Transcript
Speaker: Welcome to Critical Matters, a sound podcast covering a broad range of topics related to the practice of intensive care medicine.
Speaker: Sound provides comprehensive critical care programs to hospitals across the country.
Speaker: To learn more about our programs and career opportunities, visit www.soundphysicians.com.
Speaker: And now your host, Dr. Sergio Zanotti.
Speaker: In today's episode of Critical Matters, we will discuss the management of critically ill patients with hyperglycemic emergencies.
Speaker: Our guest is Dr. George Willis, a practicing emergency medicine physician.
Speaker: Dr. Willis is an associate professor and associate program director for emergency medicine at the University of Texas Health Science Center in San Antonio, where he also serves as vice chair of faculty affairs.
Speaker: a recognized clinical educator with a special interest in endocrine emergencies, vascular emergencies, procedural education, and medical education.
Speaker: Dr. Willis has won numerous teaching awards, including ACEPS National Junior Faculty Teaching Award and EMRA's Top 25 Under 45 Influencers in Emergency Medicine.
Speaker: It is a true pleasure and an honor to have him with us today.
Speaker: George, welcome to Critical Matters.
Speaker: Sergio, thank you for having me.
Speaker: It is an absolute pleasure to be here.
Speaker: So I would like to start off the bat with asking you, why do you think intensivists at the bedside should care about hyperglycemic emergencies?
Speaker: Sure.
Speaker: So to be honest with you, it's
Speaker: It's really increasing.
Speaker: We, you know, when I was a resident practicing in emergency medicine, you know, 10, 15 years ago, we see a DKA patient probably once or twice a month at the most.
Speaker: Now I see so many hyperglycemic emergencies in my shift.
Speaker: It's, it's funny because my residents are like, Dr. Wells, I have a really good patient for you.
Speaker: And I'm like, I already know it's, it's gonna be a hyperglycemic emergency.
Speaker: But a part of the problem is, is that we're seeing over the trend of kind of the way that especially in the United States, the health care is gone, that obesity is taking a big predominance.
Speaker: And we're starting to see, again, an increase in the diagnosis of diabetes.
Speaker: So much so that even primary care physicians are starting to turn things such as pre-diabetes because they want health care professionals to be aware of this diagnosis.
Speaker: So diabetic emergencies are much more common.
Speaker: But the thing that's kind of led to the increase in diabetic emergencies or hyperglycemic emergencies also has to do with the fact that up until recently, you know, thankfully, we have an administration that has put a cap on insulin prices.
Speaker: Insulin used to be super expensive and we had a lot of patients who either didn't qualify for health care insurance or couldn't get health care insurance for whatever reason or refused to buy health care insurance.
Speaker: And when they get diagnosed with diabetes, they're not.
Speaker: and would be started on insulin regimens, they would find that the insulin was so expensive for them that they would be unable to afford it.
Speaker: And so they would either ration their insulin, they take it like every other day or every three days.
Speaker: And unfortunately, especially with type one diabetics, they would wait too long to start their insulin that they would develop, start to develop DKA.
Speaker: And it started leading to, you know,
Speaker: We used to think that SGLT2s were the only medications that gave patients euglycemic DKA, but we've seen a lot more euglycemic DKA just because we have so many people who are rationing off their insulin.
Speaker: So unfortunately, as a result of that, we're seeing much more hyperglycemic emergencies in the emergency department as well as in the ICUs.
Speaker: So obviously, in addition to the increased frequency that you're mentioning for all those factors, I think a lot of intensivists or ICU clinicians at the bedside sometimes get a little bit cavalier about these diseases, like do this, do this, do this.
Speaker: But these patients have real risk, right?
Speaker: I mean, there's real risk of mortality and morbidity, and there's complications, and those should all be prevented with time-sensitive interventions and a thoughtful approach.
Speaker: Absolutely.
Speaker: So the hard part is that, you know, one of the things that a lot of people don't recognize is that you have to treat these patients very carefully.
Speaker: We oftentimes think that we know what we're doing.
Speaker: And unfortunately, we actually make more mistakes with this management, especially with HHS.
Speaker: And we'll get into the kind of the nuances of HHS, but we either miss the diagnosis of HHS or even worse, we treat
Speaker: HHS not adequately.
Speaker: HHS is one of those disease processes that takes days to develop and we think that we're treating them in the emergency department for instance.
Speaker: We'll say, oh we have this patient with HHS but we fixed them in the emergency department.
Speaker: That is not a good thing.
Speaker: That's not something that you want to do.
Speaker: These patients need to be treated just as slow as they develop their disease process.
Speaker: So there's a lot of nuances to the interventions that we're that we're doing with these patients that we really need to be careful of.
Speaker: Absolutely.
Speaker: And in terms of terminology for hyperglycemic syndromes, I know that we talk about DKA, we talk about in the past non-ketotic hyperosmolar coma, and that name has changed many times.
Speaker: Could you just give us the current and accepted terminology of what is considered a hyperglycemic emergency?
Speaker: Sure.
Speaker: So DKA is still DKA.
Speaker: It's diabetic ketoacidosis.
Speaker: And we'll we'll we'll you know, when we talk about the treatment and the diagnosis, we'll we'll get into why diabetic ketoacidosis is deemed the name that it is.
Speaker: We've seen this this kind of evolution of HHS.
Speaker: And so
Speaker: When I was in training, we used to call it HONK, which I universally hated because it stands for hyperosmolar non-ketotic.
Speaker: Well, where's the hyperglycemia in that?
Speaker: The hyperglycemia is certainly going to be necessary.
Speaker: And some people say, well, HONK is actually not spelled H-O-N-K.
Speaker: It's spelled H-H-O-N-K.
Speaker: So it stands for hyperglycemic.
Speaker: hyperosmolar non ketotic syndrome.
Speaker: And the big focus that they wanted people to kind of get from that was that the patients need to be hyperglycemic, they need to be hyperosmolar, and they needed to basically have the absence of the ketoacidosis.
Speaker: So the NK or the non ketosis is where that came from.
Speaker: Now we have developed it into HHS, which I love so much more.
Speaker: So it's the hyperglycemic hyperosmolar syndrome or state.
Speaker: The only thing I hate using the term state because it almost makes it seem like it's a transient thing that's only going to last for a period of time.
Speaker: I like syndrome a little bit more.
Speaker: It makes it seem like it's a formal diagnosis.
Speaker: But that's the current terminology now is still DKA and HHS, meaning hyperglycemic hyperosmolar syndrome.
Speaker: Perfect.
Speaker: So before we start talking about the clinical management, one of the things that I recall was kind of like an epiphany for me as a medical student was understanding a little bit about the pathophysiology of DKA and HHS.
Speaker: It's really kind of triggered, I think, an interest in pathophysiology and critical illness.
Speaker: Could we start with a basic overview of maybe DKA pathophysiology, and then at the end, you can maybe contrast how HHS is different or similar?
Speaker: Sure.
Speaker: So this is this is I'm going to warn you, Sergio.
Speaker: I am a true endocrine nerd.
Speaker: True.
Speaker: Tried and true.
Speaker: I absolutely love the pathophysiology of this because it basically stimulates the part of my brain that loves endocrine diseases, which is essentially my whole brain.
Speaker: So I'm going to get really into the weeds with this because I think it's very important for understanding the management and why we do the things that we do, especially with HHS.
Speaker: So starting with DKA, the main premise for DKA is that the body thinks that it is hypoglycemic.
Speaker: So although the fact that there's plenty of sugar to go around, there's not enough insulin for that sugar or there's no insulin for that sugar to actually be utilized by the muscle and by the brain and other tissues.
Speaker: And so as a result, the body thinking that it's hypoglycemic, it actually starts a process to make more glucose.
Speaker: So the primary hormone in that, the counter-regulatory hormone in that, there's three big ones, which are
Speaker: Cortisol, which is obviously a stress hormone, that cortisol is a glucocorticoid, so it's a glucose-containing steroid.
Speaker: But cortisol also has the role of turning off insulin.
Speaker: So even if the pancreas was capable of making insulin, which in type 1 diabetics usually isn't, the pancreas,
Speaker: cortisol is going to actually tell the pancreas to stop making insulin because, again, it thinks that it's hypoglycemic.
Speaker: So this is actually the thought-to-be mechanism for how type 2 diabetics develop DKA, the thought process being that
Speaker: Type two diabetics typically can make insulin, so they usually don't go into DKA.
Speaker: But when they have some stress or some event, usually it's either overwhelming sepsis or massive infection or myocardial infarction or stroke.
