Sepsis and Septic Shock Flashcards

1
Q

What is sepsis?

A

Systemic illness caused by microbial invasion of normally sterile parts of the body

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2
Q

What is SIRS?

A

Systemic inflammatory response syndrome

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3
Q

What does the traditional model of sepsis show?

A

The relationship of infection and SIRS in causing sepsis

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4
Q

What is the definition of sepsis?

A

Life threatening organ dysfunction caused by dysregulated host response to infection

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5
Q

How can organ dysfunction be identified?

A

An acute change in total SOFA score > 2

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6
Q

How can septic shock be identified?

A

A clinical construct of sepsis with persisting hypotension requiring vasopressors to maintain MAP (>65mmHg) and a serum lactate of >2mmol/l despite adequate volume resuscitation

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7
Q

Which components make up the SOFA score of Sepsis-3?

A

PaO2/FiO2, platelets, bilirubin, MAP, GCS, creatinine and urine output

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8
Q

What are the components of qSOFA and what does it mean?

A
  • Hypotension: systolic BP <100 mmHg
  • Altered mental state
  • RR > 22
  • Score > 2 suggests a greater risk of a poor outcome (long ICU stay or death)
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9
Q

Describe the pathophysiology of sepsis

A
  • Uncontrolled inflamm. response
  • Features of immunosuppression: loss of delayed hypersensitivity, inability to clear infection and predisposition to nosocomial infection
  • Initial increase in inflamm. mediators
  • Shift toward an anti-inflammatory immunosuppressive phase
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10
Q

Which bacterial toxins are commonly released?

A
  • Gram negative: lipopolysaccharide (LPS)
  • Gram positive: microbial -associated molecular pattern (Lipoteichoic acid and Muramyl dipeptides)
  • Super-antigens: staphylococcal toxic shock syndrome toxin and streptococcal exotoxins
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11
Q

Describe the mediator role in sepsis

A
  • TH1 vs TH2
  • Pro-inflamm mediators: cause inflamm. response that characterises sepsis
  • Compensatory anti-inflamm response: can cause immunoparalysis
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12
Q

What is the effect of excessive pro-inflammatory mediators?

A
  • Promote endothelial cell-leukocyte adhesion
  • Release of arachidonic acid metabolites
  • Complement activation
  • Vasodilatation of blood vessels by NO
  • Increase coagulation by release of tissue factors and membrane coagulants
  • Cause hyperthermia
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13
Q

What is the effect of excessive anti-inflammatory mediators?

A
  • Inhibit TNF alpha
  • Augment acute phase reaction
  • Inhibit activation of coagulation system
  • Provide negative feedback mechanisms to pro-inflamm mediators
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14
Q

What are the clinical features of organ dysfunction (and therefore sepsis)?

A
  • Altered consciousness, confusion and psychosis
  • Tachypnoea, PaO2 < 70mmHg and sats <90%
  • Decreases platelets and protein C
  • Increased PT/APTT and D-dimer
  • Tachycardia and hypotension
  • Oliguria, anuria and increased creatinine
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15
Q

What are the general features of sepsis?

A
  • Fever: chills, rigors, flushes, cold sweats, night sweats etc.
  • Hypothermia (esp. elderly, young children and immunosuppressed)
  • Altered mental state
  • Hyperglycaemia in the absence of diabetes
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16
Q

What would you expect the inflammatory variables to be in sepsis?

A
  • Leucocytosis (WWC> 12,000/ml) or leucopenia (WCC < 4,000/ml)
  • Normal WCC with greater than 10% immature forms
  • High CRP
  • High procalcitonin
17
Q

What would you expect the haemodynamic variables to be in sepsis?

A
  • BP: Systolic <90mmHg or MAP <70mmHg

- SvO2 > 70%

18
Q

Which organ dysfunction variables would you expect to see in sepsis?

A
  • Arterial hypoxaemia (PaO2/FiO2 < 50mmHg)
  • Oliguria (<0.5 ml/kg/hr)
  • Increased creatinine
  • Coagulation abnormalities (PT > 1.5 or APTT > 60s)
  • Ileus
  • Thrombocytopenia
  • Hyperbilirubinaemia
19
Q

Which tissue perfusion variables might you see in sepsis?

A
  • High lactate

- Skin mottling and reduced capillary perfusion

20
Q

Which host factors may effect the sepsis presentation?

A
  • Age
  • Co-morbidities
  • Immunosuppression (acquired, drug induced and congenital)
  • Splenectomy
21
Q

Which organism factors will effect the presentation of sepsis?

A
  • Gram positive vs negative
  • Virulence factors (MRSA, toxin secretion, ESBL etc.)
  • Bioburden
22
Q

What are the components of the Sepsis 6?

A
  • Blood cultures
  • Blood lactate
  • Measure urine output (catheter if severe sepsis or septic shock)
  • Oxygen sats (aim for 94-98%)
  • IV antibiotics
  • IV fluid challenge (crystalloid bollus)
23
Q

When should a referral to HDU be considered?

A
  • BP low and responsive (?) to fluids
  • Lactate > 2 despite fluid resuscitation
  • Elevated creatinine
  • Oliguria
  • Liver dysfunction
  • Bilateral infiltrates and hypoxaemia
24
Q

When should a referral to ITU be considered?

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