ESC感染性心内膜炎预防诊断治疗指南2009版.

ESC感染性心内膜炎预防诊断治疗指南2009版.
ESC感染性心内膜炎预防诊断治疗指南2009版.

ESC GUIDELINES

Guidelines on the prevention, diagnosis, and treatment of infective endocarditis (newversion 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 (ESCMIDand by the International Society of Chemotherapy (ISCfor Infection and Cancer

Authors/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 (Spain

ESC 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 (Belgium

The disclosure forms of the authors and reviewers are available on the ESC website

https://www.360docs.net/doc/d78604757.html,/guidelines

*Corresponding author. Gilbert Habib, Service de Cardiologie, CHU La Timone, Bd Jean Moulin, 13005Marseille, France. Tel:t33491386379, Email:gilbert.habib@free.fr

The 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 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@https://www.360docs.net/doc/d78604757.html,.

European Heart Journal

doi:10.1093/eurheartj/ehp285

Table of Contents

A. Preamble . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3

B. Justi?cation/scopeof 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 for

infective 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 D

streptococci . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16 Penicillin-resistant oral streptococci and group D

streptococci . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 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 infective

endocarditis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21 I. Complications and indications for surgery in left-sided native valve infective

endocarditis. . . . . . . . . . . . . . . . . . . . . . . . . . 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-operative

complications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 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 and

reinfections . . . . . . . . . . . . . . 29 Heart failure and need for valvular surgery . . . . . . . . . . .

30 Long-term mortality . . . . . . . . . . . . . . . . . . . . . . . . . . 30 Follow-

up . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30 L. Speci?c

situations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30 Part 1. Prosthetic valve

endocarditis . . . . . . . . . . . . . . . . . . . 30 Part 2. Infective endocarditis on pacemakers and implantable

de?brillators . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 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 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 36

Abbreviations and acronyms BCNIE blood culture-negative infective endocarditis

CD cardiac device

CDRIE cardiac device-related infective endocarditis CHD congenital heart disease

CNS coagulase-negative staphylococci

CT computed tomography

ELISA enzyme-linked immunosorbent assay

HF heart failure

IA infectious aneurysm

ICD implantable cardioverter de?brillator

ICE International Collaboration on Endocarditis

IE infective endocarditis

IVDA intravenous drug abuser

LDI local device infection

MBC minimal bactericidal concentration

MIC minimal inhibitory concentration

MRI magnetic resonance imaging

MRSA methicillin-resistant Staphylococcus aureus MSSA methicillin-susceptible Staphylococcus aureus NBTE non-bacterial thrombotic endocarditis

NVE native valve endocarditis

OPAT outpatient parenteral antibiotic therapy

PBP plasma-binding protein

PCR polymerase chain reaction

PET positron emission tomography

PMP platelet microbicidal protein

PPM permanent pacemaker

PVE prosthetic valve endocarditis

TEE transoesophagal echocardiography

TTE transthoracic echocardiography

ESC Guidelines

Page 2of 45

Guidelines 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/ bene?t 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 (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 (https://www.360docs.net/doc/d78604757.html,/ knowledge/guidelines/rules.

In brief, experts in the ?eld 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/bene?t 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 prede?ned 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 of

con?icts of interest. These disclosure forms are kept on ?le at the European Heart House, headquarters of the ESC. Any changes in con?ict of interest that Task Force report received its entire ?nancial 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 ?nalized 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 ?nally 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 in?uenced 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 clinical

Table 1Classes of recommendations

practice 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. Justi?cation/scopeof the problem

Infective 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. 2

Thirdly, 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. 3,4

Several 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 pro?le, 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 ?eld of prophylaxis, where con?icting 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 providers

in 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 classi?cation of the strength of recommendation and the levels of evidence.

C. Epidemiology

A changing epidemiology

The epidemiological pro?le of IE has changed substantially over the la st few years, especially in industrialized nations. 1Once a disease affecting young adults with previously well-identi?ed (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. 15

A 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. 16

Newer 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. 20

In addition, signi?cant 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 factors

Table 2Levels of evidence

ESC Guidelines

Page 4of 45

associated 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. 23

Incidence of infective endocarditis

The incidence of IE ranges from one country to another within 3–

10episodes/100000person-years. 14,24–26This may re?ect 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. 27

Types of infective endocarditis

IE 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 de?brillator wires with or without associated valve involvement (Table 3. With regard to acquisition, the following situations can be identi?ed: community-acquired IE, health care-associated IE (nosocomial and non-nosocomial, and IE in intravenous drug abusers (IVDAs. Microbiology

According to microbiological ?ndings, 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. 28

a. Infective endocarditis due to streptococci and enterococci

Oral (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 they

Table 3Classi?cation and de?nitions of infective endocarditis

ESC Guidelines Page 5of 45

tend to form abscesses and cause haematogenously disseminated infection,often requiring a longer duration of antibiotic treat-ment.Likewise,nutritionally

variant‘defective’streptococci, recently reclassi?ed into other species(Abiotrophia and Granulica-tella,should also be distinguished since they are often tolerant to

penicillin[minimal bactericidal concentration(MBCmuch higher than the mimimal inhibitory concentration(MIC]. Group D streptococci form the‘Streptococcus

bovis/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 endocarditis

Traditionally,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 (CNSwith

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 treatment

This 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 cultures

They are usually due to fastidious organisms such as nutritionally variant streptococci,fastidious Gram-negative bacilli of the HACEK group(Haemophilus parain?uenzae,H.aphrophilus, H.paraphrophilus,H.in?uenzae,Actinobacillus actinomycetemcomi-tans,Cardiobacterium hominis,Eikenella corrodens,Kingella kingae, and K.denitri?cans,Brucella,and fungi.

