eMedicine Specialties > Emergency Medicine > Infectious Diseases

Endocarditis

Author: Keith A Marill, MD, Faculty, Department of Emergency Medicine, Massachusetts General Hospital
Contributor Information and Disclosures

Updated: Nov 23, 2009

Introduction

Background

Infective endocarditis is defined as an infection of the endocardial surface of the heart, which may include one or more heart valves, the mural endocardium, or a septal defect. Endocarditis can be broken down into the following categories:

  • Native valve (acute and subacute) endocarditis
  • Prosthetic valve (early and late) endocarditis
  • Endocarditis related to intravenous drug use

Native valve endocarditis (acute and subacute)

Native valve acute endocarditis usually has an aggressive course. Virulent organisms, such as Staphylococcus aureus and group B streptococci, are typically the causative agents of this type of endocarditis. Underlying structural valve disease may not be present.

Subacute endocarditis usually has a more indolent course than the acute form. Alpha-hemolytic streptococci or enterococci, usually in the setting of underlying structural valve disease, typically are the causative agents of this type of endocarditis.

Prosthetic valve endocarditis (early and late)

Early prosthetic valve endocarditis occurs within 60 days of valve implantation. Traditionally coagulase-negative staphylococci, gram-negative bacilli, and Candida species have been the common infecting organisms. Recent data suggest Staphylococcus aureus may now be the most common infecting organism in both early and late prosthetic valve endocarditis.1

Late prosthetic valve endocarditis occurs 60 days or more after valve implantation. Staphylococci, alpha-hemolytic streptococci, and enterococci are the common causative organisms.

Endocarditis related to intravenous drug use

Endocarditis in intravenous drug abusers commonly involves the tricuspid valve. S aureus is the most common causative organism.

Pathophysiology

Infective endocarditis generally occurs as a consequence of nonbacterial thrombotic endocarditis, which results from turbulence or trauma to the endothelial surface of the heart. Transient bacteremia then leads to seeding of lesions with adherent bacteria, and infective endocarditis develops.

Pathologic effects due to infection can include local tissue destruction and embolic phenomena. In addition, secondary autoimmune effects, such as immune complex glomerulonephritis and vasculitis, can occur.

Frequency

United States

Incidence is 1.4-4.2 cases per 100,000 people per year.

International

Incidence of disease appears to be similar throughout the developed world.

Mortality/Morbidity

  • Increased mortality rates are associated with increased age,2 infection involving the aortic valve, development of congestive heart failure, central nervous system (CNS) complications, and underlying disease such as diabetes mellitus. Mortality rates also vary with the infecting organism and seem particularly higher when Staphylococcus aureus is the infecting organism.1,3
  • Mortality rates in native valve disease range from 16-27%. Mortality rates in patients with prosthetic valve infections are higher. More than 50% of these infections occur within 2 months after surgery.

Sex

The male-to-female ratio is approximately 2:1.

Age

Although endocarditis can occur at any age, the mean age of patients has gradually risen over the past 50 years. Currently, more than 50% of patients are older than 50 years.4

Mendiratta et al found that, in their retrospective study of hospital discharges from 1993-2003 of patients aged 65 years and older with a primary or secondary diagnosis of infective endocarditis, hospitalizations for infective endocarditis increased 26%, from 3.19 per 10,000 elderly patients in 1993 to 3.95 per 10,000 in 2003.5

Clinical

History

  • Present illness history is highly variable. Symptoms commonly are vague, emphasizing constitutional complaints, or complaints may focus on primary cardiac effects or secondary embolic phenomena.
  • Primary cardiac disease may present with signs of congestive heart failure due to valvular insufficiency. Secondary phenomena could include focal neurologic complaints due to an embolic stroke or back pain associated with vertebral osteomyelitis.
  • Fever and chills are the most common symptoms.
  • Anorexia, weight loss, malaise, headache, myalgias, night sweats, shortness of breath, cough, or joint pains are common complaints.
  • As many as 20% of cases present with focal neurologic complaints and stroke syndromes.
  • Dyspnea, cough, and chest pain are common complaints of intravenous drug users. This is likely related to the predominance of tricuspid valve endocarditis in this group and secondary embolic showering of the pulmonary vasculature.

