We've discussed SEPSIS a ton on EMCrit.
- Podcast 154 – Preemptive Sepsis Panel SmaccBack
- Wee – Cliff Deutschman with Additional Thoughts on Sepsis 3.0
- Renoresuscitation: Sepsis resuscitation designed to avoid long-term complications
- Podcast 112 – A Response to the Marik Sepsis Fluids Lecture
- Podcast 169 – Sepsis 3.0 with Merv Singer
- Podcast 89 – Lessons from the STOP Sepsis Collaborative
Recently, the Surviving Sepsis Campaign released their 2016 guideline update. Overall, I think this iteration moves the guidelines closer to the best evidence out there. Of course, when you travel that path it forces a divergence from the distinctly non-evidence-based CMS guidelines. In this Practical Evidence Podcast, we will discuss the SSC guidelines, the aforementioned divergence, and various alcohol recommendations. I brought on my buddy, Jeremy Faust, to discuss the changes. Jeremy is 1/2 of the FOAMcast podcast which just discussed the new guidelines in a recent episode.
Guideline Stuff
- The SSC 2016 Guidelines
- PDF Version of the SSC 2016
- Users' Guide to the Guidelines
- Our Emergency Medicine Clinics Article
The Guideline Recommendations
The Definition of Sepsis
They basically ratified SEPSIS 3.0
(Jeremy found where he saw the remnants of the old definition; it was in the Users' guide figure 2–super contradictory)
Fluids
30 ml/kg in the first 3 hours
Crystalloid first, then maybe albumin
Use dynamic markers and/or fluid challenges
Goal MAP>65
EGDT is no longer recommended
Lactate
attempt to normalize lactate
Blood Cultures
get them before antibiotics, if obtaining them will not delay the provision of antibiotics
Antibiotics
Within 1 hour of sepsis or septic shock
Vasopressors
Norepi is the first choice, add in epi or vaso
Do not use dopamine
Steroids
200 mg Hydrocortisone for patients who are still unstable after fluids and vasopressors
Blood
In most circumstances, use a trigger of <7.0 g/dL
Glucose
goal is < 180 mg/dL
Bicarb
Not recommended if pH is >7.15 (which in no way means it is recommended for pHs less than that)
What are we Drinking?
- EMCrit is drinking South Hill Cider‘s Packbasket Still and Dry Cider (as in not sparkling)
- Jeremy is drinking a homemade Margarita made wretched by the addition of sweet and sour mix
Update
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Scott Weingart
Latest posts by Scott Weingart (see all)
- EMCrit Podcast 241 – Sepsis Update 2019 - February 21, 2019
- EMCrit Podcast 240 – Renal Compartment Syndrome & It's all about the Venous Side and We've Been Fracking it up for Years - February 10, 2019
- EMCrit 239 – Vent Alarms = Code Blue - January 26, 2019
Alex (MD, Critical Care Unit – Hamburg)
I still wonder myself what does “unstable after the use of fluids and vasopressors” mean => the degree of freedom is quite big. i am planning to read those studies carefully and see at what NA dose they started the use of hydrocortisone.
degree of freedom should be big, it is a clinical judgment
I was asking because it occured to me… we have a Sepsis SOP where we are supposed to start Hydrocortisone when the NA dosage has reached really high values (more than 60µ/min). The studies citied in the SSC randomised patients who “were on vasopressors”, so what I understand is that they could have received Hydrocortisone both at small doses of NA and at higher doses, no difference. Only in HYPRESS there are some statements about inclusion criteria related on NA dosage, but basically all P who got NA and were septic received Hydrocortison…
It would be interesting to know if there are subgroups where Hydrocortison would have made some difference (small dosage NA vs high dosage NA).
SOPs can sometimes limit one’s clinical judgment ! What is your opinion, when do you start Hydrocortisone? Do you have some time limit, like, the patient has more than 12 h of NA therapy, then he needs Hydrocortisone…
Thanks for your answer.
Alex
What is the recommendation for using LR instead of NS in sepsis if trending the lactate is important? Does LR affect the measured lactate level?
for all intents and purposes, no it should not affect trending lactate
Since LR is most likely a better option, shouldn’t LR be the fluid of choice in sepsis? What do you prefer?
Ok. Can’t resist. Isn’t SIRS merely a measure of “dysregulated host response”? Thus SIRS + infection = infection with dysregulated host response = SEPSIS?
Great review by the way!
