Endocarditis overview: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
The turbulent | The pathogenesis of infective endocarditis includes valvular damage, altered and turbulent flow, bacteremia, and lack of blood supply to the [[valve]]s.<ref name=abc> Infective endocarditis. Wikipedia (2015). URL=https://en.wikipedia.org/wiki/Infective_endocarditis#Pathogenesis Accessed on September 21, 2015</ref><ref name=endo> Endocarditis. Wikipedia (2015). URL= https://en.wikipedia.org/wiki/Endocarditis Accessed on September 21, 2015</ref> Damaged endothelium becomes a site for attachment of infectious agents in infectious endocarditis. Nonbacterial thrombotic endocarditis is related to hypercoaguable states such as [[pregnancy]] or systemic bacterial [[infection]]. The characteristic lesion of endocarditis is a vegetation.<ref name="pmid11794152">{{cite journal| author=Mylonakis E, Calderwood SB| title=Infective endocarditis in adults. | journal=N Engl J Med | year= 2001 | volume= 345 | issue= 18 | pages= 1318-30 | pmid=11794152 | doi=10.1056/NEJMra010082 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11794152}}</ref> Vegetations are composed of [[fibrin]], inflammatory cells, [[platelets]], and microorganisms.<ref name="pmid11794152">{{cite journal| author=Mylonakis E, Calderwood SB| title=Infective endocarditis in adults. | journal=N Engl J Med | year= 2001 | volume= 345 | issue= 18 | pages= 1318-30 | pmid=11794152 | doi=10.1056/NEJMra010082 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11794152 }}</ref> | ||
==Causes== | ==Causes== | ||
Revision as of 15:20, 28 September 2015
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Endocarditis Microchapters |
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2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease |
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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
Infective endocarditis is the infection of the endothelium of the heart including but not limited to the valves. While acute bacterial endocarditis is caused by an infection with a virulent organism such as staphylococcus aureus, group A or other beta-hemolytic streptococci, subacute bacterial endocarditis is an indolent infection with less virulent organisms like streptococcus viridans. Patients with unexplained fever for more than 48 hours and who are at high risk for infective endocarditis and patients among whom valve regurgitation is newly diagnosed should undergo a diagnostic workup to rule out endocarditis. The diagnosis of endocarditis depends on a thorough history and physical exam as well as on the results of the blood cultures and the findings on transthoracic echocardiogram or transesophageal echocardiogram. The modified Duke criteria is used to establish the diagnosis of endocarditis. Endocarditis is initially treated with empiric antibiotic therapy until the causative agent is identified.[1][2]
Historical Perspective
Endocarditis was first described in 1554. The inflammatory process associated with endocarditis was discovered in 1799. Vegetations were first discovered to be associated with endocarditis in 1806.[3]
Classification
Endocarditis may be classified based on the underlying pathophysiology of the process (infective vs. non-infective), the onset of the disease (acute vs. subacute or short incubation vs. long incubation), results of the cultures (culture positive vs. culture negative), the nature of the valve (native vs. prosthetic) and the valve affected (aortic, mitral, or tricuspid valve).
Pathophysiology
The pathogenesis of infective endocarditis includes valvular damage, altered and turbulent flow, bacteremia, and lack of blood supply to the valves.[4][5] Damaged endothelium becomes a site for attachment of infectious agents in infectious endocarditis. Nonbacterial thrombotic endocarditis is related to hypercoaguable states such as pregnancy or systemic bacterial infection. The characteristic lesion of endocarditis is a vegetation.[6] Vegetations are composed of fibrin, inflammatory cells, platelets, and microorganisms.[6]
Causes
The majority of cases of infective endocarditis are due to bacteria.[4] Common causes of infective endocarditis include Streptococcus viridans, Staphylococci, and Enterococcus.[4]
Differentiating Endocarditis From Other Diseases
Endocarditis must be differentiated from other causes of a fever of unknown origin (FUO) such as pulmonary embolism, deep vein thrombosis, lymphoma, drug fever, cotton fever, and disseminated granulomatoses.
Epidemiology and Demographics
The incidence of native valve infective endocarditis is approximately 1.7-6.2 cases per 100,000 individuals per year in the United States and Europe.[6] The prevalence of infective endocarditis among IV drug users ranges from 10 to 15%.The incidence of endocarditis increases with age; the median age of patients is 47 to 69 years.[4] There is an increased incidence of infective endocarditis in persons 65 years of age and older.[4] Males are more commonly affected with endocarditis than females. The male to female ratio is approximately 1.7:1.[6]
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%.[7]
Diagnosis
The Duke Criteria
The Duke criteria[3] can be used to establish the diagnosis of endocarditis. The Duke clinical criteria for infective endocarditis requires either:[8]
- Two major criteria, or
- One major and three minor criteria, or
- Five minor criteria
History and Symptoms
Common symptoms of endocarditis include fever, chills, new onset of cardiac murmum, 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.
