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Year 3 - Infection > Sepsis and Septic shock > Flashcards

Sepsis and Septic shock Flashcards

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
Q

Describe phase 2 in the pathogenesis of sepsis.

A
  • Effects of infections due to endotoxin release
  • Effects of infection due to exotoxin release
  • Mediator role on sepsis
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26
Q

What endotoxins are released by gram negative bacteria?

A

Lipopolysaccharide

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27
Q

What endotoxins are released by gram positive bacteria?

A

MAMPS = Microbial-associated molecular patterns

Eg - Lipoteichoic acid
- Muramyl dipeptides

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28
Q

Do LPS or MAMPs require a binding protein?

A

LPS - Lipopolysaccharide

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29
Q

What is the mechanism of action of lipopolysaccharide?

A

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

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30
Q

What is the mechanism of action of MAMPs (Lipoteichoic acid)?

A

1) Lipoteichoic acid is able to bind directly to macrophage via toll-like receptor 2
2) Macrophage is activated and releases mediators

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31
Q

Is a small or large dose of superantigen required to produce a response?

A

A small amount of superantigen will lead to a large release of mediators causing a cascade effect.

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32
Q

What is the mechanism of exotoxins (super antigens)?

A

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

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33
Q

What do endothelial cells release in response to exotoxins?

34
Q

What do macrophage release in response to exotoxin?

A
  • Interleukin 1

- TNF-a

35
Q

Describe phase 3 in the pathogenesis of sepsis.

A

Effects of specific excessive mediators:

  • Pro-inflammatory
  • Anti-inflammatory
36
Q

In phase 3 of sepsis what is the effect of the pro-inflammatory mediators?

A
  • 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
Q

In phase 3 of sepsis what is the effect of the anti-inflammatory mediators?

A
  • Inhibit TNF-a
  • Augment acute phase reaction
  • Inhibit activation of the coagulation system
  • Negative feedback mechanism to pro-inflammatory mediators
38
Q

There is a balance between pro-inflammatory and anti-inflammatory response in sepsis. If pro-inflammatory outweighs anti-inflammatory what is the end result?

A

Multiorgan failure and death

39
Q

There is a balance between pro-inflammatory and anti-inflammatory response in sepsis. If anti-inflammatory outweighs pro-inflammatory what is the end result?

A

Immuoparalysis with uncontrolled infection and multi organ failure

40
Q

Whos at highest risk of sepsis?

A
  • Elderly
  • Diabetics
  • Chronic renal failure
  • Pneumonia
  • Immunosuppressed (HIV, splenectomy, steroids, agammaglobulinaemia etc)
41
Q

What factors influence the clinical features of sepsis?

A
  • Host
  • Organism
  • Environment
42
Q

Sepsis clinical effects on the brain?

A
  • Altered consciousness
  • Confusion
  • Psychosis
43
Q

Sepsis clinical effects on the Blood?

A
  • Decrease platelets
  • Decrease Protein C
  • Increase D-Dimer
  • Increase PT (>1.5) or APTT (>60s)
44
Q

Sepsis clinical effects on the Lungs?

A
  • Tachypnoea
  • PaO2 <70mmHg
  • Sats <90%
45
Q

Sepsis clinical effects on the heart?

A
  • Tachycardia

- Hypotension

46
Q

Sepsis clinical effects on the Liver?

A
  • Jaundice
  • Increase liver enzymes
  • Decrease in albumin
  • Increase in PT (>1.5)
47
Q

Sepsis clinical effects on the kidneys?

A
  • Oliguria

- Anuria = Increase in creatinine

48
Q

What are the general clinical features of sepsis?

A
  • 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
Q

What are the inflammatory markers in sepsis?

A
  • Leukocytosis (WCC >12,000/ml)
  • Leukopenia (WCC <4000/ml)
  • Normal WCC with greater than 10% immature forms
  • High CRP
  • High procalcitonin
50
Q

Haemodynamic variables in sepsis?

A
  • Arterial hypotension = Systolic <90mmHg or MAP <70mmHg

- AvO2 >70%

51
Q

Tissue perfusion variablesi in sepsis?

