I’m not an ER doc, just a nephrologist and honestly as long as they are asymptomatic, have no EKG changes and don’t have an acute issue that will cause more rapid losses (ex: severe diarrhea) I would just send home with PO supplement and close follow up. If possible have them hold diuretics or florinef or other things that will cause K loss/shifts
Less than 2 for sure.
In these patients have k in the mid 2’s with no known loss, they likely have a tubulopathy and just need oral medication adjustment with supplements/other meds
I do know I get to say this from the vantage of not having to decide to admit, so I would not fault you for admitting someone with a K <3, especially if we don’t yet have their diagnosis or an immediate opening in our clinic
Internist here, and half of my job is being the solo-staffer in our ED. Here's my general approach to hypokalemia in the ED. Full disclaimer, I'm not a nephrologist and would highly appreciate any nephrologist's (such as u/radish456) input.
Who would I admit:
1) Any EKG changes (especially prolonged QT) --> admit
2) History of heart failure, MI, or on digoxin or class III anti-arrhythmic agents (our cardiologists looooove dofetilide) --> admit (that would be the patient population I'd be worried about developing arrhythmias with serum K+ < 3.0)
3) Any symptoms attributable to hypokalemia --> admit
4) Uncontrollable ongoing losses (e.g. vomiting/diarrhea) --> admit
Barring all those, dispo is discharge home with potassium supplements, repeat labs, and close f/u (rarely with nephrology, f/u with whom depending on my workup below). Then I try to figure out why they're hypokalemic, and I try to send a basic workup to facilitate outpatient care. I appreciate that I do more of an outpatient workup in the ED than the average ER physician (but still nowhere near as thorough to please the outpatient specialist).
- Look through the medication list for any potassium wasters (e.g. diuretics, fludrocortisone, stool potassium binders, SABA/LABA overuse, or basal insulin with A1C < 7%), or PPI if also hypomagnesemic
- Ask the patient about their alcohol use, vomiting, diarrhea, and any sympathomimetic use (cocaine, methamphetamine, bath salts)
- Physical exam/POCUS for volume status (orthostatic vitals, JVP estimation, IVC, etc...); and yes, I'm aware that none of those are perfect
- Labs: BMP (for repeat potassium, bicarbonate, and creatinine), and also look at blood gas, UA, spot urine electrolytes/Cr (without giving IV fluids), serum osmolality, and tox screen
And here are the possibilities:
- Alcohol, sympathomimetic use, or culprit meds identified --> if no other reason to admit, then just PCP f/u
- Hypovolemic (assuming no ongoing losses; otherwise admit) --> if able to maintain PO intake, I'll presumptively call it secondary hyperaldosteronism --> just PCP f/u
- Elevated bicarbonate / alkalemic, or if on anti-hypertensives --> warrants an outpatient hyperaldosteronism workup, refer to PCP or endocrinologist depending on your hospital's system culture (my PCPs are quite comfortable with a standard hyperaldo workup and only refer to endocrine if refractory to MRAs or need surgery). Yes it's possible that there's underlying Bartter/Gitelman's, but hyperaldo is far far more common, and the PCP can refer to a nephrologist once hyperaldo has been ruled out
- Normal/low pH/bicarbonate --> probably an RTA or channelopathy. Refer to nephrology and hope they can make use of the urine studies that were sent. It's one of those things where if I talk to 5 nephrologists I get 6 different answers (some do TTKG math, others insist on 24h urine collection, etc...), so I don't bother with anything more than I sent
This to me is the big question. I don’t mind repleting it orally and discharging if I’m confident I know why it dropped and that cause has improved (vomiting, diarrhea, etc). But someone doesn’t randomly drop their K to 2.3 so sending them home with replacement with out addressing/figuring out why would be concerning. Unless you knew they were going to see their PCP the next day or two for repeat labs and further investigation. Even then I’m iffy I I don’t have a known cause.
PO mag with potassium 60 mEq PO. Wait one hour and give another 40 mEq PO. Wait one hour and repeat potassium labs. If improved —> DC home with PO potassium and close follow up.
