Endocarditis overview: Difference between revisions
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==Diagnosis== | ==Diagnosis== | ||
===The Duke Criteria=== | |||
The [http://www.medcalc.com/endocarditis.html Duke Criteria]<ref name=Durack>{{cite journal | author = Durack D, Lukes A, Bright D | title = New criteria for diagnosis of infective endocarditis: utilization of specific echocardiographic findings. Duke Endocarditis Service. | journal = Am J Med | volume = 96 | issue = 3 | pages = 200-9 | year = 1994 | id = PMID 8154507}}</ref> can be used to establish the diagnosis of [[endocarditis]]. The Duke Clinical Criteria for Infective Endocarditis requires either: | |||
* Two major criteria, or | |||
* One major and three minor criteria, or | |||
* Five minor criteria | |||
===Major Criteria=== | |||
====1. Positive Blood Culture for Infective Endocarditis==== | |||
Typical microorganism consistent with infective endocarditis from 2 separate blood cultures, as noted below: | |||
::{{unicode|☑}} [[Viridans streptococci]], [[Streptococcus bovis]], or | |||
::{{unicode|☑}} [[HACEK]] group, or | |||
::{{unicode|☑}} Community-acquired [[Staphylococcus aureus]] or [[enterococci]], in the absence of a primary focus | |||
<center>'''''or'''''</center> | |||
Microorganisms consistent with infective endocarditis from persistently positive blood cultures defined as: | |||
::{{unicode|☑}} 2 positive cultures of blood samples drawn >12 hours apart, or | |||
::{{unicode|☑}} All of 3 or a majority of 4 separate cultures of blood (with first and last sample drawn 1 hour apart) | |||
====2. Evidence of endocardial involvement==== | |||
Positive echocardiogram for infective endocarditis defined as: | |||
::{{unicode|☑}} Oscillating intracardiac mass on valve or supporting structures, in the path of regurgitant jets, or | |||
::{{unicode|☑}} On implanted material in the absence of an alternative anatomic explanation, or | |||
::{{unicode|☑}} Abscess, or | |||
::{{unicode|☑}} New partial dehiscence of prosthetic valve | |||
<center>'''''or'''''</center> | |||
::{{unicode|☑}} New valvular regurgitation (worsening or changing of preexisting murmur not sufficient) | |||
===Minor criteria:=== | |||
::{{unicode|☑}} Predisposition: predisposing heart condition or [[intravenous drug use]] | |||
::{{unicode|☑}} [[Fever]]: temperature > 38.0° C (100.4° F) | |||
::{{unicode|☑}} Vascular phenomena: major [[arterial emboli]], [[septic pulmonary infarct]]s, [[mycotic aneurysm]], [[intracranial hemorrhage]], [[conjunctival hemorrhage]]s, and [[Janeway lesions]] | |||
::{{unicode|☑}} Immunologic phenomena: [[glomerulonephritis]], [[Osler's nodes]], [[Roth spot]]s, and [[rheumatoid factor]] | |||
::{{unicode|☑}} Microbiological evidence: positive [[blood culture]] but does not meet a major criterion as noted above (see footnote) or serological evidence of active infection with organism consistent with infectious endocarditis | |||
::{{unicode|☑}} Echocardiographic findings: consistent with infectious endocarditis but do not meet a major criterion as noted above | |||
Footnote: It should be noted that the criteria exclude single positive cultures for [[coagulase-negative staphylococci]], [[diphtheroids]], and organisms that do not commonly cause endocarditis. | |||
===Symptoms=== | ===Symptoms=== | ||
Common symptoms of endocarditis include [[fever]], [[chills]], [[anorexia]], [[malaise]],[[weight loss]], and [[back pain]]. | Common symptoms of endocarditis include [[fever]], [[chills]], [[anorexia]], [[malaise]],[[weight loss]], and [[back pain]]. | ||
Revision as of 00:00, 9 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.
