Infective Endocarditis Flashcards Preview

Cardiology 2 > Infective Endocarditis > Flashcards

Flashcards in Infective Endocarditis Deck (35)
Loading flashcards...
1

Infective Endocarditis (IE)
Definition
Causes
Four groups

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

2

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

-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

3

What is HACEK?

-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

4

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

Pseudomonas aeruginosa

5

What is vegitation?

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

6

Describe acute IE.
subacute?

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

7

NVE (native) vs PVE (prosthetic) infection sites

NVE
-infection is largely confined to leaflets

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

8

IE
Pathophysiology

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)

9

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

What is the Venturi Effect?

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)

10

IE
clinical manifestations (direct and indirect)

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

11

Factors that influence the conversion of NBTE to IE

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

12

Predisposing/risk factors of IE

-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

13

IE
Acute sx
Subacute sx
General

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

14

IE
Acute vs subacute presentation

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

15

Manifestations of IE

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

16

What are some of the classical peripheral manifestations of IE?

-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

Work up for IE (labs, imaging)

-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

What is the ESSENTIAL blood test for IE?

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

What is Duke's Critera used for?

determining Definite, Possible, or Rejected IE

20

What are the four major complications of IE?

-Embolic
-Local spread of infection
-Metastatic spread of infection
-Formation of immune complexes: glomerulonephritis and arthritis

21

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

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

Possible outcomes with metastatic spread of infection during IE?

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

23

Possible outcomes with local spread of infection during IE?

-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

Poor Prognostic factors for IE

-female
- s.aureus
-vegetation size
-prosthetic valve
-older age
-DM
-low serum albumin
-heart failure

25

Treatment of IE

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

26

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

before

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

27

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

a drug reaction

28

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

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

29

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

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

What is the tx for fungal IE?

antifungals alone are not enough.

Usually, Amphotericin B is administered in conjunction with surgery