Infective endocarditis


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Infective endocarditis

  1. 1. Infective Endocarditis 高雄醫學大學附設醫院 心臟內科
  2. 2. Infective Endocarditis <ul><li>Essential characteristics </li></ul><ul><li>General definitions and epidemiology </li></ul><ul><ul><li>NVE </li></ul></ul><ul><ul><li>I.V. drug abuse </li></ul></ul><ul><ul><li>PVE </li></ul></ul><ul><li>Pathogenesis </li></ul><ul><li>Pathophysiology </li></ul><ul><li>Clinical features </li></ul><ul><li>Treatment </li></ul>
  3. 3. Infective Endocarditis <ul><li>Febrile illness </li></ul><ul><li>Persistent bacteremia </li></ul><ul><li>Characteristic lesion of microbial infection of the endothelial surface of the heart </li></ul><ul><ul><li>Variable in size </li></ul></ul><ul><ul><li>Amorphous mass of fibrin & platelets </li></ul></ul><ul><ul><li>Abundant organisms </li></ul></ul><ul><ul><li>Few inflammatory cells </li></ul></ul>the vegetation
  4. 5. Infective Endocarditis <ul><li>Typically involves the valves </li></ul><ul><ul><li>May involve all structures of the heart </li></ul></ul><ul><ul><ul><li>Chordae tendinae </li></ul></ul></ul><ul><ul><ul><li>Sites of shunting </li></ul></ul></ul><ul><ul><ul><li>Mural lesions </li></ul></ul></ul><ul><ul><li>Infection of vascular shunts, by strict definition, is endarteritis, but lesion is the same </li></ul></ul><ul><li>Majority of cases caused by streptococcus, staphylococcus, enterococcus, or fastidious gram negative cocco-bacillary forms </li></ul>
  5. 6. Infective Endocarditis <ul><li>Gram negative organisms </li></ul><ul><ul><li>P. aeruginosa most common </li></ul></ul><ul><ul><li>HACEK - slow growing, fastidious organisms that may need 3 weeks to grow out of culture </li></ul></ul><ul><ul><ul><li>Haemophilus sp. </li></ul></ul></ul><ul><ul><ul><li>Actinobacillus </li></ul></ul></ul><ul><ul><ul><li>Cardiobacterium </li></ul></ul></ul><ul><ul><ul><li>Eikenella </li></ul></ul></ul><ul><ul><ul><li>Kingella </li></ul></ul></ul>
  6. 7. Infective Endocarditis <ul><li>Acute </li></ul><ul><ul><li>Toxic presentation </li></ul></ul><ul><ul><li>Progressive valve destruction & metastatic infection developing in days to weeks </li></ul></ul><ul><ul><li>Most commonly caused by S. aureus </li></ul></ul><ul><li>Subacute </li></ul><ul><ul><li>Mild toxicity </li></ul></ul><ul><ul><li>Presentation over weeks to months </li></ul></ul><ul><ul><li>Rarely leads to metastatic infection </li></ul></ul><ul><ul><li>Most commonly S. viridans or enterococcus </li></ul></ul>
  7. 8. Infective Endocarditis <ul><li>Case rate may vary between 2-3 cases /100,000 to as high as 15-30/100,000 depending on incidence of i.v. drug abuse and age of the population </li></ul><ul><ul><li>55-75% of patients with native valve endocarditis (NVE) have underlying valve abnormalities </li></ul></ul><ul><ul><ul><li>MVP </li></ul></ul></ul><ul><ul><ul><li>Rheumatic </li></ul></ul></ul><ul><ul><ul><li>Congenital </li></ul></ul></ul><ul><ul><ul><li>ASH or: </li></ul></ul></ul><ul><ul><ul><li>i.v. drug abuse </li></ul></ul></ul>
  8. 9. Infective Endocarditis <ul><li>Case rates </li></ul><ul><ul><li>7-25% of cases involve prosthetic valves </li></ul></ul><ul><ul><li>25-45% of cases predisposing condition can not be identified </li></ul></ul>
