Infective Endocarditis

Dr. Raid Jastania

                                               

     

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

Infective Endocarditis

• Route of infection– Bacteremia

• IV drug abusers

• Other source of infection: skin..

• Dental/surgical/catheterization

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

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

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

                                               

     

Infective Endocarditis

• Morphology:– Valve vegetations– Destruction of valves:

• Rupture of leaflets, cordae, or papillary muscle

• Regurgitation

• CHF

– Extend to myocardium: • Ring abscess, inflammation, necrosis

Infective Endocarditis

• Morphology:– Valve vegetations– Destruction of valves:– Extend to myocardium: – Emboli:

• Brain, kidneys….

• Abscess in brain kidneys….

Infective Endocarditis

• Morphology:– Valve vegetations– Destruction of valves:– Extend to myocardium: – Emboli

– Subacute: less destruction, presence of granulation tissue and chronic inflammation

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

Infective Endocarditis

• Complications:– Valve regurgitation– CHF– Myocardial abscess– Emboli– Systemic abscess– Mycotic aneurysm– Renal disease

Nonbacterial Thrombotic Endocarditis

Nonbacterial Thrombotic Endocarditis

• Deposition of small masses of fibrin and platelets

• On heart valves, common mitral

• No organisms

• No valve destruction or inflammation

Nonbacterial Thrombotic Endocarditis

• Pathogenesis– Endothelial injury– Hypercoagulable state

• Malignancy in 50% of cases

Nonbacterial Thrombotic Endocarditis

• Morphology:– Vegetation:

• multiple small nodules

• Along valve closure

– Normal healthy valves: aortic, mitral– Fibrin and platelets– No inflammation– May emboli

Libman-Sacks Endocarditis

Prosthetic Valves

Prosthetic Valves

• Bioprosthetic

• Mechanical

• Complications:– Both type: thrombosis, infective endocarditis– Bioprosthetic: calcification, stenosis, tear,

regurgitation– Mechanical: hemolysis

                                               

     

Pericardial Disease

Pericarditis

• Causes:

Pericarditis

• Causes:– Infections: mostly viruses, bacteria, fungi– Ischemic: following MI– Physical: Following surgery, radiation– Chemical: uremia– Immune: SLE– Malignancy: bloody effusion

Pericarditis

• Fate:

Pericarditis

• Fate:– Acute disease: immediate hemodynamic

complications– Resolution– Chronic fibrosing pericarditis (constrictive

pericarditis)

Pericarditis

• Clinical– Chest pain– Pericardial rub– Cardiac tamponade: weak heat sound,

hypotension/shock, distended neck veins

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