Narrator - Dr. Abel 00:00 Welcome to HelixTalk, an educational podcast for healthcare students and providers, covering real life clinical pearls, professional pharmacy topics and drug therapy discussions. Narrator - ? 00:11 This podcast is provided by pharmacists and faculty members at Rosalind Franklin University, College of Pharmacy. Narrator - Dr. Abel 00:17 This podcast contains general information for educational purposes only. This is not professional advice and should not be used in lieu of obtaining advice from a qualified health care provider. Narrator - ? 00:27 And now on to the show. Dr. Sean Kane 00:31 Welcome to HelixTalk. Episode 43 I'm your co host, Dr. Kane. I'm Dr. Schuman and I'm Dr. Patel. Today we're covering what a typical practitioner should know about diabetic ketoacidosis. So this is by no means comprehensive, but it's kind of a good overview to have a good idea of why DKA happens diabetic ketoacidosis and how we treat that. Speaker 1 00:50 And I'm really glad to be doing this episode with you, Dr. Kane, because I teach diabetes and I go over the emergent treatment of DKA, but I'm not talking from a practice perspective, where versus this is something that you see in your routine practice. So we would appreciate your clinical pros Speaker 2 01:06 here and even in the even in the world of psychiatric medicine, we see a fair amount of diabetes, insulin resistance, sometimes secondary to medication second, sometimes secondary to lifestyle choices. So it's always relevant. Dr. Sean Kane 01:18 Yeah, and I would say that, you know, DK is very common for our 17 bed ICU, it would be a typical week, would be a DKA patient a day or every other day. So we definitely see a lot of DKA in most intensive care unit settings, just by virtue of the monitoring required and the kinds of medications we give. Generally, these patients have a very brief ICU stay, typically between 12 and 24 hours, until we kind of get them stabilized. So Dr. Patel, what exactly is diabetic ketoacidosis, versus diabetes or versus many people, when they hear ketones, they think of the Atkins diet. So what is DKA? Speaker 1 01:52 Then DKA basically stands for diabetic ketoacidosis, as we discussed, in patients who have controlled diabetes, or, let's just say, slightly uncontrolled diabetes. We know there is insulin, maybe it's not utilized by the cell as nicely, and that's why your blood glucose is higher. But what happens in DKA is that your cells are completely starved, and there is not enough insulin at all, which ends up increasing the blood glucose sometimes in five hundreds or even six hundreds. Speaker 2 02:21 And to be clear, this is something that generally occurs predominantly in type one diabetes, as compared to it can occur in type two diabetes, but less commonly, maybe 10 to 30% of the cases. Dr. Sean Kane 02:32 So in thinking about the pathophysiology with DKA, keep in mind that insulin is kind of the key that gets the glucose molecule into the cell right. So the key factor with DKA is that we just don't have enough insulin to get enough glucose into the cell, so the cells are starving for energy. Speaker 2 02:48 The way I always talk about it when I'm speaking to students or patients, is again, an idea of like a conveyor belt. And so we think of this insulin as the individual who's pulling the packages off the conveyor belt, putting them where they need to go, instead of them just running right toward the end of the conveyor belt, and then they just keep and then they just keep piling up, piling up, piling up. Dr. Sean Kane 03:05 And that's why we'll see you know this high blood glucose is that the insulin isn't getting that glucose from your blood into the cell, but that's also why we'll see the Keto acids. So these ketone bodies, this is the body's way of getting energy in a non Speaker 1 03:19 glucose source. So where are these ketone bodies coming from? Dr. Sean Kane 03:23 They come from your fat cells. So lipolysis, the breakdown of fat, is how you end up with these ketones that your body can use as energy. And as we said, like with the Atkins diet, this is kind of the goal, if you will, to have a little bit of ketosis. But we don't want to have diabetic ketoacidosis, where you have this accumulation of all of these ketones to the point where you actually impact your acid base balance in your body, where you get acidic, to the point where you can have nausea and vomiting, and really bad things can happen from that. Speaker 2 03:51 So there's a couple of these. The main ones of these acids is we have with beta hydroxybutyrate and acetoacetic acid, and those are really the main