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Year 3 - Infection > Sepsis and Septic shock > Flashcards

Sepsis and Septic shock Flashcards

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1
Q

What is sepsis?

A

Systemic illness caused by microbial invasion of normally sterile parts of the body

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2
Q

What is the origin of the word sepsis?

A

Sepsis derives from the Greek work “sepo” meaning decay or decomposition

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3
Q

What is the traditional model for sepsis?

A

1) SIRS
2) Sepsis
3) Sever Sepsis
4) Septic Shock

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4
Q

What is SIRS?

A
  • Temp >38oC or <36oC
  • HR >90
  • RR >20 or PaCO2 <32
  • WBCs >12,000 or <4000 or >10% bands
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5
Q

What is sepsis?

A

SIRS + Infection

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6
Q

What is Severe sepsis?

A

Sepsis + End organ damage

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7
Q

What is Septic shock?

A

Severe sepsis + Hypotension

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8
Q

What is sepsis defined as?

A

Sepsis is defined as life-threatening organ dysfunction caused by dysregulated host response to infection

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9
Q

What is Septic shock?

A

Septic shock can be 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

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10
Q

qSOFA?

A
  • Hypotension = Systolic BP <100 mmHg
  • Altered mental status
  • Tachypnea RR >22/min
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11
Q

What is survival in septic shock directly based on?

A

Antimicrobial delay - For each hour’s delay in administering ABx there is an increased mortality by 7.6%

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12
Q

What. is the mortality rates in sepsis?

A

Third leading cause of death ICNARC data 2006 -Roughly 53,000 deaths

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13
Q

What is the main intervention in curbing sepsis?

A

Sepsis 6

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14
Q

What is your bodies defence against sepsis?

A
  • Physical barrier = Skin, mucosa, epithelial lining
  • Innate immunity system - IgA in GI tract, dendritic cells/macrophage
  • Adaptive immunity = Lymphocytes, immunoglobulins
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15
Q

What are common origins of sepsis?

A
  • Breach in integrity of host barrier (Either physical or immunological)
  • Organism enter the bloodstream creating septic shock
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16
Q

Pathophysiology of sepsis?

A

1) Uncontrolled inflammatory response

2) Features of immunosuppression:
- Loss/delayed hypersensitivity
- Inability to clear infection
- Predisposition to nosocomial infection

3) Change of the sepsis syndrome over time:
- Initially, an increase in inflammatory markers
- Later, there isa shift toward an anti-inflammatory immunosuppressive phase
- Dependant on the health of an individual patient

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17
Q

What are the three phases pf the pathogenesis of sepsis?

A

1) Release of bacterial toxins
2) Release of mediators
3) Effects of specific excessive mediators

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18
Q

What are the three phases pf 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

Describe phase 1 in the pathogenesis of sepsis.

A

1) Bacterial Invasion
2) Release of toxins:
- Gram negative = LPS
- Gram positive = MAMP or superantigens

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20
Q

What is LPS?

A

Lipopolysaccharide is a toxin released by gram negative bacteria

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21
Q

What are MAMPs?

A

Microbial-associated molecular patterns released by gram positive bacteria.

Examples:

  • Lipoteichoic acid
  • Muramyl dipeptides
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22
Q

What are superantigens?

A

Antigens released by some gram positive bacteria:

  • Staphylococcal toxic shock syndrome toxin
  • Streptococcal exotoxins
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23
Q

What superantigens are associated with Staphylococcus aureus?

A

Staphylococcal toxic shock syndrome toxin

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24
Q

What superantigens are associated with Streptococcus?

