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LAM I > Equine Endotoxemia > Flashcards

Equine Endotoxemia Flashcards

1
Q

MODS

A

multiple organ dysfunction syndrome

  • most common cause of death in the ICU
  • associated with ARDS and DIC
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2
Q

SIRS

A 
systemic inflammatory response syndrome
criteria for Dx: 2 of the following:
- leukopenia, leukocytosis, >10% bands
- hyper/hypothermia
- tachycardia
- tachypnea
- sepsis in foals (look at sclera)
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3
Q

Endotoxemia

A

endotoxin in circulation
LPS on cell wall of gram negative bacteria
pathogen recognition by host receptor –> inflammatory response that can’t be contained (endotoxic shock)
rapid proliferation - bacteria translocates from GIT and overpopulates an area

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4
Q

Lipid A region

A

most responsible for toxic effects of bacteria, well conserved among species
hydrophobic inner portion

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5
Q

Polysaccharide O region

A

accounts for serological differentiation

polar outer portion

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6
Q

Core acidic polysaccharide

A

connects lipid A region to polysaccharide O region

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7
Q

T/F: E. coli in the guy always causes endotoxemia

A

no! is normally found in the gut BUT if translocates to circulation see severe endotoxemia

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8
Q

4 preventative mechanisms against endotoxemia

A

1) mucosal epithelium = physical barrier
- restrict bacterial movement across wall
- secrete lysozyme, enzymes and antibodies to limit invasion of mucosal lining
2) In circulation
- removal of endotoxin from portal blood -> eliminated in liver
- intravascular macrophages, endothelium, platelets, lymphocytes and neutrophils
3) Monocytes
- kupffer cells = effective LPS scavengers
4) Circulating anti-endotoxin antibodies
- directed at core region

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9
Q

5 stages of endotoxemia

A

1) physical barrier breach
2) Endotoxins stimulate macrophages
3) TNF + IL-1 act on neutrophils and endothelium
4) compromised organ perfusion
5) Recovery

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10
Q

Colic

A

abdominal pain, usually pain coincides with severity

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11
Q

Colic and banamine/flunixin meglumine

A

if horse pawing with high HR, give banamine/flunixin meglumine

  • if improvement, not as concerning
  • if animal still showing signs of pain, worry because NSAIDs not enough to manage pain, need to sedate, keep comfortable to see what is happening, give fluids, possible Sx
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12
Q

What does bloat indicate in a colicy horse?

A

sign that therapy isn’t sufficient

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13
Q

Reperfusion injury

A

untwisting GI may lead to repercussion injury + influx of endotoxins into circulation

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14
Q

horse throwing itself around due to colic

A

prone to develop endotoxemia

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15
Q

Enteritis and endotoxemia

A

inflammation of SI, reduced motility leads to reflux, increased risk of bacteremia - no signs of pain

Tx with prophylactic antibiotics - ahminoglycosides or sulphas (but cant give sulphas if reflux bc is a PO drug)

  • if you Tx a horse with banamine and not showing pain but showing reflux, is a clue to enteritis
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16
Q

Colitis and endotoxemia

A

inflammation of large colon, damage to GI walls then bacterial translocation
Potomac horse fever - neorickettsia ristcii, damages walls of LI = back easily translocates to circulation, difficult to Tx
Sand colic - sand grinds on mucosal layer - damages walls and bacteria can translocate, check diarrhea for sand
Carb overload - bacterial overgrowth in colon, degeneration of mucosa
Drug induced colitis - antibiotics, NSAIDs (Banamine and phenylbutazone)

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17
Q

Respiratory causes of endotoxemia

A

Pleuropneumonia - infection b/wn pleural space and lungs, commonly bacterial, can cause endotoxemia and laminitis
- need to drain thorax, do thoracotomy if will not drain

Choke - esophageal obstruction, can aspirate gram - and result in severe pleuropneumonia

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18
Q

Integument causes of endotoxemia

A

bacterial infections - Clostridium myositis - post banamine IM injections, tissue necrosis
gram - infection even though primary infection gram +

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19
Q

Reproductive causes of endotoxemia

A

retained placenta
- considered retained after 2 hours, 3 hours = BAD
- give oxytocin to promote passage
- will develop endotoxemia, laminitis may be first CS
Uterine rupture- leakage into abdominal cavity, not as life threatening
Severe metritis - possible but unlikely

20
Q

Urinary causes of endotoxemia

A

uncommon, infection, obstruction, traumatized bladder

21
Q

Endocrine and endotoxemia

A

Equine metabolic syndrome - lipotoxicity (excessive conversion of glucose to fat)
- disruption of insulin receptors –> resistance
- oxidative stress and inflammation, endotoxemia and transient resistance
Hyperglycemia = poor prognosis

Cushings - old horses in hypercortisolemic state

22
Q

Bacteremia and endotoxemia

A

registered by innate immune system

attack LPS readily but no memory - same threat on 2nd and 3rd exposure

23
Q

What does LPS bind to?

