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infective endocarditis Flashcards

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1
Q

What is IE?

A
  • an infection of the heart’s endocardial surface
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2
Q

What are th 4 groups of IE?

A
  • NVE
  • PVE
  • IVDAE
  • nosocomial IE
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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

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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
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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
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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
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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
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8
Q

Vegetation of IE?

A
  • variable in size
  • amorphous mass of fibrin and platelets
  • abundant organisms
  • few inflammatory cells
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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
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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
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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
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12
Q

Pathophys of IE?

A
    1. turbulent blood flow: disrupts the endocardium making it sticky
    1. bacteremia: delivers the organisms to the endocardial surface
    1. adherence of the organisms to the endocardial surface
    1. eventual invasion of the valvular leaflets
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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
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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
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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)
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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
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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
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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
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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
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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
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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
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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
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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)
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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
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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
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