Risk factors prior IE, presence of a prosthetic valve or cardiac device, or history of valvular or congenital heart disease) and noncardiac factors (intravenous drug use, indwelling intravenous catheter, immunosuppression, or a recent dental or surgical procedure). (

++++++++++++++++++

 

●IE is associated with a broad array of systemic complications; these include cardiac and neurologic complications, septic emboli, metastatic infection, and systemic immune reactions. Clinical manifestations reflecting these complications may be present at the time of initial presentation and/or may develop subsequently. Clinical manifestations of a complication of IE warrant independent diagnostic evaluation, concurrent with evaluation for IE. (See 'Complications as presenting symptoms' above.)

●The diagnosis of IE should be suspected in patients with fever (with or without bacteremia) in the setting of relevant cardiac and noncardiac risk factors. The diagnosis is established based on clinical manifestations, blood cultures (or other microbiologic data), and echocardiography. The accepted criteria for diagnosis of IE are the modified Duke criteria, which are summarized above and in the tables (table 1 and table 2) (calculator 1). (See 'Overview of diagnostic approach' above and 'Modified Duke criteria' above.)

●At least three sets of blood cultures should be obtained from separate venipuncture sites prior to initiation of antibiotic therapy. For patients who are clinically stable, antimicrobial therapy may be deferred while awaiting the results of blood cultures and other diagnostic tests. For patients with signs of clinical instability, initiation of empiric antimicrobial therapy (after three blood cultures have been obtained) is appropriate. (See 'Overview of diagnostic approach' above.)

●Typical microorganisms consistent with IE include Staphylococcus aureus, viridans streptococci, Streptococcus gallolyticus (formerly S. bovis), HACEK (Haemophilus, Aggregatibacter, Cardiobacterium, Eikenella, Kingella) organisms, or community-acquired enterococci. (See 'Modified Duke criteria' above.)

●Culture-negative IE should be suspected in patients with negative blood cultures and persistent fever with one or more clinical findings consistent with infective endocarditis (eg, stroke or other manifestations of emboli). Culture-negative IE should also be suspected in patients with vegetation on echocardiogram and no clear microbiologic diagnosis. (See 'Culture-negative endocarditis' above and "Culture-negative endocarditis: Epidemiology, microbiology, and diagnosis".)

●Echocardiography should be performed in patients with suspected IE (table 1 and table 2 and algorithm 1). In general, transthoracic echocardiography (TTE) is the first diagnostic test for patients with suspected IE. Transesophageal echocardiography (TEE) has higher sensitivity than TTE and is better for detection of cardiac complications such as abscess, leaflet perforation, and pseudoaneurysm. In some circumstances, it is reasonable to forgo TTE and proceed to TEE. (See 'Echocardiography' above.)

●Additional evaluation for patients with suspected IE includes electrocardiography, chest radiography, other radiographic imaging tailored to clinical manifestations, and dental evaluation. (See 'Overview of diagnostic approach' above.)

ACKNOWLEDGMENT — The editorial staff at UpToDate would like to acknowledge Vance G Fowler, Jr, MD, who contributed to an earlier version of this topic review.

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death may occur in a few days or weeks

 


Valve infection probably begins when minor trauma, with or without accompanying valve disease, impairs the antihemostatic function of valve endocardium. Infection usually first appears along the coapting surface of the leaflets, suggesting a role for valve opening and closing. This hypothesis is supported by the observation that the ranking of valves in order of frequency of infection corresponds to the ranking of valves according to the force acting to close the valve (mitral > aortic > tricuspid > pulmonic).

This minor trauma may cause the formation of a microscopic thrombus on the leaflet surface. A small noninfected thrombus on the leaflet is called nonbacterial thrombotic endocarditis (NBTE). The next step is infection of the fibrin matrix of the thrombus by blood-borne organisms, which appear briefly in blood under many circumstances, such as toothbrushing, defecating, or other mucus membrane manipulation. When transient bacteremia coincides with the presence of an NBTE lesion, organisms may adhere to the valve leaflet and begin to proliferate.

This theory for the pathogenesis of endocarditis is supported by observations regarding the circumstances under which endocarditis occurs and the particular organisms involved. Patients with endocarditis sometimes tell of a preceding event that likely resulted in transient bacteremia. The common infecting organisms are those that gain entry to the blood because they colonize body surfaces and are adapted for attachment and proliferation in the NBTE lesion (see Clinical Syndromes).

2. Growth of vegetations

Vegetations begin near the coaptation line of the leaflet on the side that contacts the opposite leaflet during valve closure. Mitral valve vegetations are typically attached within 1–2 cm of the leaflet tip on the left atrial side and prolapse into the left atrium during systole. Aortic valve vegetations usually occur on the left ventricular (LV) side of the mid or distal portions of the aortic cusps and prolapse into the LV outflow tract during diastole. A similar distribution of lesions occurs on the tricuspid and pulmonic valves.

 

 

Infective endocarditis is infection of the endocardial surface of the heart and may involve one or more heart valves, a septal defect or an intracardiac device.

 Infection of the endothelium of blood vessels occurs only at sites markedly altered by disease or surgery, such as the severely atherosclerotic aorta or the suture lines of vascular grafts.

By contrast, infection of the cardiac valve leaflet endothelium (endocardium) is not rare and occurs even in the absence of identifiable preexisting valve disease.

 

 

 

 

 

 

Its intracardiac effects include valvular insufficiency, which may progress to intractable congestive heart failure and myocardial abscesses.

Infective endocarditis produces a wide variety of systemic signs and symptoms through both sterile and infected emboli and various immunologic phenomena.

 

  • Glomerulonephritis (streptococci) may develop in children who present with subacute IE as a consequence of immune-mediated disease.
  • Other immunologic sequelae (ie, Roth's spots, Janeway lesions, and Osler nodes) are less common in children than they are in adults.

 

 

 

 

 

 

Content 3

Content 13

Content 11

 

Which of the following is accurate about the etiology of infective endocarditis?

Answer Overall, S aureus infection is the most common cause of infective endocarditis, including PVE, acute infective endocarditis, and IVDA infective endocarditis. Approximately 35%-60.5% of staphylococcal bacteremias are complicated by infective endocarditis. More than one half of all cases are not associated with underlying valvular disease.

The mortality rate of S aureus infective endocarditis is 40%-50%. S aureus infection is the second most common cause of nosocomial bloodstream infections, second only to coagulase-negative staphylococci infection.


 

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