eMedicine Specialties > Pediatrics: Cardiac Disease and Critical Care Medicine > Cardiology

Endocarditis, Bacterial

Brian Keith Eble, MD, Assistant Professor of Pediatrics, Section of Cardiology, University of Arkansas for Medical Sciences, Arkansas Children's Hospital
Gerardo Reyes, MD, Clinical Assistant Professor, Department of Pediatrics, University of Illinois at Chicago; Director of Pediatric Critical Care Outreach and Development, Midwest NeoPed Associates, Ltd
Contributor Information and Disclosures

Updated: Dec 10, 2008

Introduction

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 temporal aspect, etiology, anatomic site of infection, and relevant pathogenic risk factors is essential in therapeutic and prognostic considerations.

Pathophysiology

A high-velocity flow through a stenotic or incompetent valve or an abnormal communication between systemic and pulmonary circulations causes turbulence downstream from the opening. This turbulence damages or denudes the endothelium, to which platelets and fibrin adhere, and a small, sterile" nonbacterial thrombotic endocardial lesion" forms. In addition, indwelling intravascular catheters in the right heart may directly traumatize the endocardium or valvular endothelium. Circulating bacteria and inflammatory cells adhere to and grow in these thrombi, forming an infected vegetation. Infection may occur (1) on the wall, where the turbulent jet strikes, or (2) downstream, near the orifice, where the flow eddies. Once vegetation forms, the constant blood flow may result in embolization to virtually any organ in the body. A brisk immunologic response is produced.

Frequency

United States

The incidence of endocarditis is approximately 1 case per 1000 pediatric hospital admissions. 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 a rare cause of endocarditis. In contrast, the advent of sophisticated cardiac procedures and early intervention has led to an increase in the incidence of endocarditis in children with congenital heart disease. Preexisting cardiac abnormalities are found in approximately 75-90% of children with bacterial endocarditis.

Mortality/Morbidity

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. Mortality is mostly due to secondary congestive heart failure (CHF).

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

Race

No racial predilection is observed.

Sex

No predilection for either sex is noted.

Age

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

Clinical

History

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

  • Patients with bacterial endocarditis may present with many nonspecific symptoms; however, 85-99% of patients are febrile. Patients with congenital heart disease and fever require special consideration.
  • Other historical features include fatigue, chills, sweats, anorexia, malaise, a cough, a headache, myalgia and/or arthralgia, and confusion.
  • Patients with acute bacterial endocarditis present with an acute, toxic, febrile illness and symptoms that have lasted less than 2 weeks. A history of intravenous (IV) drug use may be elicited. S aureus is the most common cause of acute bacterial endocarditis.
  • Patients with subacute bacterial endocarditis present with a more nonspecific flulike illness and symptoms that have lasted more than 2 weeks. Subacute bacterial endocarditis is more common in patients with an underlying congenital heart defect.

Physical

Physical findings are nonspecific and vary. Factors such as the duration of illness, microbiologic etiology, and patient's age may vary.

  • Fever is present in 85-99% of patients with endocarditis. Fever is usually low grade with a temperature rarely exceeding 39°C that is remittent and is typically not associated with rigors.
  • A new or changing heart murmur is noted in 20-80% of patients. These murmurs may be difficult to identify in patients with subacute endocarditis or in infants and young children who may already have a clinically significant murmur secondary to congenital heart disease.
  • 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.
  • Peripheral symptoms may be observed.
    • Extracardiac manifestations of endocarditis are less common in children than in adults. Petechiae are the most common of these symptoms (20-40%). They are found on the palpebral conjunctiva, the buccal or palatal mucosa, and the extremities. However, petechiae are not specific for endocarditis.
    • Splinter and subungual hemorrhages are dark red, linear streaks in the nail beds of the fingers and toes.
    • Osler nodes are small, tender, subcutaneous nodules that develop in the pulp of the digits.
  • 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. Heart failure with aortic insufficiency is associated with high mortality rates.
  • Hepatosplenomegaly is noted in approximately 15-20% of patients.
  • Renal insufficiency, as a result of immune complex–mediated glomerulonephritis, occurs in less than 15% of patients with endocarditis and may cause hematuria but rarely azotemia.
  • In neonates, endocarditis commonly produces septic embolic phenomena, such as osteomyelitis, meninigitis, and pneumonia. Neonates with endocarditis may also have feeding problems, respiratory distress, tachycardia, or neurologic symptoms.
  • The diagnosis of endocarditis with the modified Duke criteria is based on pathologic or clinical findings.1 Pathologic criteria for definite infectious endocarditis include microorganisms on cultures or histology in a vegetation or histologic confirmation of active disease in a vegetation or intracardiac abscess. Clinical criteria for definite infectious endocarditis includes 2 major, 1 major and 3 minor, or 5 minor criteria, as follows:
    • Major criteria
      • Positive blood cultures (2 separate cultures for a typical endocarditis microorganism, such as Streptococcus viridans or HACEK organism [Haemophilus parainfluenzae, Haemophilus aphrophilus, Haemophilus paraphrophilus, Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, or Kingella species], persistently positive blood cultures, or evidence of infection with a Coxiella organism and/or Q fever)
      • Positive echocardiographic findings (eg, oscillating mass and/or vegetation, paravalvular abscess, or dehiscence of a prosthetic valve)
      • New valvular regurgitation
    • Minor criteria
      • Predisposition (history of IV drug use or congenital heart disease)
      • Fever with a temperature of more than 38°C
      • Vascular phenomena (arterial emboli, septic pulmonary infarcts, intracranial hemorrhage, conjunctival hemorrhage, Janeway lesions [painless, hemorrhagic lesions on palms and soles])
      • Immunologic phenomena (glomerulonephritis, Osler nodes, Roth spots, positive result for rheumatoid factor)
      • Positive blood culture findings without meeting the criteria above or serologic evidence of active infection consistent with endocarditis

Causes

Risk factors for bacterial endocarditis may be divided into those associated with high-risk conditions and those from high-risk procedures.

