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]