The last thing I was asked to talk about is electrolyte emergencies. Again, I was asked to talk about a lot of them in 15 minutes. That's going to be awful hard. So we'll try to do the best we can. I want to leave you with a couple of principles. The first is identify the cause of the change, just like we talked about with AKI and with acid-based status. You've got to understand what's causing the problem, OK, because resolution of the change requires correction of the cause. The next is that clinical manifestations and symptoms are not specific, really. So when you've got your textbooks in medical school and everything, and we all said, oh, hyponatremia makes you feel this way and hyperkalemia does this. In reality, there's a ton of overlap. OK, so if the patient is completely undifferentiated in the emergency department, it could be any one of these things. Fortunately, we get so many labs on our patients nowadays that usually they're not undifferentiated that long. And we usually have a sense pretty quickly of what the problem is. The next thing is that clinical circumstances and symptoms should determine the urgency of therapy, not the absolute electrolyte value. OK, so who has called nephrology for the K of like seven and a half in the ESRD patient and a nephrologist barely woke up in the middle of the night? OK, right. You need to you need to tell them something else to get them awake because we're not going to care so much about the absolute value. It's probably been that high for four days. And then frequent reassessment is really recurred. So I am going to shamelessly say that I got a number of cases from FCCS because the FCCS electrolyte thing is very good. But in case you haven't done that, I'm just going to show you some of these cases. So an 80 year old woman came with hypertension, heart failure, confusion, poor oral intake, a little bit tachycardic and has some non-sustained VT on the monitor. So does the patient have any risk factors for electrolyte disorders? What are they? She's old. Heart failure, so she's probably on some sort of diuretic or something like that, right? She may not be eating super well. There's all sorts of issues right here, potentially. What electrolyte disorder does she have? What's that? Hypokalemia, I heard someone say. Right. But she's also sort of altered and everything, right? And she's lethargic, could be low sodium, too, right? There's all sorts. It could be high sodium, right? So the point is, is that all of this is very difficult to sort of just pinpoint based on history. OK, so in this case, her K was 2.5. All right. So what do you do now? How do we evaluate and sort of treat this patient? So let's think about hypokalemia. So if the K is really, really low and they or if they're on digoxin, we sort of divide them into life threatening or non life threatening symptoms. If they're life threatening, then we need to put a central line in and correct this pretty quickly, right? If they're not life threatening, then we can even we can even correct it entrally. Has anybody done that? I mean, like, you know, we sometimes rush to do, you know, IV stuff and we don't necessarily need to. OK, if the K is less than 3.5, but greater and they have no symptoms, then it really should be enteral. OK. All right. 80 year old, the same 80 year old woman now with hypertension, heart failure, complaining of feeling weak, has an EKG that looks like this and a K of 7.8. Very similar symptoms, right? All right. So are you concerned now? Yeah, you bet. All right. So muscle weakness, cardiac arrhythmia, so those are peak T waves, loss of P waves, right? I had a patient actually just last week in my unit who went into just basically like a sudden junctional rhythm and no other EKG changes. And the K was like five and a half. And I wasn't putting a lot of it on to it. Other reason to potentially go into junctional rhythm. But we corrected the K, adjusted her dialysis. And then sure enough, the whole thing solved itself. The junctional rhythm. OK, so what causes hyperkalemia? Increased intake, cellular shift or decreased urinary excretion. OK, the increased intake really does have to be paired usually, though, with decreased GFR, because if your GFR is normal, you should have no trouble excreting the extra intake. And the three biggest ones in hospitalized patients or even in non-hospitalized patients are potatoes, tomatoes and citrus. Who thought it was bananas? OK, it's potatoes, tomatoes and citrus or anything that contains those products like potato chips, you'd be surprised how many times I have to tell that to patients. Potato salad, lemonade, grapefruit juice, orange juice, tomato soup, tomato sauce, tomato slices, you know, fried tomatoes where I'm from. OK, a few of these other ones. I've never had a burnt match heads, I must say, head situation. But I put it there just to let you know. Cellular shift, acidosis and like cellular lysis. So like big hematomas that are being reabsorbed or like rhabdo. Those are your big causes of cellular shift and breakdown. Hyperglycemia, usually because of inadequate insulin, beta blocker overdose, all of those. And then decreased urinary excretion is usually going to be patients who have some impairment in the kidney's ability to get rid of potassium. And this is almost always going to be CKD patients or patients with like AKI. There are some rare other disorders where you can affect potassium excretion, but those are going to be few