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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