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INFECTION OF THE ENDOCARDIUM
LINING LAYER OF THE HEART
Infective endocarditis
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VALVE LEAFLETSMost commonly affectedMay also affect
ChordaeChamber wallsParaprosthetic tissue
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PATHOGENESIS
First changeAlteration of the valve surface
Produced by various local and systemic stresses, including blood turbulence
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mNONBACTERIAL THROMBOTIC ENDOCARDITIS
Deposition of platelets and fibrinSterile vegetation
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mPLATELET-FIBRIN DEPOSITIONOccurs spontaneously
Abnormal valvesCardiac endothelial injuryCardiac inflammation
These deposits are called NBTE
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BACTEREMIA Microorganisms adhere during bacteremia to initiate IE
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BACTEREMIAConverts nonbacterial thrombotic endocarditis to IE
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BACTERIA
Certain strains adhere better
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VEGETATION Consists of
FibrinPlatelet aggregatesBacterial masses
Neutrophils and red blood cells are rare
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SITE OF VEGETATIONS
Site of infectionUsually located along the line of closure of a valve leaflet
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WHERE DO VEGETATIONS DEVELOP?
Atrial surfaceAtrioventricular valves
Ventricular surfaceSemilunar valves
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LARGE VEGETATIONS
Acute IEFungal endocarditis
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LARGE VEGETATIONS
High incidence of systemic emboli
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WHEN DO LARGE EMBOLI CAUSE MAJOR VESSEL OCCLUSION?
Fungal endocarditisMarantic endocarditis
Intracardiac myxoma
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NORMAL ENDOTHELIUM
Resistant to infectionBacteremia frequent
Endocarditis rare
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mTWO FACTORS IMPORTANT IN THE FORMATION OF NBTE
Endothelial injury
Hypercoagulable state
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HYPERCOAGULABILITY Valvular heart disease Intracardiac catheters SLE Malignancy Increasing age DIC Uremia
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HIGHEST RISK OF BACTEREMIA
Gingival trauma
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RISK OF BACTEREMIA
Less with surgical procedures involving GU and GI tracts
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ESSENTIAL FOR IEHigh velocity jet streamBlood passing through a narrow orifice with a high-pressure gradient
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HIGH VELOCITY JET
Mitral regurgitationAortic stenosisVSD
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HIGH VELOCITY JET
Damage to surface epithelium
Formation of a sterile thrombus
Nonbacterial thrombotic endocarditis
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MITRAL STENOSIS AND ASD
No high-pressure jet
IE is very rare
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mMOST COMMON UNDERLYING LESION IN INDIA
Rheumatic heart disease
MV > 85%
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mOTHER PREDISPOSING CONDITIONS
1. PDA2. VSD3. COA4. TOF5. Bicuspid AV 6. Prosthetic valves
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ELDERLY Congenital bicuspid aortic valve
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MARANTIC ENDOCARDITIS
1. Malignancy 2. SLE3. Antiphospholipid
antibody syndrome
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DIAGNOSIS OF APSClotting
Arterial or venousRepeated fetal lossesTwo positive tests for aPL > 6 weeks apart
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HIV INFECTIONHigh incidence of antiphospholipid antibodies
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HIVNot a risk factor for IEUnless associated with IV drug abuse
HIV-infected IV drug abusersIE is frequent
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m> 90% OF THE ORGANISMS IN VEGETATIONS
Metabolically inactiveNot growing
Resistant to killing by antibiotics
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WHICH BACTERIA COMMONLY CAUSE IE?
1. Streptococci2. Staphylococci3. Enterococci4. GNB
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S. AUREUSCan adhere directly to intact endothelium or exposed subendothelial tissue
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LESS VIRULENT MICROORGANISMS
Adhere to thrombi
Proliferate to form dense colonies
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ACUTE IE
Duration < 6 weeksS.aureus
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ACUTE AR OR MRVirulent organisms
(e.g., staphylococcus aureus) attack normal valves
Rapid destruction of the valve
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METASTATIC INFECTIONS
Hematogenous spread to other organs
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WHEN TO SUSPECT ACUTE IE
High fever Marked toxicityValvular destruction
Metastatic infection
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SUBACUTE IEEvolves over weeks to months
Only rarely causes metastatic infection
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VIRIDANS STREPTOCOCCI
Most common organism causing IE
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VIRIDANS STREPTOCOCCI
Originate from the oral cavity
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ALPHA-HEMOLYTIC STREPTOCOCCI
Viridans streptococci includes S. salivariusS. mitisS. sanguisS. mutans
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WHY S.VIRIDANS?Transient viridans streptococcal bacteremia induced byEatingTooth-brushing
Can adhere to biologic surfaces.
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COAGULASE-NEGATIVE STAPHYLOCOCCI
Second most common organism
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ENTEROCOCCIThird most common cause
First cause– streptococci Second cause - staphylococcus
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ENTEROCOCCINormal inhabitantGITAnterior urethra
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