ESC感染性心内膜炎指南
2023 ESC心内膜炎管理指南更新要点
2023 ESC心内膜炎管理指南更新要点新增建议1.对接受牙科手术且感染性心内膜炎（IE）风险增加的心血管疾病患者进行预防性抗生素治疗➤对于IE高危和中危人群，建议采取一般预防措施。
（I，C）➤建议使用心室辅助装置的患者预防性使用抗生素。
（I，C）➤心脏移植受者可考虑预防性使用抗生素。
（IIb，C）2.高危患者IE预防建议➤对于接受呼吸系统、胃肠系统、泌尿生殖系统、皮肤或肌肉骨骼系统侵入性诊断或治疗手术的高危患者，可考虑进行全身抗生素预防。
（IIb，C）3.心脏手术中IE预防建议➤建议对植入部位采取最佳的术前无菌措施，以预防心血管植入式电子装置（CIED）感染。
（I，B）➤在导管室环境下进行导管插入和操作时，建议采取标准的外科无菌措施。
（I，C）➤在经导管主动脉瓣置换术（TAVI）和其他经导管瓣膜手术之前，应考虑对常见的皮肤菌群（包括肠球菌和金黄色葡萄球菌）进行抗生素预防。
（IIa，C）4.超声心动图在IE中的作应用建议➤在患者病情稳定后，建议在由抗生素静脉给药转为口服治疗之前进行经食管超声心动图（TOE）。
（I，B）5.关于CT、核成像和磁共振在IE中的应用建议➤对于可能存在自体瓣膜心内膜炎（NVE）的患者，推荐行心脏计算机断层扫描血管造影（CTA）检查，以发现瓣膜病变，明确IE诊断。
（I，B）➤对于可能发生人工瓣膜心内膜炎（PVE）的患者，推荐行¹⁸F-氟脱氧葡萄糖正电子发射计算机断层扫描（[18F]FDG-PET）/CT(A)和心脏CTA检查，以发现瓣膜病变，明确IE诊断。
（I，B）➤对于可能的CIED相关IE，可考虑[18F]FDG-PET/CT(A)以明确IE诊断。
（IIa，B）➤对于超声心动图不能明确诊断，推荐在NVE和PVE中进行心脏CTA检查来诊断瓣膜旁或假体周围并发症。
（I，B）➤对于有症状的NVE和PVE患者，建议进行脑和全身影像学检查（CT、[18F]FDG-PET/ CT和/或磁共振[MRI]），以检查外周病变或增加次要诊断标准。
《2023 ESC心内膜炎管理指南》解读PPT课件
诊断心内膜炎需要进行一系列检查，包括血液检查（如血常规、血培养等）、心电图、超声心动图、心脏核磁共 振等。对于疑似感染性心内膜炎的患者，医生还会进行微生物学检查，如血培养、心内膜组织活检等，以确定病 原体类型和制定治疗方案。
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2023 ESC心内膜炎管理指南要 点解读
诊断策略
临床表现与体格检查
开展医生培训与教育项目，提高医生对指 南的认知和接受程度，确保指南的正确实
施。
A 加强医疗资源建设
政府和相关部门应加大投入，提高 医疗资源配置，确保指南实施所需
的资源充足。
B
C
D
完善医疗保障政策
政府应完善医疗保障政策，减轻患者经济 负担，提高指南的普及率和实施效果。
患者教育与宣传
加强患者教育与宣传，提高患者对指南的 信任度和依从性，促进治疗效果的提升。
新增了免疫学和分子生物学 诊断标准，提高了诊断准确 性。
影像学检查推荐
强调了经胸超声心动图（ TTE）和经食管超声心动图 （TEE）在诊断中的价值，并 给出了具体检查建议。
感染性心内膜炎诊断
新增了感染性心内膜炎的诊 断流程和治疗方案，强调了 早期识别和治疗的重要性。
治疗方面更新亮点
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抗生素治疗策略
诊疗技术不断发展
临床需求迫切
临床医生和患者对于心内膜炎的诊疗 和管理有着迫切的需求，需要权威性 的指南进行指导。
随着医疗技术的进步，心内膜炎的诊 断和治疗手段也在不断更新和完善。
指南目的和意义
规范心内膜炎管理
通过制定心内膜炎管理指南，规范心内膜炎的诊断、治疗和预防等 方面的管理，提高医疗质量。
降低发病率和死亡率
对未来发展趋势进行展望预测
ESC2009感染性心内膜炎抗菌治疗
标准治疗
剂量用法 1200~1800万U，iv，分6次给药 100~200mg/kg/d，分4-6次 2g/d,iv 或im，一次 1200~1800万U，iv，分6次给药 100~200mg/kg/d，分4-6次 2g/d,iv或im，一次 3mg/kg/d，iv或im，一次 4-5mg/kg/d，iv一次 3mg/kg/d，iv，分两次
真菌类
常见于PVE和IE，静脉药瘾者及免疫力 低下者多见。 真菌性IE死亡率高（大于50%），常 需双重抗真菌药及瓣膜置换。大多数可 选用两性霉素B单用或联用唑类抗真菌 药。口服唑类需要长期甚至终身应用。
3.经验治疗
抗生素应用前，应行3组血培养，标本取血间隔 30min.经验性治疗取决于以下几点：
少见微生物为肺炎球菌，淋球菌，流感 杆菌，肠球菌，表皮葡萄球菌，真菌及 立克次体、衣原体。
细菌仍是主要病原体，但近年真菌已成为重 要病因之一，立克次体、衣原体、螺旋体、 病毒等亦可引起。 草绿链球菌，90-95%至目前25-40% 葡球菌—金葡、白葡、表皮葡… 肠球菌，比例不断上升 G-杆菌引人注意 真菌，可能与广谱抗生素、皮质激素、免 疫抑制剂的广泛应用及有创技术开展有关
Duke诊断标准
主要诊断标准
两次血培养阳性，而且病原菌完全一 致，为典型的感染性心内膜炎致病菌。 ② 超声心动图发现赘生物，或新的瓣膜关 闭不全
①
次要诊断标准：
① ② ③ ④ ⑤ ⑥
基础心脏病或静脉滥用药物史 发热，体温≥38℃ 血管现象：栓塞、细菌性动脉瘤、颅内出血、结膜瘀点 及Janeway损害 免疫反应：肾小球肾炎、Osler结节、Roth斑及类风湿 因子阳性 血培养阳性，但不符合主要诊断标准 超声心动图发现符合IE,但不符合主要诊断标准
ESC 感染性心内膜炎指南
ESC 感染性心内膜炎指南ESC 感染性心内膜炎（Infective Endocarditis, IE）是一种严重的心脏病，可导致心脏瓣膜损害，脓肿形成，心力衰竭，甚至死亡。
本指南旨在提供对 ESC 感染性心内膜炎的基本认识、预防与管理策略的介绍。
感染性心内膜炎概述定义感染性心内膜炎是一种由病原微生物感染引起的瓣膜或心内膜的炎症疾病。
可导致瓣膜受损、赘生物形成、瓣膜功能不全和心肌梗死等。
病原微生物可来自心内膜瓣膜、血液、脊髓液和腹腔等部位。
分类感染性心内膜炎可分为急性和亚急性两种类型。
•急性感染性心内膜炎常由金黄色葡萄球菌等荚膜阳性细菌引起，起病急骤，病情进展较快。
•亚急性感染性心内膜炎一般由口腔、皮肤和胃肠道菌群引起，发病较缓，病情进展较慢。
症状感染性心内膜炎症状多样，常有以下表现：•发热、寒战、盗汗等全身炎症反应症状•体重减轻、无力、疲劳等全身不适症状•贫血、皮疹、眼、肾、脑等部位的出血、感觉障碍、脑卒中等表现•心脏相关症状，如心肌炎、心包炎、房室传导阻滞、心脏瓣膜受损、心力衰竭等。
预防预防ESC 感染性心内膜炎的关键是预防感染、及时诊断和治疗病原微生物感染。
以下是常用的预防策略：防止感染•定期接种疫苗，如肺炎球菌、流感、乙型肝炎等疫苗。
•正确使用抗生素，避免滥用，预防耐药菌株的产生。
•维持良好的个人卫生习惯，如勤洗手、避免口腔溃疡、减少亲密接触等。
•避免接触病原微生物，如污染的水、食物、接触感染源等。
高危人群的预防•有心内膜或心脏瓣膜结构缺陷的人需进行定期心脏检查，避免无菌手术和操作时引起的感染。
•心脏瓣膜置换手术前一定要采取有效的抗生素预防。
诊断早期诊断 ESC 感染性心内膜炎是预防并发症、减少心脏损害的关键。
以下是诊断 ESC 感染性心内膜炎的一些指标：体征•费用氏现象：可见到指（趾）甲床的色素沉着或出血。
•罗斯班格征：颈静脉搏动幅度增强。
•坎普维格现象：仰卧时，踝部向下压迫数分钟后迅速地向上抬高，可见到不同程度水肿。
2023ESC心内膜炎指南解读ppt课件
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总结与展望
对临床实践指导意义
规范诊断流程
新指南强调了心内膜炎诊断的规范化流程，包括临床表现、影像学 检查及实验室检查等综合评估，有助于提高诊断准确性。
优化治疗方案
根据新指南，针对不同类型和严重程度的心内膜炎，医生可制定更 合理的治疗方案，包括抗生素选择、手术时机等。
改善患者预后
通过遵循新指南建议，医生可更好地控制心内膜炎患者的炎症反应、 减少并发症发生，从而改善患者预后和生活质量。
抗凝药物
对于合并心内膜炎相关血 栓的患者，应使用抗凝药 物进行预防和治疗，降低 血栓栓塞事件的发生率。
营养支持
对于营养不良或不能进食 的患者，应给予肠内或肠 外营养支持，保证机体能 量和营养需求。
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非药物治疗方法探讨
手术治疗适应证与术式选择
手术治疗适应证
对于感染性心内膜炎合并心脏瓣膜穿孔、破裂、赘生物形成 或难治性心力衰竭的患者，应考虑手术治疗。
未来研究方向与挑战
新型抗感染治疗策略
针对心内膜炎病原体耐药性问题，研 究新型抗感染治疗策略，如靶向药物 、免疫疗法等。
早期诊断与预防
加强心内膜炎早期诊断方法的研究， 提高早期诊断率，同时探索有效预防 措施，降低发病率。
跨学科合作与治疗
促进心脏内外科、感染科、影像科等 多学科合作，共同制定心内膜炎综合 治疗策略，提高治疗效果。
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指南的推广和应用有助于降低感染性心内膜炎的误诊率和死亡
率，改善患者预后。
促进多学科协作
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指南强调多学科团队协作在感染性心内膜炎诊疗中的重要性，
有助于推动相关学科之间的交流与合作。
指南制定过程
组建专家团队
由心血管病学、感染病学、微 生物学等领域的专家组成指南
感染性心内膜炎的诊断与治疗ESC指南
感染性心内膜炎的诊断与治疗ESC指南一、诊断：1.临床表现：对于具有诱发因素（如心脏瓣膜病变、人工瓣膜等）的发热患者，应高度怀疑感染性心内膜炎，并进行详细的临床评估和观察。
2.血培养：对疑似感染性心内膜炎患者进行定期的血培养，有助于确定病原体。
连续两次阳性血培养或者单次阳性血培养且存在心脏瓣膜病变表现时可确诊感染性心内膜炎。
3.心脏超声：心脏超声检查是诊断感染性心内膜炎的重要方法，可以检测心脏瓣膜破坏和心内膜炎附壁凸起等特征性表现。
4.其他辅助检查：如炎症指标（C-反应蛋白、血沉等）升高，心电图、胸部X线等。
二、治疗：1.抗菌治疗：治疗感染性心内膜炎的首选药物是青霉素类抗生素。
根据病原体的不同，青霉素类可分为青霉素敏感菌和青霉素耐药菌两种。
对于青霉素敏感菌感染，完全静脉给药至少4-6周；对于青霉素耐药菌感染，需加用氨基糖苷类抗生素或万古霉素。
药物的选择和剂量根据当地的耐药情况和病原微生物的检测结果而定。
2.手术治疗：对于无反复感染性心内膜炎史或没有明确耐药菌株的患者，瓣膜置换是必要的。
因感染性心内膜炎所致升主动脉瘤、穿孔、心内膜炎附壁脓肿等需要手术干预的并发症，也需要尽早手术。
3.并发症的处理：感染性心内膜炎可以引起多种并发症，包括心力衰竭、心律失常等。
应根据具体情况进行相应的处理，如补充液体、应用正性肌力药物、施行心电复律等。
在治疗过程中1.早期治疗：早期通过临床评估和相关检查尽早诊断，并开始抗菌治疗和手术干预（如需要），可以提高患者的预后。
2.个体化治疗：根据患者的具体情况，包括年龄、病原体的敏感性等，制定个体化的治疗方案。
同时，还要根据治疗反应进行调整，并定期进行复查评估。
3.治疗后的预防：治疗完成后，需要加强心脏健康管理，坚持长期使用心脏抗生素预防性治疗，避免反复感染性心内膜炎的发生。
通过临床评估、血培养、心脏超声等方法进行诊断，采用抗菌治疗和手术治疗的综合措施，早期干预并个体化治疗，可以提高感染性心内膜炎的治疗效果，减少并发症的发生，提高患者的生存率和生活质量。
《ESC2015：感染性心内膜炎的管理指南》解读
《ESC2015：感染性心内膜炎的管理指南》解读The interpretation of 《2015 ESC Guidelines for the management of infective endocarditis》（1）.CHEN Yan，CHEN Yabei，TAO Rongfang.Department of cardiology，Mingguang Hospital of TCM，Mingguang，Anhui，239400，ChinaCorresponding author：CHEN Yan.Email：mgyc2394@Abstract：This paper introduced 《2015 ESC Guidelines for the management of infective endocarditis》.Key words：Endocarditis；Valve disease；Echocardiography；Prognosis；Guidelines；Prosthetic heart valves；Congenital heart disease当地时间2015年8月29日－9月2日欧洲心脏病学会年会在英国伦敦举行。
全球2.7万余名医生参加了会议。
会议推出了5部指南。
现将《感染性心内膜炎的管理指南》介绍于下。
该指南由Gilbert Habib，Patrizio Lancellotti及Manuel J. Antunes等20位学者执笔，全文54页，15部分（序言，问题的正当理由/范围，预防，“心内膜炎团队”，诊断，入院预后评估，抗菌治疗：原则和方法，左心瓣膜感染性心内膜炎的主要并发症及管理，感染性心内膜炎的其他并发症，手术治疗的原则和方法，出院后结果随访和远期预后，特定情况的处理，指南信息中应做和不应做的，附录，参考文献），参考文献483篇，推出推荐128条，其中Ⅰ类推荐73条，占57.03%。
ESC感染性心内膜炎预防诊断治疗指南2009版
ESC GUIDELINESGuidelines on the prevention,diagnosis,and treatment of infective endocarditis (new version 2009)The Task Force on the Prevention,Diagnosis,and Treatment of Infective Endocarditis of the European Society of Cardiology (ESC)Endorsed by the European Society of Clinical Microbiology and Infectious Diseases (ESCMID)and by the International Society of Chemotherapy (ISC)for Infection and CancerAuthors/Task Force Members:Gilbert Habib (Chairperson)(France)*,Bruno Hoen (France),Pilar Tornos (Spain),Franck Thuny (France),Bernard Prendergast (UK),Isidre Vilacosta (Spain),Philippe Moreillon (Switzerland),Manuel de Jesus Antunes (Portugal),Ulf Thilen (Sweden),John Lekakis (Greece),Maria Lengyel (Hungary),Ludwig Mu¨ller (Austria),Christoph K.Naber (Germany),Petros Nihoyannopoulos (UK),Anton Moritz (Germany),Jose Luis Zamorano (Spain)ESC Committee for Practice Guidelines (CPG):Alec Vahanian (Chairperson)(France),Angelo Auricchio(Switzerland),Jeroen Bax (The Netherlands),Claudio Ceconi (Italy),Veronica Dean (France),Gerasimos Filippatos (Greece),Christian Funck-Brentano (France),Richard Hobbs (UK),Peter Kearney (Ireland),Theresa McDonagh (UK),Keith McGregor (France),Bogdan A.Popescu (Romania),Zeljko Reiner (Croatia),Udo Sechtem (Germany),Per Anton Sirnes (Norway),Michal Tendera (Poland),Panos Vardas (Greece),Petr Widimsky (Czech Republic)Document Reviewers:Alec Vahanian (CPG Review Coordinator)(France),Rio Aguilar (Spain),Maria Grazia Bongiorni (Italy),Michael Borger (Germany),Eric Butchart (UK),Nicolas Danchin (France),Francois Delahaye (France),Raimund Erbel (Germany),Damian Franzen (Germany),Kate Gould (UK),Roger Hall(UK),Christian Hassager (Denmark),Keld Kjeldsen (Denmark),Richard McManus (UK),Jose´M.Miro ´(Spain),Ales Mokracek (Czech Republic),Raphael Rosenhek (Austria),Jose´A.San Roma ´n Calvar (Spain),Petar Seferovic (Serbia),Christine Selton-Suty (France),Miguel Sousa Uva (Portugal),Rita Trinchero (Italy),Guy van Camp (Belgium)The disclosure forms of the authors and reviewers are available on the ESC website/guidelines*Corresponding author.Gilbert Habib,Service de Cardiologie,CHU La Timone,Bd Jean Moulin,13005Marseille,France.Tel:þ33491386379,Email:gilbert.habib@free.frThe content of these European Society of Cardiology (ESC)Guidelines has been published for personal and educational use only.No commercial use is authorized.No part of the ESC Guidelines may be translated or reproduced in any form without written permission from the ESC.Permission can be obtained upon submission of a written request to Oxford University Press,the publisher of the European Heart Journal and the party authorized to handle such permissions on behalf of the ESC.Disclaimer.The ESC Guidelines represent the views of the ESC and were arrived at after careful consideration of the available evidence at the time they were written.Health professionals are encouraged to take them fully into account when exercising their clinical judgement.The guidelines do not,however,override the individual responsibility of health professionals to make appropriate decisions in the circumstances of the individual patients,in consultation with that patient,and where appropriate and necessary the patient’s guardian or carer.It is also the health professional’s responsibility to verify the rules and regulations applicable to drugs and devices at the time of prescription.