Transcript Modified Duke criteria for diagnosis of infective endocarditis

Infective Endocarditis
AL-ANOUD AL-JIFRI
Consultant internal medicine ,ID
Infective Endocarditis:
Definition
A microbial infection of a cardiac valve or the endocardium
caused by bacteria, fungi, or chlamydia.
 Often categorized as acute or subacute based on the
rapidity of the clinical course
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Alternatively described by type of risk factor e.g., nosocomial,
prosthetic valve, intravenous drug use - associated
Pathological findings include the presence of friable
valvular vegetations containing bacteria, fibrin and
inflammatory cells.
There is often valvular destruction with extension to adjacent
structures.
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Embolic lesions may demonstrate similar findings.
Epidemiology of Endocarditis
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Incidence the same or slightly increased
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The age of subjects with endocarditis has increased over the past 60 years
(30-40 to 47-69).
Among injecting drug users the incidence is as high as 150 2000/100,000
person years.
There has been a major shift in nature of underlying valvular disorders.
There has also been a change in the microbiology of cases
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–1.7-6.2/100,000 depending on the population
Increasing incidence of staphylococci.
There has been an increasing incidence of nosocomial endocarditis
- both native and prosthetic valve.
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There is an increased risk of IE among injecting drug users, patients on longterm hemodialysis, patients with intravenous catheters, diabetics and HIVinfected patients.
Risk Factors for Infective Endocarditis
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Dental procedures, poor dental hygiene
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viridans streptococci, nutritionally variant streptococci,
HACEK
Prosthetic valves
Early: coagulase negative staphylococci, S. aureus
 Late: coagulase negative staphylococci, viridans
streptococci
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Gastrointestinal or genitourinary procedures
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enterococci or S. bovis (colon carcinoma)
Nosocomial
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S. aureus (including MRSA), Gram negatives , Candida
species
Brouqui and Raoult, Clin Microbiol Rev, 2001
Risk Factors for Infective Endocarditis
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HIV
 S. aureus,MRSA.
Animal or farm exposure
 Coxiella , Chlamydia ,Brucella.
History of homelessness, alcoholism (body lice)
 Bartonella
Pathogenesis of IE
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The development of IE is the net result of the complex interaction between
the bloodstream pathogen with matrix molecules and platelets at sites of
endocardial cell damage.
In addition, many of the clinical manifestations of IE origenate
from the host’s immune response to the infecting microorganism.
 The following sequence of events is thought to result in IE:
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4.
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formation of nonbacterial thrombotic endocarditis (NBTE) on the surface of a
cardiac valve or elsewhere that endothelial damage occurs
bacteremia
adherence of the bacteria in the bloodstream to NBTE
proliferation of bacteria within a vegetation.
Dissemination of infection to other tissue sites and elicitation of systemic
findings.
Pathogenesis of IE
Mucous membranes - other
peripheral tissue
Valvular endothelium
Congenital abnormalities,
turbulent blood flow
Trauma - damage at
tissue surface
Nonbacterial thrombus,
Native valves
Transient bacteremia
Adherence and colonization
Platelet adherence, fibrin
deposition - vegetation
formation
Elaboration of bacterial
enzymes, proteases
HISTORY
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history of prior cardiac lesions/or rheumatic heart
disease.
historical clues pointing toward a recent source of
bacteremia:
 indwelling
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intravascular catheters
intravenous drug use.
