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
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
Anorexia Changing murmur
Weight loss Neurological sign 30-40
Malaise Embolic event
Cough Sphenomegaly
Stroke Clubbing
Headache Osler’s node
Nausea/vomiting Splinter hemorrhage
Myalgia/arthralgia Petechiae
Chest pain Janeway’slesion
Back pain Roth’s spots
confusion

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

17. through thorax echocardiogram(TTE) the sensitive about 80~90%
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. a) at least 10ml~20ml blood should placed
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. It can find metastatic abscesses in lungs or enlargement of heart
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 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 gm/kg im or iv every 8hr
Ampicilline 12gm/24hr
Gentamicin gm/kg im or iv every 8hr
vancomycin mg/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 mg/kg/24h in two equally divided doses
If methicillin-resistant staphylococci the
vancomyccis should be first chosen

35. 4. Staphylococci in PVE
Vancomyccis
Rifampine mg 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!