Speaker: Some other large stressor the.
Speaker: Cortisol that gets secreted in that high stress state causes the pancreas to not make any insulin.
Speaker: And subsequently, they end up going into DKA despite having a pancreas that's actually functioning.
Speaker: So there's cortisol.
Speaker: Then there's catecholamines, which causes the neuro glycopenic effects.
Speaker: So your increased heart rate, your increased blood pressure, diaphoresis, agitation, diabetes.
Speaker: And then the last one, which is the very important one, which is glucagon.
Speaker: So glucagon does a couple of things.
Speaker: One, it starts gluconeogenesis.
Speaker: So it starts the creation of more glucose.
Speaker: Second thing it does is it breaks down glycogen in the liver to, again, make more glucose.
Speaker: And then the primary thing that it does, which is actually the big problem with DKA, is that it starts the process of ketogenesis.
Speaker: And so it starts making ketone bodies to essentially feed the brain.
Speaker: And those ketone bodies being negatively charged are beta-hydroxybutyrate or beta-hydroxybutyric acid and acetoacetate or acetoacetic acid.
Speaker: And the large predominance of those ketone bodies in the blood and ketonemia is what actually leads to the keto acidotic state.
Speaker: So that in a nutshell is what's happening with DKA.
Speaker: And we'll get into the meat in the treatment, but essentially insulin and glucagon are polar opposites of each other.
Speaker: So when glucagon causes ketogenesis and ketoacidosis, insulin reverses everything that glucagon does.
Speaker: And so we'll get a little bit more into that when we get into treatment.
Speaker: Now, HHS is significantly
Speaker: different.
Speaker: So in this scenario, the body still makes insulin in most of these circumstances.
Speaker: But again, it's not making enough insulin.
Speaker: So what ends up happening is that is there is a significant
Speaker: elevation in the glucose level.
Speaker: And so, you know, we see HHS usually in patients who have blood sugars who are greater than a thousand.
Speaker: But what happens here is those same counter-regulatory hormones still are made, but glucagon doesn't really come into the picture in this scenario.
Speaker: So there is no ketoacidosis.
Speaker: There's no ketone bodies that are being formed.
Speaker: And so, but the body's still
Speaker: predominantly increasing the amount of glucose due to stress levels and things like that.
Speaker: So what ends up happening in the long run over time is that the elevated blood sugar causes there to be an increase in free water in the bloodstream.
Speaker: So these patients, this is where we see that pseudo hyponatremia that occurs very typically with hyperglycemia.
Speaker: And so that's what happens at the beginning.
Speaker: But then over time, as the body starts to have that osmotic diuresis, that the body actually starts to spill that free water in the urine.
Speaker: And what the body's trying to do essentially there is to lower the glucose the best way that it can.
Speaker: Unfortunately, it's...
Speaker: not that strong of a response and so what ends up happening is that the body starts to lose that free water and inside the blood they actually maintain normal or eunatremia so the body develops normal sodium the problem with that is that remembering that osmolarity is primarily driven by sodium so if you look at the osmolarity equation
Speaker: You have two times the sodium.
Speaker: And then at the end, you have glucose divided by 18.
Speaker: So if you think about that logistically, to raise osmolarity, you could raise the sodium by one point, and that raises the osmolarity by two points.
Speaker: Whereas glucose, and this is where a lot of people mistake HHS is they'll see a patient who's just hyperglycemic, normal mentation, and they think, oh, this person has a blood sugar of 1600.
Speaker: They are very clearly in HHS.
Speaker: Well, that patient is simply hyperglycemic.
Speaker: What happens with HHS is that the osmolarity is really affecting the brain and the central nervous system, which is why these patients will come in with some form of altered sensorium.
Speaker: Most of the time it's a stupor or confusion, and then it progresses to obtundation or coma.
Speaker: So if you think about it from the sodium perspective, basically,
Speaker: What's happening here is that looking at the sodium being about normal, if you correct the sodium based off of the glucose level, their sodium is actually hypernatremic.
Speaker: And so these patients who will be hyperglycemic with normal sodiums,
Speaker: that sodium is affecting the osmolarity so much that the brain is actually starting to be affected.
Speaker: And so that's the big pathophysiology for HHS.
Speaker: It's not really the glucose.
Speaker: The glucose is the cause, but the sodium is the problem.
Speaker: The sodium is driving the osmolarity up so high that they're actually starting to be starting to have some effects in the central nervous system.
Speaker: And that's what ends up being the big problem.
Speaker: And so what ends up happening with these patients, normally when you're hyperglycemic, you start to feel, you know, thirsty, you have that polyuria, that polydipsia, and so you feel that thirst.
Speaker: But as that central nervous system starts to become affected, your thirst response is
Speaker: is suppressed and so you don't drink water to keep your your blood levels and your sodium at a regulated level and so you just continue to exacerbate the process which is why again this process takes days to weeks to really manifest and and really needs to be kind of repaired and corrected in that same fashion
Speaker: And I think also explains, obviously, why the treatment that really makes a difference is fluids and not necessarily the insulin.
Speaker: But I think there's a great, I mean, overview and explanation.
Speaker: And I think it's important as clinicians to keep pathophysiology always in mind to explain the why of what we're trying to do.
Speaker: But also what I find, George, is that people who don't connect the pathophysiology to the bedside get in trouble when things don't follow the protocol.
Speaker: So anybody can start a DKA protocol, I'm sure.
Speaker: But not every patient responds the same way.
Speaker: And understanding what might be going on and what you need to adjust, I think, is guided by pathophysiology first and foremost.
Speaker: You hit that nail right on the head.
Speaker: And what a lot of people, you know, the thing that really kind of drives me up the wall with especially these both of these these disease processes is that you'll have something else that's going on.
Speaker: And we'll talk about this a little bit.
Speaker: But when we get to diagnostic criteria, you focus so much on the fact that this patient has.
Speaker: hyperglycemia and a metabolic acidosis with an anion gap and they'll think oh this is clearly dka when the patient has a lactate of 17 or they have aspirin overdose on board or they have a toxic alcohol on board and they oftentimes miss the forest for the trees and so
Speaker: I really encourage people to think outside the box with a lot of these diagnoses.
Speaker: But certainly if patients present very typically or classically, you certainly don't want to miss this diagnosis as well.
Speaker: And I think what you just explained also hits on a recurrent theme that more and more I see in medicine, which is we are programmed to find quick answers.
Speaker: We should program ourselves to ask more questions, right?
Speaker: Always ask what else, what could be causing, what am I missing?
Speaker: So I think that, like you said, it's very easy to just, oh, just label it as DKA, but there might be something else going on.
Speaker: that we didn't really pay attention to that ultimately can cause significant harm to our patients.
Speaker: 100%.
Speaker: Absolutely.
Speaker: So let's talk about clinical presentation and diagnosis.
Speaker: Let's start with DKA, diagnostic criteria.
Speaker: My understanding from reading some of your excellent review papers is that there's not a lot of agreement here.
Speaker: You can quote ADA, but the British say something different.
Speaker: Some people say, I mean, you know when you see it.
Speaker: I mean, can you tell us kind of how you think about this?
Speaker: Sure.
Speaker: So we'll talk about diagnostic criteria first, because interestingly, you
Speaker: Hot off the press in June of 2024, the ADA, the British Society of... The British Society.
Speaker: Now I'm forgetting the name.
Speaker: Give me a second.
Speaker: It's the British Society of...
Speaker: Joint British Diabetes Societies for Inpatient Care, the European Association for the Study of Diabetes, and the American Association of Clinical Endocrinology all got together and came up with a new set of diagnostic criteria.
Speaker: This is the first time that anyone has really put together a joint set of criteria for the diagnosis of DKA and HHS.
Speaker: The ADA guidelines were based off of a study or a paper that was written by Katabji et al.
Speaker: in 2009.
Speaker: And we've been using that criteria since 2009.
Speaker: But so much has changed.
Speaker: We've we've developed so much different knowledge bases now with with with DKA.
Speaker: I'm so glad that they've actually made an adjustment.
Speaker: So these new criteria now.
Speaker: Excuse me.
Speaker: are the following one, um, the, the glucose definition.
Speaker: So it used to be a glucose greater than two 50.
Speaker: They've lowered that now to 200 and added the stipulation or a previous diagnosis of diabetes.
Speaker: And what they're doing there is they're essentially making, um, constellations for the fact that there is this disease process called euglycemic decay.
Speaker: And that commonly is, um,
Speaker: seen in patients who are on diabetic medications.