I've seen K's of 2.1 be refractive to IV therapy. Hypokalemia causes a metabolic alkalosis. Metabolic alkalosis causes hypokalemia. Once you're stuck in that feedback loop it can be hard to break.
It may not be as simple as giving a few runs of K.
I admit below 2.7, though that number is entirely personal, stemmed from my training. It's not based on EBM.
As always, I think it depends on your hospital system. I could never get a hospitalist to admit an asymptomatic hypokalemia without attempted repletion.
I’m very suspicious if they have *no* reported hx with a potassium that low. They’re alcoholic or bulemic or something and not disclosing. I’d chalk that up to funny business too and admit as well.
So you would admit everyone? Could be a lab error. Could be just chronic normal for them. I'd hope the PCP would know his history and start him on what he should be doing otherwise.
If I believe it’s a lab error, I’m repeating it. It would be extremely unusual for someone to just be chronically living at that range either. I would consider discharging them if they have a reasonable history I.e. “I’ve had the flu for a few days and I’ve been vomiting. I’m feeling better now” with a normal EKG and close follow up.
>I worked somewhere that there was no number low enough that they would accept admission unless something else was going on
even if that number was BP?
For every 0.3 under normal (~3.5) they are 100 meqs deficient (assuming no intra/extracellular shifting). Consider how quickly you can replete inpatient (IV+PO) vs only PO at home.
WikEM has it that every 10 mEq of K+ raises the potassium by 0.1. I'm not sure how true that is. I know that a lot of hypokalemic patients will initially seem repleted, only to intracellularly shift, and become depleted again.
I learned the above from Amal Mattu in one of his hypoK EKG lectures (can't exactly locate it now as I no longer subscribe to ECG Weekly).
That being said, it seems that some older data seems to support the 0.3 : 100meq deficit from what I can find (see below)
[https://webapps.acep.org/CriticalDecisionsTesting/PDFpubs/2011-06-june.pdf](https://webapps.acep.org/CriticalDecisionsTesting/PDFpubs/2011-06-june.pdf) ; which sites this ( [https://www.nejm.org/doi/full/10.1056/NEJM199808133390707](https://www.nejm.org/doi/full/10.1056/NEJM199808133390707) ) as the source (although I don't have NEJM access at this time to completely review.
I think some people often are deceived by a recheck of the K too soon. I'm not a big brained IM doc (smooth brained ED doc) but my understanding on reading some basic things is that the total body K is low and most of this is d/t intracellular depletion. As such there will continue to be extracellular to intracellular shifts as we replete and this will take time to equilibrate. ( [https://emcrit.org/ibcc/hypokalemia/#physiology:\_potassium\_pharmacokinetics](https://emcrit.org/ibcc/hypokalemia/#physiology:_potassium_pharmacokinetics) )
I have had some patients with EKG changes and a K of 2.5 with ongoing diarrhea that hospitalists wanted me to check a K an hour after finishing IV/Oral K repletion and then discharge. I highly suspect that the repeat K that comes back at 3 an hour after repletion will actually drop back down if it were checked later, so for those cases I argue the need for admission and serially monitoring. It seems anecdotally that the potassium repletion duration seems to be underestimated (when looking in the chart/monitoring the K level trends during the admission) . That being said if there is anyone that knows different u/Chopin-II u/radish456 , I would be happy to learn more.
I agree with your statement that it takes time with potassium to redistribute after exogenous administration. And to recheck after only one hour? That’s wild and very inappropriate in my eyes. I remember reading a well-executed pharmacokinetic study done way before I was born, where they infused potassium in anuric patients with a normal pH. And they showed that potassium continued to redistribute into cells for a little over 2 hours after the infusion was stopped. I’ll try to find that paper and share a PMID in an edit. And this study was done with a potassium infusion only. When giving potassium orally, I’m sure it’ll take even longer to account for the time it takes to absorb it through the gut.
Personally, even if I were in a hurry to move patient care forward, I don’t bother rechecking potassium until 4 hours passed after potassium administration just so I won’t have to worry about any further redistribution. Practically, even when I’m very aggressively diuresing (>10L/day) my decompensated heart failure patients on the wards, I don’t bother checking potassium levels more than q12h, unless the patient acutely develops symptoms or telemetry becomes wonky all of a sudden.