Physical

  • Fever, possibly low-grade and intermittent, is present in 90% of patients.
  • Heart murmurs are heard in approximately 85% of patients. Change in the characteristics of a previously noted murmur occurs in 10% of these patients and increases the likelihood of secondary congestive heart failure.
  • One or more classic signs of infective endocarditis are found in as many as 50% of patients. They include the following:
    • Petechiae - Common but nonspecific finding; note the petechial rash in the image below

    • A middle-aged man with a history of intravenous d...

      A middle-aged man with a history of intravenous drug use who presented with severe myalgias and a petechial rash. He was diagnosed with right-sided staphylococcal endocarditis.

      A middle-aged man with a history of intravenous d...

      A middle-aged man with a history of intravenous drug use who presented with severe myalgias and a petechial rash. He was diagnosed with right-sided staphylococcal endocarditis.

    • Splinter hemorrhages - Dark red linear lesions in the nailbeds
    • Osler nodes - Tender subcutaneous nodules usually found on the distal pads of the digits
    • Janeway lesions - Nontender maculae on the palms and soles
    • Roth spots - Retinal hemorrhages with small, clear centers; rare and observed in only 5% of patients.
  • Signs of neurologic disease occur in as many as 40% of patients. Embolic stroke with focal neurologic deficits is the most common etiology. Other etiologies include intracerebral hemorrhage and multiple microabscesses.6
  • Signs of systemic septic emboli are due to left heart disease and are more commonly associated with mitral valve vegetations. Multiple embolic pulmonary infections or infarctions are due to right heart disease.
  • Signs of congestive heart failure, such as distended neck veins, frequently are due to acute left-sided valvular insufficiency.
  • Splenomegaly
  • Other signs
    • Stiff neck
    • Delirium
    • Paralysis, hemiparesis, aphasia
    • Conjunctival hemorrhage
    • Pallor
    • Gallops
    • Rales
    • Cardiac arrhythmia
    • Pericardial rub
    • Pleural friction rub