&The European Society of Cardiology 2009.All rights reserved.For permissions please email:journals.permissions@.European Heart Journaldoi:10.1093/eurheartj/ehp285Table of ContentsA.Preamble (3)B.Justification/scope of the problem (4)C.Epidemiology (4)A changing epidemiology (4)Incidence of infective endocarditis (5)Types of infective endocarditis (5)Microbiology (5)D.Pathophysiology (6)E.Preventive measures (7)Evidence justifying the use of antibiotic prophylaxis forinfective endocarditis in previous ESC recommendations..7 Reasons justifying revision of previous ESC Guidelines (7)Principles of the new ESC Guidelines (8)Limitations and consequences of the new ESC Guidelines.10 F.Diagnosis (10)Clinical features (10)Echocardiography (11)Microbiological diagnosis (12)Diagnostic criteria and their limitations (14)G.Prognostic assessment at admission (15)H.Antimicrobial therapy:principles and methods (15)General principles (15)Penicillin-susceptible oral streptococci and group Dstreptococci (16)Penicillin-resistant oral streptococci and group Dstreptococci (16)Streptococcus pneumoniae,b-haemolytic streptococci(groupsA,B,C,and G) (16)Nutritionally variant streptococci (16)Staphylococcus aureus and coagulase-negative staphylococci.18 Methicillin-resistant and vancomycin-resistant staphylococci19 Enterococcus spp (19)Gram-negative bacteria (19)Blood culture-negative infective endocarditis (19)Fungi (20)Empirical therapy (20)Outpatient parenteral antibiotic therapy for infectiveendocarditis (21)plications and indications for surgery in left-sided native valve infective endocarditis (23)Part1.Indications and optimal timing of surgery (23)Heart failure (23)Uncontrolled infection (24)Prevention of systemic embolism (25)Part2.Principles,methods,and immediate results of surgery (26)Pre-and peri-operative management (26)Surgical approach and techniques (26)Operative mortality,morbidity,and post-operativecomplications (26)J.Other complications of infective endocarditis............27Part2.Other complications(infectious aneurysms,acute renal failure,rheumatic complications,splenic abscess,myocarditis, pericarditis).. (28)K.Outcome after discharge and long-term prognosis (29)Recurrences:relapses and reinfections (29)Heart failure and need for valvular surgery (30)Long-term mortality (30)Follow-up (30)L.Specific situations (30)Part1.Prosthetic valve endocarditis (30)Part2.Infective endocarditis on pacemakers and implantabledefibrillators (32)Part3.Right-sided infective endocarditis (33)Part4.Infective endocarditis in congenital heart disease (35)Part5.Infective endocarditis in the elderly (36)Part6.Infective endocarditis during pregnancy (36)M.References (36)Abbreviations and acronymsBCNIE blood culture-negative infective endocarditisCD cardiac deviceCDRIE cardiac device-related infective endocarditisCHD congenital heart diseaseCNS coagulase-negative staphylococciCT computed tomographyELISA enzyme-linked immunosorbent assayHF heart failureIA infectious aneurysmICD implantable cardioverter defibrillatorICE International Collaboration on EndocarditisIE infective endocarditisIVDA intravenous drug abuserLDI local device infectionMBC minimal bactericidal concentrationMIC minimal inhibitory concentrationMRI magnetic resonance imagingMRSA methicillin-resistant Staphylococcus aureusMSSA methicillin-susceptible Staphylococcus aureusNBTE non-bacterial thrombotic endocarditisNVE native valve endocarditisOPAT outpatient parenteral antibiotic therapyPBP plasma-binding proteinPCR polymerase chain reactionPET positron emission tomographyPMP platelet microbicidal proteinPPM permanent pacemakerPVE prosthetic valve endocarditisTEE transoesophagal echocardiographyTTE transthoracic echocardiographyESC GuidelinesPage2of45Guidelines and Expert Consensus Documents summarize and evaluate all currently available evidence on a particular issue with the aim of assisting physicians in selecting the best management strategy for an individual patient suffering from a given condition, taking into account the impact on outcome,as well as the risk/ benefit ratio of particular diagnostic or therapeutic means.Guide-lines are no substitutes for textbooks.The legal implications of medical guidelines have been discussed previously.A great number of Guidelines and Expert Consensus Docu-ments have been issued in recent years by the European Society of Cardiology(ESC)as well as by other societies and organizations. Because of the impact on clinical practice,quality criteria for devel-opment of guidelines have been established in order to make all decisions transparent to the user.The recommendations for for-mulating and issuing ESC Guidelines and Expert Consensus Docu-ments can be found on the ESC website(/ knowledge/guidelines/rules).In brief,experts in thefield are selected and undertake a com-prehensive review of the published evidence for management and/ or prevention of a given condition.A critical evaluation of diagnos-tic and therapeutic procedures is performed including assessment of the risk/benefit ratio.Estimates of expected health outcomes for larger societies are included,where data exist.The level of evi-dence and the strength of recommendation of particular treatment options are weighed and graded according to predefined scales,as outlined in Tables1and2.The experts of the writing panels have provided disclosure statements of all relationships they may have which might be per-ceived as real or potential sources of conflicts of interest.These disclosure forms are kept onfile at the European Heart House, headquarters of the ESC.Any changes in conflict of interest that Task Force report received its entirefinancial support from the ESC and was developed without any involvement of the pharma-ceutical,device,or surgical industry.The ESC Committee for Practice Guidelines(CPG)supervises and coordinates the preparation of new Guidelines and Expert Consensus Documents produced by Task Forces,expert groups, or consensus panels.The Committee is also responsible for the endorsement process of these Guidelines and Expert Consensus Documents or statements.Once the document has beenfinalized and approved by all the experts involved in the Task Force,it is sub-mitted to outside specialists for review.The document is revised,and finally approved by the CPG and subsequently published.After publication,dissemination of the message is of paramount importance.Pocket-sized versions and personal digital assistant (PDA)-downloadable versions are useful at the point of care. Some surveys have shown that the intended users are sometimes unaware of the existence of guidelines,or simply do not translate them into practice.Thus,implementation programmes for new guidelines form an important component of knowledge dissemina-tion.Meetings are organized by the ESC,and directed towards its member National Societies and key opinion leaders in Europe. Implementation meetings can also be undertaken at national levels,once the guidelines have been endorsed by the ESC member societies,and translated into the national language. Implementation programmes are needed because it has been shown that the outcome of disease may be favourably influenced by the thorough application of clinical recommendations. Thus,the task of writing Guidelines or Expert Consensus docu-ments covers not only the integration of the most recent research, but also the creation of educational tools and implementation programmes for the recommendations.The loop between clinical research,writing of guidelines,and implementing them into clinicalTable1Classes of recommendationspractice can then only be completed if surveys and registries are performed to verify that real-life daily practice is in keeping with what is recommended in the guidelines.Such surveys and registries also make it possible to evaluate the impact of implementation of the guidelines on patient outcomes.Guidelines and recommen-dations should help the physicians to make decisions in their daily practice,However,the ultimate judgement regarding the care of an individual patient must be made by the physician in charge of his/her care.B.Justification/scope of the problemInfective endocarditis (IE)is a peculiar disease for at least three reasons:First,neither the incidence nor the mortality of the disease have decreased in the past 30years.1Despite major advances in both diagnostic and therapeutic procedures,this disease still carries a poor prognosis and a high mortality.Secondly,IE is not a uniform disease,but presents in a variety of different forms,varying according to the initial clinical manifestation,the underlying cardiac disease (if any),the microorganism involved,the presence or absence of complications,and underlying patient characteristics.For this reason,IE requires a collaborative approach,involving primary care physicians,cardiologists,surgeons,microbiol-ogists,infectious disease specialists,and frequently others,including neurologists,neurosurgeons,radiologists,and pathologists.2Thirdly,guidelines are often based on expert opinion because of the low incidence of the disease,the absence of randomized trials,and the limited number of meta-analyses.3,4Several reasons justify the decision of the ESC to update the pre-vious guidelines published in 2004.3IE is clearly an evolving disease,with changes in its microbiological profile,a higher incidence of health care-associated cases,elderly