4.Infective endocarditis associated with constantly negative blood cultures

They 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 ampli?cation.D.Pathophysiology

The valve endothelium

The 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 of?brin 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 blood?ow,electrodes or catheters,in?ammation,as in rheumatic ca rditis,or degenerative changes in elderly individuals,which are associated with in?am-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 in?ammation without valve lesions may also promote IE.Local

in?ammation 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 circulating?bronectin to the endothelial surface while S.aureus and some other IE pathogens carry?bronectin-binding proteins on their surface.Hence,when activated endothelial cells bind?bro-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 bacteraemia

The 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.26,36

Microbial 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.?brinogen,?bronectin, platelet proteinsand trigger platelet

activation.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 measures

Evidence justifying the use of antibiotic prophylaxis for infective endocarditis in previous ESC recommendations

The 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.40

Reasons justifying revision of previous ESC Guidelines

Within 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 activities

The 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,?ossing,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.These?ndings emphasize the importance of good oral hygiene and regular denta l review to prevent IE.44 2.Risks and bene?ts of prophylaxis

The following considerations are critical with respect to the assumption that antibiotic prophylaxis can ef?ciently prevent IE in patients who are at increased lifetime risk of the disease:(aIncreased lifetime risk of IE is not an ideal measure of the

extent to which a patient may bene?t 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.

(bIn the majority of patients,no potential index procedure pre-

ceding the?rst clinical appearance of IE can be identi?ed.26 Even if effectiveness and compliance are assumed to approxi-mate100%,this observation leads to two conclusions:(iIE prophylaxis can at best only protect a small proportion of

patients;47and(iithe bacteraemia that causes IE in the majority of patients appears to derive from another source.

(cAntibiotic 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

(dWidespread and often inappropriate use of antibiotics may

result 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.44

https://www.360docs.net/doc/d78604757.html,ck of scienti?c evidence for the ef?cacy of infective endocarditis prophylaxis

Studies reporting on the ef?cacy 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 suf?cient 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.52

感染性心内膜炎优秀教案

解放军105医院临床学院 教案 (2011/2012学年第二学期) 系(部) 临床医学 课程名称感染性心内膜炎

任课班级2009级 教师姓名何传飞 解放军临床学院教案首页 授课时间:2012年5月教案完成时间:2012年05月 授课名称感染性心 内膜炎 2009级临床医学授课时间2012.5 学时 2 授课教师何传飞专业技术职 务 主治医师教案班学生数60 教案目的及任务 掌握感染性心内膜炎的临床表现、诊断方法、标准和治疗原则及方法;熟悉该病的病理过程和相关并发症;了解其病因和发病机理。 教案内容、步骤及时间分配: l.简述什么是心内膜炎(5分钟) 2.了解心内膜炎的病因病理病生(20分钟) 3.掌握心内膜炎的症状与体征及并发症(30分钟) 4.了解心内膜炎的实验室检查(25分钟) 5.掌握心内膜炎的诊断及治疗(30分钟)

单元重点心内膜炎的症状与体征,诊断与治疗原则。 本单元难点心内膜炎的病因、病理、病生。 教案方法及准备 讲述、启发相结合。了解学生已学课程,收集整理教案素材(图片、动画),制作PPT教案课件。 所用教材《内科学》第7版陆再英等主编,人民卫生出版社。 参考资料1.实用内科学第十一版人民卫生出版社 2.心脏病学第二版人民卫生出版社 3 感染性心内膜炎诊治进展中国医刊 研室审阅意见 (教案续页) 基本内容注解(进展、辅助 手段和时间分配) 感染性心内膜炎 Infective Endocarditis 【定义】—感染性心内膜炎为心脏表面的微生物感染,伴赘生物 形成。 赘生物特点:大小不等、形状不一的血小板和纤维素团,内 含大量微生物和少量炎性细胞。 受累部位:最常累及瓣膜,也可发生在间隔缺损部位、腱索 或心壁内膜。 病程分类——急性心内膜炎 亚急性心内膜炎 【特征】 急性感染性心内膜炎中毒症状明显,病程进展迅速,数天至数周,, 引起瓣膜损害,感染迁移多见,病原菌主要为金黄色葡萄球菌 亚急性感染性心内膜炎病原体以草绿色链球菌多见,其次为肠球 菌,中毒症状轻,病程数周至数月,感染迁移少见 【分类】 自体瓣膜心内膜炎 人工瓣膜心内膜炎 静脉药瘾者心内膜炎 第一节自体瓣膜心内膜炎 【病因】

