Chapter 61 Patent Ductus Arteriosus
PATHOPHYSIOLOGY
The ductus arteriosus is a large vessel that connects the main pulmonary trunk (or left pulmonary artery) with the descending aorta approximately 5 to 10 mm from the origin of the left subclavian artery. Patent ductus arteriosus (PDA) is the persistent patency of the ductus arteriosus after birth, which results in the shunting of blood directly from the aorta (higher pressure) into the pulmonary artery (lower pressure). This left-to-right shunting causes the recirculation of increased amounts of oxygenated blood in the lungs, which raises demands on the left side of the heart. The additional effort required of the left ventricle to meet this increased demand leads to progressive dilation and left atrial hypertension. The cumulative cardiac effects cause increased pressure in the pulmonary veins and capillaries, which results in pulmonary edema. The pulmonary edema leads to decreased diffusion of oxygen and hypoxia, with progressive constriction of the arterioles in the lungs. Pulmonary hypertension and failure of the right side of the heart ensue if the condition is not corrected through medical or surgical treatment. Most PDAs are a left-to-right shunting of blood, but right-to-left ductal shunting may occur with associated pulmonary disease, left-heart obstructive lesions, and coarctation of the aorta. Closure of the PDA depends primarily on the constrictor response of the ductus to the oxygen tension in the blood. Other factors affecting ductus closure include the action of prostaglandins, pulmonary and systemic vascular resistances, the size of the ductus, and the condition of the infant (premature or full-term). PDA occurs more frequently in premature infants; it is also less well tolerated in these infants, because their cardiac compensatory mechanisms are not as well developed and left-to-right shunts tend to be larger.
INCIDENCE
1. Precise incidence varies depending on gestational age and according to the means of diagnosing (clinical signs as opposed to echocardiography).
2. Approximately 5% to 10% of infants with PDAs have additional cardiac defects (coarctation of the aorta, ventricular septal defect, aortic stenosis).
3. PDA is present in 60% to 70% of infants with congenital rubella infection.
4. PDA occurs 2 to 3 times more often in girls than in boys.
5. PDA is found in approximately 45% of infants <1750 g; and in infants <1000 g, the incidence is 80%.
CLINICAL MANIFESTATIONS
The disorder may be manifest at birth, but usually it is first noticed on days 1 to 4 of life. Manifestations of PDA in premature infants are often clouded by other problems associated with prematurity (e.g., respiratory distress syndrome). Signs of ventricular overload are not apparent for 4 to 6 hours after birth. Infants with small PDAs may be asymptomatic; infants with large PDAs may manifest signs of congestive heart failure (CHF):
1. Persistent murmur (systolic, then continuous; heard best at left upper sternal border)
2. Hyperactive precordium (result of increased left ventricular stroke volume)
3. Prominent to bounding pulses
4. Wide pulse pressure (higher than 25 mm Hg)
5. Decreased mean arterial blood pressure
6. Tachypnea (respiratory rate higher than 70 breaths/min)
7. Increased ventricular requirement (associated with pulmonary problems)
8. Tachycardia (apical pulse higher than 170 beats/min); usually associated with congestive heart failure
COMPLICATIONS
1. Cardiovascular: arrhythmias (digitalis toxicity)
2. Respiratory: concurrent pulmonary disorder (e.g., respiratory distress syndrome or bronchopulmonary dysplasia), pulmonary hemorrhage
3. Gastrointestinal (GI): necrotizing enterocolitis, GI hemorrhage (decreased platelet count), failure to thrive, decreased blood flow to intestines with use of indomethacin
4. Renal: hyperkalemia (decreased urinary output), decreased blood flow to kidneys with indomethacin
5. Hematologic: sepsis secondary to impaired white blood cell motility with use of indomethacin
LABORATORY AND DIAGNOSTIC TESTS
1. Echocardiography—two-dimensional echocardiographic visualization of the ductus with Doppler measurements is sensitive and specific for identifying PDA; M-mode measurements of left atrial to aortic root ratio greater than 1.4:1 in full-term infants or greater than 1.0 in preterm infants (caused by increased left atrial volume as a result of left-to-right shunt)
2. Doppler color flow mapping—to evaluate blood flow and its direction
3. Chest radiographic study—prominent or enlarged left atrium and left ventricle (cardiomegaly); increased pulmonary vascular markings
4. Electrocardiography (ECG)—findings vary with degree of severity: no abnormality noted with small PDA; left ventricular hypertrophy is typically seen as tall R waves in V6 with large PDA, limited value in assessment
5. Cardiac catheterization—performed only when further evaluation of confusing echocardiographic or Doppler findings is needed or when additional defects are suspected to be present
MEDICAL AND SURGICAL MANAGEMENT
Interrupting the left-to-right flow of blood is the goal of management for the uncomplicated PDA. When the shunt is hemodynamically significant, conservative measures may be tried initially. Conservative management consists of fluid restriction and medications. Furosemide (Lasix) is used along with fluid restriction to promote diuresis and minimize the effects of cardiovascular overload. Fluid restriction alone is unlikely to cause PDA closure and, in combination with diuretics, may lead to electrolyte abnormalities and dehydration as well as caloric deprivation, which impairs growth.
