Infective endocarditis

Infective endocarditis

1. INFECTIVE ENDOCARDITIS DR. KALAIMANI SENIOR RESIDENT GENERAL MEDICINE MGMCRI

2. Overview Introduction Classification Etiology/Epidemiology Pathogenesis Clinical features Complications Diagnostic criteria Management

3. INTRODUCTION What is infective endocarditis? infection of a native or prosthetic heart valve, the endocardial surface , or an indwelling cardiac device What is infective endarteritis? arteriovenous shunts, arterio -arterial shunts (patent ductus arteriosus), or a coarctation of the aorta What is a vegetation? is a mass of platelets, fibrin, microcolonies of microorganisms, and scant inflammatory cells

4. Classification Acute endocarditis: Toxic Develops within few days Valvular destruction and embolic manifestation Most commonly by Staph aureus Subacute endocarditis: Develops in weeks to months More associated with immunologic phenomena Mostly caused by streptococci and others

5. Etiology Bacteria Fungi

6. Etiology /Epidemiology Health care associated NVE  S. aureus , CoNS,enterococci ( 55% nosocomial onset, 45% community onset) PVE within 2 months of surgery  nosocomial 68 – 85% of CoNS causing IE  resistant to methicillin IVDU related IE  most common S.aureus Polymicrobial endocarditis  IVDU Negative culture  5 – 15% (1/3 to ½ due to prior antibiotics)

7. High velocity jet striking endothelium Flow from high to low pressure chamber Flow across a narrow orifice at high velocity Malignancy SLE Antiphospholipid antibody syndrome DIC Endothelial injury Hypercoagulable state NBTE (sterile platelet fibrin ) + Bacteremia Bacteria adhere to damaged endothelium and/or sterile platelet-fibrin nidus Bacteria multiply Further platelet and fibrin binding Local tissue destruction Embolization Hematogenous spread Antibody response Growth of vegetation PATHOGENESIS

8. Marantic endocarditis - uninfected vegetations seen in patients with malignancy and chronic diseases Libman sacks endocarditis – bland vegetations in SLE

9. ADHESION MOLECULES Clumping factor Fss2 Ace Ebp pili Glucans Fim A Staph aureus Enterococcus fecalis Streptococci

10. Clinical manifestations

11. Clinical presentation

12. ORGANISMS CAUSING ENDOCARDITIS

13. CLINICAL MANIFESTATIONS

14. CLINICAL AND LAB FEATURES OF IE

15. EMBOLISATION RIGHT LEFT

16. MODIFIED DUKE CRITERIA- MAJOR CRITERIA Positive blood culture Typical microorganisms for IE from 2 separate blood cultures Or Persistently positive blood culture, defined as recovery of a microorganism consistent with infective endocarditis from:  Blood cultures drawn >12 h apart; or  All of 3 or a majority of ≥4 separate blood cultures, with first and last drawn at least 1 h apart Or Single positive blood culture for Coxiella burnetii or phase I IgG antibody titer of >1:800 2. Evidence of Endocardial involvement Positive echocardiogram  Oscillating intracardiac mass on valve or supporting structures or in the path of regurgitant jets or in implanted material, in the absence of an alternative anatomic explanation, or  Abscess, or  New partial dehiscence of prosthetic valve, Or New valvular regurgitation (increase or change in preexisting murmur not sufficient)

17. MODIFIED DUKE CRITERIA- MINOR CRITERIA 1. Predisposition: predisposing heart conditions or injection drug use Fever ≥38.0°C ( ≥100.4°F ) 3. Vascular phenomena: Major arterial emboli Septic pulmonary infarcts Mycotic aneurysm Intracranial hemorrhage Conjunctival hemorrhages Janeway lesions 4. Immunologic phenomena: Glomerulonephritis Osler’s nodes Roth’s spots Rheumatoid factor 5. Microbiologic evidence: positive blood culture but not meeting major criterion or serologic evidence of active infection with an organism consistent with infective endocarditiS

18. DEFINITE INFECTIVE ENDOCARDITIS Pathologic criteria Microorganisms demonstrated by results of cultures or histologic examination of a vegetation, a vegetation that has embolized , or an intracardiac abscess specimen; or Pathologic lesions; vegetation, or intracardiac abscess confirmed by results of histologic examination showing active endocarditis Clinical criteria 2 major criteria, or 1 major criterion and 3 minor criteria, or 5 minor criteria Possible Infective Endocarditis 1 major criterion and 1 minor criterion, or 3 minor criteria

