Question on liver disease pt, MAP, and lactate level

tcvnurse, BSN, RN · Jan 7, 2017

A lactic acid is telling you that there is a mismatch between oxygen supply and demand, namely, not enough for what is bring required. In this case, I suspect because of the hypotension, which is why you gave some albumin (to pull fluid back into the vascular circulation) as well as crystalloid. You recheck the lactic a little while later after your boluses are complete to evaluate whether the treatment helped or what. Did the lactic keep rising? More aggressive treatment may be necessary. Did it come down? Great.

I can't speak directly to liver patients as I do cardiac surgery nursing, but our goal is to keep map greater than 65 to perfuse the kidneys. Hope this helps.

Wile E Coyote, ASN, RN · Jan 7, 2017

In the setting of an impaired liver, Lactate levels mean even less than we've lately come to realize they do. Said another way, there is strong evidence to suggest our understanding of oxygen debt has been wrong. High lactate doesn't necessarily equal tissue hypoerfusion, so strike one.

Strike two is that, if the liver function is poor enough, then the liver's role in the normal Cori Cycle (Lactic Acid Cycle) is impaired. Thus, in this particular patient, abnormal serum lactate levels are more attributable to impaired liver function vs tissue perfusion.

Ostensibly, the following article seems to be irrelevant, as it discusses lactate as it relates to sepsis, but read further down.

Sepsis-associated hyperlactatemia | Critical Care | Full Text

KatieMI, BSN, MSN, RN · Jan 7, 2017

The patient just lost huge amount of EXTRACELLULAR fluid (ascitis). Therefore, her body tried to "compensate" by shifting fluid from intracellular/intercell spaces, but due to lack of oncotic pressure (albumin) was not able to keep fluid there, so INTRAVASCULAR volume remained low. Add to that general "hypotensive" effect of advanced cyrrhosis (mostly produced by estrogens, bradykinin and some other substances which are supposed undergo liver elimination) and you'll get why the patient was persistently hypotensive. Albumin could help if ordered in larger amount (which could kill the kidneys, so never ordered).

These patients may or may not "deserve" MAP of 65 depending on their baseline. Treat patient, not the number.

Lactate was first time ordered for SBP exclusion within "sepsis workup", second probably for CMA reason. SBP can be with any amount of pain, from 0 to 10.

Cowboyardee · Jan 7, 2017

This gets pretty complicated, so apologies in advance - I may not be able to explain all the factors here completely.

For one, yes peritonitis is often painful. But I don't know anything about your patient, their mental status, what kinds of medications they were on, etc. So it's difficult to make a hard rule. I wouldn't go so far as to say that lack of pain excludes the possibility of bacterial peritonitis.

Elevated lactic acid levels tend to indicate the presence of anaerobic metabolism, which in turn often indicates inadequate perfusion. That's the major reason it can be elevated in shock states. It's also why a LA level was initially ordered in this case - to differentiate hypoperfusing hypotension (a shock state) from baseline compensated hypotension. (Incidentally, lactic acid can also be elevated as a response to catecholamines, which is why it is often used as a marker for sepsis even when the septic patient is not actually in septic shock, hypoxic, or hypoperfused - FYI). The first elevated LA level in your patient tended excluded one possibility - that your patient was fine, just in their baseline compensated hypotensive state.

So, what's left? In your patient's case, an elevated lactic acid level could have been caused by simple hypovolemic shock (inadequate blood volume after ascites removal and fluid shifts), septic shock (vascular dilation leading to hypoperfusion caused by bacterial peritonitis or any other systemic infection), or adequately perfused sepsis (bacterial peritonitis superimposed over a well compensated baseline hypotension).

One of the factors that complicates this is that lactic acid is cleared from the blood stream most primarily in the liver. So in the case of your patient, I'm not sure how quickly we should expect her to normalize her lactic acid level even if her perfusion was corrected.

Your doctor most likely ordered the second lactic acid to see if the albumin and IV fluid corrected the patient's apparent/possible hypoperfusion, and/or get a feel for a possible progression of sepsis.

The real devil here is still in the details though. The initial LA level was not super elevated. I cannot personally give you much guidance as to interpreting the severity of the results here. What exactly is a clinically significant LA level in a patient with baseline liver dysfunction? How quickly would we expect an LA level to clear in such a patient whose hypoperfusion was [possibly] corrected? How high might we expect it to go if the patient truly had SBP? How fast? These are questions I cannot answer. And of course it is possible I am missing some crucial piece of the puzzle.

Please do ask the doctor who was caring for the patient. He can certainly tell you more than I can.

Boomer MS, RN · Jan 7, 2017

Love all the replies and review about pathophysiology. More teaching moments!

