Case Conference

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ericL said:
good refresher for this stuff! Its been a while since I had to consider this stuf...

Looks like a metabolic acidosis (the anion gap is like 40 correct?) with respiratory compensation. Perhaps with some element of contraction alkalosis?
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here we go 👍

now if you both just combine what you have...
 
ericL said:
Looks like the gap is 40ish? Or am I reading this wrong?

So some sort fo metabolic acidosis with respiratory compensation? Maybe some contraction alkalosis too?
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sorry, I meant combine what you and choirboy have
 
ericL said:
something like an aspirin overdose?
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that's a good guess but not quite.

keep looking at the history and the acid base numbers (you are on the right track with the anion gap; many forget to do that).
 
ericL said:
metabolic acidosis with respiratory alkalosis as (partial) compensation? Contraction alkalosis thrown in the mix too?
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explain what you mean by contraction alkalosis. you're very close.
 
ericL said:
his kidney's are perceiving a low flow type state and clamping down-retaining water and losing K/H+?
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oh you are talking about the ras?

it's even more simpler than that.
 
ericL said:
Rta?
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oooo renal tubular acidosis?

even simpler than that although I like your style 😀

budding nephrologist?

ps- I see you there choirboy. don't give up on it.
 
surge55 said:
let's see what you guys got (note, it's being worked on/solved on page 2 but give it a go before you scroll onward)

A homeless white man is discovered unconscious in the park and is brought to the emergency department. He reeks of alcohol, is unkempt, and incoherent.

Physical examination shows a BP of 90/50 mmHg, heart rate of 120 beats/min, temperature of 39°C, slight scleral icterus and dullness, and bronchial breath sounds over the right lower lung fields.

Laboratory data:
Renal Panel:
Na 131 mEq/L
K 2.9 mEq/L
Cl 70 mEq/L
CO2 21 mEq/L
BUN 34 mg/dl
Creatinine, 1.4 mg/dl
Glucose, 240 mg/dl
Albumin 3.8 g/dL
Serum osmolality 320 mOsm/kg of H2O
Serum ketones weakly positive;
ABG: pH, 7.53; PaCO2, 25 mmHg; PaO2, 60 mmHg;

what's his acid-base status? ie what would you call his acid-base disturbance?
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Gap acidosis, metabolic alkalosis, and a resp alkalosis
 
jdh71 said:
Gap acidosis, metabolic alkalosis, and a resp alkalosis
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here's kind of what I was getting at eric; you pretty much had everything but I was wondering how you were explaining the contraction alkalosis.

jdh and others - how would you explain all three? what's causing them?
 
surge55 said:
here's kind of what I was getting at eric; you pretty much had everything but I was wondering how you were explaining the contraction alkalosis.

jdh and others - how would you explain all three? what's causing them?
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Well, the acidosis is likely secondary to ethylene glycol or similar because of the high osmolar gap, but it's also conceivable that this is a simply a drunk on ethanol guy with DKA. He's also hypotensive, tachycardic, febrile, with an exam that sounds like a pneumonia, and sepsis could also give you an elevated lactate, contributing to the gap acidosis.

If he's in DKA and urinating on top of drinking which makes you need to drain the weasel more often, you could easily also get a contraction alkalosis, and while we don't get this on history, drunk and DKA are also both reasons to do a lot of vomiting.

He's breathing fast because he has a pneumonia (needing to breath faster to make up for the amount lung that is not participating in ventilation to maintain minute ventilation) and liver disease (these patient's run around tychypneic).
 
jdh71 said:
Well, the acidosis is likely secondary to ethylene glycol or similar because of the high osmolar gap, but it's also conceivable that this is a simply a drunk on ethanol guy with DKA. He's also hypotensive, tachycardic, febrile, with an exam that sounds like a pneumonia, and sepsis could also give you an elevated lactate, contributing to the gap acidosis.

If he's in DKA and urinating on top of drinking which makes you need to drain the weasel more often, you could easily also get a contraction alkalosis, and while we don't get this on history, drunk and DKA are also both reasons to do a lot of vomiting.