patients,and patients with intra-cardiac devices or prostheses.Conversely,cases related to rheu-matic disease have become less frequent in industrialized nations.In addition,several new national and international guidelines or state-of-the-art papers have been published in recent years.3–13Unfortunately,their conclusions are not uniform,particularly in the field of prophylaxis,where conflicting recommendations have been formulated.3,4,6,8–13Clearly,an objective for the next few years will be an attempt to harmonize these recommendations.The main objective of the current Task Force was to provide clear and simple recommendations,assisting health care providersin clinical decision making.These recommendations were obtained by expert consensus after thorough review of the available litera-ture.An evidence-based scoring system was used,based on a classification of the strength of recommendation and the levels of evidence.C.EpidemiologyA changing epidemiologyThe epidemiological profile of IE has changed substantially over the last few years,especially in industrialized nations.1Once a disease affecting young adults with previously well-identified (mostly rheu-matic)valve disease,IE is now affecting older patients who more often develop IE as the result of health care-associated procedures,either in patients with no previously known valve disease 14or in patients with prosthetic valves.15A recent systematic review of 15population-based investi-gations accounting for 2371IE cases from seven developed countries (Denmark,France,Italy,The Netherlands,Sweden,the UK,and the USA)showed an increasing incidence of IE associated with a prosthetic valve,an increase in cases with underlying mitral valve prolapse,and a decrease in those with underlying rheumatic heart disease.16Newer predisposing factors have emerged—valve prostheses,degenerative valve sclerosis,intravenous drug abuse—associated with increased use of invasive procedures at risk for bacteraemia,resulting in health care-associated IE.17In a pooled analysis of 3784episodes of IE,it was shown that oral streptococci had fallen into second place to staphylococci as the leading cause of IE.1However,this apparent temporal shift from predominantly streptococcal to predominantly staphylococcal IE may be partly due to recruit-ment/referral bias in specialized centres,since this trend is not evident in population-based epidemiological surveys of IE.18In developing countries,classical patterns persist.In Tunisia,for instance,most cases of IE develop in patients with rheumatic valve disease,streptococci predominate,and up to 50%may be associated with negative blood cultures.19In other African countries,the persistence of a high burden of rheumatic fever,rheumatic valvular heart diseases,and IE has also been highlighted.20In addition,significant geographical variations have been shown.The highest increase in the rate of staphylococcal IE has been reported in the USA,21where chronic haemodialysis,diabetes mellitus,and intravascular devices are the three main factorsTable 2Levels of evidenceESC GuidelinesPage 4of 45associated with the development of Staphylococcus aureus endocar-ditis.21,22In other countries,the main predisposing factor for S.aureus IE may be intravenous drug abuse.23Incidence of infective endocarditisThe incidence of IE ranges from one country to another within 3–10episodes/100000person-years.14,24–26This may reflect methodological differences between surveys rather than true vari-ation.Of note,in these surveys,the incidence of IE was very low in young patients but increased dramatically with age—the peak inci-dence was14.5episodes/100000person-years in patients between70and80years of age.In all epidemiological studies of IE,the male:female ratio is!2:1,although this higher proportion of men is poorly understood.Furthermore,female patients may have a worse prognosis and undergo valve surgery less frequently than their male counterparts.27Types of infective endocarditisIE should be regarded as a set of clinical situations which are some-times very different from each other.In an attempt to avoid overlap,the following four categories of IE must be separated, according to the site of infection and the presence or absence of intracardiac foreign material:left-sided native valve IE,left-sided prosthetic valve IE,right-sided IE,and device-related IE(the latter including IE developing on pacemaker or defibrillator wires with or without associated valve involvement)(Table3).With regard to acquisition,the following situations can be identified: community-acquired IE,health care-associated IE(nosocomial and non-nosocomial),and IE in intravenous drug abusers(IVDAs). MicrobiologyAccording to microbiologicalfindings,the following categories are proposed:1.Infective endocarditis with positive blood cultures This is the most important category,representing 85%of all IE. Causative microorganisms are most often staphylococci,strepto-cocci,and enterococci.28a.Infective endocarditis due to streptococci and enterococciOral(formerly viridans)streptococci form a mixed group of microorganisms,which includes species such as S.sanguis,S.mitis, S.salivarius,S.mutans,and Gemella morbillorum.Microorganisms of this group are almost always susceptible to penicillin G.Members of the‘leri’or‘S.anginosus’group(S.anginosus, S.intermedius,and S.constellatus)must be distinguished since theyTable3Classification and definitions of infective endocarditisESC Guidelines Page5of45to penicillin[minimal bactericidal concentration(MBC)much higher than the mimimal inhibitory concentration(MIC)]. Group D streptococci form the‘Streptococcus bovis/Streptococcus equinus’complex,including commensal species of the human intestinal tract,and were until recently gathered under the name of Streptococcus bovis.They are usually sensitive to penicillin G,like oral streptococci.Among enterococci, E.faecalis, E.faecium,and to a lesser extent E.durans,are the three species that cause IE.b.Staphylococcal infective endocarditisTraditionally,native valve staphylococcal IE is due to S.aureus, which is most often susceptible to oxacillin,at least in community-acquired IE.In contrast,staphylococcal prosthetic valve IE is more frequently due to coagulase-negative staphylococci (CNS)with oxacillin resistance.However,in a recent study of 1779cases of IE collected prospectively in16countries,S.aureus was the most frequent cause not only of IE but also of prosthetic valve IE.22Conversely,CNS can also cause native valve IE,29–31 especially S.lugdunensis,which frequently has an aggressive clinical course.2.Infective endocarditis with negative blood cultures because of prior antibiotic treatmentThis situation arises in patients who received antibiotics for unexplained fever before any blood cultures were performed and in whom the diagnosis of IE was not considered;usually the diagnosis is eventually considered in the face of relapsing febrile episodes following antibiotic discontinuation.Blood cul-tures may remain negative for many days after antibiotic discon-tinuation,and causative organisms are most often oral streptococci or CNS.3.Infective endocarditis frequently associated with negative blood culturesThey are usually due to fastidious organisms such as nutritionally variant streptococci,fastidious Gram-negative bacilli of the HACEK group(Haemophilus parainfluenzae,H.aphrophilus, H.paraphrophilus,H.influenzae,Actinobacillus actinomycetemcomi-tans,Cardiobacterium hominis,Eikenella corrodens,Kingella kingae, and K.denitrificans),Brucella,and fungi.4.Infective endocarditis associated with constantly negative blood culturesThey are caused by intracellular bacteria such as Coxiella burnetii, Bartonella,Chlamydia,and,as recently demonstrated,Tropheryma whipplei,the agent of Whipple’s disease.32Overall,these account for up to5%of all IE.Diagnosis in such cases relies on serological testing,cell culture or gene amplification.infection by circulating bacteria.However,mechanical disruption of the endothelium results in exposure of underlying extracellular matrix proteins,the production of tissue factor,and the deposition offibrin and platelets as a normal healing process.Such non-bacterial thrombotic endocarditis(NBTE)facilitates bacterial adherence and infection.Endothelial damage may result from mechanical lesions provoked by turbulent bloodflow,electrodes or catheters,inflammation,as in rheumatic carditis,or degenerative changes in elderly individuals,which are associated with inflam-mation,microulcers,and microthrombi.Degenerative valve lesions are detected by echocardiography in up to50%of asymp-tomatic patients over60years,33and in a similar proportion of elderly patients with IE.This might account for the increased risk of IE in the elderly.Endothelial inflammation without valve lesions may also promote IE.Local inflammation triggers endothelial cells to express integrins of the b1family(very late antigen).Integrins are transmembrane proteins that can connect extracellular deter-minants to the cellular cytoskeleton.Integrins of the b1family bind circulatingfibronectin to the endothelial surface while S.aureus and some other IE pathogens carryfibronectin-binding proteins on their surface.Hence,when activated endothelial cells bindfibro-nectin they provide an adhesive surface to circulating staphylo-cocci.Once adherent,S.aureus trigger their