Teri Campbell, RN, BSN, CEN, CFRN discusses the features of pediatric DKA including the often missed presentation, risk factors, treatment goals and potential complications. She unravels the complicated pathology of DKA so It is easy to understand.
[MUSIC PLAYING] TERI CAMPBELL: My name's Teri Campbell. I'm lecturing I'm pediatric DKA. Are there any PICU people in the audience? OK, so lower your expectations. All right. So my intended audience for this lecture are people that don't specialize in pediatrics. So I'm intending to speak to EMS, ED, and maybe adult ICU people that occasionally see kids, despite their best efforts to avoid them. OK, so my lecture is when kids are as sweet as sugar, and sick as snot. We'll just say that's what it is. OK. So what is DKA? DKA is a complex metabolic state, which can be the spectrum, right? It's on that spectrum of badness. It can be anywhere from an emergency situation to a life threatening situation. So who in the room is old enough to remember the TV show Emergency? All right. Thank you for making me feel better, right? OK, so I love Dixie. Dixie is like the kick ass nurse, right? She has her hat. She does high heels, right? She answers the radio. She triages. She takes care of the patients. She flirts with the medics, and keeps the doctors in line, just like real ER nurses, right? Exactly. OK, so DKA is the number one reason for hospitalization for known diabetic kiddos. And cerebral edema is their biggest risk, or their biggest area of concern. So that's what we're trying to avoid. And we're going to talk more about that in a little bit. So what are our objectives? Well, we're going to start out simple. We're going to define what DKA is. We're going to talk about some of those precipitating factors. Because our children don't always presents with common presentation, right? So you can read about everything in the textbook. But kids don't always read that book. And they don't always present that way. So we're going to talk about that. For my pre-hospital folks, your stabilization priorities are going to be different than they are in the ED, and different than they are in the PICU. So we're going to talk about some of that. And then we're going to talk about different treatment options. And then we're going to also end up talking about some potential complications that we're all hoping to avoid. So let's start with the definition. So DKA is a triad of badness. So first, we've got hyperglycemia. Then we've got ketonemia and acidemia. So what's that mean? That's a whole lot of emias, right? There's rarely good things that end in emia. So we know that the word, the end of the word emia for all of us, for our strong Latin skills, means that it's in the blood. So hyperglycemia, so you've got too much sugar in the blood. You've got ketones in the blood. And you've got acid in the blood. So does acid ever belong in the blood? Not so much, right? So we know that these kiddos can be pretty sick. So by strict definition, these kids are going to have a blood glucose of above 250 milligrams per deciliter. pH, these kiddos are going to be acidotic. Don't worry so much about writing down all of this stuff for the definition. Because when we go over the pathophys, you're going to get it. And you're going to go, oh. That's why these kiddos are acidotic. So their serum bicarb is also low. So let's use some common sense. Why is their bicarb low? Because they're acidotic, right? They're trying to balance out. They're trying to make that a little bit more homeostatic there. Urinary ketones and serum ketones are both going to be elevated. And you'll understand that why in just a minute. And serum osmolality, that amount of sponge or pull in the blood is going to be variable. So we're going to talk about that also. So what are the stats? So incidence and frequency-- well, you know, this is the fun part about lecturing is, you know, you can admit when you're like, I don't really know. There really isn't clear definition at how often DKA happens. We think it's about four to eight kids out of every 1,000 kids. But again, some populations may be a little bit higher than others. That's for your primary diabetics, so the type one diabetics. We use-- the insulin-dependent diabetics. Now the type 2 diabetics, we're actually seeing an increase in incidence in the United States. I don't think that surprises anybody, does it? We've got kids that are staying inside, playing video games, that are eating tons of junk food. So we're having a more sedentary and obese childhood and adolescent problem. So probably the largest population where we're seeing an increase in type two is with our young, obese, African Americans. So let's talk about race. Does that mean that African Americans have a higher incidence than Caucasians? Actually, that's not the case. So with type 1 