12.4: Sepsis Flashcards

1
Q

What component for gram negative organisms can cause shock?

A
  • Lipid polysaccharide

- It is actually the host response to to this and infection that cause shock

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is SIRS? Criteria?

A

“Systemic inflammatory response syndrome”
- Massive inflammatory rxn from systemic cytokine release
Must include 2 of the following:
1. Temp > 38 or 90
3. RR > 20 or PaCO212k or 10% immature

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is Sepsis?

A
  • SIRS + documented cultured infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is severe sepsis?

A
  • Sepsis + organ dysfunction or hypoperfusion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Signs of severe sepsis?

A
  1. Lactic acidosis
  2. Oliguria: insul to kidney
  3. Hypoxemia
  4. Acute change in mental status
  5. Edema
  6. HYPERglycemia
  7. Tachycardia / tachypnea
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is septic shock?

A
  • Refractory hypotension plus hypoperfusion organ abnormalities
  • BP cannot be brought up
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is ileus?

A
  • Absent normal bowl sounds from inability of intestine to contract normally and move waste out of body
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Causes of SIRS?

A
  1. Bacteremia
  2. Burn
  3. Trauma
  4. Acute pancreatitis
  5. Acute adrenal insufficiency
  6. Ischemic tissue injury
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Percent of septic ptns with positive cultures?

A
  • 50%

- Close to 50/50 split between gram +/- and some fungi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is gram negative LPS?

A

“Lipopolysaccharide”

  • Found in all gram negative orgs
  • On the outer membrane of molecule
  • LIPID A is core unit it which biologic activity resides
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Where does bioactive capability of LPS reside?

A
  • Lipid A

- Long chain fatty acids in outer membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Can organisms without LPS cause sepsis? Examples?

A

Yes

  1. Gram positives
  2. Fungi
  3. Parasites
    * **Exotoxins and other components of cell wall can cause
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are TLRs?

A

“Toll like receptors”

- Recognizing PAMPs and DAMPs on molecules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What does TLR2 recognize?

A
  • Peptidoglycan of gram positives
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What does TLR4 recognize?

A
  • LPS from gram negatives
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What does binding to TLR cause?

A
  • Intracellular signalling leading to transcription of proinflammatory cytokines
17
Q

What is LPB?

A

“LPS binding protein”

  • Acute phase reactant that binds to LPS
  • Complex binds CD4 receptor on inflammatory cells activating inflammatory genes
  • Can also complex with endothelial cells causing adhesion and cytokine release
18
Q

What are the proinflammatory cytokines?

A
  1. TNF Alpha
  2. IL-1
  3. Il-2
  4. IL-6
  5. IL-8
  6. IL-10
19
Q

Which two cytokines are major players in sepsis

A
  1. TNF Alpha

2. IL-1

20
Q

What are the anti inflammatory cytokines?

A
  1. IL4

2. IL 10

21
Q

How is coagulation cascade activated in sepsis?

A
  • TNF alpha increases expression of tissue factor on macs

- Intrinsic factor XII can be activated as well

22
Q

What does TNF activate?

A
  • Coagulation cascade via TF on macs
  • Plasminogen
  • Leads to DIC with microthrombi
23
Q

Mediators of dilation in sepsis?

A
  1. Kinin system: activated by factor XII
  2. NO: activated by TNF IL1 and LPS
  3. Impaired ADH secretion
24
Q

Main cause of cellular injury in sepsis?

A
  1. Ischemia from adherance and microcirculatory lesions

- Direct cytotoxicity and apoptosis issues as well

25
Q

Which part of host immune system activated in sepsis?

A
  • Innate via TLR leading to inflammatory cytokine release
26
Q

Other systems activated in sepsis?

A
  1. Coagulation/Fibrinolytic = DIC
  2. Complement
  3. Kinin
  4. NO
27
Q

3 major clinical components of clinical shock?

A
  1. Systemic arterial hypotension
  2. Clinical signs of hypoperfusion
  3. Hyperlactatemia: > 1.5mmol/L
28
Q

Definition of systemic arterial hypotension in sepsis?

A

Systolic

29
Q

What are the 3 windows into HYPOperfusion in sepsis?

A
  1. Skin – cold, clammy, vasoconstriction, cyanosis

2. Renal – UOP

30
Q

Clinical studies in SIRS?

A
• WBC >12,000 or 10% immature forms)
• Elevated CRP
• Elevated Procalcitonin
• Glucose >140 in absence of diabetes – SEPSIS
• Decreased O2 saturation or PaO2
• Elevated creatinine
• Elevated bilirubin, other liver tests
• Thrombocytopenia, elevated INR
Elevated lactate
31
Q

Fluid management in sepsis?

A
  1. Replace .5L in first 30 min
    - Crystalloid fluids are preferred
  2. Central venous catheter: want CVP 8-12
32
Q

Target for MAP in septic ptn.?

A

> 65

33
Q

When should antibiotics be administered in sepsis?

A
  • Empirical broad spectrum IV within first hour

- Not waiting for culture results

34
Q

Next volume step after fluids?

A
  • Vasopressors: NE
35
Q

Bundle to be completed in first 3 hours of sepsis?

A
  1. Measure lactate
  2. Culture blood
  3. Broad spectrum antibiotics
  4. 30ml/kg crystalloid fluids
36
Q

Bundle to be completed in first 6 hours of sepsis?

A
  1. Vasopressors for refractory hypotension: MAP>65

2. Remeasure lactate

37
Q

Steroids effective in controlling septic shock?

A

Hydrocortisone (200 mg/day) in patients in
whom hypotension persists despite adequate
fluid resuscitation and vasopressor therapy

38
Q

Are there host modifying drugs for sepsis?

A

No