感染性心内膜炎

模块二 任务7 感染性心内膜炎病人的护理 【案例】 王先生,48岁,心脏杂音病史20年,发热6周住院。查体:睑结膜见瘀点,心尖部闻及双期杂音。超声心动图检查示二尖瓣增厚、回声增强,二尖瓣狭窄并关闭不全,二尖瓣叶可见赘生物。化验类风湿因子(+),白细胞计数10×109/L。 初步诊断:亚急性感染性心内膜炎 思考: 1.该患者为进一步明确诊断应检查什么 2.在检查过程中要注意哪些 【职业综合能力培养目标】 1.专业职业能力:具备正确采集血培养操作的能力、对高热患者进行物理降温的能力。 2.专业理论知识:掌握感染性心内膜炎病因、临床表现、治疗原则及护理措施。 3.职业核心能力:具备对感染性心内膜炎患者病情评估的能力,具备对合并栓塞患者抢救配合能力、在护理过程中进行有效沟通的能力;具备为感染性心内膜患者制定健康指导方案的能力。 【新课讲解】 走进讲堂:(视频) 一、概念 感染性心内膜炎是心脏内膜表面的微生物感染,伴赘生物形成。赘生物为大小不等、形状不一的血小板和纤维团块,内含大量微生物和少量炎性细胞。赘生物最常见的附着部位是二尖瓣和主动脉瓣. 根据病情和病程,分为急性和亚急性。急性感染性心内膜炎特点是:①中毒症状明显; ②病程进展迅速,数天或数周引起瓣膜损害;③病原体主要为金黄色葡菌球菌。亚急性感染性心内膜炎特点是:①中毒症状轻②病程长,可数周至数月③病原体以草绿色链球菌多见。根据瓣膜类型可分为自体瓣膜心内膜炎、人瓣膜心内膜炎和静脉药引者心内膜炎。(图片) 二、病因 感染性心内膜炎主要发生于器质性心脏病的基础上,以心脏瓣膜病为主,其次为先天性心脏病。急性感染性心内膜炎致病菌以金黄色葡萄球菌最常见,亚急性感染性心内膜炎以草绿色链球菌最常见,其他病原微生物有肠球菌、其他葡萄球菌、溶血性链球菌、大肠埃希菌、真菌及立克次体等。 致病微生物可因上呼吸道感染、咽峡炎、扁桃体炎及扁桃体切除术、拔牙、流产、导尿、泌尿道器械检查及心脏手术等途径侵入血流,静脉药瘾者,通过静脉将皮肤致病微生物带入血流而感染心内膜。正常情况下,自不同途径进入血液循环中的致病微生物可被机体的防御

内科学(第七版)循环系统疾病第九章 感染性心内膜炎

第九章感染性心内膜炎 感染性心内膜炎(infective endocarditis,IE)为心脏内膜表面的微生物感染,伴赘生物形成。赘生物为大小不等、形状不一的血小板和纤维素团块,内含大量微生物和少量炎症细胞。瓣膜为最常受累部位,但感染也可发生在间隔缺损部位、腱索或心壁内膜。而动静脉瘘、动脉瘘(如动脉导管未闭)或主动脉缩窄处的感染虽属动脉内膜炎,但临床与病理均类似于感染性心内膜炎。根据病程分为急性和亚急性,急性感染性心内膜炎特征:①中毒症状明显;②病程进展迅速,数天至数周引起瓣膜破坏;③感染迁移多见;④病原体主要为金黄色葡萄球菌。亚急性感染性心内膜炎特征:①中毒症状轻;②病程数周至数月;③感染迁移少见;④病原体以草绿色链球菌多见,其次为肠球菌。感染性心内膜炎又可分为自体瓣膜、人工瓣膜和静脉药瘾者的心内膜炎。 第一节自体瓣膜心内膜炎【病因】 链球菌和葡萄球菌分别占自体瓣膜心内膜炎(native valve endocarditis)病原微生物的65%和25%。急性者,主要由金黄色葡萄球菌引起,少数由肺炎球菌、淋球菌、A族链球菌和流感杆菌等所致。亚急性者,草绿色链球菌最常见,其次为D族链球菌(牛链球菌和肠球菌),表皮葡萄球菌,其他细菌较少见。真菌、立克次体和衣原体为自体瓣膜心内膜炎的少见致病微生物。 【发病机制】 (一)亚急性 至少占据2/3的病例,发病与以下因素有关: 1.血流动力学因素亚急性者主要发生于器质性心脏病,首先为心脏瓣膜病,尤其是二尖瓣和主动脉瓣;其次为先天性心血管病,如室间隔缺损、动脉导管未闭、法洛四联症和主动脉缩窄。赘生物常位于血流从高压腔经病变瓣口

或先天缺损至低压腔产生高速射流和湍流的下游,如二尖瓣关闭不全的瓣叶心房面、主动脉瓣关闭不全的瓣叶心室面和室间隔缺损的间隔右心室侧,可能与这些处于湍流下部位的压力下降内膜灌注减少,有利于微生物沉积和生长有关。高速射流冲击心脏或大血管内膜处可致局部损伤,如二尖瓣反流面对的左心房壁、主动脉反流面对的二尖瓣前叶有关腱索和乳头肌,未闭动脉导管射流面对的肺动脉壁的内皮损伤,并易于感染。本病在压差小的部位,如房间隔缺损和大室间隔缺损或血流缓慢时,如心房颤动和心力衰竭时少见,瓣膜狭窄时较关闭不全少见。 约3/4的感染性心内膜炎患者有基础心脏病。随着风湿性心脏病发病率的下降,风湿性瓣膜病的心内膜炎发生率也随之下降。由于超声心动图诊断技术的普遍应用,主动脉瓣二叶瓣畸形、二尖瓣脱垂和老年性退行性瓣膜病的诊断率提高,以及风湿性瓣膜病心内膜炎发病率的下降,近年来,非风湿性瓣膜病的心内膜炎发病率有所升高。 2.非细菌性血栓性心内膜炎实验研究证实,当内膜的内皮受损暴露其下结缔组织的胶原纤维时,血小板在该处聚集,形成血小板微血栓和纤维蛋白沉着,成为结节样无菌性赘生物,称非细菌性血栓性心内膜炎,是细菌定居瓣膜表面的重要因素。无菌性赘生物偶见于正常瓣膜,但最常见于湍流区、瘢痕处(如感染性心内膜炎后)和心外因素所致内膜受损区。 3.短暂性菌血症各种感染或细菌寄居的皮肤黏膜的创伤(如手术、器械操作等)常导致暂时』生菌血症;口腔组织创伤常致草绿色链球菌菌血症;消化道和泌尿生殖道创伤和感染常引起肠球菌和革兰阴性杆菌菌血症;葡萄球菌菌血症见于皮肤和远离心脏部位的感染。循环中的细菌如定居在无菌性赘生物上,感染性心内膜炎即可发生。 4.细菌感染无菌性赘生物:此取决于①发生菌血症之频度和循环中细菌的