Speaker: And so you are not
Speaker: I don't know if it's possible.
Speaker: It's certainly possible in my thought process that it could happen.
Speaker: It would be very difficult to happen.
Speaker: But you're not going to see a new onset diabetic come in and euglycemic DKA in most circumstances.
Speaker: So most of the euglycemic DKA that we see are typically patients who've already been previously diagnosed with diabetes.
Speaker: So I love the fact that they actually changed this as a diagnostic criteria for
Speaker: to lower the glucose and then add whatever glucose that they have.
Speaker: If they have a history of diabetes, they could be at risk for DKA.
Speaker: The second one's unchanged.
Speaker: They have to have ketonuria or ketonemia.
Speaker: They now have added beta-hydroxybutyrate levels because a lot of hospitals and emergency departments have the ability to check a beta-hydroxybutyrate level in a relatively rapid fashion.
Speaker: And so beta-hydroxybutyrate is now added into the diagnostic criteria, and they say a beta-hydroxybutyrate level greater than 3.0 is diagnostic or a ketone level that's measured, whether it's in the blood or in the urine, of 2 plus or greater.
Speaker: Now, this one I'm going to actually beat up just slightly in that ketone assay in both the blood and the urine typically checks for acetoacetate.
Speaker: And beta-hydroxybutyrate is actually the predominant ketone body that's made.
Speaker: And so that acetoacetic level or acetoacetate level changes.
Speaker: that's present in the urine and the blood assays may be lower than 2+, but that doesn't mean necessarily that the person doesn't meet criteria for DKA.
Speaker: And then the last one is an anion gap metabolic acidosis.
Speaker: That one, again, is unchanged, pH less than 7.3 or a serum bicarb level of less than 18.
Speaker: So those are the diagnostic criteria for DKA.
Speaker: HHS, their definition for HHS really hasn't changed significantly since the 2009 paper that we discussed.
Speaker: So the first diagnostic criteria is that they have to have an elevated blood sugar and that blood sugar is going to classically be greater than 600 milligrams per deciliter.
Speaker: So that definition hasn't changed in years.
Speaker: They use for hyperosmolarity two different measures for osmolarity.
Speaker: There's an effective serum osmolarity, which is greater than 300 milliosms or the total serum osmolarity, which is the classic, you know, two times the sodium.
Speaker: glucose grade glucose divided by 18 and a bun divided by 2.8 and all of those added up and they say a total serum osmolarity level greater than 320 milliliter milliosms and then they here's where the definition kind of changes they obviously say
Speaker: absence of ketonemia and so if the ketones in the urine or the serum are less than two plus or the beta hydroxybutyrate is less than 3.0 so this is the one change that they did make
Speaker: And then absence of acidosis.
Speaker: So that's unchanged.
Speaker: The thing that is a little frustrating is they used to have a diagnostic criteria for mental status.
Speaker: They've taken that out for some reason that I'm still unsure of why.
Speaker: In the grand scheme of things, again, we talked about the mental state.
Speaker: So these patients are going to come in with some element of altered mental status.
Speaker: But from the diagnostic criteria, they have taken that part out of the diagnostic criteria for HHS.
Speaker: So in terms of clinical presentation, what I typically am looking for in patients who come in with diabetic ketoacidosis, usually they are a type 1 diabetic.
Speaker: And we talked about the ways that people can present with type 2 diabetes.
Speaker: We're still more commonly going to see that in type one diabetics.
Speaker: These patients usually will present with abdominal pain and nausea and or vomiting.
Speaker: And all of those symptoms are traditionally as a result of the ketoacidosis that's present.
Speaker: It's not the hyperglycemia that's causing that.
Speaker: It is the ketoacidosis that's causing that.
Speaker: They may have an element of altered mental status when their pH starts to drop into the less than seven range.
Speaker: So you may see some element of altered mental status as well.
Speaker: And then what we call the Kussmaul respirations is the kind of pathognomonic thing that we see with patients with DKA, being that deep, rapid breathing area.
Speaker: So if you see a patient who has a respiratory rate that's 24, 30, and it's a deep, rapid respirations, then that patient is compensating for their metabolic acidosis.
Speaker: So that's kind of the classic picture for DKA.
Speaker: For HHS, there's there's.
Speaker: Classically, you're going to see this in type two diabetics.
Speaker: Type one diabetics typically won't get high enough before they're developing DKA.
Speaker: So you won't typically see HHS in type one diabetics.
Speaker: It's more commonly going to be in type two diabetics.
Speaker: And you're going to probably see this more commonly in the elderly population.
Speaker: However, recently we've had an increase in childhood obesity and subsequent re
Speaker: terrifyingly, we've seen a larger number of type two diabetics getting diagnosed in the pediatric population.
Speaker: And so there are case reports of kids developing HHS as well, which is just debilitating to even think about that we get, you know, the pediatric population with blood sugars in the 1000s and 2000s.
Speaker: So, but the classic presentation here, they typically are going to be missing your ketoacidosis symptoms.
Speaker: So they're not going to have the abdominal pain.
Speaker: They're not going to have the nausea and vomiting unless they have some disease process that's causing them to be hyperglycemic, you know, again, getting to that stressor.
Speaker: And then the again, getting back to the mental status.
Speaker: So the mental status in these patients is is frequently going to be significantly altered compared to their baseline.
Speaker: So it can be any type of neurologic symptom they can have.
Speaker: I've seen patients with HHS who've had stroke like symptoms.
Speaker: I've seen patients with HHS have paresthesias.
Speaker: But the classic.
Speaker: presentation for HHS is going to be some element of altered sensorium where they're globally confused.
Speaker: They have, you know, stupor and they develop as time progresses, they will eventually get to the point where they're uptunded and then subsequently go into a comatose state.
Speaker: So those are the kind of classic presentations for patients who present clinically.
Speaker: Perfect.
Speaker: And as you suspect that they either have DKA or HHS based on their presentation, could you comment on the initial workup and how do you think about trigger and causes and differential diagnosis?
Speaker: Sure.
Speaker: So whenever I think about patients who come in with hyperglycemia, I think of the four, what I call the four I's.
Speaker: And so those four I's are the very much the most common reasons why patients develop hyperglycemia.
Speaker: The last one is the one that we more commonly see, but I put it last because I want it to be the diagnosis of exclusion or the etiology of exclusion.
Speaker: So number one cause of hyperglycemia worldwide is infection.
Speaker: So these patients will have more commonly you're going to see urinary tract infections and pneumonias be the primary cause.
Speaker: But bacteremia, really any infection can do this.
Speaker: I've seen patients with new onset diabetes who have had fourniase.
Speaker: I've seen lots of septic patients who have developed new onset diabetes as well or worsened diabetes.
Speaker: hyperglycemia in patients who are already diabetic.
Speaker: So infection needs to be one of the things that we certainly consider.
Speaker: Number two is ischemia.
Speaker: So that can be myocardial ischemia.
Speaker: That can be
Speaker: central nervous system ischemia so strokes one that a lot of people oftentimes forget about is mesenteric ischemia so they can present with abdominal pain nausea and vomiting which is what diabetic ketoacidosis looks like and so a lot of people will mistakenly think oh this patient's simply in dka and be missing mesenteric ischemia
Speaker: So any infarction or ischemia is another eye to think about in terms of etiology.
Speaker: Third is infancy.
Speaker: So basically being pregnant.
Speaker: So obviously our patients who are in their age of childbearing age,
Speaker: They will they can present with hyperglycemia as well.
Speaker: There's obviously gestational diabetes, which gestational diabetes doesn't classically give you diabetic ketoacidosis in most circumstances, because most people think that gestational diabetes is more of an insulin resistance as opposed to a deficiency.
Speaker: But again, if these patients develop some type of stressor that can certainly throw the cortisol into the picture, they can develop diabetic ketoacidosis due to that stressor as well.
Speaker: And then the last I is insulin being insulin noncompliance.
Speaker: And so a common mistake that a lot of people make is that they assume that patients who come in in DKA or HHS have simply not taken their insulin like they're supposed to.
Speaker: And so they end up missing some infection or ischemia or they don't check a pregnancy test in a patient, a female of childbearing age.
Speaker: And so my diagnostic workup for the most part is going to be to look for any of these four eyes.
Speaker: You know, if a patient comes in with.
Speaker: Doc, I'm sorry.
Speaker: I have not been taking my insulin like I'm supposed to.
Speaker: I know that I'm in DKA because I haven't taken my insulin in like a week.
Speaker: I apologize, but unfortunately it was just too expensive.