active internalization into valve endothelial cells,where they can either persist and escape host defences and antibiotics,or multiply and spread to distant organs.34Thus,there are at least two scenarios for primary valve infection:one involving a physically damaged endo-thelium,favouring infection by most types of organism,and one occurring on physically undamaged endothelium,promoting IE due to S.aureus and other potential intracellular pathogens. Transient bacteraemiaThe role of bacteraemia has been studied in animals with catheter-induced NBTE.Both the magnitude of bacteraemia and the ability of the pathogen to attach to damaged valves are important.35Of note,bacteraemia does not occur only after invasive procedures, but also as a consequence of chewing and tooth brushing.Such spontaneous bacteraemia is of low grade and short duration[1–100colony-forming units(cfu)/ml of blood for,10min],but its high incidence may explain why most cases of IE are unrelated to invasive procedures.26,36Microbial pathogens and host defences Classical IE pathogens(S.aureus,Streptococcus spp.,and Enterococ-cus spp.)share the ability to adhere to damaged valves,trigger local procoagulant activity,and nurture infected vegetations in which they can survive.37They are equipped with numerous surface determinants that mediate adherence to host matrix mol-ecules present on damaged valves(e.g.fibrinogen,fibronectin, platelet proteins)and trigger platelet activation.Following coloni-zation,adherent bacteria must escape host defences.Gram-be the target of platelet microbicidal proteins(PMPs),which are produced by activated platelets and kill microbes by disturbing their plasma membrane.Bacteria recovered from patients with IE are consistently resistant to PMP-induced killing,whereas similar bacteria recovered from patients with other types of infection are susceptible.38Thus,escaping PMP-induced killing is a typical characteristic of IE-causing pathogens.E.Preventive measuresEvidence justifying the use of antibiotic prophylaxis for infective endocarditis in previous ESC recommendationsThe principle of prophylaxis for IE was developed on the basis of observational studies in the early20th century.39The basic hypoth-esis is based on the assumption that bacteraemia subsequent to medical procedures can cause IE,particularly in patients with pre-disposing factors,and that prophylactic antibiotics can prevent IE in these patients by minimizing or preventing bacteraemia,or by altering bacterial properties leading to reduced bacterial adherence on the endothelial surface.The recommendations for prophylaxis are based in part on the results of animal studies showing that anti-biotics could prevent the development of experimental IE after inoculation of bacteria.40Reasons justifying revision of previous ESC GuidelinesWithin these guidelines,the Task Force aimed to avoid extensive, non-evidence-based use of antibiotics for all at-risk patients under-going interventional procedures,but to limit prophylaxis to the highest risk patients.The main reasons justifying the revision of previous recommendations are the following:1.Incidence of bacteraemia after dental procedures and during daily routine activitiesThe reported incidence of transient bacteraemia after dental pro-cedures is highly variable and ranges from10to100%.41This may be a result of different analytical methods and sampling pro-cedures,and these results should be interpreted with caution. The incidence after other types of medical procedures is even less well established.In contrast,transient bacteraemia is reported to occur frequently in the context of daily routine activities such as tooth brushing,flossing,or chewing.42,43It therefore appears plaus-ible that a large proportion of IE-causing bacteraemia may derive from these daily routine activities.In addition,in patients with poor dental health,bacteraemia can be observed independently of dental procedures,and rates of post-procedural bacteraemia are higher in this group.Thesefindings emphasize the importance of good oral hygiene and regular dental review to prevent IE.44 2.Risks and benefits of prophylaxisThe following considerations are critical with respect to the assumption that antibiotic prophylaxis can efficiently prevent IE in patients who are at increased lifetime risk of the disease:extent to which a patient may benefit from antibiotic prophy-laxis for distinct procedures.A better parameter,the procedure-related risk,ranges from1:14000000for dental procedures in the average population to1:95000in patients with previous IE.45,46These estimations demonstrate the huge number of patients that will require treatment to prevent one single case of IE.(b)In the majority of patients,no potential index procedure pre-ceding thefirst clinical appearance of IE can be identified.26 Even if effectiveness and compliance are assumed to approxi-mate100%,this observation leads to two conclusions:(i)IE prophylaxis can at best only protect a small proportion of patients;47and(ii)the bacteraemia that causes IE in the majority of patients appears to derive from another source.(c)Antibiotic administration carries a small risk of anaphylaxis.However,no case of fatal anaphylaxis has been reported in the literature after oral amoxicillin administration for prophy-laxis of IE.48(d)Widespread and often inappropriate use of antibiotics mayresult in the emergence of resistant microorganisms.However,the extent to which antiobiotic use for IE prophy-laxis could be implicated in the general problem of resistance is unknown.44ck of scientific evidence for the efficacy of infective endocarditis prophylaxisStudies reporting on the efficacy of antibiotic prophylaxis to prevent or alter bacteraemia in humans after dental procedures are contradictory,49,50and so far there are no data demonstrating that reduced duration or frequency of bacteraemia after any medical procedure leads to a reduced procedure-related risk of IE. Similarly,no sufficient evidence exists from case–control studies36,51,52to support the necessity of IE prophylaxis.Even strict adherence to generally accepted recommendations for pro-phylaxis might have little impact on the total number of patients with IE in the community.52Finally,the concept of antibiotic prophylaxis efficacy itself has never been investigated in a prospective randomized controlled trial,53and assumptions on efficacy are based on non-uniform expert opinion,data from animal experiments,case reports, studies on isolated aspects of the hypothesis,and contradictory observational studies.Recent guideline committees of national cardiovascular societies have re-evaluated the existing scientific evidence in thisfield.6,9–11 Although the individual recommendations of these committees differ in some aspects,they did uniformly and independently draw four conclusions:(1)The existing evidence does not support the extensive use ofantibiotic prophylaxis recommended in previous guidelines.(2)Prophylaxis should be limited to the highest risk patients(patients with the highest incidence of IE and/or highest risk of adverse outcome from IE).(3)The indications for antibiotic prophylaxis for IE should bereduced in comparison with previous recommendations.。
2023ESC心内膜炎指南解读PPT课件
不同类型心内膜炎治疗策略差异
急性感染性心内膜炎
非感染性心内膜炎
早期、足量、联合使用抗生素，控制 感染；对于瓣膜穿孔、破裂等并发症 ，及时手术治疗。
针对原发病进行治疗，如系统性红斑 狼疮、类风湿性关节炎等；对于瓣膜 病变严重者，可考虑手术治疗。
亚急性感染性心内膜炎
针对病原菌选用敏感抗生素，疗程较 长；对于瓣膜赘生物较大、影响心脏 功能者，考虑手术治疗。
04
并发症预防与处理措施
常见并发症类型及危险因素
心力衰竭
由于心内膜炎导致心肌受损，心 脏泵血功能下降，表现为乏力、 呼吸困难等症状。危险因素包括 感染严重程度、病原体毒力等。
心律失常
心内膜炎可能导致心肌电生理异常 ，引发心律失常，如房颤、室性心 动过速等。危险因素包括心肌受损 程度、电解质紊乱等。
指南制定目的与意义
01
提高诊断水平
通过提供最新的诊断标准和方法 ，帮助医生更准确、及时地诊断 心内膜炎。
02
03
规范治疗流程
改善预后
为医生提供心内膜炎治疗的推荐 方案，确保患者接受到最恰当的 治疗。
通过遵循ESC指南，有望降低心 内膜炎患者的死亡率、复发率等 不良预后。
02
诊断方法与标准
临床诊断依据
心脏功能监测
密切监测患者心脏功能，及时发现心力衰竭、心律失常等并发症迹象 ，采取相应治疗措施。
并发症处理方案及效果评估
01
心力衰竭处理
给予利尿剂、ACEI/ARB等药物改善心脏功能，必要时使用正性肌力药
物如多巴胺、米力农等。效果评估可通过观察患者症状改善情况、心脏
超声等指标进行。
02
心律失常处理
根据心律失常类型选择相应药物治疗，如β受体阻滞剂、胺碘酮等。对
《2023 ESC心内膜炎管理指南》解读 PPT课件
抗感染治疗策略调整
根据病原体类型和严重程度，制定个体化抗感染治疗方案，提高 治疗效果。
免疫治疗策略引入
针对免疫相关心内膜炎，引入免疫抑制剂和生物制剂治疗，降低复 发率。
手术时机选择
对于复杂性心内膜炎，提倡早期手术干预，降低并发症发生率和死 亡率。
预防措施优化方向
加强口腔卫生
定期口腔检查和治疗，降低 口腔感染导致心内膜炎的风 险。
临床诊断
01
02
03
病史询问
详细了解患者的病史，包 括感症状、心脏疾病史 、手术史等。
体格检查
注意患者的心脏杂音、心 脏扩大等体征，评估心功 能状况。
临床症状
关注患者是否出现发热、 乏力、贫血等全身症状， 以及心脏相关表现。
影像学诊断
超声心动图
检测心脏结构和功能，评估瓣膜受损程度和赘生物形 成情况。
优化医疗器械使用
严格无菌操作，减少医源性 感染风险。
提高公众认知
加强心内膜炎防治知识宣传 ，提高公众对心内膜炎的认 知和重视程度。
06
总结与展望
心内膜炎管理现状总结
诊断方法进步
随着诊断技术的不断发展，心内膜炎的诊断准确率得到提高。目前，超声心动图、血培养和分子生物学检测等方法在 心内膜炎的诊断中发挥着重要作用。
解读目的与结构
解读目的
通过对《2023 ESC心内膜炎管理指 南》的解读，帮助临床医生更好地理 解和掌握心内膜炎的管理理念和方法 ，提高患者的诊断和治疗水平。
解读结构
本解读将按照指南的章节顺序进行， 重点关注诊断、治疗、预防和康复等 方面的内容，同时结合最新的研究进 展和临床实践进行阐述。
02
诊断方法与标准
CT和MRI
ESC感染性心内膜炎预防诊断治疗指南2009版.
