Sepsis: Lactate clearance vs scvo2

This forum made possible through the generous support of SDN members, donors, and sponsors. Thank you.

iridesingltrack

Full Member
10+ Year Member
5+ Year Member
15+ Year Member
Joined
Dec 28, 2007
Messages
139
Reaction score
3
Ahhh sepsis, blocking and tackling for EM.

I came accross this article recently and was wondering if some of you had already essentially been doing this or if this was going to change your practice in any way. Here is the link to the PDF: http://jama.ama-assn.org/cgi/reprint/303/8/739.

Essentially, Jones et al. via a well designed non-blinded RCT show non-inferiority of lactate clearance (defined as a change in lactate of 10% at 2 hrs) as compared to continuous scvo2 monitoring. I know, for a variety of reasons, people don't love continuous scvo2. So, I think it will be interesting to see how these data effect practice patterns. Is lactate clearance going to be one of the new sepsis resus targets and we'll see the Edwards catheter go the way of the dinosaur?

Members don't see this ad.
 
Ahhh sepsis, blocking and tackling for EM.

I came accross this article recently and was wondering if some of you had already essentially been doing this or if this was going to change your practice in any way. Here is the link to the PDF: http://jama.ama-assn.org/cgi/reprint/303/8/739.

Essentially, Jones et al. via a well designed non-blinded RCT show non-inferiority of lactate clearance (defined as a change in lactate of 10% at 2 hrs) as compared to continuous scvo2 monitoring. I know, for a variety of reasons, people don't love continuous scvo2. So, I think it will be interesting to see how these data effect practice patterns. Is lactate clearance going to be one of the new sepsis resus targets and we'll see the Edwards catheter go the way of the dinosaur?

i hope not. i love those edwards catheters a ton. i've also used them for people in cardiogenic shock (instead of sepsis) and paired em with the FloTrac addition to get indexes and cardiac outputs to augment my pressor choices.
 
The question I had on that article is: how do you titrate dobutamine based on the 2 hr lactate? It may have equal prognostic significance, but in terms guiding therapeutics I don't see it as being as helpful.
 
Members don't see this ad :)
Ahhh sepsis, blocking and tackling for EM.

I came accross this article recently and was wondering if some of you had already essentially been doing this or if this was going to change your practice in any way. Here is the link to the PDF: http://jama.ama-assn.org/cgi/reprint/303/8/739.

Essentially, Jones et al. via a well designed non-blinded RCT show non-inferiority of lactate clearance (defined as a change in lactate of 10% at 2 hrs) as compared to continuous scvo2 monitoring. I know, for a variety of reasons, people don't love continuous scvo2. So, I think it will be interesting to see how these data effect practice patterns. Is lactate clearance going to be one of the new sepsis resus targets and we'll see the Edwards catheter go the way of the dinosaur?

First a couple of disclaimers: (1) I am just a resident and (2) I don't have time to read the article (yet) and am just going off the OP's summary.

1. not so sure continuous ScvO2 is all that better that intermittent ScvO2; and why not if you are going to be getting intermittent lactates (?use of Edwards catheter)

2. if only following lactate "clearance", one must be aware of the frequently seen phenomenon of increasing lactates after initiation of proper therapy in the severely hypovolemic, truly septic patient. as starved tissues begin to receive improved circulation, "built-up" lactate can then be released. this can show an increased lactate initially that is not indicative of mismanagement.

3. i know of plenty of folks who already are using intermittent ScvO2 and lactates as guides; no Edwards at our shop except for patients enrolled in #4 (see next)

4. the ProCESS data (initial paper and then the onslaught of papers looking at subsets of the data that will follow) should provide answers to this and so many other related questions...we'll see

HH
 
The question I had on that article is: how do you titrate dobutamine based on the 2 hr lactate? It may have equal prognostic significance, but in terms guiding therapeutics I don't see it as being as helpful.

This is a great point. The protocol Jones et al. used for titration is not discussed in the paper. They report that at the two hour mark, if lactate was not down 10% and if Hgb was >30% then they started dobutamine. They titrated on q1hr lactate. Currently, with scvo2 continious monitoring we are making titration changes with immediate feedback. With that said, based on their data the delay in titration of dobutamine didn't seem to play a significant role in overall outcome. I guess this is somewhat analogous to taking samples for mixed venous o2 as opposed to continuous monitoring, as Hamhock described is his practice.

Presently, do most of you use continuous scvo2 or do you do intermittant spot checks? I have tended to put edwards catheters in my septic shock pts but have followed lactate and spot checks in my severe sepsis.

iride
 
i hope not. i love those edwards catheters a ton. i've also used them for people in cardiogenic shock (instead of sepsis) and paired em with the FloTrac addition to get indexes and cardiac outputs to augment my pressor choices.

I'm not sold on the reliability of the FloTrac in cardiogenic shock. We have it available for use in our ICU, and it is frequently used for sepsis patients with high cardiac output states and seems somewhat reliable. I have found it very unreliable in patients with sepsis who develop septic myocardial depression and in patients with cardiogenic shock when directly compared with Swan Ganz derived data in the patient while monitoring with the FloTrac. Several of these patients had the Swan Ganz catheter placed because the data provided by the FloTrac seemed inconsistent with exam findings (cold mottled feet etc.) Additionally, when the Precep catheter tip is in the superior vena cava a few patients had a large discrepancy between the ScVO2 and the "real" SvO2. In many cases data provided by the Swan Ganz catheter altered the course of treatment for the patient. Because of the lack of agreement, we have chosen to restrict the use of the FloTrac to patients with high cardiac output states. My 0.02.
 
