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RTL- Ep 90- Hyperkalemia
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RTL- Ep 90- Hyperkalemia
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[Dr. Smith] Welcome back to Run the List, a medical education podcast in partnership with McGraw Hill Medical. Our hosts are Dr. Navin Kumar, Dr. Walker Redd, Dr. Emily Gutowski, Dr. Joyce Zhou, and myself, Blake Smith. As a quick disclaimer, this podcast is meant for informational and educational purposes only, and should not be understood as medical advice under any circumstances.
[intro music] [intro music] [intro music] [Dr. Gutowski] Welcome back to Run the List. I'm Emily Gutowski, and today we are back in our nephrology series with part two on hyperkalemia. We have with us Dr. Rahul Maheshwari, who joined us last episode for AKI, welcome back, Rahul. [Dr. Maheshwari] Hey, it's a pleasure to be back.
Thanks so much. [Dr. Gutowski] So today we have with us a 72-year-old gentleman who has chronic kidney disease, insulin-dependent diabetes and CHF, who comes in to the ED with muscle cramps. He tells you that he'd just recently started on metoprolol, lisinopril and spironolactone. He's not been feeling well for a couple hours, and he tells you he forgot to take his insulin at home earlier today.
His vital signs on admission are within normal limits, and his labs are notable for a potassium of 6.6 and a glucose of 360. So Rahul, what exactly is hyperkalemia? [Dr. Maheshwari] Yeah, so this is a really interesting case of hyperkalemia with lots of different causes, so let's start at the beginning. When we think about defining hyperkalemia, that's a potassium level of greater than 5 to 5.5 mEq/L that's measured in the serum.
The actual potassium distribution in the body is predominantly intracellular with approximately 90% of the potassium stored within the cells. And so even any small alterations in how that potassium is distributed can result in pretty significant changes in the serum levels of potassium. So that's why we worry about even incremental changes going from 5 to 5.5 to 6, when we think about comparing it to sodium which has an average serum sodium concentration of about 140 mEq/L.
And so those differences again, can be pretty substantial. So again, the approximate range of normal is about 3.5 to 5.2, this can change depending on your local laboratory values and anything higher than that would be hyperkalemia. [Dr. Gutowski] Great, so you mentioned there's a couple of different potential causes of hyperkalemia in this patient, but backing up a little bit, do you have a general framework for thinking about the potential causes of hyperK?
[Dr. Maheshwari] Yeah, definitely. So the first thing you want to do is actually verify the fact that this potassium elevation is real. The number one cause of hyperkalemia is usually hemolysis and some laboratory errors. And so this can occur due to a variety of reasons but usually what ends up happening is, the blood products within the test tube break down. And we just talked about how there's lots of potassium within the intracellular compartment.
And so even small amounts of hemolysis can artificially make it look like the serum potassium level is high, making you concerned even though that may not truly represent what's going on within the body. Pseudohyperkalemia is something else we also have to think about, which can happen sometimes in patients who have elevated platelet counts or leukocytosis that's fairly extreme as well. Once you've verified however, that the patient does have a true hyperkalemia and you've thought about these other causes of pseudohyperkalemia, I could try and think about hyperkalemia in three main categories of in, shift, and out.
So first of all, when we think about the in category, you just have a high load of potassium that's coming into the body. So usually speaking, in somebody who has normal kidney function, taking in lots of potassium is a very uncommon cause of hyperkalemia as your normal renal handling of potassium should be able to manage that potassium load, and I'll get there in terms of exactly how the body manages potassium loads in a minute.
However, in patients who have CKD and advanced CKD, their GFR is decreased significantly, and so you have fewer nephrons that can actually handle that potassium load. And so with patients who have CKD 4, CKD 5, we're explicitly telling them actually to manage how much potassium they're getting in to avoid hyperkalemia coming in from the diet. Secondly, we have to think about iatrogenic causes of hyperkalemia as well.
So predominantly we think about blood product transfusions or RBC transfusions. I mentioned hemolysis, and so in those blood products, RBCs can be lysed a little bit and that's actual potassium that's going into the body. And so that can also be an excess load of potassium. And then finally we have to think about other reasons that potassium is getting into the body somewhat indirectly or getting into the serum indirectly.
