Clinical Concepts - Electrolyte Management

Hey future doctors. Thanks for joining me on Spoonful of Sugar, a podcast made for medical students by medical students to help the medicine go down. My name is Rhea Mulherker. I'm currently a radiation oncology resident in Pittsburgh, Pennsylvania. And I will be your host today. I'm sure everyone vividly remembers their experience as a third year med student in surgery. And I'll never forget how every morning I would arrive at 4.45 in the morning. I'd print out a list of my patients for the day, draw a fish bone next to each of their names. And then I'd proceed to record each of their labs. And then I would circle the abnormal ones. I'd make copies for the rest of my team. And then the interns on the team were responsible for addressing any electrolyte abnormalities. And at the time, all I did was, you know, feel sorry for myself for having to wake up that early in the morning. But, you know, I really don't think I understood what they were doing when they were repeating the electrolytes. They just kind of said that they were doing it, that it was important, and we kind of moved on. And it was something that I barely considered. And then it really hit me as an intern when this was my job every single day. And I remember as a medical student, you know, thinking about the electrolytes and knowing that they were a problem, but never really knowing how to manage them. And so, in this episode, in this clinical concept series, I'd really like to go over the main electrolytes and kind of discuss, you know, why they're important in principles of management. I think that once you're an intern, whether it's medicine or surgery, you know, it's going to be your job to complete the electrolyte, so you'll get very accustomed to the ins and outs and what doses and what specific formulation to order. So, that's not really something I want you to worry about as much. What I want you to be able to take away is to understand the normal ranges of common electrolytes. What happens when they're low or when they are in excess and when that's relevant? And, you know, what can really happen clinically and how to manage the situation? I really think that, you know, once it's your job and it's your day-to-day business, you're going to get used to the doses and the formulations and I'll mention them. But what I really want you to pay more attention to is why it's clinically relevant and understand the physiology of how we manage it more so than the actual ins and outs. And so, you know, the main electrolytes that we're going to cover today are going to be potassium, magnesium, phosphorus, calcium, and at the end, I'll kind of touch on sodium and we'll talk about why that's a more complicated one and we'll address principles of management. Okay. So, I'm going to start by talking about potassium, which I think is probably one of the most important ones as an intern to be really, you know, aware of. So, we'll start with low and then we'll go with high. But before that, even, let me ask you, what is a normal potassium level? Any idea? So, a normal potassium level is going to be around four milli-equivalence per liter. Okay. So, just remember the number four for potassium. And a useful mnemonic I learned is two, three, four for magnesium, phosphorus, potassium. So, mag should be two, phosphorus should be three and K should be four. Okay. Two, three, four, MPK. So, just remember that kind of moving forward in this episode and remember that a normal potassium level is somewhere around four. And another important thing to know is what is a dangerously high potassium level? Like, when should you maybe start to break a sweat, be a little bit worried about your patient? I would say anything above six should be concerning. When you're actually taking care of patients, sometimes you'll find that six is not necessarily as concerning, but I think six should really be your threshold to start taking some kind of action or at least think about, you know, doing something about that potassium. And why is potassium such an important electrolyte? Why do we worry about keeping it in balance and keeping that level around four milli-equivalence per liter? So, remember, potassium is a really key electrolyte that's involved in sending electrical signals. Remember, there's a lot of sodium, potassium, ATPase channels. There's all those exchanges in the cell membranes. And they're really important for nerves and, you know, signaling muscles. And which muscular organ heavily relies on electrical impulses in order to function and keep you alive? Can you think of an organ like that? How about the heart, right? The heart relies so heavily on potassium. And so any kind of abnormalities in potassium will cause electrical imbalances within the heart. And that can quickly lead to arrhythmias as well as cardiac arrest. And there's a ton of other organs, you know, anything with muscles and nerves that will