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Infective Endocarditis Flashcards

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1
Q

Definition of Infective endocarditis?

Classified into four groups. What are they?

A

an infection of the heart’s endocardial surface

Classified into four groups:

  1. Native Valve IE
  2. Prosthetic Valve IE
  3. Intravenous drug abuse (IVDA) IE
  4. Nosocomial IE
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2
Q

What part of the heart does endocarditis involve?

but may involve 3

A 
Typically involves the valves
May involve all structures of the heart
1. Chordae tendinae
2. Sites of shunting
3. Mural lesions
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3
Q

What bacteria cause endocarditis?

4

A

Majority of cases caused by

  1. streptococcus*****
  2. staphylococcus,
  3. enterococcus, or
  4. fastidious gram negative cocco-bacillary forms
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4
Q

Why are Staph, Strep, Enterococcus such a problem?

3 reasons

A
  1. They contain adhesins that attach to the fibrin platelet matrix of non-bacterial thrombotic endocarditis (NBTE)
  2. Adhesins also attach to the matrix proteins that coat implanted medical devices
  3. Bacterial extracellular structures form biofilm on surface of implanted devices
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5
Q

What is the most common gram negative organism that causes endocarditis?

Leading cause of culture negative endocarditis? 5

A

Pseudomonas aeruginosa most common

Normal oral flora…leading cause of culture negative endocarditis

  1. Haemophilus sp.
  2. Actinobacillus
  3. Cardiobacterium
  4. Eikenella
  5. Kingella
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6
Q

Clinical presentation of endocarditis?

4

A
  1. Febrile illness
  2. Persistent bacteremia
  3. A microbial infection of the endocardium
  4. Characteristic lesion of microbial infection of the endothelial surface of the heart (THE VEGETATION)
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7
Q

What is the vegetation made of?

A

Variable in size
Amorphous mass of fibrin & platelets
Abundant organisms
Few inflammatory cells

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8
Q

Acute IE:

  1. What does it affect?
  2. Onset of destruction?
  3. What kind of foci?
  4. What bacteria?
  5. Progressive of disease?
A
  1. May affect normal heart valves
  2. Rapidly destructive
  3. Metastatic foci
  4. Commonly Staph.
  5. If not treated, usually fatal within 6 weeks
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9
Q

Subacute IE:

  1. Affects what kind of valves?
  2. onset?
  3. Progession of disease?
A
  1. Usually affects damaged heart valves
  2. Indolent nature
  3. If not treated, usually fatal by one year
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10
Q

Endocarditis Pathology

  1. NVE infection is largely confined to ______?
  2. PVE infection commonly extends beyond valve ring into ________________ tissue?
  3. What will this cause? 4
  4. Invasive infection more common in ______ position and if onset is early
A
  1. leaflets
  2. annulus/periannular
    • Ring abscesses
    • Septal abscesses
    • Fistulae
    • Prosthetic dehiscence
  4. aortic
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11
Q
  1. WHAT disrupts the endocardium making it “sticky”?
  2. WHAT delivers the organisms to the endocardial surface?
  3. WHAT of the organisms to the endocardial surface?
  4. WHAT of the valvular leaflets?
A
  1. Turbulent blood flow
  2. Bacteremia
  3. Adherence
  4. Eventual invasion
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12
Q

Describe the three steps in the pathogenesis of infective endocarditis.

A

Endotheilial damage
Platelet-fibrin thrombi
Microorganism adherence

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13
Q

IE Pathogenesis

  1. Turbulent blood flow (from congenital or acquired heart dz) leads to?
  2. Platelets and fibrin deposit on damaged endothelium leads to?
  3. Bacteremia leads to? Which leads to?
A
  1. →Endothelial trauma
  2. → Nonbacterial Thrombotic Endocarditis (NBTE)
  3. → Colonization of NBTE → Bacterial Vegetation
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14
Q

Describe how nonbacterial thrombotic endocarditis occurs?
(what two things result in the problem and what is that problem)