感染性心内膜炎诊断标准

感染性心内膜炎诊断标 准 Company Document number:WUUT-WUUY-WBBGB-BWYTT-1982GT

感染性心内膜炎诊断标准除了感染本身的症状,IE的临床表现还与下列因素有关:(1)心内感染导致的局部结构破坏;(2)感染性赘生物碎片远处栓塞导致梗死与感染;(3)持续性菌血症导致感染血源性播散;(4)病原体及其损伤组织诱导的免疫反应。 临床栓塞发生率为11%~43%,多半为卒中,而尸解病理学证实的栓塞发生率为45%~65%。静脉毒品相关的三尖瓣IE肺栓塞通常为脓毒性的,发生率为66%~75%。金黄色葡萄球菌、溶血性链球菌或其他毒力较强的化脓性细菌性IE,往往并发迁徙性感染,导致局部症状体征和持续发热。迁徙性感染影响抗生素的选择,例如并非脑膜炎时,应选择能进入脑脊液的抗生素。 影像学,特别死超声心动图,在IE的诊断和治疗中起重要作用。它还对IE患者有预后评估价值,应用于治疗期间的随访,外科术中及术后。首先必须做TTE,但在大多是怀疑和确诊IE的患者都应最终完成TTE和TEE。三种超声心动图结果被认作诊断IE 的主要标准,包括赘生物、脓肿以及人工瓣膜新的裂隙。 约85%的IE患者血培养阳性。BCNIE主要与之前应用抗生素有关,在这种情况下需要停用抗生素和复查血培养,常常会延迟诊断和初始治疗,对临床预后有重要影响。BCNIE也可以见于难以培养的微生物和细胞内的细菌;其诊断依赖于血清学检测、免疫学技术、分子生物学技术或组织学方法。 ESC2015年修订的感染性心内膜炎诊断中术语定义,修改部分用黑体标记 主要标准 1.IE血培养阳性 a.2次血培养均培养出符合IE的典型病原体: ·草绿色链球菌,没食子酸链球菌(牛链球菌),HACEK组,金黄色葡萄球菌;或

最新感染性心内膜炎健康教育 护理篇

感染性心内膜炎健康教育 概念 感染性心内膜炎为心脏内膜表面的微生物感染,伴赘生物形成。赘生物为大小不等、形状不一的血小板和纤维素团块,内含大量微生物和少量炎症细胞。 症状 一、发烧,发烧前可能会寒战,一般来说,这种发烧都很厉害,而且治疗很长时间都不好。 二、多数都有基础病变,如果先天性心脏病或者做过瓣膜手术的病人出现长时间发烧,需提高警惕。 三、由于感染坏死的东西会脱落,造成一些小血管的栓塞,可以出现相应的症状,如肢体出现小出血斑点、指(趾)甲下出血等,严重者会出现腹痛、脾栓塞等。 四、如出现心脏结构损害,会有心力衰竭的表现,如咳喘、憋气、晚上不能平卧,饭后腹胀、腿肿等表现。 治疗 一、抗生素治疗。 抗生素的选择要根据血培养的结果来定。应用要求足量、足疗程。 二、手术治疗:有些严重感染抗生素无效,或者感染造成心脏结构损坏,需结合手术。

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感染性心内膜炎诊断标准

感染性心内膜炎诊断标准 Prepared on 22 November 2020

感染性心内膜炎诊断标准除了感染本身的症状,IE的临床表现还与下列因素有关:(1)心内感染导致的局部结构破坏;(2)感染性赘生物碎片远处栓塞导致梗死与感染;(3)持续性菌血症导致感染血源性播散;(4)病原体及其损伤组织诱导的免疫反应。 临床栓塞发生率为11%~43%,多半为卒中,而尸解病理学证实的栓塞发生率为45%~65%。静脉毒品相关的三尖瓣IE肺栓塞通常为脓毒性的,发生率为66%~75%。金黄色葡萄球菌、溶血性链球菌或其他毒力较强的化脓性细菌性IE,往往并发迁徙性感染,导致局部症状体征和持续发热。迁徙性感染影响抗生素的选择,例如并非脑膜炎时,应选择能进入脑脊液的抗生素。 影像学,特别死超声心动图,在IE的诊断和治疗中起重要作用。它还对IE患者有预后评估价值,应用于治疗期间的随访,外科术中及术后。首先必须做TTE,但在大多是怀疑和确诊IE的患者都应最终完成TTE和TEE。三种超声心动图结果被认作诊断IE 的主要标准,包括赘生物、脓肿以及人工瓣膜新的裂隙。 约85%的IE患者血培养阳性。BCNIE主要与之前应用抗生素有关,在这种情况下需要停用抗生素和复查血培养,常常会延迟诊断和初始治疗,对临床预后有重要影响。BCNIE也可以见于难以培养的微生物和细胞内的细菌;其诊断依赖于血清学检测、免疫学技术、分子生物学技术或组织学方法。 ESC2015年修订的感染性心内膜炎诊断中术语定义,修改部分用黑体标记 主要标准 1.IE血培养阳性 a.2次血培养均培养出符合IE的典型病原体: ·草绿色链球菌,没食子酸链球菌(牛链球菌),HACEK组,金黄色葡萄球菌;或

