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Infective Endocarditis
Outlines
• Definitions
• Pathogenesis
• Pathophysiology
• Clinical features
• Treatment
• Prevention
Definition
Infectious Endocarditis (IE):
• An infection of the heart’s endocardial surface
• Vegetation
– Variable in size
– Amorphous mass of fibrin & platelets
– Abundant organisms
– Few inflammatory cells
• Classified into four groups:
• Native Valve IE
• Prosthetic Valve IE
• Intravenous drug abuse (IVDA) IE
• Nosocomial IE
PREDISPOSING CONDITIONS ASSOCIATED WITH
INCREASED RISK OF ENDOCARDITIS
More Common
• Rheumatic heart disease
• Mitral valve prolapse with murmur
• Degenerative valvular disease
• Intravenous drug use
• Prosthetic valve
• Congenital abnormalities (valvular or septal
defect)
Less Common
• Hypertrophic obstructive cardiomyopathy
• Pulmonary-systemic shunts
• Coarctation of the aorta
• Previous endocarditis
Infecting Organisms
Common bacteria
– S. aureus
– Streptococci
– Enterococci
Uncommon bacteria
– Fungi
– Pseudomonas
– The HACEK grop
» Haemophilus sp.
» Actinobacillus
» Cardiobacterium
» Eikenella
» Kingella
Acute V Sub-acute
• Acute
– Toxic presentation
– Progressive valve destruction & metastatic infection
developing in days to weeks
– Most commonly caused by S. aureus
• Subacute
– Mild toxicity
– Presentation over weeks to months
– Rarely leads to metastatic infection
– Most commonly S. viridans or enterococcus
Infective Endocarditis
• Intravenous Drug Abuse
- S. aureus
– Increased frequency of gram negative infection
such as P. aeruginosa & fungal infections
– High concordance of HIV positivity & IE
• HIV status does not in itself modify clinical
picture
• Survival is decreased if CD4 count < 200/mm3
Pathophysiology
• Turbulent blood flow disrupts the
endocardium making it “sticky”
• Bacteremia delivers the organisms to the
endocardial surface
• Adherence of the organisms to the
endocardial surface
• Eventual invasion of the valvular leaflets
Infective Endocarditis
• Pathology
– NVE infection is largely confined to leaflets
– PVE infection commonly extends beyond valve
ring into annulus/periannular tissue
• Ring abscesses
• Septal abscesses
• Fistulae
• Prosthetic dehiscence
Pathophysiology
• Local destructive effects
• Valvular distortion/destruction
• Chordal rupture
• Perforation/fistula formation
• Paravalvular abscess
• Conduction abnormalities
• Purulent pericarditis
• Functional valve obstruction
• Clinical Features Clinical manifestations
– Direct
• Constitutional symptoms of infection (cytokine)
– Indirect
• Local destructive effects of infection
• Embolization – septic or bland
• Hematogenous seeding of infection
» N.B. may present as local infection or persistent fever,
metastatic abscesses may be small, miliary
• Immune response
» Immune complex or complement-mediated
Clinical Features
Clinical Features
• Interval between index bacteremia &
onset of sx’s usually < 2 weeks
• Systemic manifestation like any other AFIs
• Fever most common sign
• Murmur present in 80 – 85%
• Generally indication of underlying lesion
• Frequently absent in tricuspid IE
• Changing murmur
Modified Duke criteria
Major criteria include---- Table-I
1. Positive blood culture with typical IE microorganism, defined as one of the
following:
– Typical microorganism consistent with IE from 2 separate blood cultures, as
noted below:
• Viridans-group streptococci, or
• Streptococcus bovis including nutritional variant strains, or
• HACEK group, or
• Staphylococcus aureus, or
• Community-acquired Enterococci, in the absence of a primary focus
– Microorganisms consistent with IE from persistently positive blood cultures
defined as:
• Two positive cultures of blood samples drawn >12 hours apart, or
• All of 3 or a majority of 4 separate cultures of blood (with first and last
sample drawn 1 hour apart)
• Coxiella burnetii detected by at least one positive blood culture or
antiphase I IgG antibody titer >1:800
…Modified Duke criteria
2. Evidence of endocardial involvement with
positive echocardiogram defined as
– Oscillating intracardiac mass on valve or
supporting structures, in the path of regurgitant
jets, or on implanted material in the absence of an
alternative anatomic explanation, or
– Abscess, or
– New partial dehiscence of prosthetic valve or new
valvular regurgitation (worsening or changing of
preexisting murmur)
…Modified Duke criteria
Minor criteria include:
• Predisposing factor: known cardiac lesion, recreational drug
injection
• Fever >38°C
• Evidence of embolism: arterial emboli, pulmonary infarcts,