3

A
  1. Endothelial injury
  2. Hypercoagulable state

lead to

  1. Platelet-fibrin thrombi
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15
Q

In nonbacterial thrombotic endocarditis what are seen at coaptation points of valves?
and where specifically? 2

A

LESIONS

  1. Atrial surface mitral/tricuspid
  2. Ventricular surface aortic/pulmonic
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16
Q

Modes of endothelial injury
in IE?
3

A
  1. High velocity jet
  2. Flow from high pressure to low pressure chamber
  3. Flow across narrow orifice of high velocity
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17
Q

Direct clinical manifestations of IE?

A
  1. Constitutional symptoms of infection (cytokines)
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18
Q

Indirect clinical manifestations of IE?

4

A
  1. Local destructive effects of infection
  2. Embolization – septic or bland
  3. Hematogenous seeding of infection
  4. Immune response
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19
Q

Describe the Hematogenous seeding of infection?

3

A

may present as

  1. local infection or
  2. persistent fever,
  3. metastatic abscesses may be small, miliary
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20
Q

Local destructive effects
of IE?
7

A
  1. Valvular distortion/destruction
  2. Chordal rupture
  3. Perforation/fistula formation
  4. Paravalvular abscess
  5. Conduction abnormalities
  6. Purulent pericarditis
  7. Functional valve obstruction
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21
Q

High risk for embolization
in IE. How do they present?
4

A
  1. Large > 10 mm vegetation
  2. Hypermobile vegetation
  3. Mitral vegetations (esp. anterior leaflet)
  4. Pulmonary (septic) – 65 – 75% of i.v. drug abusers with tricuspid IE
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22
Q

COnversion of NBTE to IE is determined by?

2

A
  1. Frequency & magnitude of bacteremia

2. Resistance of organism to host defenses

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23
Q

Frequency & magnitude of bacteremia is characterized by what?
3

A
  1. Density of colonizing bacteria
    - -Oral > GU > GI
  2. Disease state of surface
    - -Infected surface > colonized surface
  3. Extent of trauma
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24
Q

Resistance of organism to host defenses is characterized by what?

