Sepsis and Septic Shock Flashcards

(50 cards)

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

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2
Q

What does SIRS stand for?

A

Systemic inflammatory response syndrome

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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

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4
Q

Sepsis is a combination of…

A

SIRS and infection

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5
Q

Severe sepsis is a combination of….

A

Sepsis and end organ damage

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6
Q

Septic shock is a combination of….

A

Severe sepsis and hypotension

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7
Q

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

A

No

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8
Q

Definition of organ dysfunction due to sepsis

A

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

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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)

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10
Q

qSOFA variables

A
Respiratory rate (>22/min tachypnoea)
Mental status altered
Systolic BP (<100mmHg)
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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
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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

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13
Q

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

A

2 or more

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14
Q

What can survival in septic shock be based on?

A

Antimicrobial delay

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15
Q

3Rs of sepsis kills

A

Recognise
Resuscitate
Refer

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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
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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

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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
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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)

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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

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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
What are the effects of anti-inflammatory mediators?
Inhibit TNF alpha Augment acute phase reaction Inhibit activation of coagulation system Provide negative feedback mechanisms to pro-inflammatory mediators
26
If pro-inflammatory > compensatory anti-inflammatory, results in...
Septic shock with multiorgan failure and death
27
If Compensatory anti-inflammatory > pro-inflammatory results in....
Immunoparalysis with uncontrolled infection and multi organ failure
28
Clinical presentation of sepsis depends on....
Host organism environment
29
Presentation of sepsis (general)
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
Organ dysfunction features of sepsis
``` 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
Inflammatory variables in sepsis
``` Leucocytosis (WCC > 12000) Leucopenia (WCC < 4000) Normal WCC with > 10% immature forms High CRP High prolactonin ```
32
Haemodynamic variables in sepsis
``` Arterial hypotension (systolic <90 or MAP < 70) SvO2 > 70% ```
33
Tissue perfusion variables in sepsis
High lactate | Skin mottling and reduced capillary perfusion
34
Effects of host on sepsis presentation
``` 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
Effect of organism on presentation of sepsis
Gram +ve more likely up Gram -ve more likely down Virulence factors e.g. MRSA, toxin secretion Bioburden
36
Effect of environment on presentation of sepsis
occupation travel (esp. if present with chest infection or gastroenteritis) Hospitalisation
37
Sepsis 6
``` GIVE 3 TAKE 3 Blood cultures Blood lactate Urine output Oxygen (aim sats 94-98% IV antibiotics IV fluid challenge ```
38
At least how many blood cultures should be taken in sepsis?
2
39
What is blood lactate a marker of?
Generalised Hypoperfusion Severe sepsis Poorer prognosis General metabolism problems
40
What is low urine output a marker of?
Renal dysfunction
41
When should antibiotics be given in sepsis?
Within 1st hour of recognition
42
Two types of lactate
Type A = Hypoperfusion | Type B = mitochondrial toxins, malignancy, alcohol, metabolism errors
43
Fluid challenges require the definition of 4 compartments
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
What level of serum lactate is associated with increased severity of illness and poorer outcomes (even if hypotension not yet present)?
>4mmol/L (36 mg/dL)
45
When to consider for HDU referral with sepsis
``` Low BP response to fluids Lactate > 2 despite fluid resuscitation Elevated creatinine Oliguira Liver dysfunction, Bil, PT, Plt Bilateral infiltrates, hypoxaemia ```
46
When to consider ITU for sepsis
Septic shock | Multi organ failure
47
What is CURB 65?
A score for mortality risk assessment in hospital for pneumonia
48
Scores for CURB65
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
What heart problem can sepsis lead to?
AF
50
What is the quickest way to determine lactate content?
VBG or ABG