affect patients with lower high potassium. So kind of at less extreme sometimes, patients will describe they're getting muscle cramps or weakness, especially patients who are undioretics for congestive heart failure, for example. You know, they're peeing out all their potassium. And so with that low potassium, they sometimes get muscle cramps. So anything really anything with nerves and muscles is going to be affected. And the major organ we worry about is the heart because if potassium is severely out of balance, it'll cause extreme arrhythmias. And that can kill a person. So let's start with hypocholemia, low potassium. What level is considered hypocholemia? Typically for inpatients in the hospital, anything about less than four million equivalents per liter, we try to repeat that. And what happens in patients with hypocholemia? So we talked about the muscle changes, right? You can get muscle cramps, muscle spasms or can be weakness. Are there any specific EKG changes you can think about associated with hypocholemia? So you waves can appear, which are little waves that show up in the EKG after T waves. And you can also start to see flattening of the T waves. So those are some specific EKG changes to associate with hypocholemia, you waves and flattened T waves. And what's the treatment of hypocholemia? So it's pretty logical. If potassium is low, you just repeat, right? So generally a 10 MEQ PO or IV formulation is expected to increase your serum potassium level by 0.1. So if a patient's potassium is 3.8 and you want to make it 4, you can give them 20 MEQ of PO potassium chloride, for instance. And potassium comes both in the oral as well as the IV form. So potassium chloride can either be oral or IV. You can also get potassium by carbonate, which is in the oral form. And rather than being a pill, it's actually kind of something that dissolves. So it's better for patients who can't swallow a pill. And then you should know that IV replacement of electrolytes in general tends to better increased levels than oral replations. But with IV potassium, especially, it tends to burn. So sometimes you can actually infuse lidocaine into the solution to kind of alleviate the pain that patients get when that potassium goes in. It's a burning sensation. So generally, I only used IV potassium if patients potassium was really low. Anything below 3.4 or so, I would just give IV as an intern for better absorption. And you can also do both. So if you want to give 60 MEQ of potassium to raise the potassium level by 0.6, you can maybe give 40 IV and 20 PO and then recheck it or something like that. And whenever you're repleting potassium, it's really, really important to be aware of renal function. Because if you overreplete potassium in a patient with some kind of kidney injury, you know, they're not as good at processing that. And so then their potassium levels can actually become dangerously high. And that's super dangerous as well, which we'll talk about. So, you know, whenever you're repleting potassium, it's really, really important to always check the patient's creatinine. And if you're unsure, if it's safe to give a certain level of potassium for a certain creatinine, then, you know, you need to ask a senior. And that kind of brings me to hyperkalemia. So what level, again, did I mention that is a level that should kind of worry you? 6. Anything 6 or higher, you really should worry. And you don't keep an eye if it's creeping up if it's like 5.5, next day, it's 5.8. You know, look at their kidney function. Is there kidney failing? Why is there potassium getting high all of a sudden? Are you giving them too much potassium? So keep an eye on that. And why do we worry? Why is hyperkalemia so dangerous? It can cause fatal arrhythmias. You know, do you guys know the specific EKG changes that can happen with hyperkalemia? I think this is a really important concept to know. There's a specific sequence of EKG changes that happens in patients with hyperkalemia, you know, when potassium's really high, like 7, 7.5. And you should know the sequence. So initially, you'll start to get tall, peaked T-waves. The PR interval will start to get prolonged. Then the QRS complex will start to widen. And then eventually, you can lose your P-waves entirely and start to just get a sinusoidal wave. And when you see that the EKG looks like a sine wave, the next step is a code, like a code blue. They're going to be in a lifetime. threatening arrhythmia. So tall peaked T-waves, long PR interval, wide QRS, and then the sine waves, and that's really, really bad. So what do we do in the case of hypercalemia? You know, let's say that you're checking labs in the morning, the patient's completely fine. You know, they're monitor, they're just beeping normally, you've not heard anything, they're not complaining of anything. But you check, and their potassium is 6.2. So it's easy to panic in this kind of situation, and I probably would