He's breathing fast because he has a pneumonia (needing to breath faster to make up for the amount lung that is not participating in ventilation to maintain minute ventilation) and liver disease (these patient's run around tychypneic).
Click to expand...

We don't have an ethanol level so the missing osms are likely accounted for by alcohol. With a glucose in the 200s, etoh ketoacidosis seems more likely than DKA. Alcohol is mild diuretic, but people usually urinate more because of the volume, not the alcohol (just drink shots at the bar next time and see for yourself.) So I doubt his contraction is from increased diuresis. I bet this is just a drunk guy with etoh hep (scleral icterus), who's been vomiting and aspirated.

This would give his anion gap acidosis, contraction alkalosis, and respiratory alk (from infection/pna and liver failure).

What are his LFTs?
 
HarryGary said:
We don't have an ethanol level so the missing osms are likely accounted for by alcohol. With a glucose in the 200s, etoh ketoacidosis seems more likely than DKA. Alcohol is mild diuretic, but people usually urinate more because of the volume, not the alcohol (just drink shots at the bar next time and see for yourself.) So I doubt his contraction is from increased diuresis. I bet this is just a drunk guy with etoh hep (scleral icterus), who's been vomiting and aspirated.

This would give his anion gap acidosis, contraction alkalosis, and respiratory alk (from infection/pna and liver failure).

What are his LFTs?
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well done! everyone sort of contributed but this is the answer I was looking for 👍

not sure on those LFT's. this was my attending's patient.
 
HarryGary said:
We don't have an ethanol level so the missing osms are likely accounted for by alcohol. With a glucose in the 200s, etoh ketoacidosis seems more likely than DKA. Alcohol is mild diuretic, but people usually urinate more because of the volume, not the alcohol (just drink shots at the bar next time and see for yourself.) So I doubt his contraction is from increased diuresis. I bet this is just a drunk guy with etoh hep (scleral icterus), who's been vomiting and aspirated.

This would give his anion gap acidosis, contraction alkalosis, and respiratory alk (from infection/pna and liver failure).

What are his LFTs?
Click to expand...

You don't need a high glucose to have DKA and the LFTs are irrelevant.

There simply isn't enough information in this case to say this alcoholic ketoacidosis.

I admit this guy about once a month and it's never the same story but with similar labs. Don't get dogmatic with your critical care.

Also, aspiration RARELY gives you a bacterial pneumonia.
 
jdh71 said:
You don't need a high glucose to have DKA and the LFTs are irrelevant.

There simply isn't enough information in this case to say this alcoholic ketoacidosis.

I admit this guy about once a month and it's never the same story but with similar labs. Don't get dogmatic with your critical care.

Also, aspiration RARELY gives you a bacterial pneumonia.
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you have a point too. this was kind of vague in that regard. but he has it exactly as how the patient was.
 
surge55 said:
I like your insight.
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Sorry, wrote the answer without seeing page 2's responses, didn't want to beat a dead horse.

Although, a "." is about as insightful as offering mnemonics, which I despise.
 
KRichards62 said:
Sorry, wrote the answer without seeing page 2's responses, didn't want to beat a dead horse.

Although, a "." is about as insightful as offering mnemonics, which I despise.
Click to expand...

:laugh: fair enough. I was just messing with you.

mnemonics help some people though. it's how I remember certain things like this.
 
Damn, I got paged right as I was logging in and only had time to put likely etiology.

Overall, it was a nice example of a mixed, triple acid-base disorder and textbook case of AKA from presentation to w/u.

Although both present as an anion-gap and osmolar gap ketoacidosis, I think there were several clues in the labs which (aside from hx) leaned more towards AKA vs. DKA. The first as HarryGary already mentioned is the serum glucose, which while elevated is not markedly so, and is more compatible with a diagnosis of AKA though as jdh71 mentioned it could still have been DKA.

The second clue which can be useful in differentiating the two was the weakly positive serum ketones. The test is usually negative or weakly positive in AKA but has a much stronger reaction in DKA due to the type of ketone formation. The test reacts to acetoacetate which is the predominant ketone in DKA, but not much to beta-hydroxybutyrate which is predominant in AKA. Not exactly definitive but it can be quite useful.

