Lactic acid >24

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VentdependenT

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50ish obese F with htn, dm, etoh, cocaine use feeling sick for 3
days with loose stools, lethargy, malaise, brought in by family for AMS.

No hx of mi, cva, food aversion, bloody stools, fevers, travel, sick contacts, recent hospitalizations.

Hypotensive, afebrile.

Wbc 50 with some weird promyelocytes on diff, often misread by computer in past. Hb 16, plt 400, inr 1.8. ABG 6.7/30's/100's on Fio2 1

Bun 40, Cre 4, Bicarb 3, agap sky high, Na/k/cl/glucose normal enough. Tubed. 6L in ER. 3 pressors. Neg ct head, kub, cxr. Lactate is >24. Serum tox neg. UDS cocaine. Markers essentially normal. Lfts ast 130, alt 80, rest nml. Uric acid wnl. No other source for gap really.

Meds: insulin, metformin on for 6 months off for a months then restarted "recently", some bp stuff.

Was highly functional and independent.

I pick this pt up from day team for night float at 7pm. Lactate 20 after 18L, nonoliguric atn, MODS, looks like baloon, Ph 6.8

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50ish obese F with htn, dm, etoh, cocaine use feeling sick for 3
days with loose stools, lethargy, malaise, brought in by family for AMS.

No hx of mi, cva, food aversion, bloody stools, fevers, travel, sick contacts, recent hospitalizations.

Hypotensive, afebrile.

Wbc 50 with some weird promyelocytes on diff, often misread by computer in past. Hb 16, plt 400, inr 1.8. ABG 6.7/30's/100's on Fio2 1

Bun 40, Cre 4, Bicarb 3, agap sky high, Na/k/cl/glucose normal enough. Tubed. 6L in ER. 3 pressors. Neg ct head, kub, cxr. Lactate is >24. Serum tox neg. UDS cocaine. Markers essentially normal. Lfts ast 130, alt 80, rest nml. Uric acid wnl. No other source for gap really.

Meds: insulin, metformin on for 6 months off for a months then restarted "recently", some bp stuff.

Was highly functional and independent.

I pick this pt up from day team for night float at 7pm. Lactate 20 after 18L, nonoliguric atn, MODS, looks like baloon, Ph 6.8

Comfort care. There was no point in continuing once the initial lactate came back 24. I guess seeing as she's highly functional and only 50 its worth a full 24 hour push, but after 24 hours of maximal EGDT her lactate is still 20. This is not compatible with life.

My record book is 21.1 and that was Immediately postop for an infected, excoriated fempop graft in a 45 year old. But I got her down to 11 at the 8 hour mark. And she barely lived.

20 after 24 hours......toast.
 
50ish obese F with htn, dm, etoh, cocaine use feeling sick for 3
days with loose stools, lethargy, malaise, brought in by family for AMS.

No hx of mi, cva, food aversion, bloody stools, fevers, travel, sick contacts, recent hospitalizations.

Hypotensive, afebrile.

Wbc 50 with some weird promyelocytes on diff, often misread by computer in past. Hb 16, plt 400, inr 1.8. ABG 6.7/30's/100's on Fio2 1

Bun 40, Cre 4, Bicarb 3, agap sky high, Na/k/cl/glucose normal enough. Tubed. 6L in ER. 3 pressors. Neg ct head, kub, cxr. Lactate is >24. Serum tox neg. UDS cocaine. Markers essentially normal. Lfts ast 130, alt 80, rest nml. Uric acid wnl. No other source for gap really.

Meds: insulin, metformin on for 6 months off for a months then restarted "recently", some bp stuff.

Was highly functional and independent.

I pick this pt up from day team for night float at 7pm. Lactate 20 after 18L, nonoliguric atn, MODS, looks like baloon, Ph 6.8

Was she on metformin? Probably. It's cheap. Using it prior to her binge and GI upset??

More history about the drug use and the loose stools please (if you have it)

I've pulled more than one high lactic acidosis secondary to metformin +/- secondary etiologies out of it. Too soon to comfort cares for my tastes.
 
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Was she on metformin? Probably. It's cheap. Using it prior to her binge and GI upset??

More history about the drug use and the loose stools please (if you have it)

I've pulled more than one high lactic acidosis secondary to metformin +/- secondary etiologies out of it. Too soon to comfort cares for my tastes.