two of what we call keto acids. And then when practice, we commonly test for beta hydroxybutyrate, and that's the one we use to commonly test for DKA. Speaker 1 04:08 When you have higher ketone bodies present, it acts as a GI irritant. So you see a lot of GI issues such as nausea and vomiting, and then it further deteriorates the problem of dehydration, because you're putting out all that volume outside. Yeah. Dr. Sean Kane 04:21 So as the patient is getting more nauseous and they're vomiting, on top of that, they're also peeing a lot. So if you can't keep up with your oral intake, in terms of your hydration status, you're going to get dehydrated, not just because of the nausea and vomiting, but because you have this osmotic diuresis, because your blood sugar is super high, you know, 600 or 700 something like that. So these patients will get dehydrated, and that's really like the core acute management of DK. It's actually not correcting the blood sugar, it's rehydrating the patient so that their blood pressure is better, so that their kidney function returns. You know, we see a lot of acute kidney injury where these patients get pre renal where they have inadequate flow to the kidney. So. They don't make urine. They have poor GFR. Speaker 2 05:02 And then when we talk about dehydration, again, it's not just in fluids, but also we have electrolyte deficiencies. We can see so potassium phosphates and magnesium as well. Yeah. Dr. Sean Kane 05:13 So really, the long story short is that the cells aren't getting the energy that they need from glucose because there's not enough insulin that causes the cells to break down the fat stores, so we have lipolysis that causes these ketone bodies to form that are acids in the body that causes nausea, vomiting, dehydration, and on top of that, because the glucose is in the blood instead of in the cells, the kidneys will say, Hey, I got to pee out all this glucose that causes this osmotic diuresis of electrolytes and fluid that really contributes more to the dehydration that causes hypotension, acute kidney injury, and a lot of the manifestations that we see in terms of the clinical picture of a DKA patient. Speaker 1 05:53 And so let's talk about what are the different factors that contributes to our precipitation of situation like DKA. So we talked about pathophysiology, that there is not enough insulin available. Maybe this is just a pure medication non compliance, that the patient who needs insulin around the clock is probably not getting it, or if they are getting it through a pump, maybe there is some sort of pump failure — for example, the insulin pump has come out and they're not getting enough insulin delivery. Speaker 2 06:21 And another big piece of it's going to be stressors. And so one, one big stressor, you see, is going to be infection. And again, anytime there's a stressor, the body can go into fight or flight mode, where the idea is the body needs to gain energy to be able to fight off, whether it's sickness, fear, whatever it is. So the body is pouring out sugar. And so if the insulin is not there to be able to take that sugar and use it, you start to see the sugar piling up. And so a lot of times when we do have somebody come in, we want to rule out any sort of infection that has led to that stressor. So looking for things like urinalysis, CXR, things like that. Dr. Sean Kane 06:53 Then on top of the stressors, infection is definitely the most common stressor that we see. And sometimes it can even kind of be a subtle sub clinical infection, and that's why we're looking for a urinalysis, even if the patient isn't complaining of UTI type symptoms. But on top of that, we're also worried about non infectious stressors that are less common but may be more severe. So as an example, acute am I is something that is always at the top of our mind, and that's why we'll commonly get an EKG on these patients to look for any signs of ischemic damage. On top of that, we're worried about things like pulmonary embolism, strokes, this can be precipitated by a recent trauma or a recent surgery. So our workup is kind of twofold. One fold is that we're looking at what's going on with the dka aspect of it, and then also the second part is trying to figure out why they're in DKA. If it's as simple as non compliance because they can't afford their insulin, then it's we still have to do part of that work up. But our interest in identifying why they went into DKA is a little bit lower if they confirm compliance and they exactly know what their insulin dose should be, and they say, you know, I've picked up everything. I've been doing. It just fine. This