Episode Transcript
[00:00:08] Speaker A: Welcome back to another episode of the code 321 podcast. Today, I have Riley Hoch here with me today. Hello, Riley. How are you?
[00:00:14] Speaker B: I'm doing good, Nick.
[00:00:15] Speaker A: Thanks for being an impromptu guest this month with little to no notice, but if one guy can pull it off, it is definitely you and your brain. So thank you for being here.
[00:00:23] Speaker B: I appreciate the compliment.
[00:00:24] Speaker A: Yeah, no problem. So today, what we want to take a couple minutes and talk about is diabetic ketoacidosis. And this is a really interesting one for me because I feel like you spend maybe a few hours on it in paramedic school, and you see it a couple times throughout your career. And it wasn't until I came here to healthnet doing critical care, where I really dug into, like, the actual chemistry behind what's going on. Um, and let me tell you, there's definitely a lot going on for sure. So I thought, who better than a mICU nurse to help us kind of take those strands and pull them apart a little bit and kind of see what's going on? So if you don't mind, do you want to tell the guests just a little bit about how did you get involved in medicine, and how did you end up doing the job that you're doing right now?
[00:01:06] Speaker B: Well, I kind of took a long, winding path to get to where I am today.
When I was in college doing my first undergraduate degree, I joined a fire department, got super involved into first response, and discovered that in order to make a career out of that, I would need to also have an EMT certification. So I went to EMT, you know, school, got my first EMT basic certification, realized that I really loved the medicine and taking care of sick people, and so kind of started to pursue that, decided that I'd like to become a nurse.
But I was already three quarters of the way done a degree that was nothing related to healthcare. So I finished that degree, got a job as an EMT, working for the hospital where I work now.
And everybody that I worked with there said that, don't become a paramedic, go to nursing school. You'll make way more money to do the same job. And so I went to nursing school, got out of nursing school, went straight into the medical intensive care unit here at UVM Medical center, got to work with some really great doctors and nurses, Josh Varkus being one of them, which is who has inspired this little podcast episode.
After I did my three years in the ICU, I applied for and got a job with healthnet critical care transport, where I became a ground and flight critical care transport nurse, and I've been here for five years.
[00:02:32] Speaker A: All right, so, as we start talking about DK here, let's just start with, like, a basic definition of DK. And when we say DK, we're referring to diabetic ketoacidosis. And so my understanding of this is really that this is a type of blood sugar problem where there's ketone production and there's some type of acidosis. What can you add that you've learned from your career that can really help us narrow down, like, what is DKA? Or how can we start to think that this is at play?
[00:03:03] Speaker B: So, I think the important thing to address straight out of, straight out of the gate here is that while DKA does involve a sugar problem, it is primarily an acid base problem. Um, so, essentially, the pathophysiology behind DKA is your body's not producing insulin or not producing enough insulin to keep up with the demand, and your cells, for whatever reason, are not being supplied with enough glucose, and they sense this kind of, like, hypoglycemic state, and as a result, will start to trigger the body into, what is it? Gluconeogenesis, which is the release of glucagon in order to break down glycogen stores in the body. And that drives an increase in blood sugar, which, due to the lack of insulin, is not actually making it to the cells. So it's just this whole, you know, process of, like, putting the foot down on the gas and not stopping. Um, so the blood sugar climbs, the body releases more glucagon, and the byproduct of the glycogen breakdown is the ketoacids that you can measure and test for, either in the urine or in the blood.
[00:04:22] Speaker A: Yeah, and we dont want that. And the big issue here is the change in ph. And then we have all kinds of weird electrolyte imbalances. And so its really easy, when we talk about DKA, to see that first word, the diabetic, youre like, oh, man, this is definitely a sugar problem. And I think for many years, in my nine to one career, it really was kind of correlated as, oh, thats super high blood sugar. Oh, that person has DKA. And as weve worked into critical care, ive realized more of, um, we're really thinking about, you know, the anion gap. We're thinking about the metabolic acidosis, the ph, the potassium. There's a lot of other players behind the scenes, and we will talk about this in a second. But showing up and just hammering them with insulin and taking their blood sugar from 1200 down to 80 probably isn't going to be the best plan for that patient.
[00:05:07] Speaker B: That is, that is correct. Um, however, in the 911 world, identifying somebody who you think is in DKA isn't necessarily going to be harmful to the patient, because the initial management is going to be similar, because oftentimes these patients are fluid depleted due to nausea, vomiting, diarrhea, and osmotic diuresis due to the increased blood sugar. So if you identify a patient who has high reading on your 911 glucometer, giving them some fluids is never a bad idea because it's going to be the initial phase of the management also. And then the hospital can dive into the diagnostics and kind of like tease out all of these little nuances to what's actually going on there. Is it in fact DKA? Is it something that looks like DKA?
