Endocarditis
An infection of the endocardium, heart valves, or cardiac prosthesis, endocarditis results from bacterial or fungal invasion.
In infective endocarditis, fibrin and platelets cluster on valve tissue and engulf circulating bacteria or fungi. This produces friable verrucous vegetation. The vegetation may cover the valve surfaces, causing deformities and destruction of valvular tissue. It may also extend to the chordae tendineae, causing them to rupture and leading to valvular insufficiency.
Sometimes vegetation forms on the endocardium, usually in areas altered by rheumatic, congenital, or syphilitic heart disease. It may also form on normal surfaces. Vegetative growth on the heart
valves, endocardial lining of a heart chamber, or endothelium of a blood vessel may embolize to the spleen, kidneys, central nervous system, and lungs. (See Recognizing infarction sites in endocarditis.)
valves, endocardial lining of a heart chamber, or endothelium of a blood vessel may embolize to the spleen, kidneys, central nervous system, and lungs. (See Recognizing infarction sites in endocarditis.)
Recognizing infarction sites in endocarditis
In 12% to 35% of patients with subacute endocarditis, embolization from vegetating lesions or diseased valve tissue may produce typical characteristics of splenic, renal, cerebral, or pulmonary infarction or peripheral vascular occlusion.
Splenic infarction causes pain in the left upper quadrant, radiating to the left shoulder, and abdominal rigidity.
Renal infarction causes hematuria, pyuria, flank pain, and decreased urine output.
Cerebral infarction causes hemiparesis, aphasia, and other neurologic deficits.
Pulmonary infarction causes cough, pleuritic pain, pleural friction rub, dyspnea, and hemoptysis. These signs are most common in right-sided endocarditis, which typically occurs among I.V. drug abusers and after cardiac surgery.
Peripheral vascular occlusion causes numbness and tingling in an arm, leg, finger, or toe or signs of impending peripheral gangrene.
Endocarditis can be classified as native valve endocarditis, endocarditis in I.V. drug users, and prosthetic valve endocarditis. It can be acute or subacute. Untreated, endocarditis is usually fatal. With proper treatment, however, about 70% of patients recover. The prognosis is worst when endocarditis causes severe valvular damage—leading to insufficiency and left ventricular failure—or when it involves a prosthetic valve.
Causes
Acute infective endocarditis usually results from bacteremia that follows septic thrombophlebitis, open-heart surgery involving prosthetic valves, or skin, bone, and pulmonary infections.
The most common causative organisms are group A nonhemolytic streptococci, staphylococci, and enterococci. However, almost any organism can cause endocarditis, including Neisseria gonorrhoeae, Pseudomonas, Salmonella, Streptobacillus, Serratia marcescens, bacteroids, Haemophilus, Brucella, Mycobacterium, N. meningitidis, Listeria, Legionella, diphtheroids, enteric gram-negative bacilli, spirochetes, rickettsiae, chlamydiae, and the fungi Candida and Aspergillus.
Subacute infective endocarditis typically occurs in people with acquired valvular or congenital cardiac lesions. It can also follow dental, genitourinary (GU), gynecologic, and GI procedures. The most common infecting organisms are Streptococcus viridans, which normally inhabits the upper respiratory tract, and Enterococcus faecalis, found in GI and perineal flora.
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