sepsis and septic shock Flashcards
Systemic inflammatory response syndrome
- Temp: >38oC or <36oC
- HR >90
- RR >20 or PaCO2 <32
- WBCs > 12000 or < 4000 or >10% bands (immature forms)
- SIRS does not always indicate infection. Can occur following burns, pancreatitis, surgery.
sepsis
life threatening organ dysfunction
dysregulated host response to infection
acute change in SOFA score >2 points consequent to infection
septic shock
sepsis with persisting hypotension requiring vasopressors to maintain MAP >65mmHg and serum lactate of >2mmol/l
high mortality
serum lactate
amount of lactic acid in the blood and is a fairly sensitive and reliable indicator of tissue hypoperfusion and hypoxia. Any disorder that causes an imbalance between lactate production and clearance can lead to lactic acidosis, a serious and sometimes life-threatening condition
qSOFA score (2 or more risk of poor outcome)
Hypotension altered mental status tachypnoea systolic BP <100mmHg confusion ( not neccessarily GCS) RR>22`
pathophysiology
Breach of body's natural defence uncontrolled inflam response immunosuppresion features presdiposition to nosocomial loss of delayed hypersensitivity probably change of sepsis syndrome over time -initially increase in inflam mediators -later shift toward anti inflam immunosuppresive
pathogenesis
release of bacterial toxins commonly released toxins Gram-ve: lipopolysaccharide Gram +ve: Microbial associated molecular pattern a. lipoteichoic acid b. muramyl dipeptides Superantigens a.staphylococcal toxic shock syndrome toxin streptoccocal exotoxins
release of mediators
endotoxin release LPS need LPS binding protein LTA doesnt exotoxin -proinflam response -small amount of superantigens large mediators secreted
Mediators
TH1: Pro inflam mediators cause inflammatory response that characterise sepsis
TH2: compensatory anti inflam- can cause immunoparalysis
pro inflam mediators
promote endothelial cell- leukocyte adhesion
release of arachidonic acid metabolites
complement activation
vasodilation of blood vessels-erythema
increase coagulation by release of tissue factor
hyperthermia-> TNF alpha release
Anti-inflam mediators
inhibit TNF alpha
augment acute phase reaction
inhibit activation of coagulation system
negative feedback mechanism to pto inflam
balance
Excess anti-inflammatory: septic shock with multi-organ failure and death
Excess pro-inflammatory: immunoparalysis with uncontrolled infection and multi-organ failure
Immunoparalysis
Persistence of a marked compensatory anti-inflammatory innate immune response following an insult such as sepsis or trauma
general feature of sepsis
fever hypothermia tachycardia tachypnoea >20/min hyperhlycemia >8mmol/l absence of diabetes
inflammatory
leucocytosis (>12000) leucopenia (<4000) greater than 10% immature high CRP high procalcitonin (elevated only in patients with active infection)