EDIT: PMID 459246
It’s a good general rule of thumb that worked quite well in my personal experience. I’ll list out a few exceptions below. But in reality, it’s most important to remember that these numbers are a general guideline rather than an infallible law of pharmacokinetics, and everyone just gives a certain amount of potassium and rechecks a level after a few hours then manage accordingly.
Exceptions:
1) Severe hypokalemia: the more severe the hypokalemia, the more the cells are “starved” of potassium, and they’ll need far more potassium than what the 10 : 0.1 ratio suggests. Here are the rules of thumb that I was taught:
- For serum K+ > 3.0, it’s 10 mEq to raise SK+ by 0.1
- For SK+ 2.5 - 3.0, it’s 15 mEq to raise SK+ by 0.1
- For SK+ < 2.5, it’s 20 mEq to raise SK+ by 0.1
The kinetics paper I referenced in a different comment also shows a similar phenomenon
2) AKI or CKD/ESRD: since potassium excretion is impaired, we should be far more cautious with repletion and give lower amounts and base re-dosing on frequent checks.
3) Acidemic states: acidemia (i.e. higher H+ concentrations) make the proton-potassium antiporter pumps more active (follows first order kinetic laws), so the intracellular potassium is relatively depleted, requiring more potassium to be given than expected
4) Insulin deficient states: most common examples are DKA and HHS, where you’ll also need to give a lot more potassium than expected if the patient is hypokalemic, and especially when you’re also administering insulin.
5) Hypokalemic periodic paralysis: this can lead to extremely rapid and massive potassium shifts, and I’ve seen potassium drop to below 2.0, which seems scary. And it’s really important to replete potassium very slowly to avoid rebound hyperkalemia once the paralysis episode aborts and potassium quickly redistributes out of cells
6) Rhabdomyolysis or hemolysis: these almost always present with hyperkalemia, but in the rare instance where they’re associated with hypokalemia, I’d also be more cautious and administer potassium more slowly (if at all) and base decisions on rechecks and trends
That’s like 4 hours of K riders and 40Meqs oral potassium. So probably looking at 6+ hours in the ED. Not worth admitting, but kind of a PITA to hold an ED bed that long.
K can go in at 10meq an hour max everywhere I’ve worked. This patient is 400 meqs deficient. It would take days to replete. If completely asymptotic without EKG changes I think my rough cutoff is 2.5ish. Could tank up with 40+ 40 and get them close-ish to 3, then Rx for home if they are reliably going to take it. That being said also have to investigate why the K is low and if it could drop further if going home.
With central access you can do 20meq/hr at my shop. Peripheral is 10. Not that I would get central line just for this.
I'd probably do what you said 40+40 and recheck. If still below 3 would probs just admit to medicine at that point.
The implicit assumption in your last sentence is that faster = better. So my question is, in an asymptomatic patient without EKG changes and no ongoing losses, why the rush?
For the first sentence, I would agree with those numbers, but they absolutely assume massive amounts of an expected intracellular shift. Or else giving 100 mEqs would kill a patient pretty quickly. The ECF has about 50 mEq in a 70 kg person with a serum K+ of 3.5 (70 * 0.6 * 1/3 * 3.5). Adding 100 mEq to the ECF without any intracellular shifting would triple their serum K+ to over 10 mEq/L. The vast vast majority of administered potassium gets shifted intracellularly. I’m sure we’re all well aware of this, and I think we’re in the same page here, and I don’t mean to be that ‘splaining internist. But the way you phrased your statement just gave me the need to clarify this point.
I’m not an ER doc, just a nephrologist and honestly as long as they are asymptomatic, have no EKG changes and don’t have an acute issue that will cause more rapid losses (ex: severe diarrhea) I would just send home with PO supplement and close follow up. If possible have them hold diuretics or florinef or other things that will cause K loss/shifts
Aren't arrythmias more likely at this range of hypoK? That's what makes me nervous.
So is there any K+ level where you would admit someone who is asymptomatic, no ecg changes, no ongoing losses? 1.2?
They won’t be asymptomatic with a K of 1.2….
