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BDS2 BAMS > Sepsis > Flashcards

Sepsis Flashcards

1
Q

define sepsis

A

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

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2
Q

what triggers sepsis

A

an infection

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3
Q

what is sepsis response

A

Overwhelming/excessive immune response (to infection) that causes organ dysfunction

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4
Q

what differentiates sepsis from an infection

A

presence of organ dysfunction differentiates sepsis from an infection

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5
Q

what causes pathology in sepsis

A

organ dysfunction

not pathology

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6
Q

mortality risk due to sepsis

A

1 in 5

high

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7
Q

what can organ dysfunction be identified as

A

an acute change in total SOFA score of 2 or more

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8
Q

septic shock

A

Sepsis which is underlying circulatory and cellular and/or metabolic abnormalities are marked enough to substantially increase mortality

Clinically defined as sepsis with persisting hypotension that requires vasopressors to maintain the mean arterial pressure at less than 65mmHg and with a serum lactate concentration of greater than 2mmoll-1
- Persistent hypotension despite fluid resuscitation

Immune dysfunction is severe enough to change metabolic activity and increase mortality

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9
Q

SOFA

A

organ failure score

wide range of tests done on a variety of organs in labs

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10
Q

qSOFA

A

quick SOFA

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

  • No lab tests needed
  • can be used in community to assess sepsis risk
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11
Q

3 components measured in qSOFA

A

Respiratory ≥ 22 breaths/min
- elevated

Altered mentation (Glasgow Coma Scale <15)

Systolic blood pressure ≤ 100 mm Hg
- lower

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12
Q

3 criteria of Glasgow Coma Scale

A

eye opening

verbal response

best motor response

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13
Q

what is a disability score for Glasgow Coma Scale?

A

less than maximum 15

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14
Q

what causes sepsis

A

Any infection can trigger sepsis In susceptible individuals

- Meningitis, small cut, UTI, sore throat

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15
Q

common sites of infections in ICU

A

Lungs (64%)
Abdomen (20%)
Bloodstream (15%)
Urinary system(14%)

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16
Q

source of infections in adults in ICUs

A

Gram positive bacteria (47%)

  • most common
  • Staph aureus (20%)

Gram negative bacteria (62%)

Fungal (19%)
- Candida (17%)

Candida bloodstream infections associated with higher ICU mortality compared with bacterial infections

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17
Q

what type of infection are children more susceptible to

A

viral infections

e.g. viral meningitis

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18
Q

what 2 classes of factors contribute to infections progressing to sepsis

A

microbial and host factors

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19
Q

microbial factors that can contribute to sepsis

A

Virulence factors

  • LPS
  • Lipoteichoic acid
  • Peptidoglycan
  • Pili, fimbriae, capsule etc

Virulence contributes to pathogenicity

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20
Q

host factors that contribute to sepsis

A

Innate immunity

Adaptive immunity – protect from microbial infection

Immuno-compromised

  • HIV/AIDs, cancer, autoimmunity, organ transplantation
  • Taken immunosuppressant drugs

Pre-existing chronic conditions
- Diabetes, cirrhosis, CKD

Age

Genetics

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21
Q

what is pathogenicity determined by

A

interactions between microbes and host immune responses

Microbes are more pathogenic in immune-compromised hosts
- Weakened/ compromised

Give competitive advantage
- Easier to overcome host immune response

22
Q

who most commonly get sepsis

A

elderly (disproportionate)

medically and immune-compromised patients

23
Q

medical conditions which are immune compromised

A 
Cancer
Cirrhosis
Autoimmunity
HIV/AIDS
Organ transplantation
Diabetes
24
Q

pathophysiology of sepsis

A

Dysregulated, excessive systemic inflammation
- Leads to organ dysfunction

one or more organs begin o fail
- leads to mortality

25
Q

systemic effect of sepsis

A

Body-wide blood clotting and ‘leaky vessels’

Persistent hypotension (Septic shock – 40% in hospital mortality)
- Even after fluid resuscitation 
Unable to keep in vessels – leak into tissues
26
Q

appearance of septic shock limb

A

inflammed
shiny skin
red blotching due to leaky vessels

27
Q

what is acute inflammation in response to localised infection

A

a protective immune reaction to invading microorganisms or endogenous signals from damaged cells

gives rise to cardinal signs of inflammation
- localised to site of infection

28
Q

what is present in the localised site of acute inflammation

A

Presence of microbes or endogenous things that damage cells (PAMPS)
- pathogen associated molecular patterns

pattern recognition receptors
- Toll like receptors

DAMPS – danger associated molecular patterns

causes swelling, redness and leaky vessels localised to site of infection

29
Q

what does acute inflammation result in if it is successful

A

clearance of the source of injury and necrotic tissues
- protective clearance at site of infection

followed by tissue repair and return to homeostasis

30
Q

stages of acute inflammation in sepsis

A

Innate immune system recognises PAMPs (and DAMPs) through PRRs (pattern recognition receptors – toll like receptors)

  • Due to damage to skin
  • Microbes access underlying

Responding cells trigger inflammation through release of cytokines and chemokines.

