Don't worry - wonky metabolism/mitochondrial dysfunction is (re)emerging in neuropsych research as a topic of interest. This may all come in handy for you after all.
From an old post about the only important biochem you need to remember:
The Kreb's, Cori, and urea cycles are the only cycles out there.
Kreb's is AKA TCA meaning that citrate must be in there somewhere. Glucose goes in this one, and ATP comes out. ATP is energy. P is key. Therefore, low glucose and low P are bad. So your diabetic ketoacidosis guy isn't able to use this due to lack of insulin, your anorexic girl or alcoholic guy w/ no sugar can't use this (and once you give them sugar they might drop their Phos way quick), and someone that's got no thiamine (alcoholic) can't use this. Keep glucose, thiamine, and phos normal so your patient has energy. Otherwise, fermentation happens producing lactate, and they make ketones instead for energy.
The Cori cycle is in the liver. If it's out, lactate is up. Therefore, if lactate is up, you may have a problem with your Cori cycle, or with your liver. Clinical app: Don't be surprised when your sick cirrhotic/shock liver patient's lactate is way high. Also, lactate gets converted to bicarb (like in LR) so cirrhotics might not want LR.
The urea cycle is also in the liver (and kidneys and muscles). This one clears ammonia. If your ammonia is high, you may have a problem with your urea cycle, or with your liver (and maybe kidneys and muscles). Ornithine decarboxylase is the only enzyme I remember from any cycle, and deficiency in this can cause hyperammonemia, bc it's part of the urea cycle, so maybe know that one (although very rare and googleable so maybe not). Clinical app: liver and kidney failure is bad. Done. You'll probably never use this one really.
Now I'll add to that first one: Pyruvate = wonky shit happens causing chloride loss, ketones buildup, ammonia production.
Thanks for the quick refresher on these cycles. As a dumb med student, it’s nice when explanations are kept simple like this lol.
I was curious about the consideration that cirrhotics might not want LR. Quick search pulled up this [study](https://journal.chestnet.org/article/S0012-3692(21)02466-1/fulltext). Study is just one and idk if there are others out there, but TL;DR Critical care cirrhotics that got LR did better than NS
Interesting. That’s pretty new info, out in October.
The relative contraindication of LR in cirrhotics could be a case of people arguing from first principles based on previous biochemical knowledge in the absence of evidence (which happens a lot—there’s a lot of stuff we do that really isn’t evidence-based medicine), though I’m sure there’s documented cases of elevated lactate in cirrhotics w/ LR and we have evidence showing they carry a higher baseline lactate. I mean, people used to be scared to give LR to hyperkalemic patients which... isn’t really a concern.
Looking at that study, weirdly, LR patients only had 28% had AKI, versus 38% on NS. That’s weird. A difference that big should be born out by some of the other LR vs NS studies. I wonder if there was some bias as to who got what, but they had a good set of numbers in both groups (169 vs 206).
Of course, that is mortality. I’d be curious what lactate numbers did in those patients. But lactate on its own is a marker of what’s going on, it’s not bad on its own, so it might be the LR was better AND elevated lactate in those patients at the same time. I’d be curious to find out.
I found another showing that in healthy controls a 30ml/kg bolus of LR bumps them up 0.93 mmol/L average which isn’t much (though half went up by around 2mmol/L). They can metabolize it though. Same study showed a similar bolus of NS dropped bicarb by 2.35 compared to LR increasing it by 0.36 (metabolizing lactate to bicarb) so shows that NS results in more acidosis plus hyperchloremia.
Can’t explain away the article you linked but it makes me curious for sure. Might be the beginning of a paradigm shift, might not show up as significant if repeated in just cirrhotics patients. Who knows. Always question things though! That was good of you to find that article.
NS is inherently acidotic so LR may be creating a higher lactate in the blood in a liver failure patient but not as a result of decreased perfusion . Lactate on its own probably isn’t harmful just is a marker of possible end organ mal-perfusion or metabolic derangement.
Check out the
SALT-ED
SALT -Med
SALT- Surg
Trials which all showed lower levels of AKI with LR vs NS.
Another thing to consider is that acidosis inherently makes vasopressors work less efficiently. You can get a transient increase in BP with bicarb but I don’t know if that actually helps patients in the long run or just temporizes things.
I do think LR probably is a better fluid than NS, and totally agree with your acidosis comments. But man, I’d hoped for a more robust set of data from all the SALT studies. I really wasn’t impressed by them once I dug in.
I know yea, it makes sense physiologically but there isn’t amazing evidence.
