Transcript document

INFECTIVE ENDOCARDITIS
INTRODUCTION
• Endocarditis is defined as an infection,
usually bacterial, of the endocardial
surface of the heart.
• Infective endocarditis primarily affects the
cardiac valves, although the septa
between the chambers or the mural
endocardium may be involved in some
cases.
• infective endocarditis has been
categorized as acute or subacute,
depending on the length of symptoms
before presentation; . A classification
that considers the causative organism
and the valve involved is more clinically
relevant
ACUTE IE
• Acute IE is most commonly caused by
Staphylococcus aureus. It presents
with marked toxicity and progresses
over days to several weeks to valvular
destruction and metastatic infection
SUB ACUTE IE
• Subacute IE, usually caused by
viridans streptococci, enterococci,
coagulase-negative staphylococci, or
gram-negative coccobacilli, evolves
over weeks to months with only
modest toxicity and rarely causes
metastatic infection.
Incidence Of Infective
Endocarditis
• The incidence of infective endocarditis is
approximately 1.7-6.2 cases per 100 000
patient /year,although rates are higher in at
risk cohorts such as intravenous drug
users.
• Men are more often affected than women (in a ratio of
2:1), and the incidence progressively increases with age.
Underlying degenerative aortic and mitral valve disease
now predominate over rheumatic disease, although in
one recent French study 47% of patients with infective
endocarditis presented without previous knowledge of an
underlying cardiac disorder
PREDISPOSING CONDITIONS ASSOCIATED
WITH INCREASED RISK OF ENDOCARDITIS
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More Common
Mitral valve prolapse with murmur
Degenerative valvular disease
Intravenous drug use
Prosthetic valve.
Congenital abnormalities (valvular or
septal defect)
Less Common
• Rheumatic heart disease
• Hypertrophic obstructive
cardiomyopathy
• Pulmonary-systemic shunts.
• Coarctation of the aorta
• Complex cyanotic congenital heart
disease
Infective endocarditis:
patient groups
• Children with IE:
congenital heart disease
Staphylococcus (neonate),
Streptococcus group B (children), S. pneumonia (rare)
• Adults with IE:
Rheumatic heart disease: MV (F>M), AV (M>F)
Congenital heart disease: PDA, VSD, bicuspid AV
Infective endocarditis:
patient groups
• IV drug abusers with IE:
TV (46—78%)  MV (24—32%)  AV (8—19%)
S. aureus, GNB (Pseudomonas), polymicrobial
HIV: 73%; increased mortality (CD4 < 200)
• Prosthetic valves with IE:
early (< 60 days): surgical complication,
late (> 60 days): community or nosocomial
ring abscess, annular invasion, paravalvular regurgitation
Infective endocarditis:
nosocomial
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Infected intracardiac device and catheter
GI or GU tract surgery or instrumentation
High mortality (40—56%)
GPC ( S. aureus, CONS, Enterococcus)
S. aureus catheter related bacteremia .
Infective endocarditis:
microorganism
• Streptococcus viridans:
35 — 65% NVE
normal flora of the oropharynx
• Streptococcus pneumoniae:
alcoholism
aortic valve
concurrent pneumonia or meningitis
• Enterococcus:
normal GI tract flora and cause GU infection
5—15% NVE and PVE
Infective endocarditis:
microorganism
• Staphylococcus:
Coagulase-positive: S. aureus
highly toxic febrile
30—50% CNS involvement
Coagulase-negative: S epidermidis
Major cause of PVE
Infective endocarditis:
microorganism
• Gram negative bacteria:
upper respiratory tract and oropharyngeal flora
P. aeruginosa: most common in GNB IE
HACEK: haemophilus spp., Actinobacillus actinomycetemcomitans,
Cardiobacterium hominis, Eikenella corrodens, Kingella kingae
• Fungus:
drug abuser and prosthetic valve
common: C. albicans (PVE); C. parapsilosis
(NVE)
Pathogenesis of Endocarditis
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Inoculation of bacteria colonizing a mucosal (e.g., oral
mucosa) or peripheral tissue site into the bloodstream
Transient bacteremia of a serum-resistant pathogen
capable of adhering to a cardiac valvular surface.
