Infective Endocarditis
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Infective Endocarditis

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Infective Endocarditis Infective Endocarditis Presentation Transcript

  • MOKGWANE EUTLWETSE4TH YEAR MED14/07/2011UWI, BAHAMAS CAMPUS
  • DEFINITION Infective Endocarditis (IE) is a microbial infection ofthe endocardial (endothelial) surface of the heart. The vegetation is a variably sized amorphous mass ofplatelets and fibrin in which abundant micro-organisms and scant inflammatory cells are enmeshed.Braunwald – Heart Disease
  • CAUSES OF IE
  • -PREDISPOSINGCONDITIONSCHILDREN(%)(neonates)CHILDREN(%)(2mths-15yr)ADULTS(%)(15-60yr)ADULTS (%)>60yrRHDCHDMVPDHDParenteralDrug AbuseOtherNoneMICRBIOLOGYStreptococciEnterococciS. aureusCoagulase veStaphylococciGNBFungiPolymicrobial287215-2050-5010101042-175-9015-952-540-5042555125-3010-2010-30RARE15-3510-1525-4545-655-830-403-54-811821030101025-4030-451525-305-85RARERARE
  • RISK FACTORS FOR SPECIFICPATHOGENS 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 speciesBrouqui and Raoult, Clin Microbiol Rev, 2001
  • PATHOGENESISEndothelium resistant to bacteria and thrombus formationEndothelial injury and hypercoagulable state- high velocity jets, obstructivelesions, aberrant flows, direct invasion by virulent pathogens can lead to non-bacterial thrombotic embolism(NBTE)Mitral regurgitation, Aortic stenosis, Aortic regurgitation, Ventricular SeptalDefect, complex congenital heart disease can createNBTEMost bacteria find NBTE a convenient site or nidus foradherenceVirulent organisms- Staph. aureus, Strep. pyogenes, Strep. pneumoniae havesurface molecules which allow them to adhere to intact endothelium and toexposed sub-endothelial tissuesIf the adhering bacteria are able to survive serum cidal activity, peptides,complement , antibody etc., they multiply – infective vegetation.
  • PATHOPHYSIOLOGYThe clinical manifestation IE result from:1. The local destructive effects of intracardial infection;2. The embolization of septic fragments of vegetations todistant sites, resulting in infarction or infection;3. The hematogenous seeding of remote sites duringcontinuous bacteremia and4. An antibody response to the infecting organism withsubsequent tissue injury due to deposition of preformedimmune complexes.
  • CLINICAL MANIFESTATIONSYMPTOMS PERCENT SIGNS PERCENTFeverChillsSweatsAnorexiaWeight lossMalaiseDyspneaCoughStrokeheadacheNausea/vomitingmyalgia/arthralgiaChest painAbdominal painBack painconfusion80-9542-752525-5525-3525-4020-402513-2015-4015-2015-308-355-157-1010-20FeverMurmurChanging/newmurmurNeurologicalabnormalitiesEmbolic eventSplenomegalyClubbingPeripheralmanifestationOsler’s nodesSplinterhemorrhagePetechiaeJaneway’s lesionsRetinal lesion80-9080-9510-4030-4020-4015-5010-2010-207-105-1510-406-104-10
  • CLINICAL MANIFESTIONACUTE COURSE SUBACUTE COURSERapid onsetHigh fever >39o C30-40% may not have a murmurRapid deteriorationDeath occurs with days to weeks in 50-60 % of patientsLager vegetations therefore emboliccomplications more commonHigh virulence organismseg.Strep.pyogenes, Staph. aureus,Staph. lugdunensis, Strep. pnuemoniae,Enterococcus.Insidious onsetLow grade feverHave cardiac abnormalityProgressive valvular incompetenceLess fatal compared to acute IESmaller vegetations with less emboliccomplicationsLess virulence organisms eg.Strep.viridans, COGNS, Staph.aureus,HACEK group, Bartonella, CoxiellaburnetiiHistory of illicit drugs
  • DIFFERENTIAL DIAGNOSIS Endocarditis Systemic Lupus Erythematosus Cardiac Neoplasms, Primary Antiphospholipid Syndrome Reactive Arthritis Lyme disease
  • DIAGNOSIS OF IE Pathological criteria:Microorganisms: demonstrated by culture or histology in avegetation, or in a vegetation that has embolized, or in anintracardiac abscess, orPathological lesions: vegetation or intracardiac abscesspresent, confirmed by histology showing activeendocarditis Clinical criteria:Two major criteria, or One major and three minor criteria, orFive minor criteria.
