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Cardiology 2 > Infective Endocarditis > Flashcards

Infective Endocarditis Flashcards

1
Q

Infective Endocarditis (IE)
Definition
Causes
Four groups

A

Definition

  • an infections of the hearts endocardial surface
  • typically involves the valves, but may involve any structure of the heart

Causes

  • Strep (most common)
  • -Strep Viridans is 40-50% of Strep IE
  • Staph (20%)
  • enterococcus (10-20%)
  • fastidious gram negative cocco-bacillary forms

Four groups

  • Native valve IE
  • Prosthetic Valve IE
  • Intravenous drug abuse (IVDA) IE
  • Nosocomial IE
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2
Q

Why are Staph, Strep, and Enterococcus such a problem?

A
  • 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
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3
Q

What is HACEK?

A
  • Haemophilis sp.
  • Actinobacillus
  • Cardiobacterium
  • Eikenella
  • Kingella
  • gram negative, slow growing, fastidious organisms that may need 3 weeks to grow out of culture
  • normal oral flora… leading cause of culture negative endocarditis
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4
Q

What is the most common gram negative bug that causes IE?

A

Pseudomonas aeruginosa

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5
Q

What is vegitation?

A

An amorphous mass of fibrin and platelets, abundant organisms, few inflammatory cells, variable in size

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6
Q

Describe acute IE.

subacute?

A

Acute IE

  • may affect normal heart valves
  • rapidly destructive
  • metastatic foci
  • commonly staph
  • if not treated, usually fatal within 6 weeks

Subacute IE

  • Usually affects damaged heart valves
  • indolent nature
  • if not treated, usually fatal by one year
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7
Q

NVE (native) vs PVE (prosthetic) infection sites

A

NVE
-infection is largely confined to leaflets

PVE
-infection commonly extends beyond valve ring into annulus/periannular tissue

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8
Q

IE

Pathophysiology

A

Pathophysiology

  1. Turbulent blood flow (from congenital or acquired heart disease) disrupts the endocardium making it “sticky” (platelets and fibrin deposit on damaged endothelium)…this would be Nonbacterial thrombotic endocarditis (NBTE)
  2. Bacteremia delivers the organisms to the endocardial surface
  3. Adherence of the organisms to the endocardial surface
  4. Eventual invasion of the valvular leaflets (bacterial vegetation)
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9
Q

Where are the lesions usually seen with Nonbacterial thrombotic endocarditis (NBTE)?

What is the Venturi Effect?

A

Usually at the coaptation (the drawing together of the separated tissue in a wound or fracture) points

  • atrial surface of the mitral/tricuspid
  • ventricular surface of aortic/pulmonic

-The Venturi effect is the reduction in fluid pressure that results when a fluid flows through a constricted section (or choke) of a pipe. (this is where bacteria are deposited)

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10
Q 
IE 
clinical manifestations (direct and indirect)
A

Direct
-constitutional sx of infection

Indirect

  • local destructive effects of infection (valvular distortion/destruction, chordal rupture, perforation/fistula formation, conduction abnormalities)
  • Embolization (clinically evident in 11-43%)
  • Hematogenous seeding of infection (may present as local infection or persistent fever,metastatic abscesses may be small)
  • immune response
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11
Q

Factors that influence the conversion of NBTE to IE

A
  • density of colonizing bacteria (oral over GU over GI)
  • disease state of surface
  • extent of trauma
  • resistance of organism to host defenses
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12
Q

Predisposing/risk factors of IE

A
  • male
  • MVP**
  • rheumatic heart disease
  • congenital heart disease
  • the majority for cases after the neonatal period are associated with an underlying congenital abnormality
  • IV drug abuse (staph aureus is predominant organism)
  • Prosthetic Valve Endocarditis
  • accquired heart defects
  • Intravascular catheters
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13
Q

IE
Acute sx
Subacute sx
General

A

Acute

  • high grade fever, chills
  • SOB
  • Arthralgias/myalgias
  • abdominal pain
  • pleuritic chest pain
  • back pain

Subscute

  • low grade fever
  • anorexia
  • weight loss
  • fatigue
  • arthralgias/myalgias
  • abd pain
  • n/v

*onset of sx is usually about 2 weeks or less from the initiating bacteremia

General

  • fever (most common)
  • heart murmur (new or change in existing one)
  • nonspecific signs (petechiae, subungal hemorrhages, clubbing, splenomegaly, neuro changes)
  • Osler’s nodes: painful, red, raised lesions on hands and feet (pads of fingers and toes)
  • Janeway lesions: nontender, red, macular (flat) or nodular (raised) lesions on palms and soles
  • Roth spots: white spot surrounded by red hemorrhage in the retina
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14
Q

IE

Acute vs subacute presentation

A

Acute

  • toxic presentation
  • progressive valve destruction and 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 entercoccus
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15
Q

Manifestations of IE

A
  • systemic emboli
  • neurological sequelae (embolic stroke, mycotic aneruysm, cerebritis)
  • CHF (d/t mechanical disruption)
  • Renal insufficiency (Immune complex mediated, impaired hemodynamics, drug toxcitity)
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16
Q

What are some of the classical peripheral manifestations of IE?

