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Systemic embolization occurs in 22 per cent to 50 per cent of cases of IE. Emboli often involve major arterial beds, including lungs, coronary arteries, spleen, bowel, and extremities. Up to 65 per cent of embolic events involve the central nervous system, and 90 per cent of central nervous system emboli lodge in the distribution of the middle cerebral artery. The highest incidence of embolic complications is seen with aortic- and mitral-valve infections and in IE due to S aureus and Candida species and HACEK and Abiotrophia organisms. Emboli can occur before diagnosis, during therapy, or after therapy is completed, although most emboli occur within the first 2 to 4 weeks of antimicrobial therapy. The rate of embolic events drops dramatically during the first 2 weeks of successful antibiotic therapy, from 13 to .2 embolic events per 1000 patient-days. In general, mitral vegetations, regardless of size, are associated with higher rates of embolization (25 per cent) than aortic vegetations (10 per cent). The highest embolic rate (37 per cent) has been seen in the subset of patients with mitral vegetations attached to the anterior rather than the posterior mitral leaflet and with vegetation size > 1 cm in diameter. Staphylococcal or fungal IE appears to carry a high risk of embolization, i.e., independent of vegetation size. Large vegetations independently predict embolic events only in the setting of streptococcal IE. The embolic event rate among patients with IE and increasing vegetation size was twice that of patients with static or decreasing vegetation size over 4 to 8 weeks of therapy. The indications for surgery for persistent vegetation after systemic embolization are:
1) Anterior mitral leaflet vegetation, particularly with size > 10 mm
2) One or more embolic events during first 2 weeks of antimicrobial therapy
3) Two or more embolic events during or after antimicrobial therapy
4) Increase in vegetation size after 4 weeks of antimicrobial therapy
Pathophysiology Infective endocarditis occurs when turbulence within the heart allows causative organism to infect previously damaged valves or other endothelial surfaces.
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