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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
What are the effects of pro-inflammatory mediators?
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
What are the effects of anti-inflammatory mediators?
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
What can occur if there are too many pro-inflammatory mediators?
Septic shock with multi-organ failure and death
28
What kinds of factors can alter the clinical presentation of sepsis?
Host factors, organism factors and environmental factors.
29
Name some host factors that can alter the clinical presentation of sepsis
Age Co-morbs (COPD, DM, CCF, CRF, disseminated malignancy) Immunosupressed (HIV, steroids, chemotherapy, biologics, agammaglobulinaemia, phagocytic defects, defects in terminal complement component) Splenectomy
30
Name some organism factors that can alter the clinical presentation of sepsis
Gram +ve or –ve (+ve more common) Virulence factors – e.g. MRSA, toxin secretion, ESBL, KPC, NDM-1 Bioburden (no. of bacteria infecting)
31
What is ESBL?
Extended spectrum beta lactamases - proteins produced by bacteria that breakdown antibiotics
32
What is KPS?
Klebsiella pneumoniae carbapenemases - beta-lactamase carried by strains of klebsiella
33
What is NMD-1?
Gene responsible for resistance to antibiotics
34
Name some environmental factors that can alter the clinical presentation of sepsis
Occupation Travel Hospitalisation
35
What general features are associated with sepsis?
``` 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
What are the inflammatory variables in sepsis?
Leucocytosis/leucopenia/normal WCC | Raised CPR and procalcitonin
37
What are the haemodynamic variables in sepsis?
``` Arterial hypotension (systolic >90mmHg or MAP <70mmHg) SvO2 >70% ```
38
What are the organ dysfunction variables in sepsis?
``` 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
What are the tissue perfusion variables in sepsis?
↑lactate Skin mottling ↓Cap perfusion
40
What is involved in the risk stratification of adults and 12+ with suspected sepsis?
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
What is the high risk category for suspected sepsis?
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
What is the mod-high risk category for suspected sepsis?
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
What is the low risk category for suspected sepsis?
Normal behaviour and none of mod-high/high risk categories met
44
SEPSIS-6
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
Why does lactate increase in sepsis?
Ineffective arterial circulation due to vasodilation --> low CO --> global tissue hypoxia --> increase lactate
46
What are the two types of lactic acidosis?
A - due to hypoperfusion | B - not due to hypoperfusion, e.g. mitochondrial toxins, alcohol, malignancy, metabolic syndromes etc.
47
When would you consider an HDU referral in sepsis?
``` Low BP responsive to fluids Lactate >2 despite fluid resus Raised creatinine Oliguria Liver dysfunction Bilateral infiltrates, hypoxaemia ```
48
When would you consider an ITU referral in sepsis?
Septic shock Multi-organ failure Req. sedation, intubation and ventilation

Infection (22 decks)

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