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National Institutes of Health

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  1. Infective Endocarditis National Institutes of Health National Institute of Allergy and Infectious Diseases

  2. Talk Outline History Epidemiology Pathophysiology Risk factors Clinical presentation Causes How to diagnose Treatment Special groups

  3. Alois Alzheimer

  4. Alois Alzheimer 1906 identified an 'unusual disease of the cerebral cortex' which caused memory loss, disorientation, hallucinations and ultimately death and was associated with cerebral plaques and neurofibrillary tangles.

  5. Alois Alzheimer 1906 identified an 'unusual disease of the cerebral cortex' which caused memory loss, disorientation, hallucinations and ultimately death and was associated with cerebral plaques and neurofibrillary tangles. Died in 1915 (age 51) from endocarditis.

  6. Orville Gibson

  7. Orville Gibson Guitar manufacturer.

  8. Orville Gibson Guitar manufacturer. Died in 1918 (age 62) from endocarditis.

  9. Gustav Mahler

  10. Gustav Mahler Composer. Mahler died on May 18, 1911, at age 50 from endocarditis. He never heard the Ninth Symphony performed . The Ninth taleBy Kevin Berger / SALON

  11. Why was infective endocarditis such a bad disease in the early 1900s?

  12. Why was infective endocarditis such a bad disease in the early 1900s? No antibiotics No cardiac surgery

  13. Is infective endocarditis still a problem now?

  14. Is infective endocarditis still a problem now? YES ● AHA estimates there are 10,000-20,000 cases per year in the U.S. ● The incidence of disease (about 5 cases/100,000 pt years) has not changed in several decades!! ● Mortality is 20-30% at 1 year (for GNRs and fungi is 50%) Most common valves: Mitral valve (40%), Aortic valve (36%), then multivalvular. R sided <10% of all cases.

  15. BUT, endocarditis is NOT the same disease it was a century ago. “Almost all aspects of the disease, including its natural history, predisposing factors, sequelae, and causative organisms, are virtually unrecognisable compared with Osler’s original descriptions from the 19th century.” B.D. Prendergast Heart 2006;92;879-885.

  16. Reasons IE remains a problem and why its clinical manifestations have changed  less rheumatic heart disease  more degenerative valve disease in the elderly  replacement valves  intravenous drug use  vascular instrumentation  resistant bacteria  earlier diagnosis  detection of previously unknown pathogens

  17. Pathophysiology Damaged epithelium results in exposed stromal cells and extracellular matrix proteins. This triggers deposition of fibrin-platelet clots. Streptococci can bind to fibrin-platelet clots and Staphylococcus aureus can bind to beta-1 integrins expressed by inflamed endothelial cells. Heart 2006;92;879-885.

  18. Pathophysiology Endothelial disruption also results in coagulation at site of defect. Bacteria bind to the clot. Cycle of monocyte activation and cytokine release contribute to a progressive inflammation and enlargement of the infected vegetation. Local extension and tissue damage may result in abscess formation. Ultimately septic emboli may disseminate to brain, spleen, and kidney. Heart 2006;92;879-885.

  19. Pathophysiology Endothelial Damage Thrombus Bacterial Seeding Maturation of vegetation (deposition of fibrin, proliferation of bacteria)

  20. Pathophysiology Endothelial Damage Thrombus Bacterial Seeding Maturation of vegetation (deposition of fibrin, proliferation of bacteria) Why is endocarditis so difficult to Rx?

  21. Pathophysiology Endothelial Damage Thrombus Bacterial Seeding Maturation of vegetation (deposition of fibrin, proliferation of bacteria) Why is endocarditis so difficult to Rx? absence of vasculature makes delivery of Abx to bacteria within mature vegetation difficult

  22. Risk factors for infective endocarditis?

  23. Risk factors for infective endocarditis? ● underlying heart disease -degenerative aortic and mitral valve disease -rheumatic heart dz (less common) ● prosthetic valve or prior valve surgery ● previous infective endocarditis ● IVDU ● iatrogenic or nosocomial infection prior dental surgery?  risk likely overemphasized NOTE: in one recent study 47% of patients with infective endocarditis had no previous knowledge of an underlying cardiac disorder. JAMA 2002;288:75-81.

