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Infection > Sepsis and Septic Shock > Flashcards

Sepsis and Septic Shock Flashcards

1
Q

Define sepsis

A

Lifethreatening organ dysfunction caused by a dysregulated host immune response to an infection

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2
Q

Define organ dysfunction as referred to in the definition of sepsis

A

An acute change in SOFA score >2 due to infection

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3
Q

Define septic shock

A

Sepsis & persisting hypotension requiring vasopressors to maintain MAP >65mmHg and lactate >2mmol/L despite adequate fluid resus

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4
Q

What is the mortality associated with sepsis?

A

10%

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5
Q

What mortality is associated with septic shock?

A

40%

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6
Q

What are the SOFA variables?

A 
PaO2, FiO2
Platelet count 
Bilirubin 
MAP/administration of vaspressor (type/dose) 
Serum creatnine/OU
GCS
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7
Q

What does SOFA stand for?

A

Sequential (sepsis related) organ failure assessment score

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8
Q

How can you quickly screen someone for sepsis?

A

qSOFA

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9
Q

What does the qSOFA determine?

A

qSOFA score of 2 or more is associated with longer hospital stays, increased risk of admission to UTI and death

Score of 2 or more should be followed up by completing SOFA score

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10
Q

Describe the variables in qSOFA

A

Hypotension (<100mmHg systolic)
Altered mental status
Tachypnoea (>22RR)

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11
Q

Why is sepsis so important?

A

3rd biggest killer

Each delay in hour of giving antibiotics to someone with sepsis increases their mortality by 7.6%

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12
Q

What are the body’s barriers against sepsis?

A

Physical: skin, mucosa, epithelial lining
Innate immune system: IgA in GIT, dendritic cells/macrophages
Adaptive immune system: lymphocytes, Ig

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13
Q

What does sepsis originate from?

A

A breach in the integrity of a host barrier (physical or immunological)

Organism enters blood –> septic state

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14
Q

Patients with sepsis have features consistent with what other group of individuals? Give examples of how this is so.

A

Immunocompromised patients

They have loss of delayed hypersensitivity, inability to clear infections and are predisposed to nosocomial infection

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15
Q

True or false:
Originally there is an initial increase in inflammatory mediators but then this shifts into an anti-inflammatory suppressive phase (but this depends on the health of the individual)

A

True

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16
Q

What are the three phases of pathogenesis of sepsis?

A
  1. Release of bacterial toxins
  2. Release of mediators
  3. Effects of specific excessive mediators
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17
Q

Phase 1: release of bacterial toxins

A

Toxins may or may not be cleared by the immune system

Commonly released toxins:
Gram -ve: LPS

Gram +ve: microbial-associated molecular pattern (MAMP - lipoteichoic acid, muramyl dipeptides), superantigens (TSST, streptococcal exotoxins)

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18
Q

What are endotoxins?

A

LPS complex associated with the outer membrane of gram -ve bacteria

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19
Q

What does LPS need to bind to macrophages?

A

LPS-binding protein

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20
Q

What happens when LPS binds to macrophages?

A

Triggers release of mediators

21
Q

What are exotoxins?

A

Proteins actively secreted by gram positive and negative bacteria that create a pro-inflammatory response

22
Q

How do superantigens differ in the way they trigger the host immune respones?

A

Only a small amount of superantigens is required to produce a huge number of mediators - this is due to a cascade effect.

23
Q

Distinguish pro-inflammatory mediators from anti-inflammatory mediators

A

Pro-inflammatory mediators cause the inflammatory response that causes sepsis, they are produced by Th1 cells and examples include TNFa, interferon gamma, IL-1b, IL-2

Anti-inflammatory mediators counteract the pro-inflammatory mediators and these are produced by Th2 cells, examples include IL-4, IL-5, IL-13

24
Q

What can happen if there is too many anti-inflammatory mediators?

A

Immunoparalysis, organ failure and death

25
Q

What are the effects of pro-inflammatory mediators?

A

Promotes endothelial-leucocyte adhesion
Release of arachidonic acid metabolites (e.g. prostaglandins)
Complement activation
Vasodilation of BVs by NO
Increased coagulation by release of tissue factors/membrane coagulants
Hyperthermia

26
Q

What are the effects of anti-inflammatory mediators?

A

Inhibit TNFa (TNFa major cytokine of the acute phase)
Augment the acute phase reaction
Inhibit active of coagulation system
Provide negative feedback system for pro-inflammatory mediators

27
Q

What can occur if there are too many pro-inflammatory mediators?

A

Septic shock with multi-organ failure and death

28
Q

What kinds of factors can alter the clinical presentation of sepsis?

A

Host factors, organism factors and environmental factors.