just kind of happened. Then we're more worried about what could be causing it, anything from viral gastroenteritis all the way to an MI and our workout has to really encompass those things based on the clinical picture. Speaker 1 08:08 So when you see these cases coming through your ear, Dr. Kane, what's the most common baseline factor that you see? Dr. Sean Kane 08:14 The most common thing that I see is med non compliance. So the most common reason is someone either can't afford their insulin, because insulin is a very expensive medication, and things like patient assistance programs aren't as common with some of these insulin products as you would see with, let's say, some of the newer oral agents that have come onto the market. Speaker 1 08:33 So you're saying that if they're receiving proper care and a primary care side and getting enough medications and affordable medications, then it's very likely that we can avoid some of these decay cases altogether. Dr. Sean Kane 08:45 Oh, yeah, absolutely. So compliance is the easiest correctable factor, knowing that the social aspects of the cost of it is probably the more difficult thing to fix in someone who can't afford their medicines. You know, patient assistance programs and things like Medicaid can only get you so far, and only certain people can qualify for some of these programs, and it takes a long time to get them and things like that. Speaker 2 09:06 So now that we've looked at maybe the why of what occurs, we can look at what exactly is occurring. So in clinical presentation, one of the things you will note only to some of the dehydration we've already talked about, the diuresis, you're going to see things tachycardia, maybe the individual, again, is, if you're dehydrated, you may see some some low blood pressure there. So as the blood pressure is low, the individual is going to feel dizzy, orthostatic, and so they stand up, they may feel kind of they may stumble or feel weak. And then in compensatory mechanism for that is, they're going to see a tachycardia as well, so that you're going to try to get as much blood flowing as you can, in spite of some of that low blood pressure, Speaker 1 09:41 and one of the symptoms of the compensation for metabolic acidosis will be, you know, increased respiratory rate. So put out all that CO two that's in the in the blood, Dr. Sean Kane 09:50 and with the acetoacetic acid convert into acetone, some patients will kind of have a fruity smell on their breath. It doesn't have to be present in order for a patient to be in DKA, but if it is present, that's one of the potential findings that you can see. And then Speaker 2 10:04 just to reiterate, as Dr. Patel mentioned, nausea, vomiting and abdominal pain can occur both due to the metabolic acidosis and the nature of ketone bodies as that gastrointestinal system irritant, Dr. Sean Kane 10:14 in terms of our labs. So as we mentioned, this is an anion gap metabolic acidosis. And what that means is that all of these keto acids that are in the body create what's called an anion gap, and it's kind of beyond the scope of the podcast, but what that means is that we have these anions in the blood that are not measured in terms of they're not sodium, they're not chloride and not bicarb. And there's an equation to calculate what your gap should be, and then what you observe. So because of all these keto acids, we'll see that in the form of an anion gap metabolic acidosis. Also because of that, we'll see a low bicarb for our patients. And then also we mentioned our electrolytes. So potassium is typically it's either normal or high when a patient first walks in. And part of this is because of the shift that we see with the acid base balance. So kind of the quick and dirty way to remember it is that if you have a really acidic blood, your body wants to get rid of the acid any way it can. The way it can do that is it can hide those hydrogen ions in your cells. But to do that, it has to exchange with something else, and it exchanges with a potassium. So what happens is, as all these acids are going in your cells to kind of hide them. The potassium pops out and it ends up in your blood. So you have this intracellular shift. What will happen is, as you start correcting the blood glucose, that acid base balance corrects itself, and the potassium goes back in the cells. So it's really important, and probably if you die of DKA, the most common reason is either severe dehydration or an electrolyte problem that causes a cardiac arrhythmia. So potassium is something that we absolutely are worried about, that we're checking initially and checking pretty frequently