Turbulent blood flow across the valve
• Bacterial adherence to cardiac valvular surface
Pathogen - host tissue interaction resulting in vegetation
formation and local tissue damage
– Bacterial persistence
Dissemination of infection to other tissue sites and
elicitation of systemic findings
Factors Contributing to the Pathogenesis
of Endocarditis
• Hemodynamics - blood flow
patterns
• Bacterial properties
• Host factors
• Local destruction of intracardiac infection:
valve, chordae tendineae, fistula, paravalvular abscess,
conduction
• Distant embolization with infarct or infection:
• Hematogenous seeding with bacteremia:
metasttic infection,
• Immune-complex or antibody reaction: IgM,
IgA, IgG, Osler’s node, Rheumatoid factor, Roth’s spot
Differential Diagnosis: ABE
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Sepsis
Pneumonia
Meningitis
Brain abscess
Stroke
Malaria
Acute pericarditis
• Vasculitis
• DIC
Differential Diagnosis: SBE
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As FUO
Rheumatic fever
Osteomyelitis
Tuberculosis
Meningitis
Abdominal infection
Glomerulonephritis
• Myocardial infarction
• Stroke
• Connective tissue
diseases
• Occult malignancy
• Chronic heart failure
• Pericarditis
INFECTIVE ENDOCARDITIS:
Symptoms
– High grade fever and
chills
– SOB
– Arthralgias/ myalgias
– Abdominal pain
– Pleuritic chest pain
– Back pain
Signs
• Fever
• Changing Heart murmur
• Nonspecific signs –
• petechiae,
“splinter” hemorrhages,
• clubbing,
• splenomegaly,
• neurologic changes
• More specific signs –
• Osler’s Nodes,
• Janeway lesions,
• Roth Spots
Petechiae
1. Nonspecific
2. Often located on extremities
or mucous membranes
Splinter Hemorrhages
1. Nonspecific
2. Nonblanching
3. Linear reddish-brown lesions found under the nail bed
4. Usually do NOT extend the entire length of the nail
Osler’s Nodes
1. More specific
2. Painful and erythematous nodules
3. Located on pulp of fingers and toes
4. More common in subacute IE
Janeway Lesions
1. More specific
2. Erythematous, blanching macules
3. Nonpainful
4. Located on palms and soles
Duke Criteria For The Diagnosis Of
Infective Endocarditis
• Major Criteria
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Positive blood culture .
A). Typical micro-organism consistent with
infective endocarditis from two separate blood cultures :
i) Streptococci viridans ,Streptococcus bovis
HACEK group
OR
(ii) community-acquired Staphylococcus aureus
enterococci, in the absence of a primary focus or
• B. Micro-organisms consistent with
infective endocarditis from persistently
positive blood cultures defined as:
i) at least two positive cultures of
blood samples drawn > 12h apart or
ii) all three of these or a majority of
four or more separate cultures of blood
(with first and last sample drawn at least
1h apart).
• 2. Evidence of endocardial involvement
• A. Positive echocardiogram
for infective
endocarditis as defined as:
• (i) oscillating intracardiac
mass on valve or
supporting structures, in the path of regurgitant jets, or on
implanted material in the absence of an alternative
anatomical explanation or
(ii)
abscess
or,
(iii) new partial dehiscence of prosthetic valve.
B. New valvular regurgitation (worsening or
changing of pre-existing murmur not sufficient)
Minor Criteria
• 1. Predisposition: predisposing heart
condition or intravenous drug use
2. Fever: temperature > 38 °C
3. Vascular phenomena: major arterial
emboli, septic pulmonary infarcts,
mycotic aneurysm, intracranial
haemorrhages, and Janeway's lesions
• 4. Immunological phenomena:
glomerulonephritis, Osler's nodes, Roth
spots, and rheumatoid factor
• 5. Microbiological evidence: positive blood
culture but does not meet a major criteria or
serological evidence of active infection with
organism consistent with infective
endocarditis
• 6. Echocardiographic findings: consistent
with infective endocarditis but do not meet a
major criteria.
