Endocarditis

Question 1

Cause

Answer 1

bacterial or rarely fungal infection of valvular/mural endocardium

Question 2

Epidemio

Answer 2

• Prevalence: studies in dogs around 0.11% to 0.58%, unknown in cats
• Hu: pre existing heart disease ↑ risk
  o PDA, AI, AS, MR, MS, VSD
• Dogs w SAS predisposed according to studies
  o Older dogs ↑ prevalence
  o Medium to large breed dogs

Question 3

Characteristic lesion

Answer 3

Valvular vegetation
o Most commonly MV and AoV in dogs/horses
 TV and PV for cows → associated w hardware dz
o Rarely PV

Question 4

Layers of lesion

Answer 4

• Fresh vegetation: 3 layers
  o Larger inner layer of platelets, fibrin, RBCs, WBCs, bacterias
  o Middle layer of bacterias
  o Outer layer of fibrin
• WBCs: mostly lympho¢ and histio¢
  o Few polymorphonuclear ¢
• Mature vegetations:
  o Capillaries, fibroplasia
  o Dense fibrous tissue covered by endothelium
  o Less friable
  o Often calcified

Question 5

Pathogenesis

Answer 5

• Transient/persistent bacteremia = requirement for establishment of cardiac infection
  o Initiating episode most commonly not identified

Question 6

Predisposing events

Answer 6

mx/sx procedures involving oropharynx, GI, genitourinary tract, dental procedures, IV KT, PM implantation, immunosuppressive therapy, prior valvular infections
 Bacteremia w dental procedures: 85%

Question 7

Factors for establishment of infection

Answer 7

o Endothelial integrity
 Healthy intact endothelium = resistant to bacterial attachment
 Damaged endothelium = promote dev of platelet fibrin aggregates → susceptible nidus for bacterial invasion

o Disturbed blood flow

o Bacterial virulence
 Bacteria ability to adhere to damaged surface = major role
 If well developed mechanisms of adherence: infection at low levels of inoculation
* Exposition of extra¢ polysaccharide dextran → facilitate attachment of some species
* Valvular endothelium: rich in fibronectin = facilitate attachment of certain organisms
o Staph Aureus have fibronectin R
 To sustain infection: bacteria have to evade defense mechanisms
* Protected by layer of fibrin, RBCs, platelets
* Valves/vegetation: avascular = limit AB access, phago¢, ATB

o Host immunity

Question 8

Non bacterial thrombotic endocarditis

Answer 8

o Formation of sterile clumps of platelets, fibrin, RBCs
o Normal or superficially damaged valves
o Predisposing cause:
 High velocity/turbulent blood flow
* Valvular insufficiency/stenosis
 Hypercoagulable states: DIC

Question 9

Distribution of lesions

Answer 9

• Bacterial deposition occurs on side of flow
  o Ventricular surface of AoV
  o Atrial surface of MV

Question 10

Cardiac sequela

Answer 10

• Valvular insufficiency: most common
  o Consequence of valvular necrosis, perforation, chordae tendineae rupture
  o Destruction of valvular stroma is rapid in acute/ulcerative endocarditis from S aureus
• L CHF in most dogs w AoV, common in MV
• Extensive infection to valve annulus sinus Valsalva, pericardium, myocardium can cause
  o Abscess formation
  o Aortoarterial shunting
  o Purulent pericarditis
  o Myocarditis
  o Conduction system lesions

Question 11

Systemic sequela

Answer 11

• Systemic embolization/metastatic infection
  o Septic or sterile embolization common → infarction or metastatic infection
  o Kidney + spleen = most common sites, also heart, brain, intestines
   Renal infarction/infection, glomerulonephritis (GN) can cause death
• Immune mediated disorders
  o Persistent bacteremia → stimulate humoral/¢ immune system
  o Rheumatoid factor + antinuclear AB + immune complexes → polyarthritis, renal dz, myocarditis
   GN well known complication, prevalence vary according to organism
• Correlation btw [immune complexes] vs presence/severity of GN
   Polyarthritis: synovial tissue contain IgG, IgM, complement
• Hypertrophic osteopathy lesions: platelet clumps released from vegetation → release platelet derive GF
• Sepsis and shock
  o Sepsis syndrome: altered organ perfusion
   Altered mentation, oliguria, acidosis, hypoxemia
   Hypotension = septic shock
  o Multiple organ dsfct syndrome: septic shock progressed to DIC
   Acute resp distress, renal failure, hepatobiliary compromise, CNS dysfct
   TNFα + IL1 released from macrophages → activate endothelial ¢, lympho¢ T&B, mono¢, macrophages, neutrophils, cytokine release (IL8, IL6, TGFβ, PGE2, colony stimulating, platelet derived factors, eicosanoids, etc.)

