INFECTIVE ENDOCARDITIS

1. INFECTIVE ENDOCARDITIS Gao Xiuren

2. Definition • Infective endocarditis (IE) is a microbial infection of the endothelial surface of the heart. • The characteristic lesion, the vegetation, is a variably sized amorphous mass of platelets and fibrin in which abundant microorganisms and scant inflammatory cells are enmeshed.

3. Clinical classification • Native valve endocarditis • Prosthetic valve endocarditis • Introvenous drug abuser endocarditis

4. According to the course of disease it can be divided into acute IE and subacute IE

5. Acute IE presents with marked toxicity, progresses over days to several weeks to valvular destruction and metastatic infection. In contrast; sub-acute IE envolve over weeks to months with only modest toxicity and rarely causes metastatic infection, the infection of staphylococcus stand for about 25% in native valve IE and streptococcus stand for nearly 65% in native valve IE.

6. The acute IE mainly causes by staphylococcus aureu infection. Nevertheless; the sub-acute IE more likely causes by streptococcus, enterococcus or gram-negative coccobacilli.

7. Pathogenosis • Basically heart disease (predisposing condition) For example: rheumatic heart disease,congenital heart disease, mitral valve prolapse, degenerative heart disease, intravenouse drug abuse mitral valve regurgitatiom aortic valve regurgitation fistula It seldom occurs in valve stenosis

8. Development of nonbacterial thrombolic Endocarditis(NBET) Endothelial damage Three hemodynamic circustances may injure the endothelium initiating NBTE: a) high-velocity jet impacting endothelium b) flow from a high-to a low-pressure chamber c) flow across a narrow orifice at high velocity

9. White thrombosis The deposition of platelet-fibrin to shape the white thrombosis. The white thrombosis is more receptive to colonization by bacterial than intact endothelium

10. Red thrombosis The adherence of microorganism to NBTE is a pivotal early event in the development of IE.Certain bacterial are advantage in there ability to colonize and infect NBTE. The red blood cells, white blood cells; platelet; and fibrin deposition to form the red thrombosis(vegetation).

11. The red thrombosis is easier to rupture and involve peripheral manifestation and result in hemotogenous seeding of remote sites. Antibody response to the infection organism with subsequent tissue injury, due to antibody and antigens complexes reaction.

12. Clinical feature • Incubation The incubation of infection in NVE is short (2 weeks) in contrast the incubation of infection in PVE is relatively longer, sometimes may reach to 2~5 months.

13. Fever Nearly all patients have fever.In generally, the sub-acute IE has lower temperature (<39ºC) compare with the acute IE.

14. Symptoms and signs: The symptoms come from toxicity and periphearal organs infarction. The signs include changing/new heart murmur and peripheral manifestation.

15. Symptoms% Signs % Fever 80-85 Fever 80-90 Chills 42-75 Murmur 80-85 Sweats 25 Anemia 70-80 Anorexia 25-55 Changing murmur 10-40 Weight loss 25-35 Neurological sign 30-40 Malaise 25-40 Embolic event 20-40 Cough 25 Sphenomegaly 15-50 Stroke 13-25 Clubbing 10-20 Headache 15-40 Osler’s node 7-10 Nausea/vomiting 15-20 Splinter hemorrhage 5-15 Myalgia/arthralgia 15-30 Petechiae 10-40 Chest pain 5-15 Janeway’slesion 6-10 Back pain 7-10 Roth’s spots 4-10 confusion 10-20

16. Laboratory test 1.Anemia Anemia is found in 70-90 percent patients especially in patients with sub-acute IE • normocytic red blood cell indices • low serum iron level • low serum iron-binding capacity

17. 2. Echocardiography through thorax echocardiogram(TTE) the sensitive about 80~90% through esophagus echocardiogram(TEE) the sensitive is about 95%. It can find less than 2-3mm2 vegetation

18. 3. Blood culture Three separate sets of blood cultures, obtained over first 24 hours are recommended. a) at least 10ml~20ml blood should placed b) fist day 3 sets, second day 1-2 sets c) every hour interval

