Although infective endocarditis is a relatively uncommon diagnosis in children, it is an important cause of morbidity and mortality in the pediatric population.1 The incidence of this disease appears to be increasing in patients with known cardiac disease and in other groups as well.2,3 For these reasons, the pediatric hospitalist must be well versed in the epidemiology, causative factors, and treatment of this disorder.
Over the past several decades, altered rates of predisposing risk factors have driven changes in the epidemiology of infective endocarditis. For instance, the decline in rheumatic heart disease has meant a corresponding decline in infective endocarditis resulting from this illness. Conversely, in the United States and other developed nations, an increase in infective endocarditis has occurred among children with congenital heart disease. This includes not only children with untreated cardiac conditions, such as small ventricular septal defects, but also children who have had corrective or palliative surgery, including implanted grafts or patches, prosthetic valves, and conduits. A review of the modern epidemiology of infective endocarditis after surgery for congenital heart disease found that the highest annualized risk was in patients who had had interventions for cyanotic forms of congenital heart disease, including relief of obstructed pulmonary blood flow.3 Among the acyanotic group, a higher incidence of infective endocarditis occurred in patients who had prosthetic aortic valve placement.
In addition to the rising prevalence of infective endocarditis among survivors of congenital heart disease, the same trend is occurring in certain children without structural heart disease. As many as 8% to 10% of children with infective endocarditis have no known primary cardiovascular abnormality.4 This group includes children with chronic indwelling central venous catheters, newborns (particularly premature babies, who are increasingly subjected to invasive procedures), and adolescent intravenous drug abusers.
Studies of animal models confirm that the development of a nidus for endocardial infection requires a locus of denuded endothelium as well as exposure to bacteria.5 The disrupted endothelial surface exposes collagen to the bloodstream, which leads to the deposition of fibrin and platelets and the formation of a thrombotic vegetation. Circulating microorganisms, most commonly bacteria, can become embedded in the vegetation, resulting in an endocardial infection. Additional deposits of platelets and fibrin form protective layers that shield the pathogens from host immune defenses. As the process continues, the vegetation grows, creating layers of embedded microorganisms. The organisms sequestered within the vegetation have a great potential for proliferation.
Congenital heart lesions with high-velocity blood flow jets are most susceptible to vegetation development, owing to the potential for endothelial damage. Adding appreciably to this risk is the presence of foreign material, which itself can offer a site prone to the development of platelet and fibrin plugs. Patients with surgically placed grafts or palliative shunts (e.g. Blalock-Taussig shunts) are thus at high risk for infective endocarditis.6