infective endocarditis Flashcards
1
Q
What is IE?
A
- an infection of the heart’s endocardial surface
2
Q
What are th 4 groups of IE?
A
- NVE
- PVE
- IVDAE
- nosocomial IE
3
Q
What part of the heart does IE usually involve?-
A
valves but also may involve all structures of the heart:
chordae tendinae, sites of shunting, and mural lesions
- infection of vascular shunts is endarteritis but the lesion is the same
4
Q
What bugs are most responsible for IE?
A
- strep (most common) 60% of cases, Viridans strep (40-50% of strep IE), S. sanguis and S. mitis each account for 30-50% of these cases caused by oral viridans streptococci
- staph (10-20% of cases), enterococcus (10-20%)
or fastidious gram negative cocco-bacillary forms
5
Q
Why are staph, strep and enterococcus such a problem in IE?
A
- they contain adhesins that attach to the fibrin platelet matrix of non-bacterial thrombotic endocarditis (NBTE)
- adhesions also attach to the matrix proteins that coat implanted medical devices
- bacterial extracellular structures form biofilm on surface of implanted devices
6
Q
What gram negative organims are a problem in IE?
A
- pseudomonas aeruginosa: most comon
- HACEK: slow growing, fastidious organisms that may need 3 weeks to grow out of culture
normal oral flora - leading cause of culture negative endocarditis:
Haemophilus
actinobacillus
cardiobacterium
eikenella
kingella
7
Q
Characteristics of IE?
A
- febrile illness
- persistent bacteremia
- a microbial infection of the endocardium
- characteristic lesion of microbial infection of the endothelial surface of the heart
8
Q
Vegetation of IE?
A
- variable in size
- amorphous mass of fibrin and platelets
- abundant organisms
- few inflammatory cells
9
Q
Classification of acute IE?
A
- may affect normal valves
- rapidly destructive
- metastatic foci
- commonly staph
- if not tx: usually fatal within 6 weeks
- commonly tricuspid valve
10
Q
Classification of subacute IE?
A
- usually affects damaged heart valves
- indolent nature
- if not tx: usually fatal by one year
- can persist for months until sxs appear
11
Q
Pathology of infective endocarditis?
A
- NVE infection: largely confined to leaflets
- PVE: commonly extends beyond valve ring into annulus/periannular tissue: ring abscesses, septal abscesses, fistulae, prosthetic dehiscence (sutures pull out of valve)
- invasive infection more common in aortic position and if onset is early
12
Q
Pathophys of IE?
A
- 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
13
Q
pathogenesis of IE?
A
- enodthelial damage from turbulent blood flow (congenital or acquired heat dz) leads to platelet-fibrin thrombi that deposit on damaged endothelium - NBTE - bacteremia - colonization of NBTE - to bacterial vegetation
14
Q
Process of NBTE?
A
- endothelial injury and hypercoaguabe state - goes on to form platelet fibrin thrombi
- lesions seen at coaption pts of valves: atrial surface mitral/tricuspid
- ventricular surface aortic/pulmonic
15
Q
What are the modes of endothelial injury?
A
- high velocity jet (hitting opposite wall)
- flow from high pressure to low pressure
- flow across narrow orfice of high velocity (small ventricular defect more prone to develop endocarditis than large one)
- bacteria deposited on edges of low pressure sink or are at site of jet impaction (Venturi effect)
16
Q
Clinical manifestations of IE?
A
- direct: constitutional sxs of infection (cytokines)
- indirect: local destructive effects of infection
embolization - septic or bland
hematogenous seeding of infection: may present as local infection or persistent fever, metastatic abscesses may be small, miliary
immune response: immune complex or complement mediated
17
Q
What are the local destructive effects of IE?
A
- valvular distortion/destruction
- chordal rupture
- perforation/fisula formation
- paravalvular abscess
- conduction abnormalities (perforates aortic valve - infects area around bundle of his)
- purulent pericarditis (perforates into pericardium)
- functional valve obstruction
18
Q
Embolization process in IE?
A
- clinically evident: 11-43% of pts
- pathologically present: 45-65%
- high risk for embolization: large- greater than 10 mm vegetation
- hypermobile vegetation
- mitral vegetations (esp anterior leaflet)
- pulmonary (septic): 65-75% of IV drug users with tricuspid IE
- if you have R sided endocarditis: going to affect pulm vasculature
19
Q
Conversion process of NBTE to IE?
A
- frequency and magnitude of bacteremia: density of colonizing bacteria oral greater than GUgreater than GI - disease state of surface: infected surface is greater than colonized surface - extend of trauma
- resistance of organism to host defenses:
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
20
Q
Epidemiology of IE?
A
- varies according to location
- much more common in males
- may occur in persons of any age and increasingly common in elderly
- mortality rates from 20-30%
- case rate varies depending on incidence of IV drug abuse and age of pop
- 55-75% of pts with NVE have underlying problems:
MVP
hx of rheumatic fever
congenital
asymmetric atrial hypertrophy
IV drug abuse
21
Q
case rates of IE? murmur a factor?
A
- 7-25% of cases involve prosthetic valves
- 25-45% of cases predisposing condition can’t be ID’d
- MVP in adult pop is prominent predisposing factor: high prevelance in pop - 20% in young women, accounts for 7-30% NVE in cases not related to drug abuse or nosocomial infection
- relative risk in MVP - 3.5-8.2% largely confined to pts with murmur but also increased in men and patients greater than 45
- MVP with murmur 10x greater risk than with murmur
22
Q
Rheumatic heart disease and IE?
A
- 20-25% of cases of IE in 70s and 80s
- 7-18% of cases in recent reported series
- mitral site common in women
- aortic common in men
23
Q
Congenital heart disease and IE?
A
- 10-20% cases in young adults
- 8% of cases in older adults
- PDA, VSD, biscuspid aortic valve (especially in men older than 60)
24
Q
Pediatric pop and IE?
A
- vast majority: 75-90% of cases after neonatal period are assoc with an underlying congenital abnormality:
aortic valve, VSD, TOF - risk of post op infection in children with IE is 50%
- microbio: neonates - staph, coagulase neg staph, and group B strep
older children: 40% strep, and staph aureus
25
Q
IE and IV drug abuse?
A
- risk is 2-5% per pt/year
- tendency to involve right sided valves: distributin in clinical series: 78 pts:
mostly tricuspid, and next mitral and then aortic - underlying valve normal in 75-93% of pop
- S.aureus predom organism (especially in tricuspid cases)
- increased frequency of gram neg infection such as P. aeruginosa and fungal infections
- HIV status doesn’t in itself modify clinical picture, survival is decreased if CD4 is less than 200/mm3
26
Q
PVE rates?
A
- 10-30% cases in developed nations
- early PVE: within 60 days, nosocomial - S. epidermidis predominates
- late PVE: after 60 days: community (strep viridians, staph)
27
Q
RFs of IE?
A
- IV drug abuse
- artificial heart valves and pacemakers
- acquired heart defects:
calcific aortic stenosis
mitral valve prolapse with regurgitation - congenital heart defects
- IV catheters