diabetes, it is associated with HLA, human leukocyte antigen. And that's more common in the Caucasian populations. So there goes that theory. OK, so what's the mortality of DKA? Mortality is actually pretty low. It's about 2% to 5%. And most of the time, that's related to the underlying pathology that kind of knocked them into DKA. If we're looking at complications related specifically to the DKA, which is primarily cerebral edema, it's about 0.3 to 1%. So it's actually pretty low. Unless, of course, it's your kid, right? Then it's not so low. OK, so what are some of the precipitating factors? So about 25% of our kiddos that present in the ED or through and EMS, are brand new diabetic kids, or at least brand new diagnosed diabetic kids. Infections, so far our known diabetic kids, infections or an underlying disease is what normally knocks them into DKA. Now how about noncompliance? You think a kiddo can eat themselves into DKA? You think a teenager can? OK, actually that's not the case. More of the problem is noncompliance with monitoring the blood sugars, right? Because it's not cool to have to test your blood sugars. It's not cool to not be able to eat all the things that your friends are eating. So my oldest son is 21. And his roommate from college is as much of a knucklehead as my son is. I mean, I love them both. But they're age-appropriate knuckleheads. So Connor is an insulin-dependent diabetic. He's been diabetic since he has been about eight years old. So Jack kept calling me. Because he was really worried. Because Connor was having repetitive seizures at school. And so of course, my first question is, Connor, are you monitoring your blood sugars? He's like, Mrs. Campbell, I am monitoring my blood sugars all the time. Well, here's where the age-appropriate knucklehead comes in. So they were going out to the bars and partying. And he knew he was going to be drinking. So he upped his pump. So he'd up his pump so he could handle the boost in sugar from the alcohol. And then he bottoming himself out, and then having seizures. So again, it's not necessarily that they're eating or drinking themselves into it. But sometimes they are trying to outfox the fox. So the good thing is about Connor is he no longer drinks. And he told me, Mrs. Campbell, it's cool. I just smoke pot now. So it's fine. [LAUGHTER] It's all good. My endocrinologist says that's OK. And I'm like, rock on. Age-appropriate knuckleheads, right? Did I mention that? OK, endocrine changes. So we have girls that are reaching menarche. They're getting their periods. All those hormones are messing everything up. It's our story. We're sticking to it, right? So they can have that problem. And then caregivers, so I've got adult parents, right, moms and dads that are taking care of their kids. And the problem with their little ones that they're noncompliant? Not usually. Usually, it's lack of education. So their little one has the flu or has the gastro, and they're not eating and not drinking. So the parents think, well, I better hold the insulin. And they don't realize that their demands and their needs are actually higher. And then for our older kids, there can be pump failure also. So how do these kids present? Now, wouldn't it be nice if they showed-- if the call came in through EMS or they show up in triage, and mom said, well, you know. They've got polyuria, polydipsia, and polyphagia right? We'd be like, oh. I remember that from school, right? We would know what that was. But that's not how our kiddos are going to present. They present with fatigue. They just don't feel good. Mom says, they're not acting right. They might have some vague nausea and vomiting, but nothing really consistent. Weight loss is hard to see in our little ones, maybe in our older kids. And they may have fever. So it that a clear picture of DKA? No. What could that be? Everything, right? It could be any kind of viral illness, you know, all kinds of stuff. So you can see where this can get missed, particularly in kids that are not known diabetics. So if they're part of the 25% that this is how they're being diagnosed, you can see how that could be missed initially. So abdominal pain, abdominal pain is really common in our adolescent populations. So why? Well, remember I told you an underlying cause that sends into DKA is an infection. So maybe they've got a baseline infection in their abdomen. And that's knocking them into DKA. But there's a certain percentage of our kiddos, of our adolescent patients, that have abdominal pain. And that's a symptom of the DKA. So it's kind of that chicken or an egg thing. We don't really know how these kids are. So let me give you an example. We have a 17-year-old girl who admits that she's sexually active. And she's at her prom. She has horrible abdominal pain. Her parents pick her up. And they take her to