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Infective endocarditis

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infective endocarditis

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Infective endocarditis

  1. 1. Guide By: Dr. Meenaxi Sharda Presented By: Dr. Naresh Kumar Meghwal (Resident GMC Kota)
  2. 2. DEFINITION • Infection of the endocardial surface of the heart, which may include heart valves (native or Prosthetic) , the mural endocardium , or septal defect. • The prototypic lesion of IE is the vegetation, is a mass of platelets, fibrin, microcolonies of microorganism, and scant inflammatory cells.
  3. 3. CLASSIFICATION ACUTE ENDOCARDITIS • Rapid damage of previously normal as well as diseased heart valve, with a highly virulent organism • Hematogenoulsy seeds to extracardiac sites • If untreated, leads to death within weeks SUBACUTE ENDOCARDITIS • Organisms of low virulence causing infection in a previously damaged heart, particularly on deformed valves. • Raraly metastasizs • Follow an indolent course of weeks to month • Gradually progressive unless complicated by a major embolic event or ruptured mycotic aneurysm
  4. 4. RISK FACTOR • Intravenous drug abuse • Artificial heart valves and pacemakers • Cardiac conditions such as MR, AS, AR, MVP and CHD • Intravascular catheters ,Hemodialysis, Nosocomial wound and UTI
  5. 5. CAUSATIVE ORGANISM • Acute IE is caused by Beta-Hemolytic streptococci, S. aureus, and Pneumococci. • Subacute IE is typically caused by viridans streptococci, enterococci, CoNS and HACEK group (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, and Kingella) • Endocarditis amoung IV drug users caused by S. aureus , P. aeruginosa and candida sp.
  6. 6. PATHOGENESIS • Organism enter bloodstream from mucosal surface, skin, and site of focal infection. • Endothelial injury (at the site of impact of high velocity blood jets or on low pressure side of cardiac structrual lesion) causes turbulent blood flow and • allow either direct infection by virulent organism or the development of an uninfected platelet-fibrin thombus (NBTE).
  7. 7. Cont. • Bactereamia – microorganism in blood adhere to sites at thrombus . Organisms are proliferate and induce a procoagulant state . • Fibrin deposition combines with platelets aggregation,stimulated by tissue factor and independently by proliferating microorganism, to generate an infected vegetation.
  8. 8. Endothelial injury Un-infected platelet fibrin thrombus (NBTE) Transient bacteremia and attachment of bacteria to NBTE Proliferation and pro-coagulant state Infected friable,bulky vegetation
  9. 9. CLINICAL MANIFESTATION Occur due to : • Damage to intracardiac structures • Embolization of vegetation fragments • Hematogenous infection of sites during bacteremia • Tissue injury due to deposition circulating immune complex
  10. 10. C0NSTITUTIONAL SYMPTOMS • ACUTE IE: • High grade fever and chills • SOB • Arthralgias/ myalgias • Abdominal pain • Pleuritic chest pain • Back pain • SUBACUTE IE: • Low grade fever • Anorexia, N/V • Weight loss • Fatigue • Arthralgias/ myalgias • Abdominal pain
  11. 11. CARDIAC • Murmur (85% cases) due to valvular damage and ruptured chordae. • CHF (40% cases) usually due to valvular dysfunction. • Perivalvular abscess. • Pericarditis. • Heart block. • Myocardial infarction.
  12. 12. NONCARDIAC • Nonspecific signs – petechiae, subungal or “splinter” hemorrhages, clubbing, splenomegaly, renal dysfunction, neurologic symptoms. • More specific signs - Osler’s Nodes, Janeway lesions, and Roth Spots.
  13. 13. SUBCONJUCTIVAL HAEMORRHAGE PETECHIAE
  14. 14. ROTH’S SPOTSSPLINTER HAEMORRHAGES
  15. 15. JANEWAY LESIONS
  16. 16. OSLERS NODES
  17. 17. DIAGNOSIS • Endocarditis should be suspected in patients with fever and no obvious source of infection, and particulary if heart murmur is present. • Diagnosis of IE is established with certainty only when vegetations obtained at cardiac surgery, at autopsy, or from an artery (an embolus) are examined histologically and microbiologically. • A highly sensitive and diagnostic scheme is known as DUKE CRITERIA has developed on basis of clinical, laboratory and echo findings.
