Right-sided valvular endocarditis: Etiology, diagnosis, and an approach to therapy

Abstract

Right- and left-sided endocarditis are two distinct entities, both clinically and experimentally. As such, they require different clinical approaches. The accurate diagnosis of right-sided endocarditis rests largely on a high index of suspicion which is often raised in the case of an intravenous drug abuser with fever, especially when pulmonary infiltrates are detected. Two-dimensional echocardiography can be expected to confirm the diagnosis in approximately 80% of the cases. Measurement of the echocardiographically visualized vegetation provides both prognostic and therapeutic information. When the vegetation is <1.0 cm in diameter, antibiotic therapy can be reasonably expected to cure the infection. Despite a prolonged fever, we recommend continued medical management in these cases, as lack of response to medical management is almost exclusively seen in cases in which echocardiographically determined vegetation size is ≥1.0 cm, perhaps because of the slower metabolic rate of bacterial colonies within these large vegetations. If, however, after 3 weeks of antibiotic therapy, fevers persist in a patient in whom two-dimensional echocardiography reveals a vegetation of ≥1.0 cm, surgical intervention should be contemplated. Prior to such intervention, the physician must be careful to exclude other sources of fever, such as abscesses, phlebitis, and drug reactions, as indicated in Table III. Also, adequate antibiotic levels should be documented prior to surgical intervention. Because of the adverse effect on vegetation size upon the response to antibiotics, there may be a role for anticoagulation in order to potentiate the effects of the antibiotic therapy; however, this is purely speculative at present. Left-sided disease clearly contraindicates anticoagulant therapy and anticoagulation should only be considered if left-sided involvement can be accurately excluded. At the present time this may not be possible. We would stress that anticoagulation therapy in these patients should only be considered after appropriate laboratory and clinical trials have been performed. We would like to emphasize that at the present time there is no justification for anticoagulant usage in this setting. Persistent pyrexia will necessitate surgical intervention in approximately one third of those cases with vegetation size of ≥1.0 cm, as determined by two-dimensional echocardiography. When the initial surgery is performed, we are currently inserting a prosthetic valve and have had no difficulties with recurrent infection or prosthetic valve dysfunction.