Sepsis and Septic shock Flashcards

1
Q

What is the definition of sepsis?

A
  • Sepsis derives from the Greek work “sepo” meaning decay or decomposition - Systemic illness caused by microbial invasion of normally sterile parts of the body
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2
Q

What is the traditional pathway of sepsis?

A

SIRS (systemic inflammatory response syndrome) - Sepsis (SIRS + infection) - Severe sepsis (Sepsis and end organ damage) - Septic shock (severe sepsis and hypotension)

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3
Q

What is the definition of septic shock?

A

Identified with a clinical construct of sepsis with persisting hypotension requiring vasopressors to maintain MAP >65mmHg and having a serum lactate of >2mmol/l despite adequate volume resuscitation Patients with septic shock have a hospital mortality of 40%

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4
Q

What do we use to score sepsis and what are the scores?

A

JAMA score

0 - 4

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5
Q

What is the criteria of qSOFA?

A
  • Hypotension systolic <100mmHg
  • Altered mental status
  • Tachypnea RR >22/min
  • Score of >= 2 suggestes greater risk of poor outcome
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6
Q

Why is sepsis important?

A
  • Common condition
  • Becoming more common
  • Increased morbidity
  • Increased mortality
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7
Q

For each hour delayed in giving antibs how much does mortality increase?

A

7.6%

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8
Q

Sepsis: time is ……?

A

Life

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9
Q

In what three main ways does the body defend against sepsis?

A
  • Physical barrier: skin, mucosa, epithelial lining
  • Innate immune system: IgA in GI tract, dendritic cells, macrophages
  • Adaptive immune system - lymphocytes, immunoglobulins
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10
Q

What is the origin of sepsis?

A
  • Originates from a breach of integrity of host barrier, whether physical or immunological
  • Organism enters the bloodstream creating a septic state
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11
Q

What are the three stages of pathogenesis of sepsis?

A
  1. Release of bacterial toxins
  2. Release of mediators
  3. Effects of specific excessive mediators
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12
Q

Explain phase 1 in depth.

What are commonly released toxins in stage 1 of pathophysiology in sepsis?

A
  • Bacterial invasion into body tissues is the source of dangerous toxins
  • May/may not be cleared by innate immune system

Commonly released toxins

  • Gram negative: lipopolysaccaride
  • Gram positive: MAMP, staphylococcal toxic shock syndrome toxin
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13
Q

Elaborate on stage 2 of pathophysiology of sepsis.

A

Release of mediators in response to infection

  • Effects of infections due to endotoxin release
  • Effects of infections due to exotoxin release
  • Mediator role on sepsis
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14
Q

What occurs in the pathway of endotoxin release?

A
  • LPS needs an LPS-binding protein to bind to macrophages
  • LTA do not need such proteins
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15
Q

What two types of mediators and what are their roles in sepsis?

A
  • Two types of mediators can be released
  • Pro-inflammatory mediators – causes inflammatory response that characterises sepsis
  • Compensatory anti-inflammatory reaction – can cause immunoparalysis
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16
Q

What is stage 3 of sepsis?

A

The effects of specific excessive mediators:

  • Pro inflammatory mediators
    • 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
  • Anti-inflammatory mediators
    • inhibit TNF alpha
    • Augment acute phase reaction
    • Inhibit activation of coagulation system
    • Provide negative feedback mechanisms to pro-inflammatory mediators
17
Q

What happens when the scales are tipped towards the pro-inflammatory side of sepsis?

A
18
Q

What occurs when the scales are tipped towards the compensatory anti-inflammatory side of sepsis?

A

Immunoparalysis with uncontrolled infection and multiorgan failure

19
Q

What does the clinical features of sepsis depend on?

A
  • Dependent on a number of factors
  • Host
  • Organism
  • Environment
20
Q

How does organ dysfunction present in: brain, blood, liver, lungs, heart, kidney?

A
21
Q

What are the general clinical features of sepsis? (6)

A
  • Fever >38oC – presenting as chills, rigors, flushes, cold sweats, night sweats, etc
  • Hypothermia <36oC – especially in the elderly and very young children (remember the immunosuppressed)
  • Tachycardia >90 beats/min
  • Tachypnoea >20 /min
  • Altered mental status – especially in the elderly
  • Hyperglycaemia >8mmol/l in the absence of diabetes
22
Q

What are some of the host effects on the way sepsis presents?

A
  • Age
  • Co-morbidities (COPD, DM, CCF, CRF, disseminated malignancy)
  • Immunosuppression
    • Acquired – HIV/AIDS
    • Drug-induced – steroids, chemotherapeutic agents, biologics
    • Congenital – agammaglobulinaemia, phagocytic defects, defects in terminal complement component
  • Previous surgery - splenectomy
23
Q

What are some of the organism effects on the way sepsis presents?

A
  • Gram positive versus Gram negative
  • Virulence factors (example: MRSA, toxin secretion, ESBL, KPC, NDM-1)
  • Bioburden
24
Q

Effect of environment on sepsis presentation?

A
  • occupation
  • travel
  • hospitalisation
25
Q

What is the sepsis six?

A
  • Oxygen
  • Blood cultures
  • Antibiotics
  • FLuid challenge
  • Lactate
  • Urine output
26
Q

How do we use the sepsis six?

A

take 3: give 3

  • Blood cultures (make microbiological diagnosis)
  • BLood lactate (generalised hypoperfusion/severe sepsis/poorer prognosis)
  • Measure urine output (renal dysfunction)
  • Oxygen aim sats 94-98%
  • IV antibiotics
  • IV fluid challange
27
Q

What are the two types of lactate available and why?

A

Type A - hypoperfusion

Type B - mitochondrial toxins, alcohol, malignancy and metabolism errors

28
Q

What IV fluids do we administer?

A
  • 30ml/kg fluid challenge (expert opinion)
  • 2.1L 70kg patient
29
Q

At what point should referral to HDU be considered?

A
  • Low BP responsive to fluid
  • Lactate >2 despite fluid resuscitation
  • Elevated creatinine
  • Oliguria
  • Liver dysfunction, Bil, PT, Plt
  • Bilateral infiltrates, hypoxaemia
30
Q

When do we consider ITU?

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