成人感染性心内膜炎预防诊断和治疗专家共识

成人感染性心内膜炎预防、诊断和治疗专家共识 感染性心内膜(infective endocantitis,IE)的发生是一个复杂过程,包括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[1,2];病原菌与瓣膜基质分子蛋白及血小板相互作用等。 近十多年随着我国人口的老龄化,老年退行性心瓣膜病患者增加,人工心瓣膜置换术、植入器械术以及各种血管内检查操作的增加,IE呈显著增长趋势。静脉用药等又导致右心IE患病率增加。IE患病率我国尚缺乏确切的流行病学数据,各国资料存在差异,欧洲为每年3/10万~10/10万,随年龄升高,70~80岁老年人为每年14.5/10万,男女之比≥2∶1,主要病因由以年轻人风湿性瓣膜病转为多种原因,最常见细菌类型由链球菌转变为葡萄球菌。美国则以葡萄球菌感染增长率最高。我国从病例报告来看,链球菌和葡糖球菌感染居最前列[3,4,5,6]。本病死亡率高、预后差。 本共识系由中华医学会心血管病学分会编写,由心力衰竭学组负责实施。这是我国首部成人IE共识。学组确定的编写目标是具有科学性和先进性,有中国特色,符合我国国情,适合我国临床医师应用。心力衰竭学组认真学习近几年国内外主要的IE指南,如欧洲心脏病学学会(ESC)指南、英国抗生素学会指南以及我国儿科学的IE诊断标准等,认真复习和分析了国内外相关的研究资料,评估了各种诊断和治疗方法的证据与推荐等级,经讨论和争论逐渐形成共识。学组建立了包括感染病学、心血管病内外科、影像学、临床检验以及病理学等多学科专家组成的撰写组,初稿形成后又在全国各地广泛征求意见,并反复进行近2年的完善修改。该共识的推出必定有助于提高我国对成人IE的诊治水平。 本共识按照国际通用方式,标示了应用推荐级别和证据水平分级。推荐类别:Ⅰ类为已证实和(或)一致认为有益和有效;Ⅱ类为疗效的证据尚不一致或有争议,其中相关证据倾向于有效的为Ⅱa类,尚不充分的为Ⅱb类;Ⅲ类为已证实或一致认为无用和无效,甚至可能有害。证据水平分级:证据来自多项随机对照临床试验或多项荟萃分析为A级;证据来自单项随机对照临床试验或非随机研究为B级;证据来自小型研究或专家共识为C级。 预防措施主要针对菌血症和基础心脏病两个环节。菌血症是IE发生的必要条件,器质性心脏病患者为IE高危易感人群。 预防和减少菌血症发生:一般措施是强调口腔、牙齿和皮肤的卫生,防止皮肤黏膜损伤后的继发性感染。尽可能避免有创医疗检查和操作,如必须进行,要严格遵循无菌操作规范。 预防性应用抗生素:对高危人群如各种心脏瓣膜病、先天性心脏病、梗阻性肥厚型心肌病,以及风湿免疫性疾病而长期服用糖皮质激素治疗者[1,2,7,8,9,10],以及注射毒品的吸毒者[1],在做有创医疗检查和操作时需预防性应用抗生素。

感染性心内膜炎诊断标准

感染性心内膜炎诊断标 准 Document serial number【UU89WT-UU98YT-UU8CB-UUUT-UUT108】

感染性心内膜炎诊断标准除了感染本身的症状,IE的临床表现还与下列因素有关:(1)心内感染导致的局部结构破坏;(2)感染性赘生物碎片远处栓塞导致梗死与感染;(3)持续性菌血症导致感染血源性播散;(4)病原体及其损伤组织诱导的免疫反应。 临床栓塞发生率为11%~43%,多半为卒中,而尸解病理学证实的栓塞发生率为45%~65%。静脉毒品相关的三尖瓣IE肺栓塞通常为脓毒性的,发生率为 66%~75%。金黄色葡萄球菌、溶血性链球菌或其他毒力较强的化脓性细菌性IE,往往并发迁徙性感染,导致局部症状体征和持续发热。迁徙性感染影响抗生素的选择,例如并非脑膜炎时,应选择能进入脑脊液的抗生素。 影像学,特别死超声心动图,在IE的诊断和治疗中起重要作用。它还对IE 患者有预后评估价值,应用于治疗期间的随访,外科术中及术后。首先必须做TTE,但在大多是怀疑和确诊IE的患者都应最终完成TTE和TEE。三种超声心动图结果被认作诊断IE的主要标准,包括赘生物、脓肿以及人工瓣膜新的裂隙。 约85%的IE患者血培养阳性。BCNIE主要与之前应用抗生素有关,在这种情况下需要停用抗生素和复查血培养,常常会延迟诊断和初始治疗,对临床预后有重要影响。BCNIE也可以见于难以培养的微生物和细胞内的细菌;其诊断依赖于血清学检测、免疫学技术、分子生物学技术或组织学方法。 ESC2015年修订的感染性心内膜炎诊断中术语定义,修改部分用黑体标记 主要标准 1.IE血培养阳性 a.2次血培养均培养出符合IE的典型病原体:

