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| 1. Infective endocarditis: Invasion of the endothelial surface of the heart by microorganisms Infective microorganism may be: Bacteria Fungus Rickettsia Chlamydia Virus Commonly affects heart valves; also shunts (PDA), septal defects (VSD), coarctation of aorta 2. Predisposing Factors Congenital lesions Ventricular septal defects Tetralogy of Fallot Aortic stenosis Complex cyanotic anomalies Patent ductus arteriosus Systemic to pulmonary arterial shunts Acquired lesions Rheumatic valvular disease Degenerative cardiac lesions 3. Acute Infective Endocarditis Toxicity marked Progresses in days or weeks to valvular destruction and metastatic infection Typically due to staphylococcus aureus 4. Subacute Infective Endocarditis (SBE) Toxicity modest Progresses over weeks to months, metastatic infection rare Likely caused by streptococcus viridans, enterococci, staphylococcus epidermis, gram negative coccobacilli 5. Characteristic lesion: The Vegetation A mass of platelets, fibrin and microorganisms 6. Native valve endocarditis - occurs on normal, congenitally deformed, or diseased valves Aortic valve most common Prosthetic valve endocarditis 10-20% of cases of endocarditis Greatest risk during initial 6 months after valve surgery Staphylococcus epidermis most common cause Often extends beyond the valve into anulus and cardiac tissues 7. Pathogenesis Intact endothelium is resistant to infection Injury to heart valve endothelium leads to deposition of platelets and fibrin (nonbacterial thrombotic endocarditis) Platelet - fibrin complex receptive to bacterial colonization Bacteremia originates most commonly from oral mucosa, genitourinary or gastrointestinal tract Fibronectin binds bacteria to platelet - fibrin complex (or to normal endothelium) - The vegetation grows, sheds organisms or fragments and embolizes 8. Pathophysiology Constitutional symptom of infection Locally destructive effects of infection Embolization of vegetation Continuous bacteremia with remote infection Antibody response with tissue injury (eminent complex or antibody - complement reaction) 9. Constitutional Symptoms Fever 80 - 85% Chills 42 - 75% Anorexia 25 - 55% Malaise 25 - 40% Weight loss 25 - 35% 10. Locally Destructive Effects of Infection Perforation of valve leaflets Perforation of fistula between blood vessels or cardiac chambers Abscesses Disruption of conduction system 11. Signs Fever 80 - 90% Murmur 80 - 85% Changing or new 10-40% Peripheral signs Petechiae 10 - 40% Splinter hemorrhages 5 - 15% Oslers nodes 7 - 10% (tender subcutaneous nodules in pulp of digits) Janeway lesions 6 - 10% (erythematous, nontender lesions on palm or sole) Roth spots 4 - 10% (retinal hemorrhage with pole center) 12. Emboli Systemic emboli with infarction occur in 40% Splenic (LUQ pain) Renal (flank pain) Cerebral (stroke 10 - 15%) Coronary (common at autopsy, transmural infection rare) Mesenteric (abdominal pain, ileus) Retinal (blindness 3%) Pulmonary emboli, often septic, occur In 75% with tricuspid valve endocarditis 13. Diagnosis High index of suspicion Valvular heart disease Prosthetic heart valve Fever Murmur Positive blood culture Echocardiogram (TEE = 82 - 94% +) Vegetation Dehiscence of prosthetic valve New valvular regurgitation
14. Fungal Endocarditis
15. Fungus often difficult to culture, blood cultures typically negative
17. Surgical Treatment - Relative Indications |