and far between. Makes sense? OK, this is a busy slide. Do you really want to know this? No, you do, yeah. OK, some people are saying, yeah, so I have to give in to them. OK, so first of all. You don't lose potassium when you're given Lasix because you block the sodium, potassium and 2-chloride channel in the loop of Henle. You don't have any net potassium excretion anywhere until you get to the distal nephron. OK, and there are three things that drive potassium loss in the urine. The delivery of sodium to the distal nephron, because as you reabsorb that sodium, you have to keep the urine electrically neutral. So you're going to put out potassium and magnesium. So distal delivery of sodium, higher urinary flow rates. And then the presence of aldosterone. So when you give somebody diuretics, you're increasing the distal delivery of sodium, you're increasing the urinary flow rates and you're stimulating aldosterone production. So you're the trifecta as to why you're going to start to lose potassium. But if anything increases those issues, you're going to lose potassium in the urine. So that patient who you're giving a bunch of IV fluid to and you're making them polyuric because of their rhabdo, they're going to potentially lose more potassium in the urine. The DKA patient who is making polyuric and has had a bunch of increased urinary excretion for several days are going to be hypokalemic. Make sense? OK, those are the three factors. All right. How much time do I have left? Am I good? OK. All right. So hyperkalemia. So again, I know that if the number is eight, you know, we're all sort of clenching our sphincter a little bit there. OK. But the urgency of correction should be determined, first of all, is does the patient have any symptoms and do they have any risk factors to spontaneously go into VT? OK. And those big ones are, have they recently had their heart cut on? Have they had an MI? Do they have a history of VT or VF? OK. Those are going to be your three big ones. In the absence of any of those, then you really can get by with gentle correction. In most patients, slowly remove the potassium. Use your four D's. You know what the four D's are? Diuresis, diarrhea, dialysis or drugs. OK, I'll get into the drugs in a situation in just a minute. If they do have these issues, then we need to get urgent correction. And that means first to stabilize the myocardium, which means we need to give calcium and or hypertonic saline. Most of us give calcium because it's faster. OK. Then we need to shift. And that's insulin and beta agonists. OK. If their glucose is 700, they don't need insulin and glucose. OK, so the delivery of glucose is only to make sure they don't die from the insulin overdose you just poisoned them with. OK. So it's insulin is the treatment. It's not the dextrose is the treatment. And beta agonists, so albuterol. OK, what is missing from this? Bicarb. OK, bicarb has been shown in studies to not be effective. So don't reach for it unless they're very acidemic. But even then, it's slow. All right. And then we need to rapidly remove the potassium, which gets back to our four D's of diuresis, diarrhea, dialysis or drugs. OK. All right. So let's go through these calcium. There's no change of potassium level. It stabilizes the myocardium. Hypertonic saline improves the ECG in patients with coexisting hyponatremia. It's not really recommended if they're eutremic or hypernatremic. OK, it doesn't really do much. But if they have coexisting hyponatremia, it can be very useful. And it's probably a little bit safer if there's a didge overdose than calcium might be shifting. So insulin, I told you five to ten units decreases the potassium by 0.6 in less than five minutes. It activates the sodium potassium ATPase. And then you may need to do an insulin infusion to lower it over like 90 minutes. OK, beta adrenergic agonist. The max effect is about 30 to 60 minutes, primarily done as an inhalational, like continuous inhalation. If you don't have any access to anything else and you're like you're on an airplane or something, you could give the IV epi. But or I am epi. Sodium bicarbonate is very controversial. Boluses probably have no effect. If you're going to do it, you probably need to use an infusion over time. All right. So elimination diuretics. We talked about this a little bit. Loop diuretics and orthiazide diuretics do not use amyloride spironolactone to do this because we're going to be blocking the distal excretion of sodium, our distal reabsorption of sodium. And so therefore, we won't be able to excrete as much potassium. So we need that ENAC channel to be open. OK. You can use acetazolamide if they're not responding to the loops in the thiazides. If they're euvoleumic, think about giving IV fluids and the diuretics. OK. So like if they look like us, but they come in with a K of eight, you might want to give IV fluids and diuretics because the whole goal is to drive urine output and salt delivery, which you'll do if you give them IV fluids. So this is one of the few instances that you would do that. Dialysis. OK. So hemodialysis fixes this problem way, way. I should have put 75 greater than things here. OK. Minute by minute, CRT is not efficient. Right. so do not call me and say I need CRT when the patient's on Even if they're on four pressers and a K of nine I'm gonna call in my dialysis nurse to do dialysis and then we'll put them on CRT Okay, we're gonna have to bite the bullet for a couple of hours because you need to save this patient's life Which is not gonna happen if we do CRT for a couple of hours, okay? So rebound can happen which is why oftentimes I'll follow it up with CRT afterwards. All right, what about Drugs, so first of all, let me say that we need to stimulate diarrhea in the colon And that's all that K Xolate is good for because it's mixed with sorbitol Okay, K Xolate is good for nothing else and should not no longer be what you use All right, we have better drugs and better options and the better drugs are pteramere and sodium zirconium Cyclosylate which is much better called local ma. The first one is called Beltassa Okay, your hospital should have one of these on formulary and we have increasing studies about these These are very effective as cation exchange agents to be given even in the emergency department for hyperkalemia Kxla is a very curious drug. It was approved. It was never approved by the FDA Because it was invented before there was an FDA Okay And again, the only reason why it causes potassium to go down is because the current formulations are mixed with sorbitol So it causes a ton of diarrhea and it can certainly cause who's had a bowel necrosis and had a perforation from this Yeah, good. So let's not use it anymore. Okay. All right case three 80 year old woman Hypertension lethargy confusion oral intake see the symptoms were exactly the same but her sodium was 118 Okay All right. So how do we evaluate and think about this? This is sort of your Progressive symptoms you don't want to get to the bottom, right? Okay All right. So let's think about this. We always think about sort of hypo osmolar or hyper osmolar I make a note here this sort of pseudo Hyponatremia does not exist anymore Okay modern Chemistry machines that every hospital in America uses does not get fooled anymore and cause pseudo hyponatremia So they're either hyper osmolar or they're hypo osmolar and you got to sort of decide that a little bit the overwhelming Majority of them will be hypo osmolar Okay, so they're either this whole like Hypovolemic euvolemic or hypervolemic who remembers that from medical school, right? Okay, so if they're hypovolemic and the urine sodium is low then that's like vomiting diarrhea Volume depletion all these other ones potentially. Okay So this is like the patient who is vomiting a ton at home or having a ton of diarrhea and they're drinking water They're like, oh I got to stay hydrated. So they're drinking water, right? They really need like oral rehydration solution They need like salty water, but they're only drinking water So they're pooping out a bunch of salty water and they're replacing it with water. Does that make sense? Okay The urine sodium is being high in Hypovolemic these are gonna be weird kidney problems or diuretics these oftentimes you might need a nephrologist to help you solve This could also be like a weird adrenal insufficiency problem or something else like that. Okay Then you got your hypovolemic which are your heart failures your nephrotic syndromes of the world They're gonna have low urine sodium their total body fluid overloaded But they're having trouble with perfusion of the kidney And so their kidney is holding on to salt and instead of in an effort to hold on to water And so then again, you're gonna fix that with diuresis and then your euvolemics are the ones that we all get confused about right? Okay, so the key here is is that if the urine sodium is going to be high because the kidney has no reason to retain Sodium it's seen a normal perfusion and a normal volume status and it's saying I don't need to hold on to any of this salt So that's why the salt is high Then the question is is the urine dilute or is it concentrated if it's concentrated? Then it's one of these issues with by far the most common one being SAADH in our hospitalized patients, which is syndrome of appropriate ADH release our body ADH mechanisms respond to certain stimuli like Nausea and pain and it up regulates the production of ADH under normal mechanisms Okay I see this a lot in like young women who have had surgery for example Their bodies seem to be really up regulated a lot of times with production of ADH and that's not SIADH It's SAADH. Okay, SIADH is like a tumor producing it and it's not under any control all right, and then this one is like your Polydipsia is you can get into your Your like tea and toasters will have dilute urine a lot of times and beer podomanias and such. Okay You all know that formula volume status So we got to figure out the volume status and we got to go from there And then we have to think about how we're gonna sort of treat through all of this Okay And this is how it sort of breaks everything down if you work through this treatment pathway or a decision tree So then how are we going to do this? So If they're hypoasmolar they oftentimes have what did I say hypo Hold on. I gotta remember what I'm trying to go through on this one. Oh If they've taken it too much There's ways that patients can sometimes become have a ton of hype it this should have said hyperosmolar fluid intake I apologize about that. Okay, so there's some surgical irrigation fluids that have a ton of Like mannitol and stuff in them and they can become quite hyponatremic from hyperosmolar and then freshwater drowning But it's not been seen in humans as much. Okay. So what's the how do we let me in the interest of time? Let's get squipped to the management. So harm from aggressive or brisk correction of hyponatremia, right? We've all heard about that That causes what central pontine myelin isis, right? Are you gonna see the symptoms of that in the ICU generally not? It's gonna be 12 to 14 days Maybe 16 days later when they're at home and they're gonna come back with like alternate mental status So you're gonna have to be careful on this one. So you always need to be careful about About overcorrection of hypovolemia Excuse me hyponatremia because it's almost impossible for us to clearly say what the acuity is You know, like did this happen over like seven days or did this happen over 24 hours? It's really unusual for us to be able to see it And just be able to say for sure that it was like 12 hours ago So you need to be very careful. We used to say that sort of like 10 to 12, maybe up to 14 now We really think it's more like 8 to 10. You don't want to go above 8 to 10. Okay You want to think about DDA you want to think about hypertonic saline? It does not require a central line as someone already eloquently said and it's the mainstay of therapy for severe hyponatremia If you have over corrected there is data that supports the use of re-lowering with DDA VP and water Okay So if you have over corrected you should give DDA VP and water so that you can re-lower it back to this level It's not going to eliminate the risk, but it's going to lower the risk of central pontium myelodysis Okay If their volume contracted you need to give normal saline until their volume replete If their volume is normal or overloaded then we need to free water restrict them Don't give them any IV salt and limit conditions associated with This but just be mindful that if their volume depleted and you replace their volume They can oftentimes start over correcting very quickly because their stimulus for ADH goes down their body starts saying I'm gonna get rid of all of this water that I didn't need. Okay, so just be careful Yeah These are all the things that can cause our patients to get polyureic or a fluid over and over correct too quickly All right. What about VAP tans? So these are the v2 receptor blockers. They allow for free water to be excreted They're very costly. You can consider them if other therapies have failed The newer kid on the block is powdered urea. It tastes like lemonade You can tell your patients that they're drinking powdered pee. It really goes over Okay It's extremely effective in elevated ADH states So SADH or SIADH and the patients are very well tolerated. It's easy to administer It's cheap and it very rarely over corrects and the way it works is by stimulating the kidney to excrete extra free water Okay What about hypernatremia this again happens from Excessive sodium intake water losses or loss of water greater than loss of salt Okay These are your symptoms that you can have and the management is to replace free water either enteral or IV Okay in young people you need to be worried about the speed of correction in old people who have had Cerebral volume loss we have good data now that suggests that the risk is very very low So that nursing home patient who comes in with the sodium of 170 whose brain is really tiny You can correct that really quite quickly because they're not gonna herniate from that Okay Alright hypercalcemia We're just gonna quickly go through these the main state of management is to decrease calcium reabsorption to increase calcium Elimination you do that with forced diuresis again and or hemodialysis. I'm sorry that I cut that off down there I need to fix that slide. I will do that and send it back Hypocalcemia The symptoms are like paresthesias tetanus seizures prolonged QT In the long term. Alright hypophosphatemia. This is skeletal muscle weakness in rhabdo Who has had patients with like an ability to wean off the ventilator? In your career and then you finally check a phosphorus and it's like two and you start giving them phosphorus and they make a lot Of progress, right? Okay, our muscles need phosphorus. You can also get cardiomyopathy cardiogenic shock. This is how anorexic patients die is from hypophosphatemia Nerve dysfunction amylosis and death. Okay These are the main causes the big ones that we're gonna run into our insulin and refeeding syndromes and potentially CRT If you are using a phosphorus free solution And then you just obviously need to replace with phosphorus I tend to personally if it's less than two to two and a half. I usually give IV phosphorus, but That's that and then hypomagnesemia There's a lot of things that can cause this the big ones to be Mindful of I think in the ICU that we tend to forget is that when we give diuretics, we're gonna also lose Magnesium and then chelation when we're using like CRT with citrate anticoagulation. We're not only chelating the calcium We're chelating the magnesium. And so those patients will oftentimes need more magnesium supplementation okay, and Replacement is there and I think that's about it hypermagnesemia We Don't see this too often in significant ways and maybe you're pregnant patient who has been given too much But okay. All right. So in the interest of time I will leave you with that because you've listened to me way too long and you've been very generous with your attention I hope I didn't put anybody to sleep and I'm sorry if I did All right. I will be happy

electrolyte emergencies

hypokalemia

hyperkalemia

hyponatremia

treatment strategies

clinical symptoms