Causes

  • Native valve endocarditis
    • Rheumatic valvular disease (30% of native valve endocarditis [NVE]) - Primarily involves the mitral valve followed by the aortic valve
    • Congenital heart disease (15% of NVE) - Underlying etiologies include a patent ductus arteriosus, ventricular septal defect, tetralogy of Fallot, or any native or surgical high-flow lesion.
    • Mitral valve prolapse with an associated murmur (20% of NVE)
    • Degenerative heart disease - Including calcific aortic stenosis due to a bicuspid valve, Marfan syndrome, or syphilitic disease
    • Approximately 70% of cases are caused by Streptococcus species including Streptococcus viridans, Streptococcus bovis, and enterococci. Staphylococcus species cause 25% of cases and generally demonstrate a more aggressive acute course.
  • Prosthetic valve endocarditis
    • Early disease, which presents shortly after surgery, has a different bacteriology and prognosis than late disease, which presents in a subacute fashion similar to native valve endocarditis.
    • Infection associated with aortic valve prostheses is particularly associated with local abscess and fistula formation, and valvular dehiscence. This may lead to shock, heart failure, heart block, shunting of blood to the right atrium, pericardial tamponade, and peripheral emboli to the central nervous system and elsewhere.
    • Infection that occurs early after surgery may be caused by a variety of pathogens, including S aureus and S epidermidis. These nosocomially acquired organisms are often methicillin-resistant (MRSA).7 Late disease is most commonly caused by streptococci.
  • Endocarditis associated with intravenous drug use
    • This condition most commonly involves the tricuspid valve, followed by the aortic valve.
    • Two thirds of patients have no previous history of heart disease and no murmur on admission. A murmur may not be heard in patients with tricuspid disease because of the relatively small pressure gradient across this valve. Pulmonary manifestations may be prominent in patients with tricuspid infection: one third have pleuritic chest pain, and three quarters demonstrate chest radiographic abnormalities.
    • Diagnosis of endocarditis in intravenous drug users can be difficult and requires a high index of suspicion.
    • S aureus is the most common (<50% of cases) etiologic organism. Other causative organisms include streptococci, fungi, and gram-negative rods (eg, pseudomonads, Serratia species).8 Methicillin-resistant S aureus (MRSA) accounts for an increasing portion of S aureus infections and has been associated with previous hospitalizations, long-term addiction, and nonprescribed antibiotic use.
  • Healthcare-associated endocarditis
    • Endocarditis may be associated with new therapeutic modalities involving intravascular devices such as central or peripheral intravenous catheters, rhythm control devices such as pacemakers and defibrillators, hemodialysis shunts and catheters, and chemotherapeutic and hyperalimentation lines.4
    • These patients tend to have significant comorbidities, more advanced age, and predominant infection with Staphylococcus aureus.
    • The mortality rate is high in this group.
  • Fungal endocarditis9
    • Fungal endocarditis is found in intravenous drug users and intensive care unit patients who receive broad-spectrum antibiotics.
    • Blood cultures are often negative, and diagnosis frequently is made after microscopic examination of large emboli.
  • Diagnosis: Definitive diagnosis of infective endocarditis is generally made using the Duke criteria. Major criteria include (1) multiple positive blood cultures for the infecting organism and (2) echocardiographic evidence of endocardial involvement or a new regurgitant murmur on physical examination.10

More on Endocarditis

Overview: Endocarditis
Differential Diagnoses & Workup: Endocarditis
Treatment & Medication: Endocarditis
Follow-up: Endocarditis
Multimedia: Endocarditis
References
Further Reading

References

  1. Wang A, Athan E, Pappas PA, Fowler VG Jr, Olaison L, Pare C, et al. Contemporary clinical profile and outcome of prosthetic valve endocarditis. JAMA. Mar 28 2007;297(12):1354-61. [Medline].

  2. Durante-Mangoni E, Bradley S, Selton-Suty C, Tripodi MF, Barsic B, Bouza E, et al. Current features of infective endocarditis in elderly patients: results of the International Collaboration on Endocarditis Prospective Cohort Study. Arch Intern Med. Oct 27 2008;168(19):2095-103. [Medline].

  3. Chu VH, Cabell CH, Benjamin DK Jr, Kuniholm EF, Fowler VG Jr, Engemann J, et al. Early predictors of in-hospital death in infective endocarditis. Circulation. Apr 13 2004;109(14):1745-9. [Medline].

  4. Murdoch DR, Corey GR, Hoen B, Miro JM, Fowler VG Jr, Bayer AS, et al. Clinical presentation, etiology, and outcome of infective endocarditis in the 21st century: the International Collaboration on Endocarditis-Prospective Cohort Study. Arch Intern Med. Mar 9 2009;169(5):463-73. [Medline].

  5. Mendiratta P, Tilford JM, Prodhan P, Cleves MA, Wei JY. Trends in hospital discharge disposition for elderly patients with infective endocarditis: 1993 to 2003. J Am Geriatr Soc. May 2009;57(5):877-81. [Medline].

  6. Epaulard O, Roch N, Potton L, Pavese P, Brion JP, Stahl JP. Infective endocarditis-related stroke: Diagnostic delay and prognostic factors. Scand J Infect Dis. May 15 2009;1-5. [Medline].

  7. Chu VH, Miro JM, Hoen B, Cabell CH, Pappas PA, Jones P, et al. Coagulase-negative staphylococcal prosthetic valve endocarditis--a contemporary update based on the International Collaboration on Endocarditis: prospective cohort study. Heart. Apr 2009;95(7):570-6. [Medline].

  8. Reyes MP, Ali A, Mendes RE, Biedenbach DJ. Resurgence of Pseudomonas endocarditis in Detroit, 2006-2008. Medicine (Baltimore). Sep 2009;88(5):294-301. [Medline].

  9. Baddley JW, Benjamin DK Jr, Patel M, Miro J, Athan E, Barsic B, et al. Candida infective endocarditis. Eur J Clin Microbiol Infect Dis. Jul 2008;27(7):519-29. [Medline].

  10. Durack DT, Lukes AS, Bright DK. New criteria for diagnosis of infective endocarditis: utilization of specific echocardiographic findings. Duke Endocarditis Service. Am J Med. Mar 1994;96(3):200-9. [Medline].

  11. Casella F, Rana B, Casazza G, Bhan A, Kapetanakis S, Omigie J, et al. The Potential Impact of Contemporary Transthoracic Echocardiography on the Management of Patients with Native Valve Endocarditis: A Comparison with Transesophageal Echocardiography. Echocardiography. May 26 2009;[Medline].

  12. Choussat R, Thomas D, Isnard R, Michel PL, Iung B, Hanania G, et al. Perivalvular abscesses associated with endocarditis; clinical features and prognostic factors of overall survival in a series of 233 cases. Perivalvular Abscesses French Multicentre Study. Eur Heart J. Feb 1999;20(3):232-41. [Medline].

  13. Feuchtner GM, Stolzmann P, Dichtl W, Schertler T, Bonatti J, Scheffel H, et al. Multislice computed tomography in infective endocarditis: comparison with transesophageal echocardiography and intraoperative findings. J Am Coll Cardiol. Feb 3 2009;53(5):436-44. [Medline].

  14. Fowler VG Jr, Boucher HW, Corey GR, Abrutyn E, Karchmer AW, Rupp ME, et al. Daptomycin versus standard therapy for bacteremia and endocarditis caused by Staphylococcus aureus. N Engl J Med. Aug 17 2006;355(7):653-65. [Medline].

  15. Mekontso Dessap A, Zahar JR, Voiriot G, Ali F, Aissa N, Kirsch M, et al. Influence of preoperative antibiotherapy on valve culture results and outcome of endocarditis requiring surgery. J Infect. May 5 2009;[Medline].

  16. [Guideline] 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. Oct 9 2007;116(15):1736-54. [Medline].

  17. Wang CC, Lee CH, Chan CY, Chen HW. Splenic infarction and abscess complicating infective endocarditis. Am J Emerg Med. Oct 2009;27(8):1021.e3-5. [Medline].

  18. Bach DS. Perspectives on the American College of Cardiology/American Heart Association guidelines for the prevention of infective endocarditis. J Am Coll Cardiol. May 19 2009;53(20):1852-4. [Medline].

  19. Baddour LM, Wilson WR. Infections of prosthetic valves and other cardiovascular devices. In: Principles and Practice of Infectious Diseases. 6th ed. Elsevier Churchill Livingstone; 2005:1022-1044.

  20. Baddour LM, Wilson WR, Bayer AS. Infective endocarditis: diagnosis, antimicrobial therapy, and management of complications - executive summary. Circulation. 2005;111:3167-3184.

  21. [Guideline] Baddour LM, Wilson WR, Bayer AS, Fowler VG Jr, Bolger AF, Levison ME. 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. Jun 14 2005;111(23):e394-434. [Medline].

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

  23. Carroll KC, Cheeseman SH. Infective endocarditis and infections of intracardiac prosthetic devices. In: Irwin and Rippe's Intensive Care Medicine. Lippincott Williams & Wilkins; 2003:1000-15.