Epidemiological Clues in Etiological Diagnosis of
Culture-Negative Endocarditis
Epidemiological Feature
Common Microorganism(s)
Injection drug use
S aureus, including community-acquired
oxacillin-resistant strains
Coagulase-negative staphylococci
-Hemolytic streptococci
Fungi
Aerobic Gram-negative bacilli,
including
Pseudomonas aeruginosa
Polymicrobial
Indwelling cardiovascular medical
devices
S aureus
Coagulase-negative staphylococci
Fungi
Aerobic Gram-negative bacilli
Corynebacterium sp
Genitourinary disorders, infection,
manipulation, including pregnancy,
delivery, and abortion
Enterococcus sp
Group B streptococci (S agalactiae)
Listeria monocytogenes
Aerobic Gram-negative bacilli
Epidemiological Feature
Common Microorganism(s)
Burn patients
S aureus
Aerobic Gram-negative bacilli, including
P
aeruginosa
Fungi
Chronic skin disorders, including
recurrent infections
S aureus-Hemolytic streptococci
Poor dental health, dental procedure
Viridans group streptococci
“Nutritionally variant streptococci”
Abiotrophia defectiva
Granulicatella sp
Gemella sp
HACEK organisms
Alcoholism, cirrhosis
Bartonella sp
Aeromonas sp
Listeria sp
S pneumoniae
-Hemolytic streptococci
Epidemiological Feature
Common Microorganism(s)
Diabetes mellitus
S aureus
-Hemolytic streptococci
S pneumoniae
Early (1 y) prosthetic valve placement
Coagulase-negative staphylococci
S aureus
Aerobic Gram-negative bacilli
Fungi
Corynebacterium sp
Legionella sp
Late (1 y) prosthetic valve placement
Coagulase-negative staphylococci
S aureus
Viridans group streptococci
Enterococcus species
Fungi
Corynebacterium sp
Epidemiological Feature
Common Microorganism(s)
AIDS
Salmonella sp
S pneumoniae
S aureus
Dog–cat exposure
Bartonella sp
Pasteurella sp
Capnocytophaga sp
Contact with contaminated milk or
infected farm animals
Brucella sp
Coxiella burnetii
Erysipelothrix sp
Homeless, body lice
Bartonella sp
Pneumonia, meningitis
S pneumoniae
Solid organ transplant
S aureus
Aspergillus fumigatus
Enterococcus sp
Candida sp
Gastrointestinal lesions
S bovis
Enterococcus sp
Clostridium septicum
PHYSICAL EXAMINATION
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cardiac examination for signs of new regurgitant murmurs or heart failure.
stigmata of endocarditis evidence of small and large emboli with special
attention to the fundi, conjunctivae, skin, and digits.
Associated peripheral cutaneous or mucocutaneous lesions of IE 
petechiae, splinter hemorrhages, Janeway lesions, Osler's nodes, and Roth
spots.
involvement of other organs
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due to embolic events (eg, focal neurologic deficits, renal and splenic infarcts) or
a neurologic evaluation evidence of focal neurologic impairment.
a systemic immune reaction (eg, glomerulonephritis, arthritis).
In right-sided endocarditis, septic pulmonary infarcts may be seen.
Chest radiograph of a patient with tricuspid valve endocarditis due to S. aureus
Splinter hemorrhages in infective endocarditis
Roth spots
Osler's nodes
painful, violaceous nodules found in the pulp of
fingers and toes and are seen more often in
subacute than acute cases of IE
Janeway lesions
macular, blanching, nonpainful, erythematous
lesions on the palms and soles
Modified Duke criteria for diagnosis of infective endocarditis
Definite IE
Pathologic criteria
Microorganism: demonstrated by culture or histology in a
vegetation, or in a vegetation that has embolized, or in an
intracardiac abscess OR
Pathologic lesions: vegetation or intracardiac abscess,
confirmed by histology showing active endocarditis.
Clinical criteria
2 major criteria OR
1 major and 3 minor criteria OR
5 minor criteria
Modified Duke criteria for diagnosis of infective endocarditis
Possible IE
 1 major criterion and 1 minor criterion OR
 3 minor criteria
Rejected IE
 Firm alternate diagnosis for manifestations of endocarditis OR
 Resolution of manifestations of endocarditis, with antibiotic therapy
for four days or less OR
 No pathologic evidence of infective endocarditis at surgery or
autopsy after antibiotic therapy for four days or less
 Does not meet criteria for possible infective endocarditis, as above
Modified Duke criteria for diagnosis of infective endocarditis
Major criteria
Positive blood cultures for IE
 Typical microorganism for infective endocarditis from two separate blood cultures
 Viridans streptococci
 Streptococcus bovis, including nutritional variant strains
 HACEK group - Haemophilus spp,. Actinobacillus actinomycete comitants,
Cardiobacterium hominis, Eikenella spp, and Kingella kingae.
 Staphylococcus aureus
 Community-acquired enterococci, in the absence of a primary focus; OR
Persistently positive blood culture, defined as recovery of a microorganism consistent
with IE from:
 Blood cultures drawn more than 12 hours apart OR
 All of three or a majority of four or more separate blood cultures, with first and
last drawn at least one hour apart
Single positive blood culture for Coxiella burnetii or antiphase I IgG antibody titer
>1:800*
Modified Duke criteria for diagnosis of infective endocarditis
Evidence of endocardial involvement
Positive echocardiogram for IE
 TEE recommended in patients with prosthetic valves, rated at least
"possible IE" by clinical criteria, or complicated IE [paravalvular
abscess]; TTE as first test in other patients.