Janeway lesions, conjunctival hemorrhage
• Immunological problems: glomerulonephritis, Osler's nodes
• Positive blood culture (that doesn't meet a major criterion) or
serologic evidence of infection with organism consistent with
IE but not satisfying major criterion
• Positive echocardiogram (that doesn't meet a major criterion)
(this criterion has been removed from the modified Duke
criteria)
Classical Peripheral Manifestations
• Less common today
• Not seen in tricuspid endocarditis
• Petechiae most common
Janeway Lesions
Splinter Hemorrhage
Osler’s Nodes
Subconjunctival Hemorrhages
Roth’s Spots
Clinical Features
• Systemic emboli
• Incidence decreases with effective anti-microbial Rx
• Neurological sequelae
• Embolic stroke 15 – 20% of patients
• Mycotic aneurysm
• Cerebritis
• CHF
• Due to mechanical disruption
• High mortality without surgical intervention
• Renal insufficiency
• Immune complex mediated
• Impaired hemodynamics/drug toxicity
Additional Labs
• CBC
• ESR and CRP
• Complement levels (C3, C4, CH50)
• RF
• U/A
• Baseline chemistries and coags
Imaging
• Chest x-ray -Look for multiple focal infiltrates and calcification
of heart valves
• EKG-Rarely diagnostic Look for evidence of ischemia,
conduction
delay, and arrhythmias
• Echocardiography
TTE- - First line if suspected IE
– Native valves
• Transesophageal echocardiography (TEE)
» Prosthetic valves
» Intracardiac complications
» Inadequate TTE
» Fungal or S. aureus or bacteremi
Goals of Therapy
1. Eradicate infection
2. Definitively treat sequelae of destructive
intra-cardiac and extra-cardiac lesions
+
Antibiotic Therapy
• Effective antimicrobial treatment should lead
to defervescence within 7 – 10 days
– Persistent fever in:
• IE due to staph, pseudomonas, culture negative
• IE with microvascular complications/major emboli
• Intracardiac/extracardiac septic complications
• Drug reaction
Surgical Treatment of Intra-Cardiac
Complications
• Relative indications
– Perivalvular extension of infection
– Poorly responsive S. aureus NVE
– Relapse of NVE
– Culture negative NVE/PVE with persistent fever (>
10 days)
– Large (> 10mm) or hypermobile vegetation
– Endocarditis due to highly resistant enterococcus
2.3. IE.ppt
2.3. IE.ppt
2.3. IE.ppt

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2.3. IE.ppt

  • 2. Outlines • Definitions • Pathogenesis • Pathophysiology • Clinical features • Treatment • Prevention
  • 3. Definition Infectious Endocarditis (IE): • An infection of the heart’s endocardial surface • Vegetation – Variable in size – Amorphous mass of fibrin & platelets – Abundant organisms – Few inflammatory cells • Classified into four groups: • Native Valve IE • Prosthetic Valve IE • Intravenous drug abuse (IVDA) IE • Nosocomial IE
  • 4. PREDISPOSING CONDITIONS ASSOCIATED WITH INCREASED RISK OF ENDOCARDITIS More Common • Rheumatic heart disease • Mitral valve prolapse with murmur • Degenerative valvular disease • Intravenous drug use • Prosthetic valve • Congenital abnormalities (valvular or septal defect)
  • 5. Less Common • Hypertrophic obstructive cardiomyopathy • Pulmonary-systemic shunts • Coarctation of the aorta • Previous endocarditis
  • 6. Infecting Organisms Common bacteria – S. aureus – Streptococci – Enterococci Uncommon bacteria – Fungi – Pseudomonas – The HACEK grop » Haemophilus sp. » Actinobacillus » Cardiobacterium » Eikenella » Kingella
  • 7. Acute V Sub-acute • Acute – Toxic presentation – Progressive valve destruction & metastatic infection developing in days to weeks – Most commonly caused by S. aureus • Subacute – Mild toxicity – Presentation over weeks to months – Rarely leads to metastatic infection – Most commonly S. viridans or enterococcus
  • 8. Infective Endocarditis • Intravenous Drug Abuse - S. aureus – Increased frequency of gram negative infection such as P. aeruginosa & fungal infections – High concordance of HIV positivity & IE • HIV status does not in itself modify clinical picture • Survival is decreased if CD4 count < 200/mm3
  • 9. Pathophysiology • Turbulent blood flow disrupts the endocardium making it “sticky” • Bacteremia delivers the organisms to the endocardial surface • Adherence of the organisms to the endocardial surface • Eventual invasion of the valvular leaflets
  • 10. Infective Endocarditis • Pathology – NVE infection is largely confined to leaflets – PVE infection commonly extends beyond valve ring into annulus/periannular tissue • Ring abscesses • Septal abscesses • Fistulae • Prosthetic dehiscence