A
  • Petechiae (most common) (often located on extremities or mucous membranes)
  • Splinter Hemorrhages (nonblanching, linear red/brown lesions under the nail bed, do not extend the length of the nail)
  • Osler’s nodes (painful, red nodules on fingers and toes)
  • Janeway lesions (red, blanching macules, nonpainful, on palms and soles)
  • Roth spots (pale retinal lesions surrounded by hemorrhage)
17
Q

Work up for IE (labs, imaging)

A
  • blood cultures
  • CBC
  • ESR and CRP
  • Complement levels (C3, C4, and CH50)
  • RF
  • Urinalysis
  • baseline chemistries and coags
  • CXR (multiple focal infiltrates and calcification of heart valves)
  • EKG (rarely diagnostic)
  • echocardiography (TEE is more sensitive than TTE, although TTE is first line in suspected native valve IE, TEE for other complications such as prosthetic valves)
18
Q

What is the ESSENTIAL blood test for IE?

A

Blood cultures!

  • minimum of 3 sets
  • 3 separate venipuncture sites
  • obtain 10-20 mL in adults and 0.5-5mL in children

A positive result= typical organisms present in at least 2 separate samples

19
Q

What is Duke’s Critera used for?

A

determining Definite, Possible, or Rejected IE

20
Q

What are the four major complications of IE?

A
  • Embolic
  • Local spread of infection
  • Metastatic spread of infection
  • Formation of immune complexes: glomerulonephritis and arthritis
21
Q

Predictors of embolization in IE? Possible outcomes with embolization during IE?

A

Predictors

  • Size of vegetation
  • left sided vegetation
  • fungal pathogens, S. aureus, and Strep bovis

Possible outcomes

  • Stroke
  • Myocardial Infarction
  • Ischemic limbs
  • hypoxia from pulmonary emboli
  • abd pain
22
Q

Possible outcomes with metastatic spread of infection during IE?

A
  • Metastatic abscess (Kidney, spleen, brain, soft tissues)
  • meningitis and/or encephalitis
  • vertebral osteomyelitis
  • septic arthritis
  • pulmonary abscess (right sided endocarditis)
23
Q

Possible outcomes with local spread of infection during IE?

A
  • Heart Failure (d/t extensive valvular damage)
  • Paravalvular abscess
  • -most common in aortic valve, IVDA, and s. aureus
  • -may cause arrythmias
  • -higher rates of embolization and mortality
  • Pericarditis
  • Fistulous intracardiac connections
24
Q

Poor Prognostic factors for IE

A
  • female
  • s.aureus
  • vegetation size
  • prosthetic valve
  • older age
  • DM
  • low serum albumin
  • heart failure
25
Q

Treatment of IE

A
  • Parenteral abx
  • -high serum concentrations to penetrate vegetations
  • -prolonged tx to kill dominant bacteria clustered in vegetations
  • surgery
  • surveillance blood cultures
26
Q

If you suspect acute bacterial endocarditis, should you begin abx therapy before or after the blood cultures turn positive?

A

before

-start with broad spectrum and narrow from there. don’t wait to give abx, you can always withdraw them

27
Q

If there is a persistent fever in IE, you might suspect the cause to be…

A

a drug reaction

28
Q

How long are abx typically administered after IE? what route?

A

administered IV for 4-6 weeks (duration depends on pathogen)

29
Q

What is the drug of choice for most cases of viridians streptococcal endocarditis?

A

Penicillin

  • cure rate is above 90%
  • without tx, VSE is fatal within 6 months
  • quinolones or IV Vancomycin not recommended for prophylaxis d/t concern of creating new drug resistance
30
Q

What is the tx for fungal IE?

A

antifungals alone are not enough.

Usually, Amphotericin B is administered in conjunction with surgery

31
Q

For NYHA class III/IV CHF due to valve dysfunction and unstable prosthetic valve, surgery has a better mortality rate (less die) than medical management, true or false?

A

true

32
Q

Relative indications for surgery with IE

Indications

A

Relative

  • perivalvular extension of infection
  • poorly responsive S. aureus NVE
  • Relapse of NVE
  • culture negative NVE/PVE with persistent fever (greater than 10 days)
  • large (greater than 10 mm) or hypermobile vegetation

Indications

  • refractory CHF, severe valvular dysfunction
  • uncontrolled infection
  • valve perforation, dehiscence, fistula, abscess
  • 1 embolic event with persistent large vegetation, or more than one episode of embolization
  • prosthetic valve infection
  • fungal IE
  • new heart block
33
Q

IE prevention

A
  • dental procedures known to produce bleeding
  • tonsillectomy
  • surgery involving GU or resp mucosa
  • esophageal dilation
  • ERCP for obstruction
  • Gallbladder surgery
  • cystoscopy, urethral dilation, cath
  • I and D of infected tissue
34
Q

Who gets IE prophylaxis?

A
  • prosthetic valves
  • previous bacterial endocarditis
  • RHD and other acquired valve dysfunction
  • hypertrophic cardiomyopathy
  • MVP
  • prior IE
  • cyanotic congenital heart disease
  • surgical systemic-pulmonary shunts
  • VSD, PDA, AR, AS, MR, MS with MR
35
Q

Who are at the greatest risk of developing IE (2)?

A

IVDA and the elderly

Cardiology 2 (9 decks)

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