A

Streptococcal pyrogenic exotoxin

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25
Describe phase 2 in the pathogenesis of sepsis.
- Effects of infections due to endotoxin release - Effects of infection due to exotoxin release - Mediator role on sepsis
26
What endotoxins are released by gram negative bacteria?
Lipopolysaccharide
27
What endotoxins are released by gram positive bacteria?
MAMPS = Microbial-associated molecular patterns Eg - Lipoteichoic acid - Muramyl dipeptides
28
Do LPS or MAMPs require a binding protein?
LPS - Lipopolysaccharide
29
What is the mechanism of action of lipopolysaccharide?
1) LPS binds to LPS-binding protein 2) LPS+LBP complex bind to macrophage via toll-like receptor 4 (+CD14) 3) Macrophage are activated and release mediators
30
What is the mechanism of action of MAMPs (Lipoteichoic acid)?
1) Lipoteichoic acid is able to bind directly to macrophage via toll-like receptor 2 2) Macrophage is activated and releases mediators
31
Is a small or large dose of superantigen required to produce a response?
A small amount of superantigen will lead to a large release of mediators causing a cascade effect.
32
What is the mechanism of exotoxins (super antigens)?
1) Activated T-lymphocytes 2) T-lymphocytes release IL-2 and Interferon gamma 3) Activation of macrophage and endothethial cells 4) Release of IL-1 and TNF-a + Nitric oxide respectively 5) Cascade effect
33
What do endothelial cells release in response to exotoxins?
NO
34
What do macrophage release in response to exotoxin?
- Interleukin 1 | - TNF-a
35
Describe phase 3 in the pathogenesis of sepsis.
Effects of specific excessive mediators: - Pro-inflammatory - Anti-inflammatory
36
In phase 3 of sepsis what is the effect of the pro-inflammatory mediators?
- Promote endothelial cells --> leukocyte adhesion - Release of arachidonic acid metabolites - Complement activation - Vasodilatation (NO) - Increase in coagulation by release of tissue factors and membrane coagulants - Hyperthermia
37
In phase 3 of sepsis what is the effect of the anti-inflammatory mediators?
- Inhibit TNF-a - Augment acute phase reaction - Inhibit activation of the coagulation system - Negative feedback mechanism to pro-inflammatory mediators
38
There is a balance between pro-inflammatory and anti-inflammatory response in sepsis. If pro-inflammatory outweighs anti-inflammatory what is the end result?
Multiorgan failure and death
39
There is a balance between pro-inflammatory and anti-inflammatory response in sepsis. If anti-inflammatory outweighs pro-inflammatory what is the end result?
Immuoparalysis with uncontrolled infection and multi organ failure
40
Whos at highest risk of sepsis?
- Elderly - Diabetics - Chronic renal failure - Pneumonia - Immunosuppressed (HIV, splenectomy, steroids, agammaglobulinaemia etc)
41
What factors influence the clinical features of sepsis?
- Host - Organism - Environment
42
Sepsis clinical effects on the brain?
- Altered consciousness - Confusion - Psychosis
43
Sepsis clinical effects on the Blood?
- Decrease platelets - Decrease Protein C - Increase D-Dimer - Increase PT (>1.5) or APTT (>60s)
44
Sepsis clinical effects on the Lungs?
- Tachypnoea - PaO2 <70mmHg - Sats <90%
45
Sepsis clinical effects on the heart?
- Tachycardia | - Hypotension
46
Sepsis clinical effects on the Liver?
- Jaundice - Increase liver enzymes - Decrease in albumin - Increase in PT (>1.5)
47
Sepsis clinical effects on the kidneys?
- Oliguria | - Anuria = Increase in creatinine
48
What are the general clinical features of sepsis?
- Fever (>38oC) = Chills, riggers, flushing, cold swears, night swears etc - Hypothermia (<36oC) = Especially in the elderly, very young children and immunosuppressed - Tachycardia >90/min - Tachypnoea >20/min - Altered mental status - Hyperglycaemia >8mmol/L in the absence of diabetes
49
What are the inflammatory markers in sepsis?
- Leukocytosis (WCC >12,000/ml) - Leukopenia (WCC <4000/ml) - Normal WCC with greater than 10% immature forms - High CRP - High procalcitonin
50
Haemodynamic variables in sepsis?
- Arterial hypotension = Systolic <90mmHg or MAP <70mmHg | - AvO2 >70%
51
Tissue perfusion variablesi in sepsis?