Speaker: That may be a patient who may get very minimal workup from a diagnostic perspective.
Speaker: You know, that person can probably just get some labs to kind of see what their sugar is, what level their anti-gap acidosis is, check for ketones and things of that nature.
Speaker: In most circumstances, I'm still going to get a screening chest X-ray to make sure that they don't have a pneumonia.
Speaker: I'm getting a urine anyway to make sure they don't have an infection.
Speaker: Getting a screening EKG just to make sure that they're not showing any signs of ischemia on their EKG, as well as to look and see what their EKG looks like from a potassium perspective, which we'll talk about shortly.
Speaker: But then also, you know, having a low, very low threshold to getting blood cultures.
Speaker: and things of that nature just to make sure that I'm not missing some form of one of those four eyes to look for an etiology.
Speaker: With HHS, it's a much broader workup, primarily because these patients are coming in and they are very altered, have an altered sensorium.
Speaker: So again, low threshold to get a CT scan of the head, low threshold to check other etiologies for altered mental status, checking in ammonia level,
Speaker: maybe an alcohol level, because a lot of times these patients aren't going to be able to give you much in the way of history.
Speaker: And so I have a much, much more, much bigger workup in that patient population because of how sick those patients are.
Speaker: So that's, those are the big kind of, kind of infection or initial workups in patients who come in with hyperglycemic emergencies.
Speaker: And you talked about, obviously, other diagnostic criteria and the differences between measuring the different keto acids.
Speaker: I wanted to ask you, George, is there a role for end tidal CO2 here?
Speaker: Yes.
Speaker: One of my favorite things.
Speaker: So, you know, we can get I work at one of the ivory towers.
Speaker: And so, you know, in terms of what I have access to from a diagnosis perspective, I can get a rapid VBG in five minutes.
Speaker: I can get with lights, with electrolytes.
Speaker: So I can get a rapid VBG with electrolytes and probably.
Speaker: Five minutes.
Speaker: So I can I can know if a person's in DKA relatively quickly.
Speaker: I know that most people don't practice in an ivory tower like I do.
Speaker: And they may not have access to a rapid point of care BBG or electrolyte panel.
Speaker: So what do you have access to that you can do relatively quickly?
Speaker: Because we'll get patients who come into the to our emergency department or in our critical care setting who are hyperglycemic.
Speaker: So you can do end-tidal CO2 and quickly rule out DKA.
Speaker: So if you put an end-tidal CO2 on a patient and that end-tidal CO2 is 27 or higher, you have effectively ruled out DKA with a negative predictive value of about 99.7%.
Speaker: So it is a very useful tool.
Speaker: I use it all the time actually in the ED where I'll get patients who come in and they're like, yeah, so my doctor sent me here because my sugar is –
Speaker: high quote unquote, meaning it's greater than 600 milligrams per deciliter.
Speaker: So instead of drawing a whole bunch of labs on that patient, it's sure I may want to know what their sugar is, but I can quickly just throw in title CO2 on them.
Speaker: And within five minutes I can have an entitled CO2 level.
Speaker: And if that entitled CO2 level is greater than 27, I might just get a BMP on them just to see what their sugar actually is.
Speaker: and then give them some fluids.
Speaker: I don't necessarily have to give them any insulin or any other anti-hyperglycemic therapy.
Speaker: And those patients oftentimes go home really quickly with instructions, go follow up with the primary care physician who inappropriately sends you to the emergency department.
Speaker: When the level is less than 27, it doesn't 100% rule in DKA, it just makes DKA more likely.
Speaker: It means that they have some type of acidosis process
Speaker: That's going on that's making their entitled co2 low so I use entitled co2 very very frequently from an initial diagnosis Press perspective also I use it during my treatment I actually use it during the treatment process because it actually gives me a gauge of how well my treatment is working for the patient so if that entitled co2 started off at we'll just say 16 or 17
Speaker: And I started the patient on fluids.
Speaker: I'm giving them insulin and I'm watching their entitled CO2 start to creep up.
Speaker: I know that I'm actually improving the patient and making them better.
Speaker: If it's not moving, I do two things.
Speaker: One is I may need to start increasing my treatment or I may need to look for some other etiology.
Speaker: Does this patient have a lactic acidosis?
Speaker: Does this patient have a toxic alcohol on board that I was unaware of?
Speaker: So I start to think about other diagnoses that may be going on concomitantly with the DKA.
Speaker: So I love the use of entitled CO2 in this patient population.
Speaker: Excellent.
Speaker: And I think it's important also to highlight how there's tools that maybe you're not thinking of for DKA that can help you.
Speaker: And from what you described,
Speaker: It almost feels like a, a, akin to a D-dimer, right?
Speaker: It helps you rule out stuff, but it doesn't necessarily make the diagnosis.
Speaker: But like you said, in some circumstances and environments, such as the one you practice in, that can help you move patients efficiently and not overdo the testing when it's not needed.
Speaker: Yep.
Speaker: Awesome.
Speaker: So let's talk about management.
Speaker: And you talked about the four eyes.
Speaker: And using another analogy, it feels that one of the areas where sometimes we don't pay as much attention as we should when the high glucose, the ketones are blinking in our eyes is the cause, the underlying cause.
Speaker: And it's almost similar to source control, right?
Speaker: We have to take care of that.
Speaker: First and foremost, otherwise we're not going to get anywhere with that patient.
Speaker: And could you talk about management and start with that treatment of the underlying cause, and then we can go on to the DKA treatment?
Speaker: Sure.
Speaker: So one of the things that I think is super important here is just what you're describing.
Speaker: Because, you know, we can basically give these patients fluids and...
Speaker: Start them on an insulin drip and sure they will look like they're getting better But if there's something that's going on that's causing this there We're not going to improve them just by giving them fluids because we could get them to the point where their acidosis is improved Everything's getting better
Speaker: And then we stop all of those interventions.
Speaker: And then subsequently, they throw themselves back into decay and will mistakenly think, oh, you must have gave yourself something to eat or you must have done something wrong.
Speaker: What caused you to go back into decay?
Speaker: And it's because we missed the underlying etiology or the cause of these patients symptoms.
Speaker: And so, again, in a sick situation.
Speaker: sick DKA patient and certainly a sick, sick HHS patient, or really a lot of times any HHS patient, I have a low threshold to starting those patients on empiric antibiotics.
Speaker: If they have anything that looks even remotely like they are septic in any way, obviously still following the sepsis guidelines, they're
Speaker: We want to start those patients on empiric antibiotics early.
Speaker: And so I have a low threshold in this patient population to starting these patients on empiric antibiotics.
Speaker: And again, we're looking for sources of ischemia.
Speaker: If we find sources of ischemia, getting these patients up for timely interventions, I can think off the top of my head specifically of three patients who I had who were in HHS because of STEMIs, where the cardiologist's
Speaker: was refusing to take the patient to the cath lab.
Speaker: And I was who we got their sugar better.
Speaker: And I said, look, I can treat their sugar all day and I'm going to give them fluids and I'm going to give them insulin and put them on an insulin drip.
Speaker: But I need you to take this patient to the cath lab ASAP.
Speaker: And, you know, after some significant bargaining, um, I feel like I owe one of my children, um,
Speaker: To that cardiologist at this point in time, they ended up taking the patient to the cath lab and subsequently they've gotten better.
Speaker: So I they but the stipulation that they made was that I had to start the patient on the insulin drip before they would take them to the cath lab.
Speaker: So we took it to the cath lab and the patient, both all three of those patients had really good outcomes.
Speaker: So starting with source control is important.
Speaker: Certainly looking for those screening labs, seeing if the patient meets sepsis criteria, the screening interventions of the EKG, the chest X-ray, all of those things will help you in terms of identifying potential sources.
Speaker: But you have to treat those things as well.
Speaker: The one eye that you're obviously not going to treat is the
Speaker: the infancy.
Speaker: Obviously, if you have a pregnant lady, you're not going to get rid of the baby because she's in DKA.
Speaker: You're just going to treat that.
Speaker: And that person is probably going to need to be on an insulin regimen or some other type of treatment for their diabetes in the long run.
Speaker: So those are the big kind of source control things that I do.
Speaker: Very, very low threshold to starting antibiotics.
Speaker: Again, looking for sources of ischemia and then treating the patient appropriately from there.
Speaker: Perfect.
Speaker: So let's talk a little bit more about DKA and go through the different aspects of treatment.
Speaker: And as you explained earlier, the pathophysiology kind of links to what we're doing.
Speaker: So we start with IV fluids.
Speaker: What are your thoughts on IV fluids for DKA?
Speaker: 100% necessary.
Speaker: You have to do it the right way, though.
Speaker: We'll talk about why.
Speaker: Again, I'm going to go a little in the weeds.
Speaker: Endocrine nerds, that's me.
Speaker: So as we alluded to before, we talked about the osmotic diuresis.
Speaker: And the key thing to focus on with the osmotic diuresis is two things.
Speaker: One,
Speaker: glucose and water are like best friends.
Speaker: They go everywhere together, which includes out in the urine.
Speaker: So these patients have a very significant volume depletion that occurs intravascularly as a result of the osmotic diuresis.
Speaker: Well, when you start the patients on treatment, if you haven't adequately rehydrated them and replenished at least or started to replenish the intravascular volume, we know these patients need insulin.
Speaker: So if
Speaker: you just said this patient classically looks like DKA.
Speaker: They tell me they're in DKA.
Speaker: They quack like they're in DKA.
Speaker: This patient's in DKA.
Speaker: I know they need insulin.
Speaker: I'm just going to go ahead and start an insulin drip.
Speaker: What happens is, is that intravascularly, the body will sense the insulin presence and it will start to pull glucose out
Speaker: out of the vascular system and into the tissue.
Speaker: Well, where glucose goes, water says, bring me too.
Speaker: And so it leaves the intravascular space, which can lead to circulatory collapse.
Speaker: Subsequently, these patients will get hypotensive and can go into cardiac arrest.
Speaker: So you don't want to just blanket start these patients on insulin until you've adequately hydrated them.
Speaker: So this is where I use ultrasound to my advantage.
Speaker: I will actually assess their volume status and see what I can see in terms of looking at their IVC.
Speaker: looking at some other objective measures intravascularly to see if I can get a sense of what their true vascular status is.
Speaker: You will get some patients, for instance, who may be in stage renal disease, who may not have had that osmotic diuresis, but can subsequently still be in DKA.
Speaker: And in those patients, they may have a normal volume status.
Speaker: And so flu isn't necessarily as important in that patient.
Speaker: Or they may have developed myocardial ischemia from a massive myocardial infarction.
Speaker: And they may have developed CHF where they're not going to be able to mobilize as much fluid because their EF is low.
Speaker: So in that circumstance, I may hold or give smaller volumes of fluids, but I want to assess what their volume status is.
Speaker: The vast majority of patients who are in DKA, though, are going to be very volume down.
Speaker: And again, we don't want to just start them on insulin.
Speaker: So IV fluids is going to be the most important thing to establish rehydration and replenishing the intravascular.
Speaker: Volume in terms of which IV fluids.
Speaker: This is again where I get a little frustrated with the new criteria that just came out in June of 2024, which state that the initial fluid of choice is still isotonic crystalloids.
Speaker: Now, the thing that I do like about their statement is that they don't bad mouth the
Speaker: balanced solutions.
Speaker: They just say you can use balanced solutions.
Speaker: And there is some literature out there that says that balanced solutions leads to a quicker resolution of the decay.
Speaker: So they at least acknowledge that balanced solutions are better.
Speaker: But I make the argument that balanced solutions should be our initial go-to.
Speaker: Now, obviously, if you don't have balanced solutions, normal saline is perfectly fine.
Speaker: It's just...
Speaker: Not as quick or it's not as good as using the balance solutions The reason why normal saline really gets a bad rep is because normal saline has too much chloride So the body's chloride concentration is between 95 and 105 where there's a hundred and fifty four milliequivalents of chloride in normal saline and
Speaker: And what happens with large volumes of normal saline especially is these patients will get hyperchloremic, which if you think about the anion gap equation, you're going to increase the chloride, which is one of the negative anions,
Speaker: the thing that's being subtracted from sodium.
Speaker: And so that anion gap is going to close rather quickly, despite the fact that the acidosis is not actually moving or improving.
Speaker: And so these patients develop a non-anion gap hyperchloramic metabolic acidosis.
Speaker: And so to avoid that, you can start them on plasma light, which is my go-to or lactated ringers.
Speaker: Plasma light has a chloride concentration of 98, which is much more physiologic.
Speaker: Lactated ringers has a chloride concentration of 109.
Speaker: Again, closer to the physiologic status of the chloride concentration in the body.
Speaker: And so you don't develop that hyperchloremic non-anigap metabolic acidosis with balanced solutions versus normal saline.
Speaker: So I preferentially use...
Speaker: plasma light, um, LR is available at my hospital.
Speaker: I just find plasma light to be very easy to use the problems from a perspective of normal saline versus the balanced solutions is the balanced solutions traditionally are a little bit more expensive.
Speaker: Um, so if you want to save money, certainly you can use normal saline again, knowing that your patient is just going to be a little bit longer, um, in DKA, um, in that circumstance.
Speaker: And I think that obviously what we've seen over and over again is with normal saline and DKA is the increase of non-annion gap metabolic acidosis due to the chloride, like you explained.
Speaker: But also keeping them longer than they need to in the ICU also has a cost implication.
Speaker: Plus, I would argue that...
Speaker: The available literature in critical illness, general critical illness, supports the use of balanced solutions, right?
Speaker: Absolutely.
Speaker: So I think that from that perspective, plus like you mentioned, there are some small studies that suggest that the recovery or the resolution of the ketoacidosis is quicker with the balanced solutions.
Speaker: What I was going to ask you about the plasma light is, I guess, the only challenge with plasma light, or not a challenge, but the only wrinkle, I would say, is that there is no plasma light with dextrose, right?
Speaker: So eventually, as you move your strategy, you have to figure that out, correct?
Speaker: Correct.
Speaker: So, yeah, so just to kind of go back to your previous point, the literature, the literature is really good here.
Speaker: The previous studies that were done were done on were done in like smaller numbers.
Speaker: So, you know, I think one of the studies had 25 patients.
Speaker: Another one had 49 patients.
Speaker: The largest study, which is the study that I absolutely adored,
Speaker: was done by Self et al.
Speaker: published in November of 2020.
Speaker: And it looked at the subgroup of patients who were in DKA from the SALT-D trial and the SMART trial.
Speaker: Had 172 patients and again found that those patients had decreased time to resolution of DKA and decreased time to cessation of the insulin drip.
Speaker: So there's literature again that shows that
Speaker: You want to get these patients out of the ICU faster.
Speaker: You want to get them out of the hospital faster.
Speaker: You should start these patients on plasma light.
Speaker: Now, uh,
Speaker: There is currently as of, I think if I remember correctly, 2023, a D5 Plasmalite that is available.
Speaker: I had been under the impression that it was never going to happen.
Speaker: And I actually wrote a letter to the company to say, you should probably make this happen.
Speaker: I never heard back from them, but sure enough,
Speaker: Very shortly thereafter, there's dextrose, 5% plasma light.
Speaker: There are not a lot of hospitals that have it yet.
Speaker: I do believe that it will be coming down the pipe, but...
Speaker: D5 LR is available.
Speaker: So a lot of people know that there is a D5 LR and D5 is certainly available.
Speaker: But an alternative, which is what I traditionally do until D5 plasmalite becomes a thing in my hospital, which I've already talked to our pharmacy group to make it happen, is I'll do the two bag method.
Speaker: So the two bag method is something that's been well, well researched in the pediatric population.
Speaker: and has been shown to be helpful.
Speaker: In this circumstance, what you do is you actually start them on the fluid of choice that you have for them.
Speaker: So for instance, plasma light.
Speaker: And then on the second bag, you actually start them on a D10.
Speaker: And I use half normal saline.
Speaker: I don't like using D5W because I think it waters down the sodium.
Speaker: And I certainly don't want to affect the sodium significantly.
Speaker: So I use D10 half normal saline and that dextrose gives me enough of a concentration to actually keep the patient's blood sugar at a reasonable level.
Speaker: They've recently now studied this in the adult population and have also found it to be significantly helpful.
Speaker: So preferentially, what I typically will do is I'll start them on plasma light.
Speaker: start them on the insulin, which we'll talk about in a second.
Speaker: And then once I've started both of those interventions, when their sugar starts to get low, or if they're in you glycemic decay, then I will start that D10 drip.
Speaker: And I will just titrate up the D10 drip as I get those glucoses back to make sure that we maintain around that 200 to 300 milligrams per deciliter blood sugar while the insulin is fixing the ketoacidosis.
Speaker: Awesome.
Speaker: So let's talk about insulin.
Speaker: Oh, insulin.
Speaker: We know insulin is the savior.