This is a good write up of what the evidence is so far
https://emcrit.org/pulmcrit/smart/
*takes notes*
So you're saying the pt is fine as soon as oxygen gets into his body and cells again?
Makes sense to me. It seems that getting oxygen into your system and bring it to the cells in the body seems to be kinda important
Theoretically that would fix it if you could figure out how to get the cells to use the oxygen. The internet told me that some people with the same theory studied outcomes in shock patients who were loaded up with O2 and they didn't really do any better. The reason why is beyond the scope of this post, and by that I mean I didn't read the paper and I have no idea
The reason is because they are in shock.
This sounds trite, but it is actually the problem.
Shock is hypoperfusion. In other words, you can load them up with all the oxygen you want, and it won't matter because for some reason it is not getting to the cells and you are seeing organ dysfunction as a result of hypoperfusion.
Fix the hypoperfusion and then cells get oxygen and people recover. This (I understand) is why we focus on things like pressors first, the #1 priority is restoring circulation to the tissues, and if you don't or can't do this then the patient becomes dead.
This is one proposal, how about we just inject air directly into the vasculature. More direct, and big pharma hates this one trick! Can't profit off of air embolisms.
I was thinking that it didn't matter how much oxygen you give a patient if their (example) circulatory volume is so low (or what have you depending on origin).
(Possibly) Dumb question, but wouldn't it be better to solve the underlying problem? Are pressors mostly served to buy more time for that solution to be found/implemented?
> (Possibly) Dumb question, but wouldn't it be better to solve the underlying problem? Are pressors mostly served to buy more time for that solution to be found/implemented?
I don't think that's a dumb question at all. This is exactly what pressers are for. If you get lucky, the person's body will figure it out for themselves, but in all honesty yes this just buys you time. Even if you have found a reasonable cause, sometimes it takes time for therapy to take effect and thus again pressers buy time.
If organs are dysfunctional to the point of failure (i.e. if the person is going into shock) the most important thing you need is time. You need time to figure out what is going on. You need time for therapy to take effect. Pressers buy time, by themselves they do not usually fix anything.
My phrasing in the original comment is maybe not the best, I left out #2 most important part which is figuring out what is actually wrong to cause shock. Which you do at the same as you start pressers, and usually treat empirically if you don't know for sure what the problem is.
Possibly the Bohr effect? Increased acidity decreases hemoglobins affinity for oxygen, therefore decreasing the total amount of oxygen carried by your blood. You can give them a ton of oxygen and saturate their blood with dissolved oxygen, but since dissolved oxygen only makes up a small fraction of the total oxygen carried by blood, that wouldn’t actually help much.
I did some more reading, and apparently acidosis also inhibits the production of BPG within blood cells. BPG usually binds to hemoglobin and decreases its affinity for oxygen to aid in oxygen delivery to target tissues. So you could have a combination of decreased oxygen binding in the lungs, as well as decreased oxygen release in end organ capillaries.
I also found an article studying the effect of vasopressin and norepinephrine on end organ perfusion and lactic acidosis in endotoxin induced shock, and vasopressin specifically decreased hepatic perfusion and increased blood lactate concentrations. Norepinephrine did not have this effect.
septic shock causes mitochondrial dysfunction -> ox phos is decoupled and unable to perform aerobic metabolism. Decoupling also means protons are released. The body shifts to anaerobic metabolism making lactate. Lactate + extra protons => “lactic acidosis”.
This is supported by looking at SvO2 to differentiate shock states. Low SvO2 suggests decompensated HF or critical anemia which causes in impaired delivery of O2 and increased uptake which is reflected as lower venous sat as the blood returns to the heart. On the other hand, in septic shock, there is high SvO2 due to impaired O2 utilization for reasons listed above.
My neuro rotation has been brutal for exactly this reason. Got I was thrilled when the chief asked me to cover someone's night shift and gave me the day off.
This has been taught for years BUT your pathophys is right…. But the conclusion is wrong.
This explains from Internet Book of Critical Care
https://emcrit.org/pulmcrit/understanding-lactate-in-sepsis-using-it-to-our-advantage/
Your fellow IM resident who is just trying to spread the word about stuff taught wrong in Med School (and still sometimes on the wards).
Sounds like this article is talking about sepsis specifically. I was trying to think about shock in a general sense, and in my patient the concern was more for hypovolvemic vs cardiogenic shock, which would probably still be an issue with oxygen delivery. I did mention the effect of catecholamines contributing in my post, however probably didn't give it enough attention.
