What is endocarditis Endocarditis is an inflammation of the
inner layer of the heart, the endocardium. It usually involves the
heart valves (native or prosthetic valves). Other structures that
may be involved include the interventricular septum, the chordae
tendineae, the mural endocardium, or even the surfaces of
intracardiac devices
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Endocarditis is characterized by a prototypic lesion, the
vegetation, which is a mass of platelets, fibrin, microcolonies of
microorganisms, and scant inammatory cells. In the subacute form of
infective endocarditis, the vegetation may also include a center of
granulomatous tissue, which may fibrose or calcify. There are
several ways to classify endocarditis. The simplest classification
is based on etiology: either infective or non- infective, depending
on whether a microorganism is the source of the inflammation or
not. Regardless, the diagnosis of endocarditis is based on clinical
features, investigations such as an echocardiogram, and blood
cultures demonstrating the presence of endocarditis-causing
microorganisms.
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Endocarditis begins as endothelial damage and sterile surface
microthrombus, which, in the absence of bacteremia, regresses or
grows into macrothrombi (noninfectious endocarditis). Malformed
stenotic or regurgitant valves Malformed stenotic valves, or
especially regurgitant valves, are predisposed to endocarditis. In
the presence of bacteremia or fungemia, even transient or those
with low microbe counts, microthrombi become infected, by adhesion
and colonization of the thrombotic surfaces. Growth of organisms
results in an inflammatory response, with neutrophil infiltration,
enlargement of the thrombus, recruitment of matrix
metalloproteinases (MMPs), and eventual destruction of collagen and
cusp perforation. In approximately 25% of patients, however,
neither structural valve abnormalities nor predisposing conditions
are evident. Valve abnormalities, disease, prosthesis, and previous
surgery Congenital valve abnormalities, acquired valve disease,
prostheses, and previous cardiac surgery for structural congenital
heart disease increase the risk for endocarditis and are
indications for antibiotic prophylaxis for dental and other
invasive procedures. In nosocomial endocarditis, bacteremic
conditions are present in nearly 40% of cases and include
intravenous drug abuse, hemodialysis, catheterizations, and
intravascular devices
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Infective endocarditis Since the valves of the heart do not
receive any dedicated blood supply, defensive immune mechanisms
(such as white blood cells) cannot directly reach the valves via
the bloodstream. If an organism (such as bacteria) attaches to a
valve surface and forms a vegetation, the host immune response is
blunted. The lack of blood supply to the valves also has
implications on treatment, since drugs also have difficulty
reaching the infected valve. Normally, blood flows smoothly past
these valves. If they have been damaged (from rheumatic fever, for
example) the risk of bacteria attachment is increased
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Rheumatic fever is common worldwide and responsible for many
cases of damaged heart valves. Chronic rheumatic heart disease is
characterized by repeated inflammation with fibrinous resolution.
The cardinal anatomic changes of the valve include leaflet
thickening, commissural fusion, and shortening and thickening of
the tendinous cords. The recurrence of rheumatic fever is
relatively common in the absence of maintenance of low dose
antibiotics, especially during the first three to five years after
the first episode. Heart complications may be long-term and severe,
particularly if valves are involved. While rheumatic fever since
the advent of routine penicillin administration for Strep throat
has become less common in developed countries, in the older
generation and in much of the less- developed world, valvular
disease (including mitral valve prolapse, reinfection in the form
of valvular endocarditis, and valve rupture) from undertreated
rheumatic fever continues to be a problem.
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Subacute bacterial endocarditis Also called ( endocarditis
lenta ) is a type of endocarditis (more specifically, infective
endocarditis). It is usually caused by a form of streptococci
viridans bacteria that normally live in the mouth and throat
(Streptococcus mutans, mitis, sanguis or milleri). Other strains of
streptococci (bovis and equines) can also cause subacute
endocarditis, usually in patients who have a form of
gastrointestinal cancer. Additional causes are Enterococci (urinary
tract infections) and coagulase negative staphylococci such as
Staphylococcus epidermidis (skin).
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Diagnosis and Prognosis Osler's nodes as well as Roth's spots
can indicate this condition. Nail clubbing is also often seen in
subacute endocarditis. Underlying structural valve disease is
usually present in patients before developing subacute
endocarditis. It is less likely to lead to septic emboli than is
acute endocarditis, but subacute endocarditis has a relatively slow
process of infection and, if left untreated, can worsen for up to
one year before it is fatal. In cases of subacute bacterial
endocarditis, the causative organism (streptococcus viridans) needs
a previous heart valve disease to colonize and cause such
disease.
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On the other hand, in cases of acute bacterial endocarditis,
the organism can colonize on the healthy heart valve, causing the
disease. The standard treatment is with a minimum of four weeks of
high-dose intravenous penicillin with an aminoglycoside such as
gentamicin. The use of high-dose antibiotics is largely based upon
animal models. Leo Loewe of Brooklyn Jewish Hospital was the first
to successfully treat subacute bacterial endocarditis with
penicillin. Loewe reported seven cases in 1944.
