Oh, steroids...

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engineeredout said:
CC Nerd-The Case of the Relative Insufficiency
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One thing this trial did and at least hasn't been presented in the other trials (at least that I don't remember, though maybe I'm forgetting) is they did an odds ration between exposure to hydrocortisone and APACHE. The lower APACHE had a relative (though not significant) reduction in mortality compared to the higher APACHE which had an odds of 1. Yet, people typically use steroids on the sickest as salvage therapy, which this trial more explicitly states won't make a bit of difference. However, if you are less sick, you may have an improved outcome... though if you are less sick, the reasons for giving it are less clear.

Anyway, reading the comments for the article... there's still plenty of "But steroids do work because of reason X" that will never go away. Hopefully though, people stop p-ssing away money at this hypothesis.
 
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It makes sense that steroids work in the early phases of sepsis, by limiting "overinflammation". There is a reason they are useful in COPD exacerbations, for example. That would also explain why Marik's HAT cocktail may work spectacularly (especially by decreasing ICU LOS) in some patients.

In the late phases, beyond a critical point, it's probably not the inflammation causing the most injury, but the microbes and the ongoing damage to the microcirculation, so I can see why the main use would be for relative adrenal insufficiency.
 
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My take on it was that :

1. Steroids don’t cause harm, in fact there is slight but non-significant benefit.
2. Pressor requirements go down when hydrocortisone is added (that’s a big one for me)

Means once levophed requirements go above 0.1 mcg/kg/min, the patient gets hit with hydrocortisone 100 mg q8hrs.
 
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I suspect (although clearly have no evidence) that there are likely subgroups of patients who will derive benefits from steroids, and subgroups that wont (or get harmed), based on a whole bunch of factors (Comorbidities, genetics etc), which unfortunately we are unable to identify yet. When you average them all together, no benefit.
 
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Nephro critical care said:
My take on it was that :

1. Steroids don’t cause harm, in fact there is slight but non-significant benefit.
2. Pressor requirements go down when hydrocortisone is added (that’s a big one for me)

Means once levophed requirements go above 0.1 mcg/kg/min, the patient gets hit with hydrocortisone 100 mg q8hrs.
Click to expand...

Why the high dose? Adrenal was 200 mg continuous and other studies do 50 q6 (which is what I do in fellowship). 100 q8 seems a bit high

Also something else to consider is they just excluded all patients given etomidate so take that into consideration for external validity in our patient population where I think a majority of ER and in hospital intubations use etomidate.
 
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FFP said:
It makes sense that steroids work in the early phases of sepsis, by limiting "overinflammation". There is a reason they are useful in COPD exacerbations, for example. That would also explain why Marik's HAT cocktail may work spectacularly (especially by decreasing ICU LOS) in some patients.

In the late phases, beyond a critical point, it's probably not the inflammation causing the most injury, but the microbes and the ongoing damage to the microcirculation, so I can see why the main use would be for relative adrenal insufficiency.
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So as an oversimplification: if you are going to get better, you’ll get better faster. If you are SOL, then you are SOL?
 
Fluffhead87 said:
So as an oversimplification: if you are going to get better, you’ll get better faster. If you are SOL, then you are SOL?
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I think there may be a degree of microcirculatory and/or tissue damage after which you're SOL with the current approach. I wonder if our next cocktails won't involve some new anticoagulants/antiinflammatories (a la APC), or some peripheral vasodilators (e.g. NTG, already used by some), to prevent that critical point. The HAT protocol is a step in the former direction.

I remember reading about a study that was trying to show that cortisol levels on presentation to the ED correlate with outcomes. Interestingly, the way I remember, high cortisol levels on admission had much higher mortality. So, in a way, if you're SOL on admission, you're SOL.
 
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FFP said:
I think there may be a degree of microcirculatory and/or tissue damage after which you're SOL with the current approach. I wonder if our next cocktails won't involve some new anticoagulants/antiinflammatories (a la APC), or some peripheral vasodilators (e.g. NTG, already used by some), to prevent that critical point. The HAT protocol is a step in the former direction.

I remember reading about a study that was trying to show that cortisol levels on presentation to the ED correlate with outcomes. Interestingly, the way I remember, high cortisol levels on admission had much higher mortality. So, in a way, if you're SOL on admission, you're SOL.
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That is correct. The only correlation cortisol levels have ever shown is high cortisol level (>30) was associated with higher mortality.
 
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http://www.nejm.org/doi/full/10.1056/NEJMoa1705716?query=featured_home

How come nobody is talking about this article?

In this trial involving patients with septic shock, 90-day all-cause mortality was lower among those who received hydrocortisone plus fludrocortisone than among those who received placebo.
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Same dose of hydrocortisone we give now, plus 50ng fludrocortisone QD leading to improved mortality, ICU free days, vasopressor free days, and a host of other secondary endpoints. Why wouldn't we do this?
 
engineeredout said:
http://www.nejm.org/doi/full/10.1056/NEJMoa1705716?query=featured_home

How come nobody is talking about this article?



Same dose of hydrocortisone we give now, plus 50ng fludrocortisone QD leading to improved mortality, ICU free days, vasopressor free days, and a host of other secondary endpoints. Why wouldn't we do this?
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Annane is going to keep beating that drum.

He did this study, oh a decade and a half ago.
Effect of treatment with low doses of hydrocortisone and fludrocortisone on mortality in patients with septic shock. - PubMed - NCBI
Then the CORTICUS trial found no benefit. Now we are back to benefit again. The circle is complete.

I couldn’t see how many centers participated in the methods but I want to see multinational, multicenter data that isn’t France.

At least in combination, the studies show that steroids seem relatively harmless and get you off vasoactive medications a day early.
 
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In all fairness, corticus should be barred from all civilized discussions as it’s a crap study run by bad doctors who seemed to go out of their way to assassinate their pts
 
kimbosliced said:
Why the high dose? Adrenal was 200 mg continuous and other studies do 50 q6 (which is what I do in fellowship). 100 q8 seems a bit high

Also something else to consider is they just excluded all patients given etomidate so take that into consideration for external validity in our patient population where I think a majority of ER and in hospital intubations use etomidate.
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I agree with the etomidate bit, every single patient seems to get intubated with etomidate at my shop, I wonder how they even managed to get their numbers when etomidate patients were exlcuded.
 
wickedskillz said:
I agree with the etomidate bit, every single patient seems to get intubated with etomidate at my shop, I wonder how they even managed to get their numbers when etomidate patients were exlcuded.
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Because Australia, where most of the centres were, doesn't have etomidate.
 
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