A

LBP - lipopolysaccharide binding protein

24
Q

LPS and LBP

A

LPS bind to LBP, LBP bind to CD14 cell surface intravascular macrophages and monocytes

25
Q

Endotoxin stimulation of macrophages

A

PAMPs on organism bind PRR on host phagocytic cells
TLR 4 activation normally results in MyD88 (proinflammatory pathway, IL1 and TNF) and TRIF and TRAM pathway (anti inflammatory pathway)

in horses, only MyD88 is activated so no anti-inflammatory mediators produced

26
Q

which pathway does TLR4 activation result in?

A

MyD88 - pro-inflammatory pathway

27
Q

Chemical events of macrophage stimulation by endotoxins

A

Early: macrophages stimulate TXA2 and vasoconstrictors = vasoconstriction

Late: cytokine synthesis (IL1 and TNF) - endotoxin signal amplified, pro-coagulant activity and vasodilation

  • vasoconstriction then vasodilation*
  • pale mm. then hyperaemic mm.
28
Q

Effect of TNF and IL-1 on neutrophils and endothelium (Stage 3)

A

cytokine induced margination of neutrophils = neutropenia
neutrophils empty granular content onto endothelium. –> injury –> coagulation cascade –> poor circulation –> ischemia and necrosis
endothelium damage - hyper coagulation - intravascular coagulation
Endothelium produce prostaglandin and NO = vasodilation
abnormal vascular tone dependent on stage:
initial: hyper dynamic shock = pulmonary vasoconstriction, tachypnea, hypoxia
late: hypo dynamic shock = pulmonary vasodilation

29
Q

Stage 4: compromised organ perfusion

A

vasodilation, vascular leakage + injury, intravascular cellular plugging, coagulation, systemic arterial hypotension
protein leakage, damaged endothelium, extravasation of neutrophils
2 or more organs = multiple organ failure

30
Q

Stage 5: recovery

A

LPS induce IL-10 which results in deactivation of mononuclear phagocytes and inhibits pro-inflammatory cytokines

31
Q

Which interleukin is responsible for deactivating mononuclear phagocytes and inhibits pro-inflammatory cytokines?

A

IL-10

32
Q

Which cytokines are pro-inflammatory?

A

Il-1 and TNF

33
Q

Clinical endotoxemia: hyper vs hypo dynamic state

A

Hyperdynamic state:
- MM white or injected, CRT may be normal, strong pulses, tachycardia, tachypnea, fever

Hypodynamic state:
- MM congested, dark, toxic line, CRT >2s (long), weak pulses, tachycardia or tachypnea, cold extremities, normal or hypothermic

34
Q

Experimental Endotoxemia

A

experimental infusion of LPS into horses
– hour 4-6 definitely have endothelial damage
all horses developed laminitis

35
Q

important prevention of laminitis

A

cryotherapy

36
Q

Equine specific cell response to flagellin

A

flagellin induces pro inflammatory responses of neutrophils by TLR 5, doesn’t activate monocytes
all other mammalian species –> monocytes respond strongly to flagellin via TLR 5

37
Q

Diagnosis of endotoxemia

A

CBC: leukopenia neutropenia (toxic neutrophils), left shift
Arterial blood gas: hypoxemia and metabolic acidosis
Glc: hyperglycaemia (poor prognostic factor)
lactate: increase after supportive tx (poor prognostic facto)
platelets decrease, fibrinogen increase because DIC - prognosis is worse
limulus ameobocyte lysate assay - horseshoe crab, direct measurement of circulating endotoxins

38
Q

Prevention of endotoxemia

A

vaccination - S. typhimurium mutant
- partial protection, no benefits on foals

LPS repeat exposure

  • diminish pro-inflammatory and clinical response, decreased gene expression and TNFa production, decreased fever, tachycardia, tachypnea, pain response
  • endotoxin tolerance subsides after 14-21d
39
Q

General Tx of endotoxemia

A

CV support - maintain intravascular volume

  • Hypertonic saline (follow with balanced IV fluids)
  • plasma (helps w/ protein loss)

Remove primary cause (sx for retained placenta, colic, etc)

40
Q

PAMPs antibody tx

A

hyperimmune anti LPS core antigen plasma decrease mortality rate significantly
very expensive

41
Q

Antimicrobial tx of endotoxemia

A

can worsen clinical presentation

42
Q

LPS neutralizing agent - Polymixin B

A

interacts directly with lipid A forming a stable molecule complex
decrease TNFa and residual LPS activity
can cause renal toxicity - must hydrate prior to treating
TREATMENT OF CHOICE

43
Q

dimethyl sulfoxide :DMSO

A

decrease cytokine expression, good drug, also used for fever

44
Q

Pentoxifylline

A

phosphodiesterase inhibitor

combined with flunixin meglumine - tx hemodynamic effect of LPS

45
Q

Lidocaine CRI

A

significantly decreases severity of CS

46
Q

Ketamine

A

cytokine modulating activity may benefit in tx of equine endotoxemia

47
Q

Most important part of caring for Endotoxemia horse

A

AGGRESSIVE SUPPORTIVE CARE

LAM I (8 decks)

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