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Summary
Infective endocarditis (IE) is an infectious inflammation of the endocardium that affects
the heart valves. The condition is a result of bacteremia, which is most commonly
caused by dental procedures, surgery, distant primary infections, and nonsterile
injections. IE clinically presents with either an acute or subacute course. Acute disease
is usually caused by Staphylococcus aureus and causes rapid endocardium destruction.
Subacute progression is most commonly caused by viridans streptococci species and
generally affects individuals with pre-existing damage to the heart valves,
structural heart defects, or the presence of prosthetic valves. Unlike acute disease, in
which patients develop symptoms over a period of hours to days, subacute disease is
associated with a progression of symptoms over weeks to months. Clinical features
include constitutional symptoms (fatigue, fever/chills, malaise) in combination with
signs of pathological cardiac changes (e.g., new or changed heart murmur, heart
failure signs) and possibly manifestations of subsequent damage to other organs
(e.g., glomerulonephritis, septic embolic stroke). Diagnosis is made based on the Duke
criteria, whose main features include positive blood cultures and evidence of
endocardial involvement in echocardiography. Initial treatment of IE consists of empiric
IV antibiotic therapy, which is then adapted to blood culture results and continued for
four to six weeks. Prophylaxis is only administered in specific circumstances, e.g., in
patients with preexisting heart conditions undergoing dental or surgical procedures. If
left untreated, infective endocarditis can be fatal within a few weeks.
NOTES
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Etiology
Pathogens
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Risk factors
Demographics
o Male sex
Preexisting conditions
o Previous IE
Bacteremia
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Pathophysiology
Pathogenesis: localized infection or contamination
→ bacteremia → bacterial colonization of damaged valve areas
→ formation of fibrin clots encasing the vegetation → valve
destruction with loss of function
Clinical consequences
#-The valves consist of bradytrophic, avascular tissue and are therefore relatively susceptible to infection. However,
undamaged native valves are usually not susceptible to either colonization by most types of bacteria (except for S.
aureus) or thrombusformation.
#- Osler nodes -Painful subcutaneous nodules on the pads of the fingers and toes that typically occur in protracted cases
of infective endocarditis. The lesions are due to immune complex-mediated vasculitis that most likely occurs as a
sequelae of microthrombi occluding the vasculature.
#- The tricuspid valve is the most commonly affected valve in IV drug users!
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Clinical features
Acute bacterial endocarditis Subacute bacterial endocarditis Prosthetic valve
endocarditis
Constitutional symptoms
Fever and chills (∼ 90% of cases), tachycardia
Arthralgias, myalgias
Cardiac manifestations
New heart murmur development or change to a preexisting one
Arrhythmias
Possible arthritis
FROM JANE - Fever, Roth's spots, Osler nodes, Murmur, Janeway lesions, Anemia, Nail
bed hemorrhage, Emboli
Notes
Constitutional symptoms -A collection of nonspecific symptoms such as weight loss, fever, chills, night sweats, changes
in appetite, changes in sleep, chronic pain, fatigue, and malaise. Typically evaluated on a review of systems with further
evaluation based on pertinent positives and negatives.
Infection spreads to the valve annulus and/or cardiac septum (paravalvular extension) → abscessformation → new-onset
conduction delay → arrhythmia
Perivalvular abscess- A myocardial abscess that involves structures near the cardiac valve. Can cause conductive
abnormalities such as third-degree atrioventricular block. Typically caused by infective endocarditis due to suppurative
species (e.g., Staphylococcus aureus).
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Diagnostics
Laboratory studies
Best initial test: blood cultures
o Vascular abnormalities
o Immunologic disorder
o Microbiology
***Before starting antibiotic treatment. Transport blood cultures (3 to 5 separate sets) to the lab within 2 hours.
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Pathology
Pathogenesis
Acute disease (leading to valve insufficiency, septic embolic infarcts,
tendinous cord rupture)
1. Ulceration
Differential diagnoses
Noninfective endocarditis (nonbacterial thrombotic
endocarditis)
Description: rare, noninfectious form of endocarditis due
to sterile platelet thrombus formation on
the heart valves(usually mitral and aortic valves)
Etiology
Clinical features
Diagnostics
Clinical course
Treatment
Empirical therapy
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Prosthetic valves Generally the same antibiotic regimen as for native valves, but longer
duration (at least 6 weeks)
Exceptions for staphylococci
o Methicillin-susceptible: nafcillin (or oxacillin, cefazolin)
Condition/patient Antibiotic therapy
group
+ rifampin + gentamicin
o Methicillin-resistant: vancomycin + rifampin + gentamicin
Drug of choice
o Second-line
: ampicillin-sulbactam , IV fluoroquinolone
Duration of therapy
If blood cultures are negative, but there is strong clinical suspicion of bacterial endocarditis, treat with penicillin (or
vancomycin) plus an aminoglycoside.
Use vancomycin if the patient is beta-lactamintolerant or if simultaneous treatment of other pathogens is necessary, e.g.,
MRSA.
Infective endocarditis in prosthetic valves is much harder to treat than in native valves. Surgical valve replacement may
be required.
Because IV drug users are often noncompliant, shorter regimens that possibly include oral therapy are being
investigated. These alternative regimens should only be used if the pathogen is susceptible to them, if the patient does
not have IE of the mitral or aortic valve, and if no complications (e.g., perivalvular abscess, heart failure) have occurred.
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Prevention
Endocarditis prophylaxis:
Regimens
References: [15][32]