Endocarditis 200512-1233741644373579-2
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Transcript of Endocarditis 200512-1233741644373579-2
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Infective Endocarditis
Matthew Leibowitz, MDDavid Geffen School of Medicine at UCLA
Division of Infectious Diseases
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Epidemiology• 10-20,000 cases per year in the US• Male:Female ratio 1.7:1• New trends
– Mean age was 30 in 1926, now > 50% of patients are over 60
– Decline in incidence of rheumatic fever– More prosthetic valves– More nosocomial cases, injected drug use– More staphylococcal infection
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Epidemiology
• Mitral valve alone 28-45%• Aortic valve alone 5-36% (bicuspid
valve in 20% of all native valve IE)• Both mitral and aortic valves 0-36%• Tricuspid valve 0-6%• Pulmonic valve <1%• Right and left sided 0-4%
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Classification
• OLD– Subacute Bacterial Endocarditis
• Death in 3-6 months– Acute Bacterial Endocarditis
• Death in < 6 weeks
• NEW– Native Valve Endocarditis– Prosthetic Valve Endocarditis
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Pathogenesis• Alteration of the valvular endothelial
surface leading to deposition of platelets and fibrin
• Bacteremia with seeding of non-bacterial thrombotic vegetation (NBTE)
• Adherence and growth, further platelet and fibrin deposition
• Extension to adjacent structures– Papillary muscle, aortic valve ring abscess,
conduction system
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Pathogenesis• Low pressure side of structural lesion
– Atrial side of mitral valve (MR)– Ventricular side of aortic valve (AR, AS with R)– Congenital abnormality (MV prolapse, bicuspid AV)– Scarring from rheumatic heart disease or sclerosis
as a consequence of aging– Prosthetic valves
• Other turbulence, high-velocity jets– Ventricular septal defect– Stenotic valve
• Direct mechanical damage from catheters, pacemaker leads
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Pathogenesis• Transient bacteremia
– Traumatization of mucosal surface colonized with bacteria (oral, GI)
– Low grade, cleared in 15-30 minutes– Susceptibility to complement-mediated
bacterial killing• Leads to concept of prophylaxis
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Microbiology• Staphylococcus aureus (30-40%)• Viridans group streptococci (18%)• Enterococci (11%)• Coagulase-negative staphylococci (11%)• Streptococcus bovis (7%)• Other streptococci (5%)• Non-HACEK Gram negatives (2%)• HACEK Organisms (2%)• Fungi (2%)• “Culture negative” (2-20%)
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Characteristics of Causative Organisms
• Adherence factors critical for growth in the vegetation– Can adhere to damaged valves (Staph, Strep and
Enterococci have adhesins that mediate attachment)
– Staph adhesin binds fibrinogen and fibronectin– Bacteria trigger tissue-factor production from local
monocytes and induce platelet aggregation so the organisms become enveloped in the vegetation
– Protection from immune clearance leads to large numbers of bacteria (109-1010 per g of tissue)
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Risk Factors
• Structural heart disease– Rheumatic, congenital, aging– Prosthetic heart valves
• Injected drug use• Invasive procedures (?)• Indwelling vascular devices• Other infection with bacteremia (e.g.
