内科学课件：Infective Endocarditis

1、Case At midnight on July 2, your first night on call as an intern, you got a call from the micro lab. One of the patients your colleague admitted earlier that day, one set of the blood cultures is positive, growing gram positive cocci. The patient is a 40 y.o. female with a history of asthma. One day PTA, she was seen in the ER with several days of low grade fevers, and the initial work up was unrevealing. Blood cultures were drawn and she was sent home. She came back with persistent low grade f

2、evers, and now has pleuritic chest pain and some shortness of breath. What is the diagnosis? What should do next?Infective Endocarditis（IE）Outline Definition Epidemiology Pathogenesis Clinical Manifestations Diagnosis Complications Treatment (emphasis on early surgery) Antibiotic prophylaxis PrognosisDefinitions Infection of endocardial surfaces of the heart Any area causing high pressure jet may be involved Valves are most common affected formation of bulky fibrin mass called vegetation laden w

3、ith microorganismsA changing Epidemiology Exact incidence difficult to measure ranges 310 episodes/100 000 person-yearsis increasing as the at-risk population grows Age distribution is changing mean age of patient is up to 55 years the peak incidence was 14.5 episodes/100 000 person-years in patients between 70 and 80 Male:Female = 2-9:1Epidemiology young adults with previously well-identified valve disease ( rheumatic) 、congenital heart disease older patients who more often develop IE as the re

4、sult of health care-associated procedures（chronic haemodialysis in severe kidney disease ，catheter，intravascular devices） or in patients with prosthetic valves Diabetes mellitus Intravenous drug abuseEpidemiology Mitral valve alone 28-45% Aortic valve alone 5-36% Both mitral and aortic valve 0-36% Tricuspid 0-6% Pulmonic valve 1%Classification-time course Acute: fulminant，rapid progression of symptoms Less than 6 weeks duration Significant systemic signs/symptoms Fever Elevated systemic WBC/ lef

5、t shift with few immunologic signs. Central nerve system complications in 30-50% common pt with no underling heart disease Subacute: Slower, chronic progression of symptoms Low grade fevers Vague clinical signs/symptoms weakness, anorexia, malaise,etc.Etiology：Common85% of all IE is positive blood cultures Causative microorganisms are most often：Viridans streptococciStaphylococcus aureus enterococci According to AHA Scientific Statement 2005 and ESC guideline 2009Etiology： Viridans Streptococci

6、30-65% of native valve endocarditis Typical agents of classic “SBE” common after dental procedure, tonsillectomy, bronchoscopy. almost always susceptible to penicillin GEtiology： Staphylococci Coagulase Positive (Staph. aureus) a major causative agent 2540% case typically produces “acute” IE most often susceptible to oxacillin Coagulase Negative (Staph. epi, et al) Major cause of PVE， 3-8% of NVE with oxacillin resistanceEtiology：Uncommon Strep pneumoniae: 1-3% cases , usually in those with immu

7、ne suppression(DM and Ethanolism) Group B ，C；D Streptococci（Streptococcus bovis） Staph. Epidermidis（ PVE，SBE ，in neonates） Brucella Fungi (e.gAspergillus ，Candiada ） H. influengae Coxiella burnetii (Q fever) Etiology ：HACEK organisms Hemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella Fastidious gram negative bacilli Large vegetation, high likelihood of embolization. Slow growing: hold cultures for 3 weeks. Traditionally sensitive to beta lactams, now some produce beta lactamase.Eti

8、ology ：Fungi Commonly encountered agents: Candida, Torulopsis, Aspergillus Predispositions Prosthetic valves IVDA Immunosupression Hyperalimentation Prolonged abx treatment Large vegetations and frequent embolic events.Risk factors Structure heart disease -rheumatic, congenital, aging -prosthetic heart valve Injected drug use Invasive procedure Indwelling vascular device Other infection with bacteremia (pneumonia, menigitis) History of IEPathogenesis Multiple independent pathophysiological proce

9、sses : 3 key features “Trauma” of the heart surfaces Platelet/fibrin deposition over traumatized tissue (NBTE ：non-bacterial thrombotic endocarditis) “Bacteremia” subsequent infection of the platelet/fibrin deposition (Bacterial endocarditis) Bacterial multiplication (10 9,10 cfu/gram of tissue)Pathogenesis- endothelial damage turbulent blood flow (MVP, bicuspid AV，PV） Electrodes，leads or catheters Inflammation： rheumatic carditis，IVDA degenerative changesExtracellular matrix proteins exposure t

10、issue factor ，thromboplastin triggering coagulation NBTEPathogenesis-Transient bacteraemia invasive procedures： intravascular，dental procedures， respiratory tract procedures（Bronchoscopy）, gastrointestinal or genitorurinary procedures, dermatological or musculoskeletal procedures spontaneous bacteraemia：chewing and tooth brushing Leading to the concept of prophylaxisPathogenesisCardiac Complications Valvular abscess, perforation of a leaflet, rupture of chordae, papillary muscle or the septum Fi

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