Endocarditis overview

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Overview
Historical Perspective
Classification
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Differentiating Infective Endocarditis from other Diseases
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-in-Chief: Maliha Shakil, M.D. [2] Cafer Zorkun, M.D., Ph.D. [3]

Overview

Endocarditis is an inflammation of the inner layer of the heart, the endocardium. It usually involves the heart valves. While acute bacterial endocarditis is caused by an infection with a virulent organism such as staphylococcus aureus, group A or other beta-hemolytic streptococci, subacute bacterial endocarditis is an indolent infection with less virulent organisms such as streptococcus viridans. Patients with unexplained fever for more than 48 hours and who are at high risk for infective endocarditis and patients among whom valve regurgitation is newly diagnosed should undergo a diagnostic workup to rule out endocarditis. The diagnosis of endocarditis depends on a thorough history and physical exam as well as on the results of the blood cultures and the findings on transthoracic echocardiogram or transesophageal echocardiogram. The modified Duke criteria is used to establish the diagnosis of endocarditis. Endocarditis is initially treated with empiric antibiotic therapy until the causative agent is identified.

Historical Perspective

Endocarditis was first described in 1554. The inflammatory process associated with endocarditis was discovered in 1799. Vegetations were first discovered to be associated with endocarditis in 1806.

Classification

Endocarditis may be classified based on the underlying pathophysiology of the process (infective vs. non-infective), the onset of the disease (acute vs. subacute or short incubation vs. long incubation), results of the cultures (culture positive vs. culture negative), the nature of the valve (native vs. prosthetic) and the valve affected (aortic, mitral, or tricuspid valve).

Pathophysiology

The pathogenesis of infective endocarditis includes valvular damage, altered and turbulent flow, bacteremia, and lack of blood supply to the valves. Damaged endothelium becomes a site for attachment of infectious agents in infectious endocarditis. Nonbacterial thrombotic endocarditis is related to hypercoaguable states such as pregnancy or systemic bacterial infection. The characteristic lesion of endocarditis is a vegetation. Vegetations are composed of fibrin, inflammatory cells, platelets, and microorganisms.

Causes

The majority of cases of infective endocarditis are due to bacteria. Common causes of infective endocarditis include Streptococcus viridans, Staphylococci, and Enterococcus.

Differentiating Endocarditis From Other Diseases

Endocarditis must be differentiated from other causes of a fever of unknown origin (FUO) such as pulmonary embolism, deep vein thrombosis, lymphoma, drug fever, cotton fever, and disseminated granulomatoses.

Risk Factors

Common risk factors for endocarditis include prosthetic heart valves, valvular heart disease, congenital heart disease, intravenous drug use, age-related degenerative valvular lesions, immunosuppression, and colon cancer.

Epidemiology and Demographics

The incidence of native valve infective endocarditis is approximately 1.7-6.2 cases per 100,000 individuals per year in the United States and Europe. The prevalence of infective endocarditis among IV drug users ranges from 10 to 15%. The incidence of endocarditis increases with age; the median age of patients is 47 to 69 years. There is an increased incidence of infective endocarditis in persons 65 years of age and older. Males are more commonly affected with endocarditis than females. The male to female ratio is approximately 1.7:1.

Natural History, Complications, and Prognosis

If left untreated, patients with endocarditis may progress to develop congestive heart failure. 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, and disruption of the heart's conduction system. Endocarditis may also cause 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 of endocarditis is generally poor and the overall mortality rate for both native and prosthetic valve endocarditis ranges from 20-25%. The mortality rate for right sided endocarditis in injection drug users ia approximately 10%. The 5 year survival rate for native valve endocarditis is 70-80% and 50-80% for prosthetic valve endocarditis.

Diagnosis

Diagnostic Criteria

The Duke criteria 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 murmur, 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. Laboratory findings consistent with the diagnosis of endocarditis include elevated white blood cell count, erythrocyte sedimentation rate, rheumatoid factor, and elevated BUN and creatinine if glomerulonephritis is present.

Chest x-ray

On chest x-ray, right sided endocarditis is characterized by pleural effusions, multiple round densities, and cavitary multilobar infiltrates.

Electrocardiography

On EKG, endocarditis may be characterized by conduction abnormalities, low QRS voltage, ST elevation, heart block, ventricular tachycardia, and supraventricular tachycardia. The EKG may show ST elevation in the presence of embolization of a vegetation or clot down the coronary artery.

Cardiac MRI

Findings on cardiac MRI suggestive of infective endocarditis include valvular vegetations, valvular and perivalvular damage, and vascular endothelial involvement.

CT Scan

CT scan may be helpful in the diagnosis of endocarditis. CT scan findings suggestive of endocarditis include vegetations, paravalvular abscesses, and pseudoaneurysms.

Echocardiography

Echocardiography may be diagnostic of endocarditis. Echocardiography allows detection of microbial vegetations and the degree of valvular dysfunction. Findings on transthoracic and transesophageal echocardiogram diagnostic of endocarditis include vegetations, valvular regurgitation, pseudoaneurysms, paravalvular abscess, and fistulas.

Treatment

Medical Therapy

Antimicrobial therapy is the mainstay of therapy for endocarditis. Empiric antimicrobial therapy depends on the nature of the valve (native vs. prosthetic) and the onset of endocarditis following valve implantation (less than 1 year vs. more than 1 year). In patients with endocarditis, antithrombotic therapy may be administered when needed. The prothrombin time must be carefully monitored as anticoagulants may cause or worsen hemorrhage in patients with endocarditis. Heparin administration should be avoided if possible.

Surgery

Surgical removal of the valve is necessary in patients who fail to clear micro-organisms from their blood in response to antibiotic therapy, or in patients who develop cardiac failure resulting from destruction of a valve by infection. A removed valve is usually replaced with an artificial valve which may either be mechanical (metallic) or obtained from an animal such as a pig; the latter are termed bioprosthetic valves. Surgical treatment of endocarditis involves excision of all infected valve tissue, drainage and debridement of abscess cavities, repair or replacement of damaged valves, and repair of any associated pathology such as fistulas or septal defects.

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.

References