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Flashcards in Sepsis Deck (33)
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1
Q

is sepsis an infection

A

no

but it does not occur in the absence of infection

2
Q

define sepsis

A

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

3
Q

what is septic shock

A

sepsis in which the underlying circulatory and cellular and / or metabolic abnormalities are marked enough to substantially increase mortality
clinically defined as sepsis with persisting hypotension

4
Q

what is SOFA

A

wide range of tests done on organs involving lab tests

has to be in a hospital environment

5
Q

what is qSOFA

A

quick SOFA
• A tool is clinically characterise patients at risk of sepsis (at risk of prolonged ICU or death)
This criteria does not need lab tests and can be used in the community

6
Q

what are the criteria in qSOFA

A
  • respiratory > or equal to 22 breaths per minute (elevated respiratory rate)
  • altered mentation (glasgow coma scale < 15)
  • systolic blood pressure < or equal to 100mmHg
7
Q

what is baseline qSOFA

A

• Baseline qSOFA = 0 unless patient has pre-existing organ dysfunction BEFORE onset of infection
○ If you have a patient presenting who is diabetic or diagnosed with a CVS disease or liver disease before they get infection then they will immediately score 1

8
Q

what does a qSOFA score of > or equal to 1 tell you

A

overall 10% mortality risk - requires prompt medical intervention

9
Q

what criteria remains important to aid diagnosis of infection

A

SIRS criteria

helps with identifying infection in general and the source of infection

10
Q

what are the 3 criteria looked for in the glasgow coma scale / GCS?

A
3 criteria looking for 
	- Eye opening
	- Verbal 
	- Motor response 
Maximum score is 15
11
Q

what causes sepsis

A
Any infection can trigger sepsis 
examples:
- Meningitis 
- Small infected cut
- UTI
12
Q

what are common sites of infection to trigger sepsis?

A

Lungs - 64%
Abdomen - 20%
Bloodstream - 15%
Urinary system - 14%

13
Q

what sort of micro-organism infections trigger sepsis

A
○ Gram positive bacteria - 47% 
	§ Staph aureus - 20%
○ Gram negative bacteria - 62%
○ Fungal - 19%
	§ Candida- 17%
	□ Candida blood stream infections associated with higher ICU mortality compared with bacterial infections
14
Q

what factors cause some infections to progress to sepsis

A

Mechanisms not fully understood

Involves a combination of microbial and host factors

15
Q

what microbial factors cause some infections to progress to sepsis

A
Microbial factors
Factors that help microbes to attach colonise and invade our tissues and cause disease
○ Virulence factors
	§ LPS 
	§ Lipoteichoic acid 
	§ Peptidoglycan 
	§ Pili, fimbriae, capsule etc
○ Virulence contributes to pathogenicity 
Ability to cause disease
16
Q

what host factors cause some infections to progress to sepsis

A
○ Innate immunity 
○ Adaptive immunity 
○ Immuno-compromised 
	§ HIV/AIDS
	§ Cancer
	§ Autoimmunity
	§ organ transplantation 
	§ Immune function impaired in any way will affect the body's ability to fight infection
○ Pre-existing chronic conditions
	§ Diabetes
	§ Cirrhosis 
	§ CKD
○ Age 
○ Genetics
17
Q

what is the outcome of infection (pathogenicity) determined by?

A

Outcome of infection (pathogenicity) is determined by interactions between microbes and host immune response

18
Q

what is involved in host-microbial interactions

A

microbial colonisation

  • antigens
  • virulence factors

immune response

  • innate
  • adaptive
19
Q

what happens when the host has a weakened / compromised immune response

A

the microbial colonisation uses it’s competitive advantage and are more pathogenc

20
Q

what population are more likely to get sepsis?