感染性心内膜炎患者的药物治疗

感染性心内膜炎患者的药物治疗 发表时间:2013-04-26T14:57:44.827Z 来源:《医药前沿》2013年第7期供稿作者:彭晓红[导读] 易感人群的发病年龄有所上升,退行性瓣膜病和二尖瓣脱垂已取代风湿性心脏病而成为心内膜炎最常见的基础心脏病。 彭晓红(黑龙江省森工总医院 150040) 【中图分类号】R453 【文献标识码】B 【文章编号】2095-1752(2013)07-0300-01 感染性心内膜炎(IE)是指由病原微生物(细菌、真菌等)经血流直接侵犯心内膜、瓣膜或大动脉内膜所致的感染性疾病。其中瓣膜为最常受累部位,伴赘生物形成。 近年来,易感人群的发病年龄有所上升,退行性瓣膜病和二尖瓣脱垂已取代风湿性心脏病而成为心内膜炎最常见的基础心脏病。静脉注射毒品和临床诊治过程有创检查的增加使发生心内膜炎的危险增加。用来纠正先心病或瓣膜性疾病的生物材料也增加了这类患者发生心内膜炎的危险。另外,越来越多的心内膜炎患者没有明确的心脏病基础。 1 病因和发病机制 1.1 病因 在过去几十年来,感染性心内膜炎的病原学方面已发生了较大的变化。 1.1.1 链球菌是目前最主要的病原菌,所占比例已超过感染性心内膜炎病原菌的50%。草绿色链球菌是咽部的正常寄生菌,对青霉素高度敏感,是亚急性感染性心内膜炎最常见的病原菌。 1.1.2 肠球菌是第二位常见的病原体,常在老年男性泌尿生殖道、年轻女性分娩后引起亚急性感染,也是医源性心内膜炎最常见的病原菌,有时可导致静脉药瘾者心内膜炎。 1.1.3 葡萄球菌也是心内膜炎常见的病原菌,占所有病原菌的33%左右,常快速破坏局部组织,局部和远处并发症发生率很高。其中金黄色葡萄球菌是急性感染性心内膜炎、静脉药瘾者心内膜炎和人工瓣膜感染的主要病原菌,表皮葡萄球菌是人工瓣膜早期心内膜炎的常见病原菌。 1.1.4 革兰阴性杆菌、真菌、立克次体和衣原体等为较少见的致病微生物。其中革兰阴性杆菌毒力强、预后差;真菌性心内膜炎的特点是大赘生物和反复栓塞。 1.2 发病机制 1.2.1 由于免疫复合物的沉积、压力差造成的血液湍流或瓣膜关闭不全损伤内皮细胞,是导致心内膜炎特征性赘生物形成的始动环节。本病多发生在压力阶差较大时,在房间隔缺损、大室间隔缺损、血流缓慢、心房颤动和心力衰竭时较少见。 1.2.2 内皮受损更多见于高动力循环系统,所以左侧心瓣膜较右侧更易受累,关闭不全较狭窄更易被感染。在有高速血流通过的狭窄瓣口的前方易被侵犯,如二尖瓣关闭不全时心内膜炎常发生在左房面,主动脉瓣关闭不全时心内膜炎常发生在左室面。 1.2.3 内皮细胞受损后,内皮下由胶原纤维构成的结缔组织被暴露,促使血小板和纤维蛋白聚集形成血凝块,并逐渐增大,形成无菌性血栓性赘生物。 1.2.4 当发生短暂菌血症(感染、拔牙、器械检查或静脉注射毒品等)时,细菌侵入上述赘生物,逃避宿主的免疫防御,在局部繁殖,最终形成一种多层的感染性赘生物。 1.2.5 反复的感染导致免疫系统的激活,从而引起关节炎、肾小球肾炎、心包炎和微血管炎等。 2 抗生素治疗 早期诊断,及早确定病原体,及时使用杀菌剂,早期识别和处理潜在并发症,进行恰当的外科干预,这些是感染性心内膜炎的关键处理环节。 2.1 一般应用原则抗生素治疗为最重要的治疗措施,其一般用药原则为:①早期应用,在连续送3~5次血培养后即可开始治疗;②选用杀菌药,所选药物长时间应用后无严重毒性作用;③大剂量和长疗程,一般为4~6周以上,对耐药者或出现并发症者,疗程宜延长至8周;④静脉用药为主,保持高而稳定的血药浓度。 2.2 选用合适的抗生素 2.2.1 对青霉素敏感的草绿色链球菌或牛链球菌等可选用以下方案:①首选青霉素G钠盐,1200万~1800万U/d,分次静滴,每4小时1次,疗程4周;②青霉素G钠盐,剂量和疗程同前,并联合阿米卡星(第1~2周),剂量为0.4~0.6g/d,分次静脉注射或肌肉注射,每8小时1次;③青霉素过敏时可选择头孢曲松2g/d,静脉注射或肌肉注射,疗程4周。 2.2.2 对青霉素耐药的链球菌包括:①青霉素G钠盐,1800万U/d,分次静滴,每4小时1次,用药4周;联合应用阿米卡星(第1~2周),剂量为0.4~0.6g/d,分次静脉注射或肌肉注射,每8小时1次;②万古霉素30mg/(kg?d),分2次静滴,总量不超过2g/d,疗程4周。 2.2.3 葡萄球菌包括:①萘夫西林2g,静脉注射或点滴,每4小时1次,疗程4~6周;②严重播散者,除萘夫西林外,在第1~2周联合应用阿米卡星,0.4~0.6g/d,分次静脉注射或肌肉注射,每8小时1次;③万古霉素15mg/(kg?d),分2次静滴,疗程4~6周。 2.2.4 真菌两性霉素B,静脉滴注,首日1mg,之后每日递增3~5mg,直至25~30mg/d,总量3~5g,应注意两性霉素的毒副作用。两性霉素用够疗程后口服氟胞嘧啶100~150mg/(kg?d),每6小时1次,用药数月。真菌性心内膜炎药物通常难治愈,应在药物治疗7~10天后行病灶洁除术及瓣膜置换术。术后继续用药6~8周。 参考文献 [1]林延源;感染性心内膜炎的新诊断技术[J];国际心血管病杂志;1980年01期. [2]贝聿素;曾昭瑞;梁寿彭;董承琅;二尖瓣脱垂综合征并发感染性心内膜炎一例报告[J];上海医学;1981年11期. [3]严庆方;感染性心内膜炎的近况[J];江西医学院学报;1981年04期.