  18. 18. BLOOD CLUTURE • If endocarditis is suspected, 3 blood culture sets, separated from each other by atleast 1 hr. (20 mL each), should be obtained from different venipuncture sites within 24 hr. • When endocarditis is present and no prior antibiotic therapy was given, all 3 blood cultures usually are positive because the bacteremia is continuous; at least 1 culture is positive in 99%. • Premature use of empiric antibiotic therapy should be avoided in hemodynamically stable patients to avoid culture-negative endocarditis.
  19. 19. DUKE CRITERIA •Definite IE o 2 major criteria OR o 1 major and 3 minor criteria OR o 5 minor criteria •Possible IE o 1 major and 1 minor criteria OR o 3 minor criteria •Rejected o Firm alternate diagnosis OR o Resolution of manifestations of IE with 4 days of antimicrobial therapy OR o No pathologic evidence of IE at surgery or autopsy after 4 of antimicrobial therapy.
  20. 20. MAJOR CRITERIA Positive blood culture: • Typical microorganism consistent with IE, from two separate blood cultures  S. viridans, S. bovis, HACEK  community-acquired S. aureus or enterococci (no primary focus) • Persistently positive cultures  at least two positive cultures, drawn 12 hours apart  all of three, or a majority of four or more cultures ,with first and last sample drawn at least one hour apart • Single positive blood culture for coxiella burnetii Evidence of endocardial involvement: • Positive echocardiogram  oscillating intracardiac mass on valve or supporting structures,  myocardial abscess,  new partial dehiscence of prosthetic valve • New valvular regurgitation
  21. 21. MINOR CRITERIA Predisposition • Predisposing heart condition or IV drug abuser Fever • > 38.0º C Vascular phenomena • arterial emboli, septic pulmonary infarct, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhage, Janeway’s lesion Immunologic phenomena • glomerulonephritis, Osler’s nodes, Roth’s spots, rheumatoid factors Microbiologic evidence • positive blood culture but does not meet major criteria.
  22. 22. IMAGING • Chest x-ray: – Look for multiple focal infiltrates, calcification of heart valves, evidence of cardiac failure and cardiomegaly. • ECG: – Rarely diagnostic – Look for evidence of ischemia, conduction delay(AV block), and arrhythmias • Echocardiography
  23. 23. ECHOCARDIOGRAPHY • It allows anatomic confirmation of IE, size of vegetations, detecting of intracardiac complication, and assessment of cardic function. • Trans thoracic echocardiography (TTE): Noninvasive, First line if suspected IE, Native valves IE, cannot image vegetation <2 mm in diameter, sensitivity is 65%. • Trans esophageal echocardiography (TEE): More sensitive(>90%) than TTE , Prosthetic valves IE, or detection of myocardial abscess, valve perforation, intracardiac fistulae.
  24. 24. ADDITIONAL TESTS • CBC: Normochromic normocytic anemia and/or leukocytosis. • ESR and CRP elevated • Complement levels ↓ (C3, C4, CH50) • RF • Urinalysis: Proteinuria and Microscopic hematuria • Baseline chemistries and coagulation profile. • Circulating immune complex titer commonly increased in IE.
  25. 25. MANAGMENT • Antibiotics remain the mainstay for treatment of IE. • To cure endocarditis, all bacteria in vagetation must be killed; therefore therapy must be bactericidal and prolonged. • High dose antibiotics are administered parenterally, to maximize diffusion of antibiotic molecules into depth of vegetation. • General measures include the following: – Treatment of congestive heart failure – Oxygen – Hemodialysis (may be required in patients with renal failure). • Surgery- Intracardiac complications
  26. 26. ANTIBOTIC REGIMEN FOR INFECTIVE ENDOCARDITIS: STREPTOCOCCI • Penicillin-susceptible: – Penicillin G 2-3 mU IV 4 hourly for 4 weeks – Ceftriaxone at 2 g/d IV as a single dose for 4 weeks – Penicillin G or ceftriaxone (as above dose) PLUS gentamicin at 1 mg/kg 8 hourly for 2 weeks; – Vancomycin 15mg/kg IV 12 hourly for 4 weeks.
