A bunch of fun new ideas re: sepsis for 2019
Fluids
30 ml/kg may be based on IBW if you write in the chart that that was what you were using
Andromeda-Shock Trial
A fascinating study by Hernandez et al.1
Censer Trial
Early fixed-dose norepi use was examined in this trial.2
Procalcitonin
HiTemp Study3
Procalcitonin was poor for differentiating bacterial infections and other causes of fever in the ED.
Now on to the Podcast…
1.
Hernández G, Ospina-Tascón G, Damiani L, et al. Effect of a Resuscitation Strategy Targeting Peripheral Perfusion Status vs Serum Lactate Levels on 28-Day Mortality Among Patients With Septic Shock: The ANDROMEDA-SHOCK Randomized Clinical Trial. JAMA. 2019;321(7):654-664. [PubMed]
2.
Permpikul C, Tongyoo S, Viarasilpa T, Trainarongsakul T, Chakorn T, Udompanturak S. Early Use of Norepinephrine in Septic Shock Resuscitation (CENSER) : A Randomized Trial. Am J Respir Crit Care Med. February 2019. [PubMed]
3.
van der, Limper M, Jie K, et al. Procalcitonin-guided antibiotic therapy in patients with fever in a general emergency department population: a multicentre non-inferiority randomized clinical trial (HiTEMP study). Clin Microbiol Infect. 2018;24(12):1282-1289. [PubMed]
Additional New Information
More on EMCrit
- Septic Shock(Opens in a new browser tab)
- EMCrit 345 – I Guess We Need to Talk about CLOVERS and Fluids in Sepsis (Hopefully for the Last Time Ever)
- EMCrit 318 – SSC Guidelines 2021 – The Good, The Bad, & The Ugly and What You Need to Know in Sepsis Resuscitation
Additional Resources
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Editor-in-Chief, at EMCrit.org
An ED Intensivist from NY.
Professor
Nassau University Medical Center
No conflicts of interest (coi).
Professor
Nassau University Medical Center
No conflicts of interest (coi).
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If patient only on fluid load I can apply this study in practice. Most of septic shock patients are on vasopressors from the start. You will not wait 30-60-90-120 min to reach MAP 65 or CRT <3 s just with fluid challenges if patient is 70 over 40. Let's imagine your patient still fluid responsive but on norepi 0.4 mcg/kg/min and CRT became 2 sec. According to research, should I stop fluid load?
all of the patients in andromeda-shock were already on norepi
So, I leave patient on high dose norepi because of good CRT. And do not try to reach lower norepi dependance?
So, I leave patient on high dose norepi because of good CRT. And do not try to reach lower norepi?
I agree clinicians seldom follow guidelines and change decisions to prescribe antibiotics based on a low or normal procalcitonin. However, I’ve treated a handful of patients with sky high procalcitonins that otherwise look really well. They often come back with positive blood cultures. It may not be cost effective at this stage but much like a high lactate a high procalcitonin has some correlation with severity of disease thus making it a useful additional test in decisions regarding admission/disposition/investigations and choice/route of antibiotic treatment.
Whether or not its cost effective is another matter.
i buy all of that, but that is not the question. To use a test like this for this purpose, there needs to be interval LR that would actually quantify what the test is doing to pretest prob. quantitatively.
Great podcast! One question, I think you mentioned that both the vasopressor and inodilator test had good success rates, I am unable to find any numbers for the latter however in either the main manuscript or supplement.
the vasopressor number is definitely in there, in the actual text if I am remembering correctly. Not sure if inodilator #s are there, but I assume they are.
You are misrepresenting the HiTemp Study results. They calculate the sensitivity and specifity of PCT as a marker of infection, you mentioned in your podcast septic and bacteriemic patients.
Of course in a general ED population which will present with fever because of cellulitis or sinusitis, determining the PCT adds nothing to the diagnosis.
But to dismiss it like that… How many septic patients, especially with GNBs, did you encounter with a PCT lower than 2? Or how many febrile patients with a PCT higher than 2 or 10 did you see that ended up having a non-infectious etiology?
not sure what you are talking about. i represented the study precisely. Your secondary argument seems specious. This is the same argument made for BNP. The burden of proof is the PCT users to show this is an effective screen and pointing out obvious cases is not the way to this.
For the ANDROMEDA trial, while there was not a statistically significant difference in all cause mortality, there was an absolute difference at 28 days between the 2 groups; with the lactate guided therapy group having higher mortality.
It just seems a shame to me because at first glance the conclusion in the article sites “no statistical significance in mortality” but the 18 less dead patients in the peripheral perfusion group certainly passes my eye-test for clinical significance. Just wondering further thoughts or am I totally misguided.
Keep up the great work EMCRIT team!!!!
Hi Scott, You mention that CMS now allows clinicians to base the 30 cc fluid bolus on ideal rather than actual body weight for the core measures. I have also heard this mentioned by other commentators in the FOAM world. I am having a hard time finding this published anywhere, however. My hospital system still requires the 30 cc fluid bolus regardless of body weight (with virtually no exceptions). I discussed this with my administrators and they say they are not aware of the revision to this requirement. Additionally, I am located in NYS, and the other concern was whether… Read more »
Hi Dylan.
https://www.jointcommission.org/assets/1/6/HIQR_Release_Notes_5_5.pdf
Here are the release notes TJC when the ideal body weight was added as a second option. Not sure about the NYS DOH, but hopefully this helps.
I just want to clarify that you can only use Ideal Body Weight if the patient is obese, which is defined as a BMI > 30.
/Users/jeanniejacobs/Desktop/IBW.pdf
Scott, Haven’t harassed you in a while, but ANDROMEDA-SHOCK seems to demonstrate our fundamental lack of understanding of many of the drugs we use. An agent that functions as a vasopressor, yet seems to result in better perfusion? Could it be that we really don’t understand the location of action of Norepi? Low dose = venoconstriction, higher dose=arterial constriction? But where, large, medium, small vessels? Is it dose dependent? How does it interact with Cardiac output at different dosing? I think all of these questions simply demonstrate that things aren’t always as they seem. My 2 cents, and remember, it… Read more »
hey buddy,
i’ll be the first to state emphatically that we have no idea how most of these drugs work, at least in their entirety. I can however give you a few physiological explanations that don’t require new understandings, but of course these are all post hoc rationalizations.
I have a question. I am an ER nurse with nine years ICU experience. I have noticed a trend of critically low phosphorus levels in severely septic patients; I have even used it as a prognosis indicator (scientific, IDK). My question is, why is a phosphorus level affected is sepsis?