感染性心内膜炎的外科治疗

感染性心内膜炎的外科治疗 发表时间:2009-08-11T11:09:23.170Z 来源:《中外健康文摘》2009年第21期供稿作者:周青云1 邵国丰2 张志梁2 史信宝2 [导读] 总结感染性心内膜炎的外科治疗经验。 (1浙江大学医学院浙江杭州 310000;2浙江省宁波市医疗中心李惠利医院心胸外科 315041) 【中图分类号】R542.4+1【文献标识码】A【文章编号】1672-5085(2009)21-0070-02 【摘要】目的总结感染性心内膜炎的外科治疗经验。方法 1999年4月至2009年6月,我院120例IE患者在接受内科抗感染治疗同时采取积极的外科手术治疗。结果围术期死亡1例,远期IE复发死亡2例,其余患者经随访,心功能均恢复至I~级。结论外科手术治疗感染性心内膜炎是一种有效的治疗措施,它降低了感染性心内膜炎的死亡率。正确掌握手术时机,彻底清除感染病灶,恢复瓣膜功能以及围手术期应用有效抗生素是提高感染性心内膜炎治愈率的关键。 【关键词】心内膜炎感染性心脏外科手术 感染性心内膜炎(infective endocarditis,IE)是一种严重的心脏疾病,其病变部位主要位于心脏瓣膜,常导致心脏功能明显损害。我院1999年4月~2009年6月共手术120例IE患者,现报告如下: 1 材料与方法 本组男性83例,女性37例;年龄13~70岁。术前均有畏寒、发热病史,并有不同程度贫血及血沉加快现象。术前心脏彩超检查发现心内赘生物88例,合并主动脉瓣病变80例,二尖瓣病变45例,肺动脉瓣病变10例,三尖瓣病变5例;室间隔缺损28例,房间隔缺损1例,乏氏窦瘤破裂15例,动脉导管未闭8例,左心房粘液瘤1例。术前心功能(NYHA)I级6例,II级32例,III级61例,IV级21例。 本组病例患者在找到病原菌前常规应用青霉素及庆大霉素静脉注射,在血培养或赘生物培养找到病原菌后,可改用敏感抗生素。抗生素应用疗程:静脉用药从术前、术中一直到术后4~6周。在抗感染治疗同时,积极准备手术治疗。其中24例在感染或心力衰竭未能控制下行急诊手术,44例在未完全控制下行亚急性手术,52例行择期手术。手术均在常规体外循环下进行,打开心腔后先清理赘生物、被感染的瓣膜组织及瓣周脓肿等,用电凝逐一电灼,再用浓碘伏液涂擦瓣环及赘生物附着点,并用冰盐水反复冲洗,但应避免用稀释碘伏液直接冲洗心腔。 2 结果 围术期死亡1例(死亡率0.83%),患者因严重心内膜炎,术前发生细菌性脑栓塞,急诊行四个瓣膜置换术,术后早期恢复良好,术后6d 死于大面积脑出血。1例出院后1个月IE 复发死亡。另有1例于术后1年6个月IE复发在外院手术时死亡。其余患者经随访,心功能均恢复至I~II级。 3 讨论 有效治疗IE的目的是要彻底清除致病菌,矫治侵入性、破坏性病灶及原有心脏疾病。近年临床实践证明,单纯内科治疗死亡率高达50%~90%,在抗感染的同时采用积极的外科干预治疗可使死亡率降低至8.3%~14%。与手术死亡率相关独立危险因子包括年龄、女性患者、二次手术(置换瓣膜感染)以及中风病史。充血性心力衰竭是感染性心内膜炎最常见的死亡原因。 IE 多发生于先天性或风湿性心脏病变者,最多累及主动脉瓣,其次累及二尖瓣。根据患者原有心脏病病史,有明确的感染表现,血培养阳性,心脏彩超检查发现心内赘生物,IE 诊断并不困难。但是临床上血培养阳性率较低,心脏彩超诊断价值优于血培养。若心脏彩超发现心内赘生物或瓣膜穿孔,即可诊断为IE。对于原无心脏疾病史者,短期内出现主动脉瓣明显返流,左心衰难以控制且有贫血表现者,应高度怀疑IE 存在。本组有3例紧急手术者,均无心脏病病史,也无明显感染病史,术中证实IE 引起主动脉瓣穿孔。 IE的外科治疗主要取决于感染的部位,目标是彻底清除感染病灶;恢复瓣膜正常功能;修复心脏畸形。其中,彻底清除病灶是避免术后心内膜炎复发的重要原则,术中良好的心肌保护是保证手术成功的关键。左心系统心内膜炎病情发展快,瓣膜受损严重,手术以瓣膜置换为主,右心瓣膜内膜炎较左心瓣膜为轻,采用瓣叶修补,多可矫正关闭不全。 瓣膜替换手术后IE复发是引起死亡的高危因素,本组2例远期死亡均死于IE复发。本组全部采用机械瓣替换,术中注意彻底清除病变组织,对散在细小赘生物用电灼处理,浓碘伏反复涂擦及冰盐水冲洗,取得较好疗效。作者认为IE病人只要术中彻底清除感染组织,采用机械瓣行瓣膜替换术是合适的,如果人工机械瓣膜置换术后出现严重的心内膜炎,再次行瓣膜置换时宜用生物瓣以减少术后再次心内膜炎感染。作者强调术中不用稀释碘伏溶液直接冲洗心腔,避免碘伏溶液进入肺循环系统引起肺损伤。本组有2例因碘伏溶液直接冲洗心腔造成术后肺损伤,呼吸机支持3d才脱机。IE瓣膜替换术后大剂量敏感抗生素联合应用,且疗程足够也极为重要,我们术后常规应用4周。本组有1例因故术后静脉应用抗生素2周停药出院,2个月后IE复发导致死亡。 参考文献 [1]张希,孙培吾,童萃文,等. 感染性心内膜炎急诊外科治疗.中华胸心血管外科杂志,2001,16:330-331. [2]董超,孙立忠,王水云,等.活动期感染性自然心内膜炎的外科治疗.中华外科杂志,2005,03:358-361.

