infective endocarditis

1. Guide By: Dr. Meenaxi Sharda
Presented By: Dr. Naresh Kumar Meghwal
(Resident GMC Kota)

2. DEFINITION
• Infection of the endocardial surface of
the heart, which may include heart
valves (native or Prosthetic) , the mural
endocardium , or septal defect.
• The prototypic lesion of IE is the
vegetation, is a mass of platelets, fibrin,
microcolonies of microorganism, and
scant inflammatory cells.

3. CLASSIFICATION
ACUTE ENDOCARDITIS
• Rapid damage of previously normal as well as diseased heart
valve, with a highly virulent organism
• Hematogenoulsy seeds to extracardiac sites
• If untreated, leads to death within weeks
SUBACUTE ENDOCARDITIS
• Organisms of low virulence causing infection in a previously
damaged heart, particularly on deformed valves.
• Raraly metastasizs
• Follow an indolent course of weeks to month
• Gradually progressive unless complicated by a major embolic
event or ruptured mycotic aneurysm

4. RISK FACTOR
• Intravenous drug abuse
• Artificial heart valves and pacemakers
• Cardiac conditions such as MR, AS, AR, MVP
and CHD
• Intravascular catheters ,Hemodialysis,
Nosocomial wound and UTI

5. CAUSATIVE ORGANISM
• Acute IE is caused by Beta-Hemolytic
streptococci, S. aureus, and Pneumococci.
• Subacute IE is typically caused by viridans
streptococci, enterococci, CoNS and HACEK
group (Haemophilus, Actinobacillus,
Cardiobacterium, Eikenella, and Kingella)
• Endocarditis amoung IV drug users caused by
S. aureus , P. aeruginosa and candida sp.

6. PATHOGENESIS
• Organism enter bloodstream from mucosal
surface, skin, and site of focal infection.
• Endothelial injury (at the site of impact of high
velocity blood jets or on low pressure side of
cardiac structrual lesion) causes turbulent
blood flow and
• allow either direct infection by virulent
organism or the development of an uninfected
platelet-fibrin thombus (NBTE).

7. Cont.
• Bactereamia – microorganism in blood adhere
to sites at thrombus . Organisms are
proliferate and induce a procoagulant state .
• Fibrin deposition combines with platelets
aggregation,stimulated by tissue factor and
independently by proliferating microorganism,
to generate an infected vegetation.

8. Endothelial injury
Un-infected platelet fibrin thrombus
(NBTE)
Transient bacteremia and
attachment of bacteria to NBTE
Proliferation and pro-coagulant state
Infected friable,bulky vegetation

10. CLINICAL MANIFESTATION
Occur due to :
• Damage to intracardiac structures
• Embolization of vegetation fragments
• Hematogenous infection of sites during
bacteremia
• Tissue injury due to deposition circulating
immune complex

11. C0NSTITUTIONAL SYMPTOMS
• ACUTE IE:
• High grade fever and
chills
• SOB
• Arthralgias/ myalgias
• Abdominal pain
• Pleuritic chest pain
• Back pain
• SUBACUTE IE:
• Low grade fever
• Anorexia, N/V
• Weight loss
• Fatigue
• Arthralgias/ myalgias
• Abdominal pain

12. CARDIAC
• Murmur (85% cases) due to valvular damage
and ruptured chordae.
• CHF (40% cases) usually due to valvular
dysfunction.
• Perivalvular abscess.
• Pericarditis.
• Heart block.
• Myocardial infarction.

13. NONCARDIAC
• Nonspecific signs – petechiae, subungal or
“splinter” hemorrhages, clubbing,
splenomegaly, renal dysfunction, neurologic
symptoms.
• More specific signs - Osler’s Nodes, Janeway
lesions, and Roth Spots.

15. SUBCONJUCTIVAL HAEMORRHAGE PETECHIAE

16. ROTH’S SPOTSSPLINTER HAEMORRHAGES

17. JANEWAY LESIONS

18. OSLERS NODES

19. DIAGNOSIS
• Endocarditis should be suspected in patients with
fever and no obvious source of infection, and
particulary if heart murmur is present.
• Diagnosis of IE is established with certainty only
when vegetations obtained at cardiac surgery, at
autopsy, or from an artery (an embolus) are
examined histologically and microbiologically.
• A highly sensitive and diagnostic scheme is
known as DUKE CRITERIA has developed on basis
of clinical, laboratory and echo findings.

