Sepsis and Septic Shock Flashcards
What is sepsis?
The systemic illness caused by microbial invasion of normally sterile parts of the body. It is diagnosed as life threatening organ dysfunction caused by dysregulation of host response to infection
How can septic shock be identified?
Clinical construct of sepsis with persisting hypotension requiring vasopressors to maintain a MAP >65mmHg and a serum lactate >2mmol/L despite adequate volume resuscitation
How is severity of sepsis assessed?
qSOFA score Component parts: •Systolic BP <100mmHg •Altered mental status •Respiratory rate >22 qSOFA score of 2 or more indicates a poorer outcome
How does delay in treatment of sepsis affect outcome?
For each hour long delay in administering antibiotics in septic shock, mortality increases by 7.5%
What are the main defence systems of the body against sepsis?
Physical barriers
Innate immune system
Adaptive immune system
How does sepsis originate?
Originates from a breach of integrity of host barrier, whether that is physical or immunological, through which organisms can enter the bloodstream and create a septic state.
What are the phases in the pathophysiology of sepsis?
- Release of bacterial toxins
- Release of mediators
- Effects of specific excessive mediators
What occurs in the first phase of the pathophysiology of sepsis?
Phase one is the release of bacterial toxins, which involves bacterial invasion into body tissues creating a source of dangerous toxins. These may or may not be neutralised by the existing immune system.
What occurs in the second phase of the pathophysiology of sepsis?
Phase two = release of mediators.
Endotoxins that can be released are lipopolysaccharide (LPS) and lipoteichoic acid (LTA). LPS needs a LPS binding protein to bind to macrophages, but LTA requires no such protein. Exotoxin release is a pro-inflammatory response involving small amounts of superantigens causing a large amount of mediators to be secreted (cascade effect). The two types of mediators than can be released are Th1 and Th2. These are the pro-inflammatory mediators that cause the inflammatory response that is characteristic of sepsis. The compensatory anti-inflammatory reaction can cause immunoparalysis.
What occurs in the third phase of the pathophysiology of sepsis?
Phase three relates to the effects of specific excessive mediators
What are the possible effects of proinflammatory markers?
- Promote endothelial cell-leukocyte adhesion
- Release of arachidonic acid metabolites
- Complement activation
- Vasodilation of blood vessels
- Increase coagulation by release of tissue factors
- Hyperthermia
What are the possible effects of anti-inflammatory mediators?
- Inhibit TNF alpha
- Augment acute phase reaction
- Inhibit activation of coagulation system
- Provide negative feedback mechanisms to pro-inflammatory mediators
What are the potential outcomes of over-active proinflammatory responses?
Septic shock with multi-organ failure and death
What are the potential outcomes of over-active compensatory anti-inflammatory processes?
Immunoparalysis with uncontrolled infection with multiorgan failure
How can organ dysfunction present in sepsis?
- Altered consciousness, confusion and psychosis
- Tachypnoea, PaO2 <70mmHg and sats <90%
- Jaundice, increase liver enzymes, low albumin and increased prothrombin time
- Decreased platelets, decreased protein C and increased D-dimer
- Tachycardia and hypotension
- Oliguria, anuria and raised creatinine
