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SilversteinHopper > 91: Sepsis and Septic Shock > Flashcards

91: Sepsis and Septic Shock Flashcards

1
Q

What is the incidence and mortality rate of sepsis in veterinary medicine?

A
  • the incidence rate is not established
  • mortality ranges from 20-68%
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2
Q

What is the definition of Bacteremia?

A

presence of live bacterial organisms in the bloodstream

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3
Q

What is the definition of sepsis?

A

clinical syndrome caused by infection and the host’s systemic inflammatory response to it

can be bacterial, viral, protozoal, or fungal in origin

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4
Q

What is the definition of septic shock?

A

Acute circulatory failure and persistent arterial hypotension despite volume resuscitation, associated with sepsis

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5
Q

what is the arterial blood pressure cutoff for the definition of septic shock in veterinary and human patients?

A

the critical BP cutoff is not established in veterinary patients, but extrapolated from the human consensus:

  • In people, hypotension is defined by a systolic arterial pressure less than 90 mm Hg, a mean arterial pressure less than 60,
  • or a reduction in systolic pressure of greater than 40 mm Hg from baseline despite adequate volume resuscitation, in the absence of other causes of hypotension.
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6
Q

what is the definition of Systemic inflammatory response syndrome (SIRS)?

A

The clinical signs of systemic inflammation in response to infectious or noninfectious insults (e.g., trauma, pancreatitis, burns, snakebites, neoplasia, and heat stroke).

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7
Q

what is the definition of multiple organ dysfunction syndrome (MODS)?

A

Physiologic derangements of the endothelial, cardiopulmonary, renal, nervous, endocrine, and gastrointestinal (GI) systems associated with the progression of uncontrolled systemic inflammation and disseminated intravascular coagulation (DIC).

  • two or more organs affected
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8
Q

What are the 4 hallmarks of sepsis

A
  1. Dysregulation of vasomotor tone
  2. Increased vascular permeability
  3. Dysfunctional microcirculation
  4. Coagulation abnormalities
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9
Q

What is PIRO?

A

a concept to stage sepsis, adopted after the 2001 international sepsis definition conference

to describe clinical manifestation of the infection and the host response to it

Predisposition, Insult or Infection, Response, Organ dysfunction

not yet adapted in vet med due to lack of advanced diagnostic techniques

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10
Q

What is the most common orignin of gram negative sepsis in cats and dogs?

A

gastrointestinal and genitourinary systems

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11
Q

What is the most common origin of gram positive sepsis in dogs and cats?

A

skins, injured soft tissue, IV catheters

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12
Q

What is the most important pathogen-associated molecular pattern of gram negative bacteria?

Explain how it leads to inflammation and what receptors/cytokines/cells are involved in this pathway

A

Lipopolysaccharide (LPS) > part of the gram-negative bacterial cell wall

  • binds to lipololysacchardie binding protein (LBP) > forms LPS-LBP complex
  • LPS-LBP complex binds to macrophage membrane-bound CD14
  • macrophage activation > Toll-like receptors > signaling transfuction to the nucleus > starts transcription of inflammatory cytokines

inflammatory cytokines:

  • tumor necrosis factor-alpha (TNF-alpha)
  • IL-1, IL-6, IL-8
  • interferon gamma
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13
Q

What does CARS stand for? List 3 of its cytokines.

A

compensatory anti-inflammatory response syndrome > counter-inflammatory mediators to reduce inflammatory response

IL-4, IL-10, IL-13

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14
Q

What are the most important pathogen-associated molecular patterns (PAMPs) of gram positive bacteria?

A

cell wall components:

  • lipoteichoic acid
  • peptidoglycan
  • peptidoglycan stem peptides

bacterial DNA

exotoxins

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15
Q

why are exotoxins of gram positive bacteria “superantigens”?

A

soluble bacterial exotoxins induce widespread T cell activation > inflammatory cytokines released:

  • interferon gamma
  • TNF-alpha
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16
Q

How can neutrophils lead to extensive host tissue damage?

A

release of:

  • ROS
  • proteases
  • lysozymes
  • lactoferrin
  • cathepsins
  • defensins
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17
Q

explain the main mechanism of sepsis leading to hypotension

A

bacterial endotoxins, cytokines like TNF-alpha and IL-1, and mediators like PAF (platelet activating factor) >

> lead to accumulation of iNOS (inducible nitric oxide synthase) >

> high levels of NO produced >

> potent smooth muscle relaxant >

> loss of vasomotor tone >

> septic shock

18
Q

what are ways to quantify/measure the extent of NO production in dogs?