Bingo. I mention the metformin in my post

Tried HD to help with the lytes, pull off some metformin, but it didnt help clinically.

Only read about this never seen it. All her acute problems began when she restarted metformin. Most likely big aki on ckd then the metformin side effect.

Horrible. withdrew care w/in 24h
 
Bingo. I mention the metformin in my post

Tried HD to help with the lytes, pull off some metformin, but it didnt help clinically.

Only read about this never seen it. All her acute problems began when she restarted metformin. Most likely big aki on ckd then the metformin side effect.

Horrible. withdrew care w/in 24h

The only times I ever see lactate this high are when metformin is tossed into the equation. I think that level of lactate secondary to any other etiology is simply not really possible outside of metformin as whatever is causing your lactic acidosis becomes completely incompatible with life long before you ever get to levels like 24.

I guess when metformin is part of the picture, you're never exactly sure how much of a role it's playnig and I have pulled some of these patients through, as the lactate is kind of "artificial" - I mean it's a REAL lactate level, but the level doesn't totally represent direct tissue hopoxia.

Eh.

It's still a good case.
 
Comfort care. There was no point in continuing once the initial lactate came back 24.

You should delete this post before applying to CC fellowship.

While classic teaching that any lactate >4 has a mortality of 80%, that's anecdotally very very high.
 
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You should delete this post before applying to CC fellowship.

Was one of the meds an ACE? I could see ACE to AKI + cocaine with fibrinoid renal necrosis with meformin causing this.

And 18L? You're going to cause a really nasty hyperchloremic acidosis. Why not just start CVVHD to help with acidosis?
 
Was one of the meds an ACE? I could see ACE to AKI + cocaine with fibrinoid renal necrosis with meformin causing this.

And 18L? You're going to cause a really nasty hyperchloremic acidosis. Why not just start CVVHD to help with acidosis?

Dinno bout bp meds. Fam could only remember the metformin and insulin.

All that fluid was in before i came on and took over at 7pm. first thing i did was kvo it ( fer fuks sake she was gettin 400cc an hour in drips alone) XL fem shiley, and call the renal fellow. We had nothing to lose but $$.
 
Interesting to read this. Just had a sample come into my lab last week with a lactate that required 2 dilutions and finally came out at 21. Was very curious about it. Previous 2 hours earlier had been 24, got another later that was 19 or something.
 
You should delete this post before applying to CC fellowship.

While classic teaching that any lactate >4 has a mortality of 80%, that's anecdotally very very high.

Too me this wasn't a metformin lactic acidosis, which I've never seen. It is a patient feeling sick for 3 days, febrile, severe leukocytosis of 50k, and on 3 pressors after 18L of volume. Multiple organ failure. Lactate >20. pH 6.7

To me, this is septic shock.

Severe septic shock with although I don't have all the variables, I would presume an APACHE II of around 30.

Is it possible that metformin is contributing to the lactic acidosis...I guess it could be yes. But I have seen a lactate of 21 as I stated in pure septic shock with no metformin. This lady is on three pressors and COD'n....what makes you think that lactate is not purely ischemia? Granted the severe acidemia is rendering all of your pressors except vasopressin ineffective. Maybe tons of bicarbonate and early cvvhd would have helped the refractory acidemia and thus the shock

I thought the data was ICU admit with lactate >4 was 50% mortality not 80%, but I could be wrong.

What I do know is lactate levels correlate linearly with mortality. This lady has septic shock and massive end organ failure. Couple that to a lactate of 24 and her SOFA/APACHE, and her mortality is through the roof.

As for your CC fellowship, which I sadly am not after all applying to this July, maybe in 2 years well see how my sons are doing, I would do everything just like vent did. I just known in my mind, she's already toast. What I am doing is academic. But that's never held me back from a procedure before.....
 
We also treated for abd sepsis but dead rotten gut and liver would have to be causing a refractory LA like that. The picture didnt totally fit with massive celiac infarct ( would have to destroy liver to make LA stay high I would guess), but we'll never know.

We did, of course, use BS abx with the gut in mind.

Pulm fellow on during day didnt want to dialyse because it doesnt remove lactate BUT the fellow put pt on bicarb drip which definitely doesnt do squat for lactic acidosis.