  24. Croft LB, Donnino R, Shapiro R, et al. Age-related prevalence of cardiac valvular abnormalities warranting infectious endocarditis prophylaxis. Am J Cardiol. Aug 1 2004;94(3):386-9. [Medline].

  25. Dunmire SM. Infective endocarditis and acquired valvular heart disease. In: Emergency Medicine Concepts and Clinical Practice. Vol 2. Mosby-Year Book; 1998:1745-54.

  26. Durack DT. Prevention of infective endocarditis. N Engl J Med. Jan 5 1995;332(1):38-44. [Medline].

  27. Fowler Jr. VG, Scheld WM, Bayer AS. Endocarditis and intravascular infections. In: Principles and Practice of Infectious Diseases. 6th ed. Elsevier Churchill Livingstone; 2005:975-1022.

  28. Gilbert DN, Moellering RC, Sande MA. The Sanford Guide to Antimicrobial Therapy. 2002:18-21.

  29. Heiro M, Nikoskelainen J, Engblom E. Neurologic manifestations of infective endocarditis: a 17-year experience in a teaching hospital in Finland. Arch Intern Med. Oct 9 2000;160(18):2781-7. [Medline].

  30. Karchmer AW. Infective endocarditis. In: Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine. 7th ed. WB Saunders Co; 2005:1633-1658.

  31. Karchmer AW. Infective endocarditis. In: Harrison's Principles of Internal Medicine. 16th ed. McGraw-Hill; 2005:731-40.

  32. Miro JM, del Rio A, Mestres CA. Infective endocarditis in intravenous drug abusers and HIV-1 infected patients. Infect Dis Clin North Am. Jun 2002;16(2):273-95, vii-viii. [Medline].

  33. Mylonakis E, Calderwood SB. Infective endocarditis in adults. N Engl J Med. Nov 1 2001;345(18):1318-30. [Medline].

  34. Shively BK. Infective Endocarditis. Curr Treat Options Cardiovasc Med. Feb 2001;3(1):25-35. [Medline].

  35. Stryjewski ME, Chu VH, Cabell CH. Issues in the Management of Endocarditis Caused by Resistant Gram-positive Organisms. Curr Infect Dis Rep. Aug 2004;6(4):283-291. [Medline].

Contributor Information and Disclosures

Author

Keith A Marill, MD, Faculty, Department of Emergency Medicine, Massachusetts General Hospital
Keith A Marill, MD is a member of the following medical societies: American Academy of Emergency Medicine and Society for Academic Emergency Medicine
Disclosure: Medtronic Ownership interest None; Cambridge Heart, Inc. Ownership interest None

Medical Editor

Steven A Conrad, MD, PhD, Chief, Department of Emergency Medicine; Chief, Multidisciplinary Critical Care Service, Professor, Department of Emergency and Internal Medicine, Louisiana State University Health Sciences Center
Steven A Conrad, MD, PhD is a member of the following medical societies: American College of Chest Physicians, American College of Critical Care Medicine, American College of Emergency Physicians, American College of Physicians, International Society for Heart and Lung Transplantation, Louisiana State Medical Society, Shock Society, Society for Academic Emergency Medicine, and Society of Critical Care Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Jon Mark Hirshon, MD, MPH, Associate Professor, Department of Emergency Medicine, University of Maryland School of Medicine
Jon Mark Hirshon, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Public Health Association, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Barry E Brenner, MD, PhD, FACEP, Professor of Emergency Medicine, Professor of Internal Medicine, Program Director, Emergency Medicine, University Hospitals, Case Medical Center
Barry E Brenner, MD, PhD, FACEP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Chest Physicians, American College of Emergency Physicians, American College of Physicians, American Heart Association, American Thoracic Society, Arkansas Medical Society, New York Academy of Medicine, New York Academy of Sciences, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

 
 
HONcode

We subscribe to the
HONcode principles of the
Health On the Net Foundation

All material on this website is protected by copyright, Copyright© 1994- by Medscape.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.