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INFECTIVE ENDOCARDITIS

INFECTIVE ENDOCARDITIS. Manoj Kuduvalli. Definition. Bacterial or Fungal infection within the heart (although chlamydial and rickettsial infections are known) ; the role of viruses is unknown. ORIGINAL CLASSIFICATION (Prior to Antibiotic era). Current Criteria for Classification.

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INFECTIVE ENDOCARDITIS

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  1. INFECTIVE ENDOCARDITIS Manoj Kuduvalli

  2. Definition Bacterial or Fungal infection within the heart (although chlamydial and rickettsial infections are known) ; the role of viruses is unknown

  3. ORIGINAL CLASSIFICATION(Prior to Antibiotic era)

  4. Current Criteria for Classification Underlying Anatomy: › Native Valve Endocarditis › Prosthetic Valve Endocarditis Infecting Organism › Serves as basis for therapy and prognosis

  5. Native Valve EndocarditisUnderlying Predisposing Conditions ›› 60 - 80% of non IV Drug abusers have a predisposing condition › Mitral Valve Prolapse 30 - 50% › Rheumatic Heart Disease 20 - 40% › Degenerative Aortic and 20 - 30% Mitral valve disease › Congenital Heart Disease 10 - 20%

  6. Native Valve EndocarditisMicrobiology ›› Streptococci 50 - 70% Viridans Streptococci (50% of all Strep) ›› Staphylococci ~ 25% Mostly Coagulase +ve Staph. Aureus Staph. Epidermidis ›› Enterococci ~ 10%

  7. Viridans Streptococci Infect primarily abnormal valves Indolent clinical course Highly sensitive to Penicillins Staph. aureus Infect normal and abnormal valves Fulminant course with rapid destruction of valves and multiple metastatic abscesses Mostly resistant to Penicillins and sensitive to penicillinase resistant ß-lactams Common with soft tissue infections, and infected IV catheters Native Valve EndocarditisMicrobiology

  8. Staph. Epidermidis Indolent Course Affects abnormal valves Enterococci Normally affects damaged valves Recent history of genitourinary or gastrointestinal manipulation, disease or trauma Usually sensitive to Penicllin+Gentamicin Resistant strains prevalent Native Valve EndocarditisMicrobiology

  9. Prosthetic valve endocarditis • 5 - 15% of all Infective Endocarditis • Overall incidence 1 - 4% • Risk of PVE peaks at 15 days postop. , then rapidly declines by 150 days

  10. Early ( < 60 days ) Reflects perioperative contamination Incidence around 1% Microbiology Staph (45 - 50%) Staph. Epiderm (~ 30%) Staph. Aureus (~ 20%) Gram -ve aerobes (~20%) Fungi (~ 10%) Strep and Entero (5-10%) Late ( > 60 days) After endothelialization Incidence 0.2 -0.5 % / pt. year Transient bacteraemia from dental, GI or GU Microbiology resembles native valve endocarditis Prosthetic Valve EndocarditisClassification

  11. IE in IV Drug Abusers Right sided predilection Tricuspid Valve ~ 55% Aortic Valve ~ 25% Mitral Valve ~ 20% Pulmonary Valve 1 - 1.5% Mixed Rt. And Lt. Side 5 - 6%

  12. IE in IV Drug Abusers • Skin most predominant source of infection • Also contamination of drugs and paraphernalia • 70 - 100% of Rt. sided IE results in pneumonia and septic emboli • Microbiology • Staph aureus ~60% • Streptococci and Enterococci ~20% • Gram -ve bacilli ~10% • Fungi (Candida and Aspergillus ~5%

  13. IE in adults with congenital heart disease Common defects VSD PDA Bicuspid AV PS Coarctation of Aorta Occurs in defects with --mild or no hemodynamic consequences --high gradients --high velocity jets impinging on endocardium

  14. Microbiology very important since virulence of the infecting organism is a significant factor in determining the success rates of both medical and surgical treatment

