Pediatric Bacterial Endocarditis

Updated: Mar 31, 2016
  • Author: Michael H Gewitz, MD; Chief Editor: Syamasundar Rao Patnana, MD  more...
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Overview

Background

Bacterial endocarditis is a microbial infection of the endothelial surface of the heart. Signs and symptoms of bacterial endocarditis are diverse; therefore, the practitioner must have a high degree of suspicion to make an early diagnosis. In addition, classification that implicates the disease’s temporal aspect, etiology, anatomic site of infection, and relevant pathogenic risk factors is essential in therapeutic and prognostic considerations. [1] (See History and Physical Examination.)

Go to Infective Endocarditis for more complete information on this topic. 

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Pathophysiology

Features of bacterial endocarditis are due to bacteremia, local cardiac invasion by organisms, peripheral embolization, and the formation of immune complexes.

High-velocity flow through a stenotic or incompetent valve or an abnormal communication between systemic and pulmonary circulations causes turbulence at the valve, within the communication, or downstream where the flow eddies. This turbulence damages or denudes the endothelium, to which platelets and fibrin can adhere, and a small, sterile nonbacterial thrombotic endocardial lesion forms.

In addition, indwelling intravascular catheters may directly traumatize the endocardium or valvular endothelium. Circulating bacteria and inflammatory cells adhere to and grow in these thrombi, forming an infected vegetation. Once vegetation forms, the constant blood flow may result in embolization to virtually any organ in the body. A brisk immunologic response is produced.

Acute heart failure may be due to valve destruction or distortion and/or rupture of the chordae tendineae. Chronic heart failure may be due to progressive valvular insufficiency with worsening ventricular function. (See Epidemiology.)

Vasculitis may result from circulating immune complexes that may deposit on various endothelial surfaces. Local complement activation appears to generate an immune response that causes vascular injury. (See Epidemiology.)

Renal insufficiency resulting from immune complex–mediated glomerulonephritis occurs in less than 15% of patients with endocarditis and may cause hematuria and, rarely, azotemia, which is independent of circulatory dynamics.

Not uncommonly, and especially in neonates, infective endocarditis produces septic embolic phenomena, such as osteomyelitis, meningitis, and pneumonia. (See Etiology and Epidemiology.)

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Etiology

Microbiology

A select group of organisms causes most cases of endocarditis. Gram-positive organisms, particularly alpha-hemolytic streptococci (Streptococcus viridans), Staphylococcus aureus, and coagulase-negative staphylococci, are the most common offenders. S aureus is the most common cause of acute bacterial endocarditis.

Enterococci are rare, but dangerous, causative organisms, because they often are highly resistant to antibiotic treatment.

Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, and Kingella species (HACEK organisms) are particularly common in neonates and immunocompromised children.

Fungal endocarditis is a severe disease with a poor prognosis. Complications are common.

Culture-negative endocarditis

Culture-negative endocarditis occurs when a patient has typical clinical or echocardiographic findings of endocarditis, with persistently negative blood cultures. Common causes include recent antibiotic therapy, or infection caused by a fastidious organism that grows poorly in vitro.

Risk factors

High-risk conditions include the following:

  • Cyanotic congenital heart disease
  • Valvulopathy in a cardiac transplantation patient
  • Prosthetic valve
  • Intravenous drug use
  • Previous episode of bacterial endocarditis
  • Surgical systemic to pulmonary shunts and conduits
  • Central venous catheters (especially neonates)
  • Residual cardiac defect post surgical or catheter intervention for that defect
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Epidemiology

In the United States, the incidence of endocarditis is approximately 1 case per 1000 pediatric hospital admissions. [2] This incidence has remained essentially unchanged over the past 40 years; however, the distribution of etiologies has shifted.

