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INTRODUCTION

Infective endocarditis (IE) is a microbial infection of the endocardium. It is serious and life-threatening, with an increasing incidence in children. Over past few decades, the epidemiology of IE has changed due to increased survival of children with congenital heart disease (CHD). Concurrently, a growing proportion of cases occur in children without structural heart disease.

The clinical presentation of IE in children does not follow the classical presentation described in adults. Fever is the most common finding and may be associated with changing murmur and nonspecific symptoms. The primary site of infection, defense mechanisms of the host, and organism determine the clinical manifestations and rate of progression. IE can involve native or prosthetic cardiac valves, septal defects, mural endocardium, patent ductus arteriosus (PDA), or intravascular devices such as catheters, occlusion devices, patches, and surgically constructed shunts. Blood cultures and echocardiography are of paramount importance to aid in the diagnosis.

Despite advances in modern antimicrobial and surgical treatments strategies, IE continues to cause significant morbidity and mortality. Unfortunately, previous antibiotic prophylaxis strategies have proven ineffective. As the incidence of IE in children continues to rise, it is imperative for the general pediatrician and pediatric specialist to identify children at risk of IE, recognize its clinical presentation, and work together in planning its prevention and treatment.

PATHOGENESIS

IE is established by the interaction of a bloodstream pathogen with damaged endocardium. Intact endothelium is a poor stimulator of coagulation and is resistant to colonization by microorganisms; however, damaged endothelium is a potent inducer of thrombogenesis and provides a nidus to which bacteria adhere. Turbulent flow produced by certain congenital or acquired heart diseases causes sheer stress and damages the endothelium. Thrombogenesis ensues and results in the deposition of sterile clumps of platelets, fibrin, and the formation of nonbacterial thrombotic endocarditis (NBTE). NBTE may also be produced in structurally normal hearts when indwelling intravenous catheters damage the endocardium or valvar endothelium. NBTE can then be converted to an infected vegetation in a patient with transient bacteremia or fungemia. Activities of daily living, such as chewing, toothbrushing, and flossing, account for most bloodstream seeding of an NBTE. Bacteremia may also be caused by entry of organisms at the site of entry of percutaneous catheters, via the catheter lumen, or as a result of direct infection of an indwelling device at the time of placement. Bacteremia, however, does not invariably produce IE. The propensity to adhere to an NBTE depends on the type of microorganism. Gram-positive microorganisms are most commonly responsible for IE in children because they possess specific surface components that facilitate adherence.

EPIDEMIOLOGY

Before the 1970s, rheumatic heart disease (RHD) was the underlying substrate for IE in 30% to 50% of children. While RHD remains an important substrate for IE globally, its incidence in developed countries has diminished substantially. CHD is the predominant underlying condition for ...

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