Cytokines activate endothelial cells, vasodilation and vascular permeability.
- Immune cells can move out of blood into infected tissue to remove infection and dead tissue

Large amounts of cytokines (e.g. TNFa) activate acute phase proteins in the liver, platelet activation and symptoms of fever.

  • Significant cut/very ill
  • More of an endocrine function – travel in bloodstream to liver to activate coagulation system

Activation of complement

31
Q

what is the function of acute inflammation

A

Function is to contain infection and localise it

- Stop spreading through blood stream

32
Q

what happens in most inflammatory cases

A

the pathogen is eliminated

33
Q

what type of process is the resolution of inflammation

A

active process

involving several regulatory mechanisms

34
Q

what causes immune suppression

A

anti-inflammatory mediators

e.g. IL-10 and TGF-b

35
Q

what happens in inflammation in sepsis

A

the immune response fails to eliminate the pathogen

pathogen persists
- can spread into the blood stream to other sites

36
Q

what do patients with sepsis demonstrate

A

excessive inflammation and immune suppression

37
Q

excessive inflammation causes

A

tissue injury

38
Q

what is strongly activated in excessive inflammation

A

Strong activation of innate immunity via PAMPs and DAMPs

  • Cytokines released in large amounts
  • Start to damage host cells
  • Host cells release DAMPS - activate immune system more
  • Microbes persisting as well - circulate body

sustained hyperinflammation

39
Q

which 3 systems are activated in sepsis

A

complement
coagulation
vascular

40
Q

which immune systems are activated in immune suppression

A

both innate and adaptive immunity

41
Q

what occurs in immune suppression

A

apoptosis of T cells and B cells

dysfunctional dendritic cells

delayed apoptosis of immune dysfunctional neutrophils

widespread impairment of adaptive immune system
- cannot fight of infection

42
Q

how to treat sepsis

A

mostly treating the signs and symptoms
- hard to understand cause

IV antibiotics is essential to limit spread of infection

Given fluids immediately in ICU

  • Colloids
  • crystalloid

Vasopressors for septic shock

  • Norepinephrine
  • Epinephrine
  • vasopressin

lung protective ventilation

urinary catheter

insulin

Time delivery and dosage is unknown

43
Q

why should dentists care about sepsis

A

Sepsis is a rare but potentially serious complication of acute dental infections

NICE requires all health care professionals, including dental care professionals to be trained in identifying people who may have sepsis
- state, “all healthcare staff involved in assessing people’s clinical condition are given appropriate training in identifying people who may have sepsis”

44
Q

what oral conditions could be potential source of sepsis

A

Caries
- complicated by abscess

Fungal infections

MRSA

45
Q

what factors of dental abscesses make them a risk factor for sepsis

A

Fistula can develop – drain into the mouth or cheek lead to severe local consequence

Erode into neck or floor of mouth

  • Can spread to other tissue sites
  • Bacteria in pus can disseminate throughout body
46
Q

when would a dental abscess develop

A

as a consequence of acute inflammatory response to bacterial infection

47
Q

what is contained in a dental abcess

A

immune cells, dead tissue and LIVE bacteria

- highly infectious

48
Q

how to treat a dental abscess

A

excision and drainage

49
Q

how to treat a periapical abscess

A

root canal and extraction

50
Q

when are antibiotics ineffective in treating abscess

A

ineffective (in the absence of spreading dental infection)

- No signs or symptoms of spreading infection

51
Q

where can an infection in oral cavity (e.g. abscess) spread to

A

floor of mouth

neck (most worrying - enter blood stream)

cheek

via fistula
route determined by complicated anatomy of head and neck

52
Q

red flag signs and symptoms of spreading dental infection

A

Temp < 36 or >38

Elevated breathing rate (> 20 breaths/min)

Elevated or reduced heart rate

Varying degrees of facial swelling

Trismus

Dehydration
- Reduced urine output can be sign of renal dysfunction

BDS2 BAMS (54 decks)

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