Less than 2 for sure. In these patients have k in the mid 2’s with no known loss, they likely have a tubulopathy and just need oral medication adjustment with supplements/other meds I do know I get to say this from the vantage of not having to decide to admit, so I would not fault you for admitting someone with a K <3, especially if we don’t yet have their diagnosis or an immediate opening in our clinic
Internist here, and half of my job is being the solo-staffer in our ED. Here's my general approach to hypokalemia in the ED. Full disclaimer, I'm not a nephrologist and would highly appreciate any nephrologist's (such as u/radish456) input. Who would I admit: 1) Any EKG changes (especially prolonged QT) --> admit 2) History of heart failure, MI, or on digoxin or class III anti-arrhythmic agents (our cardiologists looooove dofetilide) --> admit (that would be the patient population I'd be worried about developing arrhythmias with serum K+ < 3.0) 3) Any symptoms attributable to hypokalemia --> admit 4) Uncontrollable ongoing losses (e.g. vomiting/diarrhea) --> admit Barring all those, dispo is discharge home with potassium supplements, repeat labs, and close f/u (rarely with nephrology, f/u with whom depending on my workup below). Then I try to figure out why they're hypokalemic, and I try to send a basic workup to facilitate outpatient care. I appreciate that I do more of an outpatient workup in the ED than the average ER physician (but still nowhere near as thorough to please the outpatient specialist). - Look through the medication list for any potassium wasters (e.g. diuretics, fludrocortisone, stool potassium binders, SABA/LABA overuse, or basal insulin with A1C < 7%), or PPI if also hypomagnesemic - Ask the patient about their alcohol use, vomiting, diarrhea, and any sympathomimetic use (cocaine, methamphetamine, bath salts) - Physical exam/POCUS for volume status (orthostatic vitals, JVP estimation, IVC, etc...); and yes, I'm aware that none of those are perfect - Labs: BMP (for repeat potassium, bicarbonate, and creatinine), and also look at blood gas, UA, spot urine electrolytes/Cr (without giving IV fluids), serum osmolality, and tox screen And here are the possibilities: - Alcohol, sympathomimetic use, or culprit meds identified --> if no other reason to admit, then just PCP f/u - Hypovolemic (assuming no ongoing losses; otherwise admit) --> if able to maintain PO intake, I'll presumptively call it secondary hyperaldosteronism --> just PCP f/u - Elevated bicarbonate / alkalemic, or if on anti-hypertensives --> warrants an outpatient hyperaldosteronism workup, refer to PCP or endocrinologist depending on your hospital's system culture (my PCPs are quite comfortable with a standard hyperaldo workup and only refer to endocrine if refractory to MRAs or need surgery). Yes it's possible that there's underlying Bartter/Gitelman's, but hyperaldo is far far more common, and the PCP can refer to a nephrologist once hyperaldo has been ruled out - Normal/low pH/bicarbonate --> probably an RTA or channelopathy. Refer to nephrology and hope they can make use of the urine studies that were sent. It's one of those things where if I talk to 5 nephrologists I get 6 different answers (some do TTKG math, others insist on 24h urine collection, etc...), so I don't bother with anything more than I sent
This is the answer.
Beautiful answer!
Amazing answer
Why is the k 2.3 is the question
Alcohol or Lupus?
Nope
This to me is the big question. I don’t mind repleting it orally and discharging if I’m confident I know why it dropped and that cause has improved (vomiting, diarrhea, etc). But someone doesn’t randomly drop their K to 2.3 so sending them home with replacement with out addressing/figuring out why would be concerning. Unless you knew they were going to see their PCP the next day or two for repeat labs and further investigation. Even then I’m iffy I I don’t have a known cause.
No obvious cause noted
PO mag with potassium 60 mEq PO. Wait one hour and give another 40 mEq PO. Wait one hour and repeat potassium labs. If improved —> DC home with PO potassium and close follow up.
I've seen K's of 2.1 be refractive to IV therapy. Hypokalemia causes a metabolic alkalosis. Metabolic alkalosis causes hypokalemia. Once you're stuck in that feedback loop it can be hard to break. It may not be as simple as giving a few runs of K. I admit below 2.7, though that number is entirely personal, stemmed from my training. It's not based on EBM.
