Endocarditis overview: Difference between revisions
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==Overview== | ==Overview== | ||
'''Endocarditis''' is an [[inflammation]] of the inner layer of the [[heart]], the [[endocardium]]. The most common structures involved are the [[heart valve]]s. | '''Endocarditis''' is an [[inflammation]] of the inner layer of the [[heart]], the [[endocardium]]. The most common structures involved are the [[heart valve]]s. | ||
==Classification== | ==Classification== | ||
Revision as of 23:30, 8 October 2012
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Endocarditis Microchapters |
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Diagnosis |
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Treatment |
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2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease |
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Case Studies |
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Endocarditis overview On the Web |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-in-Chief: Cafer Zorkun, M.D., Ph.D. [2]
Overview
Endocarditis is an inflammation of the inner layer of the heart, the endocardium. The most common structures involved are the heart valves.
Classification
Endocarditis is classified based upon the underlying pathophysiology of the process (infective versus non-infective), the acuity of the process (acute versus subacute or short incubation versus long incubation), the fastidiousness of the infectious agent (i.e. how hard it is to culture and isolate as culture positive versus culture negative), the type of valve involved (native versus prosthetic) and the valve infected (aortic, mitral, or tricuspid valve).
Pathophysiology
The turbulent blood flow around the heart valves is a risk factor for the development of endocarditis. The valves may be damaged congenitally, from surgery, by auto-immune mechanisms, or simply as a consequence of old age. The damaged endothelium of these areas becomes a site for attachment of infectious agents in infectious endocarditis. Dental procedures, colorectal cancer, urinary tract infections and intravenous drug use are the most common routes of introducing the infectious agent into the bloodstream. In non-bacterial thrombotic endocarditis (NBTE), the damaged part of a heart valve becomes covered with a blood clot which organizes. Many types of organism can cause infective endocarditis. These are generally isolated by blood culture, where the patient's blood is sampled under sterile conditions, and any growth is noted and identified. It is therefore important to draw blood cultures before initiating antibiotic therapy. 70% of cases of endocarditis are due to the following three pathogens:
- Alpha-haemolytic streptococci, that are present in the mouth will often be the organism isolated if a dental procedure caused the bacteraemia.
- If the bacteraemia was introduced through the skin, such as contamination in surgery, during catheterization, or in an IV drug user, Staphylococcus aureus is common.
- A third important cause of endocarditis is Enterococci. These bacteria enter the bloodstream as a consequence of abnormalities in the gastrointestinal or urinary tracts. Enterococci are increasingly recognized as causes of nosocomial or hospital-acquired endocarditis. This contrasts with alpha-haemolytic streptococci and Staphylococcus aureus which are causes of community-acquired endocarditis.
Differentiating Endocarditis From Other Disorders
Endocarditis often presents as an unexplained fever and must be distinguished from other causes of a fever of unknown origin (FUO). Causes of a fever of unknown origin which endocarditis must be differentiated from include a drug fever, lymphoma, pulmonary embolism, and deep vein thrombosis. Disseminated granulomatoses such as Tuberculosis, Histoplasmosis, Coccidioidomycosis, Blastomycosis and Sarcoidosis can also cause a FUO. Blood cultures prior to the administration of antibiotics and echocardiography are critical in differentiating endocarditis from these other syndromes.
Diagnosis
Symptoms
Common symptoms of endocarditis include fever, chills, anorexia, malaise,weight loss, and back pain.
Physical Examination
Common signs on physical examination of endocarditis include fever, rigors, Osler's nodes, Janeway lesions and evidence of embolization. Aortic insufficiency with a wide pulse pressure, mitral regurgitation or tricuspid regurgitation may be present depending upon the valve that is infected.
Treatment
High dose antibiotics are administered by the intravenous route to maximize diffusion of antibiotic molecules into vegetation(s) from the blood filling the chambers of the heart. This is necessary because neither the heart valves nor the vegetations adherent to them are supplied by blood vessels. Antibiotics are continued for a long time, typically two to six weeks. Specific drug regimens differ depending on the classification of the endocarditis as acute or subacute (acute necessitating treating for Staphylococcus aureus with oxacillin or vancomycin in addition to gram-negative coverage). Fungal endocarditis requires specific anti-fungal treatment, such as amphotericin B.[1]
Surgical removal of the valve is necessary in patients who fail to clear micro-organisms from their blood in response to antibiotic therapy, or in patients who develop cardiac failure resulting from destruction of a valve by infection. A removed valve is usually replaced with an artificial valve which may either be mechanical (metallic) or obtained from an animal such as a pig; the latter are termed bioprosthetic valves.[1]
References
- ↑ 1.0 1.1 Baddour Larry M., Wilson Walter R., Bayer Arnold S., Fowler Vance G. Jr, Bolger Ann F., Levison Matthew E., Ferrieri Patricia, Gerber Michael A., Tani Lloyd Y., Gewitz Michael H., Tong David C., Steckelberg James M., Baltimore Robert S., Shulman Stanford T., Burns Jane C., Falace Donald A., Newburger Jane W., Pallasch Thomas J., Takahashi Masato, Taubert Kathryn A. (2005). "Infective Endocarditis: Diagnosis, Antimicrobial Therapy, and Management of Complications: A Statement for Healthcare Professionals From the Committee on Rheumatic Fever, Endocarditis, and Kawasaki Disease, Council on Cardiovascular Disease in the Young, and the Councils on Clinical Cardiology, Stroke, and Cardiovascular Surgery and Anesthesia, American Heart Association-Executive Summary: Endorsed by the Infectious Diseases Society of America". Circulation. 111 (23): 3167–84. PMID 15956145.