19. Rejected Diagnosis of Infective Endocarditis Firm alternate diagnosis explaining evidence of suspected IE, or Resolution of IE syndrome with antibiotic therapy for ≤4 days, or No evidence of IE at surgery or autopsy, on antibiotic therapy for ≤4 days, or Does not meet criteria for possible IE

20. INVESTIGATIONS Blood cultures – 3 sets from different sites atleast 1 hour apart. Why? Complete blood count Leucocytosis Thrombocytosis Thrombocytopenia Anemia ESR, CRP Serology

21. Electrocardiography to assess for conduction abnormalities (such as varying and progressive degrees of atrioventricular [AV] block) suggestive of abscess formation, which are particularly associated with aortic valve endocarditis Ischemic/infarct changes suggestive of coronary emboli CXR Evidence of HF (pulmonary edema) Septic emboli, particularly in IV drug users with suspected right-sided endocarditis

22. Transthoracic Echo ( tte ) TTE may detect valvular vegetations with or without positive blood cultures It is used to characterize the hemodynamic severity of valvular lesions in known IE It can also assess for complications of IE (e.g. abscesses, perforation, and shunts) TTE can be used to reassess high-risk patients (e.g., those with a virulent organism, clinical deterioration, persistent or recurrent fever, new murmur, or persistent bacteremia )

23. ECHO Vegetations attached to Aortic valve Aortic regurgitation ( Colour doppler )

24. Transesophageal Echo (TEE) Assess the severity of valvular lesions in symptomatic patients with IE if TTE is nondiagnostic Diagnose IE in patients with valvular heart disease and positive blood cultures if TTE is nondiagnostic Diagnose complications of IE with potential impact on prognosis and management (e.g. abscesses, perforation, and shunts) First-line diagnostic study to diagnose PVE and to assess for complications

25. TREATMENT ORGANISM Streptococi Penicillin sensitive Relatively penicillin resistant Moderately penicillin resistant DRUG ( DURATION) Penicillin G x 4 weeks Ceftriaxone x 4 weeks Vancomycin x 4 weeks Penicillin G + Gentamicin x 2 weeks Penicillin G or Ceftriaxone x 4 weeks plus Gentamicin x 2 weeks Vancomycin x 4 weeks Penicillin or Ceftriaxone x 6 weeks plus gentamicin x 6 weeks Vancomycin x 4 weeks

26. TREATMENT ORGANISM Enterococci DRUG ( DURATION) Penicillin G + Gentamicin x 4 - 6 weeks Ampicillin + gentamicin x 4 - 6 weeks Vancomycin + gentamicin x 4 - 6 weeks Ampicillin + ceftriaxone x 6 weeks

27. TREATMENT ORGANISM DRUG ( DURATION) Staphylococi Native valve MSSA Nafcillin, Oxacillin or Flucloxacillin x 4 – 6 weeks Or Cefazolin x 4 – 6 weeks Or Vancomycin x 4 – 6 weeks MRSA Vancomycin x 4 – 6 weeks Prosthetic valve MSSA Nafcillin, Oxacillin or Flucloxacillin x 6 – 8 weeks plus Gentamicin x 2 weeks plus Rifampicin x 6 – 8 weeks MRSA Vancomycin x 6 – 8 weeks plus Gentamicin x 2 weeks plus Rifampicin x 6 – 8 weeks

28. Treatment ORGANISM Coxiella burnetii Bartonella spp. DRUG ( DURATION) Doxycycline + x 18 months (NVE) Hydroxychloroquine x 24 months (PVE) Ceftriaxone or Ampicillin x 6 weeks or doxycycline plus Gentamicin x 3 weeks

29. DRUG DOSAGE Penicillin G 4 mU iv q4h Ceftriaxone 2 g iv qd Vancomycin 15mg/kg iv q12h Gentamycin 3 mg/kg iv or im single dose Or 1 mg/kg iv q8h Ampicillin 2 g iv q4h Nafcillin/ Oxacillin 2 g iv q4h / Flucloxacillin Cefazolin 2 g iv q8h Rifampicin 300 mg PO q8h

30. INDICATIONS FOR SURGERY

31. TIMING OF SURGICAL INTERVENTION

32. REFERENCES Harrison’s Principles of Internal Medicine 19 th edition Braunwald’s Heart disease 10 th edition