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Infection > Sepsis and Septic Shock > Flashcards

Sepsis and Septic Shock Flashcards

1
Q

What is the definition of sepsis?

A

Life threatening organ dysfunction caused by dysregulation host response to infection
Organ dysfunction can be identified by SOFA score more than 2 (mortality risk)

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2
Q

What is the definition of septic shock?

A

Can be identified with a clinical construct of sepsis with persisting hypotension requiring vasopressors to maintain MBP > 65mmHg and having serum lactate over 2 mmol/l

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3
Q

What is sepsis?

A

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

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4
Q

What is included in SIRS - systemic inflammatory resp. sydnrome?

A

Temp. above 38C or under 36C, HR>90, RR>20 or PaCO2 <32
WBC >12000 or <4000 or >10% bands

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5
Q

What is qSOFA?

A

3 categories which score 1 point each
Hypotension - systolic BP <100mmHg
Altered mental state
Tachypnoea - RR > 22
Score of above 2 suggests greater risk of poor outcome

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6
Q

Why is sepsis important?

A

Common condition, increased mortality and increased morbidity

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7
Q

How much does mortality increase when hour delay in administering antibiotics in septic shock?

A

Mortality increases by 7.6%

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8
Q

What is the body’s defence against sepsis?

A

Physical barrier - skin, mucosa and epithelial lining
innate immune system - IgA in GIT, dendritic cells/ macrophages
Adaptive immune system - lymphocytes and immunoglobulins

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9
Q

Describe the origin of sepsis

A

Originates from breach of integrity of host barrier, whether physical or immunological
Organism enters the bloodstream creating a septic state

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10
Q

Describe the pathophysiology of sepsis

A

Uncontrolled inflammatory response
Probable change of the sepsis syndrome over time - initially increase in inflammatory mediators, then later shift towards anti-inflammatory immunosuppressive phase

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11
Q

What features are consistent with patients with sepsis having immunosuppression?

A

Loss of delayed hypersensitivity
Inability to clear infection
Predisposition to nosocomial infection

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12
Q

What are the 3 phases of pathogenesis of sepsis?

A

Release of bacterial toxins
Release of mediators
Effects of specific excessive mediators

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13
Q

Describe phase 1 - release of bacterial toxins

A

Bacterial invasion into body tissues
May or may not be neutralised and cleared by existing immune system
Commonly released toxins - gram negative is LPS and gram positive - MAMP and super antigens

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14
Q

Describe phase 2 - release of mediators in response to infection

A

Effects of infection due to endotoxin release
Effects of infections due to exotoxin release
Mediator role of sepsis

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15
Q

What is involved in endotoxin release?

A

LPS needs an LPS binding protein to bind to macrophages
LTA do not need these proteins

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16
Q

What is involved in exotoxin release?

A

Pro-inflammatory response
Small amounts of super antigens will cause a large amount of mediators to be secreted - cascade effect

17
Q

Describe the mediator role in sepsis

A

Two types of mediators can be released - Th1 and Th2
Th1 - pro-inflammatory mediators which cause inflammatory response which characterises sepsis
Th 2 - compensatory anti-inflammatory reaction which causes immunoparalysis

18
Q

What are some main pro-inflammatory and anti-inflammatory mediators?

A

Pro - TNF-alpha and IL1b,-2,-8 and -15
Anti- IL-1RA,- 4, -10, and -13

19
Q

What are the effects of pro-inflammatory mediators?

A

Promotes endothelial cells - leukocyte adhesion
Release if arachidonic acid metabolites
Complete activation
Vasodilatation of blood vessels by NO
Increase coagulation
Causes hypothermia

20
Q

What are the effects of anti-inflammatory mediators?

A

Inhibits TNF alpha
Augment acute phase reaction
Inhibits activation of coagulation system
Provides negative feedback mechanisms to pro-inflammatory mediators

21
Q

What happens if there is more pro-inflammatory response?

A

Septic shock with multiorgan failure and death

22
Q

What happens if there is more compensatory anti-inflammatory response?

A

Immuno-paralysis with uncontrolled infection and multi-organ infection

23
Q

What can show signs of organ dysfunction in sepsis?

A

Altered conscious state
Tachypnoea - PaO2< 70mmHg and sats <90%
jaundice as increased liver enzymes, PT and decreased albumin
Oliguria, anuria and increased creatinine
Tachycardia and hypotension
Decreased platelets and protein C
Increased D-dimer

24
Q

What are the general features of sepsis?

A

Fever more than 38C - chills, rigors, flushes, cold and night sweats
Hypothermia - elderly and young children
Tachycardia and tachypnoea
Altered mental status
Hyperglycaemia > 8mmol/l

25
Q

What are the inflammatory variables in sepsis?

A

Leucocytosis WCC > 12000
Leukopenia WCC <4000
Normal WCC with greater than 10% immature bands
High CRP
High procalcitonin

26
Q

What are the haemodynamic variables in sepsis?

A

Arterial hypotension - systolic <90mmHg or MAP <70mmHg
SvO2 >70%

27
Q

What are organ dysfunction variables in sepsis?

A

Arterial hypoxaemia
Oliguria
Creatinine increase compared to baseline
Coagulation abnormalities
Ileus - lack of peristalsis
Thrombocytopenia
Hyperbilirubinemia

28
Q

What are tissue perfusion variables in sepsis?

A

High lactate
Skin mottling and reduced capillary perfusion

29
Q

What effects can the host have on sepsis presentation?

A

Age, co-morbidities, immunosuppression and previous surgery - splenectomy

30
Q

What effects of an organism have on presentation of sepsis?

A

Gram positive vs Gram negative
Virulence factors
Bioburden

31
Q

What effects of environment have on presentation of sepsis?

A

Occupation, travel and hospitalisation

32
Q

Describe the SEPSIS 6

A

Take 3, Give 3
Blood cultures, blood lactate and measure urine output
Oxygen aim sats 94-98%, IV antibiotics, and IV fluid challenge

33
Q

Why is lactate measured?

A

Marker of generalised hypoperfusion/ severe sepsis/ poorer prognosis

34
Q

Why are blood cultures taken?

A

Makes microbiological diagnosis
If spike in temp. then take 2 sets

35
Q

What is type A lactate?

A

Hypoperfusion

36
Q

What is type B lactate?

A

Mitochondrial toxins, alcohol, malignancy and metabolism errors

37
Q

What IV fluids are given?

A

30ml/kg fluid challenge
Ex. 2.1L for 70kg patient

38
Q

When should the patient be referred to HDU?

A

Low BP responsive to fluids
Lactate more than 2 despite fluid resuscitation
Elevated creatinine
Oliguria
Liver dysfunction
Bilateral infiltrates and hypoxaemia

39
Q

When is ITU considered?

A

Septic shock
Multi-organ failure
Requires sedation, intubation and ventilation

Infection (13 decks)

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