Endocarditis overview
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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.
Endocarditis can be classified by etiology as either non-infective or infective, depending on whether a microorganism is the source of the problem.
Traditionally, infective endocarditis has been clinically divided into acute and subacute (because the patients tend to live longer in subacute as opposed to acute) endocarditis. This classifies both the rate of progression and severity of disease. Thus subacute bacterial endocarditis (SBE) is often due to streptococci of low virulence and mild to moderate illness which progresses slowly over weeks and months, while acute bacterial endocarditis (ABE) is a fulminant illness over days to weeks, and is more likely due to Staphylococcus aureus which has much greater virulence, or disease-producing capacity.
This terminology is now discouraged. The terms short incubation (meaning less than about six weeks), and long incubation (greater than about six weeks) are preferred.
Infective endocarditis may also be classified as culture-positive or culture-negative. Culture-negative endocarditis is due to micro-organisms that require a longer period of time to be identified in the laboratory. Such organisms are said to be 'fastidious' because they have demanding growth requirements. Some pathogens responsible for culture-negative endocarditis include Aspergillus species, Brucella species, Coxiella burnetii, Chlamydia species, and HACEK bacteria.
Finally, the distinction between native-valve endocarditis and prosthetic-valve endocarditis is clinically important. Prosthetic-valve endocarditis constitutes 10-20% of cases of endocarditis. The greatest risk is during the first 6 months after valve surgery. Staphylococcus epidermidis is the most common cause. The infection often extends into the anulus and cardiac tissues.
Patients who inject narcotics intravenously may introduce infection which will travel to the right side of the heart. In other patients without a history of intravenous exposure, endocarditis is more frequently left-sided.
Diagnosis
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.
Non-infective endocarditis
Non-infective or marantic endocarditis is rare. A form of sterile endocarditis is termed Libman-Sacks endocarditis; this form occurs more often in patients with lupus erythematosus and the antiphospholipid syndrome. Non-infective endocarditis may also occur in patients with cancer, particularly mucinous adenocarcinoma.
Infective endocarditis
Given the poor vascular supply of the heart valves, entrance of infection fighting components of the bloodstream (such as white blood cells) are reduced. So if an organism (such as bacteria) establishes a foothold in the valves, the bodies ability to fight the infection inside the valve structures is reduced.
Normally, blood flows smoothly through these valves. If they have been damaged (for instance in rheumatic fever) the trauma of non-laminar flow can increase the risk of infection.
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.