So crush injuries are a big cause as well. And so if you have patients who have been in significant motor vehicle accidents that have had a large limb crush injury, they're going to have a huge infusion of potassium that goes into the serum as well. Now the next category I mentioned was shift. And so how does the body shift potassium from the intracellular to the extracellular compartments?
And this is predominantly dependent on the sodium-potassium ATPase pump. So if you go back a little bit and think about your biochem, think about what the different factors are that affect the ATPase pump. So some of those, especially in this patient, include insulin regulation or appropriate amounts of insulin as essentially insulin can up-regulate your sodium potassium ATPase.
And so again, the ATPase brings in potassium into the cell and takes sodium out into the extracellular component. And so if you don't have insulin to up-regulate that, you're going to have an excess of potassium outside the cell, and so in this patient that can be one cause of the hyperkalemia. Secondly, beta agonists can also have an impact on the sodium potassium ATPase, and so if you have beta blockers for example that can actually down-regulate the sodium potassium ATPase function.
And finally, acidosis can also have a negative impact on how that function occurs as well. So all that comes down to that single transporter, but insulin, beta blockers and acidotic states can all result in a shifting of potassium to the extracellular component instead of the normal shift intracellularly. And lastly, in the in, shift, out framework, we think about how is potassium leaving the body?
So I mentioned thinking about how the body actually handles potassium. So 90% of potassium excretion or even greater than that actually occurs via renal handling or through the kidneys. And so if you have any kind of issues with the kidneys, if that's an AKI, if that's somebody with advanced CKD, how they are able to regulate that potassium will significantly decrease as the renal function decreases. Now, secondly then, if we think about medications, those can impact how the kidneys are functioning and therefore how they're able to handle any kind of potassium, and so a big category of medications includes RAS inhibitors, so ACE inhibitors, ARBs, mineralocorticoid receptor antagonists, trimethoprim, sulfamethoxazole.
Interestingly, heparin is actually a pretty common cause of hyperkalemia that happens in the hospital. And this includes both systemic or intravenous heparin that you think about for patients that have PEs or MIs, as well as subQ heparin. This is less of a concern although it's still there for medications like enoxaparin as well or the brand name Lovenox. And finally, there are some pathologies such as RTAs, or specifically RTA type 4.
The way I kind of think about this is almost this is like an acquired tubulopathy, that's not actually what it is, but it's a good way to think about how does this disease state affect how the renal tubules are actually handling potassium? And if there's some kind of derangement there that can also result in hyperkalemia. So again, just to very briefly summarize, we talked about in, shift, and out.
So the in, is there a large infusion of potassium that's coming in dietary, from transfusions, from large limb injuries? For shifting, is there something that's affecting the balance of how the potassium in the body is shifting out of the intracellular space due to derangements in the sodium-potassium ATPase pump? And finally excretion, essentially is there anything that's impacting how the kidneys are handling how potassium is able to leave the body?
Now just briefly, because we're going to talk about this in a second here, but I mentioned that greater than 90% of potassium that leaves body occurs via renal handling, via the urinary tract, but the rest of it is predominantly the GI tract. You theoretically lose some potassium in the sweat but that's essentially negligible. [Dr. Gutowski] Okay, great. Thanks for taking us through that. So back to our patient, he has multiple potential etiologies for his hyperkalemia, again, just to go back over the case, he forgot to take his insulin, he's on these new medications, he mentioned a beta blocker, an ACE inhibitor, and a mineralocorticoid receptor antagonist.
And this is all in the background of CKD, so he already has impaired handling of potassium. Maybe he ate a couple of bananas or avocados today, and is not excreting them as well as someone with normal kidneys would. So moving on to next steps, what's your approach in work-up? [Dr. Maheshwari] Yeah, so there is what we would ideally do, and then what actually happens in the hospital, but in the ideal scenario first what I want to do is actually confirm this is a true hyperkalemia, so get a repeat measurement.
The practical part of that is that a repeat measurement is going to take anywhere from like half an hour to two hours depending on how backed up the lab is, and so at the same time, the biggest thing we worry about with hyperkalemia is if they're going to develop any arrhythmia, and so you want to get an EKG pretty quickly. Now there's a whole spectrum of EKG changes that we see that's associated with hyperkalemia, and seeing them is another kind of confirmatory way to really prove that this patient is hyperkalemic.
