Schoenwald - Sepsis Flashcards
bacteria in the bloodstream
bacteremia
t/f: not all bacteremia is sepsis
T
2 indications of bacteremia
positive blood cultures
fever/chills
systemic response to infxn → organ failure - can be fatal
sepsis
what do you think when you see SIRS
sepsis
SIRS in the setting of infxn, when associated w. acute organ dysfxn
severe sepsis
infxn + SIRS + organ dysfxn = sepsis
life-threatening organ dysfxn caused by dysregulated host response to infxn
sepsis
subset of sepsis in which underlying circulatory and cellular/metabolic abnormalities are profound and increase mortality
septic shock
how is organ dysfxn identified in sepsis
SOFA score →
sequential organ failure assessent
SOFA score doesn’t take into account
lactic acid
using SOFA score, the higher the score,
the worse the prognosis
components of the SOFA score (6)
respiration
coagulation
liver
CVD
CNS
renal
problem w. SOFA score
can’t be done fast/bedside
2 or higher on SOFA score reflects
overall mortality risk of 10% in hospitalized pt
2 or higher on SOFA score reflects
overall mortality risk of 10% in hospitalized pt
what sepsis score can be done bedside
qSOFA
problem w. qSOFA
not very sensitive
components of qSOFA
2 of 3:
RR 22 or higher
GCS < 13
SBP 100 or less
for sepsis dx, 2021 guidelines use (2)
SIRS criteria
qSOFA
pathway of sepsis (4)
inflammation → coagulation → fibrinolysis → coagulopathy
driving force of acute organ dysfxn in sepsis
coagulopathy
major class of bacteria associated w. sepsis
gram negative → lipopolysaccharide wall
3 proinflammatory mediators activated in sepsis
TNF
interleukins
platelet activating factors
clotting factors driven to areas of inflammation
4 classic signs of inflammation
rubor → redness
calor → heat
tumor → swelling
dolor → pain
interleukins that down regulate initial proinlammatory response
IL4
IL10
- repair existing damage*
- limit new damage*
why does such a massive systemic rxn occur in sepsis
regulation of initial response of Il4 and IL10 is lost
what mediators are responsible for cytokine storm in sepsis
TNF
IL1
IL6
what indicates activation of clotting
d-dimer
is d-dimer used as a sepsis screening tool
no
normal process to remove clots that is suppressed in sepsis
fibrinolysis
key inhibitor of fibrinolysis
plasminogen activated inhibitor-1 (PAI-1)
PAI-1 is produced by
endothelial cells
what increases activity of PAI-1
endotoxins released by gram negative rods
system responsible for vast majority of O2 delivery to tissues
microcirculation
injury to microvascular system leads to
leaky capillaries → edema
leaky capillaries lead to (6)
neutrophil migration/adhesion
increased coagulation
decreased fibrinolysis
increased inflammation
endothelial injury/loss of barrier integrity
altered microcirculatory perfusion
results of sepsis (4)
decreased O2 delivery dt capillary damage
decreased cardiac output
increased anaerobic metabolism
DIC