Infective Endocarditis

1. Infective Endocarditis Tintinalli’s Chap. 145

2. epidemiology • Incidence ranges from 2.4 to 11.9 cases per 100,000 patient-years • Higher in urban vs. rural populations • 25% of cases in pts < 30 y.o. • 50% of cases in pts ages 31-60 • 25% of cases in pts > 60 y.o. • Uncommon in kids • Related primarily to congenital heart dz, rheumatic heart dz, or nosocomial • Aortic valve most commonly affected • Then mitral, tricuspid, pulmonic valves

3. risk factors • IVDA • Indwelling catheters (vascular) • Poor dental hygiene • HIV • Prosthetic heart valves • Risk greatest in first 6 mos after surgery • MVP (most common predisposing cardiac lesion) • Rheumatic heart dz still leading RF in developing countries

4. pathophysiology • Normal endothelium is resistant to infxn & thrombus formation • Turbulent blood flow & damage to endocardium/endothelium • Endothelial damage promotes deposition of platelets & fibrin • Form sterile vegetations called nonbacterial thrombotic endocarditis (NBTE)

5. pathophysiology • Transient bacteremia may result in colonization of vegetations & conversion of NBTE to IE • Highly invasive orgs like S. aureus can also directly invade the endocardium and stimulate the adherence of platelets & fibrin

6. Vegetations (arrows) due to viridans streptococcal endocarditis involving the mitral valve

7. microbiology • Table 145-1 • Bacteria are most common cause • S. aureus is most common bacteria • Fungi, Rickettsia, Chlamydia species

8. native valve endocarditis • Non-IVDA • Streptococcus is org in > 50% of cases • Then staph & enterococci • Preexisting valvular abnormalities • Rapid destruction of valves • Multiple distal abscesses • Myocardial abscesses • Conduction defects • Pericarditis • May have negative blood cxs

9. IVDA-associated IE • Contaminants include normal skin flora or injection devices • S. aureus (>50% of cases) • Then strep, enterococci, gm-neg bacilli like Pseudomonas, & fungi (Candida)

10. prosthetic valve endocarditis • Contamination during perioperative period • S. epidermidis • Then strep, aspergillus & candida • Valve dysfunction • Fulminant clinical course

11. clinical features • Acute • Rapid onset • High fever/rigors • Hemodynamic deterioration • Death • S. aureus

12. clinical features • Subacute • Indolent course • Progressive constitutional sxs • Gradual deterioration • S. viridans • See Table 145-2

13. clinical features • Bacteremia • Heat murmurs • In right-sided IE <50% of pts have detectable murmurs on admission • CHF (leading cause of death in IE) • Valvular abscesses • Pericarditis • Heart blocks; arrhythmias • Distal embolisms (bland or septic)

14. clinical features • Stroke (MCA most common) • SAH • Retinal artery emboli (monocular blindness) • Pulmonary infarction • Pneumonia • Empyema • Pleural effusions • MI • Myocarditis • Splenic infarction • Renal emboli • Mesenteric emboli • Acute limb ischemia

15. Janeway lesions

16. Osler nodes

17. Roth spots

18. diagnosis • Duke criteria • Major & minor • Sensitivity about 90% • Table 145-3

19. Table 145-3 Definitions of Major and Minor Criteria Used in the Duke Criteria* Major criteria   Positive blood culture for IE Typical microorganism consistent with IE from two separate blood cultures* as noted below: Streptoccocus bovis, Viridans streptococci, HACEK group, or Community-acquired Staphyloccocus aureus or enterococci in the absence of a primary focus, or   Microorganisms consistent with IE from persistently positive blood cultures defined as:    At least two positive cultures of blood samples drawn >12 h apart, or All of three or a majority of four or more separate blood cultures (with first and last sample drawn at least 12 h apart)  Evidence of echocardiographic involvement     Positive echocardiogram for IE defined as: Oscillating intracardiac mass on valve or supporting structures, in the path of regurgitant jets, or on implanted material in the absence of an alternative anatomic explanation, or Abscess, or New partial dehiscence of prosthetic valve  New valvular regurgitation (worsening or changing of preexisting murmur not sufficient) Minor criteria Predisposition: predisposing heart condition or injection drug use   Fever: temperature >38°C Vascular phenomena: major arterial emboli, septic pulmonary conjunctival hemorrhages, and Janeway lesions   Immunologic phenomena: glomerulonephritis, Osler nodes, Roth spots, and rheumatoid fever Microbiologic evidence: positive blood culture but does not meet a major criterion as noted in Table 145-4* or serologic evidence of active infection with organism consistent with IE   Echocardiographic findings: consistent with IE but do not meet a major criterion as noted in Table 145-4 *Excludes single positive cultures for coagulase-negative staphylococci and organisms that do not cause IE. Abbreviations: HACEK = Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, and Kingella; IE = infective endocarditis. Source: From Durack et al.19

20. Table 145-4 Definitions of Infective Endocarditis According to the Duke Criteria Definite infective endocarditis   Pathologic criteria     Microorganisms demonstrated by culture or histologic examination of a vegetation or in a vegetation that has embolized, or in an intracardiac abscess, or     Pathologic lesions: vegetation or intracardiac abscess present, confirmed by histology showing active endocarditis   Clinical criteria, using specific definitions listed in Table 145-3 Two major criteria, or     One major and three minor criteria, or     Five minor criteria. Possible infective endocarditis Findings consistent with infective endocarditis, that fall short of "definite," but not "rejected." Rejected   1. Firm alternate diagnosis for manifestations of endocarditis, or   2. Resolution of manifestations of endocarditis, with antibiotic therapy for 4 d or less, or   3. No pathologic evidence of infective endocarditis at surgery or autopsy after antibiotic therapy for 4 d

21. differential diagnosis • Viral illnesses • HIV-related fevers • Acute rheumatic fever • Systemic complications of collagen vascular disorders • Drug reactions

22. evaluation • Blood cxs (done in ED!) • Prior to axbx • 3 separate sites • 1 hr between 1st & last set • EKG • CXR • CBC • ESR • U/A • Echo

23. A. Apical four-chamber view demonstrating a large tricuspid valve vegetation (arrow). B. Parasternal long axis view demonstrating a vegetation (arrow) on the anterior valve leaflet

24. treatment & prophylaxis • ABC’s • Empiric axbx • Native valve IE • Penicillinase-resistant penicillin or cephalosporin + aminoglycoside • Pts w/ complications (IVDA, CHD) • Add vancomycin to above regimen • Table 145-5

25. treatment & prophylaxis • Empiric axbx cont. • PVE • Vancomycin + aminoglycoside + rifampin • Definitive axbx tx as soon as cxs reveal causative orgs • Tx for 4-6 wks • Surgical tx for sev. valvular dysfxn. • Acute CHF or hemodynamic instability

26. treatment & prophylaxis • Axbx given to pts with RF’s for endocarditis (see Table 145-6) • Pts w/ prosthetic heart valves, congenital cardiac malformations, acquired valvular dysfunction, hypertrophic cardiomyopathy, MVP w/ documented regurgitation or hx of endocarditis • Procedures include dental work, bronchoscopy, cystoscopy, urethral instrumentation & ERCP