Oftentimes sick people, especially diabetics, will have a massively high blood sugar in these times of illness and stress, because it's the body's natural response, which is why you see sometimes these days, especially with the rise in metabolic syndrome and those profile of diseases, you get what would classically have been called type two diabetes, or non insulin dependent diabetics, kind of in the state of DKA, even though they do produce insulin, because their body cant keep up with the insult to their system, whether its an infection or cancer or any other kind of massive acute process.
[00:06:35] Speaker A: Yeah, and I think its really important what you just said there, that this can either be our type one insulin dependent diabetics that are getting insulin every day by injection, or it can be our folks that may or may not be getting injectable insulin every day are type two s. And so I remember going through paramedic school and some other programming. There were instructors I had who were like, oh, you know, DKA is always a type one and Hhns is always a type two. And they tried to separate into those two things, but really, um, theres some more nuances than that. And we can definitely have a type two diabetic who is not receiving injectable insulin every day, who has some sort of stressor, like, lets say, Covid-19 or any type of infectious process, usually like a sepsis is a classic one too, that can actually put them in this DKA. Um, and sometimes with these patients that are sick and have all these compounding problems, it can be difficult to, like you said, kind of tease out like, is this a DK? Is this some other issue um, so let's talk a little bit about, say you get a sick patient, you get them in from 911, or they get landed in the ICU, and you're starting to kind of pick this apart. How do you go about trying to decide if this is DKA or not? What are some tests you can do? What are some interventions and things that you look for?
[00:07:45] Speaker B: So depending on the environment that you're in and what diagnostic tests you have available, there's kind of a wide variety of ways you can approach the diagnostic portion of DKA.
In our setting, in critical care transport, we have a point of care istat which will give us a blood sugar blood gas panel, including ph and bicarb status and CO2 and these sorts of things, as well as sodium and potassium.
We do not get a chloride can be problematic when it comes to diagnosing DKA. So sometimes you have to work with the lab values given to you by whatever facility you're transporting from.
One of the hallmarks is acidosis. However, due to nausea and vomiting, you can have a normal ph or relatively normal ph and still be in DKA. So it's not a definitive test.
You usually see elevated potassium due to the acidosis.
The level of bicarb also can help indicate at least the severity of DKA.
Most cases are mild to moderate.
So moderate DKA is considered a bicarb of five to ten. Below that would be severe and above ten would be mild. So oftentimes, early on, at least, our cases are going to be in the mild to moderate.
That's not to say we don't also see severe blood sugar being elevated is another good sign of DKA. In combination with these other things, however, it is also possible to have euglycemic DKA. It just kind of depends on the patient and where they're at in their disease process.
Not everybody reads the textbook, and all of these things present differently. So just because the blood sugar is, quote unquote, within normal limits, which could be, I think, by definition, anything less than 300 would be considered euglycemic DKA. It is possible.
Anion gap is another good one, really. We calculate that by subtracting the chloride and the bicarb from the sodium. It doesn't need to be more complicated than that. You don't need to do special corrections for albumin and fluid deficits, just sodium minus chloride minus bicarb. And you want that number to be, hopefully below twelve. If it's above twelve, you have signs of an anion gap, metabolic acidosis. So in combination with the elevated blood sugar, the acidosis, and these other things going on, you can usually safely say in that scenario that this person probably has dka, and you can facilitate the treatment of that. The gold standard for diagnostic, though, would be the presence of ketones. A lot of emergency departments can do a urine dipstick and give you ketones in the urine to help diagnose DKA. In the ICU where I worked, we often drew what's called a beta hydroxybutyrate, which is a ketone body that shows up in the blood that we can easily test for. And the standard for that in DKA is a greater than three millimoles, greater than six would be severe DKA, and normal would be zero to 0.6.
[00:11:09] Speaker A: And those things kind of all kind of knit together in this complicated fabric of trying to figure out if someone's in DKA or not. And I know it can be very tempting just to be like, oh, we have high blood sugar, and they're urinating, they're vomiting, they're sweating, they're defecating.
