Pediatric Bacterial Endocarditis

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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. 

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.)

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 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.

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

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.

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.

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%.

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.

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.

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.

Baddour LM, Wilson WR, Bayer AS, Fowler VG Jr, Bolger AF, Levison ME, et al. Infective endocarditis: diagnosis, antimicrobial therapy, and management of complications: a statement for healthcare professionals from the Committee on Rheumatic Fever, Endocarditis, and Kawasaki Disease, Council on Cardiovascular Disease in the Young, and the Councils on Clinical Cardiology, Stroke, and Cardiovascular Surgery and Anesthesia, American Heart Association: endorsed by the Infectious Diseases Society of America. Circulation. 2005 Jun 14. 111(23):e394-434. [Medline].

Pasquali SK, He X, Mohamad Z, McCrindle BW, Newburger JW, Li JS, et al. Trends in endocarditis hospitalizations at US children’s hospitals: impact of the 2007 American Heart Association Antibiotic Prophylaxis Guidelines. Am Heart J. 2012 May. 163(5):894-9. [Medline]. [Full Text].

Johnson JA, Boyce TG, Cetta F, Steckelberg JM, Johnson JN. Infective endocarditis in the pediatric patient: a 60-year single-institution review. Mayo Clin Proc. 2012 Jul. 87(7):629-35. [Medline]. [Full Text].

Ware AL, Tani LY, Weng HY, Wilkes J, Menon SC. Resource utilization and outcomes of infective endocarditis in children. J Pediatr. 2014 Oct. 165 (4):807-12.e1. [Medline].

Russell HM, Johnson SL, Wurlitzer KC, Backer CL. Outcomes of surgical therapy for infective endocarditis in a pediatric population: a 21-year review. Ann Thorac Surg. 2013 Jul. 96(1):171-4: discussion 174-5. [Medline].

Wilson W, Taubert KA, Gewitz M, Lockhart PB, Baddour LM, Levison M, et al. Prevention of infective endocarditis: guidelines from the American Heart Association: a guideline from the American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee, Council on Cardiovascular Disease in the Young, and the Council on Clinical Cardiology, Council on Cardiovascular Surgery and Anesthesia, and the Quality of Care and Outcomes Research Interdisciplinary Working Group. Circulation. 2007 Oct 9. 116(15):1736-54. [Medline].

Martin JM, Neches WH, Wald ER. Infective endocarditis: 35 years of experience at a children’s hospital. Clin Infect Dis. 1997 Apr. 24 (4):669-75. [Medline].

Li JS, Sexton DJ, Mick N, Nettles R, Fowler VG Jr, Ryan T, et al. Proposed modifications to the Duke criteria for the diagnosis of infective endocarditis. Clin Infect Dis. 2000 Apr. 30(4):633-8. [Medline].

Habib G. Management of infective endocarditis. Heart. 2006 Jan. 92(1):124-30. [Medline]. [Full Text].

Gerber MA, Baltimore RS, Eaton CB, Gewitz M, Rowley AH, Shulman ST, et al. Prevention of rheumatic fever and diagnosis and treatment of acute Streptococcal pharyngitis: a scientific statement from the American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee of the Council on Cardiovascular Disease in the Young, the Interdisciplinary Council on Functional Genomics and Translational Biology, and the Interdisciplinary Council on Quality of Care and Outcomes Research: endorsed by the American Academy of Pediatrics. Circulation. 2009 Mar 24. 119(11):1541-51. [Medline].

Baltimore RS, Gewitz M, Baddour LM, et al, for the American Heart Association Rheumatic Fever, Endocarditis, et al. infective endocarditis in childhood: 2015 update: a scientific statement from the American Heart Association. Circulation. 2015 Oct 13. 132 (15):1487-515. [Medline].

Nichols KR, Israel EN, Thomas CA, Knoderer CA. Optimizing guideline-recommended antibiotic doses for pediatric infective endocarditis. Ann Pharmacother. 2016 Feb 25. [Medline].

Patel J, Kupferman F, Rapaport S, Kern JH. Preprocedure prophylaxis against endocarditis among United States pediatric cardiologists. Pediatr Cardiol. 2014 Oct. 35 (7):1220-4. [Medline].

Thornhill MH, Dayer MJ, Forde JM, et al. Impact of the NICE guideline recommending cessation of antibiotic prophylaxis for prevention of infective endocarditis: before and after study. BMJ. 2011 May 3. 342:d2392. [Medline]. [Full Text].

Michael H Gewitz, MD Physician-in-Chief, Chief, Section of Pediatric Cardiology, Maria Fareri Children’s Hospital at Westchester Medical Center; Professor and Vice Chairman, Department of Pediatrics, New York Medical College

Michael H Gewitz, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Association for Physician Leadership, American Heart Association, American Pediatric Society, American Society of Echocardiography, New York Academy of Medicine, New York Academy of Sciences, Royal Society of Medicine, Society of Pediatric Echocardiography

Disclosure: Nothing to disclose.

Brian Keith Eble, MD Associate Professor of Pediatrics, Section of Cardiology, University of Arkansas for Medical Sciences, Arkansas Children’s Hospital

Brian Keith Eble, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Heart Association, Arkansas Medical Society, Society for Cardiovascular Angiography and Interventions

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Julian M Stewart, MD, PhD Associate Chairman of Pediatrics, Director, Center for Hypotension, Westchester Medical Center; Professor of Pediatrics and Physiology, New York Medical College

Julian M Stewart, MD, PhD is a member of the following medical societies: American Academy of Pediatrics, American Autonomic Society, American Physiological Society

Disclosure: Received research grant from: Lundbeck Pharmaceuticals<br/>Received grant/research funds from Lundbeck Pharmaceuticals for none.

Syamasundar Rao Patnana, MD Professor of Pediatrics and Medicine, Division of Cardiology, Emeritus Chief of Pediatric Cardiology, University of Texas Medical School at Houston and Children’s Memorial Hermann Hospital

Syamasundar Rao Patnana, MD is a member of the following medical societies: American Academy of Pediatrics, American Pediatric Society, American College of Cardiology, American Heart Association, Society for Cardiovascular Angiography and Interventions, Society for Pediatric Research

Disclosure: Nothing to disclose.

Jeffrey Allen Towbin, MD, MSc FAAP, FACC, FAHA, Professor, Departments of Pediatrics (Cardiology), Cardiovascular Sciences, and Molecular and Human Genetics, Baylor College of Medicine; Chief of Pediatric Cardiology, Foundation Chair in Pediatric Cardiac Research, Texas Children’s Hospital

Jeffrey Allen Towbin, MD, MSc is a member of the following medical societies: American Academy of Pediatrics, American Association for the Advancement of Science, American College of Cardiology, American College of Sports Medicine, American Heart Association, American Medical Association, American Society of Human Genetics, New York Academy of Sciences, Society for Pediatric Research, Texas Medical Association, Texas Pediatric Society, Cardiac Electrophysiology Society

Disclosure: Nothing to disclose.

The authors and editors of eMedicine gratefully acknowledge the contributions of previous authors Gerardo Reyes, MD, and Dwight Bailey, MD, to the development and writing of the source article.

Pediatric Bacterial Endocarditis

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