Right-sided bacterial endocarditis and endarteritis

Two-stage replacement of tricuspid valve in active endocarditis.

“…These authors drew attention to the possibility of tricuspid valve involvement. In this form of endocarditis cardiac symptoms are initially often obscure (Bain et al, 1958;Conway, 1969;Arbulu et al, 1973;Graham et al, 1973), and the diagnosis and treatment may be delayed. Later in the course of the disease, typical signs of tricuspid regurgitation (Banks et al, 1973) and increasing heart size are frequent.…”

“…Right-sided endocarditis, mainly involving the tricuspid valve, is no longer a rare disease, its frequency increasing from less than 5 per cent (Thayer, 1931;Bain et al, 1958) to 10 to 20 per cent in the past decade (Roberts and Buchbinder, 1972;Arbulu et al, 1973); this can be ascribed largely to the increased incidence of narcotic addiction (Conway, 1969;Banks et al, 1973;Graham et al, 1973;Svanbom et al, 1973).…”

Multiple Pulmonary Artery Aneurysms

“…Blumgart (1933) and Barker (1949) reported the relative infrequency of positive blood cultures in cases of right-sided endocarditis, although Bain, Edwards, Scheifley, and Geraci (1958) found positive cultures in 17 of 18 cases seen at the Mayo Clinic. It is not clear why the filtering action of the lung, observed experimentally by Wright (1927), should be so efficient in these cases and yet apparently nonexistent in cases of generalized septicaemia or pyaemia.…”

Renal Complications of Bacterial Endocarditis

“…Initially, the clinical and morphologic features of the renal involvement were attributed to emboli from an infected valve with the kidney lesions representing injury and reaction to repeated microembolization. However, the presumed embolic etiology of the renal lesions was questioned particularly when focal glomerulonephritis was reported in cases of right-sided endocarditis [16,17], Indirect evidence for an immune etiology of the renal lesion was first advanced from the observation of low serum complement in 8 cases of endocarditis with mod erate to severe renal disease, in whom the complement level became normal as renal insufficiency abated [18], Subsequently, the demonstration of circulating immune complexes [19], electron-dense, immunoglobulin and complement deposits along the glomerular basement membrane [20], and ultimately the isolation of bacterial antigen [21] and antibody [22] from the glomerular eluate provided convincing evidence for an immune-mediated etiology of the glomerulonephritic lesions of bacterial endocarditis [23].…”

“…33,37]. Antibiotics have resulted in a decrease in the incidence of focal glomerulonephritis to 18-25% [28,33,34], The lesion is less common in cases of acute bacterial endocarditis, where the reported range is less than 15% [37,41,42], and is rare in cases of right-sided endocardi tis [17,40], Focal glomerular lesions frequently occur along the edges of renal infarcts ( fig. 4), while the major ity of adjacent glomeruli are totally spared [38].…”