  9. 10. Infective Endocarditis <ul><li>Pediatric population </li></ul><ul><ul><li>The vast majority (75-90%) of cases after the neonatal period are associated with an underlying congenital abnormality </li></ul></ul><ul><ul><ul><li>Aortic valve </li></ul></ul></ul><ul><ul><ul><li>VSD </li></ul></ul></ul><ul><ul><ul><li>Tetralogy of Fallot </li></ul></ul></ul><ul><ul><li>Risk of post-op infection in children with IE is 50% </li></ul></ul><ul><li>Microbiology </li></ul><ul><ul><li>Neonates: S. aureus, coag – staph, group B strep </li></ul></ul><ul><ul><li>Older children: 40% strep, S. aureus </li></ul></ul>
  10. 11. Infective Endocarditis <ul><li>Adult population </li></ul><ul><ul><li>MVP – prominent predisposing factor </li></ul></ul><ul><ul><ul><li>High prevalence in population </li></ul></ul></ul><ul><ul><ul><ul><li>2-4% </li></ul></ul></ul></ul><ul><ul><ul><ul><li>20% in young women </li></ul></ul></ul></ul><ul><ul><ul><li>Accounts for 7 – 30% NVE in cases not related to drug abuse or nosocomial infection </li></ul></ul></ul><ul><ul><li>Relative risk in MVP ~3.5 – 8.2, largely confined to patients with murmur, but also increased in men and patients >45 years old </li></ul></ul><ul><ul><ul><li>MVP with murmur – incidence IE 52/100/000 pt. years </li></ul></ul></ul><ul><ul><ul><li>MVP w/o murmur – incidence IE 4.6/100,000 pt. years </li></ul></ul></ul>
  11. 12. Infective Endocarditis <ul><li>Adult population </li></ul><ul><ul><li>Rheumatic Heart Disease </li></ul></ul><ul><ul><ul><li>20 – 25% of cases of IE in 1970’s & 80’s </li></ul></ul></ul><ul><ul><ul><li>7 – 18% of cases in recent reported series </li></ul></ul></ul><ul><ul><ul><li>Mitral site more common in women </li></ul></ul></ul><ul><ul><ul><li>Aortic site more common in men </li></ul></ul></ul><ul><ul><li>Congenital Heart Disease </li></ul></ul><ul><ul><ul><li>10 – 20% of cases in young adults </li></ul></ul></ul><ul><ul><ul><li>8% of cases in older adults </li></ul></ul></ul><ul><ul><ul><li>PDA, VSD, bicuspid aortic valve (esp. in men>60) </li></ul></ul></ul>
  12. 13. Infective Endocarditis <ul><li>Intravenous Drug Abuse </li></ul><ul><ul><li>Risk is 2 – 5% per pt./year </li></ul></ul><ul><ul><li>Tendency to involve right-sided valves </li></ul></ul><ul><ul><ul><li>Distribution in clinical series </li></ul></ul></ul><ul><ul><ul><ul><li>46 – 78% tricuspid </li></ul></ul></ul></ul><ul><ul><ul><ul><li>24 – 32% mitral </li></ul></ul></ul></ul><ul><ul><ul><ul><li>8 – 19% aortic </li></ul></ul></ul></ul><ul><ul><li>Underlying valve normal in 75 – 93% </li></ul></ul><ul><ul><li>S. aureus predominant organism (>50%, 60-70% of tricuspid cases) </li></ul></ul>
  13. 14. Infective Endocarditis <ul><li>Intravenous Drug Abuse </li></ul><ul><ul><li>Increased frequency of gram negative infection such as P. aeruginosa & fungal infections </li></ul></ul><ul><ul><li>High concordance of HIV positivity & IE (27-73%) </li></ul></ul><ul><ul><ul><li>HIV status does not in itself modify clinical picture </li></ul></ul></ul><ul><ul><ul><li>Survival is decreased if CD4 count < 200/mm 3 </li></ul></ul></ul>
  14. 15. Infective Endocarditis <ul><li>Prosthetic Valve Endocarditis (PVE) </li></ul><ul><ul><li>10 – 30% of all cases in developed nations </li></ul></ul><ul><ul><li>Cumulative incidence </li></ul></ul><ul><ul><ul><li>1.4 – 3.1% at 12 months </li></ul></ul></ul><ul><ul><ul><li>3.2 – 5.7% at 5 years </li></ul></ul></ul><ul><ul><li>Early PVE – within 60 days </li></ul></ul><ul><ul><ul><li>Nosocomial ( s. epi predominates) </li></ul></ul></ul><ul><ul><li>Late PVE – after 60 days </li></ul></ul><ul><ul><ul><li>Community ( same organisms as NVE ) </li></ul></ul></ul>