Agree with jdh71 about LFTs. They are irrelevant as is serum ethanol level. Given the pt's hx, I would also want to be sure to r/o other differentials for AKA (e.g. methanol, ethylene glycol poisoning) at least with a U/A looking for crystals or serum levels, and especially considering the fact the guy is homeless and was found unconscious as management would differ from plain AKA with aspiration pneumonia.

As an aside, as I was logging out last time I saw a banner ad for the Heat vs. Pacers game tonight. Thought it was kinda weird to show up on SDN. Probably not the best use of ABC's ad dollars.

Thanks surge55 and jdh71 for posting the cases.
 
jdh71 said:
You don't need a high glucose to have DKA and the LFTs are irrelevant.

There simply isn't enough information in this case to say this alcoholic ketoacidosis.

I admit this guy about once a month and it's never the same story but with similar labs. Don't get dogmatic with your critical care.

Also, aspiration RARELY gives you a bacterial pneumonia.
Click to expand...

To get the osmotic diuresis in DKA you generally need sugars > 300. He's probably a type II though, and HHNK with sugars of 200 seems unlikely to me, especially when etoh ketoacidosis makes a lot more sense.

Agree most aspiration events cause pneumonitis not pneumonia, but in a homeless alcoholic with (likely) poor dentition and who's (probably) been altered for prolonged periods of time, I wouldn't be surprised if he has a true aspiration pneumonia. I'd want to know the LFTs and Coags so I could assess his liver function. He has scleral icterus. Liver failure can cause a primary respiratory alkalosis. It's also where lactate is cleared, so it might be contributing to his anion gap. If he has etoh hepatitis, that information is relevant to his care.
 
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wooster201106 said:
Damn, I got paged right as I was logging in and only had time to put likely etiology.

Overall, it was a nice example of a mixed, triple acid-base disorder and textbook case of AKA from presentation to w/u.

Although both present as an anion-gap and osmolar gap ketoacidosis, I think there were several clues in the labs which (aside from hx) leaned more towards AKA vs. DKA. The first as HarryGary already mentioned is the serum glucose, which while elevated is not markedly so, and is more compatible with a diagnosis of AKA though as jdh71 mentioned it could still have been DKA.

The second clue which can be useful in differentiating the two was the weakly positive serum ketones. The test is usually negative or weakly positive in AKA but has a much stronger reaction in DKA due to the type of ketone formation. The test reacts to acetoacetate which is the predominant ketone in DKA, but not much to beta-hydroxybutyrate which is predominant in AKA. Not exactly definitive but it can be quite useful.

Agree with jdh71 about LFTs. They are irrelevant as is serum ethanol level. Given the pt's hx, I would also want to be sure to r/o other differentials for AKA (e.g. methanol, ethylene glycol poisoning) at least with a U/A looking for crystals or serum levels, and especially considering the fact the guy is homeless and was found unconscious as management would differ from plain AKA with aspiration pneumonia.

As an aside, as I was logging out last time I saw a banner ad for the Heat vs. Pacers game tonight. Thought it was kinda weird to show up on SDN. Probably not the best use of ABC's ad dollars.

Thanks surge55 and jdh71 for posting the cases.
Click to expand...

I would say the serum ethanol level is relevant. As JDH mentioned he may have an osmolar gap. If you account for etoh in your osms gap and it is still elevated, the guy may have ingested something truly toxic, i.e. this is not simple run of the mill AKA. If so, he may need dialysis.
 
HarryGary said:
To get the osmotic diuresis in DKA you generally need sugars > 300.
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No you don't

He's probably a type II though, and HHNK with sugars of 200 seems unlikely to me, especially when etoh ketoacidosis makes a lot more sense.
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Why is he probably a "type II" based on what information?

This is a great example of why you need to keep your differential broad. This is the biggest problem I see in residents. They get married to a diagnosis and miss other possibilities.

I'd want to know the LFTs and Coags so I could assess his liver function. He has scleral icterus. Liver failure can cause a primary respiratory alkalosis. It's also where lactate is cleared, so it might be contributing to his anion gap. If he has etoh hepatitis, that information is relevant to his care.
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He has liver disease. Knowing the specifics of his LFTs or the coags here do not help you with the case here at all. While I tend agree its information that you will eventually need for his global care, it doesn't matter here.

