Jane W. Newburger
Infective endocarditis (IE) is defined as an infection of the endocardium, generally involving cardiac valves and their valvular apparatus such as the chordae tendinae, interventricular septum, mural endocardium, or intracardiac devices. IE may occur in children with or without antecedent underlying cardiac disease. The diagnosis of IE rests on a constellation of clinical features and laboratory investigations, including blood cultures and echocardiography.1 Most often, IE presents with fever, positive blood cultures, a new murmur, or vegetations by echocardiography. Vascular findings and immunologic phenomena are common. The presenting symptoms, rate of progression, morbidity, and mortality of infective endocarditis depend, in part, upon the underlying heart disease, the etiologic organism, and host factors. Whereas most infective endocarditis is accompanied by positive blood cultures, 5% to 7% are culture negative, sometimes due to administration of antibiotics before blood cultures were obtained.1 Compared to adults, children have a lower incidence and fatality rate of IE.2,3 The most common causes of bacterial endocarditis in children are viridans group streptococci and Staphylococcus aureus; other principal pathogenic agents include coagulase-negative staphylococci, Streptococcus pneumoniae, HACEK organisms (Haemophilus species, Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, and Kingella species), and enterococcus species.4-6 Emergence of antibiotic resistance to these common pathogens has serious ramifications for the morbidity and mortality of IE. It is therefore essential that pediatricians and pediatric cardiologists work in concert with specialists in infectious diseases in planning the treatment of IE.
CLINICAL FEATURES AND DIFFERENTIAL DIAGNOSIS
Infective endocarditis (IE) is readily diagnosable in children with at least 2 positive blood cultures, structural heart disease, and vegetations as identified by echocardiography. However, the diagnosis can be challenging, for example, when a patient with structural heart disease has bacteremia. To aid diagnosis and facilitate epidemiologic and clinical research efforts, the modified Duke criteria have become the gold standard for diagnosis of infective endocarditis. These criteria classify endocarditis as definite, possible, or rejected, based upon particular pathologic findings or combinations of major and minor clinical criteria.13 (See Table 490-1.)
A typical history for the patient with subacute IE includes nonspecific symptoms, such as low-grade fever, malaise, fatigue, weight loss, headache, arthralgias, and myalgias. Presentation may also be fulminant, with acute symptoms and high fever. Careful daily physical examination reflects changes in cardiac structure or function, as well as embolic, vascular, or immune phenomena. Specifically, IE may cause new or changing heart murmurs, and worsening valvular regurgitation may cause congestive heart failure. Occlusion of a systemic to pulmonary artery shunt in a child with cyanotic heart disease may decrease oxygen saturation. Septic emboli may cause ischemia or hemorrhage in, for example, the kidneys, spleen, or brain. Patients with right-sided endocarditis may have septic pulmonary emboli. Mycotic aneurysms in the central nervous system or viscera are at risk for rupture. Vascular and immune phenomena include petechiae, most commonly present on the extremities, oral mucosa (eg, palate), or conjunctivae, best seen on eversion of the upper and lower eyelids. Splinter hemorrhages are nonblanching lines of maroon color under the proximal nail beds. Roth spots are retinal hemorrhages with white or pale centers composed of coagulated fibrin caused by immune complex deposition. Janeway lesions are painless hemorrhagic cutaneous lesions on the palms or soles due to a microabscess of the dermis formed by deposition of circulating immune complexes in small blood vessels. Osler nodes are painful subcutaneous lesions on the distal fingers caused by immune complex deposition. Glomerulonephritis and splenomegaly may also be caused by immune phenomena.
For definite clinical diagnosis: 2 major criteria or 1 major and 3 minor criteria or 5 minor criteria.
For possible clinical diagnosis: 1 major criterion and 1 minor criterion or 3 minor criteria.
For rejection of diagnosis: Firm alternative diagnosis explaining the findings of infective endocarditis, resolution of symptoms and signs after antimicrobial therapy for ≤ 4 days, no pathologic evidence of infective endocarditis found during surgery or autopsy, or failure to meet the clinical criteria for possible endocarditis.
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