  • DIAGNOSIS OF IEMAJOR CRITERIA Positive blood cultureTypical microorganism for infective endocarditis from two separate blood culturesViridans streptococci, Streptococcus bovis, HACEK group orCommunity-acquired Staphylococcus aureus or enterococci in the absence of a primaryfocus, orPersistently positive blood culture, defined as recovery of a microorganism consistent withinfective 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 atleast 1 hr apartEvidence of endocardial involvement Positive echocardiogramOscillating intracardiac mass, on valve or supporting structures, or in the path of regurgitantjets, or on implanted material, in the absence of an alternative anatomical explanation, orAbscess, 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, mycoticaneurysm, intracranial hemorrhage, conjunctival hemorrhages, Janeways lesions Immunological phenomena: glomerulonephritis, Oslers nodes, Roths spots,rheumatoid factor Microbiological evidence: positive blood culture but not meeting major criterion asnoted previously or serologic evidence of active infection with organism consistent withinfective endocarditis Echocardiogram: consistent with infective endocarditis but not meeting major criterionAdapted from Durack DT, Lukes AS, Bright DK: New criteria for diagnosis of infectiveendocarditis: Utilization of specific echocardiographic findings. Am J Med96:200, 1994.
  • DIAGNOSIS OF IEOTHER TESTS ECHOCARDIOLOGY Transthoracic Echocardiology(TTE) 65% sensitive Transoesaphageal Echocardiology(TEE) >90% sensitive, 6 – 18% falsenegatives Repeat in 7 – 10 days CBC Sed. Rate C Reactive Protein Immune Complexes
  • TREATMENTANTIBIOTICS Ideal therapy includes a cell wall-active agent plus an effectiveaminoglycoside 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 orCeftriaxone 2 g/d - 4weeks orVancomycin 15mg/kg q 12 hrly - 4weeksPen G 2-3 Mu q 4 hrly - 2weeks plusGentamicin 1mg/kg q 8hrly – 2weeks.
  • TREATMENT- ANTIBIOTICS Streptococci (relatively resistant- mic. > 0.01)PenG 4 mU q 4 hrly IV -4weeks orCeftriaxone 2g/d IV – 4weeks plusGentamicin 1mg/kg q 8hrly IV -2weeks orVancomycin 15mg/kg q 12 IV hrly – 4 weeks Streptococci (moderately resistant) Gemella, nut.variantsPen G 4-5 mU q 4hrly IV -6 weeks orCeftriaxone 2g/d IV – 6weeks plusGentamicin 1mg/kg q 8hrly IV – 6weeks
  • TREATMENT- ANTIBIOTICS Enterococci: Pen G 4-5 mU q 4hrly IV - 4-6weeks orAmp 2g q 4hrly IV- 4 -6weeks orVancomycin 15mg/Kg q 12 hrly IV - 4– 6weeksplusGentamicin 1mg/kg q8hrly IV -4-6weeks. Staphylococci (Methicillin Sensitive):Nafcillin/Oxacillin 2gq4hrly IV 4-6 wksplusGentamicin 1mg/Kg q 8 hrlyIV 3-5 days orCeftriaxone 2g /d IV 4-6 weeks orVancomycin 15mg/Kg q 12hrly IV 4-6wks
  • TREATMENT- ANTIBIOTICSStaphylococci (Methicillin Resistant):Vancomycin 15mg/Kg q 12hrly IV 4-6wksStaphylococci (Prosthetic Valve) (Methicillin Sensitive):Nafcillin/Oxacillin 2g q 4hrly IV 6-8wks plusGentamicin 1mg/Kg q 8 hrly IV – 2wks plusRifampin 300mg PO q 8hrly - 6-8wksStaphylococci (Prosthetic Valve) (Methicillin Resistant):Vancomycin 15mg/Kg q 12hrly IV – 6-8wks plusGentamicin 1mg/Kg q 8hrly IV 2wks plusRifampin 300 mg PO q 8hrly 6-8wks
  • TREATMENT-ANTIBIOTICSHACEK Group(Haemophilus, Actinobacillus,Cardiobacterium, Eikenella, Kingella):Ceftriaxone 2g /d IV 4wks orAmpicillin/Sulbactam 3g q 6hrly 4wksRosendorff- Essential Cardiology
  • TREATMENTSURGICAL THERAPY Moderate to severe congestive heart failure due tovalve 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 transplantationAmoxicillin 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 procedureCeftriaxone 1g IV 1hour before surgeryClindamycin 600mg IV 1hour before procedure
  • REFERENCE1. Braunwald: Heart Disease: A Textbook of CardiovascularMedicine, 6th ed: Copyright © 2001 W. B. Saunders Company2. Hugh D. A.: et al: Moss and Adams Heart Disease in Infants,Children, and Adolescents Including the Fetus and Young Adult6th ed (November 2000)3. Robbins et al: Pathologic Basis of Disease: 6th ed: Copyright ©1999 W.B. Saunders Company4 . Rosendorff C: Essential Cardiology Principles and Practices: 2nded: Copyright © 2005 Humana Press Inc.
  • END!!!