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.
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.
Shown below is a Janeway Lesion which is a flat, painless, erythematous lesions seen on the palm of this patient's hand:
Shown below is an Osler's Node:
Laboratory Studies
In endocarditis, the white blood cell count and erythrocyte sedimentation rate are elevated. The rheumatoid factor is elevated in half of patients. The BUN and Cr may be elevated in the presence of glomerulonephritis.
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
The goals of echocardiography in the patient with endocarditis include the following:
- Determine the presence, location and size of vegetations
- Assess the damage to the valve apparatus and determine the magnitude of regurgitation, perforation or leak
- To assess the dimensions and function of the ventricle(s)
- To identify any abscess formation
- To determine the need for surgical intervention
- Echocardiography may be useful for risk stratification. Although the data are inconsistent, some evidence suggests that vegetation size is associated with embolic complications.
Echocardiographic Features in Infective Endocarditis
- Irregular echogenic mass attached to valve leaflet
- The attachment of the vegetation is on the upstream side of the valve leaflet
- There is chaotic independent movement of the mass relative to the valve
- The minimum size of a vegetation that is identifiable on trans thoracic echocardiography is 3 mm and by transoesophageal echocardiography route is 2 mm.
- With treatment and time, the vegetation shrinks and can become fibrosed or calcified. It may not disappear completely.
- Large vegetations occur with fungal endocarditis or staph. aureus endocarditis.
- The hemodynamic effects are mostly due to valvular regurgitation as a result of valve destruction.
The valve and the surrounding anatomy should be carefully inspected for the following complications:
- Fistula
- Perforation
- Prosthetic dehiscence
- Aneurysm
- Vegetations
- Valve ulcers or erosions
- Rupture of chordaes
- Endocardial jet lesions
- Flail leaflets or cusps
- Abcess formation (annular and ring)
Performance of Transesophageal Echocardiography (TEE) Versus Transthoracic Ehcocardiography (TTE)
In general, transthoracic echocardiography (TTE) is often adequate for the diagnosis of infective endocarditis in cases where cardiac structures-of-interest are well visualized. The transthoracic echocardiogram has a sensitivity and specificity of approximately 65% and 95% if the echocardiographer believes there is 'probabable' or 'almost certain' evidence of endocarditis[3][4].
Specific situations where transesophageal echocardiography (TEE) is preferred over TTE include:
- The presence of a prosthetic valve
- Poor trans thoracic views
- Continuing sepsis despite adequate antibiotic therapy
- New PR prolongation
- No signs of endocarditis on trans thoracic echocardiography, but high clinical suspicion
- Suspected periannular complications
- Children with complex congenital cardiac lesions
- Patients with S. Aureus caused bacteremia and pre-existing valvular abnormalities that make TTE interpretation more difficult (e.g. calcific aortic stenosis).
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. Blood cultures should be drawn prior to instituting antibiotics to identify the etiologic agent and to determine its antimicrobial susceptibility. Antibiotic therapy for subacute or indolent disease can be delayed until results of blood cultures are known; in fulminant infection or valvular dysfunction requiring urgent surgical intervention, begin empirical antibiotic therapy promptly after blood cultures have been obtained.Older antibiotics such as penicillin G, ampicillin, nafcillin, cefazolin, gentamycin, ceftriaxone, rifampin and vancomycin are the mainstays of therapy. Fungal endocarditis requires specific anti-fungal treatment, such as amphotericin B.[1]
Duration of Antibiotic Therapy
The duration for native valve endocarditis is often 4 weeks. For prosthetic valve endocarditis (including the presence of a valve ring), treatment should be continued for 6 to 8 weeks. For each infective agent, the preferred antimicrobial agent, dose, and duration is listed below.
Treatment Based Upon Infectious Agent[1]
Penicillin-Susceptible Strep Viridans and Other Nonenterococcal Streptococci
Penicillin G
- If Minimum inhibitory concentration [MIC] <0.2 µg/ml.
- Dose: 12–18 million units I.V. daily in divided doses q. 4 hour for 4 weeks.
Penicillin G + gentamicin
- Dose: Penicillin G, 12–18 million units I.V. daily in divided doses q. 4 hour for 4 weeks plus gentamicin, 3 mg/kg I.M. or I.V. daily in divided doses q. 8 hour for 2 weeks (peak serum concentration should be ~ 3 µg/ml and trough concentrations < 1 µg/ml).
Ceftriaxone
- Dose: 2 g I.V. daily as a single dose for 2 weeks.
Vancomycin
- Vancomycin can be administered to patients with a history of penicillin hypersensitivity.
- Dose: 30 mg/kg I.V. daily in divided doses q. 12 hour for 4 weeks.