And it can be easy just to move right to DKA. But we're looking at that beta hydroxybutyrate. We're looking at the acidosis. By definition, if you don't have an acidosis and you don't have an anion gap, it can be difficult to really, like, say that we have DK. So I like how you mentioned talking about the bicarb level as a diagnosis for acidosis. And I think it's important just to touch on, for those of you that aren't interpreting lab results or aren't maybe going through, like, paramedic programs where we do acid based balance, to remember that really, the two things that we're looking at to try to determine what type of acid base balance we are dealing with here is we're looking at the ph to determine if this patient is alkalotic or acidotic. And then we're also looking at the CO2, meaning, like, the bicarb level, as well as the CO2 that the respiratory system is either getting rid of or retaining. So if we have a low bicarb, low base, then that means that we probably are having some type of either mixed disturbance or metabolic acidosis, because the metabolic acidosis eating up all that bicarb to try to make it into that carbonic acid and get rid of it in the kidneys, does that kind of make sense? Yeah, for the most part. All right, cool. Whereas if, with our cop deers, if they're retaining CO2, they can't, they can't expel that through the respiratory tract. That's what's going to be causing that, that system to, to lower its ph and become more acidotic. So we're looking at these values, we're determining we have an acidosis. And it's important to remember that whatever system is, is having the problem, the other system is going to try to compensate. So in this particular case, we have a metabolic acidosis. So our compensatory mechanism is going to be our respiratory system. So you'll see an increase in tidal volume and minute ventilation. The body's trying to remove as much air as possible that contains CO2 to try to drop that acidic ph level or, sorry, drop the acid and raise the ph level. So the way I always describe this to people is think about if you're starting to run on the treadmill, your body is going to naturally increase its respiratory rate, partly to get more oxygen, but primarily because its sensing an increase in the production of CO2, because your metabolic rate has increased. So its trying to compensate for the same reason. So when we have a patient with DKA, you walk in, you have that classic kusmal respirations, right? The kind of little bit of a shorter breath in, deep breath out, moving as much air as possible, rapid, that kind of that classic pattern that we only see in DKA. It can be very tempting if you were to open your EMT textbook to say, oh, this patient's definitely breathing more than 30 times a minute. We need to start bagging this patient and slow them down. But that actually would make them profoundly worse. Do you want to touch on a little bit about why we try to avoid intubation and intervening on the respiratory system with DK if possible?
[00:14:13] Speaker B: Yeah, definitely. I think you did a really great job summarizing the acid base balance were looking at. We can certainly with DKA and other metabolic disorders get really, really into the weeds when were talking about acid base balances. And there are different formulas that we use to really tease out exactly whats going on to pick out the intervention. But at the heart of it in DKA, your ph will be low, meaning youre acidotic sometimes in the six range.
And as a result, bicarb drops significantly lowers the ph. And then our CO2, as in PCo two, the partial pressure of carbon dioxide in the blood also falls to compensate.
Kind of create respiratory alkalosis to compensate for that metabolic acidosis.
And the body is doing a really, really great job taking massive breaths, sometimes more than what we can provide. With a BVM or a ventilator, safely expelling all of the CO2 that it doesn't need in the bloodstream in an effort to compensate. So if we try to take that over using a mechanical ventilator or BVM, we are not going to be able to keep up.
You know, the body, the body's respiratory drive and inhalation process is a negative pressure system, meaning the pressure in the lungs falls to less than atmospheric pressure to allow that breath to come in. If we are breathing for the patient, it's a positive pressure system. And so in order to match those, like, lung volumes, we have to be driving that air in, which can cause trauma to the respiratory system, which we want to try to avoid.
Then, when you factor in the mechanical ventilation post intubation, especially, you have to keep in mind that we've oftentimes used a paralytic in order to facilitate the endotracheal tube insertion. And so we are managing that patient's respiratory rate 100%, and there's almost no way that we can keep up with that level of minute ventilation. Mechanically, however it does happen, it's super not ideal.
But if you see a patient who has DKA and they are starting to fail in a respiratory situation, you see that accessory muscle use or that they're starting to tire out. Bipap, high flow cpap. All good options for managing respiratory support without causing any kind of patient harm.
BIPAP is typically a little bit better than CPAP, but I know that in the certain EMS agencies, all you have available is CPAP, and it'll still help you support that respiratory drive by forcing fresh air deep down into the respiratory system to allow a little less work to draw an equal amount of breath.
