Liver failure and lactic acid

[ArmaniX, MSN, APRN]

Just curious to everyone's experience and knowledge here. Perhaps my mindset is wrong here so, please, educate me. When a patient is in liver failure they are going to have an elevated lactate.

The liver is damaged. It can't do its job. There is a build up of lactate and lab calls to inform me that my patients lactic acid is 15. I'm not surprised.

What I'm not understanding is why the doctors order serial lactic acids q4 ... What is the reasoning for this or the EBP?

I feel I must be missing something because I bring it up in rounds with the doctors and their response is always "oh keep doing them just so we can monitor."

In reference, I'm discussing a scenario which involves a patient in the ICU on multiple pressors, MODs, CRRT. The whole buffet.

[WestCoastSunRN, MSN, CNS]

This sounds like a sepsis patient? The serial lactate levels can guide treatment and be helpful in determining prognosis. It's like another sort of vital sign in determining response to treatments aimed at reversing hypoxia -- however that is debated (whether increased lactate levels are in fact related to perfusion issues). Some say increased lactate is a compensatory response that is actually beneficial. But this doesn't explain why liver failure patients with high lactates have worse outcomes.

So, bottom line -- it is interesting to watch what the lactate is doing and it doesn't mean the same thing in every patient. I'd be curious enough to ask the medical team what their specific rationale is for following them.

[Natasha A., CNA, LVN]

I am curious to know the connection as well. I know that lactic acid can build up primarily in the liver and kidneys. And yes lactic acid does have a compensation mechanism. I would believe to monitor the timing of the lactic acid progression from compensation to compromise state.

[PaSSiNGaS, MSN]

Patients who have liver disease do not routinely have a lactic acidosis without some other underlying condition like decreased perfusion, sepsis, or some other pathology like a G6P deficiency or something like that.

Normal metabolism is done using oxygen and the Crebs cycle. You make daily lactate just from glycolysis regardless of having oxygen or not so then that lactate goes to the liver and by the Cori cycle gets turned into glucose. A decrease in oxygen/perfusion from something like sepsis will cause an increase in anaerobic metabolism and increase the already forming lactate in the blood which should be metabolized by the liver, but in a cirrhotic patient that is compromised even worse because it cannot metabolize the lactate to begin with.

Monitoring lactate levels is a good reference to how well tissue perfusion is getting and if the pressors and other treatments are working.

[PresG33]

So there is an excess of lactic acid, which is buffered by the body and turned into lactate, which is what we measure. The body has a relatively small amount of buffer available, so if there is extra acid it is difficult to make more (especially when someone is sick). Therefore, if the measurements of lactate are decreasing, it means that the body is more effectively buffering the acid and is "doing better". It is difficult to say what is doing this (fluids, abx, better perfusion from pressors), but it is a general idea that things are headed in the right direction. If lactate continues to rise, it is a hint that other interventions need to be made (CRRT, inotropes, etc).