Relatively Penicillin-Resistant Streptococci
If MIC 0.2–0.5 µg/ml
Penicillin G + gentamicin
- Dose: Penicillin G, 20–30 million units I.V. daily in divided doses q. 4 hour for 4 weeks; gentamicin, 3 mg/kg I.M. or I.V. daily in divided doses q. 8 hr for 2 wk (peak serum concentration should be ~ 3 µg/ml and trough concentrations < 1 µg/ml).
If MIC > 0.5 µg/ml
Penicillin G + gentamicin
- Dose is penicillin G, 20–30 million units I.V. daily in divided doses q. 4 hour for 4 week; gentamicin, 3 mg/kg I.M. or I.V. daily in divided doses q. 8 hour for 4 week (peak serum concentration should be ~ 3 µg/ml and trough concentrations < 1 µg/ml).
Vancomycin
- Regimen for patients with history of penicillin hypersensitivity.
- Dose: 30 mg/kg I.V. daily in divided doses q. 12 hour for 4 weeks.
Enterococci
In general, treatment of enterococcal endocarditis requires combination therapy with two antibiotics:
Penicillin G + gentamicin
- Dose is penicillin G, 20–30 million units I.V. daily in divided doses q. 4 hr for 4–6 weeks; gentamicin, 3 mg/kg I.M. or I.V. daily in divided doses q. 8 hour for 4–6 weeks (peak serum concentration should be ~ 3 µg/ml and trough concentrations < 1 µg/ml).
Ampicillin + gentamicin
- Dose is ampicillin, 12 g I.V. daily in divided doses q. 4 hour for 4–6 weeks; gentamicin, dose as above.
Vancomycin + gentamicin
- This regimen is for patients with history of penicillin hypersensitivity.
- Dose: Vancomycin, 30 mg/kg I.V. daily in divided doses q. 12 hour for 4–6 weeks; gentamicin, dose as above.
Staphylococci (Methicillin Susceptible) in the Absence of Prosthetic Material
Nafcillin or oxacillin + gentamicin (optional)
- Dose: Nafcillin or oxacillin, 12 g I.V. daily in divided doses q. 4 hour for 4–6 weeks; gentamicin, 3 mg/kg I.M. or I.V. daily in divided doses q. 8 hr for 3–5 days (peak serum concentration should be ~ 3 µg/ml and trough concentrations <1 µg/ml).
Cefazolin + gentamicin (optional)
- Alternative regimen for patients with history of penicillin hypersensitivity.
- Dose: Cefazolin, 12 g I.V. daily in divided doses q. 4 hour for 4–6 weeks; gentamicin, dose as above.
Vancomycin
- Alternative regimen for patients with history of penicillin hypersensitivity.
- Dose: 30 mg/kg I.V. daily in divided doses q. 12 hr for 4–6 weeks.
Staphylococci (Methicillin Resistant) in the Absence of Prosthetic Material
Vancomycin
- Dose: 30 mg/kg I.V. daily in divided doses q. 12 hour for 4–6 weeks.
Staphylococci (Methicillin Susceptible) in the Presence of Prosthetic Material
Nafcillin or oxacillin + rifampin + gentamicin
- Dose: Nafcillin or oxacillin, 12 g I.V. daily in divided doses q. 4 hour for 6–8 weeks plus rifampin, 300 mg p.o., q. 8 hour for 6–8 weeks plus gentamicin (administer during the initial 2 weeks), 3 mg/kg I.M. or I.V. daily in divided doses q. 8 hour for 2 weeks.
Staphylococci (Methicillin Resistant) in the Presence of Prosthetic Material
Vancomycin + rifampin + gentamicin
- Dose: Vancomycin, 30 mg/kg I.V. daily in divided doses q. 12 hour for 6–8 weeks plusrifampin, 300 mg p.o., q. 8 hour for 6–8 weeks plus gentamicin (administer during the initial 2 weeks), 3 mg/kg I.M. or I.V. daily in divided doses q. 8 hour for 2 weeks.
HACEK Organisms
These agents are more indolent and the infection is less complicated.
Ceftriaxone or another third-generation cephalosporin
- Dose: 2 g I.V. daily as a single dose for 4 weeks.
Ampicillin-Sulbactam
Ciprofloxacin
- This is listed as an alternative, there is not a lot of data to support its regular use.
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.
- ↑ Shively B, Gurule F, Roldan C, Leggett J, Schiller N (1991). "Diagnostic value of transesophageal compared with transthoracic echocardiography in infective endocarditis". J Am Coll Cardiol. 18 (2): 391–7. PMID 1856406.
- ↑ Erbel R, Rohmann S, Drexler M, Mohr-Kahaly S, Gerharz C, Iversen S, Oelert H, Meyer J (1988). "Improved diagnostic value of echocardiography in patients with infective endocarditis by transoesophageal approach. A prospective study". Eur Heart J. 9 (1): 43–53. PMID 3345769.