Infective Endocarditis: Difference between revisions

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(Created page with "==Introduction== Infective endocarditis (IE) is an infectious and inflammatory process of endothelial lining of the heart structures and valves. It is most commonly caused by ...")
 
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==Diagnosis==
==Diagnosis==
Several diagnostic criteria have been proposed for the diagnosis of IE. In clinical practice, it is the global clinical picture that leads to decision making in the diagnosis and treatment of endocarditis. The modified DUKE criteria for diagnosis is often widely used, with a sensitivity and specificity approaching ~80%<cite>xiv</cite> The DUKE criteria divides into Definite IE, Possible IE, or Rejected IE. It uses Major criteria (microbiology, valvular abnormalities) and Minor criteria (systemic symptoms described below). Using the diagnostic criteria for IE should not override clinical judgment.
Several diagnostic criteria have been proposed for the diagnosis of IE. In clinical practice, it is the global clinical picture that leads to decision making in the diagnosis and treatment of endocarditis. The modified DUKE criteria for diagnosis is often widely used, with a sensitivity and specificity approaching ~80%<cite>xiv</cite> The DUKE criteria divides into Definite IE, Possible IE, or Rejected IE. It uses Major criteria (microbiology, valvular abnormalities) and Minor criteria (systemic symptoms described below). Using the diagnostic criteria for IE should not override clinical judgment.


===Definite IE:===
===Definite IE:===
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*Does not meet criteria for IE, as above
*Does not meet criteria for IE, as above


{| class
{| class="wikitable" cellpadding="0" cellspacing="0" border="0" width="700px"
|-
|-
!Major Criteria (microbiology)
!colspan="2"|Major Criteria (microbiology)
!
|-
|-
|Typical organisms x 2 blood cultures |e.g S. viridans, S. bovis, HACEK (Haemophilus spp, Aggregatibacter, Cardiobacterium hominis, Eikenella spp, Kingella kingae), S. aureus, Enterecoccus with no primary source
|Typical organisms x 2 blood cultures
Persistent bacteremia With blood cultures drawn >12 hours apart OR 3 out of 3, or 3 out of 4 positive blood cultures
|e.g S. viridans, S. bovis, HACEK (Haemophilus spp, Aggregatibacter, Cardiobacterium hominis, Eikenella spp, Kingella kingae), S. aureus, Enterecoccus with no primary source
Single positive blood culture for Coxiella burnetti or antiphase I IgG antibody titer >1:800
|-
Major Criteria (valve)
|Persistent bacteremia
Echocardiogram with evidence of vegetation TTE or TEE
|With blood cultures drawn >12 hours apart OR 3 out of 3, or 3 out of 4 positive blood cultures
New valvular regurgitation
|-
Minor Criteria
|Single positive blood culture for Coxiella burnetti or antiphase I IgG antibody titer >1:800
Predisposing cardiac condition or IV drug use
|
Fever >38 degrees celsius or >100.4 fahrenheit)
|-
Vascular phenomena major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhage, janeway lesions
!colspan="2"|Major Criteria (valve)
Immune phenomena glomerulonephritis, Osler nodes, Roth spots, positive RF
|-
Positive blood culture not meeting above major criteria or serological evidence of active infection with organism consistent with IE
|Echocardiogram with evidence of vegetation
|TTE or TEE
|-
|New valvular regurgitation
|
|-
!colspan="2"|Minor Criteria
|-
|Predisposing cardiac condition or IV drug use
|
|-
|Fever
|>38 degrees celsius or  


The sensitivity of detecting on echocardiogram varies. Transthoracic and transesophageal echocardiogram sensitivities for detecting vegetations are 50% and 90% respectively .
>100.4 fahrenheit)
|-
|Vascular phenomena
|major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhage, janeway lesions
|-
|Immune phenomena
|glomerulonephritis, Osler nodes, Roth spots, positive RF
|-
|Positive blood culture not meeting above major criteria or serological evidence of active infection with organism consistent with IE
|
|}
 
The sensitivity of detecting on echocardiogram varies. Transthoracic and transesophageal echocardiogram sensitivities for detecting vegetations are 50% and 90% respectively.<cite>xvxvi</cite>


Endocarditis of prosthetic mitral valve  
===Endocarditis of prosthetic mitral valve===


http://www.echopedia.org/images/2/24/E00404.swf
http://www.echopedia.org/images/2/24/E00404.swf
http://www.echopedia.org/images/6/6a/E00405.swf
http://www.echopedia.org/images/6/6a/E00405.swf


Endocarditis of the aortic valve
===Endocarditis of the aortic valve===


http://www.echopedia.org/images/1/10/E00114.swf
http://www.echopedia.org/images/1/10/E00114.swf
http://www.echopedia.org/images/5/5b/E00117.swf
http://www.echopedia.org/images/5/5b/E00117.swf


Roth Spots
===Roth Spots==
[[Image: |Roth Spots]]
 
Roth Spots
 


==Therapy==
==Therapy==
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As soon as blood cultures become available antibiotics should be adjusted to target the identified microorganisms.  
As soon as blood cultures become available antibiotics should be adjusted to target the identified microorganisms.  