on our DKA Speaker 2 11:50 patients, and then we'll talk about it, I'm sure, later, when we get into treatment. But again, just to emphasize with something, when I cover Dr. Kane in my nutritional lectures, we talk about refeeding syndrome, and again, things like sodium, or, excuse me, like potassium and magnesium and then our phosphates. Again, as we start getting back into a mode of, you know, using that energy and using that sugar, those things start acting as CO factors to help bring sugar in. So again, it becomes really, really important at all stages to be monitoring those electrolytes. Dr. Sean Kane 12:17 And the other thing that we'll see is with sodium in patients that have very high blood glucoses, more than 400 500 we'll actually see what's called the pseudo hyponatremia, where the lab value of their sodium is falsely low versus what it truly is in their blood. It's kind of a lab assay problem, and there's a correction equation for this, but clinically, we actually don't really do much different until we start correcting that blood glucose and seeing where their true sodium level is. And then finally, we mentioned acute kidney injury is very common with the dehydration. These patients are pre renal, where they need more volume to kind of rehydrate the kidney. So we'll see high bun to serum creatinine. Ratio is greater than 20. We'll see the serum creatinine and the bun be elevated, but within about a 12 to 24 hour period, unless this was a very prolonged dehydration phase, these patients turn around very quickly from a renal standpoint, and it would be extremely rare that there need anything like renal replacement therapy or progressive chronic kidney disease. Speaker 1 13:12 So in general, when we are looking at after this clinical presentations, when we're looking at diagnosis, you know, there are some Hallmark diagnosis or factors to be considered, and one of them is looking at the blood glucose. So you're going to see usual blood glucose levels as high as 250 and they can go up to even 600 sometimes. Dr. Sean Kane 13:31 And then, as we mentioned, we'll see an anion gap, which is a mathematical equation making up sodium chloride and bicarb. We'll see a low bicarb less than 15, and we'll see a pH in the blood less than 7.3 remember, this is diabetic ketoacidosis. This isn't diabetic keto alkalosis. So you should see an acidic pH. Generally, this pH is from the venous side. From a venous blood draw, you can get it from an arterial side, but it's more invasive, and most experts don't really care if it's from the venous or the arterial side. Just note the pH on the venous side is a teeny tiny bit lower than what you'll get in terms of a pH on the arterial side. And then Speaker 2 14:07 just once again, to talk about the way we measured so we see ketones in the urine that's gonna be the urinalysis, or in the blood via that beta hydroxybutyrate, which I mentioned earlier. And then there's also this interesting variant of DKA called HHS, or hyperosmolar hyperglycemic state, and in that case, the blood glucose values can be even higher, 600 and even well above 1000 and there can be altered mental status, but no gap acidosis, Dr. Sean Kane 14:31 yeah, so that's why it's not called DKA, is that you won't have a gap and these patients present basically with altered mental status, without any acidosis, without any bicarb change, and we basically treat them the same, with the caveat that we're not using things like their anion gap and their bicarb to decide when the decay is resolved. It's more about their mental status. But in terms of our basic treatments, it's very, very, very similar. Speaker 1 14:55 And as we talked about earlier, you know, if you can't rule out just simple medication, non compliance. Ins, then we probably should be looking a little bit larger workup to identify if there is underlying infection, or MI or PE, some of the other ideologies we had mentioned. Speaker 2 15:10 All right, so now we're ready to treat her, right? We'll go ahead and give them insulin right off the bat. Unknown Speaker 15:14 That's the wrong answer. Dr. Truman, Dr. Sean Kane 15:16 so unfortunately, it seems so intuitive that all you have to do is fix their blood sugar and the dka is resolved. We really have a number of other things that we're worried about before that point. The first thing, as we mentioned, is rehydration. So the first therapy that you get for DKA is a crystalloid, like normal saline. Speaker 1 15:33 And this is the first goal of DKA therapy as well, is restore hydration. Dr. Sean Kane 15:38 So most patients will get a couple liters, so one to two liters over the