  15. 16. Infective Endocarditis Frequency of preexisting cardiac lesion in Patients with IE   Age (%) Lesion Under 2 years 2-15 years 15-50 years >50 years IVDU adults No known heart disease 50-70 10-15 10-20 10 50-60 Congenital heart disease 30-50 70-80 25-35 15-25 10 Rheumatic heart disease Rare 10 10-15 10-15 10 Degenerative heart disease 0 0 Rare 10-20 Rare Previous cardiac surgery 5 10-15 10-20 10-20 10-20 Previous endocarditis Rare 5 5-10 5-10 10-20
  16. 17. Infective Endocarditis
  17. 18. Organisms Causing Infective Endocarditis
  18. 19. Infective Endocarditis
  19. 20. Infective Endocarditis
  20. 21. IE Clinical Manifestations Systemic Manifestation
  21. 22. Infective Endocarditis <ul><li>Pathology </li></ul><ul><ul><li>NVE infection is largely confined to leaflets </li></ul></ul><ul><ul><li>PVE infection commonly extends beyond valve ring into annulus/periannular tissue </li></ul></ul><ul><ul><ul><li>Ring abscesses </li></ul></ul></ul><ul><ul><ul><li>Septal abscesses </li></ul></ul></ul><ul><ul><ul><li>Fistulae </li></ul></ul></ul><ul><ul><ul><li>Prosthetic dehiscence </li></ul></ul></ul><ul><ul><li>Invasive infection more common in aortic position and if onset is early </li></ul></ul>
  22. 23. Infective Endocarditis <ul><li>Pathogenesis </li></ul>Endothelial damage Platelet-fibrin thrombi Microorganism adherence
  23. 24. Infective Endocarditis <ul><li>Nonbacterial Thrombotic Endocarditis </li></ul><ul><ul><ul><ul><ul><li>Endothelial injury </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>Hypercoagulable state </li></ul></ul></ul></ul></ul><ul><ul><li>Lesions seen at coaptation points of valves </li></ul></ul><ul><ul><ul><li>Atrial surface mitral/tricuspid </li></ul></ul></ul><ul><ul><ul><li>Ventricular surface aortic/pulmonic </li></ul></ul></ul><ul><li>Modes of endothelial injury </li></ul><ul><ul><ul><li>High velocity jet </li></ul></ul></ul><ul><ul><ul><li>Flow from high pressure to low pressure chamber </li></ul></ul></ul><ul><ul><ul><li>Flow across narrow orifice of high velocity </li></ul></ul></ul><ul><ul><li>Bacteria deposited on edges of low pressure sink or site of jet impaction </li></ul></ul>Venturi Effect Platelet-fibrin thrombi
  24. 25. Venturi Effect
  25. 26. Conversion of NBTE to IE <ul><li>Frequency & magnitude of bacteremia </li></ul><ul><ul><ul><li>Density of colonizing bacteria </li></ul></ul></ul><ul><ul><ul><ul><ul><li>Oral > GU > GI </li></ul></ul></ul></ul></ul><ul><ul><ul><li>Disease state of surface </li></ul></ul></ul><ul><ul><ul><ul><ul><li>Infected surface > colonized surface </li></ul></ul></ul></ul></ul><ul><ul><ul><li>Extent of trauma </li></ul></ul></ul><ul><li>Resistance of organism to host defenses </li></ul><ul><ul><ul><li>Most aerobic gram negatives susceptible to complement-mediated bactericidal effect of serum </li></ul></ul></ul><ul><ul><ul><li>Tendency to adhere to endothelium </li></ul></ul></ul><ul><ul><ul><ul><ul><li>Dextran producing strep </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>Fibronectin receptors on staph, enterococcus, strep, Candida </li></ul></ul></ul></ul></ul>