(Describe the bacteria 2 and name some types -2 kinds)
4

A
  1. Most aerobic gram negatives susceptible to complement-mediated bactericidal effect of serum
  2. Tendency to adhere to endothelium
  3. Dextran producing strep
  4. Fibronectin receptors on staph, enterococcus, strep, Candida
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25
55-75% of patients with native valve endocarditis (NVE) have underlying valve abnormalities such as? 5 What is the most prominent predisposing factor?
1. MVP*** 2. History of rheumatic fever 3. Congenital 4. Asymmetric atrial hypertrophy 5. i.v. drug abuse
26
In IE caused by Rheumatic heart disease what is the most common site for men? women? What valves are often affected in congential heart disease? 3
Mitral site more common in women Aortic site more common in men 1. PDA, 2. VSD, 3. bicuspid aortic valve
27
The vast majority (75-90%) of cases after the neonatal period are associated with an underlying congenital abnormality such as? 3 What are the most common bacterias? Neonates? 3 Older children? 2
1. Aortic valve 2. VSD 3. Tetralogy of Fallot Neonates: 1. S. aureus, 2. coagulase negative staph, 3. group B strep Older children: 1. 40% strep & 2. S. aureus
28
IE for drug users tends to affect which valves? Predominant organism?
right sided S. aureus
29
Prosthetic Valve Endocarditis (PVE) 1. Early PVE – within 60 days. Which organism? 2. Late PVE – after 60 days Which organism?
1. Nosocomial (S. epidermidis predominates) | 2. Community (same organisms as NVE)
30
Top three Risk Factors for IE? 3
1. IVDA, 2 prosthetic heart valves and pacemakers 3. structural heart disease.
31
Symtpoms of acute IE? | 6
1. High grade fever and chills 2. SOB 3. Arthralgias/ myalgias 4. Abdominal pain 5. Pleuritic chest pain 6. Back pain
32
Symptoms of subacute IE? 7 The onset of symptoms is usually how long from infection?
1. Low grade fever 2. Anorexia 3. Weight loss 4. Fatigue 5. Arthralgias/ myalgias 6. Abdominal pain 7. N/V ~2 weeks or less from the initiating bacteremia
33
IE clinical presentation: Acute 1. _____ presentation 2. What is developing in days to weeks? 2 3. Most commonly caused by _ ______? Subacute 1. Mild _____? 2. Presentation over how long? 3. Rarely leads to _______ infection 4. Most commonly what two bacteria?
1. Toxic 2. Progressive valve destruction & metastatic infection 3. S. aureus 1. toxicity 2. weeks to months 3. metastatic 4. S. viridans or enterococcus
34
1. What is the most common sign? 2. What is present in 80-85% of cases but often absent in tricuspid IE? 3. Nonspecific signs of IE? 5 4. More specific signs? 3
1. Fever 2. Heart Murmur 3. - petechiae**** - subungal or “splinter” hemorrhages (on finger) - clubbing - splenomegaly - neurologic changes 4. - Osler’s Nodes, - Janeway lesions - Roth Spots
35
Clinical Features of IE? 4
1. Systemic emboli 2. Neurological sequelae (Mycotic aneurysm, Cerebritis) 3. CHF (high mortality) 4. Renal insufficiency (immune mediated)
36
What are Janeway lesions? | 3
1. Erythematous, blanching macules 2. Nonpainful 3. Located on palms and soles
37
What are Roth spots?
Pale retinal lesions surrounded by hemorrhage, usually near optic disk
38
The workup for IE? | 2
1. Blood cultures 2. Echocardiography TTE – 60% sensitivity TEE – 80 – 95% sensitive
39
Whats the minimum number of cultures? What is considered a positive result? 2
Minimum of three blood cultures Three separate venipuncture sites Obtain 10-20mL in adults and 0.5-5mL in children2 1. Typical organisms present in at least 2 separate samples 2. Persistently positive blood culture (atypical organisms)
40
Additional Labs for IE? 6
1. CBC 2. ESR and CRP 3. Complement levels (C3, C4, CH50) 4. RF 5. Urinalysis 6. Baseline chemistries and coags
41
What are we looking for with the following in IE: 1. CBC 2 2. ESR and CRP 3. RF 4. Urinalysis
