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INFECTIVE ENDOCARDITISMOKGWANE EUTLWETSE
4TH YEAR MED14/07/2011
UWI, BAHAMAS CAMPUS
DEFINITIONInfective Endocarditis (IE) is a microbial
infection of the endocardial (endothelial) surface of the heart.
The vegetation is a variably sized amorphous mass of platelets and fibrin in which abundant micro-organisms and scant inflammatory cells are enmeshed.
Braunwald – Heart Disease
CAUSES OF IE
-
PREDISPOSING CONDITIONS
CHILDREN(%)(neonates)
CHILDREN(%)(2mths-15yr)
ADULTS(%)(15-60yr)
ADULTS (%)>60yr
RHDCHDMVPDHDParenteral Drug AbuseOtherNone
MICRBIOLOGYStreptococciEnterococciS. aureusCoagulase ve StaphylococciGNBFungiPolymicrobial
28
72
15-20
50-5010
10104
2-175-9015-95
2-5
40-504255
51
25-3010-2010-30RARE15-35
10-1525-45
45-655-830-403-5
4-811
82103010
1025-40
30-451525-305-8
5RARERARE
RISK FACTORS FOR SPECIFIC PATHOGENS THAT CAUSE IE
Dental procedures, poor dental hygiene - viridans streptococci,nutritionally variant streptococci, HACEK• Prosthetic valves – Early: coagulase negative staphylococci, S. aureus – Late: coagulase negative staphylococci, viridans
streptococci• Gastrointestinal or genitourinary procedures - enterococci or
S. bovis (colon carcinoma)• Nosocomial - S. aureus (including MRSA), Gram negatives,Candida species
Brouqui and Raoult, Clin Microbiol Rev, 2001
PATHOGENESISEndothelium resistant to bacteria and thrombus formation
Endothelial injury and hypercoagulable state- high velocity jets, obstructive lesions, aberrant flows, direct invasion by virulent pathogens can lead to non-bacterial thrombotic embolism(NBTE)
Mitral regurgitation, Aortic stenosis, Aortic regurgitation, Ventricular Septal Defect, complex congenital heart disease can create
NBTEMost bacteria find NBTE a convenient site or nidus for adherenceVirulent organisms- Staph. aureus, Strep. pyogenes, Strep. pneumoniae have
surface molecules which allow them to adhere to intact endothelium and to exposed sub-endothelial tissues
If the adhering bacteria are able to survive serum cidal activity, peptides, complement , antibody etc., they multiply – infective vegetation.
PATHOPHYSIOLOGY
The clinical manifestation IE result from:
1. The local destructive effects of intracardial infection;2. The embolization of septic fragments of vegetations
to distant sites, resulting in infarction or infection;3. The hematogenous seeding of remote sites during
continuous bacteremia and4. An antibody response to the infecting organism with
subsequent tissue injury due to deposition of preformed immune complexes.
CLINICAL MANIFESTATIONSYMPTOMS PERCENT SIGNS PERCENT
FeverChillsSweatsAnorexiaWeight lossMalaiseDyspneaCoughStrokeheadacheNausea/vomitingmyalgia/arthralgiaChest painAbdominal painBack painconfusion
80-9542-752525-5525-3525-4020-402513-2015-4015-2015-308-355-157-1010-20
FeverMurmurChanging/new murmurNeurological abnormalitiesEmbolic eventSplenomegalyClubbingPeripheral manifestationOsler’s nodesSplinter hemorrhagePetechiaeJaneway’s lesionsRetinal lesion
80-9080-9510-40
30-40
20-4015-5010-2010-20
7-105-15
10-406-104-10
CLINICAL MANIFESTIONACUTE COURSE SUBACUTE COURSE
Rapid onsetHigh fever >39o C30-40% may not have a murmurRapid deteriorationDeath occurs with days to weeks in 50 -60 % of patientsLager vegetations therefore embolic complications more commonHigh virulence organisms eg.Strep.pyogenes, Staph. aureus, Staph. lugdunensis, Strep. pnuemoniae, Enterococcus.
Insidious onsetLow grade feverHave cardiac abnormalityProgressive valvular incompetenceLess fatal compared to acute IESmaller vegetations with less embolic complicationsLess virulence organisms eg. Strep.viridans, COGNS, Staph.aureus, HACEK group, Bartonella, Coxiella burnetiiHistory of illicit drugs
DIFFERENTIAL DIAGNOSIS Endocarditis Systemic Lupus Erythematosus Cardiac Neoplasms, Primary Antiphospholipid Syndrome Reactive Arthritis Lyme disease
DIAGNOSIS OF IEPathological criteria:Microorganisms: demonstrated by culture or histology
in a vegetation, or in a vegetation that has embolized, or in an intracardiac abscess, or
Pathological lesions: vegetation or intracardiac abscess present, confirmed by histology showing active endocarditis
Clinical criteria:Two major criteria, or One major and three minor
criteria, or Five minor criteria.
