Patent Ductus Arteriosus
• Definition: Ductus open in all newborns at delivery, closure occurs rapidly after birth; closure in 90% of healthy FT infants by 48th hr of life
• A ductus open beyond 72 hr is considered persistently patent
• Epidemiology: ↑ risk PDA w/ prematurity, RDS, excess fluid admin in 1st d of life, asphyxia, congenital syndromes (Trisomy 13), birth at high altitude, cong heart dz
• Clinical manifestations
• Heart murmur (usually continuous, accentuated in systole, loudest at 2nd or 3rd intercostal space), bounding periph pulses (2/2 diastolic runoff through PDA), hyperactive precordium, resp deterioration may be gradual or rapid, HoTN
• Diagnostic studies: Ductus can be visualized directly by echocardiography
• Management: Indications to Rx controversial: Spontaneous closure in neonates born at >27 wk GA; however, ibuprofen not as effective in closure after ∼DOL#5
• Ibuprofen (NeoProfen): Nonselective COX-inhib; inhib prostaglandin prod vs. Indomethacin (Cochrane Rev 2010;(4):CD003481)—same efficacy for closure
• Ibuprofen has fewer side effects compared to indomethacin: Does not reduce mesenteric and renal blood flow (N Engl J Med 2000;343:674)
• Indomethacin has more neuroprotective effects than Ibuprofen (NeoReviews 2008;9:e477)
• Fluid restriction as much as possible to decrease PDA shunt
• Surgery: Considered after failure of NeoProfen therapy, or w/ hemodynamically significant PDA, or a contraindication to the use of COX inhibitor
Persistent Pulmonary Hypertension of the Newborn (PPHN)
• Definition: Pulm HTN 2/2 ↑ pulm vasc resistance (PVR) and Δ in pulm vasoreactivity leading to R-to-L extrapulmonary shunting across PDA and foramen ovale
• Pathophysiology: 2/2 underdeveloped vasc lung bed or maladaptation of pulm vascular bed to transition to extrauterine life
• Vasodilatory & vasoconstrictive factors (leukotrienes & thromboxanes) regulate vascular tone during transition. Nitric oxide (NO) an important vasodilator
• Assoc d/o (Pediatrics 2007;120:e272): Lung dz (meconium aspiration, RDS, PNA, pulm hypoplasia, cystic lung disease), systemic disorders (polycythemia, hypoxia, sepsis), congenital heart disease, perinatal factors (asphyxia, C-section, LGA, etc.)
• Clinical manifestations
• Cyanosis, respiratory distress, lability in oxygenation within 1st 4–8 hr of life
• Large A-a gradient leading to large decrease in arterial oxygenation
• Pre- and postductal O2 sats may demonstrate gradient (R-to-L shunt through PDA)
• Treatment: Supplemental O2: Oxygen is a potent vasodilator; consider mechanical ventilation in infants w/ significant respiratory distress and CO2 retention
• Adeq SBP w/ vol support; consider dopamine to ↓ the R-to-L shunt by ↑ing SVR
• Adequate sedation, minimize handling to avoid stimulation
• Avoid acidemia, consider NaHCO3 and mild hyperventilation
• Inhaled nitric oxide: Start dose of 20 ppm; may improve PVR and oxygenation
• ECMO may be indicated in those failing mechanical ventilation