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Infective endocarditis: Clinical practice

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Infective endocarditis: Clinical practice

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A 62-year-old woman presents to the primary care physician for preoperative clearance for surgical placement of false teeth. The patient has a history of aortic stenosis and had a bioprosthetic replacement five years ago. The patient has no allergies. Which of the following describes the best treatment regimen prior to the surgery?  

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Content Reviewers:

Rishi Desai, MD, MPH

Infective endocarditis is an infection of the endocardium, the inner layer of the heart.

Most cases are due to a bacterial or fungal infection of the endocardial lining the heart valves.

But in order to reach the heart valves, a microbe has to first get into the bloodstream.

There are a few ways that might happen - microbes can hop into a blood vessel near an open wound or an abscess, or during a dental or surgical procedure, or they can go directly in when a person gets injected with an infected needle which sometimes happens while using illicit drugs.

Microbes generally like to latch onto heart valves that are already damaged, because it makes it easier for them to adhere and form vegetations.

Risk factors for infective endocarditis include cardiac factors, like prior infective endocarditis, a prosthetic valve or implantable cardiac device like a pacemaker, or valvular or congenital heart disease; and noncardiac factors like intravenous drug use, having an intravenous catheter, immunosuppression, or a recent dental or surgical procedure.

Clinically, infective endocarditis is categorized as either native valve endocarditis when it affects a previously normal heart valve, or prosthetic valve endocarditis when it affects an artificial heart valve.

Native valve endocarditis is mainly caused by Staphylococcus aureus, viridans Streptococci, and is often seen in intravenous drug users, since these bacteria are normally present in the skin.

Prosthetic valve endocarditis is mostly caused by Staphylococcus aureus as well - specifically methicillin resistant Staphylococcus Aureus or MRSA, since it’s frequently nosocomial.

Infective endocarditis causes fever, fatigue, dyspnea, and weight loss.

Typically there’s an acute infection, which occurs within two weeks, but in some cases it might be subacute or chronic and happen over a few months.

Upon auscultation, there’s usually a heart murmur from blood flowing past the vegetation and creating turbulence.

Sometimes, vegetations can detach from the valve, and float through the bloodstream—called septic emboli.

These septic emboli can then lodge under the fingernails, causing splinter hemorrhages, or in the palms and soles of the feet, causing small painless, flat, and erythematous lesions, called Janeway lesions.

Brain embolization may also occur, leading to an embolic stroke or intracerebral hemorrhage.

Other complications of septic emboli may include arterial emboli, pulmonary infarcts, and conjunctival hemorrhage.

Separately, there may be an immune reaction to bacterial proteins that results in antibodies.

Bacterial antigen-antibody complexes can form and deposit in different parts of the body. In the fingers and toes, these complexes result in painful lesions called Osler’s nodes, in the eye these deposits can lead to Roth spots, and in the kidney they can lead to glomerulonephritis.

In anyone suspected of having infective endocarditis, the first step is collecting three sets of blood cultures of 10 milliliters each from separate venipuncture sites, one for aerobic bacteria, one for anaerobic bacteria, and one for fungi.

Echocardiography should be done for all individuals with suspected infective endocarditis to look for vegetations or subtler clues like the way a valve is moving.

Transthoracic echocardiography is usually done first because it’s non-invasive and cheap, but it has a lower sensitivity.

In contrast, transesophageal echocardiography has higher sensitivity, allowing it to identify really small vegetations, but it’s invasive and typically requires sedation.

In some cases transesophageal echocardiography is done right away - like for individuals with prosthetic valves, implantable cardiac device, those with prior valve abnormalities including previous endocarditis, and individuals who are obese or have a chest wall deformity.

Diagnosis is confirmed using Duke’s criteria, which has major and minor criteria.

The first major criterion relates to having microbiologic evidence of an organism that’s likely to cause infective endocarditis.

Drilling down a bit, that might mean getting two blood cultures taken from separate sites on the body with microorganisms that commonly cause infective endocarditis, like Staphylococcus aureus; Viridans group Streptococci; Streptococcus bovis; or a HACEK group organism, which stands for Haemophilus, Aggregatibacter, Cardiobacterium, Eikenella, and Kingella.

Another way to meet the first criteria is to have a blood culture of community-acquired enterococcus, without an obvious source of infection like a urinary tract infection.

The first criterion can also be met if there’s evidence of persistent bacteremia.

For example if there are at least two positive cultures of blood samples drawn from a single site on the body more than 12 hours apart, or if more than three cultures are drawn, then if a majority of the cultures are positive, as long as the first and last sample are drawn at least one hour apart.

One microbe - Coxiella burnetii - is particularly hard to culture, so the first major criterion is met if there’s one positive blood culture or an IgG antibody titer of over 1:800.

Now, some individuals may have clinical findings of infective endocarditis, but the cultures are negative, and those situations are called culture-negative endocarditis.

This may occur in individuals that took antimicrobial treatment before collecting their blood samples, or in those infected by bacteria that don’t easily grow in standard cultures, such as the HACEK organisms.

Fortunately, some causes of culture-negative endocarditis can be identified using serology or polymerase chain reaction.

And because of the possibility of a culture-negative endocarditis, the second major criterion relates to seeing evidence of endocardial disease - usually that means new valvular regurgitation, or an echocardiogram showing a vegetation, abscess, or partial dehiscence of a prosthetic valve.

The five minor criteria are having a predisposing factor, like a known cardiac lesion or history of recreational drug injections; having a fever; having evidence of septic emboli, like arterial emboli, pulmonary infarcts, Janeway lesions, or conjunctival hemorrhage; having autoimmune conditions like glomerulonephritis, Osler's nodes, Roth's spots, or even a positive Rheumatoid factor; and having microbiologic or serologic evidence that doesn’t satisfy a major criteria.

Diagnosis of infective endocarditis can be definite or possible.

A definite diagnosis meets either two major criteria, one major criteria and three minor ones, or all five of the minor criteria.

A possible diagnosis meets one major and one minor criteria, or three minor criteria.

If infective endocarditis is suspected, an ECG should be done. It might show a heart block or conduction delay with just an isolated prolonged PR interval.

In addition, if there’s evidence of cardiac ischemia, that suggests septic emboli may have gotten into the coronary circulation.