Schoenwald - Sepsis Flashcards by Alice Richards

bacteria in the bloodstream

bacteremia

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t/f: not all bacteremia is sepsis

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2 indications of bacteremia

positive blood cultures

fever/chills

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systemic response to infxn → organ failure - can be fatal

sepsis

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what do you think when you see SIRS

sepsis

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SIRS in the setting of infxn, when associated w. acute organ dysfxn

severe sepsis

infxn + SIRS + organ dysfxn = sepsis

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life-threatening organ dysfxn caused by dysregulated host response to infxn

sepsis

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subset of sepsis in which underlying circulatory and cellular/metabolic abnormalities are profound and increase mortality

septic shock

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how is organ dysfxn identified in sepsis

SOFA score →

sequential organ failure assessent

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SOFA score doesn’t take into account

lactic acid

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using SOFA score, the higher the score,

the worse the prognosis

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components of the SOFA score (6)

respiration

coagulation

liver

CVD

CNS

renal

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problem w. SOFA score

can’t be done fast/bedside

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2 or higher on SOFA score reflects

overall mortality risk of 10% in hospitalized pt

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2 or higher on SOFA score reflects

overall mortality risk of 10% in hospitalized pt

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what sepsis score can be done bedside

qSOFA

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problem w. qSOFA

not very sensitive

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components of qSOFA

2 of 3:

RR 22 or higher

GCS < 13

SBP 100 or less

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for sepsis dx, 2021 guidelines use (2)

SIRS criteria

qSOFA

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pathway of sepsis (4)

inflammation → coagulation → fibrinolysis → coagulopathy

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driving force of acute organ dysfxn in sepsis

coagulopathy

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major class of bacteria associated w. sepsis

gram negative → lipopolysaccharide wall

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3 proinflammatory mediators activated in sepsis

TNF

interleukins

platelet activating factors

clotting factors driven to areas of inflammation

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4 classic signs of inflammation

rubor → redness

calor → heat

tumor → swelling

dolor → pain

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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

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

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

1. measure lactate 2. obtain cultures 3. abx 4. rapid admin of crystalloid 5. 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