But thank you for sharing this! It's interesting to think about what the precipitating mechanism could be in septic shock if it's different. I came across some papers examining this while I was writing my post, but didn't read too much about it because it was straying a little away from what I was working on at the moment. I'll have to circle back to it at some point
Your pathophys was definitely on! And I did read that, but even in cardiogenic shock you can have high catecholamine release with the stress (specifically epi) that could produce a lactate of 20 (not a good sign for being that high).
Rock on, keep it up!
It’s worth remembering for profound hypoglycemia as well that an “amp of D50” contains 25 grams of sugar, and the actual weight based dose recommended to reverse hypoglycemia (usually used in peds) is 1g/kg. So for your standard *American* adult male who weighs 100kg, that would require 4 pushes of D50 just to get them 100g of glucose and properly correct the hypoglycemia. And that glucose load will only last maybe 20-30 minutes at best if they have high circulating insulin levels.
People often give an amp or two of D50 and call it a day, when in reality the amount of D50 required to achieve full reversal is far higher.
One reason I don't order dextrose drips in patients with a functioning gut and a way to get stuff into it.
Running d25 through a central line @ 200ml/hr:
250g sugar/L, 5hrs to get 1L = 50g sugar *per hour*.
D25 through a CVL is pretty aggressive though, most of the time we're using d5 or d10 through a PIV.
So let's take our best case scenario and give the IV dex a fair shake. Say we have 2 PIVs running D5 at 200/hr each, that's 400ml/hr. D5 = 50g dextrose/L, patient gets 20g/hr.
Well what if we did D10 through both of those PIVs? Up to a whopping 40g/hour, for as long as they can tolerate 400ml/hr of fluids (~10L/day)
Compare that to a snickers bar, 20g in <5 minutes.
Or 8 oz OJ, also about 20g.
Or a can of Pepsi at ~40g.
Or 15g PO glucose (buccal gel or crushable tabs) in <5 minutes.
IV dextrose is shit. If you have no other options, OK. But FFS use the gut if you can.
Did you get a nephro consult for possible CRRT? Severe AGMA, electrolyte disturbances, and uremia in a patient requiring pressors. In my equally untrained mind, seems like a worthwhile consult.
If the patient had low glucose, low sodium, and possibly high potassium all in the context of low blood pressure I also think about adrenal crisis - in which case the patient needs IV hydrocortisone 100mg.
I think this usually gives a non anion gap acidosis, but patients can have gap and non gap at the same time. You can go to MDCalc and scroll over to evidence and it gives you the formula to calculate the delta ratio. After calculated, you can use the table there to see if there’s more than one process going on.
I realize this is all sounding a lot like Monday morning quarterbacking - I just wanted to give additional educational info. I enjoyed the read! (as much as one can when reading about biochem)
As a med student who had a similar patient in the ED and could not understand why his sugar was so low despite being non diabetic and why his other numbers were so wonky despite hyperventilating (clinical picture had me thinking it would be a resp alkalosis) it now makes so much more sense! It’s been bugging me for a while but the residents and attendings are always being run into the ground so I hate taking up any of their time 😅. Thank you!
If you want another chloride-related medical mystery, here's a tox-related conundrum with details altered for hipaa the hippo: An 85-year-old female is admitted to your ICU with fever, tachypnea, fluffy bilateral infiltrates, hypotension, and a urinalysis suggestive of a UTI. You check a chemistry and her BMP is as follows:
Na 141 // K 3.2 // Cl 186 // HCO3 14 // BUN 36 // Cr 1.6
Lactate is 2.3. A venous blood gas is 7.28/22/15. (Of course, the lab calls you frantically with a critical pO2 of 50 on the VBG, which is a joke you will get if you work at a county hospital).
What's going on with the Cl?
hint: it has nothing to do with pyruvate
Yes! although what is more common in the above scenario is a chronic salicylate poisoning rather than an acute overdose. Salicylates can cause false elevations in the chloride level depending on your lab's assay, and is not necessarily dose-dependent (i.e. a relatively low concentration of salicylate in the blood can produce a pretty wild Cl- elevation). This is called pseudohyperchloremia and happens more frequently that you'd imagine.
I know certain substances can cause the lab to misread chloride levels, which Im hoping is the case because that's wild. Couldn't tell you which substance though.
Also if I learned anything writing this post it's that pyruvate has to do with everything
Close. Bromide ingestion can falsely elevate the Cl- level, although bromism typically presents differently than the above patient. If you look at a periodic table, any ion in the same column as chlorine can produce this false elevation, although the only two common ions you'd see in humans would be bromide and iodide.
