Sepsis Flashcards

1
Q

Define Sepsis

A

Sepsis is a life-threatening organ dysfunction due to dysregulated immune response to infection.
Clinically its SIRS + a confirmed infection.

Essentially bacteria invade a sterile comparment e.g. blood or abdominal cavity and release endo/exotoxins leading to uncontrolled inflammatory resposne

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2
Q

Define SIRS?

A

Systemic Inflammatory Response Syndrome.
A set of symptoms that occur during systemic inflammation e.g. infection, burns, trauma or pancreatitis.

2 or more from:

  • High or low Temp
  • Tachypnoea or Low PaCO2
  • Tachycardia
  • Leucocytosis or Leucopenia or >10% band cells (immature WCs)
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3
Q

How do we assess a patient’s organ dysfunction when we suspect Sepsis?

A
SOFA score (Sepsis Organ Failure Assessment)
or qSOFA to identify patients at high risk or death/requiring ICU
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4
Q

Whats included in qSOFA?

A

High risk is 2 or more of:

  • Hypotension <100mmhg
  • Altered Mental Status
  • Tachypnoea >22breaths/min
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5
Q

Define Septic Shock?

A

Sepsis (i.e. infection + SIRS) along with refractory hypotension.
I.e. the hypotension requires vasopressors to maintain MAP >65mmHg and serum lactate remains >2mmol/l despite fluids.

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6
Q

Inflammatory mediators released in response to infection can be pro/anti-inflammatory. What happens if there’s an excess of either?

A

Pro-inflammatory = Septic Shock -> Multi-organ failure and death

Anti-inflammatory = Immunoparalysis -> Uncontrolled infection -> Multi-organ failure and death

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7
Q

How may sepsis present? Think about the different potential organ dysfunctions

A

Brain - Altered Mental Status
Lungs - Tachypnoea or Low O2
Heart - Tachycardia & Hypotension
Kidneys - Oliguria/anuria and high creatinine
Liver - Jaundice, raised enzymes, INR &bilirubin and low albumin
Systemic - Fever (and associated symptoms e.g. sweat, chills), hypothermia, hyperglycaemia, leucopenia/cytosis, thrombocytopenia, high CRP and +ve D-dimer (clotting)

Along with signs of source infection e.g. wound, peritonitis or pneumonia.

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8
Q

What factors can effect how sepsis presents?

A

Host - Age, immunosuppression, co-morbidities or surgery
Organism - Virulence factors, bioburden & Gram +ve vs -ve
Environment - Occupation, travel & hospitalisation

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9
Q

What tests can you run for Sepsis?

A
FBC
Glucose
U&amp;E + Creatinine
LFTs
D-dimer &amp; Coagulation study (sepsis causes hypercoagulation)
CRP
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10
Q

How do you manage Sepsis?

A

With the Sepsis 6:
Give 3:
- IV fluid Challenge (30ml/kg/day) (if BP doesnt improve = shock)
- IV Abx (specific to suspected source & cultures)
- O2

Take 3:

  • Blood cultures
  • Serum Lactate type A (marker of hypoperfusion and poor clinical outcome)
  • Urine output monitoring
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11
Q

What tests would you do?

A

WCC : leucocytopenia( lower WCC)/ leucocytosis (higher WCC)
CRP- HIGH
Procalcitonin- HIGH
U&Es: creatinine increase, oliguria
LFT: hyperbilirubinemia, low albumin, raised enzymes, raised INR
Lactate: increase
02 : decreased capillary perfusion

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12
Q

when would you refer to the HDU?

A
  • Low BP despite fluids
  • Lactate> 2
  • Elevated creatinine
  • Oliguria
  • Liver dysfunction
  • Hypoxemia
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13
Q

When would you refer to ITU?

A
  • Septic shock
  • Multi-organ failure
  • Requires sedation, intubation, ventilation
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14
Q

Phases of development

A

1- release of toxins

2- release of mediators

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15
Q

What are the toxins which can be released

A

Gram Negatives:
- LPS - lipopolysaccharides

Gram Positives

  • superantigens
  • microbial associated molecular patterns
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16
Q

What are the mediators released? what do they do?

A

Pro-inflammatory mediations

  • hyperthermia
  • increased adhesion of leucocytes to endothelial surfaces
  • vasodilation
  • increase coagulation
  • leads to complement activation

Anti-inflammatory mediators

  • Inhibit complement activation
  • Inhibit TNF- alpha
  • Increase acute phase reaction
  • Provide negative feedback to pro-inflammatory mediators