first one to two hours is an initial management sometimes as quickly as two liters over the first hour, depending on how dehydrated the patient is. And then, as we'll talk about, they're going to get a number of liters of fluid over the 12 to 24 hour course that they're in the ED and the ICU. And it really depends on how dehydrated there are. If they have comorbidities like heart failure, that there would be at risk for pulmonary edema. But a general rule of thumb is at least a couple of liters within the first couple hours to help rehydrate the patient. Speaker 2 16:09 And then again, we really have to watch those electrolytes, because we know for a fact that once you start getting more insulin in, once you start getting the sugar into the cells, you're going to start taking as potassium moves due to some of the changes in pH, as well as due to the changes of potassium's role with insulin. You're going to just like again, just like we talked about in refeeding syndrome. Here, you're going to see potassium and so we drop. And so we really need to plan ahead by giving some so if potassium is below about 3.3 or so, you need to give potassium chloride. Speaker 1 16:41 And if you look at the ADA 2009 statement of hyperglycemia crisis management in adults, it kind of breaks down different levels of potassium and what doses of potassium you should be given. And sometime it it seems like, you know, patients potassium is just fine, but we are still giving them potassium. It's because all the reasons we mentioned earlier, there is that interest out of their shift of potassium as the blood glucose decreases and it normalizes it, but the total body potassium can be decreased, so that's why we want to replenish it. Dr. Sean Kane 17:11 These patients will get quite a bit of potassium, typically, anywhere from, let's say, 60 to 120 mEq within the first 12 to 24 hours, depending on how bad they were dehydrated and how long they were in DKA. For the key here, though, is that twofold. One, we're going to be giving potassium when it seems like their potassium level is pretty good. Then two, if their potassium level is less than around 3.3 or 3.5 depending on who you ask, you do not give insulin until you fix the potassium. Speaker 2 17:38 All right, so we talked about rehydration. We've talked about giving potassium. Now, can we give the insulin? Speaker 1 17:43 Yes, we can go ahead and give the insulin, and it's going to be given by the route of a continuous IV infusion. So it's not going to be your normal outpatient, you know, subcutaneous injection type of insulin management. And with this, because we were giving it continuously, the rule of thumb is that we monitor the blood glucose every one to two hours. We will talk about the different dosing strategies. But in general, we need to keep in mind that the goal of blood glucose decrease or drop is not too drastic. We want to keep it anywhere from 50 to 75 milligram per deciliter per hour, and we don't want to decrease it too fast, because Dr. Sean Kane 18:20 so you can see osmotic changes that cause demyelination of the central nervous system. So you have to be gentle but firm in making that blood glucose drop quickly, but just not too Speaker 2 18:31 quickly, right? And again, that's the same as is anytime where we're shifting, you know, we're looking at some of some of those osmotic pressures. So again, whether it's talking about fluids or TBI, anything like that. There's just another case where that, but osmotic demyelination syndrome becomes, becomes a big issue. See, again, you want to always do things carefully and do kind of checks as you go along to make sure you're not Speaker 1 18:50 going too fast. And so in one way to assure that you're not going too fast is, you know, we can do a bolus and then, like a continuous infusion type of treatment, that bolus will be point one unit per kilogram and then continue point one unit per kilogram per hour rate of the infusion. Or we can alternatively give them just point 14 unit per kilogram per hour, without the use of that initial bolus itself. Dr. Sean Kane 19:16 So just to put that into perspective for an 80 kilo patient, that means that you either get an eight unit bolus with eight units per hour to start off, or you start at a slightly higher rate, around like 11 units per hour. The ADA guidelines say that they don't care if you pick a bolus with a lower dose or no bolus with a higher dose. It's actually a really interesting topic because of the limited amount of evidence that we have to bolus or not to bolus. It actually would make a really good journal club for any student, especially