sepsis Flashcards
define sepsis
Life threatening organ dysfunction caused by a dysregulated host response to infection
is sepsis considered infection?
it is NOT an infection, it is only triggered by infection
it is fundamentally an inflammatory disease
qSOFA 3 criteria
- respi
- GCS
- BP
quick sepsis related organ failure assesment
- Respiratory > 22 breaths per minute
- Altered mental status from baseline of 0; Glasgow coma scale <15
- Systolic blood pressure < 100mmHg
What causes sepsis
- Infection
- Bacteria
o S aureus - Fungal
o Candida
Which organ does sepsis usually appear?
- Lungs
- Abdomen
- Bloodstream
- Urinary system
who is at risk of sepsis
- Aging population
- Immunocompromised patients
what is the pathophysiology of sepsis? 4 points
1 body wide clotting
2 leaky vessels, vasodilation
3 organ failure
4 persistent hypotension, fluids cannot be maintained within vessels
immunopathogenesis of sepsis
5 categories
1 innate immunity
2 complement system
3 vascular endothelium
4 coagulation system
5 adaptive immunity
how to treat sepsis
- Systemic Antibiotics
- Vasopressor
- Fluids
- Insulin therapy
- Lung ventilation
- Urinary catheter
Describe the local and potential systemic consequences of dental abscesses with ref to appropriate antibiotic use
Acute dental infections can cause sepsis
o Abscesses
o Odontogenic
o Perio
o Caries
o Any infection really
how do dental abscesses form
- Immune response to acute bacterial infection of pulp space
What do dental abscesses contain?
- Immune cells
- Dead tissues
- Live bacteria
2 keys factors making dental abscesses risk for sepsis
- Highly infectious
- Can spread easily, leading to local and systemic consequences
what other anatomical regions are closely related to the teeth
a. Nasal passages, maxillary sinus, Mylohyoid muscle, Buccinator muscles, oral cavity, tongue, orbit etc
potential for spread of dental abscess
how to treat dental abscess
- Drain abscess and disinfect
- Prescribe antibiotics
Describe red flag signs and symptoms of spreading dental infections, with ref to appropriate referral
- Temp <36 or >38
- Elevated breathing rate >20 breaths per minute
- Elevated or reduced heart rate
- Facial swelling
- Trismus
- Dehydration
- Refer to oral or maxillofacial surgeon
what is PAMP and DAMP
Pattern associated molecular patterns
- exogenous factors expressed by pathogen
damage associated molecular patterns
- endogenous factors released from cell damage
when the innate immunity is activated during sepsis, what occurs
activation of inflammatory signaling pathways
PAMP and DAMPs (LPS, peptidoglycan and Nucleic acids/proteins) bind to the TLR and other receptors on the cell surface
release of chemokines, cytokines, IFN
this causes vasodilation, increased inflammatory response, cytokine storm
macrophages secrete TNF alpha
what is TNF alpha and how is it related to sepsis
TNF alpha is released by macrophages in innate immunity
TNF alpha coordinates local containment of infection but when it enters systemic circulation, it drives sepsis
how does TNF alpha coordinate local containment of infection
- Expression of adhesion molecules, Recruits immune cells
- Triggers blood clotting, Clot stops pathogens from spreading via blood
what happens when TNF alpha enters systemic circulation
drives sepsis
- Systemic vasodilation
- Increased vascular permeability
- Loss of blood pressure
- Systemic blood clotting of microvasculature
when is the complement system activated
immediately upon the recognition of PAMPs and DAMPs
what does the complement system do
generates C3 and C5
C5 drives immunopathogenesis
o Potent chemoattractant (opsonization)
Membrane attack complex
o Further amplifies inflammation
o Vasodilation
o Tissue damage
o Organ failure
how does the vascular endothelium change in response to inflammation
Endothelial barrier dysfunction
endothelium loses its anticoagulative function
theres slow blood flow
loss of tight junctions
leaky vessels
body wide blood vlotting
why is there body wide blood clotting in sepsis
the body enters a hypercoagulative state due to the coagulation system being activated more
what happens in hypercoagulation
o Micro vascular thrombi
o Fibrin deposition
o Neutrophils extracellular trap formation
o Endothelial injury
what is the adaptive immunity
patients with sepsis demonstrate excessive inflammation AND immune suppression
what mediates excessive inflammation
- pro inflammatory mediators
- coagulation activation
- endothelium dysfunction
- complement system activation
- leukocyte recruitment
all these drives
1 vasodilation and leaky vessles
2 hypotension
3 body wide blood clotting
4 organ failure
immune suppression associated with what type of cells
INCREASED APOPTOSIS of t cells and b cells
dysfunctional DC cells
delayed apoptosis of immature dysfunctional neutrophils
