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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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