infective endocarditis dr. raid jastania. infective endocarditis inflammation of the endocardium...
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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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Nonbacterial Thrombotic Endocarditis
• 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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Prosthetic Valves
• 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