Infective Endocarditis Flashcards
Definition of Infective endocarditis?
Classified into four groups. What are they?
an infection of the heart’s endocardial surface
Classified into four groups:
- Native Valve IE
- Prosthetic Valve IE
- Intravenous drug abuse (IVDA) IE
- Nosocomial IE
What part of the heart does endocarditis involve?
but may involve 3
Typically involves the valves May involve all structures of the heart 1. Chordae tendinae 2. Sites of shunting 3. Mural lesions
What bacteria cause endocarditis?
4
Majority of cases caused by
- streptococcus*****
- staphylococcus,
- enterococcus, or
- fastidious gram negative cocco-bacillary forms
Why are Staph, Strep, Enterococcus such a problem?
3 reasons
- They contain adhesins that attach to the fibrin platelet matrix of non-bacterial thrombotic endocarditis (NBTE)
- Adhesins also attach to the matrix proteins that coat implanted medical devices
- Bacterial extracellular structures form biofilm on surface of implanted devices
What is the most common gram negative organism that causes endocarditis?
Leading cause of culture negative endocarditis? 5
Pseudomonas aeruginosa most common
Normal oral flora…leading cause of culture negative endocarditis
- Haemophilus sp.
- Actinobacillus
- Cardiobacterium
- Eikenella
- Kingella
Clinical presentation of endocarditis?
4
- Febrile illness
- Persistent bacteremia
- A microbial infection of the endocardium
- Characteristic lesion of microbial infection of the endothelial surface of the heart (THE VEGETATION)
What is the vegetation made of?
Variable in size
Amorphous mass of fibrin & platelets
Abundant organisms
Few inflammatory cells
Acute IE:
- What does it affect?
- Onset of destruction?
- What kind of foci?
- What bacteria?
- Progressive of disease?
- May affect normal heart valves
- Rapidly destructive
- Metastatic foci
- Commonly Staph.
- If not treated, usually fatal within 6 weeks
Subacute IE:
- Affects what kind of valves?
- onset?
- Progession of disease?
- Usually affects damaged heart valves
- Indolent nature
- If not treated, usually fatal by one year
Endocarditis Pathology
- NVE infection is largely confined to ______?
- PVE infection commonly extends beyond valve ring into ________________ tissue?
- What will this cause? 4
- Invasive infection more common in ______ position and if onset is early
- leaflets
- annulus/periannular
- Ring abscesses
- Septal abscesses
- Fistulae
- Prosthetic dehiscence
- aortic
- WHAT disrupts the endocardium making it “sticky”?
- WHAT delivers the organisms to the endocardial surface?
- WHAT of the organisms to the endocardial surface?
- WHAT of the valvular leaflets?
- Turbulent blood flow
- Bacteremia
- Adherence
- Eventual invasion
Describe the three steps in the pathogenesis of infective endocarditis.
Endotheilial damage
Platelet-fibrin thrombi
Microorganism adherence
IE Pathogenesis
- Turbulent blood flow (from congenital or acquired heart dz) leads to?
- Platelets and fibrin deposit on damaged endothelium leads to?
- Bacteremia leads to? Which leads to?
- →Endothelial trauma
- → Nonbacterial Thrombotic Endocarditis (NBTE)
- → Colonization of NBTE → Bacterial Vegetation
Describe how nonbacterial thrombotic endocarditis occurs?
(what two things result in the problem and what is that problem)
3
- Endothelial injury
- Hypercoagulable state
lead to
- Platelet-fibrin thrombi
In nonbacterial thrombotic endocarditis what are seen at coaptation points of valves?
and where specifically? 2
LESIONS
- Atrial surface mitral/tricuspid
- Ventricular surface aortic/pulmonic
Modes of endothelial injury
in IE?
3
- High velocity jet
- Flow from high pressure to low pressure chamber
- Flow across narrow orifice of high velocity
Direct clinical manifestations of IE?
- Constitutional symptoms of infection (cytokines)
Indirect clinical manifestations of IE?
4
- Local destructive effects of infection
- Embolization – septic or bland
- Hematogenous seeding of infection
- Immune response
Describe the Hematogenous seeding of infection?
3
may present as
- local infection or
- persistent fever,
- metastatic abscesses may be small, miliary
Local destructive effects
of IE?
7
- Valvular distortion/destruction
- Chordal rupture
- Perforation/fistula formation
- Paravalvular abscess
- Conduction abnormalities
- Purulent pericarditis
- Functional valve obstruction
High risk for embolization
in IE. How do they present?
4
- Large > 10 mm vegetation
- Hypermobile vegetation
- Mitral vegetations (esp. anterior leaflet)
- Pulmonary (septic) – 65 – 75% of i.v. drug abusers with tricuspid IE
COnversion of NBTE to IE is determined by?
2
- Frequency & magnitude of bacteremia
2. Resistance of organism to host defenses
Frequency & magnitude of bacteremia is characterized by what?
3
- Density of colonizing bacteria
- -Oral > GU > GI - Disease state of surface
- -Infected surface > colonized surface - Extent of trauma
Resistance of organism to host defenses is characterized by what?