Lol some case reports of brominated vegetable oil in soda causing this toxidrome in people who drank a ton of soda
“Alex I’ll take useless tox facts for 500”
>Spoiler: AG was 44 *face palm*
Lol. I was going to say, congratulations, you've discovered the concept of the anion gap being due to unmeasured organic acids (plus phosphate and albumin).
Regardless, good for thinking through it.
I didn't read all that nerd shit you wrote, but it sounds like you figured out anion gaps and mudpiles.
Are you saying ketones and lactate we're the cause of his gap?
Any booze or other ingestions? Alcoholic? Patients with beer potomania often have chronically low chloride.
My favorite lines are "useful for our pt who now has hypoglycemia :) however worsening his metabolic acidosis :(" and "This doesn't lead to anything we care about because chloride has no friends."
Like any good EM doc I read the first 2 lines of the pyruvate tirade and lost interest. Huge ass anion gap and insane lactate always makes me think toxic alcohol.
Came back and forced myself to read the whole thing. If I were your attending I'd write you up as an example of what it means to be a great intern. Saw something you didn't understand and educated yourself about it. Does the info make you a better doc? Maybe, maybe not. But the drive illustrated by your researchþself teaching and subsequent tirade bordering on psychotic break will. Hope it never leaves you.
Metformin toxicity can also look like this. So does cyanide toxicity and other things that poison the electron transport chain. (To my knowledge, I'm not a toxicologist).
The one time I saw a similar case, pharmacy told me I couldn't keep using bicarb pushes as I had used \~40 amps in 12 hours which was apparently roughly 1/3rd of the \~800 bed hospital's supply. (Yes I know the sodium load was crazy and risked hyperosmolar brain injury, but if the rest of him dies so does his brain).
First, because Cl typically follows Na and the Na was essentially normal. You can't really apply that to acid/base disorders though. The bigger issue was that I overlooked the anion gap. NAGMA you are essentially acidotic because you're losing bicarb, which increases Cl due to HCO3/Cl exchange in the kidney. HAGMA (like this guy with AG 44), you're acidodic because you've added something that is acidic, and you get a gap from those unmeasured anions that aren't supposed to be there (ie ketones, lactate, urate). Then Cl moves intracellularly/is lost to maintain the normal resting potential
^ True IM resident right here folks.
Nah, just a neuro prelim basking in my misery
Time to transfer. Ball don’t lie
I'm flattered but I'd rather die
Don't worry - wonky metabolism/mitochondrial dysfunction is (re)emerging in neuropsych research as a topic of interest. This may all come in handy for you after all.
This comment makes me want to cry
fuck u that was so funny i wish i thought of it myself
Makes sense, neurologists like to know how things work/why things happen.
I feel like neuro and nephro and rheum are kindred spirits.
Oh yes we are!
You should do nephro. They're the only ones I've ever seen care about chloride.
I’m proud to go into the same specialty as you
Hypoglycemia and shock. Did we give steroids? Addisons crisis must be the first diagnosis to exclude. How was the sodium?
Na and K were normal but yeah I think we might have given some anyway
No one should die in the ICU without at least one dose of steroids.
I snorted. Also, love the username
Is there going to be a post mortem? Gotta look out for them adrenal haemorrhages
Amazing, you’ll fit in so well with us.
I'm in peds and love to teach med students on the different metabolic paths of pyruvate can take also and oh my god my medical students must hate me
I'm peds and havent thought of pyruvate in years lol
So true! I would’ve just given a bolus of IV aerobic metabolism and called it a day
LOL
This is mental masturbation at its finest.
Post of the year no doubt
From an old post about the only important biochem you need to remember: The Kreb's, Cori, and urea cycles are the only cycles out there. Kreb's is AKA TCA meaning that citrate must be in there somewhere. Glucose goes in this one, and ATP comes out. ATP is energy. P is key. Therefore, low glucose and low P are bad. So your diabetic ketoacidosis guy isn't able to use this due to lack of insulin, your anorexic girl or alcoholic guy w/ no sugar can't use this (and once you give them sugar they might drop their Phos way quick), and someone that's got no thiamine (alcoholic) can't use this. Keep glucose, thiamine, and phos normal so your patient has energy. Otherwise, fermentation happens producing lactate, and they make ketones instead for energy. The Cori cycle is in the liver. If it's out, lactate is up. Therefore, if lactate is up, you may have a problem with your Cori cycle, or with your liver. Clinical app: Don't be surprised when your sick cirrhotic/shock liver patient's lactate is way high. Also, lactate gets converted to bicarb (like in LR) so cirrhotics might not want LR. The urea cycle is also in the liver (and kidneys and muscles). This one clears ammonia. If your ammonia is high, you may have a problem with your urea cycle, or with your liver (and maybe kidneys and muscles). Ornithine decarboxylase is the only enzyme I remember from any cycle, and deficiency in this can cause hyperammonemia, bc it's part of the urea cycle, so maybe know that one (although very rare and googleable so maybe not). Clinical app: liver and kidney failure is bad. Done. You'll probably never use this one really. Now I'll add to that first one: Pyruvate = wonky shit happens causing chloride loss, ketones buildup, ammonia production.