a p4 student that wants to know more about what is the evidence surrounding the recommendation. In my view, I don't view the data for a no bolus option as strong as I would like, and classically, we give bolus with the point one infusion, but I have no problem either way. Just wish that the guidelines would have had a little bit more data to work with, which, unfortunately, is something that is very common in most clinical practices that we see. Speaker 2 20:08 And then most institutions do have a nursing driven generally, but an insulin titration table. And so what they're going for is to try to drop it by 50 to 75 milligrams per deciliter every hour or so. And so you try to adjust the regimen to try to fit within that range. Dr. Sean Kane 20:22 And it seems intuitive, again, with diabetic ketoacidosis, that we want to correct the acidemia. And typically, the way that you correct an acidosis is by giving bicarb. But generally speaking, in most critical care settings, including DKA, giving sodium bicarb is generally not preferred, generally will treat the underlying cause. So for DKA, the only time that you're actually giving sodium bicarbonate is if you have a really, really, really bad pH to the point where the patient their bodily functions are not working anymore because they're so acidic. So we're talking somewhere like a pH of 6.9 or seven, which is a very, very acidic pH. That's when you may consider bicarb. But for most DKA patients, you will not be giving bicarb, you'll be rehydrating and giving them insulin and electrolytes, and that will fix the acidosis on its own. Yeah, I Speaker 1 21:05 think there are a couple of issues when we are giving bicarb. Is that we have to keep monitoring the abg, so it's not very easy to do for a patient, because it's an arterial draw of the blood. And then second thing is that we have to the bicarb doesn't get infused itself. It's usually combined with sodium bicarb, then we have to worry about the sodium load that we're giving the patient to Speaker 2 21:24 and the more we're working against. You know also the some of the continuing to cause shifting of some of those other electrodes, again, that potassium is going to be shifting again and again, depending upon how we put up the pH. So it may be best to then allow it to compensate on its own, so that we see more of a steady influx reflux, rather than just kind of a back and forth. Dr. Sean Kane 21:42 So in terms of the follow up, once we've kind of done this initial management, most of our follow up consists of checking electrolytes fairly frequently. So this could be as frequent as every four every six hours, for things like potassium and magnesium, we may check phosphate, or we will check phosphate. But in terms of our repletion of phosphate, we don't have to be very aggressive with it. Most of the data says that it won't change your clinical outcome and it may actually cause harm in terms of hypocalcemia and things like that. Obviously, we'll be checking blood glucose, the blood pressure of the patient, their hydration status, as we mentioned, most patients will get a number of liters over the first 12 to 24 hours of a crystalloid like normal saline. Most patients will probably get between 60 and 120 mEq of potassium within that same time period. And really, our treatment is going to continue on this path until we get our blood glucose slowly down to around the 200 to 250 mark. And at that point, we kind of change our management strategy, yeah. Speaker 1 22:37 And we talked about how the management strategy for HHS, it's very similar to DKA, although we are not talking about HHS here, but something we need to also look at is look at the patient clinically. Is their mental status improving as they are, they becoming more lucid to as to where they are compared to where they you know, were when they came into the ER. So for Speaker 2 22:58 most individuals, again, the blood sugar is going to normalize before all the Keto acids are gone. So what we still need to do then is get rid of some of those keto acids that are building up. And so we need to consider adding a dextrose source. You can either use d5 normal saline, or you can use d5 and half normal saline, or 0.45% sodium chloride for those detail oriented and you want to keep the insulin drip going to really get rid of all the Keto acids. Dr. Sean Kane 23:21 Yeah. So like you mentioned, the problem is that the insulin is the treatment to get rid of keto acids, and if we didn't give a glucose source, the patient will be hypoglycemic. So we have to keep the insulin going until we get rid of the Keto acidosis, and we give the dextrose