Infective Endocarditis Flashcards
Infective endocarditis
Microbial infection of mural endocardium and heart valves
Where does IE occur?
Close to congenital or acquired heart defects
Natural valves- affected by congenital heart defects/RHD
Prosthetic valves - early (staph epidermis) within 60 days of surgery HAI
Prosthetic valves- late (staph aureus/strep viridans/actinobaccilus) within 2-6 months of surgery CAI
Heart valves
LHS- mitral (bicuspid) aortic (tricuspid)
RHS- tricuspid and pulmonary (tricuspid)
Etiology
B/V/P/fungi (candida)
IVDU (staph aureus/tricuspid valve/affects young people)
Hemodialysis P (staph aureus)
Epidemiology
<1% of general population affected Increases with increasing age (less immunity more heart defects) Young females (20% incidence)
Risk factors
ARF males (aortic valve) females (mitral valve) Prosthetic valves IVDU hemodialysis history of IE
Predisposing conditions
Mitral valve prolapse (in males over 45 years) Degenerative calcific valvular stenosis Aortic valve disease IVDU prosthetic valves Congenital heart defect Idiopathic 25%
Clinical course
Acute- highly virulent organism (staph aureus) infect normal HV and lots of necrotising destruction
Subacute- less virulent organism (strep viridans) infect abnormal HV and less necrotising destruction
Paediatric IE
Usually due to underlying heart defect
Ventricular septal defect
Alteration in patency of ductus arteriosus
Tetralogy of fallout - overriding aorta/RV hypertrophy/changes in aortic valve/pulmonary valve stenosis
Pediatric IE Etiology
Neonates- staph aureus/coagulase negative staph/group B strep
Children- staph aureus/strep viridans
Adults IE
1st predisposing factor is MVP
P w/ murmurs at risk
Biscuspid aortic valve defect (M. >60 years) at risk
Congenital heart disease increases risk
Pathophysiology
Injury to Ep barrier at gut/skin/oral cavity leading to bacteremia
Affects Natural valve- confined to valve leaflets
Affects prosthetic valve- extend beyond valve ring to annular and peri annular tissue (septal and ring abscess/PV splitting/fistula)
Early invasive infections can affect aortic valve
Clinical manifestations
Fever/chills/weakness/fatigue/flu like symptoms
Mortality ass. To glomerulonephritis/valve dysfunction/HF
Cardiac lesions histology
Vegetations mitral/aortic valves Friable/bulky/destructive to underlying myocardium Affect RHS HV in IVDU Single or multiple Made of B/PC/platelets/fibrin In SLE 50% P have sterile vegetatios
Embolic lesions
Friable cardiac lesions that break away and travel to many extra cardiac sites