Sepsis management Flashcards
Sepsis definition
life threatening organ dysfunction in response to infection
Septic Shock
Subset of sepsis w. circulatory dysfunction and high mortality
Hemodynamic Shock Cause
Review
Identify source of loss - repair active bleeding w/ surgical hemostasis
Hemorrhage:
* replace blood (PRBCs or FFP)
* reverse anticoagulation
GI losses, burns, third spacing
* Fluids (crystalloids, albumin)
Cardiogenic shock causes
Review
MI: revascularization CABG
Arrythmias: achieve sinus rhythm
Advance methods: LVADs
* Intraaortic balloon pump
* Impella
* HeartMate and Tandem Heart
ECMO
left ventricular assist devices
Managing septic shock
- Correct underling cause
* Abx
* Source control - Fluid
- Pressors
- Inotropes
- Corticosteroids
Identifying Sepsis
- qSOFA = rapid bedside score
- SIRS
- SOFA = stage organ dysfunction (for research)
qSOFA criteria
at least 2 of the following
* SBP < 100 mmHg
* RR > 22
* Altered mentation
SIRS criteria
at least two of the following
* Temp >38C or <36C
* HR >90
* RR > 20
* WBC >12 or <4
(+) sirs not = sepsis
Septic Shock 1 hour bundle
- Get initial lactate, if >2 re-measure
- Get blood culture asap
- Give broad spectrum abx
- Rapid bolus 30ml/kg crystalloid if hypotension or lactate ≥4
- Add pressors if hypotensive to maintain MAP ≥65
Why draw culture prior to abx admin?
Higher chance to ID bug – otherwise abx may “sterilize” the culture
Wait for culture b4 abx given as long as it doesn’t delay abx initiation
* delay abx = increased mortality
Harms of unnecessary abx use
- allergic rxn
- kidney injury
- thrombocytopenia
- C.diff
- abx resistance
Importance of source control
Just abx alone not always enough
* Ventillator associated infection = clean vent
* infected hardware = surgery
* Necrotizing fascitis = debridement
If sepsis is possible but not in shock, when do you give abx?
assess infectious vs other cause of illness
give abx within 3 hours if infection concern persists
in all other circumstances give abx asap - ideally within 1 hr or recogn
MRSA patient specific risk factors
- prior hx MRSA infection OR colonization
- Recent IV abx use
- Recent hospitalization
- Hx recurrent skin infection/chronic wound
- Presence of invasive devices
- Hemodialysis
- Severity of illness
Use VANCO or PipTazo coverage MRSA
MDR patient specific risk factors
use TWO gram negative agents to cover empirically
- proven infection/colonization with resistant organism in the last year
- broad spectrumm IV abx use last 90 days
- Travel highly endemic country last 90 days
- local prevalence of MDR
- hospital acquired infection
Goal of fluid therapy
Increase stroke volume (depends on preload)
Increase cardiac output
Increase DO2 (delivery)
Fluid therapy
BOLUSES
30ml/kg over 15-30min
then 10ml/kg bolus prn
more conservative if HF, cardiogenic shock
LR vs NS vs Albumin
- LR
- NS
- Albumin (colloid)
LR considerations
may produce hyponatremia
lactate not an issue - metabolized rapidly
NS considerations
may produce
* hypernatremia
* hypercholremia
* metabolic acidosis
* risk of increased AKI
1 L crystalloid = ____ intravascular volume?
250 mL
Respectively, albumin 1L = 500-1000 mL intravascular
Albumin considerations
available as 2 concentrations
efficacy equivalent to crystalloid
benefit not justified by cost
1L = 500-1000 mL intravascular
* SAFE trial: albumin for ICU = possible benefit for mortality
* ALBIOS trial: albumin for sepsis = no difference mortality
Starches considerations
hetastarch, hydroxyethyl starch 6%
dont use it for septic shock
increased risk of mortality, AKI, bleed
b1 agonism on organs
heart, GI, kidney, fat
* increased HR/contractility
* decreased GI tone/motility
* Increased renin secretion
* Lipolysis
no arteriole/lung/muscle/liver involvmement
b2 agonist on organs
everything but kidney
* increased HR/contractility
* Arteriole dilation
* bronchial relaxation
* decreased GI tone/motility
* Glycogenolysis/gluconeogenesis
* Increased K+ uptake
* Lipolysis
b2 dilation - counteract in shock with other a1 agonism
a1 agonism on organs
- Arteriole constriction
- decreased GI tone/motility
- Decreased renin secretion
- Glycogenolysis/gluconeogenesis
- Lipolysis
arteriole, GI, kidney, liver, fat
a2 agonism on organ
- arteriole constriction
- decreased Gi tone/motility
V1 agonism
arteriole constirction
V2 agonism
arteriole dilation
water reabsorption
D1 agonism
artetriole dilation
receptors w/ arteriole dilation
b2, v2, d1
receptors with increased HR/contractility
b1, b2
Receptors with arteriole constriction
a1,a2,v1
decreased renin secretion
a1
Increased renin secretion
b1
water reabsorption
v2
NE receptor affinity
- a1
- b2
= increased SVR
Dobutamine receptor affinity
- b1 =inotropic
- b2
±a1
= increased CO
decreased SVR
cardiogenic shock, pump failure
EPI receptor affinity
- a1, b1
- b2
= increased CO
low dose = low SVR
high dose = high SVR
Dopamine receptor affinity
Low: d1>b1(CO)
med: d1=b1(CO,SVR)
high: a1=d1=b1(SVR)
Catecholamine effects
a=more SVR (PE,, NE, EPI)
* distributibe
* hypovolemic
* code
middle = dopamine
b= more CO (Dobutamine, ISO)
* cardiogenic
* cardiomyopathy
Pressors tx
- NE
- ADH
- EPI if previous not working
- Dobutamine: if need more CO (cardiogenic)
- AGII = vasoconstriction for refractory shock (distributive)
- PE: not used, purely alpha constriction
use of steroids in sepsis
improves physiologic response to sepsis in refractory shock
1. regualtes inflammation
2. inhibits inducible NOS
3. reverses adrenergic receptor desensitization (pressor works better)
4. increases Na and water retention (increase volume) - MC
use when poor response to fluid+pressor
Choosing steroid for septic shock
- Hydrocortisone 200 mg IV QD x 3-7 days
- Fludrocortisone 50mcg PO daily (MC effect only)
fludricortisone usually adjunct to HC for additional MC effect