ESC GUIDELINESGuidelines on the prevention, diagnosis, and treatment of infective endocarditis (newversion 2009The Task Force on the Prevention, Diagnosis, and Treatment of Infective Endocarditis of the European Society of Cardiology (ESCEndorsed by the European Society of Clinical Microbiology and Infectious Diseases (ESCMIDand by the International Society of Chemotherapy (ISCfor Infection and CancerAuthors/TaskForce Members:Gilbert Habib (Chairperson(France*, Bruno Hoen (France,Pilar Tornos (Spain,Franck Thuny (France,Bernard Prendergast (UK,Isidre Vilacosta (Spain,Philippe Moreillon (Switzerland,Manuel de Jesus Antunes (Portugal,Ulf Thilen (Sweden,John Lekakis (Greece,Maria Lengyel (Hungary,Ludwig Mu¨ller (Austria,Christoph K. Naber (Germany,Petros Nihoyannopoulos (UK,Anton Moritz (Germany,Jose Luis Zamorano (SpainESC Committee for Practice Guidelines (CPG:Alec Vahanian(Chairperson(France,Angelo Auricchio(Switzerland,Jeroen Bax (TheNetherlands, Claudio Ceconi (Italy,Veronica Dean (France,Gerasimos Filippatos (Greece,Christian Funck-Brentano (France,Richard Hobbs (UK,Peter Kearney (Ireland,Theresa McDonagh (UK,Keith McGregor (France,Bogdan A. Popescu (Romania,Zeljko Reiner (Croatia,Udo Sechtem (Germany,Per Anton Sirnes (Norway,Michal Tendera (Poland,Panos Vardas (Greece,Petr Widimsky (CzechRepublic Document Reviewers:Alec Vahanian (CPGReview Coordinator (France,Rio Aguilar (Spain,Maria Grazia Bongiorni (Italy,Michael Borger (Germany,Eric Butchart (UK,Nicolas Danchin (France,Francois Delahaye (France,Raimund Erbel (Germany,Damian Franzen (Germany,Kate Gould (UK,Roger Hall(UK,Christian Hassager (Denmark,Keld Kjeldsen (Denmark,Richard McManus (UK,Jose´M. Miro ´(Spain,Ales Mokracek (CzechRepublic, Raphael Rosenhek (Austria,Jose´A. San Roma ´n Calvar (Spain,Petar Seferovic (Serbia,Christine Selton-Suty (France,Miguel Sousa Uva (Portugal,Rita Trinchero (Italy,Guy van Camp (BelgiumThe disclosure forms of the authors and reviewers are available on the ESC website/guidelines*Corresponding author. Gilbert Habib, Service de Cardiologie, CHU La Timone, Bd Jean Moulin, 13005Marseille, France. Tel:þ33491386379, Email:gilbert.habib@free.frThe content of these European Society of Cardiology (ESCGuidelines has been published for personal and educational use only. No commercial use is authorized. No part of the ESC Guidelines may be translated or reproduced in any form without written permission from the ESC. Permission can be obtained upon submission of a writtenrequest to Oxford University Press, the publisher of the European Heart Journal and the party authorized to handle such permissions on behalf of the ESC.Disclaimer. The ESC Guidelines represent the views of the ESC and were arrived at after careful consideration of the available evidence at the time they were written. Health professionals are encouraged to take them fully into account when exercising their clinical judgement. The guidelines do not, however, override the individual responsibility of health professionals to make appropriate decisions in the circumstances of the individual patients, in consultation with that patient, and where appropriate and necessary the patient’s guardian or carer. It is also the health professional’s responsibility to verify the rules and regulations applicable to drugs and devices at the time of prescription.&The European Society of Cardiology 2009. All rights reserved. For permissions please email:journals.permissions@.European Heart Journaldoi:10.1093/eurheartj/ehp285Table of ContentsA. Preamble . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3B. Justification/scopeof the problem . . . . . . . . . . . . . . . . . . . 4C. Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4 A changing epidemiology . . . . . . . . . . . . . . . . . . . . . . . 4 Incidence of infectiveendocarditis . . . . . . . . . . . . . . . . . 5 Types of infectiveendocarditis . . . . . . . . . . . . . . . . . . . 5Microbiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5D. Pathophysiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6E. Preventive measures . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7 Evidence justifying the use of antibiotic prophylaxis forinfective endocarditis in previous ESC recommendations . . 7 Reasons justifying revision of previous ESC Guidelines . . . 7 Principles of the new ESCGuidelines. . . . . . . . . . . . . . . 8 Limitations and consequences of the new ESC Guidelines . 10 F. Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10 Clinical features . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10Echocardiography . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11 Microbiologicaldiagnosis . . . . . . . . . . . . . . . . . . . . . . . 12 Diagnostic criteria and theirlimitations. . . . . . . . . . . . . . 14G. Prognostic assessment at admission . . . . . . . . . . . . . . . . . 15H. Antimicrobial therapy:principles and methods . . . . . . . . . . 15 General principles . . . . . . . . . . . . . . . . . . . . . . . . . . . 15 Penicillin-susceptible oral streptococci and group Dstreptococci . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16 Penicillin-resistant oral streptococci and group Dstreptococci . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16 Streptococcus pneumoniae , b -haemolytic streptococci (groups A, B, C, and G . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16 Nutritionally variant streptococci . . . . . . . . . . . . . . . . . 16 Staphylococcus aureus and coagulase-negative staphylococci . 18 Methicillin-resistant and vancomycin-resistant staphylococci 19 Enterococcus spp. . . . . . . . . . . . . . . . . . . . . . . . . . . . . 19 Gram-negative bacteria . . . . . . . . . . . . . . . . . . . . . . . . 19 Blood culture-negative infective endocarditis . . . . . . . . . . 19 Fungi . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 20 Empirical therapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . 20 Outpatient parenteral antibiotic therapy for infectiveendocarditis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21 I. Complications and indications for surgery in left-sided native valve infectiveendocarditis. . . . . . . . . . . . . . . . . . . . . . . . . . 23 Part 1. Indications and optimal timing of surgery . . . . . . . . . . . 23 Heart failure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23 Uncontrolled infection . . . . . . . . . . . . . . . . . . . . . . . . 24 Prevention of systemic embolism. . . . . . . . . . . . . . . . . . 25 Part 2. Principles, methods, and immediate results of surgery. . . 26 Pre-and peri-operative management . . . . . . . . . . . . . . . 26 Surgical approach and techniques . . . . . . . . . . . . . . . . . 26 Operative mortality, morbidity, and post-operativecomplications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26 J. Other complications of infective endocarditis . . . . . . . . . . . . 27 Part 2. Other complications (infectiousaneurysms, acute renal failure, rheumatic complications, splenic abscess, myocarditis,pericarditis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 28 K. Outcome after discharge and long-term prognosis . . . . . . . . 29 Recurrences:relapses andreinfections . . . . . . . . . . . . . . 29 Heart failure and need for valvular surgery . . . . . . . . . . .30 Long-term mortality . . . . . . . . . . . . . . . . . . . . . . . . . . 30 Follow-up . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30 L. Specificsituations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30 Part 1. Prosthetic valveendocarditis . . . . . . . . . . . . . . . . . . . 30 Part 2. Infective endocarditis on pacemakers and implantabledefibrillators . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 32 Part 3. Right-sided infective endocarditis . . . . . . . . . . . . . . . . 33 Part 4. Infective endocarditis in congenital heart disease . . . . . . 35 Part 5. Infective endocarditis in the elderly . . . . . . . . . . . . . . . 36 Part 6. Infective endocarditis during pregnancy . . . . . . . . . . . . 36 M.References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 36Abbreviations and acronyms BCNIE blood culture-negative infective endocarditisCD cardiac deviceCDRIE cardiac device-related infective endocarditis CHD congenital heart diseaseCNS coagulase-negative staphylococciCT computed tomographyELISA enzyme-linked immunosorbent assayHF heart failureIA infectious aneurysmICD implantable cardioverter defibrillatorICE International Collaboration on EndocarditisIE infective endocarditisIVDA intravenous drug abuserLDI local device infectionMBC minimal bactericidal concentrationMIC minimal inhibitory concentrationMRI magnetic resonance imagingMRSA methicillin-resistant Staphylococcus aureus MSSA methicillin-susceptible Staphylococcus aureus NBTE non-bacterial thrombotic endocarditisNVE native valve endocarditisOPAT outpatient parenteral antibiotic therapyPBP plasma-binding proteinPCR polymerase chain reactionPET positron emission tomographyPMP platelet microbicidal proteinPPM permanent pacemakerPVE prosthetic valve endocarditisTEE transoesophagal echocardiographyTTE transthoracic echocardiographyESC GuidelinesPage 2of 45Guidelines and Expert Consensus Documents summarize and evaluate all currently available evidence on a particular issue with the aim of assisting physicians in selecting the best management strategy for an individual patient suffering from a given condition, taking into account the impact on outcome, as well as the risk/ benefit ratio of particulardiagnostic or therapeutic means. Guide-lines are no substitutes for textbooks. The legal implications of medical guidelines have been discussed previously.A great number of Guidelines and Expert Consensus Docu-ments have been issued in recent years by the European Society of Cardiology (ESCas well as by other societies and organizations. Because of the impact on clinical practice, quality criteria for devel-opment of guidelines have been established in order to make all decisions transparent to the user. The recommendations for for-mulating and issuing ESC Guidelines and