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Infective endocarditis (IE) in pediatric patients is often associated
with an underlying congenital heart defect. However, structurally normal
hearts may also be infected. Accurate diagnosis and appropriate
medical management, are required to achieve a satisfactory outcome
of this previously uniformly fatal disease.
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Establishment of infective endocarditis results from the interaction
of several host and microbial factors. Endocardial surfaces damaged
by turbulent blood flow attract platelets and fibrin, leading to
the formation of a nonbacterial thrombotic lesion. Experimental
animal models have demonstrated that healthy, intact endothelium
is resistant to colonization by circulating microbes; in contrast,
damage of endocardium (as with a plastic catheter or a jet of blood)
leads to rapid microbial colonization. The endocardium appears to be a preferential site of microbial adherence
and may have some specificity for binding with certain bacteria.1-3
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Two mechanisms, the Venturi and jet effects, combine to damage
endocardial surfaces as blood is forced from an area of high pressure
into a low-pressure sink. The Venturi effect deposits bacterial
colonies immediately beyond the orifice that separates high and
low pressure areas. Large pressure gradients are essential to these
mechanisms, which explains the low risk of infective endocarditis
in isolated atrial septal defects and the higher risk of infective
endocarditis in small, rather than large ventricular septal defects.
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Following endocardial damage, bacterial access to the bloodstream
and adherence to endocardial surfaces are required for the establishment
of infective endocarditis. It is now thought that the great majority
of infective endocarditis develops as the result of transient bacteremia
related to activities of daily life,2 but not all
bacteria are capable of initiating this process. The presence of
several factors, including bacterial surface polysaccharides, endothelial
binding proteins, and agglutinating antibodies that clump bacteria,
promote adherence of organisms to damaged endocardial surfaces. In
some cases, microbial invasiveness may be more important than host
or tissue factors in initiating infection.
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Many of the classic manifestations of infective endocarditis
(IE) are immunologically mediated. In IE patients with arthralgias
and arthritis, splenomegaly, Roth spots, glomerulonephritis, and
thrombocytopenia, circulating immune complex levels are significantly higher
than in IE patients without these manifestations. Levels of immune
complexes decline as these physical manifestations resolve.
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Bacteremia in patients with infective endocarditis is generally
low grade and continuous. As much as 10% of cases of infective endocarditis
yield consistently negative blood cultures, most often as a result
of prior antibiotic therapy. Fastidious organisms with special growth
requirements may be difficult to culture. Bacteria infecting right-sided
heart lesions may be filtered by pulmonary phagocytes, significantly
reducing the number of bacteria in a peripheral blood sample. In
evaluating patients for infective endocarditis, it is preferable to
obtain at least three separate blood cultures over a 24- to 48-hour
period if the patient is stable. Blood should not be drawn through
indwelling vascular catheters because contamination may be misleading.
If only one of several blood ...