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
IE and IV drug abuse?
- 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
PVE rates?
- 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
RFs of IE?
- IV drug abuse
- artificial heart valves and pacemakers
- acquired heart defects:
calcific aortic stenosis
mitral valve prolapse with regurgitation
- congenital heart defects
- IV catheters
28
sxs of acute IE?
- high grade fever and chills
- SOB
- arthralgias/myalgias
- abdominal pain
- pleuritic chest pain
- back pain
29
sxs of subacute IE?
- low grade fever
- anorexia
- wt loss
- fatigue
- arthralgias/myalgias
- abdominal pain
- N/V
- the onset of sxs is usually 2 weeks or less from the initiating bacteremia
30
Acute presentation of IE?
- toxic presentation
- progressive valve destruction and metastatic infection developing in days to weeks
- most commonly caused by S. aureus
31
subacute presentation of IE?
- mild toxicity
- presentation over weeks to months
- rarely leads to metastatic infection
- most commonly S. viridans or enterococcus
32
Signs of IE?
- fever (Most common sign) - this may be absent in elderly or debiliated
- heart murmur: present in 80-85%: new, change in pre-existing murmur, often absent in tricuspid IE
- nonspecific signs: petechiae, subungal or splinter hemorrhages, subconjunctival hemorrhages, clubbing, splenomegaly, neuro changes
- more specific signs: osler's nodes, janeway lesions, and roth spots
33
Other clinical features of IE?
- systemic emboli: incidence decreases with effective anti-microbial Rx
- neuro sequelae: embolic stroke: 15-20% of pts, mycotic aneurysm, cerebritis (inflamm rxn on surface of brain)
- CHF: due to mechanical disruption, high mortality without surgical intervention
- renal insufficiency: immune complex mediated, impaired hemodynamics/drug toxicity
- peripheral manifestations: are less common today, not seen in tricuspid IE, petechiae is most common
34
Splinter hemorrhages?
- nonspecific
- nonblanching
- linear reddish brown lesions found under the nail bed
- usually don't extend the entire length of the nail
35
What are osler nodes?
- more specific
- painful and erythematous nodules
- located on pulp of fingers and toes
- more common in subacute IE
36
What are janeway lesions?
- more specifc
- erythematous, blanching macules
- nonpainful
- located on palms and soles
37
What are roth spots?
- pale retinal lesions surrounded by hemorrhage, usually near optic disc
38
Work up of IE?
High index of suspicion in pts with predisposing anatomay or behavior
- if they are sick, think systemically about other organs
- want blood cultures
- echoL TTE: 60% sensitivity
TEE: 80-95% sensitivity (Suspect IE go with TEE)
39
Blood cultures?
- min of 3 blood cultures
- 3 separate venipuncture sites
- obtain 10-20 mL in adults and 0.5-5 ml in children
- positive result: typical organisms present in at least 2 separate samples, persistently positive blood culture (atypical organisms) - 2 positive blood cultures obtained at least 12 hours apart, or 3 or more positive blood cultures in which the first and last samples were collected at least 1 hr apart.
(atypical takes up to 6 weeks to grow in culture)
40
Other labs to order?
- CBC
- ESR and CRP
- complement levels (C3, C4, CH500)
- RF
- urinalysis
- baseline chemistries and coags
41
imaging tests to order?
- CXR: look for mult focal infiltrates and calcification of heart valves
- EKG: rarely dx, look for evidence of ischemia, conduction delay, arrhythmias
- echo
42
Indications for echo?
- TTE:
first line if suspected IE
native valves
```
TEE:
prosthetic valves
intracardiac complications
inadequate TTE
fungal or S aureus or bacteremia
```
43
Criteria for making the dx of IE?
- Pelletier and Petersdorf criteria
- von Reyn criteria
- duke criteria (newest - 1994)
included the role of echo in dx, and added IVDA as a predisposing heart condition
44
Major duke's criteria?
- + blood cultures with approp organism
- echo findings
- new valvular regurg
45
Minor Duke's criteria?
- high risk for IE, or h/o of IVDU
- temp above 38 C
- vascular phenomena: arterial embolism, septic pulm infarcts, mycotic aneurysm, intracranial hemorrhage, janeway lesions
- immunologic phenomena: oslers nodes, roth spots, glomerular nephritis, rheumatoid factor
- serologic factor
- blood cultures or echo results not meeting the major criteria
46
Modified Duke's criteria?
- definite IE: microorganism (via culture or histology) in a valvular vegetation, embolized vegetation, or intracardiac abscess
histologic evidence of vegetation or intracardiac abscess
- possible IE: 2 major, 1 major and 3 minor, 5 minor
- rejected IE: resolution of illness with four days or less of abx
47
4 major complications of IE?
- embolic
- local spread of infection
- metastatic spread of infection
- formation of immune complexes: glomerulonephritis and arthritis
48
How common is embolic complications in IE? predictors?
- occur in up to 40% of pts with IE
- predictors of embolizationL
size of vegetation
left sided vegetations
fungal pathogens, S aureus, and strep bovis
- incidence decreases significantly after initiation of effective abx
49
What are the embolic complications of IE?