have my first time seeing a potassium that high. But you know, the first thing you want to do if you see a high potassium is make sure that the blood sample was not hemolyzed, because hemolysis can falsely elevate the potassium. So usually in the lab, or in the lab report, if there is hemolysis, there will be a little comment that there was some hemolysis present. And if that happens, you just recheck it, draw the lab again and re-send it. But you know, let's say you, it was hemolyzed, you re-send it, now it's not hemolyzed, the potassium is still reigning at 6.1. It's important to keep in mind that, you know, the patient is sitting in their room, and they're stable, and nothing is wrong. But at the same time, you don't want to just let that high potassium sit. So if you see a really high potassium, it's really important to always order an EKG, to make sure that there is no peaked T-waves, or worse. And what if you do get an EKG, and you are seeing those tall peaked T-waves? They're right next to the QRS complex, or almost as long as tall as the QRS, and they are pointy. So that should definitely worry you, and what medication would you give? So in a situation like that, the first medication to give is calcium gluconate. Two grams IV calcium gluconate. Any idea why? So calcium will actually stabilize the cell membrane of cardiomyocytes. It causes shifts of potassium intracellularly, and it's the first medication, or the first thing that you give in response to hypercholemia, because it will stabilize cell membrane, and you really want to stabilize the cardiac cells. And then something that you can often order as part of an order set in some of your electronic medical records, you'll hear something called the hypercholemia protocol. Any idea what's included in the hypercholemia protocol? It's basically a list of all these things that can help kind of decrease your extracellular potassium and shift it intracellularly. So one of the medications that you can give is insulin in addition to glucose. Insulin is going to activate the sodium potassium pump activity, and it's actually going to cause potassium to shift intracellularly. And you give it along with glucose because if you're giving insulin, you don't want to drop blood sugars dangerously low. Another medication that acts similarly to insulin is beta agonists, such as albuterol, and like insulin, these will activate the NAK ATPase and cause potassium to shift into cells. And finally, you'll hear of bicarb, so sodium bicarbonate, and this is something that is more controversial. You don't necessarily have to give it, but you can definitely consider it if patients are also acedotic. So remember hypercholemia protocol is going to include calcium, gluconate, insulin, glucose, beta agonists, and potentially bicarb. So what have we done so far? All of these medications that we've introduced, what have they done for you? These have shifted the potassium into the cells, right? We talked about intracellular shifting of potassium by activating that NAK pump. But these are just temporizing measures because they just shifted the potassium. Potassium can shift right back out. So how do we actually get rid of the potassium in the body? Because you need to think about that in addition to just temporizing measures. So one of the options is diuretics, such as phyrosamide. Remember I mentioned that heart failure patients on diuretics will have low potassium and they'll get muscle cramps. So you can use that to your advantage to get rid of the potassium. And then another class of agents that you can use is a class called potassium binding agents. So kxolate is something that you might hear. That is a brand name for sodium polystyrene sulfate. Anyone know a potential side effect of kxolate that we worry about? So kxolate has actually been implicated in intestinal necrosis. It's in a small percentage of patients, but it's just fun fact to know. And then another medication you can potentially use is something called Pateromer. The brand name is Valtessa. It's another potassium binding agent that's considered less risky because it's not as much associated with intestinal necrosis. It's also more expensive. So big takeaway that you know, you give these temporizing measures, but then you also give something to actually eliminate the potassium from the body. You can do diuretics or potassium binding agents that just kxolate or Valtessa. Now, patients with kidney failure are going to have high potassium. Remember, and that's why I said you should be really careful about repleting potassium in patients with kidney failure because they are not able to get rid of it as effectively and it'll build up. So if patients come in with extremely high potassium, even if they don't have you know, chronic kidney disease, even if they're not on dialysis already, they might need emergent dialysis to deal with that extremely, extremely high potassium. And if a patient is a