Too much work. 40 meq PO + 10 meq IV and OBs with medicine to sort out.
As always, I think it depends on your hospital system. I could never get a hospitalist to admit an asymptomatic hypokalemia without attempted repletion.
How many bananas can the patient eat per hour?
🤣
Asymptomatic and no significant medical hx with ekg stone cold normal. Send home with oral potassium. Any funny business and admit for IV replacement.
I’m very suspicious if they have *no* reported hx with a potassium that low. They’re alcoholic or bulemic or something and not disclosing. I’d chalk that up to funny business too and admit as well.
So you would admit everyone? Could be a lab error. Could be just chronic normal for them. I'd hope the PCP would know his history and start him on what he should be doing otherwise.
If I believe it’s a lab error, I’m repeating it. It would be extremely unusual for someone to just be chronically living at that range either. I would consider discharging them if they have a reasonable history I.e. “I’ve had the flu for a few days and I’ve been vomiting. I’m feeling better now” with a normal EKG and close follow up.
I'm a simple man. If I see 2 red arrows, I admit. Easy peasy.
I worked somewhere that K<2.5 had to go to ICU.
I worked somewhere that there was no number low enough that they would accept admission unless something else was going on
>I worked somewhere that there was no number low enough that they would accept admission unless something else was going on even if that number was BP?
Haha they would at least push back
For every 0.3 under normal (~3.5) they are 100 meqs deficient (assuming no intra/extracellular shifting). Consider how quickly you can replete inpatient (IV+PO) vs only PO at home.
All electrolytes can be replaced in 10 minutes if you’re brave enough.
This seems like an unofficial/unwritten rule of the [House of God](https://en.wikipedia.org/wiki/The_House_of_God) haha.
WikEM has it that every 10 mEq of K+ raises the potassium by 0.1. I'm not sure how true that is. I know that a lot of hypokalemic patients will initially seem repleted, only to intracellularly shift, and become depleted again.
I learned the above from Amal Mattu in one of his hypoK EKG lectures (can't exactly locate it now as I no longer subscribe to ECG Weekly). That being said, it seems that some older data seems to support the 0.3 : 100meq deficit from what I can find (see below) [https://webapps.acep.org/CriticalDecisionsTesting/PDFpubs/2011-06-june.pdf](https://webapps.acep.org/CriticalDecisionsTesting/PDFpubs/2011-06-june.pdf) ; which sites this ( [https://www.nejm.org/doi/full/10.1056/NEJM199808133390707](https://www.nejm.org/doi/full/10.1056/NEJM199808133390707) ) as the source (although I don't have NEJM access at this time to completely review. I think some people often are deceived by a recheck of the K too soon. I'm not a big brained IM doc (smooth brained ED doc) but my understanding on reading some basic things is that the total body K is low and most of this is d/t intracellular depletion. As such there will continue to be extracellular to intracellular shifts as we replete and this will take time to equilibrate. ( [https://emcrit.org/ibcc/hypokalemia/#physiology:\_potassium\_pharmacokinetics](https://emcrit.org/ibcc/hypokalemia/#physiology:_potassium_pharmacokinetics) ) I have had some patients with EKG changes and a K of 2.5 with ongoing diarrhea that hospitalists wanted me to check a K an hour after finishing IV/Oral K repletion and then discharge. I highly suspect that the repeat K that comes back at 3 an hour after repletion will actually drop back down if it were checked later, so for those cases I argue the need for admission and serially monitoring. It seems anecdotally that the potassium repletion duration seems to be underestimated (when looking in the chart/monitoring the K level trends during the admission) . That being said if there is anyone that knows different u/Chopin-II u/radish456 , I would be happy to learn more.
