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Infective endocarditis (IE) is characterized by infection of the endocardium (including the valves, mural endocardium, or septal defect) manifested by many cutaneous findings. Causes are diverse and can be broadly categorized as (1) acute and subacute native valve IE, (2) early and late prosthetic valve IE, (3) intravenous (IV) drug abuse IE, and (4) iatrogenic IE. The latter is associated with recent hospital admission or a procedure causing bacteremia or endocardial damage. Staphylococcus aureus is the most common causative organism, but many other bacteria and fungi are implicated. Janeway lesions (septic emboli forming microabscesses) are nontender, small, erythematous (occasionally with central hemorrhage) macules on the palms or soles. Osler nodes (immune complex deposition resulting in small-vessel vasculitis) consist of transient, tender, purplish nodules on the pulp of the fingers and toes. Subungual splinter hemorrhages are black, linear discolorations beneath the conjunctiva and nail plate. Murmurs, retinal hemorrhages, septic arthritis, and significant embolic episodes such as pulmonary embolism or cerebral vascular embolism may also be present.
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Management and Disposition
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Admission and empiric IV antibiotic therapy are the mainstay of treatment. Obtain blood cultures prior to antibiotic administration. Consult cardiology for emergent, echocardiographic assessment of the cardiac valves. Consult infectious disease for empiric antibiotic recommendations. Emergent surgical intervention may be required for valvular dysfunction or associated abscess.
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Acute bacterial endocarditis presents with fever (> 90% of patients) and a toxic patient; this contrasts with a more insidious presentation of subacute bacterial endocarditis.
Previous episode of IE, congenital heart disease, IV drug abuse, prosthetic heart valves, recent medical procedures, and cardiac transplants with valvulopathies are risk factors.
Although splinter hemorrhages in the nail bed have long been associated with IE, the most common causes are trauma, psoriasis, and onychomycosis. Proximal nail bed splinter hemorrhages have a higher likelihood of systemic disease (including IE, drug reactions, vasculitis, antiphospholipid antibody syndrome, and trichinosis).
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