  26. 27. Pathophysiology <ul><li>Clinical manifestations </li></ul><ul><ul><li>Direct </li></ul></ul><ul><ul><ul><li>Constitutional symptoms of infection (cytokine) </li></ul></ul></ul><ul><ul><li>Indirect </li></ul></ul><ul><ul><ul><li>Local destructive effects of infection </li></ul></ul></ul><ul><ul><ul><li>Embolization – septic or bland </li></ul></ul></ul><ul><ul><ul><li>Hematogenous seeding of infection </li></ul></ul></ul><ul><ul><ul><ul><ul><li>N.B. may present as local infection or persistent fever, metastatic abscesses may be small, miliary </li></ul></ul></ul></ul></ul><ul><ul><ul><li>Immune response </li></ul></ul></ul><ul><ul><ul><ul><ul><li>Immune complex or complement-mediated </li></ul></ul></ul></ul></ul>
  27. 28. Pathophysiology <ul><li>Local destructive effects </li></ul><ul><ul><ul><li>Valvular distortion/destruction </li></ul></ul></ul><ul><ul><ul><li>Chordal rupture </li></ul></ul></ul><ul><ul><ul><li>Perforation/fistula formation </li></ul></ul></ul><ul><ul><ul><li>Paravalvular abscess </li></ul></ul></ul><ul><ul><ul><li>Conduction abnormalities </li></ul></ul></ul><ul><ul><ul><li>Purulent pericarditis </li></ul></ul></ul><ul><ul><ul><li>Functional valve obstruction </li></ul></ul></ul>
  28. 29. Pathophysiology <ul><li>Embolization </li></ul><ul><ul><ul><li>Clinically evident 11 – 43% of patients </li></ul></ul></ul><ul><ul><ul><li>Pathologically present 45 – 65% </li></ul></ul></ul><ul><ul><ul><li>High risk for embolization </li></ul></ul></ul><ul><ul><ul><ul><ul><li>Large > 10 mm vegetation </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>Hypermobile vegetation </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>Mitral vegetations (esp. anterior leaflet) </li></ul></ul></ul></ul></ul><ul><ul><ul><li>Pulmonary (septic) – 65 – 75% of i.v. drug abusers with tricuspid IE </li></ul></ul></ul>
  29. 30. Clinical Features <ul><li>Interval between index bacteremia & onset of sx’s usually < 2 weeks </li></ul><ul><ul><ul><li>May be substantially longer in early PVE </li></ul></ul></ul><ul><li>Fever most common sign </li></ul><ul><ul><ul><li>May be absent in elderly/debilitated pt. </li></ul></ul></ul><ul><li>Murmur present in 80 – 85% </li></ul><ul><ul><ul><li>Generally indication of underlying lesion </li></ul></ul></ul><ul><ul><ul><li>Frequently absent in tricuspid IE </li></ul></ul></ul><ul><li>Changing murmur </li></ul>
  30. 31. Classical Peripheral Manifestations <ul><li>Less common today </li></ul><ul><li>Not seen in tricuspid endocarditis </li></ul><ul><li>Petechiae most common </li></ul>
  31. 32. Janeway Lesions
  32. 33. Splinter Hemorrhage
  33. 34. Osler’s Nodes
  34. 35. Subconjunctival Hemorrhages
  35. 36. Roth’s Spots
  36. 37. Clinical Features <ul><li>Systemic emboli </li></ul><ul><ul><ul><li>Incidence decreases with effective anti-microbial Rx </li></ul></ul></ul><ul><li>Neurological sequelae </li></ul><ul><ul><ul><li>Embolic stroke 15 – 20% of patients </li></ul></ul></ul><ul><ul><ul><li>Mycotic aneurysm </li></ul></ul></ul><ul><ul><ul><li>Cerebritis </li></ul></ul></ul><ul><li>CHF </li></ul><ul><ul><ul><li>Due to mechanical disruption </li></ul></ul></ul><ul><ul><ul><li>High mortality without surgical intervention </li></ul></ul></ul><ul><li>Renal insufficiency </li></ul><ul><ul><ul><li>Immune complex mediated </li></ul></ul></ul><ul><ul><ul><li>Impaired hemodynamics/drug toxicity </li></ul></ul></ul>
  37. 38. Diagnosis <ul><li>Published criteria for diagnostic purposes in obscure cases </li></ul><ul><li>High index of suspicion in patients with predisposing anatomy or behavior </li></ul><ul><li>Blood cultures </li></ul><ul><li>Echocardiography </li></ul><ul><ul><li>TTE – 60% sensitivity </li></ul></ul><ul><ul><li>TEE – 80 – 95% sensitive </li></ul></ul>
