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
what metabolite indicates increased anaerobic metabolism
lactic acid
widespread imbalance btw inflammation, coagulation, and fibrinolysis
DIC (disseminated intravascular coagulation)
clotting and bleeding at the same time
4 labs elevated in DIC
PT
PTT
fibrin monomers
d-dimer
3 labs decreased in DIC
protein C
fibrinogen
platelet count
4 labs elevated in sepsis
Cr
ALT/AST/bili
lactate
procalcitonin
3 things decreased in sepsis
urine output
mental status
bp
when do we start to worry about lactate
>2 mmol/L
when do we start to worry about procalcitonin
>2.0 ng/ml
what is procalcitonin
protein biomarker for bacterial infxn
usually doesn’t go >2 in viral infxn
clinical usefulness of procalcitonin
can be used to deescalate (d/c) abx
risk of abx in sepsis
collateral damage → c.diff, SJS, resistant bacterial infxn
procalcitonin > __ is highly suggestive of sepsis
2
majority of sepsis pt’s originate in
hospital
mainly ER
rf for sepsis (7)
critically ill
severe CAP
intra abd surgery
meningitis
chronic dz
decreased immune fxn
cellulitis
UTI
3 greatest risk for sepsis
65 yo+
underlying comorbidity
higher body wt
sx of sepsis
SEPSIS:
shivering/fever
extreme pain/worst ever discomfort
pale skin
sleepy - difficult to wake/confused
I feel like I might die
SOB
SIRS criteria (4)
temp >100.4 OR <96.8
HR > 90 bpm
RR > 20 OR PaCO2 < 32
>12,000 WBC
think sepsis
mimics of sepsis (7)
pancreatitis
GI bleed
SLE flare
DKA
anaphylaxis
adrenal insufficiency
PE/DVT
2 values highly suggestive of severe sepsis
cap refill 3 seconds or more
lactate > 2 mmol/L
mc cause of severe sepsis
PNA
~50%
blood cultures are positive in __ of severe sepsis
⅓
severe sepsis is caused by what 3 types of pathogens
gram negative bacteria: 62%
gram positive bacteria: 62%
fungi: 1.9%
screening for severe sepsis takes into account (3)
infxn
SIRS
acute organ dysfxn
tx for sepsis is divided into (3)
resuscitation
initial
maintenance
resuscitation phase:
initial phase:
maintenance phase:
resuscitation: 1st 6 hr
initial: 24 hr
maintenance: >24 hr
goal to start tx for sepsis
w. in 3 hr
* sooner the better*
tx for resuscitation phase of sepsis (8)
airway
pan-culture
initiate abx
IV fluids
tight glycemic control
vasopressors
sedation
steroids
abx options for sepsis (4)
vanco
quinolone
carbapenem (not ertapenem)
zosyn
2 abx commonly used for resuscitation phase
vanco
zosyn
indications for fluids in resuscitation phase (2)
MAP < 65
lactate > 4
initial rate for fluids
30 mL/kg continuous
glycemic control in resuscitation phase
continuous insulin drip
first line vasopressor in resuscitation phase
norepinephrine
also consider dobutamine, phenylephrine, vasopressin
pressor NOT recommended in sepsis
dopamine
in resuscitation phase, what should be done before starting abx
blood cultures
hour-1 sepsis bundle
- measure lactate
- obtain cultures
- abx
- rapid admin of crystalloid
- vasopressor
indications for vasopressor
hypotensive during or after fluid resuscitation
goal for bp in resuscitation phase
maintain MAP above 65
4 goals in resuscitation phase that reduce 28 day mortality rate
CVP 8-12 mmHg
MAP 65 mm Hg
urine output 0.5 ml/kg/hr
central venous O2 sat 70% OR mixed venous O2 sat 65%
what 3 scenarios indicate initiation of abx w.in 1 hr of sepsis recognition
sepsis definite or probable with OR without shock
sepsis is possible WITH shock
when should abx be administered w.in 3 hours of sepsis recognition
w.in 3 hr if infxn persists
tx for initial management phase of sepsis (3)
continue resuscitation phase
target abx to cultures
constant vasopressor monitoring
indications to cut back on fluids (2)
lactic acid
capillary refill
common respiratory condition associated w. sepsis
ARDS
management of ARDS (3)
special attention to pressures/volumes
elevate head of bead
weaning protocols
what is this showing
normal CXR
what is this showing
bilateral diffuse fluffy infiltrates
normal cardiac size
EKG wires
→ ARDS
CNS support for sepsis w.o ARDS
sedation
avoid neuromuscular blockers
CNS support for sepsis pt w. early, severe ARDS
sedation
short course of neuromuscular blocker
tx for maintenance phase of sepsis (if pt survives > 24 hr)
prevent nocosomial infxn
restore premorbid condition
tailor abx to cultures
general supportive care for sepsis (5)
bg < 180 mg/dl
dialysis for renal/hypervolemia
DVT prophylaxis
stress-ulcer prophylaxis
enteral feeding
what causes sepsis (4)
bacteria in:
lungs
urinary tract
GI
skin/soft tissue
tx for ICU pt w. severe or critical COVID19 (4)
corticosteroids (dexamethasone)
venous thromboprophylaxis
remdisivir if not ventilated
prone ventilation
tx NOT recommended for covid
hydroxychloroquine
t/f: severe sepsis is uncommon
F!
it’s common :(
critical aspect of sepsis management
early recognition