After a long and exhausting discussion with an inferior human being, a cardiologist, which happens to be an old friend, I decided to write some thoughts about lactate.
So, I’ll do like I do in my lectures, which is state my final position at the beginning. Lactate is more desirable as a severity marker than a target to be pursued. That’s it. THE END. The problem in characterizing lactate as ‘the” marker of hypoperfusion are the excessive treatments that come along, like drowning patients in fluids while attempting to clear it. Since there are lot of reasons why lactate could be high, each case should be evaluated separately. In the end, a thorough physical examination still is, in my opinion, the best way to guide a resuscitation.
I’ve seen a patient being admitted to the ICU with a “so called” septic shock due to pneumonia with a slightly low blood pressure and high lactate. After reviewing the case, the high lactate was due to a beta-adrenergic taken for asthma, and there were no pneumonia at all.
Ok, I swear I will tell the truth, the whole truth and nothing but the truth. Not that I think measuring lactate levels is useless, but I cannot deny that serial lactate measurements are a resource waste, and most of the time, don’t change anything. I really can’t recall the last time I saw a patient with the only abnormality being an ‘elevated’ lactate level and this drove me to a different path, a more aggressive conduct, or maybe a different hemodynamic approach.
But, my opinions aside, let’s see what Mercedes Garcia-Alvarez, Paul Marik and Rinaldo Bellomo said in 2014 . In this article, the authors question the theory behind hyperlactatemia. Well, since med school we all heard about hypoperfusion leading to tissue hypoxia and KABUM! The so famous type-A hyperlactatemia. They discussed a bunch of studies which failed to demonstrate the association between hypoperfusion leading to high lactate levels. Other studies showed that one of the TOP lactate producers during septic shock are the lungs. Yeah, those meat balloons we all have (well, not all of us, but you got the idea), which receive virtually all cardiac output and are responsible for the “oxygenation”, as a big producers of lactate. This theory goes against the old type-A hyperlactatemia theory.
The authors not only bring doubts about the most know theory of hyperlactatemia genesis, but also, they discuss another possible pathway to lactate production. During normal metabolism, lactate is produced from pyruvate as part of the glycolysis mechanism. There is a change in this mechanism in critically ill patients alongside with an increased adrenergic response. Therefore, there is an increase in lactate production without an adequate “clearance”, leading to increased lactate levels. This hyperlactatemia might be an adaptive mechanism since several organs, like brain and heart use lactate as energetic source.
There are some data to reinforce this possible adaptation mechanism, showing that the increased glycolysis and lactate production trough adrenergic stimulation is associated with better outcomes. Also, animals studies showed that decreased lactate levels might be associated to cardiovascular collapse and death.
A definition of lactate clearance based on the correction of hypoxia and tissue hypoperfusion conflicts with this metabolical changes. Trying to decrease the lactate levels no matter what, aiming better outcomes, might not be the best strategy. The decrease in lactate levels we see with the “sepsis bundles” and all other treatments might be due an increased lactate clearance, decreased production, dilution, and probably by a combination of these factors. Besides, trying to increase oxygen delivery to supranomal levels aiming to increase lactate clearance has been shown to increase mortality in critically ill patients.
Maybe there are lot of factors playing together, from metabolical changes to hypoperfusion, and once we improve the hemodynamic, we “correct” those metabolical changes and modulate the adrenergic response. Lactate then, would only be a marker of that improvement. However, I still don’t believe serial lactate measurements are necessary to show me that.
But OK, maybe you still miss those lactate measurements, who knows, you love it to damn much! So, what’s the difference between you, a lactate maniac, drawing blood every two hours and any other person who doesn’t give a damn about lactate? Well, in terms of lactate, none! That’s what the LACTATE study group found in 2010. Despite showing a difference in hospital mortality on the intervention group (lactate guided therapy), I think this association (lactate clearance) unlikely, since there were no difference in lactate levels between groups. The only real difference was that in the control group, the team had no access to lactate levels to guide their therapy. Of course, it’s not the act of measuring lactate itself that will change the outcomes, it’s what you’re going to do with those levels. In this study, patients in the lactate guided therapy group received more fluids and vasodilators, while the control group received more fluids from 9-72h (delayed resuscitation doesn’t work!). Again, maybe this difference in mortality might be due a type I error.
So, should I just wait and watch? Of course not you dumbasss! There is a cool study by Jan Bakker showing that serial physical examination and evaluation of peripheral perfusion can identify hemodynamically stable patients with a more severe organ dysfunction and higher lactate levels! FREE OF CHARGE!
I really don’t consider changing my practice based on lactate levels. Why should I? I do have a God given gift: my hands, and I will keep using them for good!
1. Garcia-Alvarez M, Marik P, Bellomo R. Sepsis-associated hyperlactatemia Crit Care. 2014; 18(5).
2. Marik PE, Bellomo R, Demla V. Lactate clearance as a target of therapy in sepsis: a flawed para- digm. OA Critical Care 2013 Mar 01;1(1):3
3. Wutrich Y, Barraud D, Conrad M et al. Early increase in arterial lactate concentration under epinephrine infusions is associated with a better prognosis during shock. Shock. 2010; 34(1):4-9.
4. Matejovic M, Radermacher P, Fontaine E. Lactate in shock: a high-octane fuel for the heart? Intensive Care Med. 2007; 33(3):406-408.
5. Jansen TC, van Bommel J, Schoonderbeek FJ et al. Early Lactate-Guided Therapy in Intensive Care Unit Patients Am J Respir Crit Care Med. 2010; 182(6):752-761.
6. Lima A, Jansen TC, van Bommel J, Ince C, Bakker J. The prognostic value of the subjective assessment of peripheral perfusion in critically ill patients Critical Care Medicine. 2009; 37(3):934-938.