  15. Pathogenesis Requires interaction between › Host vascular endothelium › Host haemostatic response › Adventitiously circulating organisms

  16. Pathogenesis of Vegetations

  17. Hemodynamic factors predisposing to Infective Endocarditis • High velocity abnormal jet stream • Flow from high to low pressure chamber • Narrow orifice between two chambers creating pressure gradient

  18. Pathology

  19. Common sites of origin of extravalvular spread

  20. Pathology Initially affects Valve leaflets in native valve endocarditis Can extend into annulus Annulus in prosthetic valve endocarditis Due to presence of sewing rim

  21. Pathology -Embolic Phenomena • Incidence • Clinically 15 - 45% • Pathologically 45 - 65% • More with large mobile vegetations • Fungi (Candida and Aspergillus) • Group B and G Streptococci • Staph aureus • Result in • Infarcts • Abscesses • Mycotic aneurysms

  22. PathologyImmune Complex Associated • Glomerulonephritis • Arthritis • Osler’s nodes

  23. Clinical Features Onset usually within 2 weeks of infection › Indolent course - Malaise - Fatigue - Night sweats - Anorexia - Weight loss › Explosive course - CCF - S/o severe systemic sepsis

  24. Clinical features › Fever - Usually < 39 °C, remittent - May be absent in - elderly - severe debility - CCF - Already on antibiotics › Murmurs - Appearance of new murmur or true change in existent murmur indicates infection with virulent organism

  25. Other Clinical Features • Splenomegaly ~ 30% • Petechiae 20 - 40% • Conjunctivae • Buccal mucosa • palate • skin in supraclavicular regions • Osler’s Nodes 10 - 25% • Splinter Haemorrhages 5 - 10% • Roth Spots ~ 5% • Musculoskeletal (arthritis)

  26. Complications • Congestive Cardiac Failure (Commonest complication) • Valve Destruction • Myocarditis • Coronary artery embolism and MI • Myocardial Abscesses • Neurological Manifestations (1/3 cases) • Major embolism to MCA territory ~25% • Mycotic Aneurysms 2 - 10%

  27. Complications • Metastatic infections • Rt. Sided vegetations • Lung abscesses • Pyothorax / Pyopneumothorax • Lt. Sided vegetations • Pyogenic Meningitis • Splenic Abscesses • Pyelonephritis • Osteomyelitis • Renal impairment d/t Glomerulonephritis

  28. Diagnosis • Blood Cultures • Positive in 95% cases • Other Laboratory Parameters • Anaemia • Leucocytosis (WCC may be normal in indolent infection) • Thrombocytopenia •  ESR (may be absent in CCF and renal failure) • Urine - Microscopic hematuria / proteinuria

  29. Echocardiography • Can demonstrate lesion / vegetation in 60 - 80% of cases • Difficult in prosthetic valve endocarditis • TOE better than TTE • Can demonstrate • Morphology of valve • Annular abscesses • Hemodynamics of the valves • Serial observations can contribute to decision for surgery

  30. Treatment Medical Surgical

  31. Principles of Medical Management Sterilization of Vegetations with antibiotics - prolonged Slowly metabolising bacteria due to high density, hence  sensitivity - high dose Bacteria deep inside vegetations -bactericidal

  32. Principles of Medical Management Acute onset, fulminant -Within two to three hours of clinical diagnosis. -Take cultures, but do not wait for results Timing of Therapy Subacute onset, or having received recent antibiotic -Within two to three days. -Can wait for culture reports

  33. Principles of Medical Management • Isolation of organisms very important • Therapy before isolation of organism • Native valve endocarditis and in IV drug abusers • Directed against Staph aureus • Prosthetic valve endocarditis • Broad spectrum antibiotics directed against • Staph aureus • Staph epidermidis • Gram –ve bacilli

  34. Indications for SurgeryLeft sided native valve endocarditis • Valvular disruption leading to severe insufficiency and CCF • Extravalvar extension • Embolization of vegetations • Failure of medical management Positive blood culture and systemic signs of infection after “adequate” antibiotic therapy • Resistant organisms such as MRSA, Fungi , Pseudomonas • Echo detected vegetation > 1 cm ??

