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 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:

1. Alpha-haemolytic streptococci, that are present in the mouth will often be the organism isolated if a dental procedure caused the bacteraemia.
2. 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.
3. 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 Diseases

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, cotton 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 and echocardiography are critical in differentiating endocarditis from these other syndromes.

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%.

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:

• 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.

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.