  24. Clinical Presentation of IE -SYMPTOMS-

  25. Clinical Presentation of IE -SYMPTOMS- • FEVER (90% of pts, but may be absent  esp in elderly) • Chills • Sweats • Poor appetite • Weight loss • NOTE: emboli to brain, spleen, or lung occur in 30% of patients and are often the presenting symptom • Focal neurologic change if septic embolus to CNS OR if development of a mycotic aneurysm • Cough/SOB/chest pain if septic embolus to lungs • Abdominal pain if septic embolus to spleen

  26. Clinical Presentation of IE -SIGNS-

  27. Clinical Presentation of IE -SIGNS- • HEART MURMUR (85%) • Cutaneous manifestations of DIC • Focal neurologic deficits • Embolic phenomena • Roth spots • Janeway lesions • Osler’s nodes • distal infarcts of digits

  28. Purpuric lesions on the arm of a woman with staphylococcal endocarditis.

  29. Roth spots: “white-centered” hemorrhages. Likely are microinfarcts. In addition to endocarditis, occur in HTN, HIV, connective tissue disease, severe anemia, Behçet's disease, viremia, & hypercoagulable states.

  30. Osler’s nodes • -small hemorrhages with • nodular quality on fingers, • palms, and soles • -very uncommon • -likely septic emboli • (could culture these) • -no real difference between these and Janeway lesions (some say Osler’s nodes on digit tips and tender and Janeway lesions on palms/soles and non-tender) Merk Medicus online Note: Mahler, who had streptococcal endocarditis, developed septic abscesses all over his body. We just don’t see this anymore.

  31. What about splinter hemorrhages?

  32. What about splinter hemorrhages? • Splinter hemorrhages have been reported in up to 66% of all hospital admissions and in up to 56% of all healthy adults. • (Sapira 1996)

  33. splinter hemorrhages Merk Medicus online

  34. Clinical Presentation of IE -LAB VALUES-

  35. Clinical Presentation of IE -LAB VALUES- • Nothing particularly helpful. • -Elevated ESR or CRP • -May have elevated WBC count as well as other changes in CBC. • -May see changes c/w glomerulonephritis • (due to immune complex deposition and/or septic emboli)

  36. So, how is the prognosis for patients diagnosed with infective endocarditis?

  37. So, how is the prognosis for patients diagnosed with infective endocarditis? Not good. ANNUAL MORTALITY FROM INFECTIVE ENDOCARDITIS APPROACHES 40%. Arch Intern Med 2002;162:90-4.

  38. Clinical complications of IE HEART OTHER heart failure vertebral osteomyelitis perivalvular abscess septic arthritis pericarditis metastatic abscesses Ao valve dsxn BRAIN abscess meningitis encephalopathy hemorrhage KIDNEY infarct abscess glomerulonephritis

  39. NNMC case from 8/07 (with thanks to Dr. Mark Johnson) 31yo M Symptoms for a few weeks, dental procedure 2 months prior Fevers HA Homonymous hemianopsia + MURMUR (and possible Osler’s node)

  40. TTE  large MV anterior leaflet vegetation • BlCx’s positive with Streptococcus mitis • Brain MRI c/w L MCA septic embolism • Treated with PCN/gent and, developed heart failure from mitral regurgitation • Taken to OR

  41. Had a mechanical valve placed. Placed on anticoagulation. Had a cerebral angiogram done which showed a 4mm right sided parietal “mycotic” (really, “infected” aneurysm). That vessel was then closed/filled with a glue by interventional neurology.

  42. Morbidity in this 31 yo pt

  43. Morbidity in this 31 yo pt • Stroke causing loss of vision • Infected brain aneurysm that required interventional embolization that may still have chance of bleeding. • In-hospital stay for >1 month with long course of Abx. • Had to undergo open heart surgery and now has a mechanical valve which • will probably need to be changed at some point • high risk for endocarditis • 5. On life-long anticoagulation.

  44. Because this is a highly morbid disease and because the clinical presentation is usually pretty non-focal (fever and chills), what is the best thing we can do on exam to help us think about the possibility of endocarditis?

  45. Because this is a highly morbid disease and because the clinical presentation is usually pretty non-focal (fever and chills), what is the best thing we can do on exam to help us think about the possibility of endocarditis?  Do a careful examination for a heart murmur in all patients with fever.

  46. Etiologic agents of IE

  47. Etiologic agents of IE Agent Cases (%) Streptococci 70% Viridans streptococci 35% Enterococci 10% other streptococci 20% Staphylococci 20% coagulase + 18% coagulase - 2% Aerobic GNRs 5% Fungi 2% Miscellaneous bacteria <5% Culture Negative <5-25%