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Flashcards in Sepsis Deck (16)
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1
Q

Define sepsis

A

Defined as life threatening organ dysfunction caused by dysregulated host response to infection

SOFA score >2 can identify organ dysfunction consequent to infection and indicates overall mortality risk 10%

2
Q

Describe SIRS

A

SIRS

  • temp >38 or <36
  • HR >90
  • RR >20 or PaCO2 <32
  • WBCs > 12,000 or <4000 or >10% bands
3
Q

Describe the traditional model of sepsis

A

SIRS

Sepsis; SIRS + infection

Severe sepsis; sepsis + end organ damage

Septic shock; severe sepsis + hypotension

4
Q

Describe qSOFA score

A

QUICK Sequential Organ Failure Assessment

  • GCS < 15
  • resp rate ≥ 22
  • systolic bp ≤ 100
5
Q

Define septic shock

A

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 resus

Patients with septic shock have a hospital mortality of 40%

6
Q

What are the sepsis 6?

A

TAKE 3 GIVE 3

  1. Administer Oxygen aim sats 94-98%
  2. Take blood cultures
  3. Give IV antibiotics
  4. Give IV fluids
  5. Check serial lactates
  6. Measure urinary output
7
Q

Describe the pathophysiology of sepsis

A

Uncontrolled inflammatory response

Features consistent with immunosuppression

  • loss of delayed hypersensitivity
  • inability to clear infection
  • predisposition to nosocomial infection
8
Q

Name the three phases in the pathogenesis of sepsis

A
  1. Release of bacterial toxins
  2. Release of mediators
  3. Effects of specific excessive mediators
9
Q

Describe the release of bacterial toxins in sepsis

A

Bacterial invasion into body tissues source of dangerous toxins

Might be neutralised by existing immune system

Commonly

  • Gram -ve; lipopolysaccharide
  • Gram +ve; Superantigens, microbial-associated molecular pattern
10
Q

Describe the release of mediators in response to infection in sepsis

A

Effects of infections due to endotoxin release

Exotoxin release; pro-inflammatory response

Two types of mediators; Th1 or Th2

11
Q

Describe the effects of specific excess mediators in sepsis

A

Pro-inflammatory mediators

  • promote endothelial cell; leukocyte adhesion
  • release of arachidonic acid metabolites
  • complement activation
  • vasodilation of blood vessels by NO
  • increase coag by release of tissue factors and membrane coagulants
  • cause hyperthermia

Anti-inflammatory mediators

  • inhibit TNF-alpha
  • augment acute phase reaction
  • inhibit activation of coag system
  • provide -ve feedback to pro-inflammatory mediators
12
Q

Describe clinical features of sepsis

A
  • Altered consciousness
  • fever; chills, rigors, flushes, night sweats etc.
  • confusion
  • psychosis
  • tachypnoea
  • tachycardia
  • hypothermia
  • hypotension
  • jaundive
  • hepatomegaly
  • oliguria
  • anuria
13
Q

Describe the possible effects of a host on sepsis presentation

A
Age
Co-morbidities
Immunosuppression
- acquired; HIV/AIDS
- drug induced; steroids, biologics
- congenital
Previous surgery i.e. splenectomy
14
Q

Why take lactate measurement in sepsis?

A

Marker of generalised hypoperfusion i.e. severe sepsis

15
Q

When to consider HDU referral in sepsis?

A
  • low bp unresponsive to fluids
  • lactate >2 despite fluid resus
  • elevated creatinine
  • oliguria
  • liver dysfunction, bil, PT, plt
  • bilateral infiltrates, hypoxaemia
16
Q

When to consider ITU referral in sepsis?

A
  • septic shock
  • multi-organ failure
  • require sedation, intubation, ventilation