Sepsis Flashcards
What causes sepsis
Sepsis can be due to infection spread throughout the body via blood
BUT…in some cases bloodstream infection cannot be detected
Sepsis can persist once the infection has been successfully treated
What is sepsis
Life-threatening organ dysfunction due to a dysregulated host response to infection
What does qSOFA stand for
quick-Sequential Organ Failure Assessment
How can sepsis risk be assessed
qSOFA
What is the baseline qSOFA
0 unless patient has pre-existing organ dysfunction BEFORE onset of infection
What are the criteria which make a patient at risk of sepsis
Respiratory ≥ 22 breaths/min
Altered mentation (Glasgow Coma Scale <15)
Systolic blood pressure ≤ 100 mm Hg
What is the most common site of infection
Lungs
What organs does sepsis affect
Can affect all of them
What are the common symptoms of sepsis
Neurological (altered mental status)
Pulmonary (hypoxaemia) – Acute Respiratory Distress Syndrome (ARDs)
Cardiovascular (shock)
Renal (oligouria)
What systemsdoes sepsis activate
Innate immunity
Complement system
Vascular endothelium
Coagulation System
Adaptive Immunity
What is the pathophysiology of sepsis
One or more organs begin to fail (Sepsis – 10% in hospital mortality)
Body-wide blood clotting and ‘leaky vessels’
Persistent hypotension (Septic shock – 40-50% in hospital mortality)
What is the difference between PAMPs and DAMPs
PAMPs - Conserved exogenous (non-self) factors expressed by pathogens
(LPS, peptidoglycan, nucleic acids)
DAMPs - Endogenous (host) factors released following cell damage
(Heat-shock proteins, nucleic acid)
How does TNF alpha control local infections
TNF⍺ stimulates expression of
Adhesion molecules on endothelial cells
Proteins that trigger blood clotting
Recruits immune cells to site of infection
Prevents pathogen spreading via blood
What immune cell is TNF alpha
A cytokine
How can TNF alpha become a driver of sepsis
When it is released systemically:
Systemic vasodilation
Increased vascular permeability
Loss of blood pressure
Systemic blood clotting of microvasculature
What component found inthe blood as a hallmark of sepsis
Complement
How does complement promote sepsis
Activated immediately upon recognition of ‘pathogenic surfaces’
Generation of anaphylatoxins C3a and C5a
Potent proinflammatory mediators
Uncontrolled activation causes damage to cells and tissues
Activates leukocytes/ endothelial cells/ platelets and coagulation system
How is the endothelium affected with sepsis
Becomes ‘sticky’ and endothelial barrier becomes leaky allowing immune cells to exit blood stream into tissues - fluid moving into tissues causing swelling
What does the hyperoagulative state caused by sepsis result in
Microvascular thrombi (blocking of small vessels)
AND
Haemorrhage (excessive bleeding) due to consumption of clotting factors and platelets.
How does sepsis cause immune suppression subsequently
Lymphocyte exhaustion and apoptosis is a common feature of sepsis
Loss of functioning adaptive immunity linked with increased mortality
Long-term dysfunctional immunity in patients who survive sepsis
Strategies to modulate dysregulated host immunity – largely unsuccessful
What methodsare used to treat sepsis
Antibiotics (early administration)
Fluids (colloids,crytalloids)
Vasopressors
Enteral feeding
Insulin therapy
Lung protective ventilation
Urinary catheter
What are the red flag signs and symptoms of a 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
When suspecting a potential diagnosis of sepsis due to spreading dental infection what should you do
Refer to oral or maxillofacial surgeon in a hospital setting without delay
qSOFA ≧ 2 + signs of infection = medical emergency