Lab: CBC
• Anemia
– Mild to moderate
– Normocytic normochromic
• Leukocytosis: not reliable
Routine Tests
• Elevated ESR: 90%
• Elevated CRP: 96%
• Urinalysis
– Microscopic hematuria or proteinuria: >50%
– RBC casts & heavy proteinuria: glomerulonephritis
– Gross hematuria: renal infarction
Blood Culture
• B/C should be done in all patients with
undiagnosed fever and a heart murmur
• B/C send on the first day
• Aerobic + anaerobic
• Additional B/C on day 3 if necessary
(when diagnosis is likely but B/C yielded negative
results)
ECG
• Repeated or even continuous ECG
monitoring
• Frequent APC or PVC
• Prolonged PR interval
• Myocardial infarction
Echocardiography
• The diagnosis of infective
endocarditis is frequently suggested
on the basis of echocardiography,
which is the diagnostic procedure of
choice for detecting valvular
vegetations.
• The echocardiographic features typical for
infective endocarditis are
• (a) an oscillating intracardiac mass on a valve or
supporting structure or in the path of a
regurgitation jet or on a device,
• (b) abscesses,
• (c) new partial dehiscence of a prosthetic valve,
or
• (d) new valvular regurgitation. The initial
attachment site of a vegetation is usually on the
ventricular surface of the semilunar valves and
on the atrial surface of the atrioventricular valves
Image Study: CXR
• Provide evidence of early CHF
• Valvular calcification
• Multiple small, patchy infiltrates in the
lungs of an Iv drug user with fever:
septic emboli from right-sided IE
Image Study: CT/MRI
• For defining the cause of focal
neurologic lesions
• Cerebral emboli
Image Study: Cardiac Cath
• Indication:
– In patients >40 y/o (for possible concurrent CAD)
– When surgical intervention is considered
Diagnostic Criteria
• DEFINITE INFECTIVE ENDOCARDITIS
• Pathologically proven infective endocarditis or Clinical
criteria meeting either Two major criteria or one
major and three minor criteria or five minor criteria
• POSSIBLE INFECTIVE ENDOCARDITIS
• One major or one minor or three minor criteria
• REJECTED INFECTIVE ENDOCARDITIS
• Firm alternative diagnosis or Resolution of infective
endocarditis syndrome with antibiotic therapy of ≤4
days or No pathologic evidence of infective
endocarditis at surgery or autopsy with antibiotic
therapy of ≤4 days
Culture-Negative Infective Endocarditis
• Blood cultures fail to isolate an etiologic agent in 3% to 23% of
cases . Culture-negative IE is most often associated with
antibiotic use within the previous 2 weeks. Less frequently,
intracellular pathogens not detected using standard culture
approaches may be the cause . If blood cultures are negative ,
consideration should be made to analyze serum for Bartonella,
Coxiella, and Chlamydia species antibodies . If the patient
requires valve surgery, RNA polymerase chain reaction
amplification of valve tissue often yields an etiologic agent
• the search for a causative organism remains fruitless,
consider noninfectious etiologies such as marantic or
Libman-Sacks endocarditis and atrial myxoma.
