Sepsis

Question 1

Systemic inflammation

Answer 1

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

Question 2

Systemic inflammatory response syndrome (SIRS)

Answer 2

tachypnea, tachycardia, fever/hypothermia, neutrophilia/neutropenia

Question 3

Sepsis

Answer 3

a systemic inflammatory response triggered by microbial molecules

Question 4

Endotoxemia

Answer 4

systemic inflammation triggered by gram-negative bacterial endotoxin (LPS)

Question 5

Septic shock

Answer 5

sepsis + signs of hemodynamic shock

Question 6

Sepsis pathogenesis

Answer 6

infection or mucosal damage allows microbes (usually bacteria) or microbial products to gain access to systemic circulation

• GI, respiratory, urogenital, umbilical, other mucosal surfaces

Question 7

What is the most variable component of LPS?

Answer 7

O-specific antigen

Question 8

What is the basic pathophysiology associated with sepsis?

Answer 8

Poor perfusion

• neutrophil & platelet aggregates
• thrombi-hypercoagulable (early)->later hypocoagulable with consumption of enough clotting factors
• hemodynamic shock
  
  • altered/dysregulated peripheral vascular tone (red, warm extremities)
  • poor CO
• increased vascular permeability

Tissue injury

• ischemia
• edema
• leukocyte products (reactive oxygen intermediates, degradative enzymes)

Ultimately lead to multi-organ dysfunction/failure

Question 9

Two examples of non-septic SIRS

Answer 9

• immune-mediated disease
• severe trauma

Question 10

Clinical signs of sepsis

Answer 10

• tachycardia, tacypnea
• hyper or hypothermia
• leukocytosis or leukopenia (left shift common)
• yperemic mucous membranes
• depression
• edema
• shock
  
  • prolonced CRT
  • poor peripheral pulses
  • hypotension
  • weak, trembling
  • cool extremities

Question 11

What are some lab findings that indicate systemic inflammation?

Answer 11

• high fibrinogen
• high WBC
• low mature PMN
• high bands
• low platelets

Question 12

What are some lab findings with sepsis that indicate organ/metabolic failure?

Answer 12

• high BUN, creatinine
• high GGT, AST
• hyperglycemia (usu. adult) or hypoglycemia(usu. foals)
• hematuria, proteinuria

Question 13

What are two contributing factors to high lactate?

Answer 13

• anaerobic metabolism due to poor perfusion
• cellular failure

Question 14

What is an absolutely critical goal of therapy for sepsis?

Answer 14

INCREASE PERFUSION

• increase BP
• improve blood distribution
• reduce vascular leak syndrome
• address hypercoagulation

Question 15

Fluid therapy for shock

Answer 15

Hypertonic (5% saline) or colloids followed by isotonic fluids(initial bolus and smaller boluses every 30 min if needed)

Question 16

What treatment can help reduce endothelial permeability(vascular leak syndrome)

Answer 16

• hetastarch or plasma (plasma is expensive!)

Question 17

What is a contraindication for Polymixin B administration?

Answer 17

High creatinine-drug is potentially nephrotoxic

Question 18

When is Polymixin B useful for treatment of sepsis?

Answer 18

It will block LPS binding to LPS binding protein; not useful for other causes of sepsis

Question 19

When should you use antibiotics in the treatment of sepsis?

Answer 19

• neutrophil count 1000 cells/uL or less
• septicemia is suspected or documented
• source of infection is found/documented

Question 20

What are some treatment methods to prevent laminitis?

Answer 20

• circulatory support
• flunixin
• pentoxifylline
• J5 plasma
• careful exercise
• cryotherapy-ice feet if high risk

Question 21

Describe how LPS induces CV shock

Answer 21

LPS binds LPS binding protein–>complex binds TLR and/or other receptors on macrophage–>triggers cascade–>production of pro-inflammatory mediators, toxic compounds inside cell, COX-2 upregulation–>PGE2 that is responsible for CV shock in septic patient