 Definition of positive echocardiogram
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Oscillating intracardiac mass, on valve or supporting structures, or in the
path of regurgitant jets, or on implanted material, in the absence of an
alternative anatomic explanation OR
Abscess OR
New partial dehiscence of prosthetic valve
New valvular regurgitation
Increase in or change in preexisting murmur
Modified Duke criteria for diagnosis of infective endocarditis
Minor criteria
 Predisposition - predisposing heart condition or intravenous drug use
 Fever - 38.0°C (100.4°F)
 Vascular phenomena - major arterial emboli, septic pulmonary
infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival
hemorrhages, Janeway lesions.
 Immunologic phenomena - glomerulonephritis, Osler's nodes, Roth
spots, rheumatoid factor.
 Microbiologic evidence - positive blood culture but not meeting
major criterion as noted previously (excluding single positive cultures
for coagulase-negative straphylococci and organisms that do not
cause endocarditis) OR serologic evidence of active infection with
organism consistent with IE.
Complications of IE
can be broadly categorized as:
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Cardiac
Septic
Embolic
Neurologic
Musculoskeletal
Renal
Associated with medical treatment
complications in terms of their pathogenesis, which leads to different
groupings:
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Embolic (eg, cerebral infarct)
Local spread of infection (eg, heart valve destruction)
Metastatic infection (eg, vertebral osteomyelitis)
Immune-mediated damage (eg, glomerulonephritis)
Complications of IE
CARDIAC COMPLICATIONS
 Heart failure
 Perivalvular abscesses
 extravalvular complications
Pericarditis, which may be suppurative or nonsuppurative,
can rarely cause pain or even cardiac tamponade
 Fistulous intracardiac connections (eg, aorta-atrial or
aorta-ventricular) due to extension of infection from the
valve to adjacent myocardium may rarely result in large
aneurysms, a pseudoaneurysm if the aortic wall is involved ,
or even myocardial perforation.
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Complications of IE
EMBOLIZATION
Emboli consisting of vegetation fragments can occlude or damage virtually any
blood vessel, large or small, in the systemic or pulmonary arterial
circulation.
As a result, emboli can produce:
 Stroke
 Blindness
 Painful ischemic or frankly gangrenous extremities
 Unusual pain syndromes (eg, due to splenic or renal infarction).
 Hypoxia (due to pulmonary emboli in right-sided endocarditis).
 Paralysis (due to embolic infarction of either the brain or spinal cord).
Complications of IE
NEUROLOGIC COMPLICATIONS
 Embolic stroke
 Acute encephalopathy
 Meningoencephalitis
 Purulent or aseptic meningitis
 Cerebral hemorrhage (due to stroke or a ruptured
mycotic aneurysm)
 Brain abscess or cerebritis
 Seizures (secondary to abscess or embolic infarction)
Complications of IE
RENAL DISEASE
 Renal infarction (due to emboli).
 Drug-induced acute interstitial nephritis.
 Glomerulonephritis (due to deposition of
immunoglobulins and complement in the glomerular
membrane).
 Rarely , renal abscess can occur in patients with IE.
Complications of IE
METASTATIC ABSCESSES
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Rarely, metastatic abscesses develop in the kidneys, spleen,
brain or soft tissues (eg, the psoas muscle) in the setting of IE.
MUSCULOSKELETAL COMPLICATIONS
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Vertebral osteomyelitis is a well known but relatively rare
complication of IE.
Osteomyelitis more frequently complicates S. aureus
endocarditis than IE due to other microorganis
Complications of IE
Acute septic arthritis, involving one or more joints, may be the first clue
to the presence of IE in a small percentage of patients.
IE should be strongly considered in selected cases of septic arthritis:
 When infections spontaneously arise in joints of the axial skeleton
(eg, sacroiliac, pubic, or manubriosternal joints).
 When organisms with a known propensity to cause IE (eg, S. aureus,
viridans streptococci or non-group A beta-hemolytic streptococci)
grow from a joint aspirate, particularly in patients without a history
of recent surgery, joint infection, or trauma.
 When multiple joints are infected.
COMPLICATIONS OF MEDICAL OR SURGICAL THERAPY
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Associated with prolonged parenteral antimicrobial therapy or surgery
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Aminoglycoside-induced ototoxicity or nephrotoxicity
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Secondary bacteremia due to central vascular lines
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Mediastinitis or early postoperative prosthetic valve endocarditis
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Intravenous catheter-associated phlebitis
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Drug fever
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Allergic or idiosyncratic reactions to various antimicrobial agents
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Bleeding due to disturbances in coagulation caused by anticoagulants (in
prosthetic valve endocarditis)
Principles of Therapy
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Bactericidal antibiotics must be used.
Prolonged therapy is necessary (6 weeks).
Treatment is best started after multiple sets of
blood cultures have been taken.