to prevent them from getting hypoglycemic while we're continuing to get rid of the Keto acidosis. Speaker 2 23:40 So then once they once they've come out of DKA, once we've moved beyond the issue, what do we need to be doing next? Speaker 1 23:46 So usually a patient would be transferred or disposed to the ICU unit to further monitor because, as you mentioned, we're going to be continuing the insulin drip to make sure we are getting rid of the ketone bodies. In general, there are a few criterias that we can look at that would define patient being, you know, cured of DKA usually resolves about after 24 hours. So one criteria you already mentioned, Dr. Kane, is blood glucose of less than 250 we are also looking at normalizing the anion gap and then getting the bicarbs to more than 15. Yeah. Dr. Sean Kane 24:20 So frequently, like in the ICU setting, an intensivist asks, "Is their gap closed?" What that means is that their anion gap has normalized and their bicarbonate has improved — basically, has their DKA resolved or not. Speaker 2 24:30 And then, just to be sure, you can double check, potentially, by going into the blood and checking for that beta hydroxybutyrate again. But a lot of the time, the normal anion gap will give you a pretty clear picture. Speaker 1 24:40 And so eventually we can't send patients home on IV drip of insulin, so we will have to convert everything to the subcutaneous type of insulin that a regimen that they can go home with, and that would include a basal insulin as well as the meal time insulin, so tid or QID, depending on how many meals they're taking per day off a. Short acting or rapid acting, insulin, we want to do a little overlap with their IV drip that's running for about one to two hours, and then they can go ahead and switch off the drip switch, and then keep them on just a subcutaneous regimen. Speaker 2 25:15 And as always, the goal is not just to have somebody come in, treat their episode, have them leave, have another episode, come back, treat it, go back and forth. So what you really want to do is also look at where did this come from? Is this something like, you know, we talked about, Dr. Kane mentioned non compliance. Is this an issue with the cost? Then we can get individual social workers involved to potentially find out other sources of income. Can we find out vouchers? Can we find programs, if it's non compliance, is there a way to use an intensive case management program that can help making sure, are you taking the medications? And so we can kind of get the individual in the community and still addressing some of those factors before they have to come in, Speaker 1 25:51 yeah, and if they're wearing pump, you know, maybe re educating them about how the pumps work and keep checking that pump set that it doesn't come out of the place. Dr. Sean Kane 25:59 So to kind of briefly review, with DKA again, our first line of therapy is counterintuitive, and it's really a rehydration, primarily with a few liters of normal saline over the first few hours. Speaker 2 26:10 And then our second step is knowing that we're going to see a decrease in potassium once we start to get the acidosis balanced out. Is we need to go ahead and give potassium, and we need to maybe doing higher doses of it. So we need to be gradual. We need to be careful and then monitoring for it, because if you don't correct it, you can cause an arrhythmia. We also don't want it to do it too high either. Speaker 1 26:30 The last step in the therapy would be correcting the blood sugar, and that would be by doing an IV drip of insulin. There are a couple different dosing strategies we mentioned earlier. We have to keep tracking the blood glucose, and the goal is to not drop it more than 50 to 75 milligram per deciliter per hour. Perfect. Dr. Sean Kane 26:47 So with that, I think that we've kind of had a good broad overview of DKA. Obviously, for clinicians that want more information, there's a lot more depth that we could talk about with DKA, but kind of sticking within our time constraints here, I think that that wraps it up nicely. So with that, I'm Dr. Kane, I'm Unknown Speaker 27:01 Dr. Schuman, and I'm Dr. Patel, and study hard. Narrator - Dr. Abel 27:05 If you enjoyed the show, please help us climb the iTunes rankings for medical podcasts by giving us a five star review in the iTunes Store. Search for HelixTalk and place your review there to Narrator - ? 27:16 suggest an episode or contact us. We're online at HelixTalk.com thank you for listening to this episode of HelixTalk. This is an educational production copyright Rosalind Franklin University of Medicine and Science.