the emergency room. OK? She comes to the emergency room. And she is wearing the dress made of condoms, right? So she admits that she's sexually active. She just came from prom. Now ER people, what are you thinking? [AUDIENCE RESPONSE] PID. STD. You got it. That's exactly what we're thinking. So that symptom of abdominal pain can lead us down the wrong path. It can lead us to the path of destruction. We can get duped. OK, so what's the pathology? So we know that the pathology is decreased insulin. That's the problem. DKA, the problem is not sugar. It's that the sugar is in the wrong place. It can't get into the cells. So those people that were in the end of the lunch line, you were hangry, weren't you? Right? You were-- you were so hungry, you were angry. I get that. Nobody likes-- the key having a happy flight nurse is having a well-fed flight nurse. Most of the pilots carry like granola bars and stuff like that in the helmet bag. So we don't eat anybody like them. OK, so our cells are exactly the same way. They get hangry. If they don't have glucose, they can't do their job. So cells are pretty basic. They want sugar. They want water. And they want oxygen. They're really not asking for that much. So if we take away that sugar, they get hangry. And they say, that's it. I'm not doing my job. But before that happens, they start producing. They start stimulating hormones so they can get more sugar. So that's where the endocrine comes in. And our adrenals start kicking out some of our stress hormones. So we've got catecholamines, glucagon, growth hormone, cortisol. All of those are stimulating gluconeogenesis. That's a fun word. It means the body's going to make sugar. So that's a good thing. But is our problem that we don't have enough sugar? No, that's not the problem. The problem is we can't get it inside the cells. So now we're going on to our pathology, is that we've got lots of sugar. In fact, now we have even more sugar than we know what to do with. Because our liver has been generating glucose for us. So in normal metabolism, when our cells can get oxygen, they can get fluid, and they can get sugar, it's like a great big bonfire. We're putting off lots of heat, lots of energy, lots of light. And everybody's happy, right? In DKA, because our cells can't get the sugar, they start throwing other things on the fire. Because the cells are starting to panic. The cells are thinking, oh, my god. Nobody is feeding me. They're not paying attention to my flags that I need more sugar. And so I have to start burning what's around me. So the first thing they throw on the fire is protein. And as a result of that, that byproduct that they burn off is ketones. Now they're looking around. And they're like, we need more energy. So they throw fat on the fire. Now, we'd all like to throw some fat on the fire, right? By product, though, is lactic acid. So again, instead of having our wonderful, warm bonfire, where we're cooking lots of heat and lots of energy, we've got big black tractor tires that we've thrown on top of our fire. And what happens when you burn rubber? What happens? What kind of smoke? You get black smoke. It's really acidy, really hard to breathe, right? So that's the byproducts, our ketones and our lactic acid. Do they burn? Yeah. Do they produce some heat? Yeah, but it's not as good as that nice big bonfire. But the body's trying. They're doing whatever they can. So how do our kiddos look? Well, hopefully we're going to get them before this stage. So mental status changes-- in fact, that's going to be one of the common reasons that parents will bring in their kids, particularly their little ones. Because they're going to say what? What's the common presentation in the ER? Not acting right. He doesn't look right. He's just not acting right. Those parents are smart. They know something's up. Tachycardia-- so our kiddos are going to be tachycardic. Why are they going to be tachycardic? They're dehydrated. They're dry. Exactly. Kussmaul-- so that's that rapid breathing. Why are they doing that? They're blowing up that CO2, remember. They're acidotic. So again, understanding that pathology helps to bring it all around. How often do they have that kind of fruity smell? You know, we read about that in the textbook. Not that often, only about 20% of the time. Blood pressure-- now what do you think their blood pressure is going to be? I don't know. It depends, right? Where are they in their spectrum of badness? How dehydrated are they? If your kiddos have blood pressure changes, you guys should have recognized this way earlier on. Because you have a really, really sick non-- and unresponsive kiddo. OK, and delayed capillary refill-- again, that's going to have to do with perfusion. It's going to depend on how dehydrated these kiddos are. And then they may or may not be febrile, depending