pneumonia, meningitis)• History of infective endocarditis
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Clinical Manifestations• Symptoms
– Fever, sweats, chills– Anorexia, malaise, weight loss
• Signs– Anemia (normochromic, normocytic)– Splenomegaly– Microscopic hematuria, proteinuria– New or changing heart murmur, CHF– Embolic or immunologic dermatologic signs– Hypergammaglobulinemia, elevated ESR, CRP,
RF
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Cardiac Pathologic Changes
• Vegetations on valve closure lines• Destruction and perforation of valve leaflet• Rupture of chordae tendinae,
intraventricular septum, papillary muscles• Valve ring abscess• Myocardial abscess• Conduction abnormalities
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S. Aureus mitral valve vegetation, anterior leaflet
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Pathologic Changes
• Kidney– Immune complex glomerulonephritis– Emboli with infarction, abscess
• Aortic mycotic aneurysms• Cerebral embolism
– Infarction, abscess, mycotic aneurysms– Purulent meningitis is rare
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Pathologic Changes• Splenic enlargement, infarction• Septic or bland pulmonary embolism• Skin
– Petechiae– Osler nodes: diffuse infiltrate of neutrophils, and
monocytes in the dermal vessels with immune complex deposition. Tender and erythematous
– Janeway lesions: septic emboli with bacteria, neutrophils and SQ hemorrhage and necrosis. Blanching and non-tender. Palms and soles
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Case Definition
• 1977 Pelletier and Petersdorf criteria • 1981 von Reyn criteria• 1994 Duke criteria• 2000 Modified Duke criteria
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Modified Duke Criteria• Major Criteria
– Positive blood cultures with typical organisms
– Persistently positive blood cultures– Evidence of Endocardial involvement
• Positive Echocardiogram– Oscillating intracardiac mass– Abscess– Dehiscence of prosthetic valve
• New Valvular regurgitation
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Modified Duke Criteria
• Minor Criteria– Predisposition (valvular disease or IDU)– Fever– Vascular phenomena (Arterial emboli,
septic pulmonary infarcts, intracranial hemorrhage, Osler, Janeway)
– Immunologic phenomena (GN, Osler, Roth spots, Rheumatoid Factor)
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Modified Duke Criteria• Definite IE
– Pathologic criteria– Clinical criteria
• 2 Major Criteria OR• 1 Major and 3 minor Criteria OR• 5 Minor Criteria
• Possible IE• 1 Major and 1 Minor OR• 3 Minor
• Rejected IE
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Blood Cultures• MULTIPLE BLOOD CULTURES
BEFORE EMPIRIC THERAPY• If not critically ill
– 3 blood cultures over 12-24 hour period– ? Delay therapy until diagnosis confirmed
• If critically ill– 3 blood cultures over one hour
• No more than 2 from same venipuncture• Relatively constant bacteremia
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“Culture Negative” IE• Less common with improved blood
culture methods• Special media required
– Brucella, Mycoplasma, Chlamydia, Histoplasma, Legionella, Bartonella
• Longer incubation may be required– HACEK
• Coxiella burnetii (Q Fever), Trophyrema whipplei will not grow in cell-free media
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HACEK
• Haemophilus aphrophilus, H. paraphrophilus, parainfluenzae
• Actinobacillus actinomycetemcomitans• Cardiobacterium hominis• Eikenella corrodens• Kingella kingae
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Other microbiologic methods
• PCR– Coxiella burnetii– Tropheryma whipplei– Bartonella henselae
• Serology– Coxiella burnetii– Bartonella– Brucella– Legionella– Chlamydophila psittaci
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Echocardiography
• Transthoracic– Relatively low sensitivity– Good specificity
• Transesophageal– Detection of valve ring abscess (87% vs.
28% sensitivity for TTE)– Detection of prosthetic valve IE
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When to go to TEE first?