Expert Consensus Docu-ments can be found on the ESC website (/ knowledge/guidelines/rules.In brief, experts in the field are selected and undertake a com-prehensive review of the published evidence for management and/ or prevention of a given condition. A critical evaluation of diagnos-tic and therapeutic procedures is performed including assessment of the risk/benefit ratio. Estimates of expected health outcomes for larger societies are included, where data exist. The level of evi-dence and the strength of recommendation of particular treatment options are weighed and graded according to predefined scales, as outlined in Tables 1and 2.The experts of the writing panels have provided disclosure statements of all relationships they may have which might be per-ceived as real or potential sources ofconflicts of interest. These disclosure forms are kept on file at the European Heart House, headquarters of the ESC. Any changes in conflict of interest that Task Force report received its entire financial suppor t from the ESC and was developed without any involvement of the pharma-ceutical, device, or surgical industry.The ESC Committee for Practice Guidelines (CPGsupervises and coordinates the preparation of new Guidelines and Expert Consensus Documents produced by Task Forces, expert groups, or consensus panels. The Committee is also responsible for the endorsement process of these Guidelines and Expert Consensus Documents or statements.Once the document has been finalized and approved by all the experts involv ed in the Task Force, it is sub-mitted to outside specialists for review. The document is revised, and finally approved by the CPG and subsequently published.After publication, dissemination of the message is of paramount importance. Pocket-sized versions and personal digital assistant (PDA-downloadableversions are useful at the point of care. Some surveys have shown that the intended users are sometimes unaware of the existence of guidelines, or simply do not translate them into practice. Thus, implementation programmes for new guidelines form an important component of knowledge dissemina-tion. Meetings are organized by the ESC, and directed towards its member National Societies and key opinion leaders in Europe. Implementation meetings can also be undertaken at national levels, once the guidelines have been endorsed by the ESC member societies, and translated into the national language. Implementation programmes are needed because it has been shown that the outcome of disease may be favourably influenced by the thorough application of clinical recommendations.Thus, the task of writing Guidelines or Expert Consensus docu-ments covers not only the integration of the most recent research, but also the creation of educational tools and implementation programmes for the recommendations. The loop between clinical research, writing of guidelines, and implementing them into clinicalTable 1Classes of recommendationspractice can then only be completed if surveys and registries are performed to verify that real-life daily practice is in keeping with what is recommended in the guidelines. Such surveys and registries also make it possible to evaluate the impact of implementation of the guidelines on patient outcomes. Guidelines and recommen-dations should help the physicians to make decisions in their daily practice, However, the ultimate judgement regarding the care of an individual patient must be made by the physician in charge of his/hercare.B. Justification/scopeof the problemInfective endocarditis (IEis a peculiar disease for at least three reasons:First, neither the incidence nor the mortality of the disease have decreased in the past 30years. 1Despite major advances in both diagnostic and therapeutic procedures, this disease still carries a poor prognosis and a high mortality.Secondly, IE is not a uniform disease, but presents in a variety of different forms, varying according to the initial clinical manifestation, the underlying cardiac disease (ifany, the microorganism involved, the presence or absence of complications, and underlying patient characteristics. For this reason, IE requires a collaborative approach, involving primary care physicians, cardiologists, surgeons, microbiol-ogists, infectious disease specialists, and frequently others, including neurologists, neurosurgeons, radiologists, and pathologists. 2Thirdly, guidelines are often based on expert opinion because of the low incidence of the disease, the absence of randomized trials, and the limited number of meta-analyses. 3,4Several reasons justify the decision of the ESC to update the pre-vious guidelines published in 2004. 3IE is clearly an evolving disease, with changes in its microbiological profile, a higher incidence of health care-associated cases, elderly patients, and patients with intra-cardiac devices or prostheses. Conversely, cases related to rheu-matic disease have become less frequent in industrialized nations. In addition, several new national and international guidelines or state-of-the-art papers have been published in recent years. 3–13Unfortunately, their conclusions are not uniform, particularly in the field of prophylaxis, where conflicting recommendations have been formulated. 3,4,6,8–13Clearly, an objective for the next few years will be an attempt to harmonize these recommendations. The main objective of the current Task Force was to provide clear and simple recommendations, assisting health care providersin clinical decision making. These recommendations were obtained by expert consensus after thorough review of the available litera-ture. An evidence-based scoring system was used, based on a classification of the strength of recommendation and the levels of evidence.C. EpidemiologyA changing epidemiologyThe epidemiological profile of IE has changed substantially over the la st few years, especially in industrialized nations. 1Once a disease affecting young adults with previously well-identified (mostlyrheu-matic valve disease, IE is now affecting older patients who more often develop IE as the result of health care-associated procedures, either in patients with no previously known valve disease 14or in patients with prosthetic valves. 15A recent systematic review of 15population-based investi-gations accounting for 2371IE cases from seven developed countries (Denmark,France, Italy, The Netherlands, Sweden, the UK, and the USA showed an increasing incidence of IE associated with a prosthetic valve, an increase in cases with underlying mitral valve prolapse, and a decrease in those with underlying rheumatic heart disease. 16Newer predisposing factors have emerged—valve prostheses, degenerative valve sclerosis, intravenous drug abuse—associated with increased use of invasive procedures at risk for bacteraemia, resulting in health care-associated IE. 17In a pooled analysis of 3784episodes of IE, it was shown that oral streptococci had fallen into second place to staphylococci as the leading cause of IE. 1However, this apparent temporal shift from predominantly streptococcal to predominantly staphylococcal IE may be partly due to recruit-ment/referralbias in specialized centres, since this trend is not evident in population-based epidemiological surveys of IE. 18In developing countries, classical patterns persist. In Tunisia, for instance, most cases of IE develop in patients with rheumatic valve disease, streptococci predominate, and up to 50%may be associated with negative blood cultures. 19In other African countries, the persistence of a high burden of rheumatic fever, rheumatic valvular heart diseases, and IE has also been highlighted. 20In addition, significant geographical variations have been shown. The highest increase in the rate of staphylococcal IE has been reported in the USA, 21where chronic haemodialysis, diabetes mellitus, and intravascular devices are the three main factorsTable 2Levels of evidenceESC GuidelinesPage 4of 45associated with the development of Staphylococcus aureus endocar-ditis. 21,22In other countries, the main predisposing factor for S. aureus IE may be intravenous drug abuse. 23Incidence of infective endocarditisThe incidence of IE ranges from one country to another within 3–10episodes/100000person-years. 14,24–26This may reflect methodological differences between surveys rather than true vari-ation. Of note, in these surveys, the incidence of IE was very low in young patients but increased dramatically with age—the peak inci-dence was 14.5episodes/100000person-years in patients between 70and 80years of age. In all epidemiological studies of IE, the male:femaleratio is ! 2:1,although this higher proportion of men is poorly understood. Furthermore, female patients may have a worse prognosis and undergo valve surgery less frequently than their male counterparts. 27Types of infective endocarditisIE should be regarded as a set of clinical situations which are some-times very different from each other. In an attempt to avoid overlap, the following four categories of IE must be separated, according to the site of infection and the presence or absence of intracardiac foreign material:left-sided native valve IE, left-sided prosthetic valve IE, right-sided IE, and device-related IE (the latter including IE developing on pacemaker or defibrillator wires with or without associated valve involvement (Table 3. With regard to acquisition, the following situations can be identified: community-acquired IE, health care-associated IE (nosocomial and non-nosocomial, and IE in intravenous drug abusers (IVDAs. MicrobiologyAccording to microbiological findings, the following categories are proposed:1. Infective endocarditis with positive blood cultures This is the most important category, representing 85%of all IE. Causative microorganisms are most often staphylococci, strepto-cocci, and enterococci. 