Patent Ductus Arteriosus

Original Editor - Rishab Mishra Top Contributors - Lucinda hampton and Rishab Mishra

Introduction

The ductus arteriosus is a fetal vessel that allows the oxygenated blood from the placenta to bypass the lungs in utero. At birth, the lungs fill with air with the first breaths, pulmonary vascular resistance drops, and blood flows from the right ventricle to the lungs for oxygenation. The increased arterial oxygen tension and the decreased flow through the ductus arteriosus allow the ductus to constrict. The ductus arteriosus is functionally closed by 12 to 24 hours of age in healthy, full-term newborns. Permanent (anatomic) closure is complete within 2 to 3 weeks.

Etiology

• Physiological Factors:
  • During fetal life, low oxygen tension and high levels of prostaglandins from the placenta maintain the patency of the ductus arteriosus.
  • At birth:
    • Removal of the placenta decreases prostaglandin levels.
    • Increased oxygen tension from the infant's first breaths reduces pulmonary vascular resistance, promoting closure.
  • Functional closure occurs within 12-24 hours due to contraction of ductal muscles sensitive to oxygen, acetylcholine, bradykinin, and endothelin.
  • Anatomic closure (fibrosis) typically completes within 2-3 weeks post-birth.
• Incidence:
  • Rare in healthy term newborns.
  • Increased incidence in preterm infants, especially those with respiratory distress syndrome (up to 80% in extremely premature infants by day 3).
• Genetic Associations:
  • Trisomies: 13, 18, 21.
  • Syndromes: Holt-Oram, Noonan, CHARGE, TAAD/PDA, DiGeorge.
  • Familial forms of PDA and congenital heart diseases.
• Maternal Conditions and Exposures:
  • Maternal diabetes.
  • Magnesium exposure.
  • Cocaine use.
  • Calcium channel blockers.
• Neonatal Conditions and Exposures:
  • Extreme prematurity.
  • Respiratory distress syndrome.
  • Neonatal sepsis.
  • Birth at high altitude.
  • Excessive fluid administration.
  • Use of loop diuretics, aminoglycosides, cimetidine, and heparin.

Pathophysiology

• Role of Prostaglandin E2:
  • Prostaglandin E2 promotes the patency of the ductus arteriosus during fetal life.
  • After birth, persistent patency leads to abnormal hemodynamic changes.
• Hemodynamic Consequences:
  • Blood flows from the descending aorta to the pulmonary circulation ("left-to-right" shunt) due to higher systemic pressure.
  • This results in pulmonary overcirculation, causing:
    • Pulmonary edema.
    • Pulmonary hemorrhage.
• Increased Cardiac Workload:
  • The "steal" of blood from the aorta during diastole reduces systemic perfusion.
  • To maintain adequate cardiac output:
    • The heart compensates by increasing cardiac output.
    • Extremely premature infants rely on increased heart rate due to limited ability to increase stroke volume.
• Systemic Hypoperfusion:
  • Reduced blood flow to the lower body can lead to:
    • Necrotizing enterocolitis (due to gut ischemia).
    • Renal failure (due to impaired renal perfusion).
• Secondary Complications:
  • Persistent PDA is associated with:
    • Congestive heart failure from volume overload.
    • Bronchopulmonary dysplasia (BPD) due to chronic lung injury from pulmonary overcirculation.
    • Intraventricular hemorrhage from altered cerebral blood flow dynamics.

Evaluation

• Chest Radiography:
  • May reveal increased pulmonary vascular markings.
  • Presence of pulmonary edema supports the diagnosis.
• Echocardiography:
  • Confirms the presence of a patent ductus arteriosus.
  • Flow Direction:
    • Left-to-right flow: Typical finding in PDA.
    • Right-to-left flow: Suggestive of pulmonary hypertension, with PDA as a secondary finding.
  • Hemodynamic Significance:
    • Enlarged left atrium and left ventricle on imaging.
    • Reversal of diastolic flow in the abdominal aorta at the diaphragm level (though technically challenging to detect).
• Renal Function Tests:
  • Increased serum creatinine and decreased urine output indicate renal impairment due to systemic hypoperfusion.
• Clinical Correlation:
  • Assess for systemic and pulmonary complications to determine the impact of PDA on overall hemodynamics.

Treatment

• Conservative Management:
  • Suitable for gestationally mature infants.
  • Fluid restriction: 110-130 ml/kg/day while monitoring urine output.
  • Increased PEEP: To treat pulmonary edema.
  • Avoid diuretics: Controversial in extremely premature infants due to lack of proven benefit, potential prevention of PDA closure, and risk of electrolyte imbalance.
• Pharmacologic Therapy:
  • Recommended for symptomatic preterm infants.
  • Medications:
    • Indomethacin: 3 doses, 12 hours apart; a 4th dose can be given after 24 hours if needed.
    • Ibuprofen: 3 doses, 24 hours apart; similar efficacy to indomethacin (66%-70%).
    • Acetaminophen/Paracetamol: 15 mg/kg/dose intravenously every 6 hours for 3-8 days; monitor liver enzymes for toxicity.
  • Considerations:
    • Evaluate renal function before a second course of indomethacin or ibuprofen.
    • Acetaminophen may be less effective in infants previously treated with other drugs or in extremely low birth weight infants.
• Surgical Ligation:
  • Indicated if PDA remains hemodynamically significant despite pharmacologic therapy.
  • Considered when:
    • Increased respiratory support is required.
    • Renal impairment persists.
    • Pharmacologic therapy is contraindicated.

Physiotherapy

• Chest PT(physiotherapy)
• Percurssion
• Deep breathing

Differential Diagnosisi

• Coronary artery fistula
• Sinus of valsalva aneurysm
• Aortopulmonary defect
• Persistent truncus arteriosus
• Pulmonary arteriovenous fistula
• Total anomalous pulmonary venous return

Complications

• Eisenmenger phenomenon
• Closure of the aorta during surgery
• Recurrent laryngeal nerve injury
• Necrotizing enterocolitis
• Pulmonary hypertension
• Right heart failure