Fluid Resuscitation in Sepsis

Here's to hoping. Our medical director encourages us to call "Sepsis Alerts" despite that not being in the guidelines, which I appreciate. The last one I called in was for a transfer from the VA, mid 40s guy with pneumonia (horrid lung sounds), pressure in the 80s, tachycardia, tachypneic, febrile, EtCO2 of 52, and altered. After my patch (with all of that), I get "what makes you think this patient is septic?"

grrrrrrr.

We are supposed to start carrying levophed this year, but I am curious as to how they will write the sepsis protocol with it. Even with an hour transport, infusing 30ml/kg pre-pressor is probably not likely. The EmCrits I've been listening to seem to suggest low dose levophed early on, but I am not sure we'll be able to do that if the hospitals aren't.

We're adding push dose epinephrine as a bridge to early levophed in these patients. We're giving 20mL/kg doses concurrently with levophed starting at 5mcg/min with a target SBP of 90mmHg and/or a MAP of 65. The big killer in Sepsis is MODS, from my understanding. Our MDs thought process is the shorter period of time those organs go un/under perfused the better chance they have.

I'll see if I can track down the evidence they're using for you guys as we don't do anything without a decent amount of evidence.


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Quick thread derail...

You know if WilCo EMS moved to an all ALS intercept service, I'd call it just about as close to a unicorn as one could ask for. Even still, you all have what I consider a career-service for paramedics down enticingly well.

...back to the sepsis talk.
 
For those who are interested, a nice (open access) paper out of Australia takes a pretty interesting tack:


Curious what everybody thinks!
Hospital- 30ml/kg IVF for Sepsis Alert even if they have cardiac issues. The idea is you can manage (diurese) later.

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Quick thread derail...

You know if WilCo EMS moved to an all ALS intercept service, I'd call it just about as close to a unicorn as one could ask for. Even still, you all have what I consider a career-service for paramedics down enticingly well.

...back to the sepsis talk.

Come join us...we have cookies!


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We're adding push dose epinephrine as a bridge to early levophed in these patients. We're giving 20mL/kg doses concurrently with levophed starting at 5mcg/min with a target SBP of 90mmHg and/or a MAP of 65. The big killer in Sepsis is MODS, from my understanding. Our MDs thought process is the shorter period of time those organs go un/under perfused the better chance they have.

I'll see if I can track down the evidence they're using for you guys as we don't do anything without a decent amount of evidence.


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Is there some sort of criteria for who gets pressor support + fluids and who gets fluids?

That's what I struggle with.
 
What is "low dose levophed"? What is your target blood pressure? Also, with all of the apparent controversy, what is not controversial is the need for some way to establish a basis for the dose of fluid. Does your system give any guidance in that respect?
I was listening to this http://emcrit.org/podcasts/vasopressor-basics/.
The idea I guess is to start with smaller (can't remember the number and am too tired to relisten) doses at the same time as fluids resuscitation begins. If you need it great, turn it up. If not, well it's probably well tolerated anyway.
 
The big killer in Sepsis is MODS
The way I learned it was SIRS-->sepsis-->severe sepsis-->septic shock-->MODS. Once you're in MODS (2+ more end organ failure) your chances of mortality drastically increase; even more so with 3, 4, 5 organs. MODS is a very late manifestation, and ominous sign of the sepsis "chain".

http://emedicine.medscape.com/article/169640-overview#a3
Is there some sort of criteria for who gets pressor support + fluids and who gets fluids?
My guess is it's the often adopted SIRS criteria coupled with reasonable suspicion to believe said patient has an port of entry (e.g., recent infection, weeping wound, etc.), but Robb can elaborate.
 
Is there some sort of criteria for who gets pressor support + fluids and who gets fluids?

That's what I struggle with.

Anyone who's hypotensive and doesn't rapidly respond to fluids. The answer I got is that if they haven't improved in the time it takes you to mix the levo then hang the levo.

Basically it's suspected infection then 2 of the following
HR >90
RR >20 or EtCO2 <25mmHg
Temp >100.4 or < 96.8
If they're normotensive they just get 20mL/kg. If they're hypotensive they get 20mL/kg and levophed with profoundly hypotensive patients getting push dose epi to bridge the gap while we mix the levo.