28a. Infective endocarditis due to streptococci and enterococciOral (formerlyviridans streptococci form a mixed group of microorganisms, which includes species such as S. sanguis , S. mitis , S. salivarius , S. mutans , and Gemella morbillorum. Microorganisms of this group are almost always susceptible to penicillin G. Members of the ‘ S. milleri ’ or ‘ S. anginosus ’ group (S. anginosus , S. intermedius , and S. constellatus must be distinguished since theyTable 3Classification and definitions of infective endocarditisESC Guidelines Page 5of 45tend to form abscesses and cause haematogenously disseminated infection,often requiring a longer duration of antibiotic treat-ment.Likewise,nutritionallyvariant‘defective’streptococci, recently reclassified into other species(Abiotrophia and Granulica-tella,should also be distinguished since they are often tolerant topenicillin[minimal bactericidal concentration(MBCmuch higher than the mimimal inhibitory concentration(MIC]. Group D streptococci form the‘Streptococcusbovis/Streptococcus equinus’complex,including commensal species of t he human intestinal tract,and were until recently gathered under the name of Streptococcus bovis.They are usually sensitive to penicillin G,like oral streptococci.Among enterococci, E.faecalis, E.faecium,and to a lesser extent E.durans,are the three species that cause IE.b.Staphylococcal infective endocarditisTraditionally,native valve staphylococcal IE is due to S.aureus, which is most often susceptible to oxacillin,at least in community-acquired IE.In contrast,staphylococcal prosthetic valve IE is more frequently due to coagulase-negative staphylococci (CNSwithoxacillin resistance.However,in a recent study of 1779cases of IE collected prospectively in16countries,S.aureus was the most frequent cause not only of IE but also of prosthetic valve IE.22Conversely,CNS can also cause native valve IE,29–31 especiallyS.lugdunensis,which frequently has an aggressive clinical course.2.Infective endocarditis with negative blood cultures because of prior antibiotic treatmentThis situation arises in patients who received antibiotics for unexplained fever before any blood cultures were performed and in whom the diagnosis of IE was not considered;usually the diagnosis is eventually considered in the face of relapsing febrile episodes following antibiotic discontinuation.Blood cul-tures may remain negative for many days after antibiotic discon-tinuation,and causative organisms are most often oral streptococci or CNS.3.Infective endocarditis frequently associated with negative blood culturesThey are usually due to fastidious organisms such as nutritionally variant streptococci,fastidious Gram-negative bacilli of the HACEK group(Haemophilus parainfluenzae,H.aphrophilus, H.paraphrophilus,H.influenzae,Actinobacillus actinomycetemcomi-tans,Cardiobacterium hominis,Eikenella corrodens,Kingella kingae, and K.denitrificans,Brucella,and fungi.4.Infective endocarditis associated with constantly negative blood culturesThey are caused by intracellular bacteria such as Coxiella burnetii,Bartonella,Chlamydia,and,as recently demonstrated,Tropheryma whipplei,the agent of Whipple’s disease.32Overall,these account for up to5%of all IE.Diagnosis in such cases relies on serological testing,cell culture or gene amplification.D.PathophysiologyThe valve endotheliumThe normal valve endothelium is resistant to colonization and infection by circulating bacteria.However,mechanical disruption of the endothelium results in exposure of underlying extracellular matrix proteins,the production of tissue factor,and the deposition offibrin and platelets as a normal healing process.Such non-bacterial thrombotic endocarditis(NBTEfacilitates bacterial adherence and infection.Endothelial damage may result from mechanical lesions provoked by turbulent bloodflow,electrodes or catheters,inflammation,as in rheumatic ca rditis,or degenerative changes in elderly individuals,which are associated with inflam-mation,microulcers,andmicrothrombi.Degenerative valve lesions are detected by echocardiography in upto50%of asymp-tomatic patients over60years,33and in a similar proportion of elderly patients with IE.This might account for the increased risk of IE in the elderly.Endothelial inflammation without valve lesions may also promote IE.Localinflammation triggers endothelial cells to express integrins of the b1family(very late antigen.Integrins are transmembrane proteins that can connect extracellular deter-minants to the cellular cytoskeleton.Integrins of the b1family bind circulatingfibronectin to the endothelial surface while S.aureus and some other IE pathogens carryfibronectin-binding proteins on their surface.Hence,when activated endothelial cells bindfibro-nectin they provide an adhesive surface to circulating staphylo-cocci.Once adherent,S.aureus trigger their active internalization into valve endothelial cells,where they can either persist and escape host defences and antibiotics,or multiply and spread to distantorgans.34Thus,there are at least two scenarios for primary valve infection:one involving a physically damaged endo-thelium,favouring infection by most types of organism,and one occurring on physically undamaged endothelium,promoting IE due to S.aureus and other potential intracellular pathogens. Transient bacteraemiaThe role of bacteraemia has been studied in animals with catheter-induced NBTE.Both the magnitude of bacteraemia and the ability of the pathogen to attach to damaged valves are important.35Of note,bacteraemia does not occur only after invasiveprocedures, but also as a consequence of chewing and tooth brushing.Such spontaneous bacteraemia is of low grade and short duration[1–100colony-forming units(cfu/ml of blood for,10min],but its high incidence may explain why most cases of IE are unrelated to invasive procedures.26,36Microbial pathogens and host defences Classical IEpathogens(S.aureus,Streptococcus spp.,and Enterococ-cus spp.share the ability to adhere to damaged valves,trigger local procoagulant activity,and nurture infected vegetations in which they can survive.37They are equipped with numerous surface determinants that mediate adherence to host matrix mol-ecules present on damagedvalves(e.g.fibrinogen,fibronectin, platelet proteinsand trigger plateletactivation.Following coloni-zation,adherent bacteria must escape host defences.Gram-positive bacteria are resistant to complement.However,they may be the target of platelet microbicidal proteins(PMPs,which are produced by activated platelets and kill microbes by disturbing their plasma membrane.Bacteria recovered from patients with IE are consistently resistant to PMP-induced killing,whereas similar bacteria recovered from patients with other types of infection are susceptible.38Thus,escaping PMP-induced killing is a typical characteristic of IE-causing pathogens.E.Preventive measuresEvidence justifying the use of antibiotic prophylaxis for infective endocarditis in previous ESC recommendationsThe principle of prophylaxis for IE was developed on the basis of observational studies in the early20th century.39The basic hypoth-esis is based on the assumption that bacteraemia subsequent to medical procedures can cause IE,particularly in patients with pre-disposing factors,and that prophylactic antibiotics can prevent IE in these patients by minimizing or preventing bacteraemia,or by altering bacterial properties leading to reduced bacterial adherence on the endothelial surface.The recommendations for。
2015年ESC感染性心内膜炎管理指南
2015年ESC感染性心内膜炎管理指南--五大要点∣单位：心在线作者：常三帅刘屹发布时间：2015-09-11时间：9月2日，伦敦当地时间9点地点：Excel London，2015年欧洲心脏病学会（ESC）"ESC clinical practice gui delines 2015-highlight"专场事件：最新发布临床指南亮点评析2015年ESC感染性心内膜炎（IE）管理指南是对2009年欧洲临床微生物学和传染病学会（ESCMID）、国际感染与肿瘤化疗学会（ISC）共同发布的IE防治指南的再版更新。
新指南更新内容包括心内膜炎团队管理、多模态成像、新诊断流程、抗生素预防性应用，并强调了三个"早期"（早诊断、早治疗、早手术）。
在2015年ESC年会上，该指南的主要评审者、来自英国的Petros Nihoyannopoul os教授对新版指南进行了精彩解析。
要点一抗生素预防性应用IE的预防治疗一直存在争议，目前仍未出现有说服力的新证据。
1. 指南推荐只在IE高危患者中预防性使用抗生素，包括以下几类患者：①置入人工瓣膜或使用人工材料修补心脏瓣膜者②有IE病史者③先天性心脏病患者--紫绀型先心病--通过外科手术或经皮介入技术行假体置入的先心病患者。
对于这类患者，预防性抗生素可用至术后6个月。
如果存在残余漏或瓣膜反流，则需要终生使用抗生素（Ⅱa/C）。
2. 指南不推荐对其他类型瓣膜疾病或先心病患者预防性使用抗生素。
3. 患者不能自行开始应用抗生素。
4. 指南强调了保持口腔卫生对于预防IE的重要性。
要点二心内膜炎团队指南强调，IE不是一个孤立的疾病，而是涉及多种微生物、多器官受累、存在多种症状和表现的疾病，因此需要多学科专家团队协作，包括心脏科、外科、感染科、神经科、风湿科和影像科医生及微生物学家。
对于复杂IE患者（如伴有心衰、脓肿、栓塞或神经系统并发症或先天性心脏病），可考虑及早转诊至可施行外科手术的中心（Ⅱa/B）。
感染性心内膜炎指南医学PPT
抗菌治疗
达托霉素
环脂肽类抗生素，万古霉素之后第二代糖肽类抗生素 作用机制：
通过扰乱细胞膜对氨基酸的转运，从而阻碍细菌细胞壁肽聚糖的生物合成，改变细胞 质膜的性质
通过破坏细菌的细胞膜，使其内容物外泄而达到杀菌的目的
细菌对达托霉素产生耐药性可能会比较困难
抗菌治疗：达托vs万古
抗菌谱
杀菌作用
3. 心脏或血管手术：早期(1年）人工瓣膜感染最常见病原微生物 为凝固酶阴性葡萄球菌和金葡菌。预防性治疗应该在术前立即 开始，如果术程延长，应重复应用至术后 48 小时停止
4. 不建议高危患者及天然瓣膜疾病患者进行纹身或穿刺。即使进 行这些操作，也应在严格无菌条件下实施，但不建议预防性应 用抗菌药物
IE检查还应包括诸如
多层螺旋CT，MRI， 18F- 氟脱氧葡萄糖 （FDG）正电子发射 断层扫描（PET/计算 机断层扫描（CT或其 他成像技术
18F-FDG PET/CT 在 IE 诊断中有前景，可以用 于监测抗微生物治疗的 反应
Bruun NE, Habib G, Thuny F, Sogaard P. Cardiac imaging in infectious endocarditis. Eur Heart J 2014;35:624–632.