1. normochromic normocytic anemia and/or a leukocytosis. 2. Look for an elevated erythrocyte sedimentation rate and/or an elevated C-reactive protein which are present 90-100% of the time. 3. elevated particularly in patients who have been infected for six weeks or more 4. microscopic or gross hematuria, proteinuria, and pyuria. These findings along with a low serum complement level indicate a glomerulonephritis or “immunologic phenomena”. (Minor Duke’s Criteria)
42
Imaging for IE: CXR? EKG? ECHO
1. Chest x-ray Look for multiple focal infiltrates ``` 2. EKG Rarely diagnostic Look for evidence of -ischemia, -conduction delay, and -arrhythmias ```
43
Indications for Echocardiography TTE? 2 TEE? 4
TTE 1. First line if suspected IE 2. Native valves TEE - Prosthetic valves - Intracardiac complications - Inadequate TTE - Fungal or S. aureus or bacteremia
44
Major Duke’s Criteria for IE | 3
1. (+) blood cultures with appropriate organism 2. Echo findings 3. (New valvular regurgitation)
45
DUKE's CRITERIA: 1. Definite IE 2. Possible IE 3. Rejected IE
1. Microorganism (via culture or histology) in a valvular vegetation, embolized vegetation, or intracardiac abscess Histologic evidence of vegetation or intracardiac abscess 2. 2 major 1 major and 3 minor 5 minor 3. Resolution of illness with four days or less of antibiotics
46
Four major complications for IE? 4
1. Embolic 2. Local spread of infection 3. Metastatic spread of infection 4. Formation of immune complexes – glomerulonephritis and arthritis
47
1. Embolic complications occur in what % of pts? 2. Predictors of embolization? 3 3. Incidence decreases significantly after initiation of?
1. Occur in up to 40% of patients with IE 2. Predictors of embolization - Size of vegetation - Left-sided vegetations - Fungal pathogens, S. aureus, and Strep. bovis 3. effective antibiotics
48
What kind of embolic complications are we taking about? | 5
1. Stroke 2. Myocardial Infarction - -Fragments of valvular vegetation or vegetation-induced stenosis of coronary ostia 3. Ischemic limbs 4. Hypoxia from pulmonary emboli 5. Abdominal pain (splenic or renal infarction)
49
Additional Metastatic Spread of Infection | 5
1. Metastatic abscess - -Kidneys, spleen, brain, soft tissues 2. Meningitis and/or encephalitis 3. Vertebral osteomyelitis 4. Septic arthritis 5. Pulmonary abscess (R. sided endocarditis)
50
Local Spread of Infection | 4
1. Heart failure - -from extensive valvular damage 2. Paravalvular abscess (30-40%) 3. Pericarditis 4. Fistulous intracardiac connections
51
1. Paravalvular abscess (30-40%) is most common in? 3 2. May extend to where? 3. Higher rates of what?
1. Most common in - aortic valve, - IVDA, and - S. aureus 2. May extend into adjacent conduction tissue causing arrythmias 3. Higher rates of embolization and mortality
52
Poor Prognostic Factors 12
1. Female 2. S. aureus 3. Vegetation size 4. Aortic valve 5. Prosthetic valve 6. Older age 7. Diabetes mellitus 8. Low serum albumin 9. Apache II (Acute Physiology and Chronic Health Evaluation) score 10. Heart failure 11. Paravalvular abscess 12. Embolic events
53
Treatment | 3
1. Parenteral antibiotics 2. Surgery 3. Surveillance
54
What kind of parenteral antibiotics? | 2
1. High serum concentrations to penetrate vegetations | 2. Prolonged treatment to kill dormant bacteria clustered in vegetations
55
Goals of Therapy 2
1. Eradicate infection | 2. Definitively treat sequelae of destructive intra-cardiac and extra-cardiac lesions
56
Treatment tailored to etiologic agent (how is it tailored)? | 2
- Important to note MIC/MBC relationship for each causative organism and the antibiotic used - High serum concentration necessary to penetrate avascular vegetation
57
Antibiotic Therapy needs to be when? 2
Treatment before blood cultures turn positive 1. Suspected Acute Bacterial Endocarditis 2. Hemodynamic instability
58
Antibiotic Therapy Effective antimicrobial treatment should lead to defervescence within what time period? Persistent fever? Then its due to what? 4
7 – 10 days 1. IE due to staph, pseudomonas, culture negative 2. IE with microvascular complications/major emboli 3. Intracardiac/extracardiac septic complications 4. Drug reaction
59
1. How long will antobiotics be administered for? | 2. Drug of choice?