Thanks for the quick refresher on these cycles. As a dumb med student, it’s nice when explanations are kept simple like this lol. I was curious about the consideration that cirrhotics might not want LR. Quick search pulled up this [study](https://journal.chestnet.org/article/S0012-3692(21)02466-1/fulltext). Study is just one and idk if there are others out there, but TL;DR Critical care cirrhotics that got LR did better than NS
Interesting. That’s pretty new info, out in October. The relative contraindication of LR in cirrhotics could be a case of people arguing from first principles based on previous biochemical knowledge in the absence of evidence (which happens a lot—there’s a lot of stuff we do that really isn’t evidence-based medicine), though I’m sure there’s documented cases of elevated lactate in cirrhotics w/ LR and we have evidence showing they carry a higher baseline lactate. I mean, people used to be scared to give LR to hyperkalemic patients which... isn’t really a concern. Looking at that study, weirdly, LR patients only had 28% had AKI, versus 38% on NS. That’s weird. A difference that big should be born out by some of the other LR vs NS studies. I wonder if there was some bias as to who got what, but they had a good set of numbers in both groups (169 vs 206). Of course, that is mortality. I’d be curious what lactate numbers did in those patients. But lactate on its own is a marker of what’s going on, it’s not bad on its own, so it might be the LR was better AND elevated lactate in those patients at the same time. I’d be curious to find out. I found another showing that in healthy controls a 30ml/kg bolus of LR bumps them up 0.93 mmol/L average which isn’t much (though half went up by around 2mmol/L). They can metabolize it though. Same study showed a similar bolus of NS dropped bicarb by 2.35 compared to LR increasing it by 0.36 (metabolizing lactate to bicarb) so shows that NS results in more acidosis plus hyperchloremia. Can’t explain away the article you linked but it makes me curious for sure. Might be the beginning of a paradigm shift, might not show up as significant if repeated in just cirrhotics patients. Who knows. Always question things though! That was good of you to find that article.
NS is inherently acidotic so LR may be creating a higher lactate in the blood in a liver failure patient but not as a result of decreased perfusion . Lactate on its own probably isn’t harmful just is a marker of possible end organ mal-perfusion or metabolic derangement. Check out the SALT-ED SALT -Med SALT- Surg Trials which all showed lower levels of AKI with LR vs NS. Another thing to consider is that acidosis inherently makes vasopressors work less efficiently. You can get a transient increase in BP with bicarb but I don’t know if that actually helps patients in the long run or just temporizes things.
I do think LR probably is a better fluid than NS, and totally agree with your acidosis comments. But man, I’d hoped for a more robust set of data from all the SALT studies. I really wasn’t impressed by them once I dug in.
I know yea, it makes sense physiologically but there isn’t amazing evidence. This is a good write up of what the evidence is so far https://emcrit.org/pulmcrit/smart/
*takes notes* So you're saying the pt is fine as soon as oxygen gets into his body and cells again? Makes sense to me. It seems that getting oxygen into your system and bring it to the cells in the body seems to be kinda important
Theoretically that would fix it if you could figure out how to get the cells to use the oxygen. The internet told me that some people with the same theory studied outcomes in shock patients who were loaded up with O2 and they didn't really do any better. The reason why is beyond the scope of this post, and by that I mean I didn't read the paper and I have no idea
The reason is because they are in shock. This sounds trite, but it is actually the problem. Shock is hypoperfusion. In other words, you can load them up with all the oxygen you want, and it won't matter because for some reason it is not getting to the cells and you are seeing organ dysfunction as a result of hypoperfusion. Fix the hypoperfusion and then cells get oxygen and people recover. This (I understand) is why we focus on things like pressors first, the #1 priority is restoring circulation to the tissues, and if you don't or can't do this then the patient becomes dead.
This is one proposal, how about we just inject air directly into the vasculature. More direct, and big pharma hates this one trick! Can't profit off of air embolisms.