WestCoastSunRN, MSN, CNS · Jan 7, 2017

In the setting of an impaired liver, Lactate levels mean even less than we've lately come to realize they do. Said another way, there is strong evidence to suggest our understanding of oxygen debt has been wrong. High lactate doesn't necessarily equal tissue hypoerfusion, so strike one.
Strike two is that, if the liver function is poor enough, then the liver's role in the normal Cori Cycle (Lactic Acid Cycle) is impaired. Thus, in this particular patient, abnormal serum lactate levels are more attributable to impaired liver function vs tissue perfusion.
Ostensibly, the following article seems to be irrelevant, as it discusses lactate as it relates to sepsis, but read further down.
Sepsis-associated hyperlactatemia | Critical Care | Full Text

Great article, Wile. I'm not sure about there not being a correlation between tissue hypoxia and high lactate levels. While the above article challenges that understanding -- much of the data came through measuring muscle perfusion. The article concedes the fact that there are certainly areas of microcirculation where we see decreased perfusion in septic patients. Lactate seems to be pretty complex in the uptake and release of various tissue/organs. Maybe increased levels are related to a compensatory response of some sort, but what we do know is high levels correlate with severity of illness. Fortunately we have other indices besides lactate to guide resuscitation in sepsis -- and as with anything else, you look at the whole picture.

As for the liver patient -- yes you would expect high values since so much lactate is metabolized by liver... but this doesn't mean lactate levels are irrelevant.

This is a good topic to devote more study to!

Wile E Coyote, ASN, RN · Jan 7, 2017

Great article, Wile. I'm not sure about there not being a correlation between tissue hypoxia and high lactate levels...but this doesn't mean lactate levels are irrelevant.

Thank you, but please note that I didn't encourage such either/or conclusions. I did go through the thought process on refining a differential Dx. This patient's management would better be driven by procalcitonin and serum protein levels. (Protein levels

Cowboyardee · Jan 7, 2017

Thank you, but please note that I didn't encourage such either/or conclusions. I did go through the thought process on refining a differential Dx. This patient's management would better be driven by procalcitonin and serum protein levels. (Protein levels
Good information. But I wonder if there is still something you're missing. If you feel I'm wrong, please do explain...
The thing about this situation is that along with SBP in the differential diagnosis are several possibilities, at least from what we know so far.
1) The patient has no infectious process but is still in a hypoperfused state, most likely secondary to insufficient intravascular volume.
2) The patient has no acute disease process at all and is merely hypotensive within her compensated baseline range.
3) The patient has some other form of sepsis besides SBP, which is a possibility given that she lacks some of the common symptoms of peritonitis.
With this in mind, the first lactic acid level wasn't a way of asking, "does this patient have SPB?" or even "does this patient have sepsis?" It was asking, "is there something wrong here in the first place?" or "can we eliminate option #2 above?"
The patient was then administered fluid and volume expanders. A second lactic acid level was then obtained, and this second lactic acid could be thought of as a way to ask "does adding volume improve whatever is wrong in this case?" We still don't have a our differential diagnosis pared down to a single possibility, but the second level might give us hints about whether it would be a good idea to start abx empirically, transfer to a higher level of care, etc - especially if, like where I work, procalcitonin levels aren't performed in house anyway.
I suspect you may be right that a lactic acid in this particular patient of 2.6 wasn't even enough to answer the first question. Not being there (and not being a doctor), it's hard to know. Still, in this case, it seems reasonable to me to 'ask' not only whether the patient has SBP, but also whether that patient is sick at all. Once again, please challenge any arguments I've made that seem questionable to you.

WestCoastSunRN, MSN, CNS · Jan 8, 2017

Thank you, but please note that I didn't encourage such either/or conclusions. )

I was referring to the assertions made in the article, not by you.

NurseKatie08, MSN · Jan 8, 2017

The patient just lost huge amount of EXTRACELLULAR fluid (ascitis). Therefore, her body tried to "compensate" by shifting fluid from intracellular/intercell spaces, but due to lack of oncotic pressure (albumin) was not able to keep fluid there, so INTRAVASCULAR volume remained low. Add to that general "hypotensive" effect of advanced cyrrhosis (mostly produced by estrogens, bradykinin and some other substances which are supposed undergo liver elimination) and you'll get why the patient was persistently hypotensive. Albumin could help if ordered in larger amount (which could kill the kidneys, so never ordered).
These patients may or may not "deserve" MAP of 65 depending on their baseline. Treat patient, not the number.
Lactate was first time ordered for SBP exclusion within "sepsis workup", second probably for CMA reason. SBP can be with any amount of pain, from 0 to 10.

A little confused about why you say high doses of Albumin are never ordered because it will kill the kidneys. I find quite the opposite to be true as a liver nurse. We give large doses of Albumin as part of our SBP protocol on day 1 & 3 for renal protection (1.5g/kg on day 1, 1g/kg on day 3), as well as to aide in pushing fluid where it belongs. NS boluses for hypotension in liver patients are ill advised because they'll just go right to the belly. Hoping you can explain what you mean.

Wile E Coyote, ASN, RN · Jan 8, 2017

I was referring to the assertions made in the article, not by you.

Got it, thank you for clarifying.