Speaker: This is the thing that's going to stop the ketoacidosis, stop the ketogenesis.
Speaker: So it's going to reverse everything that glucagon does.
Speaker: Now, how do we administer the insulin?
Speaker: So the classic teaching was the insulin infusion.
Speaker: Thankfully, we have gotten rid of the insulin bolus plus the insulin infusion.
Speaker: In pediatric population, again, bolus is completely contraindicated.
Speaker: In the adult population, you can go ahead and do it if you feel like it's necessary.
Speaker: In most circumstances, though, the literature has borne out that you don't have to start the insulin infusion.
Speaker: And then I'm sorry, the insulin bolus and then the insulin infusion.
Speaker: So do you have to start everybody on an insulin infusion?
Speaker: I'm a beat up two things here.
Speaker: One, you don't have to do everybody on an insulin infusion.
Speaker: And then the second thing we're going to talk about is the insulin titration protocols, which drives me up the wall.
Speaker: So from an insulin infusion,
Speaker: If they're in severe DKA, the literature has borne out that you still should start the patient on an insulin infusion.
Speaker: So if their pH is 7.1 or less, you should go ahead and start that patient on an insulin infusion.
Speaker: If they are in moderate or mild DKA, you can actually do something called the SQUID protocol, which stands for subcutaneous insulin in diabetic ketoacidosis.
Speaker: What the squid or subcutaneous insulin uses is they use aspart or lispro insulin, which is an ultra rapid acting insulin.
Speaker: You give it subcutaneously.
Speaker: You still do it every hour.
Speaker: You do if their blood sugar is high, you start them on point two units per kilogram.
Speaker: And then if their blood sugar is closer to that 250 range, then you start them on point one units per kilogram.
Speaker: And the unfortunate thing with the squid protocol is it's exceptionally nurse intensive.
Speaker: So if you're in the ICU, this is probably a fine place to do it.
Speaker: If you're on a medical floor or a med-surg tele floor, this is probably not a great protocol to use because it's going to be very similar to what they experience in the ICU.
Speaker: They're going to be Q1 hour finger sticks,
Speaker: They're going to be Q1 hour insulin and insulin boluses subcutaneously.
Speaker: But they found that comparing subcutaneous insulin versus the insulin infusion, the outcomes were pretty much the same.
Speaker: But they actually got out of the hospital and out of the emergency department faster when you did the subcutaneous insulin.
Speaker: So now I preferentially actually in patients who are your kind of, you know, classic insulin.
Speaker: Insulin non-compliance.
Speaker: There's no source of infection.
Speaker: No sources of ischemia They just you know haven't been taking their insulin for whatever reason and they don't have to necessarily be admitted to the ICU I will preferentially start those patients on the squid protocol giving subcutaneous boluses and Get those patients out of the emergency department as quickly as possible.
Speaker: So like, yeah, it makes sense.
Speaker: I mean, to try to avoid the ICU, right?
Speaker: But once they go to our world in the ICU, you're almost as equally off just with the insulin drip.
Speaker: And if there's other things going on, the drip might be actually helpful just to minimize nurse bandwidth and focus on other things.
Speaker: But I do think it's important for people to be aware of that.
Speaker: Absolutely.
Speaker: 100 percent.
Speaker: Yeah, I think that's that.
Speaker: I'm sorry to cut you off, Sergei.
Speaker: No, no, go ahead.
Speaker: I think I think you hit the nail right on the head.
Speaker: I think a lot of times it's just easier to put the patients on the on the infusion.
Speaker: And in other than like the description that I said before.
Speaker: If the patient has some other thing that's going on, if they have some other eye that's an etiology for why they're hyperglycemic, there's almost no reason not to start them on the infusion.
Speaker: So it's reasonable to just start the infusion.
Speaker: There's been a very few circumstances where I've done the squid protocol.
Speaker: And again, those patients, it is just simply a, I'm noncompliant for whatever reason,
Speaker: I just need a couple of doses of insulin and I will probably be fine.
Speaker: And getting those patients out of DKA and either admitted to the hospital or subsequently discharged from the emergency department, I think is great.
Speaker: But in most circumstances, these patients are going to need the infusion to be going in and to fix everything that they need to be fixed.
Speaker: Excellent.
Speaker: And the other thing that I wanted to talk about, it's easy to start up, like you said, but it's the middle and the end that sometimes people have a little more difficulty with insulin.
Speaker: So could you talk about, obviously, you mentioned the pathophysiology that we might correct the hyperglycemia before we correct the ketosis, which forces us to continue the insulin a little bit longer.
Speaker: But could you talk about that portion and how you transition to longer acting insulin?
Speaker: I know that that's not something probably that happens all the time in the ED, but just curious, I mean, how you see this.
Speaker: So this is a great transition point because...
Speaker: I do.
Speaker: I do do this a lot in my emergency department because we are, we have a lot of busy ICUs.
Speaker: So one of the things that's really hit emergency medicine in the United States is a problem with boarding.
Speaker: And so we actually do transition a lot of patients.
Speaker: So this is actually very pertinent.
Speaker: So with DKA, as we alluded to earlier, the insulin is going to be the big, big, big fixer here.
Speaker: So when the patient's acidosis is corrected, in other words, their anti-gap is closed, closer to that normal range of about 10 to 12, their bicarb or their pH is around that normal level.
Speaker: I will transition those patients to getting ready to turn off the insulin infusion.
Speaker: In order to do that, though, they still need insulin in place.
Speaker: And so the classic insulin to start these patients on is glargine.
Speaker: Glargine is a long-acting insulin that lasts about 23 to 24 hours.
Speaker: The teaching is that it's 23 hours.
Speaker: But what Glargine does is Glargine is essentially like a basal...
Speaker: insulin infusion that's just long-acting you can kind of think about it like a depot shot that's just basically sitting in the system giving a low dose but sufficient dose of insulin over that 23-hour period the other great thing about glargine is that there's no peak on it so it basically you can think about it as it reaches a maximum
Speaker: dose level at about two hours and then it maintains that dose level for the next 21 hours or 22 hours.
Speaker: And so it's essentially replacing your insulin drip, but you have to have that two hour period where it's reaching the maximum dose effect before you can actually turn the drip off.
Speaker: And so if I know that their acidosis is better, their, um, anion gap is better and their glucose is at a reasonable level, I can, um,
Speaker: give them the glargine and then I wait about two hours and then I can turn the insulin drip off.
Speaker: And then essentially that glargine has started the drip for me.
Speaker: Now that two hour period is certainly going to, um, they're still going to be on the drip and things like that.
Speaker: And the unfortunate thing is that sometimes, you know,
Speaker: Nurses get busy.
Speaker: That insulin drip is going to run for maybe three hours or maybe four hours.
Speaker: And oh, my gosh, I completely forgot to turn the insulin drip off.
Speaker: So there's a study that has recently come out and it needs to be repeated.
Speaker: And it's something that's in interest of mine is why wait?
Speaker: until they are getting close to the end of the treatment, you could potentially start it on right when you start the insulin infusion.
Speaker: And there's been safety.
Speaker: The study that was done was a safety study, which basically said people were scared to give glargine at the same time as starting the insulin infusion because they thought the patients would develop more hypoglycemia and more hypokalemia.
Speaker: And what this safety study showed is that the incidence of hypoglycemia and hypokalemia was the same whether you started the glargine at the beginning versus started the glargine at the end.
Speaker: So you can start the glargine at the beginning of the insulin infusion.
Speaker: And when their acidosis corrects, you can just turn the drip off and the glargine's in the system.
Speaker: Obviously, once the patient...
Speaker: has been on the Glargine, you know, if the insulin drip is, is going for 24 hours, you know, maybe they were really sick decay, their pH was 6.8 or 6.7 and they're on the insulin infusion for a long period of time.
Speaker: You may have to redose the Glargine, but it's an interesting concept to think, why don't we just start the Glargine at the same time as the insulin infusion?
Speaker: And they may actually still get better in the same amount of time.
Speaker: But you you lose that.
Speaker: You know, I forgot to turn the insulin drip off.
Speaker: Oh, my gosh.
Speaker: If you turn the insulin drip off when their acidosis corrects, you've got that glargine on board and is essentially is doing its job.
Speaker: So an interesting area of research.
Speaker: So we'll see what happens.
Speaker: But that's how I transition.
Speaker: Give them the glargine once the ketoacidosis has resolved and then wait two hours, turn the insulin infusion off.
Speaker: And then they can go on about, you know, being treated with the glargine that's in their system.
Speaker: Excellent.