dialysis patient who already has kidney failure and relies on dialysis, it's really important for them to go to dialysis regularly. Otherwise, their potassium can build up and it can get extremely high. And believe it or not, I have heard of a patient who skipped dialysis multiple times in a row and twice in her life, she had coded, literally coded and you know, died because her potassium was so high because she missed dialysis. So keep this in mind that, you know, patients who missed dialysis, you will see their potassium skyrocket and you can give them those temporizing measures, but ultimately, the solution is going to be dialysis. So let me give you another, you know, scenario, say you're repleting and repleting the patient's potassium, but it's just not improving, you know, every time you check it, it's been low, it's been around 3.6. Every time you check it, it, it's not improved. Can you guys think of another lab that you should check to make sure that you've been repleting the potassium correctly? So magnesium, magnesium is actually needed for potassium absorption. Now, do you guys remember what normal mag level is? Around 2, remember, 2, 3, 4, mag, fosk. So normal magnesium level should be somewhere around 2. And what can happen if magnesium is low? So there is a very specific EKG finding that you should know for hypomagnesemia. Any idea what that is? It's called Torsade de point. So Torsade de point is, you know, French term and it basically means twisting around a point. And it's a type of polymorphic V-tac. It's really, really bad and it's, you know, it's a step before the patient has cardiac arrest. So Torsade de point is really terrible, polymorphic V-tac. The patient is very likely to arrest. And that is a finding that's seen with hypomagnesemia. And then hypomagnesemia is also associated with hypocalcemia as well as tetany. So then how do you replete magnesium? Any idea? It's also available in the PO and the IV form. You can get magnesium oxide pills. They come in 200 and 400 milligrams. And then you can also give IV magnesium sulfide with which is in 1 to 2 grams IV. And then what happens in hypermagnesemia if it's too high? So you can get decreased tendon reflexes, lethargy, bradycardia. And then similar to potassium and hyperkalemia if the mag level is too high, you can also give calcium gluconate in this case. Moving on then to phosphorous. Remember what the normal level of phosphorous is? That would be three. And what happens if phosphorous is low? Can you think of a disease that occurs in children that's associated with low phosphorous levels? Rickets, absolutely. And how about an adult? Osteomalacia. So essentially phosphorous is a huge component of bones. And so with hypophosphatemia you're going to get bone loss. So Rickets and children, osteomalacia, and adults. And phosphorous replicion is a little bit more complicated. And you tend to not need it as frequently as potassium or magnesium. So I won't go into too much detail. I'll just tell you that IV form is available. 15-millimal equivalents and there's different reference charts that you can look at how many millimoles you need to give for what level of phosphorous. And generally, we don't actively check phosphorous in our in-patients. Can you think of a circumstance where we actually would be concerned about phosphous levels and check them pretty vigilantly? If you are concerned about refeeding syndrome, so patients who have not eaten for a while, let's say they've had numerous surgeries, they've been NPO for days, they haven't eaten for like seven to ten days and they're starved. They will switch into an anabolic state as soon as they're exposed to food, right? insulin will be secreted, there'll be uptake of glucose, uptake of thymine, there'll be increased uptake of potassium, magnesium, phosphorous. And so in this situation is called refeeding syndrome and the levels of these electrolytes can drop dangerously low. So if you're concerned about a patient developing this, you know, if you're feeding a patient for the first time in a week or so, the nutritionists will often recommend that you monitor their electrolytes every eight hours. So every eight hours you'll check their potassium, their phosphorous and your magnesium and you'll repeat it pretty aggressively. Moving on now, let's talk about calcium. Any idea what normal level of calcium is? So normal calcium level is around eight and a half to ten and a half milligrams per desoleter, okay, 8.5 to 10.5. So let's talk about hypocalcemium. Let's say you have a patient who has advanced cirrhosis and their calcium is 6.5. Should you repeat? Yes, right, because it's slow and we just said that the normals are on 8.5 to 10.5 there at 6.5. I'm trying to trick you here. If you're thinking that you need to check another lab, you're absolutely right. You need to check for albumin and correct the calcium level for albumin. So the cirrhosis was actually a clue because remember, albumin is made in the liver and patients with cirrhosis will have lower albumin levels. So you have to actually correct the calcium for albumin and why would that be? Serum calcium is actually bound in the blood to protein such as albumin. So if your albumin is low, it may not accurately reflect the free calcium. So there's actually two ways to figure out what is the free calcium in the blood. So one of the ways is to just use a formula to correct for albumin. So you can use MD Calc or you can just learn the formula which is pretty easy. The formula is you take the measured calcium plus 0.8 times the quantity of 4 minus albumin. Let's break that down. 4 is the normal level of albumin. So you just subtract the patient's albumin. So let's say the cirrhosis patient's albumin is 2, you would do 4 minus 2 equals 2. And then you do 0.8 times that value. So 0.8 times the quantity of 4 minus 2 is 1.6. So 1.6 is the correction factor and then you just add that to the measured calcium. So the measured calcium in our patient's case was 6.5. So we do 6.5 plus 1.6. And we find that their corrected calcium is actually 8.1. So it wasn't as bad as we thought. And then the second way to, if the albumin is low and then their calcium level is low, you can check their ionized calcium because that'll tell you there's another normal value for ionized calcium and if that's within the normal range it tells you that their calcium actually isn't low. So remember two ways to check and the formula that you should know is measured calcium plus 0.8 times the quantity of 4 minus albumin. We always correct calcium for albumin. Now what happens when calcium is low? How do patients present? They can have tetany, seizures, spasm because remember calcium is another key player in the muscles. They can also have QT prolongation. And then there's two specific signs that you might get tested on. Any idea what those, there's special names for those signs and you should kind of be familiar with them. So what if you tap a person's cheek and their facial muscles start to twitch? What's that called? Chvostech sign. And then what if you put a blood pressure cuff on a patient's arm and you inflate it to systolic pressure and then their hand starts to twitch, it's the spasm of their hand and their wrist? That's true so sign. Okay. So remember Chvostech is the cheek and true so is the wrist with the blood pressure cuff. If calcium levels are truly low you can replete them with calcium and gluconate. And then the next one that we should know is hypercalcemia. So what happens if calcium level is too high, how do patients present? For whatever reason this is probably my favorite mnemonic in first aid. But the mnemonic for hypercalcemia is stones, bones, groans, thorns and psychiatric overtones. So kidney stones, bone pain, groans refers to abdominal pain, thorns refers to toilet because increased urinary frequency and then psychiatric overtones so they can have anxiety or altered mental status. So just remember stones, bones, groans, groans and psychiatric overtones. And what's the treatment for hypercalcemia? How do you manage it? This is also my favorite treatment because it's easy to remember if a patient is hypercalcemia you just give IV fluids, normal saline or LR just give IV fluids. Now you might be wondering if I forgot sodium. It is the first electrolyte that we write in the fishbone so it must be pretty important. And I did not forget it but unlike hypercalcemia sodium abnormalities are my absolute least favorite because they can get very, very complicated. In terms of how they affect the body, any idea what happens with high or low sodium? It's pretty similar. Any abnormalities in sodium whether it's high or low can lead to stupor, coma, malaise, irritability. What you should really understand about sodium is that abnormalities in sodium really tend to reflect what's going on with the water in the body, right? Because we always learn with osmosis water follows the salt. So if sodium is high, it generally means that the person is dehydrated and another clue that a person is dehydrated can be higher levels of all of the electrolytes and kind of all of the lab because they tend to get concentrated. So high sodium should make you think of a person being dehydrated. And low sodium can sometimes mean that they are over hydrated and treatment can sometimes involve, pretty often it can actually involve water restriction, sometimes salt tabs of extreme. But just think of high sodium as dehydration. And low sodium can often mean a state of over hydration but you can also have hypolimic hyponatremia. So we'll talk about it really quickly. I just want you to remember when we talk about sodium though that this is a very, very complicated topic and it could probably be a lecture or a podcast episode in itself. So I'm going to try to give you kind of the major highlights regarding sodium. And then I'm going to encourage you to go read more about it or hopefully down the line we'll have a more comprehensive episode on hyponatremia. Because these are important topics to understand, especially if you're going into medicine. But they can be very complex and difficult to explain in a condensed kind of way. So there are some algorithms actually to figure out, to help you address both situations of hyponatremia. And there's an excellent set of graphics in the book Step Up to Medicine which is one of the resources that I used when I was studying for my Step 2 exam. And those graphics go really well into how you should kind of map out hyponatremia in your head. So my first question to you is going to be what is a normal level of sodium? Around 136 to 146 million equivalent per liter is a normal level of sodium, okay? And let's say a patient is hyponatremic. So their sodium is 128. What's the first step to kind of diagnosing their hyponatremia? So the first thing you want to do is actually measure their serum-osmolality. And that's a lab that you can order. And if there's serum-osmolality, so I guess first I should ask you what's normal serum-osmolality? It's around 280 to 295. okay, 280 to 295. So if their serum osmolality is high, like it's, let's say it's 310, that generally indicates a hypertonic hyponatremia, okay. So there's some kind of osmotic substance present, whether it's sugar, it can happen in hyperglycemia where you get a falsely elevated sodium, and then there's also a special formula to correct the sodium for the sugar level, which you can actually look up on MD-Calc, but in hypertonic hyponatremia, there's some kind of osmotic substance present, whether it's glucose, in hyperglycemia, or manitol, or glycerol, that's one branch. If the osmolality is normal, 280 to 295, this is generally pseudo-hyponatremia. So in this case, something else is high, and it's generally something like proteins, or triglycerides, or abnormally high, and so their sodium levels are actually normal, but they're just looking falsely high because of the proteins, or triglycerides. Okay, and then if your serum osmolality is truly low, if it's less than 280, this is when you have true hyponatremia, okay. So when you have hyponatremia, and the sodium is low, the first thing you need to check is the tenicity. So if they're hypertonic, or they're normatonic, there's other explanations. If they're hypotonic, and it's a hypotonic hyponatremia, this is a true hyponatremia, okay. And then after you check for the tenicity, the next thing you need to check for is the volume. So you need to assess the patient's volume status, and this is something that you'll get used to as you do physical exams on patients. If a patient appears dry, if they are hypovalemic, then, you know, their total body sodium is low. And in this situation, it's generally recommended to measure their urine sodium, because if the urine sodium is high, then that tells you that they're losing sodium in their kidney, and they're losing sodium as well as volume in their kidney, because remember, water follows sodium. So if they're excessively using diuretics, if they're aldosterone levels are low, if they have acute tubular necrosis, they're going to be just, you know, dumping sodium into their urine, water is going to follow the sodium, and they're going to have renal salt loss, and they're going to have a hypolimic hyponatremia. If their urine sodium is low, though, they're losing the salt elsewhere in the body. It's not leaving through the kidney, but perhaps it's leaving through the GI system. They may have diarrhea or vomiting. They may be sweating, or they may be third spacing. So, you know, if they have a true hyponatremia, and it's a hypovalemic hyponatremia, you need to figure out where they're losing the sodium from, because they're losing the sodium, and then they're losing the water, because water follows sodium. So it's either through the kidney or through some other place in the body. So if the urine sodium is high, then your source is a kidney, and if it's low, then it's going out from somewhere else, such as the GI system. Now, what if you assess their volume status, and their hypervalemic? They're really, really swollen. They have three plus pinning a D-million bilateral lower extremities. They have a sitease. They almost have anusarca. What are certain conditions that can cause that state? So, anytime you think of hypervalemia systemically in the body, there's three organs that should come to mind as the likely culprits. The heart, the kidney, and the liver, okay? Congestive heart failure, nephrodix syndrome, and liver disease, or cirrhosis, are all three conditions that can give you a diffuse state of hypervalemia. Hypervalemia can, it's a lot of water in the body, and think of it as just flooding your sodium. So tons of water in the body, low sodium, that's a hypervalemic hyponatremia. And then, finally, the last option, if they're non-hypovalemic, they're non-hypervalemic, let's say they're uvalemic. They appear perfectly normal, like you and me, and they're not dehydrated, they're not overhydrated. They're uvalemic. What are some causes of uvalemic hyponatremia? So, Si-ADH syndrome of inappropriate ADH is a condition that can cause a uvalemic hyponatremia. This can also happen with hypothyroidism, and interestingly, it can also happen in psychogenic polydipsia. If a person just drinks a ton of water, they can actually get a uvalemic hyponatremia. So, these are some kind of important, this is an important algorithm to know. And then, the management of hyponatremia really depends on how severe the hyponatremia is. If it's mild, let's say their sodium is just 120 to 130 millimoles per liter, we generally just withhold free water, and we restrict their water intake and allow the patient to kind of re-equilibrate spontaneously, because your kidneys are amazing, and if they're working properly, they will do that for you. So mild hyponatremia, 120 to 130, just withhold water. If they have moderate hyponatremia, 110 to 120 millimoles per liter, we generally give loop diuretics, and they can sometimes be given even with saline to prevent the kidneys from concentrating the urine. So, if it's moderate at this point, we do want to give an intervention, and that intervention is typically loop diuretics along with saline potentially. And then, finally, if a patient's sodium is extremely low, like less than 110, or if they're symptomatic, and, you know, levels that lower super dangerous, because you can have seizures even, and very low sodium levels are sometimes criteria for ICU admission because they need to be closely monitored for their neurologic status. So, if sodium levels are severely low, or if the patient is symptomatic, you give hypertonic saline, and you actually want to increase the serum sodium, 1 to 2 million equivalents per liter per hour until the symptoms improve. And why doesn't matter to monitor how quickly the sodium levels are increasing? Why is that important? So, another excellent mnemonic that I got from first aid. From low to high, so from low sodium to high sodium, the ponds will die. If you repeat the sodium too rapidly, you can get an extremely dangerous condition called central pontein demyelination. And this is, you know, it permanently affects the patient for life. There was an episode in Grey's Anatomy about this, actually, if you are Grey's Anatomy fan. But from low to high, ponds will die, and you can get central pontein demyelination if you repeat the sodium too rapidly. And then the other part of the mnemonic is from high to low, the brains will blow. So, if your pitas, I mean, I'm sorry, if your sodium is high, and you bring it down too quickly, you can get cerebral edema. So, both ways you want to be really, really careful, and you want to monitor these patients. And that is why sodium is one of my least favorite electrolyte abnormalities because it involves checking labs very frequently. Q2 or Q4 hours, and you have to make sure the sodium is right. And it never does what you want to do, even if you do the intervention that you think will help them. So, these can get really complicated. They typically involve an effrology consult, and they can be very mind-boggling. But, you know, having a basic idea of the algorithm, so for hyponatremia, we start by calculating the tenicity, and then we assess the ECF status and try to kind of actually figure out what's happening. That's important to know. And then, for hyponatremia, you also want to assess the ECF volume, okay? So, assess the patient's volume status. If they're depleted, it's a hypotholimic hyponatremia where they're losing water more than sodium. So, this can also be from diuretics. It can be from osmotic dioresis. For example, if they have excess sugar in their urine, it can be from renal failure. It can also be extra renal losses, kind of like we talked about with hyponolimic. So, if, you know, if their volume status appears depleted, and if they're hyponolimic, think about these causes. If they're hypervalimic, you know, if they appear a demonis, it seems that they have gained more salt than water. And this can also be multifactorial. It can be, it can be itatrogenic. It can be from sodium bicarb therapy. It can be from transparentaryl nutrition. It can be from exogenous glucocorticoids or cushing syndrome. Or it can be from primary hyper-aldosteronism. So, think about, you know, your adrenal hormones. Any of those can be implicated in hypervalimic hypernatremia. as well as eye atrogenic causes and then finally a very common cause of or I guess I should say a commonly tested cause of norisolvalemic hypernatremia. Can you think of one? It's diabetes insipidus. So remember diabetes insipidus is a condition where your body does not react to ADHD and it can be either central where your body is not producing ADHD or it can be nephrogenic or forever reason your kidneys are not responding to ADHD. But the anti-diuretic hormone is secreted but it's not acting and so you're just losing water through the urine and this actually causes a uvalemic hypernatremia and it's something that you should know. And then in terms of management it differs depending on what is the cause of the hypernatremia but I'll start by asking you about isolvalemic hypernatremia and the most common example that's used on tests being diabetes insipidus. So if a patient has diabetes insipidus how can you treat that? So if the problem is central and they're not secreting the ADHD then you can give them vasopressin you can also give them fluids or D5 if the patient can drink. So D5W is just water with dextrose and there's you know there's no salt in it. And then for hypervalemic hypernatremia we typically give diuretics with D5 to remove the excess sodium. For hypervalemic hypernatremia we typically give isotonic sodium chloride to kind of restore their hemodynamics. And another calculation that can be useful to have on rounds with you whenever you're dealing with a patient whose hypernatremia is to calculate their free water deficit. Because remember what I said earlier the concept is that water follows salt. So whatever the salt is doing is actually an indicator of more importantly what the water is doing. So if the salt is high I mean if the sodium is high then that means that they're dehydrated so there's a water deficit and you can use the calculator to figure out what the free water deficit is and that can be a helpful tool to help you figure out how much fluid you actually need to give. So I'm a little bit out of breath from talking so much about sodium which is a topic that I've spent a lot of time trying to kind of wrap my head around and it still continues to baffle me a lot. But from this episode the major takeaways that I wanted you to have were kind of understanding the basics of the main electrolyte, potassium, magnesium, phosphorus, calcium, and sodium. You know understand why we check these levels in the hospital whenever we do check them very rigorously and why it's important to replete them what can happen in the principles of management. If you're at least familiar with that concept then when the time comes and you're you know you're assigned a patient whose sodium level is low at least you have a starting point and you know you know what algorithm to look up or you know that there even is an algorithm to look up so that you can then go from there. You know I say this time and time again in my episodes but everything we do in medicine has a reason and I think that understanding that reason and understanding the physiology and the clinical applications of that you know of that intervention or of that lab that we check it's so so important because that builds your foundation and if you are solid in that knowledge then whenever you're faced with a situation of unknown and you have a situation that you're not exactly sure what's going on with the patient you can use your basic knowledge to kind of puzzle through and I really think that's the beauty of medicine because there's so many questions and there's so many puzzles that are presented to us and it's the basic fundamental knowledge understanding the why behind literally everything that is extremely important and I think that makes learning medicine fun and I think that makes you know that's an important part of our job so that we can do what we do and help people every day. So thank you so much for joining me on that episode I hope that this was useful to you you know electrolyte management is hard and again don't feel bad if you don't remember the exact doses and formulations of things when you're an intern and you're doing this every day you'll know them really well and then if you go into a specialty like me and radiation oncology you'll quickly forget that as well but that's not the most important part the most important part is understanding the why like I just said so with that I'll let you be thank you so much again for your time it's really really appreciated as we're getting closer to the end of the year I'm starting to put together just a list of statistics regarding how many followers we've gained and how many viewers we've gained and how many people have joined our team and it's really you know it warms my heart to see how many of you guys are listening to our podcast so thank you for your continued support if you have any questions comments or concerns please log on to our website at spoonfulofsugar.org and you can post them under the link for this website if you're interested in joining our team this season is actually coming to a close but we are definitely looking for people for next year because we'll definitely be coming back so please reach out and we'll keep you in mind and you know in the meantime just remember spoonfulofsugar is always here to help the medicine go down thank you