on what that underlying pathology was that sent them into DKA to begin with. So we know that our kids have high serum glucose, right? We know that's a problem. So what you might not know is that sugar is like a great big sponge, like SpongeBob. So any of us that like to go to Oberweis or Baskin Robbins and eat lots of ice cream, how do you feel afterwards, besides completely satisfied? Thirsty, right? So if you have lots and lots of sugar, it makes you very thirsty. So glucose is a big sponge. So the body is going to go through these periods and this progressive dehydration. It's going to start out with intracellular dehydration. So remember, glucose is inside the cell or outside the cell? Outside the cell. So where's the sponge? Outside the cell. So the first thing that happens is the intracellular department gets depleted. That sponge is pulling fluid from the cell outside of the cell. So where's our fluid going to go? Extracellular. This is not that hard, right? So now I've got an engorgement in my extracellular space. So let's talk about our electrolytes, potassium and sodium. Potassium normally lives inside the cells. Sodium lives outside the cells. So if I add more water to my extracellular space, what's going to happen to my sodium? It's going to get diluted, right? So think of a glass of Kool-Aid. And I've just added twice the amount of water. So I'm going to end up hyponatremic initially. Now, that fluid's not going to stay extracellular. It's going to continue to move. Because where's all that sugar? It's in the intravascular compartment, right? So that sponge is going to continue to pull. And the fluid is going to go into the blood vessels. It goes to the kidneys. And the kidneys say wee, wee, wee all the way home, right? Kidneys are completely volume-driven. They love the fact that they're getting all of this. Now the problem is we have an excessive amount of fluid water losses over our sodium losses. So that sodium initially gets diluted. But as that body gets more and more dehydrated, as that volume is pulled into the intravascular compartment and then gets peed off, we end up with hypernatremia. So the sodium actually goes high. So the body is going to respond. Because remember, I told you the kidneys are completely volume-driven. So after awhile, as they're getting more and more dehydrated, they're starting to whine. They're starting to complain. And they're like, hey, I'm not digging this. I know. I know how I can get more volume. I'm going to retain glucose. So the kidneys send a signal back to the brain to hang on to glucose. Because they know that glucose is a big sponge. That's exactly why you can't pee off your sugar. OK, so acidosis-- we've got two main culprits. We already started to talk about it. So do you guys remember Scotty from I'm the Starship Enterprise? I totally grew up in the '80s, in case you didn't figure this out. I had really big hair. OK, Scotty was the engineer. And Captain Kirk, whenever there was a problem, he calls Scotty to the deck. And he'd be like, you know, Scotty. We need more power. We need more thrust. We need more energy. And what would Scotty always say? [AUDIENCE RESPONSE] Captain, I'm giving her all she's got, right? Or something better than that. But OK, so that's exactly where our body is right now. Our body is throwing everything on the fire that it can. Because it cannot get hold of the sugar. So we know from burning the proteins, we've got ketones. And from burning the fats, we've got lactic acid. But in addition to that, as our body is getting more more and more dehydrated, and we're having more and more tissue hypoperfusion, that's also kicking out lactic acid, so all that bad byproduct of the poor stuff that we're burning on the fire. So hyperosmolality-- now, this is going to be directly related to two things, the hyperglycemia and the dehydration. And so since they go together, that's what's going to be affecting our serum and our cerebral osmoles. So as our blood osmolality, which is that sponginess of the blood, increases, it's going to also be increasing in the brain. So serum osmoles, so osmoles pull, osmotic pull into the blood vessel. Is that a horrible thing? Not initially, until our patients get good and dehydrated. How about in the brain? Do I want to be pulling a lot of fluid into the brain? No. So that's what our problem's going to be later on when we talk about cerebral edema. OK, so electrolyte disturbances-- we started to talk about this. So initially, our sodium is going to be low. Because as my fluid goes from the intrava-- I mean, from the intracellular compartment to the extracellular compartment, my Kool-Aid's diluted. As that osmotic pull pulls that fluid into the intravascular compartment, the salt stays. So it's like having a glass of salt water that dehydrates. And you have all that