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Endocarditis
Posted by: admin in Diseases
- An acute or subacute inflammation and infection of the endothelial layer of the heart and cardiac valves.
Causes and Incidence Acute bacterial endocarditis (ABE) is usually caused by Staphylococcus aureus. Hemolytic streptococcus, pneumococcus, and gonococcus have also been implicated. Subacute bacterial endocarditis (SBE) is usually caused by a streptococcal species but may also be caused by staphylococcal and Haemophilus organisms. Individuals at risk include those with a history of rheumatic heart disease, valvular disease, and congenital heart defects; those with prosthetic valves, pacemakers, or arteriovenous shunts; IV drug abusers; immunosuppressed individuals; and individuals who have had invasive cardiac procedures or surgery. Estimates of the incidence range from 0.16 to 5.4 cases per 100,000 hospital admissions. Men are more susceptible, and the mean age is about 55 years. The overall mortality rate is about 25%, but it rises to as high as 70% in elderly patients.
Disease Process The bacterial agent travels to the heart via the bloodstream after a transient bacteremia. They are attracted to and colonize a fibrin-platelet vegetation that formed as a result of previous endothelial damage. The pathogens are resistant to normal host defense mechanisms because the vegetation prevents access of the defense mechanisms to the microorganisms.
Symptoms
SBE
Onset is insidious with malaise, night sweats, chills, aching, anorexia, weight loss, intermittent fever, headache, and dyspnea over a period of weeks; when embolization occurs, petechiae of the skin and mucous membranes, splinter hemorrhages of the fingernails, macules on the palms and soles, retinal hemorrhage, and neurologic sequelae are also present; late signs include clubbing of the fingers and splenomegaly
ABE
Rapid onset of high fever, chills, and severe aching; rapid course with embolization and manifestations of various complications
Potential Complications The course of endocarditis is progressive and fatal without treatment. Complications include stroke, congestive heart failure, renal failure, meningitis, subarachnoid hemorrhage, and heart failure.
Diagnostic Tests
Clinical evaluation
History of symptoms, risk factors; heart murmur
Complete blood count
Anemia, leukocytosis, elevated erythrocyte sedimentation rate
Blood cultures
To identify causative agent
Echocardiography
To detect vegetations, abscesses, damaged valves, regurgitation
Urinalysis
Proteinuria, hematuria with renal involvement
Rheumatoid factor
Positive in 50% of individuals with SBE of at least 6 weeks’ duration
Treatments
Surgery
Removal of thrombi, valve replacement in cases of uncontrollable sepsis.
Drugs
Antiinfective drugs targeted at causative agent; aspirin for fever, aches.
General
Rest; forcing fluids during temperature elevation; high-calorie supplements; monitoring for complications.
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