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Also called infective endocarditis and bacterial endocarditis, endocarditis is an infection of the endocardium, heart valves, or a cardiac prosthesis, resulting from bacterial or fungal invasion. This invasion produces vegetative growths on the heart valves, the endocardiallining of a heart chamber, or the endothelium of a blood vessel that may embolize to the spleen, kidneys, central nervous system, and lungs.

In endocarditis, fibrin and platelets aggregate on the valve tissue and engulf circulating bacteria or fungi that flourish and produce friable verrucous vegetations. Such vegetations may cover the valve surfaces, causing ulceration and necrosis; they may also extend to the chordae tendineae, leading to their rupture and subsequent valvular insufficiency.

Untreated endocarditis is usually fatal, but with proper treatment, about 70% of patients recover. The prognosis is worst when endocarditis causes severe valvular damage, leading to insufficiency and heart failure, or when it involves a prosthetic valve.


Bacterial endocarditis occurs when bacteria in the bloodstream (bacteremia) lodge on abnormal heart valves or other damaged heart tissue. Certain bacteria normally live on parts of your body, such as the mouth and upper respiratory system, the intestinal and urinary tracts, and the skin. Some surgical and dental procedures cause a brief bacteremia. Bacteremia is common after many invasive procedures, but only certain bacteria commonly cause endocarditis.

Signs and symptoms

Early clinical features of endocarditis are usually nonspecific and include malaise, weakness, fatigue, weight loss, anorexia, arthralgia, night sweats, chills, valvular insufficiency and, in 90% of patients, an intermittent fever that may recur for weeks. A more acute onset is associated with highly pathogenic organisms such as S. aureus.

Endocarditis often causes a loud, regurgitant murmur that is typical of the underlying heart lesion. A suddenly changing murmur or the discovery of a new murmur in the presence of fever is a classic physical sign of endocarditis.

In about 30% of patients, embolization from vegetating lesions or diseased valvular tissue may produce the following features of splenic, renal, cerebral, or pulmonary infarction or peripheral vascular occlusion:

  • splenic infarction: pain in the left upper quadrant, radiating to the left shoulder; abdominal rigidity
  • renal infarction: hematuria, pyuria, flank pain, decreased urine output
  • cerebral infarction: hemiparesis, aphasia, or other neurologic deficits
  • pulmonary infarction (most common in right-sided endocarditis, which usually occurs in I.V. drug abusers and after cardiac surgery): cough, pleuritic pain, pleural friction rub, dyspnea, hemoptysis
  • peripheral vascular occlusion: numbness and tingling in an arm or a leg, finger, or toe or signs of impending peripheral gangrene.

Other signs include splenomegaly; petechiae of the skin (especially common on the upper anterior trunk) and the buccal, pharyngeal, or conjunctival mucosa; and splinter hemorrhages under the nails. Rarely, endocarditis produces Osler's nodes (tender, raised subcutaneous lesions on the fingers or toes), Roth's spots (hemorrhagic areas with white centers on the retina), and Janeway lesions (purplish macules on the palms or soles).


Three or more blood cultures in a 24­to 48-hour period identify the causative organism in up to 90% of patients. The remaining 10% may have negative blood cultures, possibly suggesting fungal infection or infections that are difficult to diagnose, such as Haemophilus parainfluenzae. Other abnormal but nonspecific laboratory test results include:

  • normal or elevated white blood cell count
  • abnormal histiocytes (macrophages)
  • elevated erythrocyte sedimentation rate
  • normocytic, normochromic anemia (in 70% to 90% of endocarditis cases)
  • positive serum rheumatoid factor (in about one-half of all patients with endocarditis after the disease is present for 3 to 6 weeks).

Echocardiography may identify valvular damage; electrocardiography may show atrial fibrillation and other arrhythmias that accompany valvular disease.


The goal of treatment is to eradicate the infecting organism. Anti-microbial therapy should start promptly and continue over 4 to 6 weeks. Selection of an antibiotic is based on identification of the infecting organism and on sensitivity studies. While awaiting test results or if blood cultures are negative, empiric antimicrobial therapy is based on the likely infecting organism.

Supportive treatment includes bed rest, aspirin for fever and aches, and sufficient fluid intake. Severe valvular damage, especially aortic or mitral insufficiency, may necessitate corrective surgery if refractory heart failure develops or in cases in which an infected prosthetic valve must be replaced.


Not all cases of endocarditis can be prevented, because we don't always know when a bacteremia occurs. However, preventive antibiotics are often given to people with predisposing heart conditions before dental procedures or surgeries involving the respiratory , urinary, or intestinal tract. Continued medical follow-up is advised for people with a history of endocarditis.

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