[00:17:16] Speaker A: Yeah, absolutely. And one thing you mentioned about the innovation is remembering that if we paralyze that person, just thinking about our minute ventilation equation, our breaths per minute and our tidal volume, if we paralyze someone, even if we only paralyze them for 30 seconds before we start ventilating again, they may have taken 30 breaths in those 30 seconds that we paralyze them for. And think about 30 breaths of 500 mls per breath. I mean, we're already behind the eight ball, and we have to make that up somewhere, or it is like, ipso facto going to literally continue to drop the ph lower. So even 30 seconds of delay might be too big of a gap for us to catch up on. And even that small bump in ph can cause a cardiac arrest, which is why we are so careful when it comes to intubating our DKA patients or any profoundly acidotic patient. Not to mention, fun fact of the day with your ph is down below seven, your vasoactive drugs start to not work as well because all your enzymes get destroyed. So now we're talking about those of you that are like, well, we'll just give push dose epi, we'll just give Norepi. Those drugs get less and less effective as the ph gets lower and lower and lower. So it's not like something where we can just give ten mics of epi and be right back where we started with a ph of 6.8 or 6.7. It's just not going to give us the same bang for the buck that you might see at 7.4.
Let's say we're taking care of this patient, we're starting to treat them, and let's just use the critical care level. What are some initial actions that we're going to be doing to try to stabilize this patient? What are some initial meds? What are some initial goals that we're going to have as we start to slowly untangle this cluster problem that they're running into?
[00:18:52] Speaker B: Yeah. So we are assuming now that we've diagnosed DKA definitively, and we're going to start down this treatment pathway, the first thing that's important to do is get a baseline set of like, basic metabolic panel, chem seven, whatever you want to call it. You get your sodium, your potassium, your chloride, your bicarb or tco two, depending on what your shop uses as a lab value. They're both the same. You'll get a bun, a creatinine and a blood sugar.
And, you know, some places are also, you know, getting a magnesium and a calcium and, you know, some other, other lab values in there. But, you know, that chem seven is really the important one. We're going to get that and start the clock, and we're going to repeat that every two to 4 hours.
And it's important because when we think about our treatment for DKA, we need to start an insulin trip as soon as we can.
The problem with insulin, though, is it's going to drop your potassium. We need to start with a safe level of a potassium.
As people might know, in acidosis, your potassium rises, however, due to the dehydrated state. In this acidosis.
It's very common in DKA patients for that potassium to drop very, very rapidly.
We want to make sure that we're starting at a level that's hopefully above five. But definitely above the low end of normal in your normal patients. So 3.3 or greater, preferably. We want to target greater than five for the duration of this treatment.
So once we've confirmed that the potassium is, in fact, in a safe level, we can then begin our initial treatment with DKA. Compared to maybe some other disorders, we want to start insulin sooner rather than later, because this is a problem that develops relatively quickly. And with a lot of things in medicine, if it developed quickly, we want to try to treat it on the faster side.
So get insulin started, and we also need to fluid resuscitate. Oftentimes, these patients are going to be, like I mentioned before, you know, fluid down due to, you know, physical losses through vomiting and diarrhea and osmotic diuresis due to the increased osmotic pressures and increased blood sugar. And that's why they also present, usually very thirsty. So we're going to get the fluid started, we're going to get the insulin started and continue to monitor fluid choices. Kind of varies based on, you know, the institution you're in. My particular ICU, definitely preferred plasma light or normisol, depending on the brand name that you have, and or lactated ringers. It's a much more balanced crystalloid with a lower chloride content.
And reducing the chloride input that we're giving to these patients is going to help in the long run, and it'll help reduce the non anion gap acidosis that typically develops later in the treatment phase of DKA. But some places prefer to infuse a normal saline with 20 of potassium in it to help with their staying on top of the potassium. So, you know, use what you have and kind of, you know, weigh each, you know, the needs of the patient with the fluids that you have available.
[00:22:14] Speaker A: I think one of the things I always mention, too, is, like, all the 901 services I work for always carried normal saline. They didn't carry any lactated ringers. So I've heard people who kind of do enough critical care research, just enough to be dangerous, where they're like, well, you don't want to give normal saline because it has chloride content and the ph is lower. But again, you got to take a step back and look at the big picture. If your map is like, 47 and the is a profound shock state, sometimes getting an organ perfusion, even if it's with normal saline, even if the ph is low and even if it has chloride in it, maintaining an organ perfusion and starting to, like, treat the hypovolemia is going to give you more bang for your buck in terms of the total therapy than just letting them stay hypotensive with dangerous maps because you're worried about some electrolyte problem that may come down the road. You just want to make sure that you're cognizant that every action has an equal and opposite reaction. But I think, you know, thinking back to some of the patients I've seen in 911, these patients who you can't get a blood pressure on, you can't even get iv access because they're so dehydrated and hypovolemic that you're doing I Os, like, those patients need a couple liters just to get back in the game. And if that's normal saline until you get to the hospital, like, let the hospital worry about, you know, the potassium and those other things down the line, but you got to get that map where their. Their kidneys are functioning. Otherwise, we're going to. We're going to have a lot of problems, Evan.
