• Fetal circulation (parallel) in transition to complete adult circulation (series)
  
• Is essentially a complete adult circulation in series, but with PDA and patent foramen ovale
  
• Potential for shunting exists, determined by relation between SVR and PVR
  
• Determinants of SVR
  
  
  
  • Intrinsic autoregulatory mechanisms
    
  • Environmental temperature
    
  • Radiant warmer–induced vasodilation
  
  
• Determinants of PVR
  
  
  
  • Alveolar hypoxia
    
  • Reduced total pulmonary vascular bed
    
  • Sensitization of pulmonary vascular bed by sustained asphyxia

• Prenatally, ductus arteriosus (DA) is a vascular connection between the main pulmonary artery (occasionally proximal LPA) and the aorta, diverting blood from pulmonary to systemic circulation.
  
• Postnatally, the vasa vasorum to the DA constrict, leading to necrosis of the medial muscular layer → ductal closure.
  
• In preterm infants, the DA wall thickness is proportionately less than in term infants, allowing passive diffusion of nutrients from the ductal lumen to the medial muscular layer, even after constriction of the vasa vasorum → higher rate of ductal patency.
  
• DA closed in 50% of full-term infants by 24 h, 90% by 48 h, >99% by 96 h.
  
• Incidence in term infants: ∼0.02%–0.04% (10% of all CHD in term infants).
  
  
  
  • Incidence in preterm infants: ∼45% of infants <1750 g, ∼80% of infants <1000 g.
    
  • Increased in: prematurity, hyaline membrane deficiency, asphyxia, high altitude, CHD, increased fluid administration
    
  • Decreased in: antenatal steroids, intrauterine growth restriction, prolonged rupture of membranes
  
  
• Spontaneous closure of PDA occurs in 38%–85% of babies <1500 g and in 25%–34% of those <1000 g.

Clinical Manifestations

• Large PDA can be diagnosed relatively accurately based on clinical findings.
  
• Small PDA usually requires an echocardiogram with Doppler, because findings may be similar to pulmonary disease or sepsis.
  
• Clinical findings of moderate to large PDA:
  
  
  
  • Hypotension
    
  • Murmur (Continuous, “machinery”-like, may be intermittent)
    
  • Heart failure (Poor feeding, apnea, respiratory failure)
    
  • Wide pulse pressure (>25 mm Hg)
    
  • Hyperdynamic precordium
    
  • Bounding pulses (± Palmar pulses, prominent pedal pulses)
    
  • Respiratory compromise (Increased ventilator support or inability to wean ventilatory support)

Diagnosis

• CXR
  
  
  
  • May be normal, or may see pulmonary edema or cardiomegaly (compare films serially)
  
  
• Echocardiography with Doppler
  
  
  
  • Findings associated with hemodynamically significant PDA include:
    
    
    
    • Ductal diameter >1.5 mm
      
    • Predominantly left-to-right shunt
      
    • Disturbed diastolic flow in MPA
      
    • Reversal of end-diastolic flow in postductal aorta
      
    • Left atrial/left ventricular enlargement
  
  
• Electrocardiography (no specific findings exist for PDA)
  
  
  
  • May be normal, or may see LVH, BVH, or LAE

Complications

• Pulmonary edema
  
• Heart failure
  
• Pulmonary hypertension
  
• Septic emboli (from vegetations located on the pulmonary side of PDA)

Management

• Asymptomatic PDA without need for ventilator support: No long-term benefits established with medical or surgical treatment; may continue to feed these infants
  
• Symptomatic PDA: No long-term benefits established with medical or surgical treatment, but treatment reduces the need for ventilator support and theoretically prevents progression to heart failure, pulmonary hypertension, and septic emboli
  
  
  
  • Ventilatory support (may increase PEEP to control pulmonary edema)
    
  • Fluid restriction (alone does not cause ductal closure, but excess fluid administration is associated with increased incidence of PDA)
    
  • PRBC transfusion (if significant anemia present, may reduce high-output state and decrease pulmonary overcirculation)
    
  • Definitive management (medical versus surgical [ie, indomethacin vs ligation])

Indomethacin

• Effectiveness diminishes above 1500 g and beyond 3–4 wk of life
  
• Two approaches:
  
  
  
  • Prophylactic administration (not standard practice at TCH)
    
    
    
    • Dose: 0.1 mg/kg indomethacin IV q24h for three doses
      
    • Who: All infants <1000 g with RDS necessitating surfactant
      
    • Rationale: Administering prophylactic doses during the first 3 DOL results in a greater rate of permanent ductus closure (J Pediatr 2000;136:330.)
    
    
  • Treatment of the symptomatic PDA
    
    
    
    • Dose: Administration is q12–24h, following urine output closely, and is dependent on when indomethacin is begun postnatally (see the table below)

• 
  
  
  
  • Who: Infant with evidence of significant symptoms of PDA (eg, murmur, ↑ ventilator support, signs of heart failure); must rule out a ductal dependent lesion prior to initiation of indomethacin therapy
    
  • Rationale: Treat a slightly more targeted population; risk treating those who would spontaneously close

• Treatment failure: 30%–50% of PDAs will either reopen or fail to close after treatment; if the PDA either fails to close or reopens and remains symptomatic/hemodynamically significant, options include:
  
  
  
  • Repeat: Administer one to two more 0.2 mg/kg IV doses q12–24h of indomethacin (although extended dosing has been shown to be associated with more moderate to severe retinopathy of prematurity and renal impairment in one study [J Pediatr 2008;153:183]).
    
  • Surgical ligation: Infants <28 wk gestation with Doppler evidence of ductus flow after the initial indomethacin course are unlikely to respond to a subsequent course (Pediatrics 2003;112(3 pt 1):583). Given the long-term neurodevelopmental concerns with surgical closure, many continue to favor a second course of indomethacin prior to surgical ligation. The decision to pursue further dosing of indomethacin versus surgical ligation is made on a case-by-case basis after weighing the risk:benefit ratio for each.