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BDS2 BAMS lectures > Sepsis > Flashcards

Sepsis Flashcards

1
Q

What is sepsis

A

Life threatening organ dysfunction due to a dysregulated host response to infection

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2
Q

What is sepsis triggered by

A

infection (in susceptible patients)

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3
Q

what differentiates sepsis from infection

A

presence of organ dysfunction

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4
Q

What are the major changes to the definition of sepsis between 1990s and 2016

A

1990s - focus on inflammation

2016 - focus on organ dysfunction and qSOFA score

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5
Q

What qSOFA score do you need to be at risk of developing sepsis

A

score of 2 or more

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6
Q

what is qSOFA

A

a tool to clinically characterise patients at risk of sepsis (at risk of prolonged ICU or death)

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7
Q

what is a person’s baseline qSOFA score

A

0 unless patient has pre-existing organ dysfunction before onset of infection

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8
Q

what does a qSOFA score of ≥2 mean

A

overall 10% mortality risk, requires prompt medical intervention

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9
Q

what are SIRS criteria used for

A

to aid diagnosis of infection

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10
Q

What are the SIRS criteria

A

‘Systemic inflammatory response syndrome’ (used in 1990s to define sepsis)

Patients experiencing at least 2 of the following symptoms:

  • body temp <36,>38
  • heart rate >90bpm
  • resp rate >20 breaths/pm
  • white cell count >12 x10-6l-1
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11
Q

What is the glasgow coma scale (GCS) used for

A

a way to communicate about the level of consciousness of patients in a coma

  • 3 = deep unconciousness
  • 15 = concious
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12
Q

What is assessed in the glasgow coma scale

A
  • eyes
  • verbal
  • motor response
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13
Q

What causes sepsis

A

any infection can trigger sepsis

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14
Q

what are the most common sites of infection for sepsis

why do the % not add up to 100

A
  • lungs (64%)
  • abdomen (20%)
  • bloodstream (15%)
  • urinary system (14%)

cause of multiple infections

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15
Q

What are the most common sources of infection that trigger sepsis

A
  • gram negative bacteria (62%)
  • gram positive bacteria (47%) e.g. staph aureus 20%
  • fungal (19%) e.g. candida (17%)
  • viral
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16
Q

Which is associated with higher ICU mortality? Candida or bacterial bloodstream infections

A

candida

17
Q

What factors cause some infections to progress to sepsis

A

Microbial

  • virulence factors e.g. LPS, Lipoteichoic acid, peptidoglycan, pili, finbriae, capsule etc
  • antigens
  • competitive adantage

Host factors

  • innate immunity
  • adaptive immunity
  • immuno-compromised e.g. HIV, cancer, organ transplantation
  • pre-existing chronic conditions e.g. diabetes, cirrhosis
  • age
  • genetics
18
Q

What is the outcome of infection (pathogenicity) determined by

A

interactions between microbes and host immune response

19
Q

Why are microbes more pathogenic in immunocompromised hosts

A

gives them a competitive advantage

20
Q

Who gets sepsis

A
  • older people

- immunocompromised

21
Q

Describe the pathophysiology of sepsis

A
  • dysregulated, excessive systemic inflammation
  • body-wide blood clotting and ‘leaky vessels’
  • organs begin to fail
  • persistent hypotension
22
Q

what is the difference between sepsis and septic shock

A

Sepsis: Bacteremia or another infection triggers a serious bodywide response (sepsis), which typically includes fever, weakness, a rapid heart rate, a rapid breathing rate, and an increased number of white blood cells

Septic shock: Sepsis that causes dangerously low blood pressure (shock) is called septic shock

23
Q

Describe normal acute inflammation in response to localised infection

A
  • protective immune reaction to invading microorganisms or endogenous signals from damaged cells
  • PAMPS-PRRs
  • cytokines, complement
  • cardinal signs of inflammation, localised to site of infection
  • clearance of the source of injury and necrotic tissues
  • elimination of pathogen
  • immune suppression via IL-10 and TGF-beta
  • followed by tissue repair and return to homeostasis
24
Q

Describe the immunopathogenesis of sepsis

A
  • immune response fails to eliminate the pathogen
  • localised acute inflammation progresses to acute systemic inflammation
  • excessive inflammation AND immune suppression

Excessive inflammation

  • tissue injury from sustained inflammation
  • activation of innate immunity via PAMPS/DAMPS
  • complement, coagulation and vascular endothelium activated

Immune supression

  • both innate and adaptive
  • apoptosis of T and B cells
  • dysfunctional DCs
  • delayed apoptosis of dysfunctional neutrophils
25
Q

what does qSOFA stand for

A

quick sequential organ failure assessment

26
Q

What are the aims of sepsis treatment

A

keeping the patient alive and treating symptoms (there’s a lot we don’t know)

27
Q

What are some of the treatments for sepsis

A
  • antibiotics (early administration)

- vasopressors

28
Q

Why should dentists care about sepsis

A
  • rare but serious complication of acute dental infections

- risk from dental abscesses

29
Q

What 2 factors make dental abscesses a risk factor for sepsis

A
  1. fistulas can drain into the mouth and cheek

2. abscesses can spread to other sites. Bacteria can travel throughout the body

30
Q

Why do dental abscesses develop

A

as a consequence of acute inflammatory response to bacterial infection

31
Q

What do dental abscesses contain

A

immune cells, dead tissue and LIVE bacteria

32
Q

Are dental abscesses infectious

A

highly infectious

33
Q

How are dental abscesses treated

A
  • promptly by excision and drainage
  • periapical abscesses require root canal or extraction
  • antibiotics ineffective (in the absence of spreading dental infection)
34
Q

Why can dental abscesses be dangerous

A

can spread leading to severe local and systemic consequences

35
Q

Why is the spread of dental abscesses hard to predict

A

complicated architecture of head and neck

36
Q

What are the red flag signs and symptoms of sepsis

A
  • temp <36 or >38
  • elevated breathing rate (>20 breaths per min)
  • elevated or reduced heart rate
  • varying degrees of facial swelling
  • trismus
  • dehydration

BDS2 BAMS lectures (9 decks)

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