19. The cultures should include staphylococci, steptococci, mycobateria, rickettsiae, chlamydozoan, mycoplosmal, coccobacilli, fungi, and other special organisms. Sensitive to the antibiotic drug should be done. minimal inhibitory concentration MIC minimal bactericidal concentration MBC

20. 4. Urine tests hematuria proteinuria tubular proteinuria

21. 5. ECG 6. X-ray It can find metastatic abscesses in lungs or enlargement of heart

22. Diagnosis Criteria • Major criteria • Minor criteria

23. Major criteria 1. Positive blood culture • Typical microorganism for infective endocarditis from two separate blood cultures • persistently positive blood culture, • blood cultures draw more than 12 hrs apart, All of three or a majority of four or more separate blood culture, with first and last drawn at least 1 hour apart

24. 2. Evidence of endo-cardium involvement Positive echocardiogram • Oscillating mass (vegetation) • Abscess • New/changing murmur (valvular regurgitation)

25. Minor criteria 1. Predisposition: predisposing heart condition or intravenous drug abuse 2. Fever 38°C 3. Vascular phenomena: major arterial embolic, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhages, rheumatoid factor janeway’s lesion

26. 4. Immunological phenomena • glomerulonephritis • Osler’s nodes • Roth’s spots 5. Microbiological evidence • positive blood culture but not meeting major criteria 6. Echocardiogram: other evidence of endocarditis but not meeting major criteria

27. Diagnosis of infective endocarditis • Clinical criteria: fever,chill,sweat,weight lose anemia,murmur, Osler’node,Janeway’s lesion,Roth’s spots and so on.

28. Pathological criteria • Microorganism: demonstrated by culture or histology in a vegetation, or in a vegetation that has embolized, or intracardiac abscess, • Pathological lesions: vegetation or intracardiac abscess present comfirmed by histology showing active endocarditis

29. Clinical diagnosis criteria • Two major criteria • One major and three minor criteria • Five minor criteria

30. Rejected • Not meeting pathological and clinical diagnosis criteria, predisposing other disease • no pathological evidence at surgery or autopsy, after antibiotic therapy for 4 days or less

31. antibiotic therapy • The regular antibiotic therapy include flow 1. Early use as soon as clinical diagnosis has been set up 2. High serum concentration 3. Treatment is continued for prolonged period at least 4~6 weeks 4. Bactericidal antibiotics should be chosen 5. Monitoring serum bactericidal titer 6. Combination bactericidal and bacteriostatic

32. Antimicrobial therapy for specific organisms 1.Viridans streptococci Penicillin G 12-18 million units/24 hr Ceftriaxone 2gm 1~2 doses/24hr Gentamicin 1mg/kg im or iv every 8hr Vancomycin 30mg/kg/24hr in two equally divided doses. not to exceed 2gm/24hr

33. 2. Enterococci Penicilline G. 18~30 million units /24hr Plus: Gentamicin 1gm/kg im or iv every 8hr Ampicilline 12gm/24hr Plus: Gentamicin 1gm/kg im or iv every 8hr vancomycin 30mg/kg/24hr, iv in two equally divided doses not to exceed 2gm/24hr

34. 3. Staphylococci in Native valvalar endocarditis (NVE) Nafcilline or oxacillin 2gm iv every 4hr Cefazoline 2gm iv every 8hr Vancomycin 30mg/kg/24h in two equally divided doses If methicillin-resistant staphylococci the vancomyccis should be first chosen

35. 4. Staphylococci in PVE Vancomyccis Rifampine 300mg PO every 8hr and Gentamicin Nafcilline or oxacilline

36. Surgical treatment Indications 1.Moderate to severe congestive heart failure due to valve dysfunction 2.Unstable prosthesis 3.Uncontrolled infection despite optimal antimicrobial therapy fnngi Brucellae ect. 4.Staphylococcus aureus PVE with an intracardiac complication 5.Relapse of PVE at optimal therapy

37. Relative surgical Indications 1. Perivalvular extension of infection, intracardiac fistula 2.Pooly responsive staphylococcus aureus NVE 3.Culture-negative NVE or PVE with persistent fever 4.Large hypermobile vegetation 5.Endocarditis due to highly antibiotic-resistant enterococci

38. Thank you!