These discussions amuse me.
Remember, the numbers for Swan-Ganz vs regular show non-inferiority for no PA catheter. You can guide therapies without having a box with numbers flashing for you.
 
These discussions amuse me.
Remember, the numbers for Swan-Ganz vs regular show non-inferiority for no PA catheter. You can guide therapies without having a box with numbers flashing for you.

Agreed. Not to mention the fact that the patient should be long gone to the ICU under the care of an intensivist before nursing even hooks up the SCV02 monitoring.

If you're titrating pressors based on serial lactates or SCVO2 while the patient is still in the ED, then there is something seriously wrong with patient flow in your hospital.
 
These discussions amuse me.
Remember, the numbers for Swan-Ganz vs regular show non-inferiority for no PA catheter. You can guide therapies without having a box with numbers flashing for you.


I think that there are numerous people that agree with you. In regard to FloTrac, I've had minimal exposure, ICU only. But, we routinely place the edwards catheters at our shop. What do you use to guide your sepsis therapy in the absence of continuous scvo2 monitoring?

GV, your comment definitely plays to what I thought was one of the oddities of the Jones paper. They kept the patient in the ED for 6hrs. Holy crap that is a long time. I agree the septic shock patient should be under the care of an intensivist in no time. They are an easy dispo.

But, the severe sepsis patient is often a different story: the otherwise healthy 45 y/o M, febrile with tachycardia and normal pressures with CAP and a lactate of 5. I've found that they can be tuned up and managed in step down vs. floor. So, I may keep them for a while...but, not 6 hrs if I can at all help it. FWIW, this is also the patient that I don't like doing continuous scvo2 on...seems too invasive given the apperant severity of illness. In this patient I like the idea of using serial lactates.
 
Agreed. Not to mention the fact that the patient should be long gone to the ICU under the care of an intensivist before nursing even hooks up the SCV02 monitoring.

If you're titrating pressors based on serial lactates or SCVO2 while the patient is still in the ED, then there is something seriously wrong with patient flow in your hospital.

It's not uncommon for many hospitals to be holding admitted ICU patients for prolonged periods of time. I think there's enough data that holding ICU patients is as dangerous as crossing the streams, but that doesn't seem to convince the hospital to spring for increased surge capacity for the units.

So while it is suboptimal, I don't think you can argue that it falls outside of EM anymore.
 
What do you use to guide your sepsis therapy in the absence of continuous scvo2 monitoring?

Since the patients in the ProCESS trial are few and far between, and those are the only patients we use those on, we use the old tried and true "vital signs" data. You know, how is their pressure doing. What is the pulse? Do they have evidence of perfusion? Urine output? Etc.
As before, there is plenty of evidence that "guiding" your therapy on the numbers vs guiding it on other factors has little to no difference in outcomes.

As for now, serial lactates will work just fine. If they're downstairs long enough for a second one.
 
EGDT works because it means neglecting the rest of the department for a survival benefit to your sickest patient; no different than bringing everything to a halt for STEMI or rTPA. ICU patients boarding in the ED do poorly because we've got the rest of Ellis Island competing for time with your "stable" critically-ill patient. This is another zero-sum resource allocation issue, particularly when you consider the added cost of continuous CVO2 monitoring and the Edwards catheter.
 
It's not uncommon for many hospitals to be holding admitted ICU patients for prolonged periods of time. I think there's enough data that holding ICU patients is as dangerous as crossing the streams, but that doesn't seem to convince the hospital to spring for increased surge capacity for the units.

So while it is suboptimal, I don't think you can argue that it falls outside of EM anymore.

It shouldn't matter whether or not the patient is physically in the ED. Once they are admitted and the admitting physician (or intensivist) has accepted that patient it is theirs. At that point I stop managing the patient and move on to seeing the new patients who have been stacking up while the ED staff have been taking care of the septic patient. That's why I think it's odd that any of us would be managing drips, pressors on patients who are already admitted.
 
As before, there is plenty of evidence that "guiding" your therapy on the numbers vs guiding it on other factors has little to no difference in outcomes.

As for now, serial lactates will work just fine. If they're downstairs long enough for a second one.

In general, I agree with you; however, as it specifically relates to sepsis and scvo2 monitoring, I don't think we are there yet. This very question is one of the primary goals of the ProCESS trial, as I understand it. I think the Jones et al. paper is interesting because it addresses the issue of eliminating the need for the scvo2 monitoring and that mortality and morbidity are unchanged as long as we are pretty stringent about responding to lactate levels. Vital signs in and of themselves don't help us with determining microvascular tissue hypoperfusion. That is why Rivers used the scvo2 and Jones suggested the lactate clearance. UOP and other signs are lagging features. Unfortunately, I don't think we know yet, from an EBM perspective (for what that is worth), if we can safely divorce scvo2 from EGDT.

EGDT works because it means neglecting the rest of the department for a survival benefit to your sickest patient; no different than bringing everything to a halt for STEMI or rTPA. ICU patients boarding in the ED do poorly because we've got the rest of Ellis Island competing for time with your "stable" critically-ill patient. This is another zero-sum resource allocation issue, particularly when you consider the added cost of continuous CVO2 monitoring and the Edwards catheter.

Great comment...also consider the traumatic arrest, or the coding patient in terms of the resulting neglect to the rest of the dept. At least in the STEMI, TPA, or sepsis patient we are potentially saving lives. The onslaught never stops.
 
Top