DIAGNOSIS OF IEMAJOR CRITERIA
Positive blood cultureTypical microorganism for infective endocarditis from two separate blood cultures Viridans streptococci, Streptococcus bovis, HACEK group orCommunity-acquired Staphylococcus aureus or enterococci in the absence of a primary
focus, orPersistently positive blood culture, defined as recovery of a microorganism consistent
with infective endocarditis from:Blood cultures drawn more than 12 hr apart, orAll of three or a majority of four or more separate blood cultures, with first and last
drawn at least 1 hr apartEvidence of endocardial involvement
Positive echocardiogramOscillating intracardiac mass, on valve or supporting structures, or in the path of
regurgitant jets, or on implanted material, in the absence of an alternative anatomical explanation, or Abscess, or New partial dehiscence of prosthetic valve, or New valvular regurgitation (increase or change in preexisting murmur not sufficient)
DIAGNOSIS OF IEMINOR CRITERIA
Predisposition: predisposing heart condition or intravenous drug use Fever ,38.0°C (100.4°F) Vascular phenomena: major arterial emboli, septic pulmonary infarcts, mycotic
aneurysm, intracranial hemorrhage, conjunctival hemorrhages, Janeway's lesions Immunological phenomena: glomerulonephritis, Osler's nodes, Roth's spots,
rheumatoid factor Microbiological evidence: positive blood culture but not meeting major criterion
as noted previously or serologic evidence of active infection with organism consistent with infective endocarditis
Echocardiogram: consistent with infective endocarditis but not meeting major criterion
Adapted from Durack DT, Lukes AS, Bright DK: New criteria for diagnosis of infective endocarditis: Utilization of specific echocardiographic findings. Am J Med
96:200, 1994.
DIAGNOSIS OF IE
OTHER TESTS
ECHOCARDIOLOGY Transthoracic Echocardiology(TTE) 65% sensitive Transoesaphageal Echocardiology(TEE) >90% sensitive, 6 – 18%
false negatives Repeat in 7 – 10 days
CBCSed. RateC Reactive Protein Immune Complexes
TREATMENTANTIBIOTICS Ideal therapy includes a cell wall-active agent plus an effective
aminoglycoside to achieve bactericidal synergy. Bactericidal, prolonged administration 4 – 8 weeks Given IV Knowledge of MIC of the pathogen is important.
Strep.viridans (pen.sensitive): PenG 2-3 mU q 4hrly - 4weeks or Ceftriaxone 2 g/d - 4weeks or Vancomycin 15mg/kg q 12 hrly - 4weeks
Pen G 2-3 Mu q 4 hrly - 2weeks plus
Gentamicin 1mg/kg q 8hrly – 2weeks.
TREATMENT- ANTIBIOTICS
Streptococci (relatively resistant- mic. > 0.01)
PenG 4 mU q 4 hrly IV -4weeks or Ceftriaxone 2g/d IV – 4weeks plus Gentamicin 1mg/kg q 8hrly IV -2weeks or Vancomycin 15mg/kg q 12 IV hrly – 4 weeks
Streptococci (moderately resistant) Gemella, nut.variants
Pen G 4-5 mU q 4hrly IV -6 weeks or Ceftriaxone 2g/d IV – 6weeks plus Gentamicin 1mg/kg q 8hrly IV – 6weeks
TREATMENT- ANTIBIOTICSEnterococci: Pen G 4-5 mU q 4hrly IV - 4-6weeks or
Amp 2g q 4hrly IV- 4 -6weeks or Vancomycin 15mg/Kg q 12 hrly IV - 4– 6weeks
plus Gentamicin 1mg/kg q8hrly IV -4-6weeks.
Staphylococci (Methicillin Sensitive):
Nafcillin/Oxacillin 2gq4hrly IV 4-6 wks plus Gentamicin 1mg/Kg q 8 hrlyIV 3-5 days or Ceftriaxone 2g /d IV 4-6 weeks or Vancomycin 15mg/Kg q 12hrly IV 4-6wks
TREATMENT- ANTIBIOTICS
Staphylococci (Methicillin Resistant):
Vancomycin 15mg/Kg q 12hrly IV 4-6wks
Staphylococci (Prosthetic Valve) (Methicillin Sensitive):
Nafcillin/Oxacillin 2g q 4hrly IV 6-8wks plus Gentamicin 1mg/Kg q 8 hrly IV – 2wks plus Rifampin 300mg PO q 8hrly - 6-8wks
Staphylococci (Prosthetic Valve) (Methicillin Resistant):
Vancomycin 15mg/Kg q 12hrly IV – 6-8wks plus Gentamicin 1mg/Kg q 8hrly IV 2wks plus Rifampin 300 mg PO q 8hrly 6-8wks
TREATMENT-ANTIBIOTICS
HACEK Group(Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella):
Ceftriaxone 2g /d IV 4wks or Ampicillin/Sulbactam 3g q 6hrly 4wks
Rosendorff- Essential Cardiology
TREATMENTSURGICAL THERAPY
Moderate to severe congestive heart failure due to valve dysfunction
Partially dehisced prosthetic valve
Persistent bacteremia despite optimal antibiotic therapy
In the absence of effective antibiotic therapy
Recurrent prosthetic valve endocarditis
Prevent septic emboli
PROPHYLAXISHigh risk patients only Prosthetic valves Prior endocarditis Congenital Cyanotic Heart Disease Up to Six months after repair of Congenital Heart Disease Post cardiac transplantation
Amoxicillin 2g po 1 hr before procedureAmpicillin 2g IV 1hr before procedureAzithromycin 500mg po 1 hr before procedureCephalexin 2g po 1 hr before procedureClindamycin 600mg po 1hr before procedure Ceftriaxone 1g IV 1hour before surgeryClindamycin 600mg IV 1hour before procedure
REFERENCE1. Braunwald: Heart Disease: A Textbook of
Cardiovascular Medicine, 6th ed: Copyright © 2001 W. B. Saunders Company
2. Hugh D. A.: et al: Moss and Adams' Heart Disease in Infants, Children, and Adolescents Including the Fetus and Young Adult 6th ed (November 2000)
3. Robbins et al: Pathologic Basis of Disease: 6th ed: Copyright © 1999 W.B. Saunders Company
4 . Rosendorff C: Essential Cardiology Principles and Practices: 2nd ed: Copyright © 2005 Humana Press Inc.
END!!!