Infective endocarditis is a microbial infection on the endothelial surface of the heart, which includes one or more heart valve, the mural endocardium or septal defect. IE produce a wide variety of systemic signs and symptoms through a several mechanisms, including both sterile and infected embolic and various immunological phenomena.
IE generally occur as a consequence of nonbacterial thrombotic endocarditis, which result s from turbulence or trauma to the endothelial surface of the heart. A transient bacteriemia then seeds the sterile platelet/fibrin thrombus, which IE as the end result. Pathologic effects due to infection can include local tissue destruction and embolic phenomena. In addiction, secondary autoimmune effects, such as immune complex glomerulonephritis and vasculitis, can occur.
Endocarditis can be broken down into the fallowing categories:
.Native valve endocarditis: Acute (Staphylococcus aureus, high virulence, large
vegetation on previously normal valves).
Subacute (Streptococcus viridans, low virulence,
smaller vegetation on congenitally abnormal or diseased
vales.
Sequela of dental procedures. More insidious onset)
.Prosthetic valve endocarditis, early and late.
.Intravenous drugs abuse endocarditis.
Other types include.
_Pacemaker IE.
_Nosocomial IE.
Endocarditis may also be nonbacterial secondary to malignancy or hypercoagulable state (marantic/thrombotic endocarditis).
Streptococcus bovis is present in colon cancer and staphylococcus epidermidis on prosthetic valves.
Mitral valve is most frequently involved, closely fallowed by the aortic valve, the combined mitral and aortic valve, the tricuspid valve (associated with intravenous drugs abuse), and, rarely, the pulmonic valve.
General finding:
Fever (most common symptom).
Roth’s spots (round white spot on retina surrounded by hemorrhage).
Osler’s node (tender raised lesions on finger or toes pads)
New murmur (caused by valvular damage)
Janeway lesions (small erythematous lesion on palm or sole)
Anemia.
Splinter hemorrhages on nail bed.
Signs of neurological disease: Embolic stroke with focal neurologic deficit is the most common etiology.
Signs of systemic septic emboli are due to left heart disease and are more common associated with mitral valve vegetation. Multiples embolic pulmonary infections or infarction are due to right heart disease.
Signs of congestive hear failure.
Diagnosis considerations.
The clinical criteria for definitive infectious endocarditis (Duke Criteria) include 2 major, 1 major and 3 minor, or 5 minor.
Major criteria.
Positive blood culture: 2 separate cultures for a typical endocarditis microorganism, persistently positive cultures, or evidence of infection with a Coxiella organism and/or Q fever.
Positive echocardiography finding: oscillating mass and/or vegetation, paravalvular abscess, or dehiscence of prosthetic valve.
New valvular regurgitation.
Minor criteria.
Predisposition: history of IV drug use or congenital heart disease).
Fever with a temperature of more than 38 º C.
Vascular phenomena (arterial emboli, septic pulmonary infarcts, intracranial hemorrhage, conjunctival hemorrhage, Janeway lesions).
Immunologic phenomena (glomerulonephritis, Osler node, Roth spots, a positive result for rheumatoid factor).
Positive blood culture findings without meeting the criteria above or serologic evidence of active infection consistent with endocarditis.
Treatment: Antibiotic are the mainstay of treatment. Goals to maximize treatment success are early diagnosis, accurate microorganism identification, and reliable susceptibility testing, prolonged intravenous administration of bactericide antimicrobial agents, proper monitoring of potentially toxic antimicrobial regimens, and aggressive surgical managements of correctable mechanical complications.
Prognosis largely depends on whether or not complications develop. If left untreated, IE is generally fatal. Early detection and appropriate treatment of this uncommon disease can be lifesaving.
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