  • High-risk conditions
    • Congenital heart disease (septal defects, valve disease, cyanotic heart disease)
    • Acquired valve disease
    • Prosthetic valve
    • IV drug use
    • Previous episode of bacterial endocarditis
    • Surgical systemic to pulmonary shunts and conduits
    • Central venous catheters
  • High-risk procedures (procedures that are likely to produce bacteremia involving typical microorganisms in susceptible patients)
    • Dental procedures (extractions, implants, root canals)
    • Respiratory procedures (tonsillectomy and adenoidectomy, surgical operations, bronchoscopy)
    • GI procedures (sclerotherapy, biliary tract surgery, endoscopic retrograde cholangiopancreatography [ERCP])
    • Genitourinary tract (prostatic surgery, cystoscopy, urethral dilation)
  • Microbiology
    • A select group of organisms causes most cases of endocarditis. Gram-positive organisms, particularly alpha-hemolytic streptococci (S viridans), S aureus, and coagulase-negative staphylococci, are the most common offenders.
    • 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 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.

Contents

Overview: Endocarditis, Bacterial
Differential Diagnoses & Workup: Endocarditis, Bacterial
Treatment & Medication: Endocarditis, Bacterial
Follow-up: Endocarditis, Bacterial

References

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

  2. Wilson W, Taubert KA, Gewitz 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. Oct 9 2007;116(15):1736-54. [Medline].

  3. Baddour LM, Wilson WR, Bayer AS, 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. Circulation. Jun 14 2005;111(23):e394-434. [Medline].

  4. Bayer AS, Bolger AF, Taubert KA, et al. Diagnosis and management of infective endocarditis and its complications. Circulation. Dec 22-29 1998;98(25):2936-48. [Medline].

  5. Brook MM. Pediatric bacterial endocarditis. Treatment and prophylaxis. Pediatr Clin North Am. Apr 1999;46(2):275-87. [Medline].

  6. Dajani AS, Taubert KA, Wilson W, et al. Prevention of bacterial endocarditis. Recommendations by the American Heart Association. JAMA. Jun 11 1997;277(22):1794-801. [Medline].

  7. Dodo H, Child JS. Infective endocarditis in congenital heart disease. Cardiol Clin. Aug 1996;14(3):383-92. [Medline].

  8. Ferrieri P, Gewitz MH, Gerber MA, et al. Unique features of infective endocarditis in childhood. Circulation. Apr 30 2002;105(17):2115-26. [Medline].

  9. Gewitz MH. Prevention of bacterial endocarditis. Curr Opin Pediatr. Oct 1997;9(5):518-22. [Medline].

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

  11. Hoesley CJ, Cobbs CG. Endocarditis at the millennium. J Infect Dis. Mar 1999;179 Suppl 2:S360-5. [Medline].

  12. Hoyer A, Silberbach M. Infective endocarditis. Pediatr Rev. Nov 2005;26(11):394-400. [Medline].

  13. Morris CD, Reller MD, Menashe VD. Thirty-year incidence of infective endocarditis after surgery for congenital heart defect. JAMA. Feb 25 1998;279(8):599-603. [Medline].

  14. Stamboulian D, Carbone E. Recognition, management and prophylaxis of endocarditis. Drugs. Nov 1997;54(5):730-44. [Medline].

Further Reading

Keywords

bacterial endocarditis, infective endocarditis, acute bacterial endocarditis, subacute bacterial endocarditis, fulminant endocarditis, rheumatic heart disease, congestive heart failure, CHF, left-sided endocarditis, Staphylococcus aureus, systemic-to-pulmonary shunt, heart murmur, stroke, intracerebral hemorrhage, subarachnoid hemorrhage, renal insufficiency, hepatosplenomegaly, glomerulonephritis, azotemia, septic embolic phenomena, osteomyelitis, meningitis, pneumonia, respiratory distress, arterial emboli, septic pulmonary infarcts, intracranial hemorrhage, conjunctival hemorrhage, Janeway lesions

Contributor Information and Disclosures

Author

Brian Keith Eble, MD, Assistant 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, and Society for Cardiac Angiography and Interventions
Disclosure: Nothing to disclose

Coauthor

Gerardo Reyes, MD, Clinical Assistant Professor, Department of Pediatrics, University of Illinois at Chicago; Director of Pediatric Critical Care Outreach and Development, Midwest NeoPed Associates, Ltd
Gerardo Reyes, MD is a member of the following medical societies: American Academy of Pediatrics
Disclosure: Nothing to disclose

Medical Editor

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, FAAP, FACC, FAHA 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, Cardiac Electrophysiology Society, Heart Rhythm Society, New York Academy of Sciences, Society for Pediatric Research, Texas Medical Association, and Texas Pediatric Society
Disclosure: Nothing to disclose

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock for Investment from broker recommendation; Avanir Pharma Stock for Investment from broker recommendation

Managing Editor

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
Disclosure: Nothing to disclose

CME Editor

Gilbert Herzberg, MD, Assistant Professor, Department of Pediatrics, Section of Pediatric Cardiology, New York Medical College
Gilbert Herzberg, MD is a member of the following medical societies: American Academy of Pediatrics
Disclosure: Nothing to disclose

Chief Editor

Steven R Neish, MD, SM, Director of Pediatric Cardiology Fellowship Program, Associate Professor, Department of Pediatrics, Baylor College of Medicine
Steven R Neish, MD, SM is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, and American Heart Association
Disclosure: Nothing to disclose

 
 
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