I cared about the Ph, was doing all i could to provide supportive care, and pulled the trigger on calling the renal seevice. Nothing works with a Ph of 6.8...

Intetestingly, once on sled or whatever mode renal chose the LA dropped from 22 to 15 and of course the ph was in the life compatible range. Too late however.

I have a greater respect for metformin now.
 
I have a greater respect for metformin now.[/QUOTE]

Agree with previous post, this is not MALA, it's septic shock.
 
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Too me this wasn't a metformin lactic acidosis, which I've never seen. It is a patient feeling sick for 3 days, febrile, severe leukocytosis of 50k, and on 3 pressors after 18L of volume. Multiple organ failure. Lactate >20. pH 6.7

Quick physiology question....what happens to cardiac output in severe acidemia?

To me, this is septic shock.

When all you see are horses, zebras look horse-ish......

Is it possible that metformin is contributing to the lactic acidosis...I guess it could be yes. But I have seen a lactate of 21 as I stated in pure septic shock with no metformin. This lady is on three pressors and COD'n....what makes you think that lactate is not purely ischemia?

What's the source of infection? It ain't sepsis without a source. Granted this case will be bias by Vent's bias of the case, but septic shock this bad is almost always blatantly obvious.

And there is no guessing about it, metformin can very very easily cause a lactic that high. The lowest metformin relate lactate I've seen, is 26.

Granted the severe acidemia is rendering all of your pressors except vasopressin ineffective.

Oh really? I believe the main study promoting this was done on beta-agonist receptors in lymphocytes, not cardiac tissue. Is just as likely that you're seeing the deleterious effects of acidosis itself.

T
I thought the data was ICU admit with lactate >4 was 50% mortality not 80%, but I could be wrong.

What I do know is lactate levels correlate linearly with mortality. This lady has septic shock and massive end organ failure. Couple that to a lactate of 24 and her SOFA/APACHE, and her mortality is through the roof.

I've brought many a goner with lactates >15 back, many a sicky with APACHE2 >25 back, don't ever stop looking at the patient as a patient and not a number. I once literally walked out of a room disgusted about running a code on a dead man for well over an hour with a SaO2 <50. My attending called me a ***** and told me to get back in there and man the **** up and do what needed to be done (ended up putting 2 more surgical chest tubes in the guy after already placing a pigtail and 1 surgical chest tube), son of a bitch walked out of the hospital 2 months later.
 
IM not arguing with you hern. You are an attending intensivist and I am merely a medicine resident, technically not even a third year for another week, my opinion is really worthless in the context of you and JDH. But to me, this was septic shock from a GI source with refractory acidemia. At this level pH, the majority of vasopressors have a severely reduced efficacy as they are pH sensitive, and thus the shock state persists. The patients calculated scores show a very very poor prognosis. And with a lactate still >20 after 24 hours and a clinically worsening picture, I think comfort care is a reasonable option. That's all I was saying.
 
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But to me, this was septic shock from a GI source with refractory acidemia. ... And with a lactate still >20 after 24 hours and a clinically worsening picture, I think comfort care is a reasonable option. That's all I was saying.

Yea, I'm with you there (except the bit about septic shock from a GI source). If I had this clinical picture in the ED then by all means see what happens over the next 24 hours. If this is the clinical picture you have in the ICU after 24 hours then I'd agree it's time for the comfort care talk with the family. For every anecdotal story of someone walking out of the hospital after a situation like this there are a lot of anecdotal stories of people continuing to deteriorate and crap out. If the family dug in their heels and said "no, do everything" I wouldn't say it is completely unreasonable to go on for another 24 hours, but I'd set the stage with them that we're probably going to have this talk again the following day and if there wasn't an improving trajectory my recommendations would be stronger.
 
this level pH, the majority of vasopressors have a severely reduced efficacy as they are pH sensitive,

The data is not as clear cut as you distill it down in 1 sentence. I'm more inclined to think the direct acidosis effects are more important than decreased efficacy of vasopressors based off what I've read.
 
Pulm fellow on during day didnt want to dialyse because it doesnt remove lactate BUT the fellow put pt on bicarb drip which definitely doesnt do squat for lactic acidosis. .

I'd have argued with this fellow on this, bicarb clearly does not work with pH above 7.1, and the reccomendations to use bicarb for pH worse that are based off consensus and basically state, "it sounds reasonable"

I anything, bicarb for lactic acidosis may make the intra-cellular acidosis worse, AND can increase lactic acid production.