(Describe the bacteria 2 and name some types -2 kinds)
4
- Most aerobic gram negatives susceptible to complement-mediated bactericidal effect of serum
- Tendency to adhere to endothelium
- Dextran producing strep
- Fibronectin receptors on staph, enterococcus, strep, Candida
55-75% of patients with native valve endocarditis (NVE) have underlying valve abnormalities
such as?
5
What is the most prominent predisposing factor?
- MVP***
- History of rheumatic fever
- Congenital
- Asymmetric atrial hypertrophy
- i.v. drug abuse
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
- PDA,
- VSD,
- bicuspid aortic valve
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
- Aortic valve
- VSD
- Tetralogy of Fallot
Neonates:
- S. aureus,
- coagulase negative staph,
- group B strep
Older children:
- 40% strep &
- S. aureus
IE for drug users tends to affect which valves?
Predominant organism?
right sided
S. aureus
Prosthetic Valve Endocarditis (PVE)
1. Early PVE – within 60 days. Which organism?
2. Late PVE – after 60 days
Which organism?
- Nosocomial (S. epidermidis predominates)
2. Community (same organisms as NVE)
Top three Risk Factors
for IE?
3
- IVDA,
2 prosthetic heart valves and pacemakers - structural heart disease.
Symtpoms of acute IE?
6
- High grade fever and chills
- SOB
- Arthralgias/ myalgias
- Abdominal pain
- Pleuritic chest pain
- Back pain
Symptoms of subacute IE?
7
The onset of symptoms is usually how long from infection?
- Low grade fever
- Anorexia
- Weight loss
- Fatigue
- Arthralgias/ myalgias
- Abdominal pain
- N/V
~2 weeks or less
from the initiating bacteremia
IE clinical presentation:
Acute
- _____ presentation
- What is developing in days to weeks? 2
- Most commonly caused by _ ______?
Subacute
- Mild _____?
- Presentation over how long?
- Rarely leads to _______ infection
- Most commonly what two bacteria?
- Toxic
- Progressive valve destruction & metastatic infection
- S. aureus
- toxicity
- weeks to months
- metastatic
- S. viridans or enterococcus
- What is the most common sign?
- What is present in 80-85% of cases but often absent in tricuspid IE?
- Nonspecific signs of IE? 5
- More specific signs? 3
- Fever
- Heart Murmur
- petechiae**
- subungal or “splinter” hemorrhages (on finger)
- clubbing
- splenomegaly
- neurologic changes
- Osler’s Nodes,
- Janeway lesions
- Roth Spots
Clinical Features
of IE?
4
- Systemic emboli
- Neurological sequelae (Mycotic aneurysm, Cerebritis)
- CHF (high mortality)
- Renal insufficiency (immune mediated)
What are Janeway lesions?
3
- Erythematous, blanching macules
- Nonpainful
- Located on palms and soles
What are Roth spots?
Pale retinal lesions surrounded by hemorrhage, usually near optic disk
The workup for IE?
2
- Blood cultures
- Echocardiography
TTE – 60% sensitivity
TEE – 80 – 95% sensitive
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
- Typical organisms present in at least 2 separate samples
- Persistently positive blood culture (atypical organisms)
Additional Labs
for IE?
6
- CBC
- ESR and CRP
- Complement levels (C3, C4, CH50)
- RF
- Urinalysis
- Baseline chemistries and coags
What are we looking for with the following in IE:
- CBC 2
- ESR and CRP
- RF
- Urinalysis
- normochromic normocytic anemia and/or a leukocytosis.
- Look for an elevated erythrocyte sedimentation rate and/or an elevated C-reactive protein which are present 90-100% of the time.
- elevated particularly in patients who have been infected for six weeks or more
- 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)
Imaging for IE:
CXR?
EKG?
ECHO
- Chest x-ray
Look for multiple focal infiltrates
2. EKG Rarely diagnostic Look for evidence of -ischemia, -conduction delay, and -arrhythmias
Indications for Echocardiography
TTE? 2
TEE? 4
TTE
- First line if suspected IE
- Native valves
TEE
- Prosthetic valves
- Intracardiac complications
- Inadequate TTE
- Fungal or S. aureus or bacteremia
Major Duke’s Criteria for IE
3
- (+) blood cultures with appropriate organism
- Echo findings
- (New valvular regurgitation)
DUKE’s CRITERIA:
1. Definite IE
- Possible IE
- Rejected IE
- Microorganism (via culture or histology) in a valvular vegetation, embolized vegetation, or intracardiac abscess
Histologic evidence of vegetation or intracardiac abscess - 2 major
1 major and 3 minor
5 minor - Resolution of illness with four days or less of antibiotics
Four major complications
for IE?
4
- Embolic
- Local spread of infection
- Metastatic spread of infection
- Formation of immune complexes – glomerulonephritis and arthritis
- Embolic complications occur in what % of pts?
- Predictors of embolization? 3
- Incidence decreases significantly after initiation of?
- Occur in up to 40% of patients with IE
- Predictors of embolization
- Size of vegetation
- Left-sided vegetations
- Fungal pathogens, S. aureus, and Strep. bovis - effective antibiotics
What kind of embolic complications are we taking about?