In cases of prosthetic valve endocarditis (PVE), microbiological activity depends on early (<2 months post op) or late (>2 months post op). In early PVE S.aureus accounts for 40% of the cases, followed by coagulase negative staphylococcus (17%). In late PVE coagulase negative staphylococcus accounts for 20% of cases, followed by S. aureus (18%). Coverage for enterococci, streptococci, and gram negative should be considered in empiric therapy in both groups. Rifampin + Vancomycin + Gentamicin should be initiated for PVE <12 post op. Suspected PVE >12 months post op may be treated with the same regimen as for native valves .
In cases of prosthetic valve endocarditis (PVE), microbiological activity depends on early (<2 months post op) or late (>2 months post op). In early PVE S.aureus accounts for 40% of the cases, followed by coagulase negative staphylococcus (17%). In late PVE coagulase negative staphylococcus accounts for 20% of cases, followed by S. aureus (18%). Coverage for enterococci, streptococci, and gram negative should be considered in empiric therapy in both groups. Rifampin + Vancomycin + Gentamicin should be initiated for PVE <12 post op. Suspected PVE >12 months post op may be treated with the same regimen as for native valves.<cite>xvii</cite>


The American Heart Association recommendation for specific antimicrobial therapy is shown below:
The American Heart Association recommendation for specific antimicrobial therapy is shown below:
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http://eurheartj.oxfordjournals.org/content/30/19/2369.long
http://eurheartj.oxfordjournals.org/content/30/19/2369.long


Prophylaxis
===Prophylaxis===


According the American Heart Association guidelines published in 2007 the following groups of patients are considered to be high-risk and require prophylaxis :
According the American Heart Association guidelines published in 2007 the following groups of patients are considered to be high-risk and require prophylaxis :


- Any prosthetic heart valve, or prosthetic material used for valve repair
*Any prosthetic heart valve, or prosthetic material used for valve repair
- Previous infective endocarditis
- Previous infective endocarditis
- Congenital heart disease (CHD)
- Congenital heart disease (CHD)
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Common complications arising from IE can be divided into local and systemic. Local complications often arise from direct extension of the infection into cardiac structures. Systemic complications arise from embolization and bacteremias.  
Common complications arising from IE can be divided into local and systemic. Local complications often arise from direct extension of the infection into cardiac structures. Systemic complications arise from embolization and bacteremias.  


Heart failure occurs in 26-30% of patients with endocarditis . It may occur acutely or over time, it is often times due to anatomical disruption from valve vegetations or destruction of nearby tissue. Development of heart failure in the setting of IE is correlated with worse outcomes. Heart failure occurs most commonly with aortic (29%) and mitral valve (20%) infections and less with tricuspid valve (8%). The overall in hospital mortality rate for patients diagnosed with heart failure approaches 30% .  
Heart failure occurs in 26-30% of patients with endocarditis.<cite>xxxxi</cite> It may occur acutely or over time, it is often times due to anatomical disruption from valve vegetations or destruction of nearby tissue. Development of heart failure in the setting of IE is correlated with worse outcomes. Heart failure occurs most commonly with aortic (29%) and mitral valve (20%) infections and less with tricuspid valve (8%).<cite>xxii</cite> The overall in hospital mortality rate for patients diagnosed with heart failure approaches 30%.<cite>xxiii</cite>


Conduction abnormalities, commonly characterized by heart blocks in endocarditis are associated with infection extension, increased risk of embolization and increased mortality. They are reported to be present in 26%-28% of patients .  
Conduction abnormalities, commonly characterized by heart blocks in endocarditis are associated with infection extension, increased risk of embolization and increased mortality. They are reported to be present in 26%-28% of patients .  
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==Prognosis==
==Prognosis==
Prognosis of IE is largely dependent on the patient’s comorbid conditions such as diabetes , hemodialysis, congestive heart failure , complications of endocarditis, prosthetic valve and the microorganism identified. Generally the outcome largely depends on the organism involved. According to recent data it, the over 30 day mortality is ~15% and the 1-year mortality is ~34%. Prosthetic valve endocarditis has a significant in hospital mortality of ~24%, while native valve endocarditis carries a lower in hospital mortality of 12% if treated early and surgically .
Prognosis of IE is largely dependent on the patient’s comorbid conditions such as diabetes , hemodialysis, congestive heart failure , complications of endocarditis, prosthetic valve and the microorganism identified. Generally the outcome largely depends on the organism involved. According to recent data it, the over 30 day mortality is ~15% and the 1-year mortality is ~34%. Prosthetic valve endocarditis has a significant in hospital mortality of ~24%, while native valve endocarditis carries a lower in hospital mortality of 12% if treated early and surgically .
==References==
<biblio>
</biblio>
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