Sepsis and Septic Shock Flashcards

1
Q

SIRS criteria

A

temp <36 or >38
HR > 90
RR > 22 or PaCO2 <32
WBC >12,000 or <4,000 or 10% bands

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

sepsis =

A

SIRS + infection

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

severe sepsis =

A

sepsis + end organ damage

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

septic shock =

A

severe sepsis + hypotension

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

sepsis definition

A

life threatening organ dysfunction caused by dysregulated host response to infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

how can organ dysfuction be identified?

A

acute change in total SOFA score > 2 points consequent ot the infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

how can septic shock be identified?

A

Septic shock can be identified with a clinical construct of sepsis with persisting hypotension requiring vasopressors to maintain MAP > 65 mmHg and having a serum lactate of >2 mmol/l despite adequatevolume resuscitation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is the hospital mortality of patients with septic shock?

A

40%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

how to calculate SOFA score

A

hypotension, systolic BP < 100
altered mental status
tachypnoea RR > 22

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

body defence mecahnisms

A

physical barrier - skin mucosa, epithelial lining
innate immune system - IgA in GIT, dendritic cells/macrophages
adaptive immune system - lymphocytes, immunoglobulins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

patients with sepsis have an uncontrolled inflammatory response. what features are consistent with immunosuppression?

A

loss of delayed hypersensitivity
inability to clear infection
predisposition to nosocomial infection

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

change in sepsis syndrome over time

A

increase in inflammatory mediators then there is a shift to an anti-inflammatory immunosuppressive phase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

name the 3 phases in the pathogenesis of sepsis

A

release of bacterial toxins
release of mediators
effects of specific excessive mediators

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

bacterial invasion of the body tissues is a source of what?

A

dangerous toxins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

name the commonly released gram negative toxins

A

lipopolysaccharide (LPS)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

name the commonly released gram positive toxins

A

microbial associated molecular pattern: lipoteichoic acid, muramyl dipeptides

super antigens: staphylococcal toxic shock syndrome, streptococcal exotoxins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

name the 3 components of the release of mediators in sepsis

A

effects of infections due to endotoxin release
effects of infections due to exotoxin release
mediator role on sepsis (Th1 vs Th2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

draw a diagram showing effects of infections due to endotoxin release

A

LPS needs an LPS-binding protein to bind to macrophages

LTA do not need these

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

draw a diagram to show the effects of infections due to exotoxin release

A

pro-inflammatory response

small amounts of super antigens will cause a large number of mediators to be secreted: cascade effect

20
Q

what is the mediator role on sepsis?

A

pro-inflammatory
causes inflammatory response that characterises sepsis
compensatory anti-inflammatory reaction can cause immunoparalysis

21
Q

describe the effects of pro-inflammatory mediators

A
  • Promote endothelial call – 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
22
Q

describe the effects of anti-inflammatory mediators

A
  • Inhibit TNF alpha
  • Augment acute phase reaction
  • Inhibit activation of coagulation system
  • Provide negative feedback mechanisms to pro-inflammatory mediators
23
Q

clinical features of sepsis: nervous system

A

altered consciousness
confusion
psychosis

24
Q

clinical features of sepsis: respiratory

A

tachypneoa
PaO2 <70
<90%

25
Q

clinical features of sepsis: liver

A

jaundice
increased liver enzymes
decreased albumin
increased prothrombin

26
Q

clinical features of sepsis: blood

A

decreased plateletes
increased PT/APTT
decreased protein C
increased d-dimer

27
Q

clinical features of sepsis: cardiac

A

tachycardia

hypotension

28
Q

clinical features of sepsis: renal

A

oliguria
anuria
increased creatinine

29
Q

clinical features of sepsis: general

A

fever >38
hypothermia <36
hyperglycaemia > 8 mmol/l

30
Q

inflammatory variables in sepsis

A
leucocytosis WCC > 12,000/ml
leucopoenia WCC < 4,000/ml
normal WCC with >10% immature
high CRP
high procalcitonin
31
Q

haemodynamic variables in sepsis

A

arterial hypotension - systolic < 90 or MAP < 70

SvO2 > 70%

32
Q

organ dysfunction variables in sepsis

A
arterial hypoxaemia PaO2/FiO2 < 50mmHg
oliguria < 0.5ml/kg/h
creatinine increase
coagulation abnormalities PT > 1.5 or APTT > 60s
ileus
thrombocytopaenia <150,000/ml
hyperbilirubinaemia
33
Q

tissue perfusion variables in sepsis

A

high lactate

skin mottling and reduced capillary perfusion

34
Q

how can the host affect sepsis presentation?

A

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

35
Q

how can the organism affect sepsis presentation?

A

gram positive vs gram negative
virulence factors - MRSA, toxin secretion, ESBL, KPC, NDM-1
bioburden

36
Q

how can the environment affect sepsis presentation?

A

occupation
travel
hospitalisation

37
Q

sepsis 6

A
high flow oxygen
IV antibiotics
IV fluids
Blood cultures
Serum lactate
Urine output
38
Q

antibiotic guidance in sepsis 6

A

o Based on working diagnosis from history and examination
o Local antibiotic guidelines
o Consider allergy
o Consider previous MRSA, ESBL, CPE
o Consider antibiotic toxicity/interactions

39
Q

IV fluids in sepsis 6

A

30ml/kg

40
Q

in sepsis, if there is a spike in temperature what should you do?

A

take another set of blood cultures

41
Q

what is serum lactate a marker of?

A

generalised hypoperfusion/sever sepsis/poorer prognosis

42
Q

type A serum lactate shows?

A

hypoperfusion

43
Q

type B serum lactate shows?

A

mitochondrial toxins
alcohol
malignancy
metabolism errors

44
Q

of the available biomarkers which one has the most support to identify adverse outcomes in sepsis?

A

lactate

45
Q

what is urine output a measure of?

A

renal dysfunction

46
Q

when would you consider a HDU referral in a septic patient?

A
  • Low BP responsive to fluids
  • Lactate > 2 despite fluid resus
  • Elevated creatinine
  • Oliguria
  • Liver dysfunction, bil, PT, Plt
  • Bilateral infiltrates, hypoxaemia
47
Q

when would you consider a ITU referral in a septic patient?

A

When to Consider ITU Referral
• Septic shock
• Multi-organ failure
• Requires sedation, intubation and ventilation