A

plasma nitrate and nitrite measurements

= breadown products of NO

have shown to be elevated in septic dogs with SIRS compared to healthy controls

19
Q

Briefly summarize how inflammation leads to a hypercoagulable state

A

inflammatory cytokines > upregulate TF (tissue factor) levels > TF combines with VIIa > initate coagulation cascade

TF-VIIa complex and subsequent products trigger release of even more inflammatory cytokines and cause platelet activation

downregulation of anticoagulants

  • downregulation of antithrombin, tissue factor pathway inhibitor, tissue plasminogen activator (tPA)
  • inhibition of protein C/S pathway > less active protein C
  • increased plasminogen activator inhibitor (PAI-1)
20
Q

Explain how sepsis can lead to cryptic shock

A

endothelial damage, increased vascular permeability, microcirculatory derangements from:

  • endothelial dysfunction
  • alteration and damage to the endothelial glycocalyx layer
  • rheologic changes to red blood cells
  • leukocyte activation
  • microthrombosis
  • loss of vascular smooth muscle autoregulation

⇒ decreased tissue oxygen extration ⇒ tissue hypoxia

21
Q

What is cryptic shock?

A

microcirculatory disturbances despite normal macrohemodynamic variables

22
Q

What is VEGF?

A

Vascular endothelial growth factor

  • hypoxia-responsive angiogenic factor associated with increasing vascular permeability
  • higher levels in septic dogs have been associated with increased mortality
23
Q

How does increased vascular permeability lead to tissue hypoxia?

A

increased vascular permeability ⇒ efflux of water, proteins, and solutes into the interstitial space ⇒ increased distance from RBC in capillaries to target cells and mitochondira

24
Q

what is cytopathic hypoxia?

A

primary mitochondiral dysfunction, e.g., from sepsis itself

25
Q

What are common bacteria causing sepsis from the peritoneal cavity/septic peritonitis (e.g., GI perforation)

A
  • Coagulase-negative Staphylococcus spp,
  • Enterococcus spp,
  • B-hemolytic Streptococcus spp,
  • Escherichia coli,
  • Klebsiella spp,
  • Enterobacter spp,
  • Pasteurella spp,
  • Corynebacterium spp
26
Q

What are common bacteria causing sepsis from the pulmonary parenchyma or pleura (e.g., pneumonia, pyothorax, …)

A
  • B-hemolytic Streptococcus spp,
  • E. coli,
  • Bordetella bronchiseptica,
  • Staphylococcus spp,
  • E. coli,
  • Klebsiella spp,
  • Pseudomonas spp,
  • Enterococcus faecalis,
  • Acinetobacter spp,
  • Pasteurella spp
27
Q

What are common bacteria causing sepsis from the GI tract (e.g., enterocolitis, bacterial translocartion)?

A

E. coli

28
Q

What are common bacteria causing sepsis from the reproductive tract? (e.g., pyometra, prostatitis)?

A
  • Group G Streptococcus spp,
  • Enterococcus spp,
  • B-hemolytic Streptococcus spp,
  • E. coli,
  • Klebsiella spp
29
Q

What are common bacteria causing sepsis from the urinary tract? (e.g., pyelonephritis, bacterial cystitis)

A
  • B-hemolytic Streptococcus spp,
  • E. coli,
  • Acinetobacter spp,
  • Enterococcus spp
30
Q

What are common bacteria causing sepsis from the soft tissue or bones (e.g., trauma, osteomyelitis, bite wounds)?

A
  • E. coli
  • Enterobacter spp.
31
Q

What are common bacteria causing sepsis from the cardiovascular system? (e.g., endocarditis)

A
  • Staphylococcus lugdunensis,
  • Bartonella spp,
  • S. aureus,
  • E. faecalis,
  • Granulicatella spp,
  • Streptococcus spp,
  • Brucella spp
32
Q

What are considerations to be made when chosing an empirical antimicrobial before culture results are available?

A
  • Location of the infection (and ability of antimicrobial to penetrate the site)
  • Suspected bacterial flora
  • Community versus nosocomial source
  • Duration of hospitalization à long hospitalization time makes likelihood of multidrug-resistant bacteriahigher à consider hospital antibiograms
  • Previous exposure to antimicrobials

bactericidal rather than bacteriostatic antimicrobials preferred

33
Q

How many mL of plasma are needed to raise the albumin by 0.5 g/dL?

A

22 mL/kg of plasma

34
Q

How could vasopressors worsen sepsis?

A
  • Vasopressors may also result in excessive vasoconstriction –> particularly splanchnic and renal circulation –> GI and renal ischemia
  • Splanchnic vasoconstriction may exacerbate septic state due to loss of gut barrier function and bacterial translocation
35
Q

What is the venous oxygen saturation reflective of?

A

the difference between DO2 and VO2

36
Q

what are the options for measuring venous oximetry?

A

blood sampling (blood gas)

co-oximetry

continuous fiberoptic measurement (spectrophotometry)

37
Q

Where should blood for SvO2 ideally be sampled from?

A

pulmonary artery

38
Q

By how much and why differ SvO2 and ScvO2?

A

ScvO2 is in health approximately 2-3% lower than SvO2

  • because of the high metabolic rate of the brain and the cranial part of the body
  • because of vascular circuits with low oxygen extraction (i.e., renal blood flow)
39
Q

How does the difference between the SvO2 and ScvO2 change during states of shock?

A

SvO2 becomes higher than ScvO2 due to prioritization of coronary and cerebral circulation as well as decrease in splanchnic circulation

40
Q

What ScvO2 and SvO2 target goals does the SSC recommend?

A

ScvO2 70% or greater

SvO2 65% or greater

SilversteinHopper (11 decks)

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