- stroke
- MI: fragments of valvular vegetation or vegetation-induced stenosis of coronary ostia
- ischemic limbs
- hypoxia from PE
- abdominal pain (splenic or renal infarction)
50
Spread of infection?
- metastatic abscess: kidneys, spleen, brain, soft tissue
- meningitis, and or encephalitis
- verterbral osteomyelitis
- septic arthritis
- pulmonary abscess (R sided endocarditis)
51
what occurs with the local spread of infection?
- HF: extensive valvular damage
- paravalvular abscess (30-40%): most common in aortic valve, IVDA, and S. aureus
may extend into adjacent conduction tissue causing arrhythmias.
higher rates of embolization and mortality
- pericarditis
- fistulous intracardiac connections
52
What are some poor prognostic factors of IE?
- female
- S. aureus
- vegetation size
- aortic valve
- prosthetic valve
- older age
- DM
- low serum albumin
- apache II score
- HF
- paravalvlar abscess
- embolic events
53
Tx of IE?
- parenteral abx: high serum concentrations to penetrate vegetations, prolonged tx to kill dormant bacteria clustered in vegetations
- surgery: intracardiac complications
- surveillance blood cultures
54
What are the goals of IE therapy?
- eradicate the infectio
| - definitively tx sequelae of destructive intra-cardiac and extra-cardiac lesions
55
Abx therapy for IE?
- tx tailored to etiologic agent: impt to not MIC/MBC relationship for each causative organism and the abx used
- high serum concentration necessary to penetrate avascular vegetation
- tx before blood cultures turn positive: suspected acute bacterial endocarditis, hemodynamic instability
- effective antimicrobial tx should lead to defervescence within 7-10 days.
- abx usually admin IV for 4-6 weeks, duration depends on virulence of pathogen
- DOC for most cases of viridians streptococcal endocarditis is PCN (cure rate for strep endocarditis is above 90%), w/o tx, VSE is typically fatal within 6 months
- antifungals alone are not enough to cure fungul IE, although amphotericin B is often admin in conjuntion with surgery
56
What should you think about as a causative agent if fever persists after 7-10 days?
- IE due to staph, pseudomonas, culture negative
- IE with microvascular complications/major emboli (look for atypical places for abscesses)
- intracardiac/extracardiac septic complications
- DRUG reaction
57
How do you tx resistant strep viridans?
- 13% resistant to PCN
- 26% resistant to macrolides
- 4% to clindamycin
- impact of resistance on abx prophylaxis is unknown
- quinolones or IV vanco not recommended for prophylaxis due to concern of creating new drug resistance
58
difference b/t surgical and medical mortality of tx intra-cardiac complications?
- Class III/IV CHF due to valve dysfxn:
surgical: 20-40%
medical: 50-90%
- unstable prosthetic valve: surgical - 15-55%
medical: near 100% at 6 months
- uncontrolled infection
59
What causative agents hav no effective antimicrobial tx?
- fungal endocarditis
| - brucella
60
What are relative indications for surgical tx of IE?
- perivalvular extension of infection
- poorly responsive S. aureus NVE
- relapse of NVE
- culture neg NVE/PVE with persistent fever (greater than 10 days)
= large (more than 10 mm) or hypermobile vegetation
- endocarditis due to highly resistant enterococcus Indications:
- refractory CHF, severe valvular dysfunction
- uncontrolled infection
- valve perforation, dehiscence, fistula, abscess
- 1 embolic event with persistent large vegetation, or more than 1 episode of embolization
- Prosthetic valve infection
- fungal IE
- new heart block
61
What surgeries are indications for prophylactic abx?
- dental procedures known to produce bleeding
- tonsillectomy
- surgery involving GI, respiratory mucosa
- esophageal dilation
- ERCP for obstruction
- gallbladder surgery
- cytoscopy, urethral dilation
- urethral catheter if infection present
- urinary tract surgery, including prostate
- I&D of infected tissue
62
What are high risk lesions?
- **prosthetic valves
- ** prior IE
- ** cyanotic congenitatl heart disease
- **surgical systemic pulmonary shunts
- PDA
- AR, AS, MR, MS with mR
- VSD
- coarction
63
Intermediate risk lesions?
- MVP with murmur
- pure MS
- tricuspid disease
- pulmonary stenosis
- ASH
- bicuspid aortic valve with no hemodynamic significance
64
Low/no risk lesions?
- MVP without murmur
- trivial valvular regurg
- isolated ASD
- implanted device (ICD, pacer)
- CAD
- CABG
65
What organisms are we prophylactically tx?
- strep. viridans: oral, respiratory, esophageal
- enterococcus - genitourinary, gi
- S. aureus: infected skin, mucosal surfaces
66
MOA of prophylaxic abx?
- abx may kill blood borne bacteria or interfere with their metabolism, hindering their ability to adhere to a damaged heart valve
- controversial: abx resistance increasing
- should only be admin prior to high risk surgeries and high risk pops
67
Antimicrobial proph is recommended in what pts?
```
- high risk pts:
prosthetic valves
previous bacterial endocarditis
RHD and other acquired valve dysfunction
- hypertrophic cardiomyopathy
- MVP
```
68
Std regimen for endocarditis prophylaxis in dental, oral, resp, and esophageal procedures?
- amoxicillin
| allergic to PCN: clinda, cefalexin
