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Infective
endocarditis, a microbial
infection of the endocardial surface of the heart, has been
classified as "acute" or "subacute –chronic" on the basis of
severity of the clinical presentation and the progression
of the untreated disease.
The
characteristic lesion, a vegetation, is composed of a
collection of platelets, fibrin, microorganisms, and
inflammatory cells.
It most
commonly involves heart valves but may also occur at the
site of a septal defect, on the chordae tendineae, or on
the mural endocardium.
REPORTING OF ENDOMYOCARDIAL BIOPSY
Men are more
often affected than women.
Clinical features:
Fever
; Cardiac manifestations ; Evidence of embolisms.
Fever is the
most common symptom and sign; however, it may be absent or
minimal in patients with congestive heart failure, severe
debility, chronic renal or liver failure.
Other common
symptoms of subacute infective
endocarditis include anorexia, weight loss,
malaise, and night sweats.
Most patients
with infective
endocarditis have a heart
murmur (most commonly preexisting), and patients may have
petechiae on the skin, conjunctivae, or oral mucosa, as
well as splenomegaly and other peripheral manifestations.
Unexplained
fever in a patient with a
prosthetic valve should prompt
careful evaluation for prosthetic-valve
endocarditis.
In earlier
literature the term "subacute" was used to refer infections that were
from 6 weeks to 3 months or more in duration. The term "acute" was
applied to patients who died in less than 6 weeks. Current effective
treatment has changed the course of the two varieties of endocarditis
, so there is now an overlapping in their clinical, bacteriologic and
pathologic features.
Modified Duke Criteria for the Diagnosis of
Infective Endocarditis: CLICK HERE
(NEJM)
Causative organism:
The most
frequent causative agents of endocarditis are the alpha- streptococcus
and staphylococci.
Infection by
other forms of streptococci (including enterococci), gram-negative
organisms, and various unusual organisms have increased in incidence.
Fungal
endocarditis from
Candida albicans,
Histoplasma capsulatum,
Coccidioides immitis, Aspergillus,
Cryptococcus neoformans,
Blastomyces dermatitidis, and Mucor has been reported.
Other commonly
implicated organisms include the HACEK group, (Haemophilus
aphrophilus, H paraphrophilus, H influenzae, H
parainfluenzae, Actinobacillus actinomycetemcomitans,
Cardiobacterium hominis, Eikenella corrodens, Kingella
species),
Coxiella burnetii , Bartonella
, Brucella and Legionella.
Predisposing factors:
The
development of infective endocarditis requires - i) the presence of
infective organisms in the bloodsream ; ii) preparation of the valve
surface to permit adherance and subsequent proliferarion of
circulating organism.
Conditions
associated with an increased incidence of infective
endocarditis include
poor
dental hygiene, long-term hemodialysis, and
diabetes
mellitus.
The highly
pathogenic organisms that produce endocarditis commonly arise
from infections elsewhere in the body (such as
pneumonia, skin
infections and renal infections) or may be introduced intravenously by
narcotic addicts.
Human
immunodeficiency virus (HIV) infection and infective endocarditis are
serious complications of injection drug use. Staphylococcus aureus
is the most frequent pathogen in these patients, and mortality
is higher among those with advanced HIV disease.
The presence
of underlying heart disease predisposes to infective endocarditis.
In a number of
cases of rheumatic fever organisms are implanted on the valves that
are thickened and fibrotic.
Visit:
EXAMINATION OF CARDIAC VALVES
;
CARDIAC VALVE DISEASE
.
Mitral-valve
prolapse is now the most common cardiovascular diagnosis
predisposing patients to infective
endocarditis.
Atherosclerotic
aortic valvular disease may also predispose to infective endocarditis.
Congenital
lesions predisposing to the infection include
bicuspid aortic valves , interventricular septal defects, subaoric stenosis and pulmonary
stenosis (including tetralogy of Fallot), coarction of the aorta, and
patent ductus arteriosus.
Prosthetic-valve
endocarditis accounts for a
number of cases of infective
endocarditis.
Mechanical
heart valves are probably at higher risk for infection than
are bioprostheses during the first three months after
surgery. Cases with onset within two months after surgery are called
early prosthetic-valve
endocarditis and are usually
acquired in the hospital. Cases that occur more than 12
months after surgery are called late prosthetic-valve
endocarditis and are
largely community-acquired.
All cases of
endocarditis seen at
hospitals are nosocomial. Infected intravascular devices
give rise to a number of these cases. Other sources of nosocomial
infective endocarditis
include genitourinary or gastrointestinal tract procedures
or surgical-wound infection.
Pathological Features:
The
characteristic pathologic feature of infective endocarditis is the
presence of vegetations on the valve cusps or leaflets.
The valve most
frequently affected is the
mitral .
Image1 ;
Image2;
Image3 .
The
aortic valve is the next most commonly involved. Rarely,
in narcotic addicts infective endocarditis involves the
tricuspid
valve.
Image4
The vegetations
vary in size from a few millimeters to a centimeter or more and are
gray, reddish, or brown fairly firm but friable single or multiple and
flat, filiform, fungating or polypoid.
Image5
Because the
vegetations are friable they give rise to emboli (D/D- this is absent
in
rheumatic lesions
).
The vegetations
tend to localize on the atrial surface of the atrioventricular valves
and on the ventricular surfaces of the semilunar valves.
They arise from
the contact areas of the cusps or leaflets but tend to spread along
the valve surfaces onto the adjacent mural endocardium. The chordae
tendineae may be involved. Ulceration and perforation of the valve
leaflets or cusps may develop.
Microscopic
features:
Image1
;
Image2
;
Image3
;
Image4
;
Image5
;
Image6
;
Image7 .
Microscopically, the vegetations consist of fibrin, platelets,
leukocytes, and the infecting organism, and in the underlying valve a
nonspecific inflammatory reaction with varying degrees of necrosis is
present.
In the
acute, fulminant cases, neutrophils are prominent, and there may be
extensive necrosis with abscess formation. The abscess may extend to
the valve rings.
In the prolonged
cases, varying degrees of granulation tissue and fibroblastic
proliferation with mononuclear inflammatory cells are seen.
Sometimes
foreign-body giant cells are noted in the necrotic area.
Bacterial
masses may be present in the periphery of the fibrin, in a position to
seed the bloodstream with organism.
Healing of the
vegetation may take place, particularly after antibiotic therapy,
There is invasion
of the fibrinous layer by granulation tissue, resulting in fibrosis.
Hyalinization,
calcification and endothelialization of the vegetation subsequently
occur.
If calcification is extensive a severely deformed nodular valve may
occur.
In fungal endocarditis microscopically many organisms are usually
present in the vegetations.
The inflammation
of the underlying endocardium is consistent with the nature of the
infecting organisms and includes granulomatous or acute and chronic
nonspecific inflammation with or without suppuration. |
