Sepsis and Septic Shock Flashcards
Define sepsis
Life threatening organ dysfunction caused by dysregulated host response to infection
Define septic shock
Septic shock can be identified with a clinical construct of sepsis with persisting hypotension requiring vasopressors to maintain MAP >65mmHg and having a serum lactate of >2mmol/l despite adequate volume resuscitation
(sepsis with low blood pressure and high lactate)
What is the SOFA score
Sequential organ failure assessment score
Used to track a person’s status during the stay in an intensive care unit (ICU) to determine the extent of a person’s organ function or rate of failure
What are the systems involved in the sofa score?
Respiratory (PaO2)
Nervous system (GCS)
Cardiovascular (MAP or administration of vasopressors required)
Liver (bilirubin)
Coagulation (platelets)
Kidneys (creatinine)
What is the qSOFA score?
Quick SOFA Score as an initial way to identify patients at high risk for poor outcome with an infection
Only includes three clinical criteria (low blood pressure, high respiratory rate, any altered mental state)
The presence of 2 or more qSOFA points near the onset of infection was associated with a greater risk of death or prolonged intensive care unit stay. These are outcomes that are more common in infected patients who may be septic than those with uncomplicated infection.
qSOFA basically is a good indicator for who is likely to be septic
What are the components of the bodyes defence against sepsis?
Physical barrier
Innate immune system
Adaptive immune system
- Physical barrier – skin, mucosa, epithelial lining
- Innate immune system – IgA in gastrointestinal tract, dendritic cells / macrophages
- Adaptive immune system – lymphocytes, immunoglobulins
How does sepsis arise?
Failure of host barrier (physical or immunological)
Organism enters the blod stream creating a septic state
Patients with sepsis are said to have features consistent with immunosuppression, what are these features?
- Loss of delayed hypersensitivity
- Inability to clear infection
- Predisposition to nosocomial infection
What is the probable change of the sepsis syndrome over time?
- Initially there is an increase in inflammatory mediators
- Later, there is a shift toward an anti-inflammatory immunosuppressive phase
- Depends on the health of the individual patient
What are the three phases in the pathogenesis of sepsis?
- Release of bacterial toxins
- Release of mediators
- Effects of specific excessive mediators
What are comonly released toxins?
•Gram negative:
Lipopolysaccharide (LPS)
•Gram positive:
- Microbial-associated molecular pattern (MAMP):
- •Lipoteichoic acid
- •Muramyl dipeptides
•Superantigens:
- Staphylococcal toxic shock syndrome toxin (TSST)
- Streptococcal exotoxins
What is the difference between endotoxins and exotoxins?
Exotoxins are toxic substances secreted by bacteria and released outside the cell. Pro inflammatory response, small amounts of superantigens will cause a large amount of mediators to be secreted: cascade effect
Endotoxins are bacterial toxins consisting of lipids that are located within a cell. (LPS needs a LPS binding protein to bind to macrophages, LTA (Lipoteichoic acid) does not
What are the two types of mediators that can be released in sepsis/?
- Pro-inflammatory mediators – causes inflammatory response that characterises sepsis
- Compensatory anti-inflammatory reaction – can cause immunoparalysis
Name some pro-inflammatory mediators
TNF-alpha
IL1b, IL-2, IL-8, IL-15
Neutrophil elastase
IFN-gamma
Prostaglandins, prostacyclin
Name some anti-inflammatory mediators
IL-1Ra
IL-4
IL-10
IL-13
LPS binding protein
Soluble TNF alpha receptor
Epinephrine phospholipase a2
