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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
systemic effect of sepsis
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
appearance of septic shock limb
inflammed shiny skin red blotching due to leaky vessels
27
what is acute inflammation in response to localised infection
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
what is present in the localised site of acute inflammation
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
what does acute inflammation result in if it is successful
clearance of the source of injury and necrotic tissues - protective clearance at site of infection followed by tissue repair and return to homeostasis
30
stages of acute inflammation in sepsis
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
what is the function of acute inflammation
Function is to contain infection and localise it | - Stop spreading through blood stream
32
what happens in most inflammatory cases
the pathogen is eliminated
33
what type of process is the resolution of inflammation
active process | involving several regulatory mechanisms
34
what causes immune suppression
anti-inflammatory mediators | e.g. IL-10 and TGF-b
35
what happens in inflammation in sepsis
the immune response fails to eliminate the pathogen pathogen persists - can spread into the blood stream to other sites
36
what do patients with sepsis demonstrate
excessive inflammation and immune suppression
37
excessive inflammation causes
tissue injury
38
what is strongly activated in excessive inflammation
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
which 3 systems are activated in sepsis
complement coagulation vascular
40
which immune systems are activated in immune suppression
both innate and adaptive immunity
41
what occurs in immune suppression
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
how to treat sepsis
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
why should dentists care about sepsis
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
what oral conditions could be potential source of sepsis
Caries - complicated by abscess Fungal infections MRSA
45
what factors of dental abscesses make them a risk factor for sepsis
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
when would a dental abscess develop
as a consequence of acute inflammatory response to bacterial infection
47
what is contained in a dental abcess
immune cells, dead tissue and LIVE bacteria | - highly infectious
48
how to treat a dental abscess
excision and drainage
49
how to treat a periapical abscess
root canal and extraction
50
when are antibiotics ineffective in treating abscess
ineffective (in the absence of spreading dental infection) | - No signs or symptoms of spreading infection
51
where can an infection in oral cavity (e.g. abscess) spread to
floor of mouth neck (most worrying - enter blood stream) cheek via fistula route determined by complicated anatomy of head and neck
52
red flag signs and symptoms of spreading dental infection
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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