crystallized salt in there. So our patients end up hypernatremic. So that could be a big problem later on. Because seizures don't normally help with DKA. That I can tell you. Increase in potassium-- so again, we know that potassium normally lives inside the cell. But as our cell wall is been disrupted, that potassium is moving out extracellular. So initially, we're going to have a high potassium. Guys, don't let that fool you. Because when you first get them in the ED and you draw that first set of labs, and you see that their K is high, don't be thinking that you have to be treating this kiddo right away. The potassium is probably the right level, or a little bit low. It's just in the wrong place. So we do suspect that all of our kiddos are going to end up having decreased potassium. All of these kiddos are going to end up hypokalemic. Because as we give them-- remember that fluid came out to the extracellular space and intravascular, so they're peeing off some of that potassium. As we start giving them IV fluids, and that potassium starts moving into the cell, and then we give them dextrose and sugar, and more of that potassium moves into the cell, these kiddos really end up being hypokalemic. And that's really much more of a problem than hyperglycemia. So we do want to make sure that we're treating our hypokalemia before we start the insulin. So normally, we will be assessing that potassium after the IV fluids, but before we start the insulin. So that's one of the arguments for delaying that start of insulin. Now we know that we want to treat the hypokalemia first. Otherwise, we're going to really increase the chances that these kids can have some ventricle disorders. So what are the labs? So the glucose, we know we're going to be drawing a glucose. Potassium, we already talked about. ABGs, we know that these kiddos are acidotic, right? They've been throwing all kinds of crap on the fire. And it's causing acidemia. So we're looking at the pH. We're looking at the lactate. We're seeing how we're doing with our volume resuscitation. Other electrolytes, so your chlorate is going to be following your sodium. So whatever your sodium's doing, your chlorate's along for the ride. Bicarb, again, is going to be related to your ABG. BUN and creatinine are going to be elevated. That makes sense, right? You have a dehydrated kiddo. So your BUN's going to be elevated. And your creatinine is going to be elevated because of the ketones. So once you start clearing your ketones, your creatinine will correct itself. And then phosphate follows your potassium. So usually that's a clinical sign, which we'll talk about in a minute. So we're going to draw a CBC on these kiddos. Why do I want a CBC? What am I looking at? So infection, right? So these kiddos often have a left shift. It's not always from infection, though. It could just be a stress. It could be a stress response. So typically, these kiddos have a left shift. But I do want to see if I have a 32,000 white count, right? I also want to look at that H&H. All those kind of things will give you some ideas about fluid status. Blood and urine culture, because I'm looking for that underlying disorder that's causing the badness. UA, because I'm looking at what? Glucose and ketones, exactly. Serum osmolality, because we're going to talk about that in a little bit. So if I have a kiddo that I know has hyperkalemia, or if on my EKG, I see that my kiddo has beautiful peaked T-waves, I'm probably going to get an EKG on this kid. So that's one of the indications. Now this second slide is a little bit harder to see. But remember, these kids are tachycardic. So I've got a tachycardic kid that has crazy high T-waves, what could that-- and you also have a kid that has decreased mental status and poor perfusion, poor pulses. So what could that be mixed up with? V-tach, right? So if I've got complexes that are running into each other, and I've got these huge, peaked T-waves, and a kid that I'm having a hard time feeling pulses on and he's not responding to me, you can see where this kiddo might accidentally get the a sync cardioversion. So what happens if we shock hyperkalemia? What happens to those peak T-waves? Yeah, you'll straighten that line out. That's called asystole. So we really don't want to do that. OK, so pre-hospital, so for my pre-hospital folks, A for airway, right? Mental status changes is going to be your guide. It's pretty unusual that even in our really sick DKAers that we're needing to tube them. Most of the time, if we start the IV fluid, start moving some of that fluid back in, their mentation increases. But you may need to tube them because of that. Again, they may or may not need oxygen. If you find that you're having to bag them, just do a little bit of [INAUDIBLE] so we don't fill up their little tummies. Isotonic fluid, so