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1、INFECTIVE ENDOCARDITIS,某章(或某三级学科)教学大纲要求,注:适当标记重点和难点,Infective Endocarditis,Essential characteristics General definitions and epidemiology NVE I.V. drug abuse PVE Pathogenesis,Pathophysiology Clinical features Treatment,Essential characteristics,Febrile illness Persistent bacteremia Characteristic le
2、sion of microbial infection of the endothelial surface of the heart Variable in size Amorphous mass of fibrin & platelets Abundant organisms Few inflammatory cells,the vegetation,Essential characteristics,Typically involves the valves May involve all structures of the heart Chordae tendinae Sites of
3、 shunting Mural lesions Majority of cases caused by streptococcus, staphylococcus, enterococcus, or fastidious gram negative cocco-bacillary forms,Clinical classification,NVE I.V. drug abuse PVE,Epidemiology,55-75% of patients with native valve endocarditis (NVE) have underlying valve abnormalities
4、MVP Rheumatic Congenital i.v. drug abuse,Epidemiology,Intravenous Drug Abuse Risk is 2 5% per pt./year Tendency to involve right-sided valves Distribution in clinical series 46 78% tricuspid 24 32% mitral 8 19% aortic Underlying valve normal in 75 93% S. aureus predominant organism (50%, 60-70% of t
5、ricuspid cases,Epidemiology,Intravenous Drug Abuse Increased frequency of gram negative infection such as P. aeruginosa & fungal infections High concordance of HIV positivity & IE (27-73%) HIV status does not in itself modify clinical picture Survival is decreased if CD4 count 200/mm3,Epidemiology,P
6、rosthetic Valve Endocarditis (PVE) 10 30% of all cases in developed nations Cumulative incidence 1.4 3.1% at 12 months 3.2 5.7% at 5 years Early PVE within 60 days Nosocomial (s. epi predominates) Late PVE after 60 days Community (same organisms as NVE,Infective Endocarditis,Pathology NVE infection
7、is largely confined to leaflets PVE infection commonly extends beyond valve ring into annulus/periannular tissue Ring abscesses Septal abscesses Fistulae Prosthetic dehiscence Invasive infection more common in aortic position and if onset is early,Infective Endocarditis,Pathogenesis,Endothelial dama
8、ge,Platelet-fibrin thrombi,Microorganism adherence,Infective Endocarditis,Nonbacterial Thrombotic Endocarditis Endothelial injury Hypercoagulable state Lesions seen at coaptation points of valves Atrial surface mitral/tricuspid Ventricular surface aortic/pulmonic Modes of endothelial injury High vel
9、ocity jet Flow from high pressure to low pressure chamber Flow across narrow orifice of high velocity Bacteria deposited on edges of low pressure sink or site of jet impaction,Venturi Effect,Platelet-fibrin thrombi,Venturi Effect,Conversion of NBTE to IE,Frequency & magnitude of bacteremia Density o
10、f colonizing bacteria Oral GU GI Disease state of surface Infected surface colonized surface Extent of trauma Resistance of organism to host defenses Most aerobic gram negatives susceptible to complement-mediated bactericidal effect of serum Tendency to adhere to endothelium Dextran producing strep
11、Fibronectin receptors on staph, enterococcus, strep, Candida,Case: Infection and Shock,Vegetations Opened right atrium,View of the Tricuspid Valve (from Atrial Side,Infective endocarditis,Mitral valve involved Aortic valve involved,Infective endocarditis,Tricuspid valve involved,Pathophysiology,Clin