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Roths spot
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Non-infective endocarditis Nonbacterial thrombotic endocarditis
(NBTE), also called marantic endocarditis is most commonly found on
previously undamaged valves. As opposed to infective endocarditis,
the vegetations in NBTE are small, sterile, and tend to aggregate
along the edges of the valve or the cusps. Also unlike infective
endocarditis, NBTE does not cause an inflammation response from the
body. NBTE usually occurs during a hypercoagulable state such as
system wide bacterial infection, or pregnancy, though it is also
sometimes seen in patients with venous catheters. NBTE may also
occur in patients with cancers, particularly mucinous
adenocarcinoma where Trousseau syndrome can be encountered.
Typically NBTE does not cause many problems on its own, but parts
of the vegetations may break off and embolize to the heart or
brain, or they may serve as a focus where bacteria can lodge, thus
causing infective endocarditis
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Another form of sterile endocarditis, is termed Libman- Sacks
endocarditis; this form occurs more often in patients with lupus
erythematosus and is thought to be due to the deposition of immune
complexes. Like NBTE, Libman-Sacks endocarditis involves small
vegetations, while infective endocarditis is composed of large
vegetations. These immune complexes precipitate an inflammation
reaction, which helps to differentiate it from NBTE. Also unlike
NBTE, Libman-Sacks endocarditis does not seem to have a preferred
location of deposition and may form on the undersurfaces of the
valves or even on the endocardium.
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Causative organisms The organisms responsible for most cases of
infectious endocarditis are gram-positive cocci: streptococci and,
increasingly, staphylococci. The most common microbial infection is
staphylococcus. Hospital-acquired infection is often associated
with hemodialysis, prosthetic valvular infection, malignancies, and
vascular interventions. Some cases of culture-negative endocarditis
are caused by fastidious gram-negative organisms of the Haemophilus
parainfluenzae, Actinobacillus, Actinomycetemcomitans,
Cardiobacterium hominis, Eikenella corrodens, Kingella kingae
(HACEK) group, which constitutes approximately 1-3% of cases of
community-acquired endocarditis on native and prosthetic valves,
and may have a relatively good prognosis.
Organisms responsible for nosocomial endocarditis include the
following: S aureus (60-80%; majority, MRSA) Alpha-hemolytic
streptococci (< 5%) Enterococcus (5%) Culture negative (5%)
Fungi (10%) S epidermidis (coagulase negative; < 5%) Others (eg,
E coli, Klebsiella, Corynebacterium; 5-10%) The rate of
culture-negative endocarditis varies from 7% to 33% and is
increased in community-acquired infections because of antibiotic
treatment before diagnosis. No association exists between culture
negativity and underlying etiology or risk factors. If a full
work-up is performed at a tertiary reference center, including
serology and culture for esoteric organisms and polymerase chain
reaction (PCR), an etiology is found in over 75% of cases of
endocarditis with an initial negative culture. The most common
organisms are C burnetii and Bartonella species.
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SIGNS AND SYMPTOMS Fever Chills Sweating Malaise Weakness
Anorexia weight loss Splenomegaly flu like feeling cardiac murmur
heart failure patechia of anterior trunk Janeway's lesions
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Diagnosis Examination of suspected infective endocarditis
includes a detailed examination of the patient, complete history
taking, and especially careful cardiac auscultation, various blood
tests, ECG, cardiac ultrasound (echocardiography). In the overall
analysis of blood revealed the typical signs of inflammation
(increased erythrocyte sedimentation rate, leukocytosis). It is
also necessary to sow twice venous blood in order to identify the
specific pathogen (this requires two samples of blood). Negative
blood cultures, however, does not exclude the diagnosis of
infective endocarditis. The decisive role is played by
echocardiography in the diagnosis (through the anterior chest wall
or transesophageal), with which you can reliably establish the
presence of microbial vegetation, the degree of valvular and
violations of the pumping function of the heart
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TREATMENT Treatment of infectious endocarditis includes
antibiotics, and, possibly, surgery if the valve is irreversibly
insufficient. Surgical options include replacement, and repair if
possible. In general, between 14% and 37% of cases require
surgery.
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PROGNOSIS The overall mortality of infectious endocarditis is
approximately 20-25%, and it is increased with advanced patient
age, left- sided disease, methicillin-resistant S aureus (MRSA)
infection, and chronic renal failure. For staphylococcal
endocarditis, mortality is associated with age 60 years or older,
female sex, community- acquired infection, absence of heart murmur,
presence of congestive heart failure, and central nervous system
involvement. The mortality rate of MRSA endocarditis in
hemodialysis patients is as high as 90%. The long-term prognosis of
patients with negative blood culture infective endocarditis has
been found to be similar to that of patients with positive blood
culture infective endocarditis across all age ranges.
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