感染性心内膜炎课件_13

Infective Endocarditis Introduction Infective endocarditis (IE) is a disease that produces vegetations on the endocardium. A heart valve or endothelium of adjacent large artery is usually involved. Two major predisposing causes are: a susceptible cardiovascular substrate and a source of bacteremia. Majority of cases caused by streptococcus, staphylococcus, enterococcus, or fastidious gram negative cocco-bacillary forms. MicrobiologysxsF) Associated medical conditions : Long term HD DM Poor dental hygiene HIV (independent) Congenital defects MVP (100/100,000 pt-yr, in advanced countries) MR Thickened leaflets ASD, VSD Injection-drug use (TV) Long-term indwelling intravenous catheters Rheumatic heart dz. (primarily the young in developing countries) Pathophysiology Clinical manifestations Direct Constitutional symptoms of infection (cytokine) Indirect Local destructive effects of infection Embolization septic or bland Hematogenous seeding of infection N.B. may present as local infection or persistent fever, metastatic abscesses may be small, miliary Immune response Immune complex or complement-mediated Pathophysiology (cont.) Local destructive effects Valvular distortion/destruction Chordal rupture Perforation/fistula formation Paravalvular abscess Conduction abnormalities Purulent pericarditis Functional valve obstruction Pathophysiology(cont.2) Embolization Clinically evident 11 43% of patients Pathologically present 45 65% High risk for embolization Large 10 mm vegetation Hypermobile vegetation Mitral vegetations (esp. anterior leaflet) Pulmonary (septic) 65 75% of i.v. drug abusers with tricuspid IE Clinical Features Symptoms % Signs % Fever80-85Fever80-90 Chills42-75Murmur80-85 Sweats25Changing/new murmur10-40 Anorexia25-55Neurological abnormalities 30-40 Weight loss25-35Embolic events20-40 malaise25-40Splenomegaly15-50 dyspnia20-40Clubbing10-20 Cough25Peripheral manifestation Stroke13-20 Oslers nodes7-10 Headache15-40 Splinter hemorrhage5-15 Nausea / vomiting15-20 Petechiae10-40 Myalgia / arthralgia15-30 Janeway lesion6-10 Chest pain8-35Retinal lesion/ Roth spot4-10 Abdominal pain5-15 Back pain7-10 Confusion10-20 ABE and SBE Acute Toxic presentation Progressive valve destruction 95: 1686-1784 Differential Diagnosis AIE: Septicemia (S. pneumonia, Staph. Aureus, G (-) bacilli, etc.) SIE: Rheumatic fever, Tb, SLE, myxoma, Lymphoma, glomerulonephritis, etc. Treatment Goal of Therapy lEradicate infection lDefinitively treat sequelae of destructive intra-cardiac and extra-cardiac lesions Antibiotic Therapy Treatment tailored to etiologic agent Important to note MIC/MBC relationship for each causative organism and the antibiotic used High serum concentration necessary to penetrate a vascular vegetation Combination therapy (synergic effect, eg. PG + aminoglycosides ) Antibiotic Therapy(2) Treatment before blood cultures turn positive Suspected ABE Hemodynamic instability Neither appropriate nor necessary in patient with suspected SBE who is hemodynamically stable Antibiotic Therapy(3) Effective antimicrobial treatment should lead to defervescence within 7 10 days Persistent fever in: IE due to staph, pseudomonas, culture negative IE with microvascular complications/major emboli Intracardiac/extracardiac septic complications Drug reaction Adequate therapy (4-6 w) Surgical Treatment of Intra- Cardiac Complications NYHA Class III/IV CHF due to valve dysfunction Surgical mortality 20-40% Medical mortality 50-90% Unstable prosthetic valve Surgical mortality 15-55% Medical mortality near 100% at 6 months Uncontrolled infection Surgical Treatment of Intra- Cardiac Complications(2) Unavailable effective antimicrobial therapy Fungal endocarditis Brucella S. aureus PVE with any intra-cardiac complication Relapse of PVE after optimal therapy Surgical Treatment of Intra- Cardiac Complications(3) Relative indications Perivalvular extension of infection Poorly responsive S. aureus NVE Relapse of NVE Culture negative NVE/PVE with persistent fever ( 10 days) Large ( 10mm) or hypermobile vegetation Endocarditis due to highly resistant enterococcus Prevention Prophylactic regimen targeted against likely organism Strep. viridans oral, respiratory, eosphogeal Enterococcus genitourinary, gastrointestinal S. aureus infected skin, mucosal surfaces Prevention the procedure Dental procedures known to produce bleeding Tonsillectomy Surgery involving GI, respiratory mucosa Esophageal dilation ERCP for obstruction Gallbladder surgery Cystoscopy, urethral dilation Urethral catheter if infection present Urinary tract surgery, including prostate Incision 129:761-9. IV drug users and nosocomial cases excluded. Nonbacterial Thrombotic Endocarditis Sterile platelet-fibrin deposits Occur at sites of eddy currents or jet streams created by pre-existing cardiac disease Create the “soil” for bacterial deposition. Characteristically, non-inflammatory Infection Growth of vegetation by platelet-fibrin deposition yields a sanctuary for bacteria. Streptococci in IE Viridans Streptococci 30-65% of native valve endocarditis Normal oral commensals A group, composed of several species: S. mitior, S. sanguis, S. mutans,etc. Alpha-hemolytic, non-typable Typical agents of classic “SBE” Other Streptococci S. bovis Lancefield group D Gut flora: associated with GI pathology S. pneumonia 1-3% of cases of IE with predilection for AV Usually, in those with immune suppression DM and Ethanolism Group B Streptococci Elderly with chronic disease Enterococcus Normal inhabitant of GI tract. Frequently encountered in UTIs. Up to 40% of cases without identified underlying predisposition to IE. Difficult to treat due to drug resistance. Staphylococci Coagulase Positive (Staph. aureus) a major causative agent in all populations of IE typically produces “acute” IE fulminant, rapidly progressive with few immunologic signs. CNS complications in 30-50% Coagulase Negative (Staph. epi, et al) Major cause of PVE. 3-8% of NVE. Fungi Commonly encountered agents: Candida, Torulopsis, Aspergillus Predispositions Prosthetic valves IVDA Immunosupression Hyperalimentation Prolonged abx treatment Large vegetations and frequent embolic events. Other Organisms Pseudomonas Brucella Diphtheroids Listeria Bartonella Coxsiella Chlamydia Diagnosis Frequently difficult to diagnose with certainty. Highly variable and often non-specific presentation. Overdiagnosis and Underdiagnosis are common. Diagnosis Classic Clinical Approach: Von Reyn (Beth Israel) Criteria Limitations: No Use of Echo. IVDA not identified as a predisposition Lacks sensitivity for “acute” cases. Incorporation of Echo: Durack (Duke) Criteria Increases proportion of definite diagnoses. Use of Echo in Diagnosis of IE Native Valves-ACC Guidelines: Detection/characterization of valvular lesions Detection of vegetations and characterization of lesions in patients with CHD Detection of associated abnormalities Reevaluation studies in complex IE Evaluation of patients with high suspicion of culture-negative IE Use of Echo in Diagnosis of IE Prosthetic Valves-ACC Guidelines: Detection/characterization of valvular lesions Detection of associated abnormalities Reevaluation in complex IE Evaluation of suspected IE and negative cultures Evaluation of persistent fever without known source Use of Echo in Diagnosis of IE TEE: Prosthetic valves Poor visualization on TTE and high suspicion Detection of associated complications Preoperative Reevaluation in complex IE Medical Management Tailor therapy to results of susceptibility testing. Use parenteral drugs. Plan for prolonged courses of abx. Be vigilant for adverse drug effects. Use bactericidal agents. Synergistic combinations are useful. Monitor levels of aminoglycosides. Culture Negative Endocarditis Most common cause is recent use of abx. Fastidious organisms Fungal Intracellular agents: Bartonella, chlamdia, viruses. Non-infectious (marantic) Anticoagulation “If anticoagulation is indicated for another reason it should be continued. Anticoagulation does not prevent embolization due to IE.” ACC guidelines on Diagnosis and Management of Infective Endocarditis. Class I Indications for Surgery Acute AR or MR with heart failure. Acute AR with tachycardia and early closure of the MV. Fungal endocarditis. Annular or aortic abscess. Sinus or aortic aneurysm. Persistent bacteremia and valve dysfunction After 7-10 days of appropriate antibiotics. Circulation. 98(18):1949-1984, 1998 Other Indications for Surgery Class IIa Recurrent emboli after appropriate abx. Agent with known poor response to abx (GNR) with valve dysfunction. Class IIb Mobile vegetations 10 mm. Class III Early infections of MV that can likely be repaired. Persistent pyrexia and leucocytosis with negative blood cultures. Circulation. 98(18):1949-1984, 1998 Bayer AS, et al. Circ 98:25, 2936-48. 22/29 Dec 98 Features of High Risk for Complications Prosthetic cardiac valves Left-sided IE Staphylococcus aureus Fungal IE Prior IE Features of High Risk for Complications Prolonged symptoms (9 months) Cyanotic CHD Pulmonary-to-systemic shunts Poor response to antimicrobial therapy Complications Occur in Over Half of All Cases Embolic: CNS and Peripheral Ischemic Hemorrhagic Septic: mycotic aneurysm metastatic abscess Local invasive Conduction abnormalities Valvular dysfunction CHF Glomerulonephritis CHF High associated mortality Accounts for 80-90% of IE deaths Leading indication for surgery More common with AV involvement More common with Staph aureus? Surgery is strongly indicated in most cases. In-house death reduced from 51% to 9%. Once CHF develops, surgery should be performed promptly. Embolic Events Occurs in 22-50% of cases. 65% of events occur in CNS 90% of these in MCA distribution Associated with high mortality Highest incidence with S. aureus, Candida sp., and HACEK organisms. Embolic Events Risk for embolism drops dramatically within two weeks of antibiotic therapy institution. 13 to AV disease, AML disease the highest. Size of vegetation and embolic potential remain incompletely explained. Embolic Events: an Aggressive Approach Clinical Embolic Event (CNS or peripheral) CT/MR of Brain Small, ischemic infarcts a calling, not a business; a calling in which your heart will be exercised equally with your head. Often the best part of your work will have nothing to do with potions and powders, but with the exercise of an influence of the strong upon the weak, of the righteous upon the wicked, of the wi