Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Infection > Sepsis and Septic Shock > Flashcards

Sepsis and Septic Shock Flashcards

1
Q

Definition of sepsis

A

A systemic illness caused by microbial invasion of normally sterile parts of the body and a dysregulated host response to the infection

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

What does SIRS stand for?

A

Systemic inflammatory response syndrome

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

SIRS is when there is 2 or more of….

A

Temp > 38 or < 36
HR > 90
RR > 20 or PaCO2 < 32
WBCs > 12000 or <4000 or > 10% Ioand

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

Sepsis is a combination of…

A

SIRS and infection

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

Severe sepsis is a combination of….

A

Sepsis and end organ damage

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

Septic shock is a combination of….

A

Severe sepsis and hypotension

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

If have SIRS, does it always mean that there is an infection?

A

No

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

Definition of organ dysfunction due to sepsis

A

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

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

Definition of severe sepsis

A

Sepsis-induced tissue Hypoperfusion or organ dysfunction (any of the following through to be due to the infection)

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

qSOFA variables

A 
Respiratory rate (>22/min tachypnoea)
Mental status altered
Systolic BP (<100mmHg)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

SOFA variables

A 
PaO2/FiO2 ratio 
GCS
Mean arterial pressure (MAP)
Administration of vasopressors by type and dose rate of infusion 
Serum creatinine or urine output 
Bilirubin 
Platelet count
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is qSOFA for?

A

Patients with suspected infection who are likely to have prolonged ICU stay or die in the hospital can be promptly identified with qSOFA

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

What score of qSOFA suggests a greater risk of a poor outcome

A

2 or more

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

What can survival in septic shock be based on?

A

Antimicrobial delay

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

3Rs of sepsis kills

A

Recognise
Resuscitate
Refer

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

Body’s defence against sepsis

A 
Physical barrier
- skin 
- mucosa
- epithelial lining
Innate immune system 
- IgA in GI tract 
- dendritic cells/macrophages
Adaptive immune system 
- lymphocytes
- immunoglobulins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Pathology of sepsis

A

Uncontrolled inflammatory response
Patients with sepsis have features consistent with immunosuppression
- loss of delay hypersensitivity
- inability to clear infection
- predisposition to nosocomial infection
Probable changes of sepsis syndrome over time
- initially an increase in inflammatory mediators
- later a shift towards an anti-inflammatory immunosuppressive phase
- Depends on health of patient

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

3 stages in the pathogenesis of sepsis

A
  1. release of bacterial toxins
  2. release of mediators
  3. effects of specific excessive mediators
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Commonly released toxins in sepsis

A

Gram -ve
- lipopolysaccharide (LPS)
Gram +ve
- microbial assisted molecular pattern (MAMP) - lipoteichoic acid
- superantigens - staphylococcal toxic shock syndrome toxin (TSST)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Effects of release of mediators in sepsis

A

Effects of infections due to endotoxin release (LPS)

Effects of infections due to exotoxin release (pro-inflammatory response and small amounts of super antigens will cause large amounts of mediators to be released -> cascade effects)

Mediator role on sepsis
- Th1 vs Th2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What does Th1 mediator do?

A

Pro-inflammatory mediator - causes inflammatory response that characterises sepsis

22
Q

What does Th2 mediator do?

A

Compensatory anti-inflammatory reaction - can cause immunoparalysis

23
Q

Release of mediators in sepsis can lead to either;

A

apoptosis

an inflammatory reaction

24
Q

What are the effects of pro-inflammatory mediators?

A

Promote endothelial cell leukocyte adhesion
Release of arachidonic acid metabolites
Complement activation
Vasodilation of blood vessels by NO
Increase coagulation by release of tissue factors and membrane coagulants
Causes hyperthermia

25
Q

What are 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

26
Q

If pro-inflammatory > compensatory anti-inflammatory, results in…

A

Septic shock with multiorgan failure and death

27
Q

If Compensatory anti-inflammatory > pro-inflammatory results in….

A

Immunoparalysis with uncontrolled infection and multi organ failure

28
Q

Clinical presentation of sepsis depends on….