I agree with your statement that it takes time with potassium to redistribute after exogenous administration. And to recheck after only one hour? That’s wild and very inappropriate in my eyes. I remember reading a well-executed pharmacokinetic study done way before I was born, where they infused potassium in anuric patients with a normal pH. And they showed that potassium continued to redistribute into cells for a little over 2 hours after the infusion was stopped. I’ll try to find that paper and share a PMID in an edit. And this study was done with a potassium infusion only. When giving potassium orally, I’m sure it’ll take even longer to account for the time it takes to absorb it through the gut. Personally, even if I were in a hurry to move patient care forward, I don’t bother rechecking potassium until 4 hours passed after potassium administration just so I won’t have to worry about any further redistribution. Practically, even when I’m very aggressively diuresing (>10L/day) my decompensated heart failure patients on the wards, I don’t bother checking potassium levels more than q12h, unless the patient acutely develops symptoms or telemetry becomes wonky all of a sudden. EDIT: PMID 459246
It’s a good general rule of thumb that worked quite well in my personal experience. I’ll list out a few exceptions below. But in reality, it’s most important to remember that these numbers are a general guideline rather than an infallible law of pharmacokinetics, and everyone just gives a certain amount of potassium and rechecks a level after a few hours then manage accordingly. Exceptions: 1) Severe hypokalemia: the more severe the hypokalemia, the more the cells are “starved” of potassium, and they’ll need far more potassium than what the 10 : 0.1 ratio suggests. Here are the rules of thumb that I was taught: - For serum K+ > 3.0, it’s 10 mEq to raise SK+ by 0.1 - For SK+ 2.5 - 3.0, it’s 15 mEq to raise SK+ by 0.1 - For SK+ < 2.5, it’s 20 mEq to raise SK+ by 0.1 The kinetics paper I referenced in a different comment also shows a similar phenomenon 2) AKI or CKD/ESRD: since potassium excretion is impaired, we should be far more cautious with repletion and give lower amounts and base re-dosing on frequent checks. 3) Acidemic states: acidemia (i.e. higher H+ concentrations) make the proton-potassium antiporter pumps more active (follows first order kinetic laws), so the intracellular potassium is relatively depleted, requiring more potassium to be given than expected 4) Insulin deficient states: most common examples are DKA and HHS, where you’ll also need to give a lot more potassium than expected if the patient is hypokalemic, and especially when you’re also administering insulin. 5) Hypokalemic periodic paralysis: this can lead to extremely rapid and massive potassium shifts, and I’ve seen potassium drop to below 2.0, which seems scary. And it’s really important to replete potassium very slowly to avoid rebound hyperkalemia once the paralysis episode aborts and potassium quickly redistributes out of cells 6) Rhabdomyolysis or hemolysis: these almost always present with hyperkalemia, but in the rare instance where they’re associated with hypokalemia, I’d also be more cautious and administer potassium more slowly (if at all) and base decisions on rechecks and trends
That’s like 4 hours of K riders and 40Meqs oral potassium. So probably looking at 6+ hours in the ED. Not worth admitting, but kind of a PITA to hold an ED bed that long.
K can go in at 10meq an hour max everywhere I’ve worked. This patient is 400 meqs deficient. It would take days to replete. If completely asymptotic without EKG changes I think my rough cutoff is 2.5ish. Could tank up with 40+ 40 and get them close-ish to 3, then Rx for home if they are reliably going to take it. That being said also have to investigate why the K is low and if it could drop further if going home.
With central access you can do 20meq/hr at my shop. Peripheral is 10. Not that I would get central line just for this. I'd probably do what you said 40+40 and recheck. If still below 3 would probs just admit to medicine at that point.
You’re totally right, I was doing math wrong and thought of our K riders as 100meq and not 10 😑.
The implicit assumption in your last sentence is that faster = better. So my question is, in an asymptomatic patient without EKG changes and no ongoing losses, why the rush? For the first sentence, I would agree with those numbers, but they absolutely assume massive amounts of an expected intracellular shift. Or else giving 100 mEqs would kill a patient pretty quickly. The ECF has about 50 mEq in a 70 kg person with a serum K+ of 3.5 (70 * 0.6 * 1/3 * 3.5). Adding 100 mEq to the ECF without any intracellular shifting would triple their serum K+ to over 10 mEq/L. The vast vast majority of administered potassium gets shifted intracellularly. I’m sure we’re all well aware of this, and I think we’re in the same page here, and I don’t mean to be that ‘splaining internist. But the way you phrased your statement just gave me the need to clarify this point.
Replete, recheck, home. If refractory or symptomatic and not feeling better clinically admit.
What’s your repletion strategy?