Clinical Criteria
• 2 major
• 1 major + 3 minor
• 5 minor
INDICATIONS FOR SURGERY IN
ENDOCARDITIS
Indication
NATIVE VALVE ENDOCARDITIS
• Acute aortic insufficiency or mitral regurgitation with heart
failure I
• Acute aortic insufficiency with tachycardia and early
closure of the mitral valve on echocardiogram I
• Fungal endocarditis I
• Evidence of annular or aortic abscess; sinus or aortic true
or false aneurysm; valve dehiscence, rupture, perforation,
or fistula I
• Evidence of valve dysfunction and persistent infection
after a prolonged period (7–10 days) of appropriate therapy,
provided there are no noncardiac causes for infection I
• Recurrent emboli after appropriate antibiotic therapy I
• Infection with gram-negative organisms or organisms with
a poor response to antibiotics in patients with evidence of
valve dysfunction I
• Anterior mitral leaflet vegetation
(especially >10 mm) or persistent
vegetation after systemic embolization IIa
• Increase in vegetation size despite
appropriate antimicrobial therapy IIb
• Early infections of the mitral valve that can
probably be repaired III
• Persistent fever and leukocytosis with
negative blood cultures III
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PROSTHETIC VALVE ENDOCARDITIS
Early prosthetic valve endocarditis (<2
months after surgery) I
Heart failure with prosthetic valve
dysfunction I
Nonstreptococcal endocarditis I
Evidence of perivalvar leak, annular or
aortic abscess, sinus or aortic true or
false aneurysm, fistula formation, or
new-onset conduction disturbances I
• Persistent bacteremia after 7–10 days of
appropriate antibiotic therapy without
noncardiac causes for bacteremia IIa
• Recurrent peripheral embolus despite
therapy Iia
• Vegetation of any size seen on or near the
prosthesis IIb
• Class III: Conditions for which there is
evidence and/or general agreement that
the procedure/treatment is not useful and
in some cases may be harmful
PROPHYLAXIS
AGAINST INFECTIVE
ENDOCARDITIS
PROPHYLACTIC
ANTIBIOTIC
REGIMENS
Dental , oral , respiratory &
oesophageal procedures
Oral Amoxycillin 2 gm 1 hour before the
procedure
• if allergic to penicillin :
Clindamycin 600 mg or
Azithromycin or clarithromycin 500
mg 1 hour before the procedure
Gastrointestinal &
Genitourinary procedures
parenteral amoxicillin 2 gm +
gentamycin 1.5 mg / kg
1 hour before and 6 hours after the
procedure
• if allergic to penicillin :
Vancomycin 1 gm over 1-2 hours +
gentamycin 1.5 mg / kg IV or IM
Patients receiving antibiotics
for other reasons
• the main danger is resistant organisms
• Clindamycin , Azithromycin or
Clarithromycin are alternatives
Patients undergoing cardiac
surgery or procedures
involving infected tissue :
• Clindamycin or Vancomycin +
Aminoglycosides are effective
• Prognosis
• Untreated, infective endocarditis is uniformly fatal.
Aggressive medical and surgical management, however,
has dramatically improved the outcome. Mortality overall
from both native and prosthetic valve endocarditis remains
fairly high, ranging from 17 to 36%. Certain subgroups carry
a lower risk of death (endocarditis related to viridans
streptococci); endocarditis due to S. aureus, fungal
endocarditis, and zoonotic endocarditis have higher
mortalities. Heart failure and CNS events are the most
frequent causes of death.
• Endocarditis recurs in 12 to 16% of patients and is more
common in injection drug users, elderly people, and
patients with prosthetic valves. The rate of relapse also
varies according to the causative organism. Easily treated
infections, such as those with α-hemolytic streptococci,
have a low rate of relapse (∼5%), whereas infections with
organisms that are more difficult to eradicate may have
significantly higher rates.
• Future Directions
• As cardiac imaging technology continues to improve, the
duration of treatment of endocarditis may be dictated in
part by the characteristics of visualized vegetations. In
addition, now that large vegetations have been
demonstrated to cause more embolic events, interventions
to remove vegetations “prophylactically” (e.g., valve repair
and vegectomy) or to introduce agents that prevent the
formation or promote the dissolution of vegetations may be
feasible. Finally, novel therapeutic approaches (for
instance, antibacterial antibodies and cell wall–specific
enzymes) that act as adjuncts to antibiotics in facilitating
bacteriologic clearance are in development.
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