Cite this post as:
Scott Weingart, MD FCCM. Practical Evidence Podcast 015 – Surviving Sepsis Campaign (SSC) Guidelines 2016 (in 2017). EMCrit Blog. Published on January 22, 2017. Accessed on September 19th 2024. Available at [https://emcrit.org/emcrit/ssc-guidelines-2016/ ].
Financial Disclosures:
The course director, Dr. Scott D. Weingart MD FCCM, reports no relevant financial relationships with ineligible companies. This episode’s speaker(s) report no relevant financial relationships with ineligible companies unless listed above.
CME Review
Original Release: January 22, 2017
Date of Most Recent Review: Jul 1, 2024
Termination Date: Jul 1, 2027
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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… Read more »
TYPO: false POSITIVES that SIRS brings along….
TYPO: false POSITIVES that SIRS brings along.
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… Read more »
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… Read more »
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… Read more »
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?
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… Read more »