Laboratory Tests
Two blood cultures should be ordered when infective endocarditis is suspected. BUN and Cr may be elevated in the presence of glomerulonephritis. In endocarditis, the white blood cell count and erythrocyte sedimentation rate are elevated. The rheumatoid factor is elevated in half of patients.
Electrocardiography
The EKG can show conduction abnormalities such as AV block in the presence of a myocardial abscess. The EKG can show ST elevation in the presence of embolization of a vegetation or clot down the coronary artery.
Echocardiography
A transthoracic echocardiogram must be ordered for the diagnosis of infective endocarditis. A transesophageal echocardiogram should be ordered in some cases such as a non diagnostic TTE in a suspected infective endocarditis, presence of clinical complications, intracardiac device leads, staphylococcus aureus bacteremia without a known cause among others. The findings on echocardiography include:
- Oscillating intracardiac mass on valve or supporting structures, in the path of regurgitant jets, or on implanted material in the absence of an alternative anatomic explanation, or
- Abscess, or
- New partial dehiscence of prosthetic valve, or
- New valvular regurgitation
Treatment
Medical Therapy
Blood cultures should be drawn prior to instituting antibiotics to identify the etiologic agent and to determine its antimicrobial susceptibility. Older antibiotics such as penicillin G, ampicillin, nafcillin, cefazolin, gentamycin, ceftriaxone, rifampin and vancomycin are the mainstays of therapy.
Surgery
Early valve surgery should be scheduled when there is heart failure due to the valve dysfunction, left sided infective endocarditis due to staphylococcus aureus, fungal or highly resistant organisms, or a heart block, annular or aortic abscess or destructive lesions. Other indications include persistent bacteremia or fever 5 to 7 following the initiation of the antibiotics, relapse of the infection depsite a complete course of antibiotics in prosthetic valve endocarditis when no portal of infection can be identified, recurrent emboli and persistent vegetations despite antibiotic therapy, and mobile vegetations with a length more than 10 mm in native valve endocarditis.[2]
Prevention
Prevention of infective endocarditis can be achieved through the administration of antiobiotic prophylaxis to high risk subjects who are undergoing high risk procedures. The choice of antibiotic prophylaxis depends on whether the subject can tolerate oral intake or not, as well as on whether patient has allergy to penicillin or not.[9][1]
References
- ↑ 1.0 1.1 "2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease: Executive Summary". Retrieved 4 March 2014.
- ↑ 2.0 2.1 Baddour, LM.; Wilson, WR.; Bayer, AS.; Fowler, VG.; Bolger, AF.; Levison, ME.; Ferrieri, P.; Gerber, MA.; Tani, LY. (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: endorsed by the Infectious Diseases Society of America". Circulation. 111 (23): e394–434. doi:10.1161/CIRCULATIONAHA.105.165564. PMID 15956145. Unknown parameter
|month=ignored (help) - ↑ Millar BC, Moore JE (2004). "Emerging issues in infective endocarditis". Emerg Infect Dis. 10 (6): 1110–6. doi:10.3201/eid1006.030848. PMC 3323180. PMID 15207065.
- ↑ 4.0 4.1 4.2 4.3 4.4 Infective endocarditis. Wikipedia (2015). URL=https://en.wikipedia.org/wiki/Infective_endocarditis#Pathogenesis Accessed on September 21, 2015
- ↑ Endocarditis. Wikipedia (2015). URL= https://en.wikipedia.org/wiki/Endocarditis Accessed on September 21, 2015
- ↑ 6.0 6.1 6.2 6.3 Mylonakis E, Calderwood SB (2001). "Infective endocarditis in adults". N Engl J Med. 345 (18): 1318–30. doi:10.1056/NEJMra010082. PMID 11794152.
- ↑ 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.
- ↑ Wilson W, Taubert KA, Gewitz M, Lockhart PB, Baddour LM, Levison M; et al. (2007). "Prevention of infective endocarditis: guidelines from the American Heart Association: a guideline from the American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee, Council on Cardiovascular Disease in the Young, and the Council on Clinical Cardiology, Council on Cardiovascular Surgery and Anesthesia, and the Quality of Care and Outcomes Research Interdisciplinary Working Group". Circulation. 116 (15): 1736–54. doi:10.1161/CIRCULATIONAHA.106.183095. PMID 17446442.