病例讨论-感染性心内膜炎.

有奖病例讨论 诊断: 1、感染性心内膜炎 2、脾栓塞 3、肾血管栓塞 4、多发性脑栓塞 脑膜脑炎可能 5、左下肺炎 6、心包积液、胸腔积液原因待查 原发型肺癌? 7、DIC 8、I型呼吸衰竭 诊断依据: 1、患者有肺部感染史,发热1个月,伴畏冷、寒战、全身酸痛,贫血、消 瘦,食欲不振等全身性感染的表现,有脾栓塞、脑栓塞等全身性栓塞的表现,心尖部可闻及2/6级收缩期吹风样杂音。UCG示:左室增大,二尖瓣前叶左房面见一大小为1.7cm×3.4cm赘生物;中度二尖瓣返流,因未明确患者是否有心脏器质型基础疾病,而且血培养阴性,故考虑感染性心内膜炎可能性大。根据血管彩超提示及尿常规示:蛋白、红细胞明显增多,故脾栓塞肾、血管栓塞可诊断。患者意识障碍、反应迟钝、言语欠清,有持续性头痛伴视物模糊,四肢麻木,右巴氏征阳性,结合头颅CT,可诊断脑栓塞,定位于左侧颞枕叶、右侧枕叶,因颅脑CT示:病灶为低密度影、显示欠清,

故定性为脑栓塞。因患者表现右侧周围性面瘫,不排除面神经及脑干核团受损,一过性双侧听力下降,考虑可能相应血管一过性栓塞。 患者有颈抵抗,结合病史,有发热、意识障碍,考虑脑膜脑炎可能 2、患者发热1个月,伴畏冷、寒战、全身酸痛,经“抗炎”治疗后体温有所 下降,2天前再度出现高热。血常规WBC14.3×10^9/L,N80.2%。外院胸部CT提示左肺下叶小斑片影。故左下肺炎可诊断。 3、心包积液、胸腔积液原因待查,原发性肺癌?:患者有胸腔积液、心包积 液,因肺癌筛查示TPA、NSE、cyfra均升高,LDH明显升高,故不可排除肺癌可能,可以行胸部CT检查、心包、胸腔诊断性穿刺,积液检查培养,以协助诊断明确。 4、患者有感染的诱因,DIC全套示:3P试验阳性,FDP>40ug/ml,PT18s, APTT36.5s,D-二聚体3.15mg/L。血凝全套:蛋白C活性降低,蛋白S活性增高,抗凝血酶Ⅲ活性降低,故DIC可诊断。 5、患者未吸氧血气分析示:PO2:59mmHg,PCO2:30mmHg,故I型呼吸衰 竭可诊断。 讨论存在以下疑点: 患者有腹膜刺激征,考虑是否为赘生物脱落的带菌栓子引起腹膜炎可能; 脑膜脑炎可能由带菌栓子引起。 鉴别诊断: 1、风湿性心瓣膜病:可有发热,血象高,C反应蛋白高,多伴有二尖瓣关闭不

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