Update:
Consider Joining the RLA if you want to commit to Resuscitation
Does SIRS Suck?
- Systemic Inflammatory Response Syndrome Criteria in Defining Severe Sepsis (DOI: 10.1056/NEJMoa1415236)
- The Falsely Reported Death of SIRS [cite source='doi']10.1056/NEJMoa1415236[/cite]
We are Complicit
- Please read my post, We are Complicit, to understand why this Table 2 from SSC will make life miserable for all ED docs:
Sepsis Collaborative Triage Screen
More Recent Evidence on the Benefit of Lactate for Prognosis
- doi:10.1136/emermed-2013-203541
- doi:10.1136/emermed-2014-204305
Peripheral Pressors
Additional Posts of Interest
Additional New Information
More on EMCrit
Podcast 89 – Lessons from the STOP Sepsis Collaborative(Opens in a new browser tab)
Frequently Asked Questions (FAQ) regarding Sepsis(Opens in a new browser tab)
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).
Latest posts by Scott Weingart, MD FCCM (see all)
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Scott, excellent summation of some hot topics. As you may know, I travel all over the USA. Worked in Pacific Northwest for years, worked in the medwest, and mostly work in North Carolina now. I have seen ‘sepsis’ treated all sorts of ways to be honest. Patients either get drowned or stay relatively dehydrated with pressors thrown on. Not sure if dehydrated is the right word. A few things remain constant though. Most providers think that their way is the right way or at least they feel that their method of treatment is ‘OK’ since we really do not have… Read more »
I have seen the complete opposite in fellowship. I do feel the AKI and anuric/oliguric in early sepsis is a normal part of ‘severe sepsis/septic shock’. Patients that get pounded with fluid, which generally is NS in ED or at OSH, end up on NaHCO gtt out of fear of a ‘low’ pH (don’t get me started on my thoughts on treating a ‘low’ pH) or get RRT from the NAGMA/AGMA or are 8L + and/or don’t respond to aggressive diuretics so get RRT for volume overload. In the patients that get 3-4L, I have seen far less RRT used.… Read more »
Great counter point Matt, I suspect at our core we likely think about sepsis the same. When I was a fellow we were still doing CVP’s and IV Fluid to meet certain CVP goals. We then added pressors and sorta followed the Rivers approach. I think that in the end we gave a bit much fluid. Over that last several years as the newer literature is coming out, I have opted to be a bit more conservative and hold back my initial urge to keep giving fluids. The point I was getting at, and maybe it did not come across… Read more »
Hi Scott and Craig. Interesting to hear your descriptions of being on the receiving end of IV fluids. It makes me think of Kathryn Maitland on the sepsis panel at SMACC, when she described the treating physicians impressions of the kids treated in the fluid group of the FEAST trial. They could see that the kids got better, they were mentating better, urinary output was increasing, and everything just looked right. But the fluid group did worse when they got down to looking at the important end-points. Just makes you think… Great podcast as always! Jens Michelsen, MD Dept. of… Read more »
Great post as always. I appreciate the humility of stating that we don’t understand the mechanism of action of IV fluid and even the role of edema. Too often I hear thundering pronouncements based on lovely physiological theories…but things always turn out to be far more complicated.
Hi Scott
Loved the SMACC Sepsis panel – the best fluid choice was beer I believe!
My thoughts on the pressor / fluid debate are here:
http://broomedocs.com/2015/05/podcast-pushing-pressors-in-the-periphery/
I think we can use fluids and pressers synergistically – after all your right ventricle don’t care if it is being filled by fresh crystalloids or squeezed plasma?
I have tried to write a protocol that can be used in the most remote hospital, the peripheral pressor papers have made this do-able, so thanks for sharing that knowledge
Cheers
Casey
Thanks for the great summary, Scott!
I believe different patients need different amount of fluids.
I wonder whether individual patient data meta-analysis could show us the outcome of different amounts of fluids according to the site of infection.
My hypothesis is that pneumonia patients may need less fluids than patients with either urinary or abdominal infections.
Would it be reasonable to perform a randomized trial comparing aggressive vs restrictive fluid management in the three major infection group of patients?
Cheers
Roberto
yes, I think it would be very reasonable; but very difficult
Very Very Nice Podcast. One thing which continues to remain in the presentations made by all of us is that “sepsis” is a unified entity. That unified entity concept is fundamental to the argument high fluid volume vs low. for sepsis. We call this the geocentric model of sepsis, where the central thing “sepsis” as defined by a set of criteria is at the center of the universe with treatment flowing to it. The central thing is the sepsis syndrome as defined by the original best guessed Bone criteria. One doubts that the great Rodger Bone realized he was creating… Read more »
Nail on the head…. I totally agree… For the longest time I have been aggravated by the apples to oranges association in the medical literature regarding sepsis. I think that if you spend more than a four week rotation in residency in the ICU, you soon realize that sepsis in patient A is not the same sepsis in patient B. However, if we say it is all different, then people cant do studies as they would have difficulty randomizing randomization in columns that they later try to drawn conclusions from. I completely think that we have tried to make it… Read more »
Yes In my garden are many spider webs. Each spider species makes a different web pattern. This web pattern is not taught to the spider, it is the extended phenotype of its DNA. The Web pattern is as much a derivative of the spiders DNA as the spider itself. So too does Group A strep generate its extended phenotype within its primary host (the human). These molecular patterns are as much a derivative of the Groups A strep DNA as the cell wall of the bacteria itself. Yet these patterns of molecules are not just the ones manufactured by organism… Read more »
Scott! Greetings
I wanted to clear some things up.
When you say 30ml/kg fluid that’s a bolus… Now what about maintenance? We’ve historically been taught that we have to replace ongoing losses like insensible losses, pts on a vent, urine output, surgical drains etc…
When you say no more fluids, do you mean we shouldn’t give the maintenance? Or do you say no more boluses?
Thanks!
2nd year resident
I think we need to be looking at these pt more globally, many of the antibiotics can and do cause acute renal failure, resulting in the pulmonary failure. While the preload is important we need to support the after load with nitro and put them on BiPAP sooner and stay away from lasix causing more issues with electrolytes. This will also provide better measure of the kidney function and coupled with vasopressor’s better control of blood pressure. While I have no papers or studies to back this only experience and yes clinical judgement managing these patients both in an ICU… Read more »
May I make a comment regarding the fluid bolusing near about 20-30ml/kg. In my practice I have found that there is a subset of patients with sepsis who have pulmonary hypertension. I suspect [with no proof] that there may have been a higher incidence of this cohort in the Rivers study, hence the higher mortality. This is a group I refer to as having Hypertensive hypotension. There is a lot of discussion about looking at the LV and lungs and then give fluids. Of course the LV and lungs may be fine, but in this cohort, you should still not… Read more »
patient tailored therapy…