Discussion
PDA accounts for 5% to 10% of all congenital heart disease. [1]
A PDA that persists beyond 1 month of age is estimated to occur in 0.3–0.8–4 per 1000 live births. [2]
The size of a PDA can range from very large to <1 mm, and accordingly, the clinical findings associated with a PDA can vary considerably.
Infective endarteritis (IE) was the most common cause of death in patients with patent ductus arteriosus (PDA) prior to the introduction of antibiotic therapy and surgical closure of the defect, though nowadays it is a rare complication. Infective endarteritis is especially unusual in asymptomatic patients, more so when the PDA is silent on cardiac auscultation, with very few reports of this type of case to be found in the relevant literature. [3]
An unrepaired PDA is a risk factor for IE, and when it occurs, vegetations usually occur on the pulmonary artery end of the ductus; embolic events are usually of the lung rather than the systemic circulation. [4]
The proposed pathogenesis of IE associated with congenital heart disease involves complex interactions among the damaged valvular or mural endocardium exposing the matrix proteins to thromboplastin and tissue factor, formation of a nonbacterial thrombotic endarteritis, and eventual microbial adherence, colonization, and replication. The turbulent blood flow through the aorta and pulmonary artery which causes endothelial injury and subsequent seeding of pathogens onto the injured endothelium is central to the proposed pathogenetic mechanisms for the development of vegetations particularly in patients with PDA. [5]
The management of mycotic aneurysm is unclear. There are no strategies or recommendations regarding the timing of surgery (before or after antibiotics), aortic reconstruction (with or without material), and the duration of post-operative antibiotic therapy. Studies suggest that combined medical and surgical treatment decreases mortality. [6]