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What are yall's experience with using epi in this case? No levo here, so epi would be the only decent option I would have.
 
What are yall's experience with using epi in this case? No levo here, so epi would be the only decent option I would have.

Adrenaline works well. It's the only vasopressor carried. I'm told there is no convincing evidence noradrenaline or one of the dopamine like drugs is better. Easy, cheap, simple to make up and administer (1 mg in one litre NaCl run at 2 drops a second initially) and no fart arseing around with syringe boluses.
 
What are yall's experience with using epi in this case? No levo here, so epi would be the only decent option I would have.
The research I did in class brought me to the conclusion that I'd rather give epi than dope. Dopamine does not have great outcomes for sepsis.
 
While a few years old, this seems to be the mainstay when talking norepi vs. dopamine with the septic patient, so I'll leave this here:

https://www.ncbi.nlm.nih.gov/m/pubmed/22036860/

And yes, many providers seem to be leaning more, and more on Epi as opposed to Dopamine as an option for septic shock patients in need of vasoactive medications.
 
Dopamine looses its effectiveness the lower the PH is. B-Hydroxyesterase ( i think) is an enzyme dopamine uses that is not apparent in a very acidotic enviroment.
 
Dopamine looses its effectiveness the lower the PH is. B-Hydroxyesterase ( i think) is an enzyme dopamine uses that is not apparent in a very acidotic enviroment.

Any pressor or inopressor is less effective the more acidotic the patient is. Dopamine is not a very predictable drug compared with epi in the best of conditions. Early on, the most potent mediator of fall in CO is loss of vasomotor tone, not contractility which is why NE (mostly alpha mild beta) is used and Epi or dopamine isn't. As things progress, if contractility becomes impaired, epi is added as opposed to dopamine because of it's greater dose/response predictability.
 
Any pressor or inopressor is less effective the more acidotic the patient is. Dopamine is not a very predictable drug compared with epi in the best of conditions. Early on, the most potent mediator of fall in CO is loss of vasomotor tone, not contractility which is why NE (mostly alpha mild beta) is used and Epi or dopamine isn't. As things progress, if contractility becomes impaired, epi is added as opposed to dopamine because of it's greater dose/response predictability.
@E tank I want to say this is what, and why our CCP instructor emphasized and was such a Levophed proponent. Basically its added benefits as it possesses both ino- and chronotropic properties.
 
The research I did in class brought me to the conclusion that I'd rather give epi than dope. Dopamine does not have great outcomes for sepsis.
That's what I am seeing too. Trying to learn more about epi, not sure how keen the docs are on letting us hang it.
 
That's what I am seeing too. Trying to learn more about epi, not sure how keen the docs are on letting us hang it.
Our guidelines are super vague about pressures (edit: ironically autocorrect changed that from "pressors"). "Refractory shock" is the indication for epi for both drip and 0.1mg push doses, refractory to what might I ask?
 
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@E tank I want to say this is what, and why our CCP instructor emphasized and was such a Levophed proponent. Basically its added benefits as it possesses both ino- and chronotropic properties.

The greatest advantage is the vasopressor property because that's what most of the problem is when you guys contact the patient. It's only a mild inotrope, but that isn't what is called for in vasoplegia 2/2 septic shock. A rise in heart rate comes at higher doses and isn't what it's used for. Raising the heart rate as a goal isn't an advantage.
 
Our guidelines are super vague about pressures. "Refractory shock" is the indication for epi for both drip and 0.1mg push doses, refractory to what might I ask?
That is kinda vague. It's non-existent here. Dopamine with cardiogenic shock, but that's it.
 
We have our choice of Epi or Dopamine in regards to cardiogenic shock in our protocol. I doubt if push came to shove on a truly septic patient that spun the right way a hospital wouldn't ok the Epi gtt in a severely symptomatic septic patient, but again, from my standpoint it seems like we're all in need of some more education, and in my case re-education regarding the pearls of EGDT.

I am seeing a lot of uncertainty, and "not sure" type answers. I'm not knocking anyone whatsoever, I'm just saying as paramedics without sounding too crude, we need to be educated to the point where we run these calls with the same sense of comfort, and confidence in treatment making as the ones that have been drilled into our heads.
 
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