  • 11. Pathophysiology • Local destructive effects • Valvular distortion/destruction • Chordal rupture • Perforation/fistula formation • Paravalvular abscess • Conduction abnormalities • Purulent pericarditis • Functional valve obstruction
  • 12. • Clinical Features Clinical manifestations – Direct • Constitutional symptoms of infection (cytokine) – Indirect • Local destructive effects of infection • Embolization – septic or bland • Hematogenous seeding of infection » N.B. may present as local infection or persistent fever, metastatic abscesses may be small, miliary • Immune response » Immune complex or complement-mediated Clinical Features
  • 13. Clinical Features • Interval between index bacteremia & onset of sx’s usually < 2 weeks • Systemic manifestation like any other AFIs • Fever most common sign • Murmur present in 80 – 85% • Generally indication of underlying lesion • Frequently absent in tricuspid IE • Changing murmur
  • 14. Modified Duke criteria Major criteria include---- Table-I 1. Positive blood culture with typical IE microorganism, defined as one of the following: – Typical microorganism consistent with IE from 2 separate blood cultures, as noted below: • Viridans-group streptococci, or • Streptococcus bovis including nutritional variant strains, or • HACEK group, or • Staphylococcus aureus, or • Community-acquired Enterococci, in the absence of a primary focus – Microorganisms consistent with IE from persistently positive blood cultures defined as: • Two positive cultures of blood samples drawn >12 hours apart, or • All of 3 or a majority of 4 separate cultures of blood (with first and last sample drawn 1 hour apart) • Coxiella burnetii detected by at least one positive blood culture or antiphase I IgG antibody titer >1:800
  • 15. …Modified Duke criteria 2. Evidence of endocardial involvement with positive echocardiogram defined as – Oscillating intracardiac mass on valve or supporting structures, in the path of regurgitant jets, or on implanted material in the absence of an alternative anatomic explanation, or – Abscess, or – New partial dehiscence of prosthetic valve or new valvular regurgitation (worsening or changing of preexisting murmur)
  • 16. …Modified Duke criteria Minor criteria include: • Predisposing factor: known cardiac lesion, recreational drug injection • Fever >38°C • Evidence of embolism: arterial emboli, pulmonary infarcts, Janeway lesions, conjunctival hemorrhage • Immunological problems: glomerulonephritis, Osler's nodes • Positive blood culture (that doesn't meet a major criterion) or serologic evidence of infection with organism consistent with IE but not satisfying major criterion • Positive echocardiogram (that doesn't meet a major criterion) (this criterion has been removed from the modified Duke criteria)
  • 17.
  • 18. Classical Peripheral Manifestations • Less common today • Not seen in tricuspid endocarditis • Petechiae most common
  • 24.
  • 25. Clinical Features • Systemic emboli • Incidence decreases with effective anti-microbial Rx • Neurological sequelae • Embolic stroke 15 – 20% of patients • Mycotic aneurysm • Cerebritis • CHF • Due to mechanical disruption • High mortality without surgical intervention • Renal insufficiency • Immune complex mediated • Impaired hemodynamics/drug toxicity
  • 26.
  • 27. Additional Labs • CBC • ESR and CRP • Complement levels (C3, C4, CH50) • RF • U/A • Baseline chemistries and coags
  • 28. Imaging • Chest x-ray -Look for multiple focal infiltrates and calcification of heart valves • EKG-Rarely diagnostic Look for evidence of ischemia, conduction delay, and arrhythmias • Echocardiography TTE- - First line if suspected IE – Native valves • Transesophageal echocardiography (TEE) » Prosthetic valves » Intracardiac complications » Inadequate TTE » Fungal or S. aureus or bacteremi
  • 29. Goals of Therapy 1. Eradicate infection 2. Definitively treat sequelae of destructive intra-cardiac and extra-cardiac lesions
  • 30.
  • 31. +
  • 32. Antibiotic Therapy • Effective antimicrobial treatment should lead to defervescence within 7 – 10 days – Persistent fever in: • IE due to staph, pseudomonas, culture negative • IE with microvascular complications/major emboli • Intracardiac/extracardiac septic complications • Drug reaction
  • 33.
  • 34. Surgical Treatment of Intra-Cardiac Complications • Relative indications – Perivalvular extension of infection – Poorly responsive S. aureus NVE – Relapse of NVE – Culture negative NVE/PVE with persistent fever (> 10 days) – Large (> 10mm) or hypermobile vegetation – Endocarditis due to highly resistant enterococcus