Endocarditis

Endocarditis – Justin Smith

Background

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  • Multiple etiologies of endocarditis:
    • Typical Bacterial
      • S. aureus, Enterococcus spp (E. faecalis most commonly), viridans group streptococci, Strep gallolyticus (formerly S. bovis)
      • HACEK: Haemophilus, Aggregatibacter, Cardiobacterium, Eikenella, Kingella
    • Other infectious
      • Culture negative: often recent antimicrobial exposure, slow growing organism
      • Coxiella, Brucella, Bartonella, Chlamydia, Legionella, Mycoplasma, Tropheryma whipplei, Propionibacterium acnes
      • Fungal: Candida and aspergillus most common
    • Non-infectious: a.k.a., marantic endocarditis, Libbman-Sacks Endocarditis
      • Rare, most common in advanced malignancy, SLE, inflammatory conditions
      • Endothelial injury with associated hypercoagulability
      • Higher risk for embolization compared to IE
      • Risk factors: IV drug use, congenital heart disease, valve abnormalities, intracardiac devices, recent cardiac surgery
  • Fever (90%), Murmur (85%), Other: splenomegaly, splinter hemorrhages, Janeway lesions, Osler Nodes, Roth Spots
  • Persistent bacteremia despite appropriate treatment, new onset cardiac dysfunction, new onset valve abnormalities, stroke, other thromboembolic events, metastatic infections/abscesses, splenic abscess, septic pulmonary emboli

 

Duke Criteria:

  • Pathologic Criteria
    • Microorganisms: culture or histology proven: vegetation, embolus, or intracardiac abscess
    • Pathologic vegetations: vegetation of abscess with histology proven endocarditis
  • Clinical Criteria
    • Major:
      • 2x positive blood cultures from a typical organism
      • Evidence of endocardial involvement
  • Minor
    • Predisposing heart condition/IVDU
    • Fever
    • Vascular phenomena (Glomerulonephritis)
    • Immunologic phenomena (Osler Nodes, Roth Spots, +Rheumatoid factor, GN)
    • Micro (Cultures that don’t fit the above, or serologic evidence of acute infection)
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  • Definite: 2 Major, 1 major and 3 minor, or 5 minor
  • Possible: 1 major and 1 minor, or 3 minor
  • Rejected: firm alternate diagnosis, resolution of evidence with <4 days of antibiotics, or absence of pathologic evidence with <4days of antibiotics

 

Evaluation

  • Physical exam: murmur, decreased peripheral perfusion, evidence of heart failure, petechiae, splinter hemorrhages, Janeway lesions/Osler nodes, organomegaly
  • Blood cultures: at least three sets from different sites over a span of several hours
  • Echo (TTE vs TEE)
    • It can be reasonable to start with TEE if pretest probability is high enough, if patient has known valvular abnormalities, or TTE will be technically difficult
  •  
  • EKG: new heart block or prolonged PR raises concern for endocardial/perivalvular abscess. Endocarditis patients should be on telemetry, monitored closely by team
  • CXR: infiltrates suggestive of septic pulmonary emboli, pulmonary edema, cardiomegaly
  • Imaging of distant affected site if concerned for septic emboli
  • Other advanced imaging in select scenario: cardiac CTA, cardiac MRI, FDG-PET/CT

 

Management

  • Empiric antibiotics:
    • If bacteria isolated from blood, reference bacteremia section for abx choice
    • If awaiting cultures
      • Native valve: Vancomycin
      • Prosthetic valve: Vancomycin and cefepime, consider gentamicin
  • Duration: determined by ID, often 4-6 weeks
  • Surgical consult, if valve dysfunction, perivalvular abscess, large (>20mm) vegetations

 

Additional Information:

  • Complications
    • Cardiac:
      • Heart failure:  usually secondary to valve dysfunction. Most common when aortic valve involved, risk also depends on organism (worst is Staph aureus)
      • Perivalvular abscess: suspect when there are conduction abnormalities on EKG; most likely when aortic valve involved, less likely with mitral valve.
      • Pericarditis: can be suppurative or non-suppurative
      • Intracardiac Fistula
    •  
    • Septic emboli and metastatic abscesses
    • Mycotic aneurysm: usually occurs at vessel branch points
  • Follow Up
    • Repeat TTE at completion of treatment to establish new baseline
    • Followed for valvular dysfunction with frequency determined by nature of the dysfunction. (MR caused by IE should be followed on a timeline like other MR)
    • Regular dental care, Prior IE is an indication for SBE prophylaxis with dental work.
  • Episode of IE is an indication for PDA or VSD closure