12、ical 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 respons
13、e Immune complex or complement-mediated,Pathophysiology,Local destructive effects Valvular distortion/destruction Chordal rupture Perforation/fistula formation Paravalvular abscess Conduction abnormalities Purulent pericarditis Functional valve obstruction,Pathophysiology,Embolization Clinically evi
14、dent 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,Fever most common sign May be absent in elderly
15、/debilitated pt. Murmur present in 80 85% Generally indication of underlying lesion Frequently absent in tricuspid IE Changing murmur,Classical Peripheral Manifestations,Less common today Not seen in tricuspid endocarditis Petechiae most common,Janeway Lesions,Splinter Hemorrhage,Oslers Nodes,Subcon
16、junctival Hemorrhages,Roths Spots,Clinical Features,Systemic emboli Incidence decreases with effective anti-microbial Rx Neurological sequelae Embolic stroke 15 20% of patients Mycotic aneurysm Cerebritis CHF Due to mechanical disruption High mortality without surgical intervention Renal insufficien
17、cy Immune complex mediated Impaired hemodynamics/drug toxicity,Tests,Repeated blood culture and sensitivity ESR CBC may show low grade, microcytic (small red blood cells) anemia Echocardiogram TTE 60% sensitivity TEE 80 95% sensitive chest X-ray CT scan of the chest ASO,临床警惕IE,器质性心脏病患者出现原因不明发热一周以上;
18、新出现的心脏杂音,或原有杂音性质发生明显改变 动脉栓塞症而无原因解释; 原因不明的心力衰竭; 心脏手术后伴持续性发热超过1周,Diagnostic Criteria,Definitive infective endocarditis pathologic criteria clinical criteria (see below) two major criteria, or one major and two minor criteria, or five minor criteria,IE 诊断(病理学依据,1)微生物:在赘生物、发生栓塞的赘生物或心内脓肿中经培养或组织学检查证实有微生物
19、(2)病理改变:赘生物或心内脓肿经组织学证实有活动性心内膜炎,IE 诊断(临床依据,主要指标: 1.血培养两次阳性,提示为典型微生物,如草绿色链球菌、 HACEK组菌 2.间隔12h两次血培养持续菌血症,或培养3次阳性为金 黄色葡萄球菌、肠球菌或表皮葡萄球菌 3. 伯氏立克次体、鹦鹉热衣原体等感染的血清学检测阳 性 4. 特殊的基因靶点分子生物学检测阳性 5. 超声检测发现赘生物、脓肿,或新出现的瓣膜反流、穿孔、人工瓣 膜或缺损补片有新的开裂 6. 血管征象:重要的动脉栓塞、脓毒性肺梗死或感染性动脉瘤,IE 诊断(临床依据,次要指标: l.易致IE的基础疾病,包括基础心血管病或静脉毒瘾 2.发
20、热,体温38伴贫血 3.原有心脏杂音改变、出现新的反流性杂音或心功能不全 4.血管征象:脾大、结膜出血、镜下血尿、颅内出血、Janeway结节、杵状指、瘀点瘀斑等 5.免疫现象:肾小球肾炎、Osler结节、Roth斑、类风湿因子阳性 6.微生物学证据:血培养阳性但不符合上述主要标准,或血清学证据符合可致IE的微生物活动性感染 7.CRP升高,ESR加快,Goals of Therapy,Eradicate infection Definitively treat sequelae of destructive intra-cardiac and extra-cardiac lesions,An
21、tibiotic 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 avascular vegetation,Antibiotic Therapy,Intravenous antibiotics. .Long-term high-dose antibiotic therapy i
22、s required, Therapy up to 6 weeks is not uncommon. .The chosen antibiotic must be specific for the organism causing the condition. This is determined by the blood culture and the sensitivities tests. .If heart failure develops as a result of damaged heart valves, surgery to replace the affected hear
23、t valve may be indicated,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 Tre
24、atment of Intra-Cardiac Complications,Unavailable effective antimicrobial therapy Fungal endocarditis Brucella S. aureus PVE with any intra-cardiac complication Relapse of PVE after optimal therapy,Prevention,Prophylactic regimen targeted against likely organism Strep. viridans oral, respiratory, eosphogeal Enterococcus genitourinary, gastrointestinal S. aureus infected skin, mucosal surfa
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