What if the LFTs were stone cold normal, how would that change your answer to the question? What if they were 4 times normal? What if they were 10 times normal?
 
surge55 said:
http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(08)61398-7/fulltext

here's a good summary on newer high anion gap causes and a mnemonic

GOLD MARK. This acronym represents Glycols (ethylene and propylene), Oxoproline, L-lactate, D-lactate, Methanol, Aspirin, Renal failure, and Ketoacidosis.
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That letter was published the month I started med school, yet I've still had to endure countless "lessons" on acid-base disorders centered around a bastardized mnemonic describing causes of acidoses from the 1940's. Can someone explain to me why we're unable to update our teaching to the modern age?
 
turkeyjerky said:
That letter was published the month I started med school, yet I've still had to endure countless "lessons" on acid-base disorders centered around a bastardized mnemonic describing causes of acidoses from the 1940's. Can someone explain to me why we're unable to update our teaching to the modern age?
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mud piles bitch!!
 
JDH: No you don't


-- A healthy proximal tubule can usually reabsorb about 330 of glucose before it fails, so typically its sugars above 330 that lead to the osmotic diuresis. It is entirely possible that his proximal tubules are not healthy, so I agree it's possible he could could get an osmotic diuresis at a lower sugar level.



JDH: Why is he probably a "type II" based on what information?

-- I have no information to suggest this, but by odds, type II diabetes is far more common. I'd also guess that in a homeless man, who probably doesn't have access to insulin, and who's now sick, if he were type I his sugars would be higher. This is all just guessing and playing stereotypes and could be wrong. It's true, he could be a type I diabetic.


JDH: This is a great example of why you need to keep your differential broad. This is the biggest problem I see in residents. They get married to a diagnosis and miss other possibilities.

-- I agree, getting married to a diagnosis early is bad, and keeping a broad differential is good. I didn't get married to any diagnosis though, I just said dka seemed less likely. I think it's entirely appropriate for me to say which diagnosis seems more likely or less likely.


JDH: He has liver disease. Knowing the specifics of his LFTs or the coags here do not help you with the case here at all. While I tend agree its information that you will eventually need for his global care, it doesn't matter here.

What if the LFTs were stone cold normal, how would that change your answer to the question? What if they were 4 times normal? What if they were 10 times normal?

-- If his LFTs were 10 times normal and his INR elevated, that information would be relevant to calculating his discriminant function, and inform on my decision as to whether or not to start steroids. In regards to the acid base status, I was able to make a reasonable guess with the information given, which apparently was correct.
 
My fav mneumonic for AG acidosis is SLUMPED

Salicilates
Lactate
Uremia
Methanol
Paraldehyde (not seen anymore)
Ethylene Gycol
DKA (and AKA, or add that to "E" for EtOH Acidosis)

It's really no better than the other, except that these patients usually arrive "SLUMPED" to the ED.
 
HarryGary said:
If his LFTs were 10 times normal and his INR elevated, that information would be relevant to calculating his discriminant function, and inform on my decision as to whether or not to start steroids.
Click to expand...

Which still wasn't relevant to the question.

And I'd be careful with those roids in a guy who seems to have a pneumonia 😉
 
aProgDirector said:
My fav mneumonic for AG acidosis is SLUMPED

Salicilates
Lactate
Uremia
Methanol
Paraldehyde (not seen anymore)
Ethylene Gycol
DKA (and AKA, or add that to "E" for EtOH Acidosis)

It's really no better than the other, except that these patients usually arrive "SLUMPED" to the ED.
Click to expand...
Switch paraldehyde for propylene glycol.

Honestly, could someone explain to me why you guys insist on teaching stuff from the 50's?
 
turkeyjerky said:
Switch paraldehyde for propylene glycol.

Honestly, could someone explain to me why you guys insist on teaching stuff from the 50's?
Click to expand...


not sure; I was told about my mnemonic from my nephrologist preceptor.
 
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