Having an elevated lactate in septic acid on admission is bad. Trending it, as studies that I have shown on this page does not change mortality. Seeing the numbers downtrend do give us that warm and fuzzy feeling inside, though. We give off a sigh of relief when that number becomes “euboxic”. This article was is from April 2019. We are commonly taught in medical school, residency, and other training that an elevated lactic acidosis is due to tissue hypoperfusion. Is this accurate?
Mechanisms for Elevated Lactic Acid
1. a deficit in oxygen delivery or extraction
2. shunting
3. stress
4. increased adrenergic stimulation
Notice that none of these mean that we have to drown the lactates with a bunch of fluids thereby diluting the value. We need to go after the etiology of it in a more specific manner. The authors of this study looked at the patients enrolled in the ALBIOS study (you know, the 2014 study where they sorted out that giving patients in septic shock albumin was good for depleting hospital resources but not a survival benefit? I guess I need to cover that trial on here and looks at more than 1700 patients with lactate and central venous oxygen saturation measurements. They did a bunch of calculations and statistics that I am not going to cover here but you can click on the link for the article and go to town on it if you so wish.
Interesting Findings
Something really interesting was found in this study. The authors found that 1017 patients had a lactic acidosis but 57% of those patients had a normal serum pH. I would’ve thought that the number would have been lower. And it’s not because these patients were on bicarbonate drip band-aids either.
The Early Goal Directed Therapy trial made us infatuated with checking central venous oxygen sats and our target was to get that to be over 70%. This study showed us that only 35% of that patients they looked at had a value less than 70%. 65% of patients with an elevated lactic acid had a normal or high ScVO2. Strange. We do know that the extremes of ScVO2 are bad and that ultimately ScVO2 has a number of limitations within itself. Anyway, I’m not going to dive too deep into all that, I’ll leave it for the authors to explain.
To conclude….
All in all, their main conclusion in this study, and the important takeaway is that lactate is not primarily created in sepsis by of the cells not receiving enough oxygen, but rather by an impairment of tissue oxygen utilization. This is a game changer. In my opinion, it doesn’t mean that fluids are the answer, but rather, to find a way to help the tissues use said oxygen. Now let’s all change our practice. Ultimately, lactic acidosis does not mean hypoperfusion.
Don’t take my word as gospel on all this, I could be wrong. Read the article for yourself. A hat tip to the authors. -EJ
Gattinoni, L., Vasques, F., Camporota, L., Meessen, J., Romitti, F., Pasticci, I., … Marini, J. J. (2019). Understanding Lactatemia in Human Sepsis: Potential Gattinoni L, Vasques F, Camporota L, et al. Understanding Lactatemia in Human Sepsis. Potential Impact for Early Management. Am J Respir Crit Care Med. 2019;200(5):582‐589. doi:10.1164/rccm.201812-2342OC
Link to Abstract
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