29
Q

Name some host factors that can alter the clinical presentation of sepsis

A

Age
Co-morbs (COPD, DM, CCF, CRF, disseminated malignancy)
Immunosupressed (HIV, steroids, chemotherapy, biologics, agammaglobulinaemia, phagocytic defects, defects in terminal complement component)
Splenectomy

30
Q

Name some organism factors that can alter the clinical presentation of sepsis

A

Gram +ve or –ve (+ve more common)
Virulence factors – e.g. MRSA, toxin secretion, ESBL, KPC, NDM-1
Bioburden (no. of bacteria infecting)

31
Q

What is ESBL?

A

Extended spectrum beta lactamases - proteins produced by bacteria that breakdown antibiotics

32
Q

What is KPS?

A

Klebsiella pneumoniae carbapenemases - beta-lactamase carried by strains of klebsiella

33
Q

What is NMD-1?

A

Gene responsible for resistance to antibiotics

34
Q

Name some environmental factors that can alter the clinical presentation of sepsis

A

Occupation
Travel
Hospitalisation

35
Q

What general features are associated with sepsis?

A 
Fever >38C (chills, rigor, flushes, cold sweats, night sweats) 
Hypothermia in old/young/immunocomp
Tachycardia>90bpm
Tachypnoea >20/min
Altered mental status (esp. elderly) 
Hyperglycaemia in non-DM (>8mmol/L)
36
Q

What are the inflammatory variables in sepsis?

A

Leucocytosis/leucopenia/normal WCC

Raised CPR and procalcitonin

37
Q

What are the haemodynamic variables in sepsis?

A 
Arterial hypotension (systolic >90mmHg or MAP <70mmHg) 
SvO2 >70%
38
Q

What are the organ dysfunction variables in sepsis?

A 
Arterial hypoxaemia (PaO2/FiO2 <50mmHg)
Oliguria (<0.5ml/kg/h)
↑Creatinine 
Coagulation abnormalities (PT>1.5 or APTT >60s) 
Ileus
Thrombocytopenia (<150, 000/ml)
Hyperbilirubinaemia
39
Q

What are the tissue perfusion variables in sepsis?

A

↑lactate
Skin mottling
↓Cap perfusion

40
Q

What is involved in the risk stratification of adults and 12+ with suspected sepsis?

A

History - evidence of new altered mental status?

Respiratory - RR, need for oxygen to maintain sats >92% (or 88% in COPD)?

BP - systolic

Circulation and hydration - HR, anuria/oliguria if catheterised

Temp

Skin appearance - mottling? cyanosis of lips/mouth/tongue? non-blanching rash?

41
Q

What is the high risk category for suspected sepsis?

A

Objective evidence of new altered mental state

RR >25/new need for O2 (>40% FiO2) to maintain saturation >92% (or 88% COPD)

Systolic <90mmHg/40 below normal

↑HR (>130bmp)
Anuria for 18h
If catheterised: UO <0.5ml/kg/h

Mottled/ashen appearance
Cyanosis skin/lips/tongue
Non-blanching rash

42
Q

What is the mod-high risk category for suspected sepsis?

A

Hx of altered behaviour/mental state
Hx of acute deterioration of functional ability
Impaired immune system
Trauma/surgery/invasive procedures wi last 6/52

RR:21-24

Systolic: 91=100mmHg

HR (91-130bmp, if preg 100-130bmp)
Anuria for 12-18h
If catheterised: UO 0.5-1ml/kg/h

Tympanic temp >36C

Signs of infection - redness, swelling, discharge at surgical site/breakdown of wound

43
Q

What is the low risk category for suspected sepsis?

A

Normal behaviour and none of mod-high/high risk categories met

44
Q

SEPSIS-6

A

A - air with oxygen (aim for sats 94-98%)
- antibiotics (IV w.i. 1h, follow local guidelines, consider allergy, resistance, DDIs)

B - blood culture (before antibx, 2 sets if temp spikes)
- blood lactate (high assoc. with poor perfusion and poorer outcomes)

C - crystalline bolus (IV fluid challenge, 30ml/kg)
- catheterise if req (measure UO - marker of renal dysfunction)

45
Q

Why does lactate increase in sepsis?

A

Ineffective arterial circulation due to vasodilation –> low CO –> global tissue hypoxia –> increase lactate

46
Q

What are the two types of lactic acidosis?

A

A - due to hypoperfusion

B - not due to hypoperfusion, e.g. mitochondrial toxins, alcohol, malignancy, metabolic syndromes etc.

47
Q

When would you consider an HDU referral in sepsis?

A 
Low BP responsive to fluids 
Lactate >2 despite fluid resus 
Raised creatinine 
Oliguria 
Liver dysfunction 
Bilateral infiltrates, hypoxaemia
48
Q

When would you consider an ITU referral in sepsis?

A

Septic shock
Multi-organ failure
Req. sedation, intubation and ventilation

Infection (22 decks)

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