pre-hospital, that's all we carry, 0.9 and LR, so that's a good thing. You're going to give one 20 cc per keg bolus. That's it. I don't care if your transport time is 10 minutes, if your transport time is 60 minutes. You're going to give one bolus. And we're going to talk about that in a little bit. What size IV are you going to get in this kiddo? Pre-hospital? Whatever you can get in, right? Is this kid going to be an easy IV stick? No, because the kid's going to be way, way, way dehydrated. Would you need to do an IO on this kid? Maybe. Maybe. Depends on his perfusion and how my kiddo's doing, right? So again, we get in whatever size spear we can get in. Like Ann was saying in her lecture, any line is a good line. We can make it pretty later on. D, so again, do they have any altered mentation? What is their history? For my pre-hospital people, they're really good at getting chems. Anytime somebody's acting like they're not supposed to act, the first thing we do is we get a blood sugar. So we rule that out, right? And for my pre-hospital people that do in interfacility transports, or do critical care transports, you may be transporting kiddos on insulin. So I would suggest that you talk to the receiving PICU that's going to be getting this patient. Because one of our biggest concerns is the blood sugar dropping too quickly. Kiddos are not going to die initially in transport, because their blood sugar's too high. But we can kill them by dropping their blood sugar too rapidly. So you may want to talk to the receiving facility to see if they want you to turn the insulin drip off for transport, right? And for those really, really sick transf-- those really, really sick kids, we try to get them with the fastest vehicle as possible. And you know, of course, we want the rocket on transport. But that doesn't really happen. I can't tell you how many times I've asked my pilot to turbo boost. And you know, he doesn't think I'm as funny as I think I am. So what are our global goals? Our global goals are to restore perfusion. Because if we can get fluid back into the cells, we could make a lot of that other badness go away. We're going to give the insulin. Because the insulin's going to piggyback that sugar back into the cell. And we're going to correct electrolyte disturbances. But by doing those first two bullets, the electrolytes are going to fix themselves. And that's particularly what we need to keep in mind with our kiddos, is that they want to be in that homeostatic balance. So those electrolytes will improve themselves. And then I loved when I was like doing my research for the lecture, you know, all the articles say, and you want to avoid complications. Well, don't we always want to avoid complications? They find me. I don't know. I'm at the bedside. And I'm like, OK, where are we going? And why am in this hand basket? Because complications tend to follow me. OK, so fluid therapy-- so for the first one to two hours of therapy, we're going to be giving them an isotonic IV fluid bolus of 20 cc per keg. So for my pre-hospital people, even though you know that they're dry as a bone, you're only going to give them one bolus. Even in the ED, we tend to get a little over-zealous with our volume. Because we realize that that's part of the problem. And we want to fix it. We want to make it better. Because in the ED, we're all about moving the meat, right? We want you to get way better. And we want you to either go home, go to another unit, or die, right? Let's face it. We got to move people. We gotta move them. OK. Fluids that we're going to use is typically 0.9. Some PICUs use 0.45. So again, it's going to depend on your institution. So at the University of Chicago, we stick with 0.9. But some PICUs will start with 0.9, and then switch to 0.45. It's fine. Whatever formula your docs use is fine. For fluid, we're going to be giving one and a half to two times maintenance. So that's how we're going to be hydrating these kids a little bit more actively. So at the University of Chicago, they use a formula, where they take 1,200 cc's per meter squared per day. And that's how they figure out what the IV fluid is going to be. So I am a nurse. And so when they told me their formula, this is exactly what I looked like. Because I'm like, oh, my gosh. Even with my shoes off, this is going to be a difficult calculation. So I'm going to make it a little bit easier for you guys, particularly for the pre-hospital and the ED people. PICU, you're on your own. But you've got calculators. OK, so fluid therapy, we're going to use the four, two, one rule. Have you guys heard of this before? It's great. It's easy math. Even I can do it. So for the 10 first kilograms in weight, your kiddo's going to get 40 cc. For their next 10 kilograms in weight, they're going to get an additional 20 cc. And for every kilogram greater