Speaker: And I think it's important for our critical care listeners to talk about glargine because a
Speaker: Basically, we always kind of think dogmatically that long-acting drugs are not friends of the ICU.
Speaker: We have the illusion of control, so we use shorter-acting insulin, we have more control.
Speaker: But the truth is, like, how you explained it, I think it makes it very, very obvious that large-ing is probably the way to go, right?
Speaker: I mean, start early and have that on board.
Speaker: And as the ketosis resolves, you can transition a lot, a lot quicker.
Speaker: Because I've also seen, I mean, sometimes rookie mistakes for some, and it might be just, I mean, miscommunication, but stopping the drip too quickly, right?
Speaker: And then you have a rebound and it just delays things.
Speaker: It doesn't help our patients.
Speaker: You mentioned hypokalemia, and I wanted to talk about electrolytes.
Speaker: Could you just tell us, I mean, how you think about electrolyte management in these patients?
Speaker: Sure.
Speaker: So as we know, insulin will also shift potassium and putting them on an insulin infusion is actually a treatment for refractory hyperkalemia.
Speaker: So if you start a patient on an insulin drip, you are going to potentially bottom out their potassium.
Speaker: What I love about the way that I treat potassium is that it actually works fast if you do it correctly.
Speaker: So
Speaker: Again, the guidelines have changed, which I again love.
Speaker: The old guidelines used to say that the numbers were 3.3 and 5.5.
Speaker: So what that essentially meant was that I'm sorry, 5.2, 3.3 and 5.2.
Speaker: So if the potassium was higher than 5.2, then you just started the insulin infusion and didn't worry about giving supplemental potassium.
Speaker: If it was between 3.3 and 5.2, you gave insulin and you gave supplemental potassium.
Speaker: And if it was less than 3.3, you give them potassium until it gets to 3.3, and then you can start the insulin infusion.
Speaker: I hate those numbers because, one, they're very hard to remember.
Speaker: Two, I feel like that 3.3 threshold is a little bit on the lower side.
Speaker: If you look physiologically at patients who are in DKA, the vast majority of them are actually hypokalemic, sometimes significantly hypokalemic because of the amount of osmotic diuresis that they've been having as well as the vomiting that they've been having.
Speaker: And if they have pHs of 7 or lower, they're
Speaker: It's a pseudo eukalemia or hyperkalemia because of the fact that the acidosis has forced the potassium out of the cell and has caused there to be a higher element of potassium in the serum when it's getting measured than what the total body potassium actually is.
Speaker: So when it's 3.3, if they have a pH that's less than 7, their potassium is in the toilet.
Speaker: So I like the 3.5 to 5.5.
Speaker: The numbers are easier to remember.
Speaker: And it gives me a higher threshold to actually thinking that that potassium is much lower than it really is and a lower threshold to actually starting potassium supplementation.
Speaker: So in terms of how I treat potassium is I actually give it to them IV and orally.
Speaker: Now, a lot of people have this mindset that oral potassium in a patient with diabetic ketoacidosis, they're not going to absorb any of the potassium that's actually present.
Speaker: And I have not found a single ounce of literature to show that to be true.
Speaker: I have anecdotal evidence that says that that's false.
Speaker: So I think it's fake news.
Speaker: I think it's certainly dependent on what else is going on with the patient.
Speaker: But if the patient can tolerate PO and there's this, I don't know, medication called Zofran or Dansetron or other antiemetics that you can give patients that will actually resolve their inability to tolerate PO that comes sometimes with acidosis, that you can give them oral potassium and it gets absorbed relatively quickly and will subsequently supplement them for diabetes.
Speaker: the infusion that's going to lower their potassium.
Speaker: So I preferentially will give them oral and IV.
Speaker: I also make sure
Speaker: Because again, these patients can develop some magnesium deficiency and we all know that they're not going to absorb the potassium if they are hypomagnesemic.
Speaker: So sometimes I will, I'm going to say prophylactically or empirically give magnesium as well to help them absorb the potassium to make sure that it's actually getting into their system.
Speaker: Another controversial electrolyte is phosphorus.
Speaker: So
Speaker: Oops, that was Alexa, sorry.
Speaker: Phosphorus is controversial because phosphorus, the thought process is that most patients who are in diabetic ketoacidosis are actually hypophosphatemic.
Speaker: The problem with phosphate is that one, it's hard to administer.
Speaker: The IV formulation comes with several other electrolytes with it, and it's not sufficient enough of that electrolyte being mainly potassium.
Speaker: But the amount of potassium that comes with that phosphorus is not sufficient to replenish the potassium that you're trying to replenish.
Speaker: So that's why I preferentially give the potassium by itself.
Speaker: And the oral formulation, one, is terrible tasting.
Speaker: So the question becomes, is it necessary?
Speaker: And what the guidelines used to say was that if the phosphorus level was less than one, you should go ahead and give it.
Speaker: In reality, which I'm glad, again, that the guidelines have changed, they now say if the patient is symptomatic from the hypophosphatemia, if they're experiencing muscle weakness, if they're having respiratory difficulties, mainly being knowing that phosphorus is one of the components of ATP.
Speaker: So certainly the muscles may be getting tired, especially with their breathing a lot.
Speaker: Those patients may have an element of respiratory depression if their phosphorus gets low.
Speaker: But if the phosphorus is low and they're experiencing symptoms, then they recommend going ahead and replenishing the phosphorus.
Speaker: But otherwise, there's no real need or indication to replenishing phosphorus.
Speaker: So I preferentially don't do it.
Speaker: I usually try to fix the acidosis as quickly as I can so that their breathing is slowed down.
Speaker: And then they subsequently can eat orally and hopefully replenish their own phosphorus.
Speaker: And then subsequently, they usually don't need anything from me.
Speaker: Excellent.
Speaker: Any comments on magnesium and sodium as we wrap up the electrolyte discussion?
Speaker: Sure.
Speaker: So sodium becomes much more important, especially when we get to HHS.
Speaker: With DKA, sodium, we kind of just watch the sodium.
Speaker: It gives us a little bit of an assessment of what their intravascular...
Speaker: Yeah.
Speaker: So I don't monitor the sodium as much in DKA patients because we fix it so quickly that it usually doesn't usually give us any problems.
Speaker: Magnesium, again, primarily I'm looking at it in the scenario of potassium replenishment.
Speaker: So if the magnesium is low, they're not going to.
Speaker: they're not going to retain any of the potassium that I'm going to replace their electrolytes with.
Speaker: So if their magnesium is low, I want to check it and replenish it.
Speaker: If they are in stage renal, their magnesium can be high.
Speaker: But again, that's not a common patient population.
Speaker: So I empirically give magnesium if I know that their potassium is very, very low.
Speaker: And again, they're very acidotic.
Speaker: If they are...
Speaker: you know, in that mild to moderate state and the potassium is pretty close to normal, I won't necessarily replenish the magnesium.
Speaker: I'll check it, but I won't empirically give it, um, unless they are very low and their pH is very low.
Speaker: What about bicarb?
Speaker: Ah, one of my pet peeves.
Speaker: So sodium bicarbonate has been shown over the years to be universally not a great medication to give.
Speaker: In the DKA patient, it is extremely controversial.
Speaker: So even now and reading the ADA guidelines, the new guidelines, they still say if the pH is less than 7.0, we should give sodium bicarb.
Speaker: I universally hate that thought process because we're treating the number and not the patient because I have had multiple as I'm sure you have as well had multiple patients who've been 6.9 6.0 6.8 playing on their phone breathing hard and breathing fast.
Speaker: I'm okay, doc.
Speaker: Doing good.
Speaker: Just sitting here playing my game.
Speaker: And they don't need bicarb.
Speaker: So I reserve sodium bicarbonate for three patient populations.
Speaker: One, profound hyperkalemia.
Speaker: So patient, you know, usually they're going to be acidotic.
Speaker: They're going to have pHs that are pretty low.
Speaker: But let's say that they are end-stage renal, for an example, and
Speaker: and their potassium is eight.
Speaker: And I'm not seeing like peaked T waves.
Speaker: I'm seeing significant prolongations of the QRS complex, maybe even a sine wave.
Speaker: That's a person who I'm going to give calcium to and a patient, because remembering that calcium only has a half-life of about two hours.
Speaker: So I may need to repeat that calcium.
Speaker: But in the interim, I'm going to also get that
Speaker: potassium out of the serum.
Speaker: And so I'm going to give those, give those patients bicarb.
Speaker: Typically I don't give pushes of bicarb.