[00:23:30] Speaker B: Oh, you're absolutely right about that. I wouldn't withhold fluids because I don't have lactated ringers or plasma light. I would absolutely send it with the normal saline and get them, you know, ball rolling on the rehydration, because that's going to help set the hospital up a little bit better for what they need to do afterwards.
And I've, for sure, taken care of patients from community hospitals where they don't have access to, necessarily all these fluids in high volume, and they do get three liters of normal saline, and it may not be the best. But we treat the DKA, the DKA resolves, and they get discharged from the hospital.
[00:24:08] Speaker A: Yeah, 100%.
[00:24:09] Speaker B: And if we have to treat a non anion gap acidosis at the tail end of the DKA management, you know, so be it. It happens even when they only get lactated ringers for a fluid.
[00:24:19] Speaker A: So, yeah, I think one of the things you told me pretty early on in my career here that I always kind of hold dear to me is, as you said, something along the lines of, like, you know, sometimes these ICU patients, they just need to be sick for a little while, and it's nothing like nine one where you're going to show up and cardiovert somebody, and then they're going to go home 12 hours later with a follow up to their cardiologist. Like these patients that develop DKA, it's going to take them, like, days, possibly weeks, to be kind of deconstructed. This Jenga tower of, like, fixing you know, the acidosis, the ketones, the blood sugar, the potassium, like, all these things have to come down in an incremental fashion, which I think is a good segue to. We give the potassium, we start this patient on insulin. We need to kind of make sure that we're slowly deconstructing this patient at the right rate. So you want to talk a little bit about what we're monitoring and how we kind of make decisions about treatment once we initiate it?
[00:25:11] Speaker B: Yeah, definitely. So as we mentioned earlier, this is DKA is a primarily an acidosis problem that has a side of a blood sugar problem. And that's really important to keep in mind as we infuse insulin over the next twelve to 24 hours.
We don't want to see massive drops in blood sugar. Even if it is 6700, we still want to bring it down 50 to 100 /hour tops. And so we have a very specific DKA insulin infusion protocol that we use in the hospital. So we do a blood sugar every hour using a finger stick glucometer situation and compare it to the last hours blood sugar. If it's in that 50 to 100 range, we leave the insulin trip as is.
Or if the blood sugar is still super high and it was 50 to 100, we might increase it a unit or two. While we're doing this, we watch the anion gap. And the anion gap is kind of our, you know, the driving force behind this treatment. As the anion gap closes, then we start to think about when we're turning the insulin trip off. And if the blood sugar gets down below 300, we start infusing dextrose containing solutions in order to kind of maximize our use of this insulin drip until such time as it needs to be turned off. And kind of along with that, we start as early as possible with subcutaneous long acting insulin injections so that when the insulin does get turned off, the anion gap doesn't open or reopen. However, even after the insulin drip stop, we still continue to monitor the blood sugar. We still continue to draw labs every 4 hours because it's super common for that to reopen. And then we need to restart the insulin drip.
And so it's, you know, very much a balancing act of monitoring potassium and sodium and fluid status and, you know, blood sugar and making sure that the nion gap closes and the acidosis resolves. And the bicarb comes up. And one of the things that we very commonly see is the anion gap closing. But the bicarb is still at the bargain basement. Level of 510 super low. And that's we see the anion gap resolving. If the bicarb isn't changing appropriately, we can identify this as now, in addition to having an anion gap acidosis, we have a non anion gap acidosis, at which point we have to start considering an isotonic bicarb infusion in order to supplement that bicarb level, you know, through medicine.
[00:27:50] Speaker A: Yeah, which is fascinating. So definitely a complicated topic. I want to give a shout out to Josh Farkus in his Internet book of critical care, if you haven't searched that and read through it. Fascinating resource. Really helpful. We definitely use that frequently, not only because he's a fellow uvmer, but also it's just a great vetted resource used across the board in critical care medicine around the country. So definitely check that out. Riley, I want to thank you for being on the show today and helping us unravel this very complicated topic. I think we probably are going to have to do DKA part two once people's brains have cooled down and they've enjoyed their summer and they're ready to tackle this topic again. But thanks for being here and hopefully you folks have learned something. So thanks, Riley.
[00:28:29] Speaker B: Yeah, thanks for having me, Nick.
