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Infection > Sepsis and Septic Shock > Flashcards

Sepsis and Septic Shock Flashcards

1
Q

What is sepsis?

A

Life-threatening organ dysfunction caused by dysregulated host response to infection

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2
Q

What is septic shock?

A

Clinical construct of sepsis with persisting hypotension requiring vasopressors to maintain MAP >65mmHg and having serum lactate of >2mmol/L despite adequate volume resuscitation

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3
Q

How is organ dysfunction identified in sepsis?

A

Organ dysfunction identified as acute change in total SOFA score >2

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4
Q

What is sepsis caused by?

A

Is a systemic illness caused by microbial invasion of normally sterile parts of the body

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5
Q

Describe the traditional model of sepsis?

A
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6
Q

What is qSOFA used for?

A

To identify if a patient is likely to require ICU or die in hospital

Score of 2 or more indicates greater risk of poor outcome

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7
Q

What does qSOFA look at?

A
  • Hypotension systolic BP <100mmHg
  • Altered mental state
  • Tachypnea RR >22/min
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8
Q

What is survival in septic shock based on?

A

Survival in septic shock is based on antimicrobial delay:

  • Each hour delay increases mortality by 7.6%

Remember “time is life”

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9
Q

What are some of the bodies defences against sepsis?

A
  • Physical barrier
    • Skin, mucosa, epithelial lining
  • Innate immune system
    • IgA in gastrointestinal tract, dendritic cells, macrophages
  • Adaptive immune system
    • Lymphocytes, immunoglobulins
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10
Q

Describe the pathophysiology of sepsis?

A

Systemic immune response results in shift of fluid to third space and microthrombi.

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11
Q

What are the 3 phases of pathogenesis of sepsis?

A
  1. Release of bacterial toxins
    1. Bacterial invasion into body tissues source of dangerous toxins
    2. May or may not be neutralised by existing immune system
    3. Commonly released toxins
      1. Gram negative
        1. Lipopolysaccharide (LPS)
      2. Gram positive
        1. Microbial-associated molecular pattern (MAMP)
          1. Lipoteichoic acid
          2. Murmyl dipeptides
        2. Superantigens
          1. Staphylococcal toxic shock syndrome toxin (TSST)
          2. Streptococcal exotoxins
  2. Release of mediators
    1. Effects due to endotoxin release
      1. LPS needs an LPS-binding protein to bind to macrophages
      2. LTA do not need such proteins
    2. Effects due to exotoxin release
      1. Pro-inflammatory response
      2. Small amounts of superantigens cause a large amount of mediators to be secreted causing cascade effect
    3. Mediator role on sepsis
    4. Two types of mediators can be released
      1. Pro-inflammatory mediators – cause inflammatory response that characterises sepsis
      2. Compensatory anti-inflammatory reaction – can cause immunoparalysis
  3. Effects of specific excessive mediators
    1. Pro-inflammatory mediators
      1. Promote endothelial cell – leukocyte adhesion
      2. Release of arachidonic acid metabolites
      3. Complement activation
      4. Vasodilation of blood vessels by NO
      5. Increase coagulation by release of tissue factors and membrane coagulants
      6. Cause hyperthermia
    2. Anti-inflammatory mediators
      1. Inhibit TNF alpha
      2. Augment acute phase reaction
      3. Inhibit activation of coagulation system
      4. Provide negative feedback mechanism to pro-inflammatory mediators
    3. Balance between pro and anti-inflammatory mediators determines outcome
      1. Pro-inflammatory stronger causes septic shock with multiorgan failure and death

Anti-inflammatory stronger causes immunoparalysis with uncontrolled infection and multiorgan failure

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12
Q

What are commonly released toxins that cause sepsis?

A

gram negative

  • lipopolysaccharide (LPS)

gram positive

  • microbial-associated molecular pattern (MAMP)
  • lipoteichoic acid
  • murmyl dipeptides

- superantigens

  • staphylococcal toxic shock syndrome toxin (TSST)
  • streptococcal exotoxins
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13
Q

What are examples of superantigens that can cause sepsis?

A
  1. Staphylococcal toxic shock syndrome toxin (TSST)
  2. Streptococcal exotoxins
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14
Q

What are the 2 types of mediators that can be released in the pathogenesis of sepsis?

A
  1. Pro-inflammatory mediators – cause inflammatory response that characterises sepsis
  2. Compensatory anti-inflammatory reaction – can cause immunoparalysis
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15
Q

What do pro-inflammatory mediators cause in relation to sepsis?

A

Cause inflammatory response that characterises sepsis

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16
Q

What do anti-inflammatory mediators cause in relation to sepsis?

A

Can cause immunoparalysis

17
Q

What are the specific effects of pro-inflammatory mediators?