Urgency in the initiation of therapy is required for
acute but not subacute endocarditis.
Synergistic combinations of antibiotics are used
when available.
Echocardiographic Features That Suggest Potential Need for Surgical Intervention
Vegetation
 Persistent vegetation after systemic embolization.
 Anterior mitral leaflet vegetation, particularly with size 10 mm.
 1 embolic events during first 2 wk of antimicrobial therapy.
 Increase in vegetation size despite appropriate antimicrobial therapy.
Valvular dysfunction
 Acute aortic or mitral insufficiency with signs of ventricular failure.
 Heart failure unresponsive to medical therapy.
 Valve perforation or rupture.
Perivalvular extension
 Valvular dehiscence, rupture, or fistula.
 New heart block.
 Large abscess or extension of abscess despite appropriate antimicrobial
therapy.
Predictors of death
Several studies have attempted to identify predictors of death in patients with IE.
Each patient may have one or more of the following:
 Infection with S. aureus , while mortality is lower with streptococcal infection.
 Heart failure.
 Diabetes mellitus.
 Embolic events .
 Perivalvular abscess .
 Larger vegetation size.
 Female gender.
 Contraindication to surgery.
 Low serum albumin.
 Persistent bacteremia.
 Abnormal mental status.
 Poor surgical candidacy.
Mimics of Infective Endocarditis
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Atrial myxoma.
Marantic endocarditis.
Left atrial thrombus.
Acute rheumatic fever with carditis.
Collagen vascular disease (SLE).
Neoplasms (carcinoid).
Antimicrobial Prophylaxis of Endocarditis
Potential Mechanisms
 Bactericidal activity.
 Reduce bacterial adherence.
 Reduce bacterial density in the wound at the
time of surgery (for prosthetic valves).
Prevention of Infective Endocarditis
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High risk
– Prosthetic valve
– Complex congenital heart disease
– Previous endocarditis
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Moderate risk
– Acquired valvular dysfunction (e.g. rheumatic valve)
– Mitral valve prolapse with regurgitation
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Negligible risk
– Mitral valve prolapse without regurgitation
– Rheumatic fever without valvular dysfunction
Cardiac Conditions Associated With the Highest Risk
of Adverse Outcome From Endocarditis for Which Prophylaxis
With Dental Procedures Is Reasonable
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Prosthetic cardiac valve or prosthetic material used for cardiac valve
repair.
Previous IE.
Congenital heart disease (CHD)
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Unrepaired cyanotic CHD, including palliative shunts and conduits.
Completely repaired congenital heart defect with prosthetic material or
device, whether placed by surgery or by catheter intervention, during
the first 6 months after the procedure.
Repaired CHD with residual defects at the site or adjacent to the site of
a prosthetic patch or prosthetic device (which inhibit endothelialization).
Cardiac transplantation recipients who develop cardiac
valvulopathy.
Dental Procedures for Which Endocarditis
Prophylaxis Is Reasonable
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All dental procedures that involve manipulation of gingival
tissue or the periapical region of teeth or perforation of the
oral mucosa.
The following procedures and events do not need
prophylaxis:
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routine anesthetic.
injections through noninfected tissue.
taking dental radiographs .
placement of removable prosthodontic or orthodontic appliances.
adjustment of orthodontic appliances.
Placement of orthodontic brackets .
shedding of deciduous teeth.
bleeding from trauma to the lips or oral mucosa.
ENDOCARDITIS PROPHYLAXIS FOR DENTAL PROCEDURES
ORAL
Adult Dosage
(30-60 minutes
before procedure)
Pediatric Dosage
(30-60 minutes
before procedure)
Amoxicillin
2 g P.O.
50 mg/kg
Penicillin allergy:
Cephalexin(Keflex,
and others)
2 g P.O.
50 mg/kg
OR
600 mg P.O.
20 mg/kg
500 mg P.O.
15 mg/kg
Clindamycin
OR Azithromycin
(Zithromax,
and others)
or Clarithromycin
(Biaxin, and others)
PARENTERAL (FOR PATIENTS UNABLE TO TAKE ORAL DRUGS)
Adult Dosage
(30-60 minutes before
procedure
Pediatric Dosage
(30-60 minutes
before procedure)
Ampicillin
2 g IM or IV
50 mg/kg IM or IV
OR Cefazolin or
Ceftriaxone
1 g IM or IV
50 mg/kg IM orIV
Penicillin allergy:
Cefazolin or Ceftriaxone
1 g IM or IV
50 mg/kg IM or IV
OR Clindamycin
600 mg IM or IV
20 mg/kg IV