Sepsis and septic shock Flashcards
define sepsis
Sepsis is defined as life-threatening organ dysfunction caused by dysregulated host response to infection, an organism enters the bloodstream creating a septic state.
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
what does qSOFA consist of?
hypotension <100 systolic, altered mental status, tachypnea >22RR. A SCORE OF 2 OR MORE SUGGESTS A GREATER RISK OF A POOR OUTCOME
what is a SOFA score?
pao2, GCS, MAP, serum creatinine or urine output, bilirubin, platelet count.
despite adequate fluid resucitation when should you suspect sespis has progressed to septic shock?
vassopressors required to maintain MAP over 65mmhg, serum lactate over 2
how much does mortality increase for each hours delay of abx administration in septic shock?
7.60%
pathophysiology of sepsis
similar to immunosuppression: loss of hypersensitivity, inability to clear infection, predisposition to nosocomial infection
what are the 3 phases in the pathogenesis of sepsis?
release of bascterial toxins, release of mediators, effects of specific excessive mediators
describe what happens in phase 1
Bacterial invasion into body tissues is a source of dangerous toxins, May or may not be neutralised and cleared by existing immune system
what are commonly 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
describe what happens in phase 2
effects of infection due to endo/exo toxin release, mediator role on sepsis (endo - LTA don’t need binding proteins to bind to macrophages) (exo - pro-inflammatory response)
what do proinflammatory mediators do? (inflammatory response that characterises sepsis)
Promote endothelial cell – leukocyte adhesion, Release of arachidonic acid metabolites, Complement activation, Vasodilatation of blood vessels by NO, Increase coagulation by release of tissue factors and membrane coagulants, Cause hyperthermia
what is a compensatory anti-inflammatory reaction?
can cause immunoparalysis
what do anti-inflammatory mediators do?
Inhibit TNF alpha, Augment acute phase reaction, Inhibit activation of coagulation system, Provide negative feedback mechanisms to pro-inflammatory mediators
what are the Clinical features of sepsis?
• Fever >38 degrees – chills, rigors, flushes, cold sweats, night sweats
• Hypothermia < 36 degrees – especially in elderly and children (anti-inflammatory response)
• Tachycardia >90bpm
• Tachypnoea >20/min
• Altered mental state
• Hyperglycaemia >8mmol/l
Arterial hypotension (systolic <90mmHg or MAP <70mmHg)
SvO2 >70%