Question 12

Dx: history

Answer 12

• Variable, non specific
• CHF: cough, labored breathing, collapse, weakness
• Lameness

Question 13

Findings on PE

Answer 13

FEVER
 Heart murmurs
 New/changed murmur
o Predictive value: depend on location and characteristic (which valve, severity)
o L diastolic basilar murmur in febrile dog = high probability of endocarditis
 AI is rare
 Alterations in character of murmur on serial PE → px
o Mild AI: holodiastolic, small ↓ intensity
o Severe AI: intensity ↓ throughout diastole, may not be audible at the end
 Equilibration of LV and Ao pressures
 Volume overload from AI → impending CHF

 Arrhythmias: 50-75%
o Secondary to myocarditis, HF, myocardial infarction, destruction of conduction system, immune mediated vasculitis
o Most commonly
 Ventricular arrhythmias: VPCs
 Paroxysmal/sustained tachyarrhythmias
 Heart block → bradycardia (damage to AV node/bundle of His)
* 1st-2nd-3rd AVB
* BBB

 Femoral pulses: bounding (waterhammer)

 Systemic abnormalities
o Vasculitis, polyarthropathy → immune mediated/septic arthritis
o Retinal hemorrhage, hyphema, epistaxis, petechion

Question 14

Criteria for dx

Answer 14

DEFINITVE
o Pathologic:
 Microorganism demonstrated by culture/histo in vegetation
 Microorganism in embolized vegetation
 Vegetation confirmed by histology
o Clinical
 2 major
 1 major + 3 minor
 5 minor

POSSIBLE: consistent findings but not definitive

REJECTED
o Firm alternative dx
o Resolution of c/s w ATB for <4days
o No pathologic evidence of endocarditis at sx/autopsy after ATB <4days

Question 15

Major clinical criteria

Answer 15

• > 2 + blood culture from typical organisms
  o Corynebacterium spp
  o Erysipelothrix rhusiopathiae
  o Streptococcus spp
  o Staphylococcus spp
  o Pseudomonas aeruginosa
  o Pasteurella
• Persistently + blood cultures (>12h or >3-4)
• Evidence of endocardial involvement
  o Echo: oscillating valvular lesion
   Abcess
   New valvular regurgitation

Question 16

Minor criteria

Answer 16

• Predisposition: SAS, chronic KT
• Fever
• Vascular phenomena
  o Major arterial emboli
  o Septic pulmonary infarcts
  o Intracranial/ onjunctival hemorrhage
• Immunologic phenomena
  o GN
  o Polyarthropathy
  o Vasculitis
• Microbiologic evidence:
  o + blood culture not meeting major criteria
  o Serologic evidence of infection
• Echo: consistent with infective endocarditis but not meeting major

Question 17

Echo changes

Answer 17

 Early changes: slight thickening/↑ echogenicity of affected valve
o No/minimal hemodynamic changes

 Vegetation: area of highly reflective leaflet thickening w pedunculated mass from tile of leaflet
o Small vegetation = difficult to visualize
 Smooth, nodular
o Large lesions are echogenic, heterogenous, irregular, pedunculated, mobile
 Move independently form valve
 Vegetations >10mm: risk for embolization
o May extend to chordae tendinae if AV valve
o May cause functional stenosis (rare)
o Poor valve motion/coaptation

 Regurgitation:
o Destroyed valve stroma
o Vegetation prevent normal coaptation

 Regional wall motion abnormality: can suggest coronary artery embolization

 Negative predictive value of high quality echo >90%
o TEE more sensitive

Question 18

M-mode echo changes

Answer 18

 High frequency diastolic fluttering of MV: highly suggest AI
o Anterior leaflet is below AoV in diastole
o Regurgitation directly on the valve

 Premature closure of MV w severe AI
o Rapid rise of LV pressure during diastole (blood from Ao)
o Reach LA pressure faster

Question 19

Doppler echo changes

Answer 19

 AI: decay rate, proximal jet area and height: estimation of reguritant volume
o Degree of LA and LV dilation

Question 20

Poor long term px indicators

Answer 20

LV dysfct
o ↓FS%/EF
o Ao flow acceleration

Question 21

Blood culture: things to consider

Answer 21

 Multiple sets should be obtained from different venipuncture sites
 Bacteremia precedes fever by 1-2h

Question 22

Complications

Answer 22

 Abscess and 2nd rupture of ventricular, atrial, great vessel walls
 Myocardial infarction → coronary embolism
 PTE if R sided lesions
 CHF 2nd to valvular insuficiency

Question 23

Treatment goals

Answer 23

o Sterilize vegetative lesions
o Attend to adverse cardiac sequelae
o Manage systemic abnormalities

Question 24

Tx

Answer 24

 Antibiotherapy
o Select ATB for ability to penetrate fibrin rich matrix of vegetations
 For at least 2w, as long as 6w
o Gentimicin/amikacin + peni/ampi/oxa/nafcillin
 Aminoglycoside toxicity: limit use to 5-7days
 Anaerobic coverage: clindamycin/metronidazole

 Heart failure and arrhythmias
o Most common cause of death
 Acute endocarditis can lead to rapid development of HF
o Severe AI/MR: poor px

Question 25

Prevention

Answer 25

prophylaxis if predisposed