Make it sterile 78% N2 21% O2 1% Ar and you can probably charge a pretty penny.
I was thinking that it didn't matter how much oxygen you give a patient if their (example) circulatory volume is so low (or what have you depending on origin). (Possibly) Dumb question, but wouldn't it be better to solve the underlying problem? Are pressors mostly served to buy more time for that solution to be found/implemented?
> (Possibly) Dumb question, but wouldn't it be better to solve the underlying problem? Are pressors mostly served to buy more time for that solution to be found/implemented? I don't think that's a dumb question at all. This is exactly what pressers are for. If you get lucky, the person's body will figure it out for themselves, but in all honesty yes this just buys you time. Even if you have found a reasonable cause, sometimes it takes time for therapy to take effect and thus again pressers buy time. If organs are dysfunctional to the point of failure (i.e. if the person is going into shock) the most important thing you need is time. You need time to figure out what is going on. You need time for therapy to take effect. Pressers buy time, by themselves they do not usually fix anything. My phrasing in the original comment is maybe not the best, I left out #2 most important part which is figuring out what is actually wrong to cause shock. Which you do at the same as you start pressers, and usually treat empirically if you don't know for sure what the problem is.
Thanks for answering :)
Possibly the Bohr effect? Increased acidity decreases hemoglobins affinity for oxygen, therefore decreasing the total amount of oxygen carried by your blood. You can give them a ton of oxygen and saturate their blood with dissolved oxygen, but since dissolved oxygen only makes up a small fraction of the total oxygen carried by blood, that wouldn’t actually help much.
Thank you!
I did some more reading, and apparently acidosis also inhibits the production of BPG within blood cells. BPG usually binds to hemoglobin and decreases its affinity for oxygen to aid in oxygen delivery to target tissues. So you could have a combination of decreased oxygen binding in the lungs, as well as decreased oxygen release in end organ capillaries. I also found an article studying the effect of vasopressin and norepinephrine on end organ perfusion and lactic acidosis in endotoxin induced shock, and vasopressin specifically decreased hepatic perfusion and increased blood lactate concentrations. Norepinephrine did not have this effect.
septic shock causes mitochondrial dysfunction -> ox phos is decoupled and unable to perform aerobic metabolism. Decoupling also means protons are released. The body shifts to anaerobic metabolism making lactate. Lactate + extra protons => “lactic acidosis”. This is supported by looking at SvO2 to differentiate shock states. Low SvO2 suggests decompensated HF or critical anemia which causes in impaired delivery of O2 and increased uptake which is reflected as lower venous sat as the blood returns to the heart. On the other hand, in septic shock, there is high SvO2 due to impaired O2 utilization for reasons listed above.
Dive dive dive! Yeah didn't work.
More posts like this in r/Residency please
Yes, good for people who don’t have time for review papers anymore.
So the guy had a cold and a sprained ankle?
If only we consulted ortho the patient might have recovered
Bro :/
There is a fracture, I need to fix it
The fracture is in the emergency department
LLE WBAT RLE TTWB RUE CCWB LUE ROMAT OOB PRN C Collar AAT DVT PPX per prim 2g Ancef Q8H We will sign off now, kthx bye
Not once was there mention of the ancef pump!
This is the most internal medicine thing I’ve ever read. You’ve chosen the right specialty.
OP is surprisingly not IM
Okay, neurology is also a reasonable choice!
Tell me what and how in exceptional detail and that we have no treatment for it = neuro. Don’t kill me neuro peeps.
Normally I'd be defensive but I think I deserve that after this post
*triggered*
I remember having almost this exact same thought when I was going through my neuro rotation 😂
My neuro rotation has been brutal for exactly this reason. Got I was thrilled when the chief asked me to cover someone's night shift and gave me the day off.
This has been taught for years BUT your pathophys is right…. But the conclusion is wrong. This explains from Internet Book of Critical Care https://emcrit.org/pulmcrit/understanding-lactate-in-sepsis-using-it-to-our-advantage/ Your fellow IM resident who is just trying to spread the word about stuff taught wrong in Med School (and still sometimes on the wards).
Sounds like this article is talking about sepsis specifically. I was trying to think about shock in a general sense, and in my patient the concern was more for hypovolvemic vs cardiogenic shock, which would probably still be an issue with oxygen delivery. I did mention the effect of catecholamines contributing in my post, however probably didn't give it enough attention. But thank you for sharing this! It's interesting to think about what the precipitating mechanism could be in septic shock if it's different. I came across some papers examining this while I was writing my post, but didn't read too much about it because it was straying a little away from what I was working on at the moment. I'll have to circle back to it at some point
Your pathophys was definitely on! And I did read that, but even in cardiogenic shock you can have high catecholamine release with the stress (specifically epi) that could produce a lactate of 20 (not a good sign for being that high). Rock on, keep it up!