  38. 39. Diagnosis <ul><ul><li>Major criteria : </li></ul></ul><ul><ul><li>Positive blood culture for Infective Endocarditis Typical microorganism consistent with IE from 2 separate blood cultures, as noted below: •  viridans streptococci, Streptococcus bovis , or HACEK group or •  community-acquired Staphylococcus aureus or enterococci, in the absence of a primary focus or Microorganisms consistent with IE from persistently positive blood cultures defined as: •  2 positive cultures of blood samples drawn >12 hours apart, or •  all of 3 or a majority of 4 separate cultures of blood (with first and last sample drawn 1 hour apart) </li></ul></ul><ul><ul><li>Evidence of endocardial involvement </li></ul></ul><ul><ul><li>Positive echocardiogram for IE defined as : •  oscillating intracardiac mass on valve or supporting structures, in the path of regurgitant jets, or on implanted material in the absence of an alternative anatomic explanation, or •  abscess, or •  new partial dehiscence of prosthetic valve </li></ul></ul><ul><ul><li>Or New valvular regurgitation (worsening or changing of preexisting murmur not sufficient) </li></ul></ul>
  39. 40. Diagnosis <ul><li>Minor criteria : </li></ul><ul><li>1.Predisposition : predisposing heart condition or intravenous drug 2. Fever : temperature > 38.4C (100.4?F) 3. Vascular phenomena : </li></ul><ul><li>major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhages, and Janeway lesions 4. Immunologic phenomena : </li></ul><ul><li>glomerulonephritis, Osler's nodes, Roth spots and rheumatoid factor 5. Microbiological evidence : positive blood culture but does not meet a major criterion as noted above¹ or serological evidence of active infection with organism consistent with IE 6. Echocardiographic findings : </li></ul><ul><li>consistent with IE but do not meet a major criterion as noted above ¹ Excludes single positive cultures for coagulase-negative staphylococci, diphtheroids, and organisms that do not commonly cause endocarditis. </li></ul>
  40. 41. Goals of Therapy <ul><li>Eradicate infection </li></ul><ul><li>Definitively treat sequelae of destructive intra-cardiac and extra-cardiac lesions </li></ul>
  41. 42. Antibiotic Therapy <ul><li>Treatment tailored to etiologic agent </li></ul><ul><ul><li>Important to note MIC/MBC relationship for each causative organism and the antibiotic used </li></ul></ul><ul><ul><li>High serum concentration necessary to penetrate avascular vegetation </li></ul></ul>
  42. 43. Antibiotic Therapy <ul><li>Treatment before blood cultures turn positive </li></ul><ul><ul><ul><li>Suspected ABE </li></ul></ul></ul><ul><ul><ul><li>Hemodynamic instability </li></ul></ul></ul><ul><ul><li>Neither appropriate nor necessary in patient with suspected SBE who is hemodynamically stable </li></ul></ul>
  43. 44. Antibiotic Therapy <ul><li>Effective antimicrobial treatment should lead to defervescence within 7 – 10 days </li></ul><ul><ul><li>Persistent fever in: </li></ul></ul><ul><ul><ul><li>IE due to staph, pseudomonas, culture negative </li></ul></ul></ul><ul><ul><ul><li>IE with microvascular complications/major emboli </li></ul></ul></ul><ul><ul><ul><li>Intracardiac/extracardiac septic complications </li></ul></ul></ul><ul><ul><ul><li>Drug reaction </li></ul></ul></ul>
  44. 45. Infective Endocarditis - Principles of Therapy