Mike
By the way. If you ever make it out west. I can introduce you to some amazing artisanal ciders!!!
Hey Mike, I’ll answer the SIRS question by saying that all of the evidence we have is that SIRS is *such* a wide net that it seems to capture both normal responses to infection (i.e. a perfectly healthy and appropriate one that shows that the body is doing what it supposed to do–fight infection) as well as dysregulated ones (i.e. maladaptive host response in which the body’s pro and anti inflammatory pathways are on overdrive and wreak havoc.) That is why SIRS is so sensitive but so TERRIBLY not specific. One way of looking at this is to look at Figure 1 of Jean-Louis Vincent’s article on SIRS and qSOFA. https://ccforum.biomedcentral.com/articles/10.1186/s13054-016-1389-z Caveat: while Dr. Vincent probably knows more about sepsis than I ever will, he’s missed the fine points of the data on how qSOFA performs..so you can ignore lot of what he says, actually. In fact, qSOFA outperformed even SOFA and SIRS in the ED setting in the original derivation paper. But it is the FIGURE in his article is what is important in terms of framework, which is what you should notice. In short, not all SIRS is sepsis nor is qSOFA. On the other hand, the recent… Read more »
TYPO: false POSITIVES that SIRS brings along….
TYPO: false POSITIVES that SIRS brings along.
To start (at least in an ALS-based EMS system, or one with ALS-intercept availability), EMS should not be transporting cardiac arrest patients to the hospital (unless there are extenuating circumstances: refractory VT/VF, pregnancy >20 weeks, hypothermia, etc.). I agree with your thoughts and highly promote the idea of dual-sequential defibrillation, along with the ideas behind mechanical CPR. From an EMS standpoint (as a Paramedic), many agencies simply can’t afford mechanical devices…so we’re stuck with old-school practices. Meds and defibrillation, however, our trends are changing to promote cardiac arrest as a “stay and play” type of event, rather than “load and go.”
I think you will see the trends swinging back the other way. What I can do in the hospital for these patients is dramatic. I think you will see in non-MD systems a move towards early transport for all but unsurvivable cases.
Andrés von Wernitz (MD Emergency Department, Madrid, Spain)
Maybe I’m not catching the correct sense of the new guidelines (or the 2012 ones) but here is my question: is there a change in the definition of sepsis-induced hypoperfusion ?
SSC2012 “sepsis- induced tissue hypoperfusion (defined in this document as hypotension persisting after initial fluid challenge or blood lactate concentration ? 4 mmol/L).”
SSC2016 “Sepsis-induced hypoperfusion may be manifested by acute organ dysfunction and/or +/- decreased blood pressure and increased serum lactate.”
Does it means that in 2012 to state that someone had sepsis-induced hypoperfusion it was necessary to first preload with the mysterious amount of 30cc/kg fluid and then confirm hypotension or lactate concentration ? 4 mmol/L and now on it is sufficient that someone presents with suspected infection and delta SOFA > 2 to defining sepsis-induced hypoperfusion (without no initial fluid infusion and not presenting hypotension and lactate > 2, i.e. Bilirubin of 3 mg/dL)?
Thanks for your answer.
As a paramedic the only pressor i have available is dopamine. Is it still worth giving if it is the only option?
With no lactate in the field we look at EtCO2.
EtCO2 less than 25 in suspected sepsis pt =high likelihood of elevated lactate. And it is an instantaneous measure.
How come EtCO2 isn’t more widely used in the ED?
[…] Infektion/sepsis: mer tjat om sepsis, här kortare podcast om nyaste guidelines […]
I believe the guidelines say lactate greater than 2 is septic shock! That doesn’t make sense
What the fuck do I do with cirrhosis (albumin 2.3), elevated lactate without shock, large transudative pleural effusion, anisocoria. Had good response with initial crystalloid of 1000ml (15ml/kg) then gave albumin followed by D5 1/2 (due to persistent hypoglycemia) at 250ml/hr. I know it says only consider albumin for fluids needed after initial 30ml/kg… but the studies I’ve seen comparing initial fluid types indicate there’s only no benefit (but no harm), using albumin sooner. And these same studies don’t seem to provide subanalyis for cirrhotic or liver failure patients.
BTW… heard of your podcast but recently started listening. Change my life. I have completely given up store bought drink mixers.
What’s your approach for intravascular volume depleted, significantly third spaced, septic patients with impaired organ perfusion requiring fluids?