11. Infective Endocarditis 7th Prt1

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    Infective Endocarditis

    DR Mohamad Jarrah

    Assistatnt Professor

    Cardiologist

    JUST

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    Definition

    Infectious Endocarditis (IE): an infection of

    the hearts endocardial surface

    Classified into fourgroups:

    Native Valve IE

    Prosthetic Valve IE

    Intravenous drug abuse (IVDA) IE

    Nosocomial IE

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    Further Classification

    Acute

    Affects normal heart

    valves

    Rapidly destructive Metastatic foci

    Commonly Staph.

    If not treated, usually

    fatal within 6 weeks

    Subacute

    Often affects damaged

    heart valves

    Indolent nature If not treated, usually

    fatal by one year

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    Etiology

    Native valve Endocardi t is-Streptococcus viridans, Staphylococci,HACEK

    - Oral cavity, skin, upper respiratory tract

    Streptococcus bovis (GIT), EnterococciIntravascular catheters, UTI, Nosocomial wound

    infections, HD- transient bacteremia

    Prosthet ic Valve Endocardi t is-Coagulase negative Staphylococci,S.Aureus, GNB, diptheroids, fungii

    Within 2 months- intra-operative contamination

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    IV Drug abuse endocardi t is:- Tricuspid valveMRSA

    More varies Etiology if left sided heart valves are involved

    Polymicrobial

    Unusual organisms- Pseudomonas Aeruginosa, Candida, Bacillus,

    Lactobacillus, Corynebacterium

    Nosocomia l -Transvenous pacemaker lead- and/or implanteddefibrillator associated endocarditis

    5-15% may be cultu re negative(?prior antibiotic exposure)

    Or fastidious organisms- Coxiella burnetti in Europe, Brucella in the Middle

    East

    Tropheryma whipplei- indolent afebrile culture negative endocarditis

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    Pathophysiology

    1. Turbulent blood flow disrupts the

    endocardium making it sticky

    2. Bacteremia delivers the organisms to

    the endocardial surface

    3. Adherence of the organisms to the

    endocardial surface

    4. Eventual invasion of the valvular

    leaflets

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    Inherently endothelium is resistant to

    infection

    Turbulent blood f lowcauses endothelial

    injury- direct infection

    OR

    Nonbacterial thrombotic endocarditis-

    platelet fibrin thrombus- site of infection

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    Epidemiology

    Incidence difficult to ascertain and varies

    according to location

    Much more common in males than in

    females

    May occur in persons of any age and

    increasingly common in elderly

    Mortality ranges from 20-30%

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    Risk Factors

    Intravenous drug abuse

    Artificial heart valves and pacemakers

    Acquired heart defects Calcific aortic stenosis

    Mitral valve prolapse with regurgitation

    Congenital heart defectsIntravascular catheters

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    Symptoms

    Acute

    High grade fever and

    chills

    SOB Arthralgias/ myalgias

    Abdominal pain

    Pleuritic chest pain

    Back pain

    Subacute

    Low grade fever

    Anorexia

    Weight loss Fatigue

    Arthralgias/ myalgias

    Abdominal pain

    N/V

    The onset of symptoms is usually ~2 weeks or less

    from the initiating bacteremia

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    Signs

    FeverClubbing

    Splenomegaly

    Neurological manifestations

    Heart murmur

    Peripheral manifestations- Oslers nodes,

    Subungual hemorrhage, Janeway lesions,

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    Anemia

    Leukocytosis

    Microscopic hematuriaElevated ESR, CRP

    Decreased serum complement

    Immune complexesRheumatoid factor

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    Cardiac Manifestations

    New regurgitant murmurs- 30-35% then85%

    CHF- 30 to 40%- valvular damage (aortic),

    myocarditis, intracardiac fistulaPerivalvular abscess

    Fistulae (Root of aorta to chambers/

    between cardiac chambers)Pericarditis

    Heart block/ MI due to embolic

    phenomena

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    Septic Pulmonary Emboli

    http://www.emedicine.com/emerg/topic164.htm

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    Non cardiac

    Septic embolization- subungual hemorrhage,Oslers nodes

    Musculoskeletal

    Skin, spleen, kidney, meninges, skeletal system-

    infarcts

    Embolic strokes

    Mycotic aneurysms (infection in vasa vasorum)

    Brain microabscesses

    Glomerulonephritis (reduced complement)

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    Petechiae

    1.Nonspecific2.Often located on extremities

    or mucous membranes

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    Splinter Hemorrhages

    1. Nonspecific2. Nonblanching

    3. Linear reddish-brown lesions found under the nail bed

    4. Usually do NOT extend the entire length of the nail

    5. vessel damage from swelling of the blood vessels (vasculitis) or

    tiny clots that damage the small capillaries (microemboli).

    http://www.nlm.nih.gov/medlineplus/ency/article/000874.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/000874.htm
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    Oslers Nodes- immune