  45. 46. Microbiologic Cure Rate for Endocarditis Virridan streptococci, group A strep 98 98 Enterococcus 90 >90 S. aureus (young IVDU) 90 >90 S. aureus (elderly patients with underlying disease 50 70 Gram negative aerobic bacilli 40 65 Native Valve Endocarditis Antimicrobial therapy alone Antimicrobial therapy plus Surgery Fungus <5 50
  46. 47. Microbiologic Cure Rate for Endocarditis Prosthetic valve endocarditis Antimicrobial therapy alone Antimicrobial therapy plus Surgery   Early PVE Late PVE Early PVE Late PVE Virridan streptococci, group A strep NA 80 NA 90 Enterococcus NA 60 NA 75 S. aureus 25 40 50 60 Coagulase negative staphylococcus 20 40 60 70 Gram negative aerobic bacilli <10 20 40 50 Fungus <1 <1 30 40
  47. 48. Surgical Treatment of Intra-Cardiac Complications <ul><li>NYHA Class III/IV CHF due to valve dysfunction </li></ul><ul><ul><li>Surgical mortality – 20-40% </li></ul></ul><ul><ul><li>Medical mortality – 50-90% </li></ul></ul><ul><li>Unstable prosthetic valve </li></ul><ul><ul><li>Surgical mortality – 15-55% </li></ul></ul><ul><ul><li>Medical mortality – near 100% at 6 months </li></ul></ul><ul><li>Uncontrolled infection </li></ul>
  48. 49. Surgical Treatment of Intra-Cardiac Complications <ul><li>Unavailable effective antimicrobial therapy </li></ul><ul><ul><li>Fungal endocarditis </li></ul></ul><ul><ul><li>Brucella </li></ul></ul><ul><li>S. aureus PVE with any intra-cardiac complication </li></ul><ul><li>Relapse of PVE after optimal therapy </li></ul>
  49. 50. Surgical Treatment of Intra-Cardiac Complications <ul><li>Relative indications </li></ul><ul><ul><li>Perivalvular extension of infection </li></ul></ul><ul><ul><li>Poorly responsive S. aureus NVE </li></ul></ul><ul><ul><li>Relapse of NVE </li></ul></ul><ul><ul><li>Culture negative NVE/PVE with persistent fever (> 10 days) </li></ul></ul><ul><ul><li>Large (> 10mm) or hypermobile vegetation </li></ul></ul><ul><ul><li>Endocarditis due to highly resistant enterococcus </li></ul></ul>
  50. 51. Prevention <ul><li>Prophylactic regimen targeted against likely organism </li></ul><ul><ul><li>Strep. viridans – oral, respiratory, eosphogeal </li></ul></ul><ul><ul><li>Enterococcus – genitourinary, gastrointestinal </li></ul></ul><ul><ul><li>S. aureus – infected skin, mucosal surfaces </li></ul></ul>
  51. 52. Prevention – the procedure <ul><li>Dental procedures known to produce bleeding </li></ul><ul><li>Tonsillectomy </li></ul><ul><li>Surgery involving GI, respiratory mucosa </li></ul><ul><li>Esophageal dilation </li></ul><ul><li>ERCP for obstruction </li></ul><ul><li>Gallbladder surgery </li></ul><ul><li>Cystoscopy, urethral dilation </li></ul><ul><li>Urethral catheter if infection present </li></ul><ul><li>Urinary tract surgery, including prostate </li></ul><ul><li>I&D of infected tissue </li></ul>
  52. 53. Prevention – the underlying lesion <ul><li>High risk lesions </li></ul><ul><ul><li>Prosthetic valves </li></ul></ul><ul><ul><li>Prior IE </li></ul></ul><ul><ul><li>Cyanotic congenital heart disease </li></ul></ul><ul><ul><li>PDA </li></ul></ul><ul><ul><li>AR, AS, MR,MS with MR </li></ul></ul><ul><ul><li>VSD </li></ul></ul><ul><ul><li>Coarctation </li></ul></ul><ul><ul><li>Surgical systemic-pulmonary shunts </li></ul></ul><ul><li>Intermediate risk </li></ul><ul><ul><li>MVP with murmur </li></ul></ul><ul><ul><li>Pure MS </li></ul></ul><ul><ul><li>Tricuspid disease </li></ul></ul><ul><ul><li>Pulmonary stenosis </li></ul></ul><ul><ul><li>ASH </li></ul></ul><ul><ul><li>Bicuspid Ao valve with no hemodynamic significance </li></ul></ul>Lesions at highest risk
