liver failure and LR

i haven't looked this up... distant memory going here.....

but the lactate byproducts can make an acidotic state worse.....????

I learned that you shouldn't give LR to patients with hepatic failure because it will cause metabolic acidosis. The reasoning is that in normal people, the lactate combines with H+ ions to form lactic acid which is then metabolized by the liver into HCO3. So LR works as a buffer in normal liver function but not so much in liver failure. Hope this helps :)

Wow, I had completely forgotten about this. Amazing the things you forget.

Noney

thanks, this helps a lot. i knew there was something to it ... just couldn't remember quite what it was. i just remember that annoying woman who gives the CCRN lectures saying that she 'saved a Dr's license' b/c she refused to give LR to a pt in liver failure

Thank you so much for this thread. This is something I did not know. My daughter has an undetermined liver disease w/fibrosis. The thought is, she has auto-immune hepatitis, but has not yet been diagnosed. Liver biopsy said she had significant fibrosis consistent w/ cirrohsis, but does not have cirrohsis. Has extremely elevated enzymes, has never drank alcohol, never taken any drugs, or smoked.

But anyway, I will remember this in case she is hospitalized and LR is ordered. Thanks again. I learn so much from this site, every day.

i think there are a lot of misconceptions about lactic acidosis associated with lactated ringers... while you are right that in hepatic failure there is no/minimal conversion of lactate to bicarbonate, you can't imply that it would cause or worsen lactic acidosis. You might have higher measurable lactate levels, but in of itself that number means nothing unless it is associated with ischemia, in which case that number is not diagnostic but purely a prognostic value (ie: a high lactate - ONLY in the setting of presumed ischemia - would suggest a higher mortality rate).

Your body produces an excess of about 20 mmols/kg/day of Lactate which is about 1500 mmols per day (which is a far cry from the 28mmols/Liter of LR) ... the implication that all of a sudden that LR would cause a lactic acidosis is a common myth propagated in the nursing literature and has no true evidence to back it up. For example in patients with chronic hepatic/end-stage liver disease, why aren't they all in lactic acidosis??? because their muscle picks it up and converts into sugar and the kidney excretes it.... the times that you see true lactic acidosis in the end-stage liver population is when they are in septic shock, have acute renal dysfunction. So you would then argue not to give LR to an end-stage liver patient with hepato-renal syndrome - well, those patients should be on CVVH or dialysis and that would mean that you could give LR since the dialysis/filtration will assist with management of the acidosis - and in the setting of sepsis they need volume and it doesn't matter at this point whether they get LR or saline....

So my point is: you can use LR for patients with hepatic dysfunction.

Tenesma - thank you for your post - i look forward to the day when i will have all that info...

i guess my question is - i know that LR isn't going to cause a sudden state of acidosis...but if someone were in such a state - why WOULD you give it -even though the chances are minimal it would exacerbate it??

Try thinking K+, look at the bag, see what LR consists of.

mittels what is your point about the K??? and what does that have to do with liver failure?

Originally posted by Tenesma

mittels what is your point about the K??? and what does that have to do with liver failure?

Critical thinking now!!!!

K+ and glucose in LR where does K+ metabolize?

Metabolic acidosis with compensation

i am fully aware of what substances LR consists of.....my point is if there are better fluids out there to use, why would LR be used in that scenario....

and.... in an acidotic state - the K+ will be more attracted to the negative vibe extracellularly thereby moving out of the intracellular space - causing a false elevation of K+ (such as happens in DKA) - so why in the world would you give an infusion of RL which could exacerbate this "false" hyperkalemia??

mittels....

1) there is no glucose in LR

2) there are 4mEq of K per liter of LR

3) potassium does not get metabolized --- what would the breakdown product be???

4) what does administering potassium have to do with metabolic acidosis???

if the patient is acidotic the patient will have a falsely elevated potassium due to the extracellular shift of potassium - so let's say the patient has a K=6.5 due the acid/base imbalance, can you please explain to me how diluting their blood with one liter of fluid containing 4 mEq of potassium is going to raise their potassium??? that doesn't make sense, if anything it would dilute their potassium.... the only time i wouldn't administer LR to a patient who is hyperkalemic is when they are in acute renal failure and are unable to excrete excess potassium... however in patients who are in hepatic failure and who have renal failure (usually due to a hepato-renal syndrom), they should be on dialysis, and when a patient is on dialysis it doesn't matter what kind of fluid you administer, since the excess K is leeched off in the dialysis bath.

the only times i would not administer LR due to the concern regarding potassium content: hyperkalemia due to TRUE excess of potassium, not simply potassium shifting in or out of cells due to acid/base status.

this time i won't make a big fuss about you telling me: "critical thinking now!!!" - next time i won't be so kind :)