Acquired Valvular Disease- Endocarditis Flashcards

1
Q

describe infective endocarditis

A
  1. inflammation of the endocardial surface of the heart with invasion by an infectious agent (bacteria, rickettsial organisms, fungal organisms)
  2. endocardial surface includes: surface of the valves, mural/wall, edges of septal defects, and chordae tendinae
  3. synonyms:
    -infective endocarditis: microbial infection (bacterial, fungal, etc.)
    -bacterial endocarditis: bacterial infection
    -vegetative endocarditis: vegetations (composed of platelets, fibrin, microorganisms, and inflammatory cells), adherent
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2
Q

contrast endocardiosis to endocarditis

A

endocardiosis: degenerative/myxomatous
-gross lesion: smooth, glistening, nodular thickening of valve margins

endocarditis: inflammatory/infectious
-gross lesion: friable, rough, irregular yellowish raised proliferative lesions (vegetative lesions)

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3
Q

describe incidence/prevalence of endocarditis

A

cows: relatively common
-important cause of hardware disease

dogs: uncommon diagnosis
-middle-aged to older, medium to large breed, purebred dogs

horses, pigs, camelids: sporadic: can be mural (wall) in camelids and cattle

cats: rare

avian: very few cases documented

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4
Q

describe pathogenesis of endocarditis

A
  1. endothelial damage/injury:
    -collagen exposure due to endocardial damage
    -healthy endothelium is resistant!! to bacterial colonization, so injury is required vie direct trauma, inflammation, or turbulent bloodflow to allow colonization
    -underlying cardiac defect is NOT present is 87-94% of vet cases, of those with lesions, 75% have congenital subaortic stenosis
    -endocardiosis is NOT a predisposing factor
  2. formation of non-bacterial thrombotic endocarditis (NBTE):
    -ECM, thromboplastin, and tissue factor trigger coagulation and formation of coagulum (fibrinogen, fibrin, platelet proteins)
    -body is just trying to heal itself!
  3. bacteremia:
    -can be transient or persistent
    -predisposing events: chronic infections, GI/GU tract surgery, immunosuppression (systemic illness: DM, cushings, or iatrogenic via corticosteroids)
  4. bacterial colonization of NBTE:
    -circulating bacteria adhere and attach to the thrombus
    -bacteria that most easily adhere to valves are most commonly involved (staph, strep)
    -bacteria have surface proteins that bind fibrin/fibrinectin
  5. activation of clotting cascade and lesion extension:
    -bacteria become embedded and trigger tissue factor production and induce platelet aggregation
    -this forms a protected environment for bacterial growth where they are shielded from host defenses and antimicrobial drug penetration
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5
Q

describe lesion pathology in small animals

A
  1. almost exclusively mitral and aortic valves (left sided valves)
  2. lesions most often associated with lower-pressure side of valve/lesions
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6
Q

describe lesion pathology in large animals

A

cows: right sided valves, esp tricuspid!
-FOR SURE ON EXAM!!!!!!!!!!
-due to dirty environment venous flow potentially

horses, pigs, camelids: left sided valves&raquo_space; right sided valves
-can be mural (or wall) as well

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7
Q

describe etiologic agents in small animals

A
  1. we only ID the agent in 60% of cases!
  2. commonly cultured in dogs:
    -staphylococcus: aureus, intermedius
    -streptococcus: canis, bovis
    -E. coli
    -bartonella spp.
  3. commonly cultured in cats:
    -pasteurella

don’t memorize bacteria according to Hammond!! (just have the MSCRAMMS, ability to stick to scab)

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8
Q

describe bartonella endocarditis in small animals

A

unique!

  1. has a strong predilection for aortic valve
  2. associated with poorer outcome: more CHF, earlier death
  3. affected dogs are usually afebrile
    -only 20% have fever
  4. difficult to isolate from blood
    -responsible for up to 20% of cases that are culture negative with routine methods
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9
Q

describe etiologic agents in large animals

A

cattle:
-trueperella pyogenes: 80% of cultures
-streptococcus spp.
-E. coli

horses:
-actinobacillus
-streptococcus spp.
-staphylococcus spp.

pigs:
-streptococcus spp.