诊断
诊断
4. 微生物诊断
血培养阳性IE 血培养阴性IE
5. IE组织学诊断
病理检查切除的瓣膜组织或栓塞碎片仍然是 IE 诊 断的金标准
手术切除的心脏瓣膜样本必须收集在无菌容器中，不 添加固定剂或培养基。整个样本应在微生物学实验室 进行最佳恢复并鉴定微生物种类
诊断
确诊
• 符合2条主要标准 • 符合1条主要标准
3. 推荐使用达托霉素和磷霉素用于治疗葡萄球菌感染性心内膜炎，使用奈 替米星治疗PG敏感的口腔链球菌和消化链球菌，若当具备达托霉素用药指 征时，给药时必须采用高剂量方案（每天1次，药量≥10 mg/kg），同时联 合第2种抗菌药物用药以增加抗菌活性、避免出现耐药性
2019ESC感染性心内膜炎指南-PPT文档资料
5%
6%
11%
18%
病原菌学变化
葡萄球菌位居首
位,链球菌已退至第 二位,其次为肠球菌
ICE=International Collaboration on Endocarditis; CoNS=coagulase-negative staphylococci. Fowler VG Jr, Miro JM, Hoen B, et al. Staphylococcus aureus endocarditis: a consequence of medical progress. JAMA. 2019;293:3012-3021.
2:1 男女比例
女性患
者预后差､接受瓣膜置换术的 概率相对小
•死亡率居高不下，仍高
达16-25%
•合并心力衰竭、脓肿形 成、栓塞或细菌性动脉 瘤破裂早期病死率4075%，晚期为20-25%
IE流行病学
感染性心内膜炎的微生物分布 ： G+ 占80%以上
8% 10%
11%
31%
金黄色葡萄球菌 凝固酶阴性葡萄球菌 草绿色链球菌 牛链球菌 其他链球菌 肠球菌 其他 培养阴性
感染性心内膜炎的管理
—2019 ESC IE管理指南
徐莹莹 南昌大学第二附属医院 心内科
IE 定义
感染性心内膜炎(IE)
是病原微生物经血行途 径直接侵袭心内膜、心 瓣膜或邻近大动脉内膜 而引起的炎症性疾病， 常伴赘生物形成
•受损的心瓣膜内膜上可形成非 细菌性血栓性心内膜炎
•瓣膜内皮损伤处聚集的血小板 形成赘生物
➢ 根据当前指南和标准的治疗流程，选择抗菌药物治疗的 类型、疗程及随访方式
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• 强调早诊断、早期应用抗菌药物及早期萄球菌性心内膜炎给出新的抗菌药物治疗方案。
2015 ESC IE管理指南
1
预防
IE团队
2
3
诊断
预后评价
4
5
抗菌治疗原则方法
合并症处理
6
7
特殊IE管理
IE预防 基础心脏 病
强调口腔、牙齿和皮 肤卫生，防止继发感 染 避免有创医疗检查和 操作，严格无菌操作
IE预防
抗菌药物的选择
2. 非口腔的侵入操作仅在感染区域进行时需应用抗菌药物治疗 3. 心脏或血管手术：早期(1年）人工瓣膜感染最常见病原微生物 为凝固酶阴性葡萄球菌和金葡菌。预防性治疗应该在术前立即 开始，如果术程延长，应重复应用至术后 48 小时停止 4. 不建议高危患者及天然瓣膜疾病患者进行纹身或穿刺。即使进 行这些操作，也应在严格无菌条件下实施，但不建议预防性应 用抗菌药物 5. 医源性感染性心内膜炎约占所有 IE 病例的 30%
IE流行病学
感染性心内膜炎的微生物分布 ： G+ 占80%以 上
8% 10% 31% 11% 金黄色葡萄球菌 凝固酶阴性葡萄球菌
草绿色链球菌
牛链球菌 其他链球菌 肠球菌 其他 培养阴性
5% 6% 11%
18%
病原菌学变化 葡萄球菌位居首 位,链球菌已退至第 二位,其次为肠球菌
ICE=International Collaboration on Endocarditis; CoNS=coagulase-negative staphylococci. Fowler VG Jr, Miro JM, Hoen B, et al. Staphylococcus aureus endocarditis: a consequence of medical progress. JAMA. 2005;293:3012-3021.
必要条件
高危人群
菌血症
高危人群预防性应用 抗生素
7
IE预防
IE预防
1、口腔操作过程中预防性应用抗菌药物主要针对口腔内的链球菌属
抗菌药物的选择
– 推荐术前 30-60 分钟应用阿莫西林或氨苄西林，成人 2 g / 儿童 50 mg/kg 口服或静滴 – 头孢唑啉或头孢曲松，成人 1 g / 儿童 50 mg/kg 静滴 – 头孢氨苄，成人 2 g/ 儿童 50 mg/kg i.v – 过敏者选用克林霉素，成人 600 mg/ 儿童 20 mg/kg 口服或静滴 – 不推荐应用喹诺酮类抗菌药物和氨基糖苷类抗菌药物
• • • • • •
千差万别，复杂多样 90％ 的发热病人伴寒战、食欲不振、体重减轻的全身性 症状 85％ 的患者存在心脏杂音 25％ 的患者诊断时合并有栓塞 存在发热和栓塞的任何患者均应考虑 IE 的可能 老年人或免疫功能低下患者其症状常不典型。这部分患者 和其他高危人群（CHD或人工瓣膜）应高度怀疑，以排 除 IE 或避免延误诊断
IE流行病学
•年发病率约3-10/10万人 •风湿性瓣膜病比例下降 •人工瓣膜、老年退形性变、经 静脉吸毒、无器质性心脏病患 者上升 •发病年龄有增加趋势 •医源性获得性IE更为常见 •因脑梗塞、急性左心衰死亡者 增加
男女比例
女性患 者预后差､接受瓣膜置换术的 概率相对小
2:1
•死亡率居高不下，仍高 达16-25% •合并心力衰竭、脓肿形 成、栓塞或细菌性动脉 瘤破裂早期病死率4075%，晚期为20-25%
心内膜炎团队
3. 心内膜炎团队的任务
• •
应定期进行病例讨论、术前讨论，并制定相应随访计划 根据当前指南和标准的治疗流程，选择抗菌药物治疗的 类型、疗程及随访方式 参加国际国内学术交流，公布中心的发病情况及死亡情 况，并参与医疗质量改进及患者教育 定期进行门诊随访
•
•
心内膜炎团队
诊断
1. 临床特点
2015 ESC IE管理指南
Eur Heart J. 2015 Aug 29
2015 ESC IE管理指南
highlight
• 强调了多模态成像技术在诊断心内膜炎中的重要作用。 • 首次推荐建设包含多学科团队（心内科医生、心脏外科医生、感染科 医生等）的转诊中心用于IE的管理。 • 对特定情况下 IE 管理的更新，包括 ICU 中、IE 合并癌症及消耗性（ 非细菌性）IE患者的诊疗建议等情况的管理。
• 无菌原则
IE预防
建议
心血管术前应用抗菌药物推荐意见 推荐心脏手术前筛查鼻部金黄色葡萄球菌携带者并加以治疗 推荐在起搏器及可植入除颤仪置入术的围手术期内预防性应 用抗菌药物 除非急诊手术，否则应在人工瓣膜或其他心脏血管内外源性 材料植入术前至少 2 周将潜在的感染灶清除 对于拟行外科手术或经导管置入人工瓣膜、血管内移植物及 其他外源性材料的患者，应在其围手术期预防性应用抗菌药 物 I I IIa IIa A B C C 推荐 证据 级别 水平
•
心内膜炎团队
2. 治疗中心的要求
•
可为患者随时进行检查，TTE、TOE、CT、MRI、核素显 像 可在患者的疾病早期随时进行心脏外科手术，尤其是复杂 性 IE 患者
•
•
治疗中心拥有多学科的专家，至少包括心内、心外、麻醉 、感染及微生物领域专家，如有可能，还应包括瓣膜疾病 、先天性心脏病、起搏器、超声心动图、神经科专家以及 神经外科手术及介入设备
IE 定义
感染性心内膜炎(IE)
是病原微生物经血行途 径直接侵袭心内膜、心 瓣膜或邻近大动脉内膜 而引起的炎症性疾病， 常伴赘生物形成
•受损的心瓣膜内膜上可形成非 细菌性血栓性心内膜炎 •瓣膜内皮损伤处聚集的血小板 形成赘生物 •菌血症时血液中的细菌黏附于 赘生物并在其中繁殖 •病原菌与瓣膜基质分子蛋白及 血小板相互作用
不推荐对未筛查金黄色葡萄球菌的患者进行系统性治疗或局 部治疗
III
C
心内膜炎团队
ESC 专家组强烈建议组建专业化团队在治疗中心对 IE 患 者进行治疗
1. 需要心内膜炎团队处理的患者类型
•
复杂性 IE 患者，如心内膜炎伴有心力衰竭、脓肿、栓塞 、神经系统并发症或先天性心脏病 非复杂性 IE 患者虽未在治疗中心进行初始治疗，但其与 治疗中心有定期沟通并经心内膜炎团队会诊，如有需要可 转入治疗中心