A
  1. Promote endothelial cell – leukocyte adhesion
  2. Release of arachidonic acid metabolites
  3. Complement activation
  4. Vasodilation of blood vessels by NO
  5. Increase coagulation by release of tissue factors and membrane coagulants
  6. Cause hyperthermia
18
Q

What are the specific effects of anti-inflammatory mediators?

A
  1. Inhibit TNF alpha
  2. Augment acute phase reaction
  3. Inhibit activation of coagulation system
  4. Provide negative feedback mechanism to pro-inflammatory mediators
19
Q

Balance of pro and anti-inflammatory markers determines outcome of sepsis, what does pro-inflammatory being stronger cause?

A
  1. Pro-inflammatory stronger causes septic shock with multiorgan failure and death
20
Q

Balance of pro and anti-inflammatory markers determines outcome of sepsis, what does anti-inflammatory being stronger cause?

A
  1. Anti-inflammatory stronger causes immunoparalysis with uncontrolled infection and multiorgan failure
21
Q

What is endotoxin release?

A
  • LPS (lipopolysaccharide) needs an LPS-binding protein to bind to macrophages
  • LTA (lipoteichoic acid) does not need such a protein
22
Q

Which of LPS and LTA needs a binding protein before binding to macrophage?

A

LPS

23
Q

A common gram negative toxin with endotoxin release is?

A

LPS

24
Q

A common gram positive toxin with endotoxin release is?

A

LTA

25
Q

What toxins have exotoxin release?

A

Superantigens

26
Q

What are some examples of pro-inflammatory markers?

A
27
Q

What are some examples of anti-inflammatory markers?

A
28
Q

What do the clinical features of sepsis depend on?

A
  • Host
  • Organism
  • Environment
29
Q

What are some signs of organ dysfunction?

A
30
Q

What are some general features of sepsis?

A
  • Fever
    • Presenting as chills, rigors, flushes, cold sweats, night sweats etc
  • Hypothermia
    • Especially in elderly and young children (remember the immunosuppressed)
  • Tachycardia
  • Tachypnoea
  • Altered mental state
    • Especially in elderly
  • Hyperglycaemia in absence of diabetes
31
Q

What are some diagnostic markers of sepsis?

A
  • Inflammatory
    • Leucocytosis (WCC > 12,000/ml)
    • Leucopenia (WCC < 4,000/ml)
    • Normal WCC with greater than 10% immature forms
    • High CRP
    • High procalcitonin
  • Haemodynamic
    • Arterial hypotension (systolic <90mmHg or MAP <70mmHg)
    • SvO2 >70%
  • Organ dysfunction
    • Arterial hypoxaemia (PaO2/FiO2 < 50mmHg)
    • Oliguria (<0.5ml/kg/h)
    • Creatinine increase compared to baseline
    • Coagulation abnormalities (PT >1.5 or APTT >60s)
    • Ileus
    • Thrombocytopenia (<150,000/ml)
    • Hyperbilirubinaemia
  • Tissue perforation
    • High lactate
    • Skin mottling and reduced capillary perfusion
32
Q

What are some effects of the host on sepsis?

A
  • Age
  • Co-morbidities
  • Immunosuppression
    • Acquired such as HIV/AIDS
    • Drug induced such as steroids, chemotherapy agents, biologics
    • Congenital
  • Previous surgery
    • Such as splenectomy
33
Q

What are some effects of the organism on sepsis?

A
  • Gram positive vs gram negative
  • Virulence factors
    • Such as MRSA, toxin secretion etc
  • Bioburden
34
Q

What are some effects of the environment on sepsis?

A
  • Occupation
  • Travel
  • Hospitalisation
35
Q

In general, what is the process for recognising and managing sepsis?

A
  1. Recognise clinical presentation of sepsis
  2. Identify source of infection
  3. Treat with antibiotics, fluids and oxygen
36
Q

What is the sepsis 6 used for management of sepsis?

A
  • Give 3
    • Blood cultures
    • Blood lactate
      • Marker of hypoperfusion/severe sepsis/poorer prognosis
    • Measure urine output
      • Low urine output is marker of renal dysfunction
  • Take 3
    • Oxygen aim sats 94-98%
    • IV antibiotics
    • IV fluid challenge
      • 30ml/kg
37
Q

When should you consider HDU referal?

A
  • Low BP responsive to fluids
  • Lactate >2 despite fluid resuscitation
  • Elevated creatinine
  • Oliguria
  • Liver dysfunction, Bil, PT, Plt
  • Bilateral infiltrates, hypoxaemia
38
Q

When should you consider ITU?

A
  • Septic shock
  • Multi-organ failure
  • Requires sedation, intubation and ventilation

Infection (18 decks)

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