Granted.......CVVHD typically uses...bicarb, but you get better fluid control and electrolyte control, and many advocates show you don't get the same fluid overload states with CVVHD that you do with massive bicarb drips.
 
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The data is not as clear cut as you distill it down in 1 sentence. I'm more inclined to think the direct acidosis effects are more important than decreased efficacy of vasopressors based off what I've read.

Ok. That's fine. Doesn't change my viewpoint. This is still shock with refractory acidemia after 24 hours that is not improving. I think the CMO talk is valid. Call me an inexperienced resident if you want, no argument there I am one .But that's my opinion
 
Is there a specific lactate level when you guys start suspecting Type B lactic acidosis?
 
With a leukocytosis that high presenting in shock with multi-organ failure I'd be very concerned about sepsis and my source would be some abdominal catastrophy. Did you follow your culture data post-withdrawal? MALA is a very real possibility, but I'd be looking very hard and persistently for infection.

I find it very weird that, with presumed days of hypotension, she comes in with likely ATN but pretty much normal LFTs. I was very much anticipating shock liver given the acidemia and hypotension..

I have seen a Burkitt's lymphoma (of the bowel) present very similarly with a sky high lactate, complicated by a perf and gram negative bacteremia.
 
With a leukocytosis that high presenting in shock with multi-organ failure I'd be very concerned about sepsis and my source would be some abdominal catastrophy. Did you follow your culture data post-withdrawal? MALA is a very real possibility, but I'd be looking very hard and persistently for infection.

I find it very weird that, with presumed days of hypotension, she comes in with likely ATN but pretty much normal LFTs. I was very much anticipating shock liver given the acidemia and hypotension..

I have seen a Burkitt's lymphoma (of the bowel) present very similarly with a sky high lactate, complicated by a perf and gram negative bacteremia.

Oh, the patient in the OP was almost certainly septic - probably the straw that broke the camel's proverbial back.

The point I and others were making was that with a lactate that high MALA was also playing a role.

It's not one or the other.
 
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Oh, the patient in the OP was almost certainly septic - probably the straw that broke the camel's proverbial back.

The point I and others were making was that with a lactate that high MALA was also playing a role.

It's not one or the other.

Good point
 
The data is not as clear cut as you distill it down in 1 sentence. I'm more inclined to think the direct acidosis effects are more important than decreased efficacy of vasopressors based off what I've read.

Do you have a link to the study in question? I am having a hard time finding it.
 
Do you have a link to the study in question? I am having a hard time finding it.

Its in some of the nephrology journals. Look up bicarb use for acidosis. Acidosis causes increased CO and bicarb makes us feel better but not the Pt. Guess what? metabolic ALKALOSIS is far more dangerous. yup.
 
Its in some of the nephrology journals. Look up bicarb use for acidosis. Acidosis causes increased CO and bicarb makes us feel better but not the Pt. Guess what? metabolic ALKALOSIS is far more dangerous. yup.

Chest 2006ish bicarb in lactic acidosis. And pull their references.
 
Quick anecdote. Had a little old asian lady with ESRD, already in the ICU for 2 weeks for sepsis IIRC, went out and came back with HAP and septic shock. At her worst lactate was 22. I remember my attending tell me he had never seen anyone survive that high a lactate. Spoke to the family about grim prognosis. We didn't expect her to survive 24hrs. Pulled through, and was sent to floor from ICU.
 
From a surgical perspective, you described a patient who very well could have infarcted off part of their gut from cocaine usage. Just as you can have spasm of the coronaries with cocain use, you can have the same occur to some of the mesenteric vasculature. This is a well described phenomen of causes of mesenteric ischemia and is not that uncommon of a cause of necrotic bowel/abd catastrophy cause these patients come from a population at times who are not actively seeking out medical care readily. Three days would be about the right time frame for a sizable portion of the colon to be dead, leading to such a high lactate. And the compromised bowel would lead to loose stool as the mucosa dies and sloughs off. I have definately seen my share of patients with dead bowel with a lactate this high. Doesn't usually end well but it is not that much of a rarity, unfortunately. However, unless you did a CT scan and saw free air/pneumotosis etc versus an exlap or an autopsy, you'll never know if this was the etiology in this patient.
 
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