1. Antibiotics are usually administered intravenously for 4-6 weeks. Duration depends on the virulence of the pathogen. 2. The drug of choice for most cases of viridians streptococcal endocarditis is penicillin.
60
Antifungals alone are not enough to cure fungal IE, although ___________ ___ is often administered in conjunction with surgery.
Amphotericin B
61
What about resistant Strep Viridans? | 3
PCN-Resistance: 13% Macrolide-Resistance: 26% Clindamycin-Resistance: 4%
62
Surgical Treatment of Intra-Cardiac Complications: Relative Indications? 7
1. Perivalvular extension of infection 2. Poorly responsive S. aureus 3 NVE 4. Relapse of NVE 5. Culture negative NVE/PVE with persistent fever (> 10 days) 6. Large (> 10mm) or hypermobile vegetation 7. Endocarditis due to highly resistant enterococcus
63
IE: Indications for surgery? | 7
1. Refractory CHF, Severe valvular dysfunction 2. Uncontrolled infection 3. Valve perforation, dehiscence, fistula, abscess 4. 1 embolic event with persistent large vegetation, or >1 episode of embolization 5. Prosthetic valve infection 6. Fungal IE 7. New heart block…
64
Prevention – the procedure When should we give prophylactic antibiotics? 10
1. Dental procedures known to produce bleeding 2. Tonsillectomy 3. Surgery involving GI, respiratory mucosa 4. Esophageal dilation 5. ERCP for obstruction 6. Gallbladder surgery 7. Cystoscopy, urethral dilation 8. Urethral catheter if infection present 9. Urinary tract surgery, including prostate 10. I&D of infected tissue
65
Prevention – the underlying lesion HIGH RISK LESIONS? (what are the 4 highest) Intermediate risk lesions? 6
1. Prosthetic valves 2. Prior IE 3. Cyanotic congenital heart disease 4. Surgical systemic-pulmonary shunts 5. PDA 6. AR, AS, MR,MS with MR 7. VSD 8. Coarctation 1. MVP with murmur 2. Pure MS 3. Tricuspid disease 4. Pulmonary stenosis 5. ASH 6. Bicuspid aortic valve with no hemodynamic significance
66
Prophylactic regimen targeted against likely organism What organism is likely in the following areas: 1. Oral, respiratory, eosphogeal? 2. Genitourinary, gastrointestinal? 3. Infected skin, mucosal surfaces?
1. Strep. viridans 2. Strep. viridans 3. Strep. viridans
67
Antimicrobial Prophylaxis Recommended in patients considered high-risk such as? 5
1. prosthetic valves 2. previous bacterial endocarditis 3. RHD and other acquired valve dysfunction 4. hypertrophic cardiomyopathy 5. MVP
68
Endocarditis Prophylaxis (no need to memorize….NOW) For Dental, Oral, Respiratory and Esophageal Procedures: 1. Standard Regimen? 1 2. Unable to take oral meds? 1 3. Allergic to Penicillin? 3 4. Allergic to penicillin and unable to take oral medications? 2
1. Amoxicillin; Adult 2.0 g: Child 50 mg/kg orally1 hr before procedure 2. Ampicillin; Adult 2.0 g; child 50 mg/kg IM or IV 30 min before procedure 3. - Clindamycin; Adult 600 mg; child 20 mg/kg orally 1 hour before procedure - Cefalexin; Adult 2.0 g; child 50mg/kg orally 1 hour before procedure - Azithromycin or Clarithromycin; Adult 500 mg; child 15 mg/kg orally 1 hour before procedure 4. - Clindamycin; Adult 600 mg; child 20 mg/kg IV within 30 min before procedure - Cefazolin; Adult 1.0 g; child 25 mg/kg IM or IV within 30 min before procedure
69
For GI/GU (excluding esophageal) Procedures: Dont memorize! 4
High Risk Patient: HIgh risk pts: -Amp & Gent; Adult 2 g IM/IV plus gent 1.5 mg/kg (not to exceed 120 mg) within 30 min of starting procedure; 6 hr later amp 1 g IM/IV or amox 1 g orally. High Risk pt allergic to PCN -Vanc plus Gent; Adult 1 g vanc IV over 1-2 hrs plus gent (IM/IV)1.5 mg/kg (not to exceed 120 mg)) complete injection/infusion within 30 min of starting the procedure Moderate Risk Patient: -Amox or amp; Adult amox 2.0 g orally 1 hr before procedure or amp 2.0 gm IM/IV within 30 of starting the procedure Moderate Risk Patient allergic to PCN -Vancomycin; Adult 1.0 g IV over 1 to 2 hrs; complete infusion within 30 min of starting procedure.
70
1. Who are at greatest risk for developing IE?
1. IVDA and the elderly
Cardiology
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