Equine Med - Sepsis

Front 1

systemic inflammation

Back 1

inflammatory response to blood borne microbial molecules, tissue derived enzymes, and other proteins, pro-inflammatory mediators

Front 2

systemic inflammatory response syndrome

Back 2

two or more of the following; tachypnea, tachycardia, fever/hypothermia,neutrophilia/neutropenia

Front 3

sepsis

Back 3

systemic inflammatory response triggered by an microbial molecules (infection, damaged gut barrier, etc)

Front 4

endotoxemia

Back 4

systemic inflammation triggered by gram negative bacterial endotoxin

Front 5

septic shock

Back 5

sepsis w/signs of shock

Front 6

what triggers inflammatory response?

Back 6

microbial molecules absorbed into blood (lipopolysacharide-endotoxin), inflammation in sepsis is triggered by specific host receptors for microbial molecules (toll like receptors-TLRs)

Front 7

wht does LPS induce?

Back 7

COX-2 protein expression and activity

Front 8

what is the pathophysiology of sepsis?

Back 8

poor perfusion (neutrophil and platelet aggregates, thrombi, **hymodynamic shock-altered dysregulated peripheral vasculartone and poor cardiac output**, increased vascular permeability) and tissue injury (ischemia, edema, leukocyte products-reactive oxygen intermediates & degradative enzymes)

Front 9

what diseases are commonly accompanied by systemic inflammation?

Back 9

septicemia, endotoxemia/absorption of other microbial products from a site of infection (colic, colitis, pleuropneumonia, metritis, peritonitis, cellulitis), immune mediated dz (non-septic SIRS), severe trauma (non-septic SIRS)

Front 10

what are the clinical signs of sepsis?

Back 10

tachycardia, tachypnea, hyper/hypothermia, leukocytosis/penia, others (hyperemic mucous membranes, depression, edema, shock-prolonged CRT, poor peripheral pulses, hypotension, weak-trembling, cool extremities)

Front 11

what are the typical lab findings on CBC of sepsis?

Back 11

hemoconcentration (high RBC count, PCV, TP), systemic inflammation (high FB, high WBC, low mature PMN, high bands, low PLT)

Front 12

what are the typical lab findings on chemistry of sepsis?

Back 12

organ dysfunction (high creatinine, high BUN, high GGT, high AST), poor perfusion (low pH, high anion gap, high lactate, low pO2v-increased extraction)

Front 13

what are the typical lab findings on UA of sepsis?

Back 13

concentrated (high SG), hematuria/proteinuria

Front 14

what are the principles of shock therapy?

Back 14

stop absorption/treat source (hasten GI mucosal healing, drain abscesses, treat infections), antagonize LPS effects, **increase perfusion-increase BP, improve blood distribution, reduce vascular leak syndrome**, control coagulation/platelet activation

Front 15

how do we use crystalloid fluids for shock?

Back 15

isotonic fluids (effective if animal is dehydrated but not effective for treating shock because redistribute quickly to interstitial space), hypertonic-5% saline (increase cardiac output, increases perfusion during endotoxic shock), pressors (dopamine, dobutamine, norepinephrine-neonates)

Front 16

how do we use colloid fluids for shock?

Back 16

plasma (6-8L/d) & hetastarch (5-10ml/kg/d or eod) commonly used, increase cardiac outpu & increase perfusion, reduce endothelial permeability (vascular leak syndrome), long lasting compared to hypertonic crystalloid fluids

Front 17

what can be used to antagonize LPS?

Back 17

polymixin B, J5 plasma

Front 18

what does polymixin B do?

Back 18

binds LPS w/high affinity, blocks LPS binding to LPS-binding protein, blocks effects of LPS in vivo, potentially nephrotoxic, 2000-6000 IU/kg IV BID

Front 19

what does J5 plasma do?

Back 19

polyclonal anti-LPS antibody, protective against septic shock in at least one human study, improved clinical appearance at 48h after plasma and reduced mortality in horses with evidence of endotoxic shock (13% mortality in the treated vs 47% control)

Front 20

what NSAID should be used for shock?

Back 20

flunixin meglumine

Front 21

what are the drawbacks of using NSAIDs for shock?

Back 21

nephrotoxicity, GI mucosal ulceration/inhibited repair of injure mucosa, COX-2 inhibitors-debatable (Eqoxx, Meloxicam) mucosal damage

Front 22

what does pentoxifylline do?

Back 22

inhibits neutrophil and macrophage activation by LPS and reduces RBC stiffness

Front 23

when should antibiotics be used?

Back 23

neutrophil count is 1000 cells/uL or less, if septicemia is suspected/documented, source of infection causing spesis is found/documented

Front 24

when should nutrition be supplemented?

Back 24

anorexic horse or horses with restricted fod intake benefit from parenteral nutrition

Front 25

when should DMSO be used?

Back 25

NEVER

Front 26

what is a general treatment plan?

Back 26

SIRS (2-4L J5 plasma, polymyxin IV, LRS, flunixin IV), hypotensive (LRS bolus and twice maintenance, if still hypotensive hetastarch, consider pressors in neonates), monitor (PE, BP, colic, feet, veins, PCV/TP, creatinine, LFTs, urine)

Front 27

how do we prevent laminitis?

Back 27

circulatory support-include colloids, antiinflammatory drugs-aspirin (reduce platelet clumping) and pentoxyifyllin (increased deformability of RBC/WBC), handwalk, icing?