  53. 54. Prevention – the underlying lesion <ul><li>Low/no risk </li></ul><ul><ul><li>MVP without murmur </li></ul></ul><ul><ul><li>Trivial valvular regurg. </li></ul></ul><ul><ul><li>Isolated ASD </li></ul></ul><ul><ul><li>Implanted device (pacer, ICD) </li></ul></ul><ul><ul><li>CAD </li></ul></ul><ul><ul><li>CABG </li></ul></ul>
  54. 55. This wallet card is to be given to patients by their physician. Healthcare professionals, please see back of card for reference to the complete statement. Name: ____________________________________________ needs protection from BACTERIAL ENDOCARDITIS because of an existing HEART CONDITION Diagnosis: __________________________________________ Prescribed by: _______________________________________ Date: ______________________________________________
  55. 56. Chemoprophylaxis <ul><li>Adult Prophylaxis: Dental, Oral, Respiratory, Esophageal </li></ul><ul><li>Standard Regimen </li></ul><ul><ul><li>Amoxicillin 2g PO 1h before procedure or </li></ul></ul><ul><ul><li>Ampicillin 2g IM/IV 30m before procedure </li></ul></ul><ul><li>Penicillin Allergic </li></ul><ul><ul><li>Clindamycin </li></ul></ul><ul><ul><ul><li>600 mg PO 1h before procedure or </li></ul></ul></ul><ul><ul><ul><li>600 mg IV 30m before </li></ul></ul></ul><ul><ul><li>Cephalexin OR Cefadroxil 2g PO 1 hour before </li></ul></ul><ul><ul><li>Cefazolin 1.0g IM/IV 30 min before procedure </li></ul></ul><ul><ul><li>Azithromycin or Clarithromycin 500mg PO 1h before </li></ul></ul>
  56. 57. <ul><li>Adult Genitourinary or Gastrointestinal Procedures </li></ul><ul><li>High Risk Patients </li></ul><ul><ul><li>Standard Regimen </li></ul></ul><ul><ul><ul><ul><li>Before procedure (30 minutes): </li></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>Ampicillin 2g IV/IM AND </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>Gentamicin 1.5 mg/kg (MAX 120 mg) IM/IV </li></ul></ul></ul></ul></ul><ul><ul><ul><li>After procedure (6 hours later) </li></ul></ul></ul><ul><ul><ul><ul><li>Ampicillin 1g IM/IV OR </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Amoxicillin 1g PO </li></ul></ul></ul></ul><ul><ul><li>Penicillin Allergic </li></ul></ul><ul><ul><ul><li>Complete infusion 30 minutes before procedure </li></ul></ul></ul><ul><ul><ul><ul><li>Vancomycin 1g IV over 1-2h AND </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Gentamicin 1.5 mg/kg IV/IM (MAX 120 mg) </li></ul></ul></ul></ul><ul><li>Moderate Risk Patients </li></ul><ul><ul><li>Standard Regimen </li></ul></ul><ul><ul><ul><li>Amoxicillin 2g PO 1h before OR </li></ul></ul></ul><ul><ul><ul><li>Ampicillin 2g IM/IV 30m before </li></ul></ul></ul><ul><ul><li>Penicillin Allergic </li></ul></ul><ul><ul><ul><li>Vancomycin 1g IV over 1-2h, complete 30m before </li></ul></ul></ul>
  57. 58. Summary <ul><li>You need to go to medical school (and graduate) in order to take care of patients with endocarditis. </li></ul>
  58. 59. Case presentation <ul><li>M-mode and trans-esophageal echocardiogram showed mobile vegetation at aortic valve </li></ul>
  59. 60. Case presentation <ul><li>Blood culture yield Streptococcal viridans </li></ul><ul><li>Despite deferverscence nearly immediately after penicillin and gentamicin treatment, he developed Rt CVA 4 days after hospitalization </li></ul>