  27. 27. Cont. • Relatively penicillin resistant streptococci – Penicillin G or Ceftriaxone PLUS gentamicin 1 mg/kg IM or IV 8 hourly for 4 weeks – Vancomycin 15mg/kg IV 12 hourly for 4 week. • Moderately penicillin resistant streptococci and nutritionally variant organisms -Penicillin G (4-5 mU IV 4 hourly) or Ceftriaxone (2 g/d IV) for 6 weeks PLUS gentamicin 1 mg/kg IM or IV 8 hourly for 4 weeks -Vancomycin 15mg/kg IV 12 hourly for 4 week
  28. 28. Cont. ENTEROCOCCI • Penicillin G (4-5 mU IV 4 h) PLUS gentamicin (1 mg/kg IM or IV 8 h) for 4-6 weeks • Ampicillin (2 g IV 4 h) PLUS gentamicin (1 mg/kg IM or IV 8 h) for 4-6 weeks • Vancomycin (15 mg/kg IV 12h)PLUS gentamicin (1 mg/kg IM or IV 8 h) for 4-6 weeks.
  29. 29. STAPHYLOCOCCI Methicillin-sensitive S aureus: • Nafcillin or oxacillin 2 g IV 4 h for 4-6 weeks • Cefazolin 2 g IV 8 h for 4-6 weeks • Vancomycin 15 mg/kg IV 12 h for 4-6 weeks Methicillin-resistant S aureus: • Vancomycin (15 mg/kg IV 12h for 6-8 weeks) PLUS gentamicin (1 mg/kg IM or IV 8 h for 2 weeks). • For infecting prosthetic valves (S/R) add rifampin 300 mg oral 8 h for 6-8 weeks. HACEK Organisms • Ceftriaxone 2 g/d IV as a single dose for 4 week
  30. 30. EMPIRICAL THERAPY • In injection drug user should cover MRSA and gram negative bacilli. The initiation of T/t with vancomycin and gentamycin immediatly after blood is obtain for cultures. • Pending the availability of diagnostic data, blood culture negative subacute NVE is T/t with ceftriaxone plus gentamycin. • If prosthetic valve are involved then above two plus vancomycin should be used.
  31. 31. MONITORING • Blood culture repeated daily until sterile. • Blood culture become sterile within 2 days after start of appropriate therapy when infection caused by viridans streptococci, enterococci,or HACEK organism. • In S. aureus ,penicillin therapy results in 3-5 days, whereas with vancomycin therapy culture positive persist for 7-9 days. • Resolution of fever within 5-7 days, when fever persists for 7 days , patients should be evaluated for paravalvular abscess and for extracardiac abscess (spleen, kidney) or complications (embolic events ).
  32. 32. INDICATIONS FOR SURGERY • Congestive heart failure refractory to standard medical therapy • Partially dehiscence unstable prosthetic valve • Persistent sepsis despite appropriate antibiotic treatment • Lack of effective microbicidal therapy (eg. Fungal or brucella) • Relapse after optimal antimicrobial therapy • Paravalvular abscess and intracardiac fistula • Large(>10mm) hypermobile vegetations with increased risk of embolism • Persistent fever (>10 day) in culture negative NVE.
  33. 33. PREVENTION High risk cardiac lesion for which prophylaxis is advised: • Prosthetic heart valves • Previous infective endocarditis • Unrepaired cyanotic CHD (including palliative shunts and conduits), • Completely repaired CHD during the 1st 6 months after surgery if prosthetic material or device was used • Incompletely repaired CHD that has residual defects at or adjacent to the site of repair • Valvulopathy developing after cardiac transplantation • Any procedure involving manipulation of gingival tissue or the periapical region of teeth, or perforation of the oral mucosa
  34. 34. REGIMEN FOR IE PROPHYLAXIS Standard oral regime: • Amoxicillin 2 g 1hr before procedure Inability to take oral medication: • Ampicillin 2g IV or IM 1hr before procedure Penicillin allergy: • Clindamycin 600 mg oral 1hr before procedure • Clarithromycin or azithromycin 500 mg oral 1hr before procedure • Cephalexin 2 g oral 1hr before procedure Penicillin allergy, inability to take oral: • Cefazolin or Ceftriaxone 1g IV or IM 30 min before • Clindamycin 600mg IV or IM 1hr before procedure Regimen for IE prophylaxis
  35. 35. OUTCOME • Older age, severe comorbid conditions, delayed diagnosis, involvment of prosthetic or aortic valve, an invasive(s.aureus) or antibiotic resistant (P. aeruginosa, yeast)pathogen, intracardiac complications, and major neurologic complications adversely impact outcome. • Prosthetic valve endocarditis beginning within 2 month of valve replacement results in mortality rate of 40-50% , whereas rate are only10-20% in later onset cases.
  36. 36. THANKS

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