20. BLOOD CLUTURE
• If endocarditis is suspected, 3 blood culture sets,
separated from each other by atleast 1 hr. (20 mL
each), should be obtained from different
venipuncture sites within 24 hr.
• When endocarditis is present and no prior
antibiotic therapy was given, all 3 blood cultures
usually are positive because the bacteremia is
continuous; at least 1 culture is positive in 99%.
• Premature use of empiric antibiotic therapy
should be avoided in hemodynamically stable
patients to avoid culture-negative endocarditis.

21. DUKE CRITERIA
•Definite IE
o 2 major criteria OR
o 1 major and 3 minor criteria OR
o 5 minor criteria
•Possible IE
o 1 major and 1 minor criteria OR
o 3 minor criteria
•Rejected
o Firm alternate diagnosis OR
o Resolution of manifestations of IE with 4 days of antimicrobial therapy OR
o No pathologic evidence of IE at surgery or autopsy after 4 of antimicrobial
therapy.

22. MAJOR CRITERIA
Positive blood culture:
• Typical microorganism consistent with IE, from two separate
blood cultures
 S. viridans, S. bovis, HACEK
 community-acquired S. aureus or enterococci (no primary focus)
• Persistently positive cultures
 at least two positive cultures, drawn 12 hours apart
 all of three, or a majority of four or more cultures ,with first and
last sample drawn at least one hour apart
• Single positive blood culture for coxiella burnetii
Evidence of endocardial involvement:
• Positive echocardiogram
 oscillating intracardiac mass on valve or supporting structures,
 myocardial abscess,
 new partial dehiscence of prosthetic valve
• New valvular regurgitation

23. MINOR CRITERIA
Predisposition
• Predisposing heart condition or IV drug abuser
Fever
• > 38.0º C
Vascular phenomena
• arterial emboli, septic pulmonary infarct, mycotic aneurysm,
intracranial hemorrhage, conjunctival hemorrhage, Janeway’s lesion
Immunologic phenomena
• glomerulonephritis, Osler’s nodes, Roth’s spots, rheumatoid factors
Microbiologic evidence
• positive blood culture but does not meet major criteria.

24. IMAGING
• Chest x-ray:
– Look for multiple focal infiltrates, calcification of
heart valves, evidence of cardiac failure and
cardiomegaly.
• ECG:
– Rarely diagnostic
– Look for evidence of ischemia, conduction
delay(AV block), and arrhythmias
• Echocardiography

25. ECHOCARDIOGRAPHY
• It allows anatomic confirmation of IE, size of
vegetations, detecting of intracardiac
complication, and assessment of cardic function.
• Trans thoracic echocardiography (TTE):
Noninvasive, First line if suspected IE, Native
valves IE, cannot image vegetation <2 mm in
diameter, sensitivity is 65%.
• Trans esophageal echocardiography (TEE): More
sensitive(>90%) than TTE , Prosthetic valves IE, or
detection of myocardial abscess, valve
perforation, intracardiac fistulae.

26. ADDITIONAL TESTS
• CBC: Normochromic normocytic anemia and/or
leukocytosis.
• ESR and CRP elevated
• Complement levels ↓ (C3, C4, CH50)
• RF
• Urinalysis: Proteinuria and Microscopic
hematuria
• Baseline chemistries and coagulation profile.
• Circulating immune complex titer commonly
increased in IE.

27. MANAGMENT
• Antibiotics remain the mainstay for treatment of IE.
• To cure endocarditis, all bacteria in vagetation must be killed;
therefore therapy must be bactericidal and prolonged.
• High dose antibiotics are administered parenterally, to
maximize diffusion of antibiotic molecules into depth of
vegetation.
• General measures include the following:
– Treatment of congestive heart failure
– Oxygen
– Hemodialysis (may be required in patients with renal failure).
• Surgery- Intracardiac complications

28. ANTIBOTIC REGIMEN FOR INFECTIVE ENDOCARDITIS:
STREPTOCOCCI
• Penicillin-susceptible:
– Penicillin G 2-3 mU IV 4 hourly for 4 weeks
– Ceftriaxone at 2 g/d IV as a single dose for 4
weeks
– Penicillin G or ceftriaxone (as above dose)
PLUS gentamicin at 1 mg/kg 8 hourly for 2
weeks;
– Vancomycin 15mg/kg IV 12 hourly for 4
weeks.

