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Infective Endocarditis Dr. Raid Jastania
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Infective Endocarditis Inflammation of the endocardium Common on heart valves Caused by infections: mostly bacteria Resulting in vegetations: thrombotic bebris and organism at the surface of the valve Acute: high virulence organism, severe, acute, on normal healthy valves Subacute: low virulence organism, mild, on diseased defective valves
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Infective Endocarditis Route of infection –Bacteremia IV drug abusers Other source of infection: skin.. Dental/surgical/catheterization
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Infective Endocarditis Factors increasing the risk of endocarditis: 1.Pre-existing cardiac abnormlity Valve disease: rheumatic valve disease, calcific aortic stenosis, mitral valve prolapse. Hemodynamic trauma: small VSD 2.Prosthetic valve: 10-20% of cases 3.IV drug abusers: right side of heart
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Infective Endocarditis Organisms: –Strep viridans: damaged valves 50-60% –Staph aureus: healthy and diseased valve 10- 20% –Others: Hemophilus, Actinobacillus… –Prosthetic valve: Staph epidermidis, Gram negative, fungi –IV drug abusers: Staph aureus, Gram -ve
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Infective Endocarditis Morphology: –Valve vegetations: Bacteria/fibrin Common on aortic and mitral Single or multiple More than one valve Starts as small lesion and enlarges Bulky friable lesion
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Infective Endocarditis Morphology: –Valve vegetations –Destruction of valves: Rupture of leaflets, cordae, or papillary muscle Regurgitation CHF –Extend to myocardium: Ring abscess, inflammation, necrosis
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Infective Endocarditis Morphology: –Valve vegetations –Destruction of valves: –Extend to myocardium: –Emboli: Brain, kidneys…. Abscess in brain kidneys….
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Infective Endocarditis Morphology: –Valve vegetations –Destruction of valves: –Extend to myocardium: –Emboli –Subacute: less destruction, presence of granulation tissue and chronic inflammation
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Infective Endocarditis Clinical: –Fever: Low-grade in subacute High-grade with chills in acute –Malaise, weight loss –Change in heart murmur –Clubbing of fingers –Emboli
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Infective Endocarditis Complications: –Valve regurgitation –CHF –Myocardial abscess –Emboli –Systemic abscess –Mycotic aneurysm –Renal disease
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Nonbacterial Thrombotic Endocarditis
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Deposition of small masses of fibrin and platelets On heart valves, common mitral No organisms No valve destruction or inflammation
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Nonbacterial Thrombotic Endocarditis Pathogenesis –Endothelial injury –Hypercoagulable state Malignancy in 50% of cases
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Nonbacterial Thrombotic Endocarditis Morphology: –Vegetation: multiple small nodules Along valve closure –Normal healthy valves: aortic, mitral –Fibrin and platelets –No inflammation –May emboli
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Libman-Sacks Endocarditis
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Prosthetic Valves
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Bioprosthetic Mechanical Complications: –Both type: thrombosis, infective endocarditis –Bioprosthetic: calcification, stenosis, tear, regurgitation –Mechanical: hemolysis
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Pericardial Disease
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Pericarditis Causes:
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Pericarditis Causes: –Infections: mostly viruses, bacteria, fungi –Ischemic: following MI –Physical: Following surgery, radiation –Chemical: uremia –Immune: SLE –Malignancy: bloody effusion
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Pericarditis Fate:
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Pericarditis Fate: –Acute disease: immediate hemodynamic complications –Resolution –Chronic fibrosing pericarditis (constrictive pericarditis)
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Pericarditis Clinical –Chest pain –Pericardial rub –Cardiac tamponade: weak heat sound, hypotension/shock, distended neck veins
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Pericardial Effusion Accumulation of fluid in the pericardial space Transudate VS. Exudate Serous, serosanguineous, chylous, bloody Hemopericardium: in rupture aortic aneurysm, rupture MI, traumatic injury
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