Infective Endocarditis عبد المهيمن أحمد

Transcription

1 Infective Endocarditis إعداد : عبد المهيمن أحمد أحمد علي

2 Infective endocarditis Inflammation of the heart valve or endocardium of the heart. The agents are usually bacterial, but other organisms can also be responsible.

3 Risk Factors Intravenous drug abuse. Artificial heart valves and pacemakers. Acquired heart defects: Calcific aortic stenosis. Mitral valve prolapse with regurgitation. Congenital heart defects. Intravascular catheters.

4 Infecting Organisms Common bacteria: S. aureus. Streptococci. Enterococci. Not so common bacteria: Fungi. Pseudomonas.

5 Pathogenesis Altered blood flow around the valves contributes to development of endocarditis. The valves may be damaged congenitally, from surgery, by autoimmune mechanisms, or simply as a consequence of old age. The damaged part of a heart valve leads to formation of a local blood clot, Altered blood flow, and thus infective endocarditis, are more likely in high pressure areas.

6 Consequently, ventricular septal defects create more susceptibility to infection than atrial septal defects. Damaged vascular endothelium will also promote platelet and fibrin deposition, upon which bacteria can proliferate. Valvular lesions are a major cause of such damage, as jet lesions resulting from ventricular septal defects or patent ductus arteriosus.

7 Classification Acute Affects normal heart valves. Commonly due to highly virulent bacteria e.g. Staph. aureus. Rapidly destructive. If not treated, usually fatal within 6 weeks. Subacute Often affects damaged heart valves or congenitally abnormal heart. Due to low virulent bacteria e.g. Streptococcus viridance less destructive. If not treated, usually fatal by one year.

8 Pathology Occurs when blood flow turbulence within the heart allows the causative organism to infect previously damaged valves or other endothelial surfaces. The classical lesion is called Vegetation which adheres to valve surface or endocardium Can break into circulation and result in embolization.

9 In both acute and subacute forms of the disease, friable bulky, and potentially destructive vegetations containing fibrin, inflammatory cells, and microorganisms are present on the heart valves. The aortic and mitral valves are the most common sites of infection, although the tricuspid valve is a frequent target in the setting of intravenous drug abuse. Vegetations may be single or multiple and may involve more than one valve ; they can erode into the underlying myocardium to produce an abscess cavity (ring abscess) As time passes, fibrosis, calcification, and a chronic inflammatory infiltrate may develop.

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12 Acute S. aureus IE with perforation of the aortic valve and aortic valve vegetations.

13 Acute S. aureus IE with mitral valve ring abscess extending into myocardium.

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16 Complications Heart failure. Extensive valvular damage. Paravalvular abscess (30-40%). Most common in aortic valve, IVDA, and S. aureus. May extend into adjacent conduction tissue causing arrythmias. Higher rates of embolization and mortality Pericarditis. Fistulous intracardiac connections.

17 Symptoms Acute High grade fever and chills. congestive heart failure. Arthralgias/ myalgias. Abdominal pain. Pleuritic chest pain. low grade fever & failure to thrive in children.

18 Subacute - Low grade fever. - Anorexia. - Weight loss. - Fatigue. - Arthralgias/ myalgias. - Abdominal pain. - The onset of symptoms is usually ~2 weeks or less from the initiating bacteremia.

19 Prevention of Infective Endocarditis Interesting article on American Heart Association website regarding prevention of IE. The current practice of giving patients antibiotics prior to a dental procedure is no longer recommended EXCEPT for patients with the highest risk of adverse outcomes resulting from BE (bacterial endocarditis). Patients at highest risk and therefore should be given prophylaxis antibiotics are those who have: Prosthetic cardiac valve. Previous endocarditis. Congenital heart disease. Cardiac transplant recipient with cardiac valvular disease.

20 Thank you