    1. More specific

    2. Painful and erythematous nodules

    3. Located on pulp of fingers and toes

    4. More common in subacute IE

    American College of Rheumatology

    webrheum.bham.ac.uk/.../ default/pages/3b5.htm www.meddean.luc.edu/.../

    Hand10/Hand10dx.html

    http://webrheum.bham.ac.uk/professional/slides/lec3b/default/pages/3b5.htmhttp://www.meddean.luc.edu/lumen/MedEd/medicine/Rheumatology/Hands/Hand10/Hand10dx.htmlhttp://www.meddean.luc.edu/lumen/MedEd/medicine/Rheumatology/Hands/Hand10/Hand10dx.htmlhttp://www.meddean.luc.edu/lumen/MedEd/medicine/Rheumatology/Hands/Hand10/Hand10dx.htmlhttp://www.meddean.luc.edu/lumen/MedEd/medicine/Rheumatology/Hands/Hand10/Hand10dx.htmlhttp://www.meddean.luc.edu/lumen/MedEd/medicine/Rheumatology/Hands/Hand10/Hand10dx.htmlhttp://webrheum.bham.ac.uk/professional/slides/lec3b/default/pages/3b5.htm
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    Janeway Lesions

    1. More specific

    2. Erythematous, blanching macules3. Nonpain fu l

    4. Located on palms and soles

    5. Microabscess of the dermis with marked necrosis and

    inflammatory infiltrate not involving the epidermis.

    http://en.wikipedia.org/wiki/Abscesshttp://en.wikipedia.org/wiki/Dermishttp://en.wikipedia.org/wiki/Necrosishttp://en.wikipedia.org/w/index.php?title=Epidermis(skin)&action=edit&redlink=1http://en.wikipedia.org/w/index.php?title=Epidermis(skin)&action=edit&redlink=1http://en.wikipedia.org/wiki/Necrosishttp://en.wikipedia.org/wiki/Dermishttp://en.wikipedia.org/wiki/Abscess
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    Roth Spots

    septic embolization, leukemia, lupus erythematosus, or pernicious anemia.

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    TheEssentialBlood Test

    Blood Cultures Minimum of three blood cultures

    Three separate venipuncture sites

    atleast 1 hour apart- over 24 hrs

    Serology-

    Brucella, bartonella, Legionella, C. Burnetti

    Schiff stain for T. whippeli

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    Imaging

    Chest x-ray

    Look for multiple focal infiltrates and

    calcification of heart valves

    EKG

    Rarely diagnostic

    Look for evidence of ischemia, conduction

    delay, and arrhythmias

    Echocardiography

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    Indications for Echocardiography

    Transthoracic echocardiography (TTE)

    First line if suspected IE

    Native valves

    Transesophageal echocardiography (TEE)

    Prosthetic valves

    High risk patients

    Intracardiac complications

    Inadequate TTE

    Fungal or S. aureus or bacteremia

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    Major Criteria

    1. Posi t ive blood cu l tureTypical organism from 2 separate cultures-

    Viridans streptococci, Strptococcus bovis,

    HACEK, S. aureus, enterococci

    OR

    Persistently + blood culture- all of three/ majority

    4 blood cultures

    OR

    Single +ve blood culture for Coxiella or phase

    IgG > 1:800

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    2. Evidence of endocardial involvement

    ECHO- oscillating intracardiac massOR

    Abscess

    ORNew partial deheiscence of prosthetic

    valve/ new regurgitation

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    Minor criteria

    Predisposing heart condition

    Fever > 100.4F

    Vascular- Emboli, pulmonary infarct,mycotic aneurysm, Janeway lesions

    Immune- Oslers nodes, Roth spots,

    glomerulonephritis

    Microbiological evidence

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    Modified Duke Criteria

    Definite IE

    Microorganism (via culture or histology) in a valvular vegetation,

    embolized vegetation, or intracardiac abscess

    Histologic evidence of vegetation or intracardiac abscess

    2 Major 1 Major + 3 minor

    5 Minor

    Possible IE

    1 major and 1 minor

    3 minor

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    Treatment

    Parenteral antibiotics

    High serum concentrations to penetrate

    vegetations

    Prolonged treatment to kill dormant bacteriaclustered in vegetations

    Surgery

    Intracardiac complications

    Surveillance blood cultures

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    Monitor for side effects

    Improvement in 5-7 days

    Repeat blood cultures till sterileAgain 4-6 weeks after therapy

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    Prophylaxis

    Amoxicillin 2 g PO I hour before procedure

    Ampicillin 2 g iv within 1 hr

    Clarithromycin/ Azithromycin 500 mg

    Cephalexin 2 g

    Clindamycin 600 mg

    Cefazolin/ceftriaxone 1 g iv 30 min before procedure

    Clindamycin 600 mg iv

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    WHO prophylaxis

    Prosthetic heart valves

    Prior history

    Unrepaired cyanotic congenital heart disease

    Completely repaired congenital heart disease within 6

    months of repair

    Incompletely repaired CHD

    Valvulopathy after cardiac transplantation

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    Poor Prognostic Factors

    Female

    S. aureus

    Vegetation size

    Aortic valve

    Prosthetic valve

    Older age

    Diabetes mellitus

    Low serum albumen

    Heart failure

    Paravalvular abscess

    Embolic events