Risk Factors
The following are risk factors for the development of endocarditis:
- Prosthetic (artificial) heart valves
- Congenital heart disease (atrial septal defect, patent ductus arteriosus, and others)
- Heart valve problems (such as mitral insufficiency)
- History of rheumatic heart disease
- Intravenous drug users are also at risk for this condition, because unsterile needles can cause bacteria to enter the bloodstream.
Epidemiology and Demographics
Incidence
The incidence of infective endocarditis is approximately 2-4 cases per 100,000 persons per year worldwide. This rate has not changed in the past 5-6 decades.
Age
Infective endocarditis may occur in a person of any age. The frequency is increasing in elderly individuals, with 25-50% of cases occurring in those older than 60 years of age.
Gender
Infective endocarditis is 3 times more common in males than in females.
Changes in Bacterial Species Causing Endocarditis
There has been a decline in streptococcus viridans endocarditis and an increase in staphylococcal endocarditis.
Complications
Complications of endocarditis can occur as a result of the locally destructive effects of the infection. These complications include perforation of valve leaflets causing congestive heart failure, abscesses, disruption of the heart's conduction system, and embolization to the brain (causing a stroke), to the coronary artery (causing a heart attack), to the lung (causing pulmonary embolism), to the spleen (causing a splenic infarct) and to the kidney (causing a renal infarct).
Prognosis
Infective endocarditis is associated with a high (10% to 25%) mortality. Operative mortality is 15 - 20%. The development of an infection of a prosthetic valve during operation for native valve endocarditis is 4%, it is higher (12 - 16%) if active endocarditis is present at the time of the surgery. Late survival at 5 years for native valve endocarditis is 70 - 80% and for prosthetic valve endocarditis is 50 - 80%.[1]
Diagnosis
The Duke Criteria
The Duke Criteria[2] can be used to establish the diagnosis of endocarditis. The Duke Clinical Criteria for Infective Endocarditis requires either:
- Two major criteria, or
- One major and three minor criteria, or
- Five minor criteria
Major Criteria
1. Positive Blood Culture for Infective Endocarditis
Typical microorganism consistent with infective endocarditis from 2 separate blood cultures, as noted below:
- Template:Unicode HACEK group, or
- Template:Unicode Community-acquired Staphylococcus aureus or enterococci, in the absence of a primary focus
Microorganisms consistent with infective endocarditis from persistently positive blood cultures defined as:
- Template:Unicode 2 positive cultures of blood samples drawn >12 hours apart, or
- Template:Unicode All of 3 or a majority of 4 separate cultures of blood (with first and last sample drawn 1 hour apart)
2. Evidence of endocardial involvement
Positive echocardiogram for infective endocarditis defined as:
- Template:Unicode Oscillating intracardiac mass on valve or supporting structures, in the path of regurgitant jets, or
- Template:Unicode On implanted material in the absence of an alternative anatomic explanation, or
- Template:Unicode Abscess, or
- Template:Unicode New partial dehiscence of prosthetic valve
- Template:Unicode New valvular regurgitation (worsening or changing of preexisting murmur not sufficient)
Minor criteria:
- Template:Unicode Predisposition: predisposing heart condition or intravenous drug use
- Template:Unicode Fever: temperature > 38.0° C (100.4° F)
- Template:Unicode Vascular phenomena: major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhages, and Janeway lesions
- Template:Unicode Immunologic phenomena: glomerulonephritis, Osler's nodes, Roth spots, and rheumatoid factor
- Template:Unicode Microbiological evidence: positive blood culture but does not meet a major criterion as noted above (see footnote) or serological evidence of active infection with organism consistent with infectious endocarditis
- Template:Unicode Echocardiographic findings: consistent with infectious endocarditis but do not meet a major criterion as noted above
Footnote: It should be noted that the criteria exclude single positive cultures for coagulase-negative staphylococci, diphtheroids, and organisms that do not commonly cause endocarditis.
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 1.2 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.
- ↑ Durack D, Lukes A, Bright D (1994). "New criteria for diagnosis of infective endocarditis: utilization of specific echocardiographic findings. Duke Endocarditis Service". Am J Med. 96 (3): 200–9. PMID 8154507.