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Infective endocarditis (IE) is the result of infection and damage to the endocardium of the heart due to either a cardiac structural abnormality or risk factors such as injection drug use, indwelling catheters, poor dental hygiene, or infection with HIV. IE most commonly involves the mitral valve and has 3 main classifications. Native valve endocarditis is the most common form (59% to 70%) and most often affects patients with mitral valve prolapse, bicuspid aortic valve, calcific aortic stenosis, or rheumatic heart disease. Streptococcus viridians, Staphylococcus aureus, and enterococcus are most commonly involved with mortality rates from 16% to 27%. Endocarditis involving injection drugs is the second classification and has an estimated incidence of 2% to 5%. There is a predilection for the tricuspid valve and is associated with high recurrence and mortality rates, particularly in HIV patients. S aureus is the main pathogen. Prosthetic valve endocarditis affects 1% to 4% of valve recipients within a year of surgery. It is divided in to early (<60 days post op) and late (>60 days). Early disease is usually nosocomial involving Staphylococcus epidermis and almost twice the mortality, whereas late is typically community acquired.

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IE presents along a continuum from acute to insidious and indolent. Symptoms are consistent with bacteremia (blood cultures are negative in approximately 5%). Fever is the most common manifestation followed by chills, weakness, and dyspnea. Cardiac manifestation such as heart murmurs are present in up to 85% of cases, although this can be difficult to hear in the ED. Dyspnea is common and often due to acute or progressive CHF, which occurs in approximately 70% of patients. Embolic phenomenon occurs about 50% of the time and is due to the embolization of friable vegetation fragments. Embolic stroke in the distribution of the MCA is the most common CNS complication followed by subarachnoid hemorrhage due to mycotic aneurysm. Other symptoms due to embolic phenomenon are chest and abdominal pain, flank pain with hematuria, and acute limb ischemia. Cutaneous findings occur in 18% to 50% of patients and include petichiae, splinter/subungual hemorrhages, Osler nodes (tender subcutaneous nodules on finger/toe pads), and Janeway lesions (hemorrhagic plaques on the palms or soles).

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Suspicion of IE requires hospital admission. Patients at risk for IE are those with unexplained fever and risk factors for the disease, such as injection drug users, patients with prosthetic valves, and those with new or changing murmurs and evidence of arterial emboli.

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The necessary components for diagnosis are blood cultures, echocardiogram, and clinical observation. Blood cultures should be drawn prior to administration of antibiotics and from 3 separate sites, with an hour elapsing between the first and last set of cultures. Echocardiography should be performed as soon as possible. Transthoracic two-dimensional echocardiography is typically the initial choice. Although nonspecific for IE, laboratory abnormalities that support the diagnosis are anemia, hematuria, and elevations in C-reactive protein, erythrocyte sedimentation rate, and procalcitonin.

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  1. Patients may present with respiratory compromise and require emergent ...

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