precordium. A heart murmur occurs in the pulmonary area; the murmur may be continuous, systolic with a short diastolic component, or only systolic. Some infants have no audible heart murmur.
Diagnosis
Diagnosis is suggested by clinical examination, supported by chest x-rays and ECG, and established by 2-dimensional echocardiography with color flow and Doppler studies.
Chest x-ray and ECG are typically normal if the PDA is small. If the shunt is significant, chest x-rays show prominence of the left atrium, left ventricle, and ascending aorta and increased pulmonary vascular markings; ECG may show left ventricular hypertrophy. Cardiac catheterization is not usually necessary.
Treatment
In premature infants with compromised respiratory status, the PDA can sometimes be closed by using a prostaglandin synthesis inhibitor (eg, indomethacin [see Table 4: Congenital Cardiovascular Anomalies: Indomethacin Dosing Guidelines (mg/kg) for doses] IV q 12 h for 3 doses; or ibuprofen 10 mg/kg po followed by 2 doses of 5 mg/kg at 24-h intervals) with or without fluid restriction. If this treatment is ineffective, surgical ligation is indicated.
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Table 4
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Indomethacin
Dosing Guidelines (mg/kg)
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Age At Dose 1
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Dose 1
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Dose 2
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Dose 3
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< 48 h
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0.2
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0.1
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0.1
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2–7 days
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0.2
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0.2
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0.2
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> 7 days
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0.2
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0.25
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0.25
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In full-term infants, indomethacin is usually ineffective. For a large PDA, surgical ligation and division are typically done electively at age 6 mo to 3 yr. If HF develops, surgery can be done earlier after medical management for HF. Nonsurgical options for PDA closure include various catheter-delivered occlusion devices (percutaneous coil occlusion, Amplatzer duct occluder, Rashkind umbrella device). These techniques have become the treatment of choice in children > 1 yr. Outcomes after PDA closure are excellent.
Before and for 6 to 12 mo after surgical or catheter-based PDA closure, all patients require endocarditis prophylaxis (see Table 4: Endocarditis: Recommended Endocarditis Prophylaxis During Oral-Dental, Respiratory Tract, or Esophageal Procedures*) before dental or surgical procedures. Patients with a residual shunt require prophylaxis indefinitely.
Last full review/revision November 2005
Content last modified November 2005
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