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10
Q

describe cardiac consequences of infective endocarditis (local disease)

A
  1. valve leaflet injury:
    -insufficiency: most common
    –bacterial enzymes destroy affected valve, leading to necrosis/perforation that leads to valvular regurgitation, followed by volume overload, left heart enlargement, and CHF

-obstruction/stenosis: increases cardiac workload, resulting in concentric hypertrophy

  1. extension of infection into surrounded tissues
    -AV/bundle branch blocks
    -abscess formation
    -purulent pericarditis
    -myocarditis
    -intracardiac perforation
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11
Q

describe systemic consequences/metastatic disease of infective endocarditis

A
  1. embolic disease:
    -end organ infarction/metastatic infection
    –in 84% of cases at necropsy, most commonly in the kidney and spleen
    –increased risk: larger, mobile vegetations (>10-15mm) or mitral valve involvement
  2. immune-mediated disease
    -cell mediated and humoral immune responses cause circulating immune complex deposition and complement activation, resulting in inflammatory tissue damage
    -most commonly affected: joints (polyarthritis), kidneys (glomerulonephritis)
  3. renal failure: up to 33% of cases
    -metastatic infection/infarction
    -glomerulonephritis
  4. septic shock
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12
Q

describe history and clinical findings of infectious endocarditis

A
  1. risk factor:
    -prior or current infection
    -immunosuppressive disease or drug history
  2. fever
  3. constitutionally ill
  4. palpable joint effusion
  5. new heart murmur:
    -ejection murmur: fever, increased slow, stenotic semilunar valve from large vegetation

-regurgitant murmur:
–AoV: diastolic, left base
–MV: systolic, left apex
–TV: systolic, right apex

  1. intermittent lameness
  2. signs of vasculitis (cutaneous hemorrhage, thrombosis)
  3. other possible cardiac findings:
    -tachycardia
    -hyperkinetic pulses
    -arrhythmia
    -signs of CHF
  4. lethargy, weight loss, inappetance, weakenss

SUPER vague, have to go hunting

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13
Q

describe diagnostics for IE

A
  1. CBC: variable
    -leukocytosis
    -anemia
  2. serum biochem: variable
    -azotemia
    -elevated globulin
  3. urinalysis:
    -pyuria
  4. modified Duke criteria: tells the probability that the patient has IE
    -major criteria:
    –positive echocardiogram: oscillating, vegetative lesion, erosive lesion, abscess
    –new valvular insufficiency
    –positive blood culture in at least 2 samples

minor criteria:
–fever
–presence of predisposing factors: med to large breed dog, suboartic stenosis
–evidence of systemic sequelae: thromboembolic disease, immune-mediated disease (polyarthritis, glomerulonephritis)
–positive blood culture not meeting major criteria
–bartonella serology

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14
Q

describe echocardiography for IE

A
  1. most important tool for antemortem dx of IE
  2. hyperechoic, oscillating, irregular-shaped (shaggy) mass adherent to endothelial cardiac surface
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15
Q

describe the modified duke criteria

A
  1. major criteria (FOR SURE KNOW THESE)

-positive echocardiogram: oscillating, vegetative lesion, erosive lesion, abscess

-new valvular insufficiency

-positive blood culture in at least 2 samples

  1. minor criteria:
    -fever

-presence of predisposing factors: med to large breed dog, suboartic stenosis

-evidence of systemic sequelae: thromboembolic disease, immune-mediated disease (polyarthritis, glomerulonephritis)

-positive blood culture not meeting major criteria

-bartonella serology

definite: 2 major criteria OR 1 major + 3 minor OR 5 minor

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16
Q

describe blood cultures for IE

A
  1. essential to support diagnosis and guide therapy!!
  2. goal: document persistent bacteremia by culturing samples taken at different times
    -ideally 3-4 aseptically obtained samples of 10ml collected over 24 hours BEFORE starting antibiotics
    -if critically ill: 2-3 samples, 1 hour apart, fever spike or trough concentration level if abx given increases liklihood of positive
  3. blood cultures are negative in 40-70% of cases!
    -bartonella: PCR, serology
17
Q

describe treatment of IE

A
  1. LONG TERM antibiotic therapy
    -goals

sterilize vegetation: aggressive, prolonged therapy
-appropriate antibiotic choice: bacteriCIDAL, penetrates fibrin, based on blood C&S
-extended duration of therapy: ideally IV abx for 1st week (impractical), so oral abx AT LEAST 12 weeks!
-want to hit gram + and - !!
-beta lactam and fluroquinolones, or beta lactam and aminoglycoside, or for bartonella: add azythromycin

address cardiac sequelae:
-standard therapy for CHF
-recheck echo at 2 then 6-8 weeks after starting abx
-surgical options: rare
-antiarrhythmic and/or pacemaker therapy, as indicated

manage systemic complications:
-anti-platelets/thrombotics are controversial: consider if PLN, DIC, or hypercoagulable state
-corticosteroids are CONTRAINDICATED (already immune suppressed, dont make it worse)
-renal failure treated routinely
-lameness treated symptomatically

18
Q

describe prognosis of IE

A
  1. dependent on:
    -microorganisms involved
    -whether infection is left or sided valves (left is worse)
  2. overall is guarded to poor
  3. majority develop CHF or embolic complications
  4. cows: unknown
    -dogs: MST 54 days; worse if on steroids prior to tx, TCP, high serum creatinine, renal complications, or thromboembolic disease
    -horses, pigs, camelids: unknown
    -cats: MST 30 days; high prevalence of CHF at time of diagnosis