Infective Endocarditis

N C Joshi
Infective Endocarditis - Introduction
Bacterial infections can cause serious cardiac disease. Two examples are endocarditis and rheumatic fever. Bacterial endocarditis occurs when certain bloodborne bacteria lodge on damaged endocardial surfaces of the heart usually an abnormal valve or on anatomic cardiac defect.

The epidemiological pattern of endocarditis has changed significantly during last few years. The term "infective endocarditis" popularized by Lerner and Weinstein (1) has gained general acceptance in recent medical literature replacing the older term "subacute bacterial endocarditis." The disease was known as acute or subacute depending on virulence of the organism. But now it is known that organisms with low virulence can produce acute disease and that virulent organisms may produce subacute disease. Factors that contributed to changing pattern include longer survival of infants and children with congenital heart disease, the widespread use of anti-microbial agents, increased use of indwelling intravenous catheters in intensive care units. The number of children hospitalized with infective endocarditis is reported at 0.55/1000 hospital admissions.

The cardiac lesions that predispose to endocarditis are those that result in high velocity turbulent flows leading to eddy currents and/or denudation of endocardial epithelium. The rheumatic valvular disease and congenital heart disease still continue to be a major predisposing factor in India. Few cases of endocarditis continue to occur in children with no apparent preexisting heart lesion.

Endocarditis is preceded by bacteremia, often caused by dental or other surgical procedures. The cyanotic patients with dental caries and periodontal disease are particularly at risk.

Bacteremia and endocardial colonization may be associated with procedures such as hemodialysis via arteriovenous fistula, barium enemas, intravenous alimentation, cardiac catheterization and can also occur following open-heart surgery.

In patients with rheumatic heart disease , the mitral valve is the most common site of involvement with an incident of 30-50%. The aortic valve is involved in 5-35% and both valves in about 35%.

Tetralogy of Fallot is the most common lesion associated with endocarditis. Children with small VSD (high velocity turbulent shunt flow) and patent ductus arteriosus are next to develop infective endocarditis. Endocarditis is also common in children with bicuspid aortic valve, aortic stenosis, and prolapsed mitral valve syndrome . It is very rare with ASD (OS) and pulmonic stenosis.

Children who undergo palliative cardiac surgery with prosthetic material for repair and in whom aortic valvulotomy have been performed continue to be at risk even after successful surgery.

Alpha hemolytic streptococci (streptococcus viridans ) continue to be most common cause of infective endocarditis in children and adults occurring in 50-60% of patients followed by staphylococcal endocarditis. Streptococcus viridans endocarditis usually follows dental procedures whereas staphylococcal endocarditis is typically associated with cardiac surgery, prosthetic valves and materials, drug addiction and endocarditis without preexisting heart disease.

Group D streptococci, now called enterococci account for less than 4% of endocarditis in children. Pneumococci, Gm-ve bacilli such as Escherichia coli, salmonella are uncommon causes. Fungi, especially candida, are not uncommon especially in patients with compromised host resistance.

The histopathologic hallmark of endocarditis is the vegetation, an amorphous clot typically harboring micro-organisms but scant inflammatory cells. The observation that organisms buried in the vegetation are protected from host defenses explains why long courses of bactericidal antibiotics are needed for reliable cure of endocarditis. In 14-30% of patients, blood culture will remain negative but does not appear to be related to prior antibiotic therapy, duration of the disease, or specific cardiac lesion.

Infective Endocarditis Infective Endocarditis 01/02/2002
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