A
• Most common among aging population
	○ 65% of sepsis cases in US
• Sepsis disproportionately affects medically and immune compromised patients
	○ Cancer
	○ Cirrhosis 
	○ Autoimmunity 
	○ HIV / AIDS 
	○ Organ transplantation
	○ Diabetes
21
Q

what is included in the pathophysiology of sepsis

A

• Dysregulated, excessive systemic inflammation
○ Leads to organ dysfunction
• Body wide blood clotting and leaky vessels
○ Leaks into tissues
• One or more organs begin to fail (sepsis - 10% in hospital mortality)
• Persistent hypotension (septic shock - 40% in hospital mortality)

22
Q

what is acute inflammation in response to localised infection

A
  • A protective immune reaction to invading micro-organisms or endogenous signals from damaged cells
  • Gives rise to cardinal signs of inflammation - localised to the site of infection
  • Leading to clearance of the source of injury and necrotic tissues
  • Followed by tissue repair and return to homeostasis
23
Q

what happens with the innate immune system?

A
  • Innate immune system recognises PAMPs (and DAMPs) through PRRs
  • Responding cells trigger inflammation through release of cytokines and chemokines
  • Cytokines activate endothelial cells, vasodilation and vascular permeability
  • Large amounts of cytokines (eg TNFa) activate acute phase proteins in the liver, platelet activation and symptoms of fever
  • Activation of complement
24
Q

what happens in the resolution of inflammation

A

• In most cases, the pathogen is eliminated
• Resolution of inflammation is an active process
• Involving several regulatory mechanisms
• Immune suppression via anti-inflammatory mediators
○ IL-10
○ TGF-beta
§ Activated during this period
• In sepsis, the immune response fails to eliminate the pathogen
○ Pathogen persists and can spread through the blood
• Localised acute inflammation progresses to acute systemic inflammation

25
Q

what is the immunopathogenesis of sepsis

A

Very complicated

Patients with sepsis demonstrate excessive inflammation and immune suppression

26
Q

how does excessive inflammation occur

A

• Sustained inflammation causes tissue injury
• Strong activation of innate immunity via PAMPs and DAMPs
○ Cytokines are released in large amounts and these start to damage the host cells
○ Host cells release DAMPs
○ Same time microbes are persisting
• Sustained hyperinflammation
○ Cycle
• Activation of complement system, coagulation system and vascular endothelium
○No longer localised - happening throughout the whole body

27
Q

what happens in immune suppression

A
• Both innate and adaptive immunity
• Apoptosis of T cells, B cells
	○ Don’t understand why this happens
	○ Adaptive immunity is impaired
• Dysfunctional DCs 
	○ Dendritic cells = DCs
	○ Cannot effectively present antigens
• Delayed apoptosis of immature dysfunctional neutrophils
28
Q

where are the main sites for sepsis to be a problem

A

CVS
blood coagulation system
leakage of fluids

29
Q

how do you treat sepsis

A

treat signs and symptoms but there is no real way to treat the cause of sepsis = focus is to keep the patient alive

  • antibiotics, IV essential, early administration
  • fluids
  • vasopressors, 1-6hours after onset
  • enteral feeding
  • insulin therapy
  • lung protective ventilation
  • urinary catheter
30
Q

why should dentists care about sepsis?

A

• Sepsis is rare but potentially serious complication of acute dental infections
• NICE requires all health care professionals, including dentists to be trained in identifying people who may have sepsis
○ “all healthcare staff involved in assessing people’s clinical condition are given appropriate training in identifying people who may have sepsis”
• What oral conditions could be a potential source of sepsis
○ Fungal infections
○ MRSA
○ Caries
§ Treatment can sometimes be complicated by abscess
•There have been cases of sepsis with odontogenic origin

31
Q

what are key points about dental abscesses

A
  • Develop as a consequence of acute inflammatory response to bacterial infection
  • Contain immune cells, dead tissues and LIVE bacteria
  • Highly infectious
  • Treated promptly by excision and drainage
  • Periapical abscesses require root canal treatment or extraction
  • Antibiotics ineffective (in the absence of spreading dental infection)
  • Dental abscesses can spread leading to severe local and systemic consequences
32
Q

what are the red flag signs and symptoms for spreading dental infection

A
  • Temp < 36 or > 38
  • Elevated breathing rate ( > 20 breaths per minute)
  • Elevated or reduced heart rate
  • Varying degrees of facial swelling
  • Trismus
  • Dehydration
33
Q

are spreading dental infections potential triggers of sepsis

A

yes

refer to oral or maxillogacial surgeon in a hospital setting without delay