endocarditis Flashcards
what is IE
◦ Definition
Infective endocarditis (IE) is an infection of the
endocardial surface of the heart.
Historically categorized as “acute” or “subacute” but now described according to etiology
◦ Epidemiology
It is traditionally associated with heart valves
(damaged by rheumatic heart disease).
- May also involve non-valvular areas of the
endocardium or implanted mechanical devices In the current era, health care contact and
injection drug use are the primary risk factors.
Most frequently mitral or aortic valvesaffected
◦ Related to degree of mechanical stress
(pressure resting on closed valve) on valve
(MV > AV > TCV > PV)
A shift in usual causative organisms from
viridans group Streptococci to
Staphylococcus aureus as leading cause
common causes organisms
Staphylococcus aureus 31.6
Viridans group streptococci 18.0
Enterococci 10.6
risk factors
Valvular Disease
• E.g. Mitral valve prolapse with regurgitation, prosthetic heart valve, acquired valvular dysfunction (rheumatic heart disease)
Previous Endocarditis
Congenital abnormalities • E.g. congenital bicuspid mitral valve or surgically constructed shunts or conduits Hypertrophic myopathy Injection Drug Use (IDU) Turbulent blood flow
sequence of events
Turbulent blood flow
Development of non-bacterial thrombus on valve Transient bacteremia exposes thrombus to
bacterial colonization
Development of IE
◦ Embolisation of septic fragments that can cause
hematogenous complications in other organs (spleen,
brain, lungs)
Incidence of Bacteremia after Various Procedures3
viridans strep ound in mouth
- poor dentition
- tooth brushing can cause bacteremia
dental extration, periodontal srugery, tonsillectomy
presentation
clinical signs
Fever 96 Heart murmur 85 Changing murmur 20 New murmur 48 Hematuria 26
clubbing (longterm), fingers - long term poor oxygenation(COPD, kung cancer)
splinter hemorrhages
conjunctival petechiae
Janeway Lesions
“numerous small hemorrhages
with slight nodular character in the
palms of the hand and soles of the feet”
Retinal Roth SpotsUsually caused by immune complex
mediated vasculitis often resulting
from bacterial endocarditis
Osler\s nodes: Found to be microabscesses in the papillary dermis together with
microemboli in the nearby dermal arterioles
not common
modified duke criteria
Pathologic Criteria (definitive):
◦ Micro-organisms demonstrated by culture or
histologic examination of a vegetation, a vegetation that has emolised, or an intra-cardiac abscess
specimen, or
◦ Pathogenic lesions; vegetation or intra-cardiac
abscess confirmed by histologic examination
showing active endocarditis
Clinical Criteria:
◦ Definitive diagnosis is made based on: 2 major criteria, 1 major criterion + 3 minor criteria, or
5 minor criteria
◦ Possible diagnosis is based on: 1 major criterion + 1 minor criterion, or 3 minor criteria
Clinical judgement is important
consideration despite criteria based
diagnosis standard
major criteria
Blood culture positive of IE
◦ Micro-organisms consistent with IE from 2 separate blood cultures (VGS, S. gallolyticus, HACEK, S. aureus), or
◦ Community acquired Enterococci, in absence of
primary focus, or
◦ Micro-organisms consistent with IE from persistently positive BC (at least 2 cultures, or all of 3 or most of > 4 separate BC), or
◦ Single positive BC for Coxiella burnetii or antiphase I IgG antibody titre > 1:800
Evidence of Endocardial involvement:
◦ Positive TEE or TTE
minor criteria
Predisposition, or predisposing heart condition, or IDU
Fever > 38℃
Vascular phenomena
◦ Major arterial emboli, septic pulmonary infarcts,
mycotic aneurysms, intra-cranial hemorrhage,
conjunctival hemorrhages, Janeway lesions
Immunologic phenomena
◦ Glomerular nephritis, Osler’s nodes, Roth’s spots,
rheumatoid factor
Microbiologic evidence – e.g. positive BC but
does not meet major criterion
Echocardiographic minor criteria eliminated
Rejected:
◦ Firm alternate diagnosis explaining evidence of IE, ◦ Resolution of IE syndrome with AB therapy < 5 d, ◦ No pathologic evidence, or ◦ Does not meet any of the criteria
tx options
Direct empiric therapy to the expected “usual” causes
◦ Staphylococcus aureus – needs vancomycin (not as good as b-lactam) and/or cloxacillin/cefazolin
- tend to use both vanco + cef/clox
◦ VGS – needs ceftriaxone (or other 3rd generation
cephalosporin)
◦ Role of aminoglycosides – consider in enterococcal
IE, prosthetic valve IE, allergic patients, and
potentially in IDU patients (where you may suspect Gram negative bacteria)
◦ Role of rifampin – generally in prosthetic valve
infections - breaks thru biofilm
Empiric
Antimicrobial Therapy
Adult Native Valve Non IDU S.aureus Viridans Streptococci Enterococcus HACEK
Acute
Vancomycin 15 mg/kg IV q8 -12h
+
Ceftriaxone 2 g IV daily
IF Severe Penicillin Allergy
Gentamicin 1 mg/kg IV q8h
+ Vancomycin 15 mg/kg IV q8 -12h
Culture positiveRefer to B+D app for pathogen directed Rx
adult native valve IDU S.aureus/MRSA Pseudomonas Enterobacteraciae Candida Enterococcus Viridans Streptococci Polymicrobial
Vancomycin 15 mg/kg IV q8 -12h +/- Gentamicin 1.5-2 mg/kg IV q8h or Tobramycin 1.5-2 mg/kg IV q8h or Ciprofloxacin 400 mg IV q12h/ 750 mg PO bid
Culture positive Refer to B+D app for pathogen directed Rx
culture directed tc
Important to understand MIC’s of
Streptococci (Enterococcus as well)
◦ Penicillin MIC ≤ 0.1 mcg/mL – highly susceptible◦ Penicillin MIC 0.12 - < 5 mcg/mL – relatively
penicillin resistant
Would need to add gentamicin to therapy
◦ Penicillin MIC ≥ 5 mcg/mL (or Enterococcus) Add gentamicin and extend treatment length Add ceftriaxone to ampicillin for Enterococcus
Potentially non-penicillin therapy (depending on
susceptibilities)
culture directed tx
role of rifampin
Role of rifampin
◦ Synergistic activity for Gram positive organisms◦ Active against the bacterial biofilm◦ Has a positive role to play in prosthetic infections◦ Powerful enzyme inducer so must be assessed for
drug interactions
◦ Need to discuss with patient the expected adverse reactions to watch for while on treatment