than that, they're going to get one cc. So let's do some math. I've got a 37 kilogram kiddo. First 10 kilogram, they're going to get 40 cc. So now my kid's 27 kg. OK? So for that second 10, they're going to get an additional 20 cc. So now I'm down to 17 kg. So they're going to get one cc for that. So this kid's maintenance fluid is going to be 77 cc. Keep it simple. Keep it simple. OK, potassium supplementation. So if I've got a kid that has profound hypokalemia, so we've rehydrate this kid. And this kid's K has dropped to 3.0, or something that I'm concerned about. Should we give it IV, or should we give oral? What do you guys think? OK, you know what? As nurses, we would tend to think IV. Because we're all about go big or go home. But actually, oral absorbs better. So these kiddos do better with the oral potassium. And there's also less complications. They don't have burning at the site, less chance of us killing them, you know, those kind of good things. OK, we want to treat before the insulin. Why? We just talked about this. What happens when I start the insulin? Shoves more potassium back into the cell. And it makes them more hypokalemic. So that's our problem. Now for our kiddos that are the opposite, that are grossly hyperkalemic, so they're over, they're 3.5 to 5. I've got a kid that's 5.5. I'm not initially going to be adding potassium to my IV. But it's probably going to be coming later on. Should I be hanging KCl or K phos? Again, it's going to depend. Most of the time, the K phos is for the kiddos that have really weak muscles. That tends to be how we determine which one we're going to do, or whatever one your lab and pharmacy decide they want you to hang, right? So again, for that slow lab, you don't have to wait for your phosphate to come back. That's a clinical exam on how strong they are. OK, so for the insulin bolus controversy. So again, where you practice doesn't mean that that's the right answer or the wrong answer. So again, I can tell you what we do at the University of Chicago. But that's just one data point for you, right? So part of it's going to depend on the institutions that you come from. So there is a controversy related to giving boluses. So if a kiddo has a blood sugar over 500, some institutions will give a bolus of insulin. Then they'll start the fluids. And then they'll start the maintenance. At the University of Chicago, they don't do that. They like to keep their kids on the sweet side. They like to be very conservative with bringing the sugars down. So we don't do that. When do you start that insulin? Again, there's controversy in the literature. At the University of Chicago, we give them the IV fluids first. We assess the potassium. And then we're going to start them on the insulin. Priming the tubing-- you know what, Kelly, I forgot to take this off. So when I was a wee little nurse in college, they told me that you had to run like 20 to 50 cc through your IV tubing, because the insulin stuck to it. And it's one of those urban legends that I think has stuck with me. And I don't really think there's anything that supports that that's true. But so anyway, I meant to take that out. OK, we're going to start our kiddos on 0.1 units per kg per hour, unless you've got a brand new diagnosed kid. Because you don't know how he's going to respond to the exogenous insulin. Or if you've got a kiddo that's less than two to three years of age, so there are more sensitive to insulin, so we start them at a lower rate. We're going to keep our insulin going til the ketones are cleared. And we're going to be hanging regular insulin, as you know, one to one. OK, so bicarb-- bicarb is rarely indicated. But that does not mean that we don't still see it clinically. So there is absolutely no evidence that shows that bicarbonate is helpful for our pediatric patients. In fact, it can be actually harmful. But again, it doesn't mean we don't see it. Typically, it's given for our kiddos that are pretty grossly acidotic. Because what it's trying to avoid is the myocardial depression that the acidemia can cause. Now, that's true for our adult patients. Our adult patients that live in an acid bath of blood, they tend to have myocardial depression. And they have a lot of ventricle dysrhythmias. Our kiddos have an underlying usually normal heart. And so they don't tend to have those hemodynamic changes. OK, so what are the problems we can have from bicarbonate? Well, one of the problems is hypokalemia. So if I've got a doc that's all excited about this low pH, and he wants to correct the numbers by giving bicarb first, and then he starts the insulin, and the fluids, our kiddos can end up swinging the other direction. Hypernatremia-- OK, what's bicarb's first name? Sodium, right? So remember, depending on where my kid is in that dehydration stage, he may already be