29. Cont.
• Relatively penicillin resistant streptococci
– Penicillin G or Ceftriaxone PLUS gentamicin 1
mg/kg IM or IV 8 hourly for 4 weeks
– Vancomycin 15mg/kg IV 12 hourly for 4 week.
• Moderately penicillin resistant streptococci
and nutritionally variant organisms
-Penicillin G (4-5 mU IV 4 hourly) or Ceftriaxone
(2 g/d IV) for 6 weeks PLUS gentamicin 1
mg/kg IM or IV 8 hourly for 4 weeks
-Vancomycin 15mg/kg IV 12 hourly for 4 week

30. Cont.
ENTEROCOCCI
• Penicillin G (4-5 mU IV 4 h) PLUS gentamicin (1
mg/kg IM or IV 8 h) for 4-6 weeks
• Ampicillin (2 g IV 4 h) PLUS gentamicin (1
mg/kg IM or IV 8 h) for 4-6 weeks
• Vancomycin (15 mg/kg IV 12h)PLUS
gentamicin (1 mg/kg IM or IV 8 h) for 4-6
weeks.

31. STAPHYLOCOCCI
Methicillin-sensitive S aureus:
• Nafcillin or oxacillin 2 g IV 4 h for 4-6 weeks
• Cefazolin 2 g IV 8 h for 4-6 weeks
• Vancomycin 15 mg/kg IV 12 h for 4-6 weeks
Methicillin-resistant S aureus:
• Vancomycin (15 mg/kg IV 12h for 6-8 weeks)
PLUS gentamicin (1 mg/kg IM or IV 8 h for 2
weeks).
• For infecting prosthetic valves (S/R) add rifampin
300 mg oral 8 h for 6-8 weeks.
HACEK Organisms
• Ceftriaxone 2 g/d IV as a single dose for 4 week

32. EMPIRICAL THERAPY
• In injection drug user should cover MRSA and gram
negative bacilli. The initiation of T/t with vancomycin
and gentamycin immediatly after blood is obtain for
cultures.
• Pending the availability of diagnostic data, blood
culture negative subacute NVE is T/t with ceftriaxone
plus gentamycin.
• If prosthetic valve are involved then above two plus
vancomycin should be used.

33. MONITORING
• Blood culture repeated daily until sterile.
• Blood culture become sterile within 2 days after
start of appropriate therapy when infection caused
by viridans streptococci, enterococci,or HACEK
organism.
• In S. aureus ,penicillin therapy results in 3-5 days,
whereas with vancomycin therapy culture positive
persist for 7-9 days.
• Resolution of fever within 5-7 days, when fever
persists for 7 days , patients should be evaluated for
paravalvular abscess and for extracardiac abscess
(spleen, kidney) or complications (embolic events ).

34. INDICATIONS FOR SURGERY
• Congestive heart failure refractory to standard medical
therapy
• Partially dehiscence unstable prosthetic valve
• Persistent sepsis despite appropriate antibiotic
treatment
• Lack of effective microbicidal therapy (eg. Fungal or
brucella)
• Relapse after optimal antimicrobial therapy
• Paravalvular abscess and intracardiac fistula
• Large(>10mm) hypermobile vegetations with increased
risk of embolism
• Persistent fever (>10 day) in culture negative NVE.

35. PREVENTION
High risk cardiac lesion for which prophylaxis is advised:
• Prosthetic heart valves
• Previous infective endocarditis
• Unrepaired cyanotic CHD (including palliative shunts and
conduits),
• Completely repaired CHD during the 1st 6 months after
surgery if prosthetic material or device was used
• Incompletely repaired CHD that has residual defects at or
adjacent to the site of repair
• Valvulopathy developing after cardiac transplantation
• Any procedure involving manipulation of gingival tissue or
the periapical region of teeth, or perforation of the oral
mucosa

36. REGIMEN FOR IE PROPHYLAXIS
Standard oral regime:
• Amoxicillin 2 g 1hr before procedure
Inability to take oral medication:
• Ampicillin 2g IV or IM 1hr before procedure
Penicillin allergy:
• Clindamycin 600 mg oral 1hr before procedure
• Clarithromycin or azithromycin 500 mg oral 1hr before
procedure
• Cephalexin 2 g oral 1hr before procedure
Penicillin allergy, inability to take oral:
• Cefazolin or Ceftriaxone 1g IV or IM 30 min before
• Clindamycin 600mg IV or IM 1hr before procedure
Regimen for IE prophylaxis

37. OUTCOME
• Older age, severe comorbid conditions, delayed
diagnosis, involvment of prosthetic or aortic
valve, an invasive(s.aureus) or antibiotic resistant
(P. aeruginosa, yeast)pathogen, intracardiac
complications, and major neurologic
complications adversely impact outcome.
• Prosthetic valve endocarditis beginning within 2
month of valve replacement results in mortality
rate of 40-50% , whereas rate are only10-20% in
later onset cases.

38. THANKS