  35. Indications for SurgeryRight sided native valve endocarditis Indications differ because: - Consequences of valve disruption and emboli are less - Success with antibiotics seems to be better --Failure of medical treatment --CCF, with its complications Indications (elective) --Recurrent pulmonary emboli with complications --Extravalvar spread (rare)

  36. Indications for surgeryProsthetic valve endocarditis • Early infection almost always require surgery • Late infection Antibiotic therapy succeeds more often with Bioprosthesis compared to mechanical valves CCF due to prosthesis dysfunction Indications Multiple emboli Persistent infection

  37. Indications for SurgerySpecial situations AIDS Not usually indicated since life expectancy due to AIDS very poor HIV +ve patient without AIDS IV Drug Abusers No change in indications since enough number survive > 10 years

  38. When to operate ? As soon as there is a major indication Valid reasons for delay Acute CNS injury --Hemorrhagic infarct (Wait for 10 days to allow healing) --Coma (very poor prognosis ) Renal failure due to Glom’nephritis Follow through the acute phase (Prerenal failure -- early operation)

  39. Principles of operation Repair or Replacement ? (More important with mitral valves) Repair contemplated only if: --Infection well controlled --Repair structurally feasible after involved tissue excised

  40. Principles of operation • Early operation once indicated • Preop. knowledgeof morphology of valve • Good exposure(may be difficult in mitrals) • Excision and debridement of all infected or involved tissue even if extensive reconstruction or permanent pacing required

  41. Principles of operation • Lookfor extravalvar extension • If present,evacuate abscess cavity and repairwith biological material such as autologous or bovine pericardium • Suturevalve onto clean and relatively strong tissue • Temporary pacing leads

  42. Stented Bioprosthesis Mechanical Which Prosthesis? Stentless Bioprosthesis Homograft

  43. Choice of prosthesis Important factor is location of infection -- Infection of cusps only: Choice does not matter, since all infected tissue is usually excised -- Perivalvar extension: No choice between mechanical and stented bioprosthesis (both with cloth sewing rims) Homograft, maybe stentless bioprosthesis have lesser incidence of infection

  44. Choice of prosthesisMechanical v/s Bioprosthetic • No difference in linearized rates for recurrent or residual infection (~1-2% per patient year) • No difference in operative mortality and complication free survival • Infected bioprosthesis more easily sterilized (since infection initially involves leaflets) • However, infection in bioprosthesis may hasten SVD due to damage to leaflets

  45. Choice of prosthesisHomograft v/s others • Hazard function for recurrent endocarditis has only low constant phase and has no high early hazard phase like other prosthesis • Homograft best choice if valved conduit is required for root replacement ( > 50% annular dehiscence or aortoventricular discontinuity)

  46. Postoperative Antibiotics To continue for 6 weeks if › Operated for --Acute fulminant infection --Failure of medical therapy --Resistant organisms › Excised valve yields positive cultures › Periannular involvement › Valve culture –ve, but organisms seen on histology › Positive blood cultures 3 – 4 days postop.

  47. Results of TreatmentNative valve endocarditisMedical Management Mortality 10 – 60 % Risk Factors Virulent organisms s/a MRSA, G-ve bacilli, fungi CCF Persistence of systemic sepsis Major septic embolus Extravalvar extension Acute renal failure

  48. Results of TreatmentNative valve endocarditisSurgical Management Hospital Mortality 5 – 20% Risk factors Virulent organisms Perivalvar extension Intractable CCF Renal and multiorgan failure

  49. Results of TreatmentNative valve endocarditisSurgical Management Recurrent Endocarditis ~ 2% Most occurs within 2 months post op. Same organism No fresh source of infection Perivalvar leaks 3-7%

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