Let's take a hypothetical scenario, you get an unexpected potassium of 6.5, it's not something you really would've expected in a different kind of patient that's not in this clinical scenario. And so you get a repeat lab value, but at the same time you want to make sure that this is not an actual urgent concern, and you get an EKG, and you start seeing these spectrum of changes.
So what are these changes? So they can start with peaked T waves, this then can progress to an increased PR interval, a widened QRS, eventually development of sine waves, and then lastly, the biggest thing that we most worry about is the evolution of a PEA or asystole cardiac arrest. And so if you're seeing any of those spectrum, it doesn't really matter what that repeat potassium serum measurement that you're waiting on is going to be, because you know it's "real hyperkalemia" that you need to actually act on.
A question that we frequently get is, at what potassium level do you get a specific EKG change? So is there a potassium level that correlates with peaked T waves? Is there a potassium level that correlates with a widened QRS? And unfortunately that's not really the case. In general, the way that you think about this, and this is additionally applicable to CKD patients is, what is the deviation from where their usual potassium level is?
If you have people with a normal baseline renal function that have a potassium that's somewhere in the floor range for example, and then they come to the hospital with a potassium of 6.5, that's a pretty significant change. However, if you have patients who have CKD and they have a baseline potassium in the low 5s and then they go to 6.5, you may not actually see changes on the EKG. Now in both cases, you're right to be worried and you should have some management, but that change in the potassium or that delta is a thing that's most concerning.
And so you may have a little bit more time to act on that CKD patient who has an outpatient lab of a potassium of 5.2 a couple weeks ago, had an out-office visit a 6.5, was sent to the emergency department, they come in, their EKG doesn't show many changes you may expect, but still you need to act on it, but you have a little bit more time compared to again, that patient with a normal potassium in the 4s, that comes in with 6.5, and you are far more likely to see peaked T waves, a widen QRS, et cetera.
So part of this has to do with adaptations essentially of the cardiac membrane that occur with patients who have kind of long-term borderline hyperkalemia. [Dr. Gutowski] Got it, so always good to keep in mind the patient's medical history and take a look at some of their more recent labs to get a sense of the chronicity. So in our patient, we repeated the measurement, which shows that his potassium is persistently elevated, so it was real.
His EKG shows mildly peaked T waves. As we start to think about treatment, what are our first steps? [Dr. Maheshwari] Yeah, so part of what's helpful about thinking about that framework of in, shift, out is that that kind of helps you think about how to treat this, but the very first step is thinking about, again, the most life-threatening concern we have with hyperkalemia is how it impacts the cardiac membrane, it can lead to arrhythmias.
So the first thing you want to do is stabilize the patient, afterwards we think about shifting, and then finally eliminating potassium. With stabilizing what we usually do is provide calcium gluconate or calcium chloride to stabilize the cardiac membrane and prevent any kind of precipitation into an unstable arrhythmia. Now one thing that's important to note is that calcium gluconate lasts roughly 30 minutes, again, it can vary from patient to patient, and so that may not be enough time for you to have implemented all of your hyperkalemia management therapies, or to actually get that potassium down enough.
So one thing that you want to see is that you have the initial EKG which shows, for example, peaked T waves, you give them calcium gluconate, your recheck an EKG, and hopefully those peaked T waves have gone away. In another 30 minutes or so you're going to want to recheck an EKG to see, did they come back or not, and do you need to re-dose of calcium gluconate or calcium chloride? That can be pretty labor intensive.
So keeping the patient on telemetry is also important to start to see that evolution of peaked T waves as the calcium gluconate starts to wear off essentially. The next bucket is to think about shifting. So we talked about all the things that can help ramp up the sodium potassium ATPase activity, if you will, and so those are going to be the exact same things that we're going to use to help treat or shift the extracellular potassium back into the cells.
So one of the therapies we talked about is insulin. So you can give insulin to the patient, that will help again increase the sodium-potassium ATPase pump, bring potassium back into the cell. Now of course, if you're giving insulin to a patient, you want to make sure they're not going to be hypoglycemic. Typically, most order sets will have either 5 or 10 units of insulin given to the patient with an amp of D50. Now in patients that are hyperglycemic you may not need this, so keep in mind just what their serum glucose is, in this patient whose presenting serum glucose I believe was in the 300s, you're probably going to be able to get away without needing any amps of glucose.
Your usual protocol will be to check an hourly point-of-care glucose, one and then two hours after, but it can vary from hospital to hospital. Now the next thing that we can use is our beta agonists, in the U.S. we usually use albuterol. Now what's important to note is that the dose of albuterol is roughly 10 times that of what we use for asthma exacerbations, and so that can be pretty significantly limited by tachycardia.
And so yes, we often give albuterol inhalers as part of our hyperkalemia cocktail in order to help try and shift again that potassium back into the cells, but you are going to be kind of coming up against a barrier as to how much is a safe amount of albuterol to give. And then lastly, you can give sodium bicarbonate. We talked about how acidosis can also cause this shift of potassium out of the cells. It's only useful if the patient is acidotic, and so if their bicarb is low, if their pH is low, then certainly you're going to derive some benefit from giving bicarb.
However, if it's not, you're not going to really be able to cause much of an improvement there. So all of these shifting strategies are temporizing ultimately, because the total body potassium is still high in these cases, and so you can't really just stop at only giving them insulin, or only giving them beta agonists, you also are going to want to get rid of some of that potassium. And so we use that to temporize a patient, because the insulin and the beta agonist and the bicarb kick in within 30 minutes to an hour, but then you want to think about your elimination strategies.
So we talked about how the body eliminates potassium predominantly through the renal handling of potassium, but also to a lesser degree, the GI tract. So from the renal perspective of things, you can use loop diuretics, classically furosemide to try and eliminate potassium. This will kick in in terms of the potassium lowering effect in roughly one to two hours, and so you can give them high doses of loop diuretic to try and have them essentially eliminate any potassium definitively from the body.
Now of course, you're going to run up into the issue of a patient who's hypovolemic, then you don't want to be giving them diuretics because that can cause its own problems, but at the same time then you can give them IV fluids concurrently. So this is one of the few indications where you would actually see someone getting both IV fluids and furosemide in order to make them try and excrete potassium more effectively and more quickly.
Finally, we think about GI binders. Now up until about 10 to 15 years ago, the most common GI binder we would be using is Kayexalate, however, one of the safety concerns that came up was bowel necrosis. As a result, there are newer binders, most notably, sodium zirconium cyclosilicate, which I will now call Lokelma for the sake of brevity, as well as patiromer or the brand name is Veltassa.
Now these are generally well tolerated. In the urgent situation, Lokelma is what's approved for the urgent management of hyperkalemia. It's fairly well tolerated, in most of the validation in initial studies, there wasn't really any bowel necrosis that was seen, which is excellent. There's one important thing to note is that there is a very high sodium load that comes with it, hence sodium is in the name.
And so if you have patients especially that have CHF or cirrhosis, you just have to note that you're getting them on a pretty high sodium load and keep that in mind. The onset of action is relatively quick, with a single 10 gram dose of Lokelma, you'll have a potassium lowering initially of just 0.2 to 0.4 within the first hour, but that can often be enough to at least mitigate those urgent concerns you have of somebody precipitating an unstable cardiac arrhythmia.
And then within the next several hours or so, you'll have further lowering of the serum potassium. Now you can give up to three doses typically within the first 24 hours, some of these studies that were done to show Lokelma's affect in the emergent situation gave three doses of Lokelma within the first 12 hours even, and so you are able to dose it up to every four hours for the first three doses to try and quickly get that potassium down.
Again, what's important to note is what we were talking about, the majority of potassium handling is going to happen through renal excretion, and so you are going to come up against a little bit of a barrier in terms of only trying to get the potassium out from the GI tract, and so you do have to think about, again, are they getting in a lot of excess potassium or are there any other reversible causes like medications or things, as you try and temporize them using Lokelma.
[Dr. Gutowski] When would we have to think about dialysis in a patient like this? [Dr. Maheshwari] Yeah, so we talked about all our management strategies in terms of medical management. You have your patient with a potassium 6.5, you've given them high doses of loop diuretics, GI binders such as Lokelma, you can bring them maybe down to the low 6s, but you're still seeing EKG changes, so certainly that's concerning, and that's the point at which you start thinking about dialysis.
So once you have tried all your medical management and you're not able to definitively improve the patient's potassium, then you're going to reach for that as a tool. Some other situations in which we often are using dialysis even if there is some improvement, is when we think about high infusions of potassium, so patients that have TLS or tumor lysis syndrome, they have a lot of intracellular lysis that's occurring.
And so maybe you are able to give them enough loop diuretics to generate a high urine output, but just because of how much intracellular lysis is going on you just can't keep up. And so that's kind of another way you would think about using dialysis even if your medications haven't "failed", they're just not able to keep up with the potassium load that's coming into the body.
[Dr. Gutowski] Got it, that makes a lot of sense. So in this patient, he gets treated initially with calcium gluconate and insulin. He didn't require D50 as we said, because he was hyperglycemic on arrival. He got a bit of Lokelma as well, and gradually his potassium returned to a normal range. His symptoms improved and his EKG changes resolved as well. He had some medication adjustments as well, he was taken off of his lisinopril, spironolactone and metoprolol.
Vitals still remain stable, and he was scheduled for close follow-up with cardiology for some adjustment of his cardiac medications. So wrapping up this episode, what are some of the main takeaways or clinical pearls you want to leave us with? [Dr. Maheshwari] Yeah, so I think the first thing to think about is how does potassium kind of move around the body?
And we talked about the in, shift, and out paradigm where is there a lot of potassium coming in, either from exogenous sources or from endogenous sources such as muscle crush injuries or TLS? Is it leaving the body appropriately? Does the patient have appropriate renal function? Are there medications that are impacting how the kidneys are handling potassium and excreting it appropriately?
And then finally, are there things that are causing the potassium to shift from the intracellular space to the extracellular space? Is the patient acidotic, are they hyperglycemic because they don't have enough insulin? Things like that. Now once you have that framework in mind and you've confirmed that the patient is truly hyperkalemic, you're going to want to actually manage them through our three buckets of management.
So stabilizing the cardiac membrane using calcium gluconate and calcium chloride, and not forgetting to monitor them with telemetry. Shifting is your next step of management, using insulin, beta agonists, or bicarbonate if indicated. And finally, elimination strategies both through, again, diuretics such as loop diuretics or GI binders. And finally, if they're not working, then thinking about calling your friendly nephrologist for dialysis.
One really important thing to think about is, is the patient anuric? And that's actually going to be one of the most important things we're going to want to know as a nephrologist when you call us. So if we have a consult for hyperkalemia, one of the first questions we're going to ask is, is the patient peeing? And that's important for the reasons that we talked about. Because if we can't rely on the body's ability to handle that 90% or greater load of potassium, then that will make us reach for dialysis far more quickly than if someone who has a good amount of urine output, and then we can actually get away with just using loop diuretics with additional volume supplementation as needed.
Finally, along that note, if a patient presents with sort of unexplained or unexpected hyperkalemia you just want to make sure that they're not suddenly obstructed. So one of the most common causes of calls that I get, especially in the middle of the night for hyperkalemia, is a gentleman who is older, has pretty significant BPH, comes in, has normal outside baseline renal function, but comes in with a creatinine of 5 and a potassium of 8s.
They get a bladder scan and they often have like a liter of urine in their bladder, and so a Foley gets placed, and they have excellent urine output, creatinine comes down, potassium comes down without any medical management. And so ruling out obstruction is going to be very important, and it's a really satisfying way of treating hyperkalemia as well. Now, in terms of when to call us, we're happy to help you guys out any point in someone with hyperkalemia, but certainly if you're getting to the point where you're approaching maximum doses of your medications and you're not able to treat their hyperkalemia, give us a call.
Or if there's urgent hyperkalemia and you're worried that you're not going to have enough time, essentially to shift or use other medications to eliminate potassium from the body, such as again, TLS like we talked about before, and you think they may end up needing dialysis anyways, feel free to give us a call. [Dr. Gutowski] Awesome. Well, we'll try and stave that off as long as possible now that we have some great tips for managing this.
So thank you so much again for this incredible episode. I think we all will be a lot more confident managing hyperkalemia from now on. [Dr. Maheshwari] Thanks, Emily, for having me. [outro music] [outro music]