hypernatremic. And now I'm going to give him sodium bicarb. So I'm going send his sodium way higher. Alkalemia-- so my kid's going to end profoundly alkalemic because the insulin, and the fluids, and the dextrose stop the ketones. They stop the ketone production. But they also break down the ketones. Guess what the byproduct of broken down ketones is? Bicarb. It's bicarb. So we can really make these kids alkalemic. And we're never going to give it IV push unless, of course, we want to practice a code. So we're not going to do that. OK, glucose-- so most of the time, we're adding glucose when our kids, we've dropped them to about 250 milligrams per deciliter. It can be D5, D10, whatever your institution uses. We're doing it because we're stopping that production of ketones. And we're preventing the hypoglycemia. Because we're starting insulin. Now what's your goal for your blood sugar? Again, this is where there can be differences in your institution. U of C, we keep our kids at 150 to 250. We keep them sweeter. We're very, very slow at reducing those blood sugars. Keep in mind, guys, just that first IV fluid bolus that you guys give pre-hospital is going to drop that blood sugar 50 to 70 points. That's significant. That's just from fluids. So closing the gap, so this is more for my hospital people. This is related to the electrolyte imbalances as a result of the DKA. So we've got-- the calculation is your positive anions, I can never say that word, minus the negative anions. I even practiced it and I still can't say it. Keep it simple. You're going to take your sodium minus your bicarb plus your chloride. So you want your values to be between six to 14. To worry about memorizing this stuff. Your lab all come with it printed. And they have the values on there. We're going to evaluate this by doing hourly blood sugars and every two hour labs. The serum osmole-- so normal range is 275 to 295. Remember that osmolality has to do with that pull, has to do with that sponge of fluids. So if my osmoles are high, I've got a higher incidence of cerebral edema. The higher my osmoles are, the slower I am at rehydrating my kiddos. Why? Because I'm concerned about cerebral edema. For whatever reason, pediatric patients and adolescents have a higher risk of cerebral edema than our adult patients. Now if you read in the literature and you try to figure out why, you get answers like, I don't know. Kids are just more spongy. So we don't really know. We just know that it is a higher incidence. Although that incidence is low, it's 0.3% to 1%, but mortality is 70%. So if it happens, it is bad. So we do want to avoid that. Risk factors-- unfortunately, we don't have great risk factors. I might have a kid that's wicked sick that has crazy high blood sugars and does just fine. And I might have another kid that really doesn't have that impressive of blood sugars. And that's the kid that has cerebral edema. So we don't really have good markers for that. Presentation-- all of our kiddos initially, because of that dehydration, are going to have some altered mental status. We give them some fluid. We water our flowers. And they perk up. And they look better. Our kiddos with cerebral edema then will either have an acute, or a more slowly deterioration in their mental status. So again, it has to do with that high blood sug-- that high serum osmolality related to the dehydration and hyperglycemia. So as your serum osmoles increase, your cerebral increase, and it pulls fluid into the brain. So how are we going to treat them? Initially, we're going to do a CAT scan. But I have to tell you, most of the time, this is a clinical diagnosis. Most of the time, it's based on mental status changes. Because our initial CTs in our kids aren't all that impressive. They're either going to show nothing, or they might show a little bit of basilar edema, but not anything that's going to really explain why these kids are acting so goofy. So choices are going to be Mannitol or 0.3. Again, it's going to depend on your institution. So just keep in mind when you're running your drugs, Mannitol is like a margarita. That's what you need to think about. It's a sweet sugar. And you know how your mouth feels the next day after lots of margaritas? So Mannitol is pulling fluid off of everywhere. 0.3 is going to pull fluid into the intravascular space. It just depends on your institution. So ARDS is very, very rare for our pediatric patients. And there's a good reason for that. Most of our kiddos have a normal heart. So that's why they don't have the problem with ARDS that our adult patients have. But it can be potentially fatal. And it has to do with us rehydrating them too quickly and with too much volume. So in conclusion, keep it slow. It took them days or weeks to become this full blown DKA. We do not need to make them better on our shift.