- High lactate | - Skin mottling and reduced capillary perfusion
52
Examples of immunosuppression?
1) Acquired: HIV/AIDs 2) Drug-induced: - Steroids - Chemotherapy - Biologics 3) Congenital: - agammaglobulinaemia - Phagocytic defects - Defects in terminal complement component 4) Previous surgery - Splenectomy
53
What is the most common cause of sepsis, gram-positive, gram-negative or fungi?
1) Gram-positive bacteria 2) Gram-negative bacteria 3) Fungi (Rising)
54
Risk stratification for suspected sepsis - High risk history?
Objective evidence of new altered mental status
55
Risk stratification for suspected sepsis - Moderate risk history?
- History of altered mental status from a friend or family member - History of acute deterioration - Impaired immune system - Trauma, surgery or invasive procedure in the last 6 weeks
56
Risk stratification for suspected sepsis - Low risk history?
Normal behaviour
57
Risk stratification for suspected sepsis - High risk respiratory?
- RR >25 breaths/min | - New need of oxygen = >40% FIO2 required to maintain saturation more than 92% (88% in COPD)
58
Risk stratification for suspected sepsis - Moderate risk respiratory?
- RR 21-24 breaths/min
59
Risk stratification for suspected sepsis - High risk BP?
- Systolic < 90mmHG or - Systolic decrease >40 mmHg below normal
60
Risk stratification for suspected sepsis - Moderate risk BP?
Systolic 91-100mmHg
61
Risk stratification for suspected sepsis - High risk circulation and hydration?
- BP >130/min - Anuria for >18hrs or - Catheterised patients passed less than 0.5 ml/kg of urine/hr
62
Risk stratification for suspected sepsis - Moderate risk circulation and hydration?
- BP 91-130/min (Pregnant woman 100-130/min) - Not passed urine in past 12-18hrs or - Catheterised patients passed less than 0.5-1 ml/kg of urine/hr
63
Risk stratification for suspected sepsis - Moderate risk temperature?
Tympanic temperature less than 36oC
64
Risk stratification for suspected sepsis - Moderate risk skin?
- Signs of infection = Redness, swelling or discharge or wound breakdown
65
Risk stratification for suspected sepsis - High risk skin?
- Mottled or ashen appearance - Cyanosis of skin, lips or tongue - Non-blanching rash of skin
66
In terms of Sepsis 6 what is meant by take 3: give 3?
Take: 1) Blood cultures 2) Blood lactate 3) Measure urine output Give: 1) Oxygen - aim for 94-98% sats 2) IV Abx 3) IV fluid challenge
67
In terms of Sepsis 6 what is meant 2As, 2 Bs, 2 Cs?
As: 1) Air enriched with O2 2) Abx after blood cultures Bs: 1) Blood culture 2) Blood gas with lactate Cs: 1) Crystalloid bolus 2) Catheter (If severe sepsis or septic shock)
68
If there is a spike in temperature within sepsis what should be performed?
A second set of blood cultures
69
Why do we measure lactate in sepsis?
It acts a marker of general hypoperfusion, indicating severe sepsis and a bad prognosis
70
Why do we measure urine output in sepsis?
A low urine output is a marker of renal dysfunction and a bad indicator
71
Type A cause of Lactate rise?
Hypoperfusion
72
Type B cause of Lactate rise?
- Mitochondrial toxins - Alcohol - Malignancy - Metabolisation errors
73
What level of serum lactate indicates increased severity in sepsis?
>4 mmol/L (36 mg/dL)
74
If someone is hypotensive or has a serum lactate >4 mmol/L what do they require?
Intravenous fluids (30ml/Kg)
75
What four components are required of fluid challenge is there?
1) Type of fluid 2) Rate of infusion 3) The end point 4) The safety limits
76
What is severe sepsis?
- Sepsis induced tissue hypoperfusion or Organ Dysfunction
77
When to consider ITU in sepsis?
- Septic shock - Multi-organ failure - Requires sedation, intubation and ventilation
78
When to consider HDU?
- Low BP responsiveness to fluids - Lactate >2 despite fluid resuscitation - Elevated creatinine - Oliguria - Liver dysfunciton - Hypoxeamia
79
What indicates septic shock?
Despite fluid resuscitation: 1) Vasopressors required to maintain MAP >65 mmHg and 2) Serum Lactate > 2 mmol/L
80
What is used to indicate pneumonia severity?
CURB 65

Year 3 - Infection (16 decks)

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