A
  • High lactate

- Skin mottling and reduced capillary perfusion

52
Q

Examples of immunosuppression?

A

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
Q

What is the most common cause of sepsis, gram-positive, gram-negative or fungi?

A

1) Gram-positive bacteria
2) Gram-negative bacteria
3) Fungi (Rising)

54
Q

Risk stratification for suspected sepsis - High risk history?

A

Objective evidence of new altered mental status

55
Q

Risk stratification for suspected sepsis - Moderate risk history?

A
  • 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
Q

Risk stratification for suspected sepsis - Low risk history?

A

Normal behaviour

57
Q

Risk stratification for suspected sepsis - High risk respiratory?

A
  • RR >25 breaths/min

- New need of oxygen = >40% FIO2 required to maintain saturation more than 92% (88% in COPD)

58
Q

Risk stratification for suspected sepsis - Moderate risk respiratory?

A
  • RR 21-24 breaths/min
59
Q

Risk stratification for suspected sepsis - High risk BP?

A
  • Systolic < 90mmHG
    or
  • Systolic decrease >40 mmHg below normal
60
Q

Risk stratification for suspected sepsis - Moderate risk BP?

A

Systolic 91-100mmHg

61
Q

Risk stratification for suspected sepsis - High risk circulation and hydration?

A
  • BP >130/min
  • Anuria for >18hrs
    or
  • Catheterised patients passed less than 0.5 ml/kg of urine/hr
62
Q

Risk stratification for suspected sepsis - Moderate risk circulation and hydration?

A
  • 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
Q

Risk stratification for suspected sepsis - Moderate risk temperature?

A

Tympanic temperature less than 36oC

64
Q

Risk stratification for suspected sepsis - Moderate risk skin?

A
  • Signs of infection = Redness, swelling or discharge or wound breakdown
65
Q

Risk stratification for suspected sepsis - High risk skin?

A
  • Mottled or ashen appearance
  • Cyanosis of skin, lips or tongue
  • Non-blanching rash of skin
66
Q

In terms of Sepsis 6 what is meant by take 3: give 3?

A

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
Q

In terms of Sepsis 6 what is meant 2As, 2 Bs, 2 Cs?

A

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
Q

If there is a spike in temperature within sepsis what should be performed?

A

A second set of blood cultures

69
Q

Why do we measure lactate in sepsis?

A

It acts a marker of general hypoperfusion, indicating severe sepsis and a bad prognosis

70
Q

Why do we measure urine output in sepsis?

A

A low urine output is a marker of renal dysfunction and a bad indicator

71
Q

Type A cause of Lactate rise?

A

Hypoperfusion

72
Q

Type B cause of Lactate rise?

A
  • Mitochondrial toxins
  • Alcohol
  • Malignancy
  • Metabolisation errors
73
Q

What level of serum lactate indicates increased severity in sepsis?

A

> 4 mmol/L (36 mg/dL)

74
Q

If someone is hypotensive or has a serum lactate >4 mmol/L what do they require?

A

Intravenous fluids (30ml/Kg)

75
Q

What four components are required of fluid challenge is there?

A

1) Type of fluid
2) Rate of infusion
3) The end point
4) The safety limits

76
Q

What is severe sepsis?

A
  • Sepsis induced tissue hypoperfusion
    or
    Organ Dysfunction
77
Q

When to consider ITU in sepsis?

A
  • Septic shock
  • Multi-organ failure
  • Requires sedation, intubation and ventilation
78
Q

When to consider HDU?

A
  • Low BP responsiveness to fluids
  • Lactate >2 despite fluid resuscitation
  • Elevated creatinine
  • Oliguria
  • Liver dysfunciton
  • Hypoxeamia
79
Q

What indicates septic shock?

A

Despite fluid resuscitation:
1) Vasopressors required to maintain MAP >65 mmHg
and
2) Serum Lactate > 2 mmol/L

80
Q

What is used to indicate pneumonia severity?

Year 3 - Infection (16 decks)

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