A

Host
organism
environment

29
Q

Presentation of sepsis (general)

A

fever > 38C (chills, rigor, flushes, cold sweats etc)
Hypothermia < 36C (elderly and very young children esp)
HR > 90 tachycardia
Tachypnoea >20/min
Altered mental status (esp. elderly)
Hyperglycaemia >8mmol/L in absence of diabetes

30
Q

Organ dysfunction features of sepsis

A 
Altered consciousness, confusion and psychosis
Tachypnoea (PaO2 < 70, stats <90%)
Jaundice
- increase liver enzymes
- decreased albumin 
- increased PT
Tachycardia and hypotension 
Oliguria, anuria and increased creatinine 
Blood
- decreased platelets
- increased PT/APTT
- decreased Protein C
- Increased D-dimer
31
Q

Inflammatory variables in sepsis

A 
Leucocytosis (WCC > 12000)
Leucopenia (WCC < 4000)
Normal WCC with > 10% immature forms
High CRP
High prolactonin
32
Q

Haemodynamic variables in sepsis

A 
Arterial hypotension (systolic <90 or MAP < 70)
SvO2 > 70%
33
Q

Tissue perfusion variables in sepsis

A

High lactate

Skin mottling and reduced capillary perfusion

34
Q

Effects of host on sepsis presentation

A 
Age
Co-morbidities
- COPD
- DM 
- CCF
- CRF
- Disseminated malignancy 
Immunosuppression 
- Acquired (HIV/AIDs)
- Drug induced (steroids, chemo, biologics)
- congenital (phagocytic defects etc)
Previous surgery 
- splenectomy
35
Q

Effect of organism on presentation of sepsis

A

Gram +ve more likely up
Gram -ve more likely down
Virulence factors e.g. MRSA, toxin secretion
Bioburden

36
Q

Effect of environment on presentation of sepsis

A

occupation
travel (esp. if present with chest infection or gastroenteritis)
Hospitalisation

37
Q

Sepsis 6

A 
GIVE 3 TAKE 3
Blood cultures
Blood lactate 
Urine output
Oxygen (aim sats 94-98%
IV antibiotics
IV fluid challenge
38
Q

At least how many blood cultures should be taken in sepsis?

A

2

39
Q

What is blood lactate a marker of?

A

Generalised Hypoperfusion
Severe sepsis
Poorer prognosis
General metabolism problems

40
Q

What is low urine output a marker of?

A

Renal dysfunction

41
Q

When should antibiotics be given in sepsis?

A

Within 1st hour of recognition

42
Q

Two types of lactate

A

Type A = Hypoperfusion

Type B = mitochondrial toxins, malignancy, alcohol, metabolism errors

43
Q

Fluid challenges require the definition of 4 compartments

A
  1. type of fluid to be administered
  2. rate of fluid infusion
  3. the end points (MAP > 65, HR < 110)
  4. the safety limits (e.g. development of pulmonary oedema)
44
Q

What level of serum lactate is associated with increased severity of illness and poorer outcomes (even if hypotension not yet present)?

A

> 4mmol/L (36 mg/dL)

45
Q

When to consider for HDU referral with sepsis

A 
Low BP response to fluids
Lactate > 2 despite fluid resuscitation 
Elevated creatinine 
Oliguira
Liver dysfunction, Bil, PT, Plt
Bilateral infiltrates, hypoxaemia
46
Q

When to consider ITU for sepsis

A

Septic shock

Multi organ failure

47
Q

What is CURB 65?

A

A score for mortality risk assessment in hospital for pneumonia

48
Q

Scores for CURB65

A

1 point for each present;
- confusion
- raised blood urea nitrogen (>7)
- Raised RR (>30)
- Low BP (<60/90)
- Age >_65
Risk of death as follows
- 0 or 1 = low risk (<3% mortality risk)
- 2 = intermediate risk (3-15% mortality risk)
- 3 to 5 = high risk (>15% mortality risk)

49
Q

What heart problem can sepsis lead to?

A

AF

50
Q

What is the quickest way to determine lactate content?

A

VBG or ABG

Infection (16 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions