Last week I posted a lecture an incredible by Paul Marik on Fluid Management in severe sepsis. The lecture is the equivalent of a bucket of ice water poured over your head. Now let's give you a towel and discuss.
Want to add a journal club to this flipped classroom?
Then read these pieces in Critical Care:
- Bellomo on Norepinephrine and the Kidney
- Rethinking Resus Goals by Dunser
- Response: Rethinking Resus Goals by Marik and Bellomo
- Pharmacodynamic Analysis of a Fluid Challenge (Crit Care Med 2016;44:880)
The Low-Fluid Volume Early Pressor Experiment has Already Been Tried
It was called standard care 15-20 years ago–patients did not do all that well.
Should we Increase DO2?
We know from that shooting for supranormal DO2 is actually harmful. The original goal-directed therapy trials did not pan out and this may be why.
There is definitely a group of Severe Sepsis patients that are receiving inadequate oxygen delivery. I have treated these patients; I have documented ScvO2s in the 50's and 60's on initial check in a EGDT-type algorithm.
Far more commonly, patients are in pure vasodilatory shock (Jones' trial patients). The latter fact doesn't disprove the former. Using the studies demonstrating the deleterious effects of shooting for above normal delivery doesn't say anything about normalizing patients with low delivery.
- Achieve adequate perfusion pressure
- Improve microcirculatory flow
- Limit Tissue Edema
All right on point; how do we get there is the question.
Rivers Trial as a Waterfall?
This is not actually what that trial showed. And the way CVP was used was not actually debunked by the 7 mares article (Note: I'm not advocating you use CVP, I'm just pointing this out! We have better ways to accomplish assessing fluid responsiveness so CVP should be sent to the junk bin)
I will make the utterly blasphemous statement that Dr. Rivers and Dr. Marik are actually in near-complete agreement if you followed both of their protocols explicitly in the ED.
MAP and Association to Survival
Not sure what this is proving: both groups (the flow-optimizers and the desert-inducers) believe in shooting for MAP goals. Patients in whom it is impossible to get the MAP up will die more frequently.
But is it Flow or Pressure that Matters?
I must say, I am still in the tissue flow camp
On to the Glycocalyx
Now this is where stuff gets really interesting. Every day, there is increasing research and more publications on the fundamental role of the vascular glycocalyx. But how do we integrate this clinically?
Now as to its relation to fluids in sepsis, we are being told hypervolemia is bad. But if the fluids are leaking from the vascular space are we ever seeing hypervolemia in the vasculature or is the problem whole body volume overload–not if we believe BNP/ANP are the root of the problem, they only respond to vasculature fluids. If we are doing a fluid responsiveness strategy, we should not be seeing the vascular overload.
Do balanced vs. unbalanced fluids have a different effect on the glycocalyx in Sepsis? I have no answers to any of these questions.
ANP/BNP damage the Glycocalyx
But are we causing Myocardial Wall Stress to generate these peptides. Well here is where things get interesting. If you really start thinking this through, CVP EGDT style would make more sense–its use solely to measure RA/RV overdistension rather than fluid responsiveness. Not advocating this in any way, just something to think about.
And is a majority of the BNP coming from fluid resuscitation or from sepsis-induced cardiomyopathy? Is the latter why higher BNP levels are associated with worse outcomes?
Do Crystalloids Stick Around?
I'm not sure, but the Bark Study quoted was a study in septic rats. [cite]23318490[/cite]. This study, if it has any practice-changing value, would be to make one consider albumin. Clinically this lacks all face validity. Start doing IVC exams on your patients, fill until there is no resp collapse. Come back in a few hours, they will have stayed fuller than when you started by a significant amount. Some of this fluid is sticking around.
Let's Talk about Marshmallow People and the Inflammatory State
I'm not sure anything we do makes a damn bit of difference when it comes to patients holding on to water if you are using a reasoned fluid responsiveness strategy, but I am open to new data telling me I am wrong.
Excess Fluid Increases Mortality
This is when the lecture really diverges from clean cause/effect progression. Associations are being taken for causation, so let's spend a bit of time on these:
I'm going to ignore the experimental trials and move to the clinical.
- Fluid Balance doesn't equal fluid administration
- Fluid balance associations certainly do not equate to fluid administration causation (SOAP, etc.)
- CVP associations with fluid administration–Is Dr. Marik, the ultimate CVP debunker, actually equating these two?
Optimal survival occured with a 3-liter positive fluid balance at the 12 hour mark?
Dr. Marik's statements on this one need to be looked at carefully. The FEAST trial was an amazing accomplishment with results contradictory to what we all expected. Giving severely ill kiddies fluid increased mortality. But what doesn't get discussed at all is this little article:
subgroup analysis (BMC Medicine 2013, 11:68 ) of why pts actually died revealed CV collapse as opposed to the expected volume overload.
Norepi to tense the Tank
- Critical Care 2007, 11(Suppl 2):P37
- Crit Care Med 2011;39(4):689-94
- Critical Care 2010, 14:R142
- Crit Care Med. 2012;40(12):3146-3153
- Crit Care Med. 2013 Jan;41(1):143-50
Then go read this editorial to get some perspective on the issues involved. [cite source='pubmed']23269148[/cite]
Would indicate that fluid accumulation in the lungs occurs only on the flat portion of the Starling Curve
Should we be using Fluid Responsiveness on all Severe Sepsis Patients?
I think we should. I think we should stop blind fluid loading; it will take a while for us to get there in many EDs.
My modification of Marik's Algorithm:
Where are the Endpoints and Is Lactate Clearance is Flawed?
I have already addressed this in a wee when Marik's article was published. See that link if you want all the nitty-gritty details, but here is the essence. Anyone who has talked about lactate clearance for the past decade has already known and perpetrated that the lactate elevation in severe sepsis is not solely from tissue hypoperfusion. We know this. This fact in no way changes that elevated lactates mirror the inflammatory response, and strategies that cause it to clear (probably to near-normal, rather than just 10%) are associated with improvement and decreased mortality.
What about Microcirculatory Endpoints?
Anyone have any good ones? I want one, I want one…
Sepsis Mortality goes Down if you Care!
Paul actually sent me this study. [cite source='pubmed']24201173[/cite] Control arm mortality has dropped consistently since 1991. If you care and do a modicum of resuscitation, I think you are seeing a vast majority of the benefit. Our Sepsis Collab data has shown the same thing.
Read the Comments of the Marik Post
Some amazing stuff buried in the comment section including an inotropy first pathway and the USCOM Device
to Chris Nickson, Cliff Reid, and Minh Le Cong for pre-publication peer review and many helpful comments
Now on to the Podcast…
- EMCrit 309 – Critically Ill Diabetic Ketoacidosis (DKA) - October 21, 2021
- EMCrit 308 – Risk Stratification and Treatment of Pulmonary Embolism (PE) 2021 – Is the PERT Wilted? - October 7, 2021
- EMCrit 307 – TTM2 Episode Retort with Ben Abella & Joe Tonna - September 23, 2021