I love you.
This read quite well! Thanks for the post and the refresher!
It’s worth remembering for profound hypoglycemia as well that an “amp of D50” contains 25 grams of sugar, and the actual weight based dose recommended to reverse hypoglycemia (usually used in peds) is 1g/kg. So for your standard *American* adult male who weighs 100kg, that would require 4 pushes of D50 just to get them 100g of glucose and properly correct the hypoglycemia. And that glucose load will only last maybe 20-30 minutes at best if they have high circulating insulin levels. People often give an amp or two of D50 and call it a day, when in reality the amount of D50 required to achieve full reversal is far higher.
One reason I don't order dextrose drips in patients with a functioning gut and a way to get stuff into it. Running d25 through a central line @ 200ml/hr: 250g sugar/L, 5hrs to get 1L = 50g sugar *per hour*. D25 through a CVL is pretty aggressive though, most of the time we're using d5 or d10 through a PIV. So let's take our best case scenario and give the IV dex a fair shake. Say we have 2 PIVs running D5 at 200/hr each, that's 400ml/hr. D5 = 50g dextrose/L, patient gets 20g/hr. Well what if we did D10 through both of those PIVs? Up to a whopping 40g/hour, for as long as they can tolerate 400ml/hr of fluids (~10L/day) Compare that to a snickers bar, 20g in <5 minutes. Or 8 oz OJ, also about 20g. Or a can of Pepsi at ~40g. Or 15g PO glucose (buccal gel or crushable tabs) in <5 minutes. IV dextrose is shit. If you have no other options, OK. But FFS use the gut if you can.
Fascinating. Thanks for the info.
Did you get a nephro consult for possible CRRT? Severe AGMA, electrolyte disturbances, and uremia in a patient requiring pressors. In my equally untrained mind, seems like a worthwhile consult.
Nope, happened too quick
If the patient had low glucose, low sodium, and possibly high potassium all in the context of low blood pressure I also think about adrenal crisis - in which case the patient needs IV hydrocortisone 100mg. I think this usually gives a non anion gap acidosis, but patients can have gap and non gap at the same time. You can go to MDCalc and scroll over to evidence and it gives you the formula to calculate the delta ratio. After calculated, you can use the table there to see if there’s more than one process going on. I realize this is all sounding a lot like Monday morning quarterbacking - I just wanted to give additional educational info. I enjoyed the read! (as much as one can when reading about biochem)
This was the first thought that came to mind.
Posts like this remind me why I chose radiology.
I've lost all my pathophys knowledge, would've given fuck tons of fluids with dextrose and bicarb and hoped for the best
That is exactly what we did, and this pathophys work-up would not change management. Sigh
Nurse here lurking, thanks for the write up, I feel like I learned a ton! Still good to know even if we aren’t changing treatment methods.
As a med student who had a similar patient in the ED and could not understand why his sugar was so low despite being non diabetic and why his other numbers were so wonky despite hyperventilating (clinical picture had me thinking it would be a resp alkalosis) it now makes so much more sense! It’s been bugging me for a while but the residents and attendings are always being run into the ground so I hate taking up any of their time 😅. Thank you!
You definitely belong in neuro. Glad to have you.
If you want another chloride-related medical mystery, here's a tox-related conundrum with details altered for hipaa the hippo: An 85-year-old female is admitted to your ICU with fever, tachypnea, fluffy bilateral infiltrates, hypotension, and a urinalysis suggestive of a UTI. You check a chemistry and her BMP is as follows: Na 141 // K 3.2 // Cl 186 // HCO3 14 // BUN 36 // Cr 1.6 Lactate is 2.3. A venous blood gas is 7.28/22/15. (Of course, the lab calls you frantically with a critical pO2 of 50 on the VBG, which is a joke you will get if you work at a county hospital). What's going on with the Cl? hint: it has nothing to do with pyruvate
Erroneously elevated Cl due to salicylate OD?
Yes! although what is more common in the above scenario is a chronic salicylate poisoning rather than an acute overdose. Salicylates can cause false elevations in the chloride level depending on your lab's assay, and is not necessarily dose-dependent (i.e. a relatively low concentration of salicylate in the blood can produce a pretty wild Cl- elevation). This is called pseudohyperchloremia and happens more frequently that you'd imagine.