5
- Stroke
- Myocardial Infarction
- -Fragments of valvular vegetation or vegetation-induced stenosis of coronary ostia - Ischemic limbs
- Hypoxia from pulmonary emboli
- Abdominal pain (splenic or renal infarction)
Additional Metastatic Spread of Infection
5
- Metastatic abscess
- -Kidneys, spleen, brain, soft tissues - Meningitis and/or encephalitis
- Vertebral osteomyelitis
- Septic arthritis
- Pulmonary abscess (R. sided endocarditis)
Local Spread of Infection
4
- Heart failure
- -from extensive valvular damage - Paravalvular abscess (30-40%)
- Pericarditis
- Fistulous intracardiac connections
- Paravalvular abscess (30-40%)
is most common in? 3 - May extend to where?
- Higher rates of what?
- Most common in
- aortic valve,
- IVDA, and
- S. aureus - May extend into adjacent conduction tissue causing arrythmias
- Higher rates of embolization and mortality
Poor Prognostic Factors
12
- Female
- S. aureus
- Vegetation size
- Aortic valve
- Prosthetic valve
- Older age
- Diabetes mellitus
- Low serum albumin
- Apache II (Acute Physiology and Chronic Health Evaluation) score
- Heart failure
- Paravalvular abscess
- Embolic events
Treatment
3
- Parenteral antibiotics
- Surgery
- Surveillance
What kind of parenteral antibiotics?
2
- High serum concentrations to penetrate vegetations
2. Prolonged treatment to kill dormant bacteria clustered in vegetations
Goals of Therapy
2
- Eradicate infection
2. Definitively treat sequelae of destructive intra-cardiac and extra-cardiac lesions
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
Antibiotic Therapy
needs to be when?
2
Treatment before blood cultures turn positive
- Suspected Acute Bacterial Endocarditis
- Hemodynamic instability
Antibiotic Therapy
Effective antimicrobial treatment should lead to defervescence within what time period?
Persistent fever? Then its due to what? 4
7 – 10 days
- IE due to staph, pseudomonas, culture negative
- IE with microvascular complications/major emboli
- Intracardiac/extracardiac septic complications
- Drug reaction
- How long will antobiotics be administered for?
2. Drug of choice?
- Antibiotics are usually administered intravenously for 4-6 weeks. Duration depends on the virulence of the pathogen.
- The drug of choice for most cases of viridians streptococcal endocarditis is penicillin.
Antifungals alone are not enough to cure fungal IE, although ___________ ___ is often administered in conjunction with surgery.
Amphotericin B
What about resistant Strep Viridans?
3
PCN-Resistance: 13%
Macrolide-Resistance: 26%
Clindamycin-Resistance: 4%
Surgical Treatment of Intra-Cardiac Complications:
Relative Indications?
7
- Perivalvular extension of infection
- Poorly responsive S. aureus
3 NVE - Relapse of NVE
- Culture negative NVE/PVE with persistent fever (> 10 days)
- Large (> 10mm) or hypermobile vegetation
- Endocarditis due to highly resistant enterococcus
IE: Indications for surgery?
7
- Refractory CHF, Severe valvular dysfunction
- Uncontrolled infection
- Valve perforation, dehiscence, fistula, abscess
- 1 embolic event with persistent large vegetation, or >1 episode of embolization
- Prosthetic valve infection
- Fungal IE
- New heart block…
Prevention – the procedure
When should we give prophylactic antibiotics?
10
- Dental procedures known to produce bleeding
- Tonsillectomy
- Surgery involving GI, respiratory mucosa
- Esophageal dilation
- ERCP for obstruction
- Gallbladder surgery
- Cystoscopy, urethral dilation
- Urethral catheter if infection present
- Urinary tract surgery, including prostate
- I&D of infected tissue
Prevention – the underlying lesion
HIGH RISK LESIONS? (what are the 4 highest)
Intermediate risk lesions? 6
- Prosthetic valves
- Prior IE
- Cyanotic congenital heart disease
- Surgical systemic-pulmonary shunts
- PDA
- AR, AS, MR,MS with MR
- VSD
- Coarctation
- MVP with murmur
- Pure MS
- Tricuspid disease
- Pulmonary stenosis
- ASH
- Bicuspid aortic valve with no hemodynamic significance
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?
- Strep. viridans
- Strep. viridans
- Strep. viridans
Antimicrobial Prophylaxis
Recommended in patients considered high-risk such as?
5
- prosthetic valves
- previous bacterial endocarditis
- RHD and other acquired valve dysfunction
- hypertrophic cardiomyopathy
- MVP
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
- Allergic to Penicillin? 3
- Allergic to penicillin and unable to take oral medications? 2
- Amoxicillin; Adult 2.0 g: Child 50 mg/kg orally1 hr before procedure
- Ampicillin; Adult 2.0 g; child 50 mg/kg IM or IV 30 min before procedure
- 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
- 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
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.
- Who are at greatest risk for developing IE?
- IVDA and the elderly
