Chris Burke, MD
What is the Ductus Arteriosus?
Ductus Arteriosus Allows blood from RV to bypass fetal lungs Between the main PA (or proximal left PA) and the descending thoracic aorta Maintains patency in utero by low O2 tension and high circulating prostaglandin levels
Ductus Arteriosus During final trimester, ductus becomes much less sensitive to prostaglandins Following birth, rise in O2 tension and lack of placental prostaglandins usually results in closure Usually complete by hours, but sometimes days-weeks Becomes ligamentum arteriosum
Patent Ductus Arteriosum Roughly 1 out of 1200 live births, more common in premature infants thought to be related to immature ductal wall being less sensitive to O2 tension Constitutes 7% of congenital heart defects Desirable in some defects including many cyanotic heart lesions; this has led to the use of PGE4 clinically
Pathophysiology Shunt volume determined by the size of ductus and ratio of pulmonary to systemic vascular resistance PVR declines over first several weeks of life, increasing left-to-right shunt across PDA Excessive shunting can lead to right heart failure
Pathophysiology Over time, pulmonary vascular obstructive disease will develop Eisenmenger syndrome is the end result, when shunting reverses to right-to-left; this is associated with irreversible pulmonary hypertension and cyanosis, eventually leading to RV failure
Morphologies
Clinical Manifestations Infants with large shunt volume may develop CHF leading to tachypnea, tachycardia, and poor feeding Physical exam findings include: widened pulse pressure and continuous “machinery murmur”, heard best along the left sternal border radiating to the back
Clinical Manifestations CXR may show increased pulmonary markings and left heart enlargement EKG may have LVH and/or left atrial enlargement Echo diagnostic method of choice Diagnostic cardiac catheterization generally only performed in adults to evaluate for pulmonary hypertension
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Treatment Pharmacologic Endovascular Surgical
Considerations Closure is performed for all symptomatic patients with left-to-right shunt Indications for closure in Asx patients: signs of left heart volume overload reversible pulmonary hypertension murmur Closure NOT recommended when Eisenmenger physiology is present or PDA is silent (controversial)
Considerations In patients with PVR greater than 8 Woods Units, closure is generally not recommended This is especially true when right-to-left or bi- direction flow is present or elevated PVR not reversed with high O2 or iNO This can lead to catastrophic RV failure, due to loss of “pop-off” mechanism
Pharmacologic Closure Indomethacin, a prostaglandin inhibitor, can be used to close a PDA mg/kg IV at 12 or 24- hour intervals for a total of three doses Rarely effective in term infants 80% effective in premature infants
Surgical Closure Dates back to 1939 Generally reserved for infants and children with lesions deemed unsuitable for percutaneous closure Good choice for larger PDAs (~ 8mm) Posterolateral thoracotomy classically, but VATS approach described
Percutaneous Closure First performed in 1967 Access via femoral artery or vein Most commonly use coils or occlusion devices Proven benefit with PDAs < 3mm Major limitation of these techniques is ductus size in one study a PDA diameter greater than 4mm had a 24-fold increased risk of incomplete closure Morphology is another significant issue!
Percutaneous Closure
Surgical Closure Still Has a Role Galal et al reported a 20% conversion or failure rate with 236 attempted percutaneous closures Hsiao et al reported reduced number of ventilator days and improved outcomes in VLBW ( 14 days old) surgical repair
Management Summary Who gets closed? Sxs with left-to-right shunt Audible murmur Reversible pulmonary HTN Left sided volume overload/heart failure
Management Summary Premies indomethacin; surgery if unsuccessful Term infants medical treatment to optimize for percutaneous closure; if this fails, then surgery Children/Adults: in general, percutaneous closure