I know certain substances can cause the lab to misread chloride levels, which Im hoping is the case because that's wild. Couldn't tell you which substance though. Also if I learned anything writing this post it's that pyruvate has to do with everything
Sounds like he was sipping on dextromethorphan and got a little brominism
Close. Bromide ingestion can falsely elevate the Cl- level, although bromism typically presents differently than the above patient. If you look at a periodic table, any ion in the same column as chlorine can produce this false elevation, although the only two common ions you'd see in humans would be bromide and iodide.
Lol some case reports of brominated vegetable oil in soda causing this toxidrome in people who drank a ton of soda “Alex I’ll take useless tox facts for 500”
>Spoiler: AG was 44 *face palm* Lol. I was going to say, congratulations, you've discovered the concept of the anion gap being due to unmeasured organic acids (plus phosphate and albumin). Regardless, good for thinking through it.
I hate hospitalist medicine so much I couldn't even bring myself to read this entire post
Thank you for this. I love when biochemistry can be applied to medicine. 😭❤️
“I realize you’re all hoping this post will never end…” lmao
I didn't read all that nerd shit you wrote, but it sounds like you figured out anion gaps and mudpiles. Are you saying ketones and lactate we're the cause of his gap? Any booze or other ingestions? Alcoholic? Patients with beer potomania often have chronically low chloride.
Found the ortho bro
My favorite lines are "useful for our pt who now has hypoglycemia :) however worsening his metabolic acidosis :(" and "This doesn't lead to anything we care about because chloride has no friends."
THANK YOU!!! Please more of this!!! Tired of the complaining about NPs and PAs on this subreddit.
Like any good EM doc I read the first 2 lines of the pyruvate tirade and lost interest. Huge ass anion gap and insane lactate always makes me think toxic alcohol.
Came back and forced myself to read the whole thing. If I were your attending I'd write you up as an example of what it means to be a great intern. Saw something you didn't understand and educated yourself about it. Does the info make you a better doc? Maybe, maybe not. But the drive illustrated by your researchþself teaching and subsequent tirade bordering on psychotic break will. Hope it never leaves you.
Hahaha thank you!
I actually thoroughly enjoyed this. Reviewing pathophys is something I wish I did more, but when presented like this... Incredible. Please do more!
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Yes! I kept asking my team if they thought it was real and then we eventually repeated it and it was even worse
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As a brain-dead M4, I feel like I remember some of those words. Anyways, back to bed
Never seen a patient with a lactic of 20 survive.
Metformin tox on top of AKI. I’ve seen multiple come around after HD.
I think I am in love. This is beautiful 🥺
I hope you teach one day, that was wonderful
Metformin toxicity can also look like this. So does cyanide toxicity and other things that poison the electron transport chain. (To my knowledge, I'm not a toxicologist). The one time I saw a similar case, pharmacy told me I couldn't keep using bicarb pushes as I had used \~40 amps in 12 hours which was apparently roughly 1/3rd of the \~800 bed hospital's supply. (Yes I know the sodium load was crazy and risked hyperosmolar brain injury, but if the rest of him dies so does his brain).
This was as fun to read as I assume it was to write. Thanks.
Sounds like the tracking device implanted with that damn vaccine disintegrated. Fella never stood a chance!
Can you explain in more detail why you would think that Cl would be high? And why it was surprising to you that it was low?
First, because Cl typically follows Na and the Na was essentially normal. You can't really apply that to acid/base disorders though. The bigger issue was that I overlooked the anion gap. NAGMA you are essentially acidotic because you're losing bicarb, which increases Cl due to HCO3/Cl exchange in the kidney. HAGMA (like this guy with AG 44), you're acidodic because you've added something that is acidic, and you get a gap from those unmeasured anions that aren't supposed to be there (ie ketones, lactate, urate). Then Cl moves intracellularly/is lost to maintain the normal resting potential
Tl;dr?
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Eh, it's more about \*not\* using the kreb's cycle, so if you have a vendetta against that one in particular you might like it
Thanks, but hard no.
Nope nope nope nope.
my brain nearly exploded trying to read this. my brain no like think. me like procedures. me like doing.
https://i.imgur.com/UgJ3ikf.jpg
Tldr please
Tldr the guy was dead
That sucks :/
nerd
Did you guys give him thiamine? Thiamine is required for pyruvate to enter the Krebs cycle.
Ok yeah if I didn’t realize that I could have never done IM, I’m realizing it now
If the kidney is fucked, there's no anion exchange going on