Rheumatic heart disease, which was once common, is now rare as a condition associated with endocarditis. In contrast, the advent of sophisticated cardiac procedures and early intervention with improved survivor rates has led to an increase in congenital heart disease as the underlying condition in children with endocarditis. Preexisting cardiac abnormalities are found in approximately 75-90% of children with bacterial endocarditis. [3] In premature neonates, the prevalent use of chronic indwelling catheters and prolonged hospitalization with frequent interventional therapies has led to an increased incidence of endocarditis even when the heart is structurally normal.

Race-, sex-, and age-related demographics

No racial or sex predilection is observed.

Bacterial endocarditis is most frequently observed in adults, but the incidence in children and infants with congenital heart disease or central indwelling venous catheters continues to rise.

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Prognosis

The prognosis of bacterial endocarditis varies with the etiologic agent. [4] Infection by a penicillin-sensitive Streptococcus, if diagnosed early, has a cure rate of nearly 100%.

Because many infections are diagnosed late or are due to resistant organisms, the average mortality rate is approximately 16-25%.

Mortality rate

The overall mortality rate for endocarditis in pediatric patients is approximately 16-25%. Improved general health care, improved dental care, early treatment, and antibiotic prophylaxis have decreased the mortality rate. [3]  Mortality is mostly due to secondary congestive heart failure (CHF) or to the complications of systemic emboli. Russell et al reported an overall mortality of 15% in children who underwent surgery. [5]

Heart failure with acute, severe aortic insufficiency is associated with high mortality rates.

Morbidity

Cardiac complications include heart failure, new valvular disease, valve ring abscess, myocardial disease or abscess, conduction abnormalities (including arrhythmia or heart block), and pericardial disease. In rare cases, coronary artery embolic events can occur.

Vasculitis may result from circulating immune complexes that may deposit on various endothelial surfaces. Local complement activation appears to generate an immune response that causes vascular injury.

Endocarditis commonly produces septic embolic phenomena, such as osteomyelitis, meningitis, and pneumonia, with neonates most prone to these complications.

Embolic complications are most common in patients with large or highly mobile lesions. Peripheral vascular complications include splenic emboli with infarction or abscess, embolization to the pulmonary artery, and emboli to the femoral artery, resulting in extremity pain and decreased pulses.

Mycotic aneurysms occur in 10-20% of patients with endocarditis. They are often multiple and may involve any vessel.

Cutaneous manifestations include petechiae, Osler nodes, Janeway lesions, and splinter hemorrhages.

Neurologic syndromes include cerebral embolism, infarction, and intracerebral hemorrhage and stroke. Seizures, meningitis, and mental status changes have also been reported. Neurologic abnormalities occur in approximately 30-40% of patients and are most frequent in endocarditis caused by S aureus. Symptoms include stroke, intracerebral hemorrhage, and subarachnoid hemorrhage.

Renal embolism and infarction occur in patients with bacterial endocarditis. This complication may result in pain in the flank or abdomen but may be asymptomatic in as many as 50% of cases. Glomerular disease is a common finding, and is usually not of serious clinical significance because renal failure rarely occurs. However, renal insufficiency resulting from immune complex–mediated glomerulonephritis occurs in less than 15% of patients with endocarditis and may cause hematuria and, rarely, azotemia.

Hepatosplenomegaly is noted in approximately 15-20% of patients.

Neonates with endocarditis may also have feeding problems, respiratory distress, or tachycardia.

Factors that increase the risk of complications include prosthetic valve endocarditis, left-sided endocarditis, infection with S aureus or fungi, previous endocarditis, cyanotic congenital heart disease, systemic-to-pulmonary shunts, and a poor response to antibiotic therapy.

Go to Neurological Sequelae of Infective Endocarditis for more complete information on this topic.

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Patient Education

American Heart Association (AHA) guidelines for the prevention of bacterial endocarditis should be emphasized to the family of each patient identified as being at high risk. These recommendations underwent significant changes in 2007. [6]

All children at risk and their families should also be instructed about the importance of maintaining the best possible oral health.

Patient and parent education is critical to ensuring appropriate antimicrobial prophylaxis before high-risk dental procedures are performed in children with cardiac conditions having a highest risk for complications from endocarditis.

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