• Limited thoracic windows = TTE low sensitivity
• Prosthetic valves• Prior valvular abnormality• S. aureus bacteremia and suspected IE• Bacteremia with organisms likely to
cause IE= high prior probability of IE
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Other tests
• Electrocardiogram– Conduction delays– Ischemia or infarction
• Chest X-ray– Septic emboli in right-sided IE– Valve calcification– CHF
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Treatment of IE
• Native vs. Prosthetic Valve• Bactericidal therapy is necessary• Eradication of bacteria in the vegetation
– May be metabolically inactive (stationary phase)
– May need higher concentrations of antimicrobial agents
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Antimicrobial Therapy
• Most patients are afebrile in 3-5 days• Long duration of therapy (4-6 weeks or
more)• Combination therapy most important for
– Shorter course regimens– Enterococcal endocarditis– Prosthetic valve infections
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Native Valve IE
• Viridans Streptococci and S. bovis– Aqueous Penicillin G 12-20 million
units/day continuously or divided q4 or q6 for 4 weeks
– If intermediate susceptibility to penicillin, aqueous penicillin G 24 million units or ceftriaxone 2 g q24 PLUS aminoglycoside for the first 2 weeks
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Native Valve IE
• Aminoglycosides for synergy– Low concentrations are adequate (1-3
mcg/ml)– Gentamicin 3 mg/kg divided q12 or q8– Little data for q24 dosing
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Native Valve IE• Enterococci, ampicillin sensitive
– High rates of failure– β-lactams are bacteriostatic, must combine with
aminoglycoside for optimal therapy– High-level gentamicin resistance occurs in 35%
• High-dose ampicillin for 8-12 weeks
• Enterococci, ampicillin resistant– Vancomycin plus gentamicin
• Enterococci, vancomycin resistant– Linezolid or daptomycin– Penicillin + vancomycin + gentamicin ?
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Native Valve IE
• S. aureus– Penicillinase-resistant semi-synthetic
penicillin (oxacillin or nafcillin) 1.5-2 g IV q4 or cephalosporin (cefazolin 1-2 g IV q8) for 4-6 weeks
– Aminoglycoside synergistic but does not affect survival, not recommended
– Short course in right-sided IE• 2 weeks of semi-synthetic penicillin and
aminoglycoside
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Native Valve IE
• Methicillin-resistant S. aureus– Vancomycin is bacteriostatic– Vancomycin plus aminoglycoside or
rifampin– Daptomycin– Linezolid
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Native Valve IE
• HACEK– Ceftriaxone 2 g IV q 24 x 4-6 weeks
• Fungal– Amphotericin– Fluconazole– Caspofungin, little data– Surgery usually necessary 1-2 weeks into
treatment
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Native Valve IE• Indications for surgery
– Refractory CHF– More than one systemic embolic event– Uncontrolled infection– Physiologically significant valvular
dysfunction– Ineffective antimicrobial therapy (e.g.
fungal)– Local suppurative complications– Mycotic aneurysm
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Prosthetic Valve IE
• Staphylococci most common– Coagulase negative staphylococci
• Enterococcus• Nutritonally variant streptococci• Fungi
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Prosthetic Valve IE
• Risk is greatest in the first 3 months and first year (early PV IE)– Coagulase-negative staphylococci in early
endocarditis, S. aureus– Late-onset more similar to native valve
disease in microbiology but more coagulase-negative staphylococci. Valve is endothelialized
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Prosthetic Valve IE
• TEE should be used first• Staphylococci
– Vancomycin or oxacillin plus rifampin for at least six weeks, gentamicin for the first two weeks (3 mg/kg q24)
– Rifampin started at least 2 days after 2 other agents to avoid resistance
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Prophylaxis of IE
• Uncertainty and controversy• No randomized trials• Indirect evidence (uncontrolled clinical
series, case-control studies)• Decision analysis
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Clinical Case
• 43 yo man ESRD, Cadaveric Renal Transplant 2004
• Recurrent UTIs, placement of nephrostomy tube
• Fevers, chills, altered mental status, sepsis syndrome
• Bradycardia to 35 and increased PR
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Clinical Case• Urine with MRSA, 4/4 blood cultures with MRSA• Initial TTE: EF 35-45%, thickened AV with moderate
AS, thickened or calcified MV mild MR– “Compared with last previous echo, 3/3/00, there is no
significant change. In the presence of valvular thickening, cannot rule out endocarditis.
• Next day TEE– thickened AV, mild to moderate AS, no AR. 2 vegetations
~1 cm on ventricular side– Markedly thickened MV, large mobile vegetation >4cm on
atrial side anterior leaflet, possible second vegetation on posterior leaflet, mild MR
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Clinical case
• Renal allograft removed the following day with abscess
• Replacement of AV and MV and resection of left ventricular abscess cavity two days later