Speaker: I usually start patients on a sodium bicarbonate drip, which is three amps of sodium bicarbonate in a liter of D five.
Speaker: So that's my preferential way of giving sodium bicarbonate in that patient population.
Speaker: Yeah.
Speaker: The second population, which is another population that I also give sodium bicarbonate infusions for, is for there's a small subset of populations who get very acidotic, who the acidosis actually affects the heart and causes decreased cardiac output.
Speaker: And so rather than starting these patients on potentially a second vasopressor, I give them a sodium bicarbonate drip to hope that it actually increases the EF and allows the heart to pump in a little bit better fashion to give me a little bit more cardiac output.
Speaker: The third population that I give sodium bicarbonate to, and this is obviously not one that I'm giving an infusion to, is a patient who's in cardiac arrest.
Speaker: Usually it's going to be as a result of the hyperkalemia, but there are obviously some patients who may have pHs of 6.5, 6.4, 6.3 that are not compatible with life.
Speaker: And so in that circumstance, I am administering sodium bicarbonate, this time in pushes, and
Speaker: to hope that it will give them some element of some ROSC that we want in that patient population to hopefully get them started on the appropriate medications in that circumstance.
Speaker: So those are the three times that I will administer sodium bicarbonate.
Speaker: Everybody else, if their pH is 6.7, I've had patients who've been 6.7 and looking like they're needing to be intubated,
Speaker: I will start them on insulin, start them on fluids.
Speaker: And usually within an hour or two, their pH has corrected to the point where they're up talking, laughing, looking perfectly fine and doing very well.
Speaker: And so I always make the one of my favorite statements is treat the patient, not the number.
Speaker: So I don't there's no blanket number for me for what their acidosis level is for me to start sodium bicarbonate.
Speaker: I will treat the patient, not the number.
Speaker: I agree, and I think it ties back to your comments on pathophysiology, right?
Speaker: And it's very similar to why when you have lactic acidosis giving bicarb, it's not going to correct the underlying process, right?
Speaker: Right, and if you think about the equation...
Speaker: If you administer sodium bicarbonate, all you're doing is increasing the carbon dioxide that they now have to subsequently breathe off.
Speaker: And so these patients most of the time are maximally compensating from a respiratory perspective.
Speaker: And so by increasing the amount of carbon dioxide, we're telling them, hey, you're breathing 40 times a minute, but I need you to breathe 50 times a minute to get rid of this carbon dioxide that I am now giving you.
Speaker: Perfect.
Speaker: So as we close the discussion on DKA, any specific comments on euglycemic DKA or DKA in pregnancy?
Speaker: Sure.
Speaker: So euglycemic DKA is going to be approached a little bit differently in that most of the time with DKA, we're seeing patients who are hyperglycemic.
Speaker: So these patients are euglycemic.
Speaker: And so I still preferentially treat them with
Speaker: IV fluids, insulin still monitor their potassium.
Speaker: But the other thing that I want to make sure that I'm doing is making sure that their glucose is not dropping.
Speaker: And the way that I do that, again, I do this a little controversially.
Speaker: This may make some people and rub them the wrong way.
Speaker: But there's this thought process that if you start a patient on an insulin infusion, that you need to keep them in PO.
Speaker: My question is,
Speaker: Why?
Speaker: What is the reasoning for that?
Speaker: I care more about them going hypoglycemic than them going hyperglycemic.
Speaker: When we discharge these patients home, we're not going to tell them we're starting you on insulin, but you're not allowed to eat while you're on insulin.
Speaker: We allow them to eat.
Speaker: And so I make the argument that if they want to eat, let them eat.
Speaker: And if they're capable of eating, you should let them eat.
Speaker: So I let my DKA patients eat, and that prevents them from going hypoglycemic.
Speaker: I give them nausea medicine to prevent vomiting because certainly we don't want them to aspirate.
Speaker: But give them food and allow them to eat because, again, we're trying to prevent them from going hypoglycemic.
Speaker: I especially do this with euglycemic DKA.
Speaker: So I will start these patients on a D10 drip, very similar to that two-bag system that I talked about earlier, in the same time that I'm starting them on an insulin infusion.
Speaker: And so what that does is, again, it prevents them from going hypoglycemic, which is what we really worry about with euglycemic DKA.
Speaker: If you look at the studies on euglycemic DKA, the incidence of hypoglycemia leaps and bounds higher than what we see in the traditional DKA population.
Speaker: So my preferential treatment is to start them on the dextrose drip with IV fluids, and
Speaker: concomitantly with the insulin infusion.
Speaker: And I let them eat while they're getting both.
Speaker: I actually check finger sticks.
Speaker: So what I traditionally do with my DKA patients is I will check their finger sticks or a BMP every other, essentially every other hour or so.
Speaker: Q1 hour finger stick and then the next hour they're getting a BMP to see what their anti-gap is doing, to see what their potassium is doing and to see what their glucose is doing and their bicarb.
Speaker: And then the next one's a finger stick and then the next one's a BMP and so on and so forth.
Speaker: And patients with euglycemic decay or anybody that I'm putting on a dextrose drip, I'm checking their finger stick every 30 minutes to basically see what level I need that dextrose drip to be at to...
Speaker: maintain euglycemia or a little bit of hyperglycemia.
Speaker: So if their sugar is 250, for instance, and I start the dextrose, the D10 drip at 125 milliliters per hour,
Speaker: If I check the finger stick in an hour and their finger stick has gone from 250 to 225 Then I know that I need to turn the dextrose drip up a little bit more if it drops precipitously if it goes from 250 to 150 then I need to turn that dextrose drip up a lot But if their sugar is 250 I turn the dextrose drip on at 125 and their sugar stays at 250 or goes a little bit higher
Speaker: Then I leave the dextrose drip alone and let them continue to get treated.
Speaker: Remembering that insulin is treating the ketoacidosis.
Speaker: I don't care about the sugar unless it gets low.
Speaker: So that's what I do for euglycemic DKA.
Speaker: Pregnancy is a difficult beast.
Speaker: And a lot of the reasons why is that most of the time these patients are going to be very, very refractory to insulin.
Speaker: So you may need to even use a higher dose of insulin in this patient population.
Speaker: I have given...
Speaker: I've started people on 0.1 units per kilogram per hour, and sometimes I've gone as high as doubling that to 0.2.
Speaker: Usually I go 0.15, and then subsequently, if that doesn't work, I may need to go to 0.2.
Speaker: The thing you have to watch for in this patient population is that they can sometimes have these ebbs and flows of insulin, we'll call it insulin resistance or acceptance, if you will.
Speaker: There have been circumstances where I've started patients on the insulin drip, seeing that sugar is continuing to either go up or
Speaker: not to go down when they're hyperglycemic, and I may need to double the dose, and then I double it, and then they precipitously drop.
Speaker: So there are really, really...
Speaker: difficult patient population to kind of deal with.
Speaker: So the other thing that I will oftentimes do is when they, I will preferentially start those patients on a D10 drip really early to prevent them from having that precipitous drop if it does occur.
Speaker: So I'm just a little bit careful with the pregnancy population.
Speaker: Remembering that these patients also, they need to be a little bit more hyperglycemic than normal because there's a second body inside the mom.
Speaker: So you don't want the baby to develop hypoglycemia because that obviously leads to worse outcomes.
Speaker: So you really want to avoid hypoglycemia in this patient population.
Speaker: So I tend to have a little bit of a higher threshold for their glucose.
Speaker: If they come in and they're in the five, six hundreds, I start the dextrose drip a little bit higher because, again, I don't want them to go hypoglycemic.
Speaker: I'd rather them be a little bit hyperglycemic compared to hypoglycemic.
Speaker: Perfect.
Speaker: No, and I think it's important to recognize, like you said, also the eucalycemic decay are increasing.
Speaker: So having that discussion, I think, is also an important refresher for all our audience.
Speaker: Absolutely.
Speaker: Could you tell us, George, in terms of like management of HHS, kind of your approach and contrasting what would be different?
Speaker: I mean, obviously, some things, as we discussed earlier, once you determine are similar, but there are some differences in anything that you want to point out or emphasize for HHS.
Speaker: Absolutely.
Speaker: So the big difference with HHS being again, as we alluded to earlier, is the sodium is much more important in this circumstance.
Speaker: A lot of people mistakenly think that glucose is the large thing that we're supposed to be monitoring.
Speaker: Glucose, again, I don't care about.
Speaker: I care more about the glucose becoming hypoglycemic than I do about the glucose being at 1,000 or 2,000 or 3,000.
Speaker: The thing to be monitoring here is the sodium.
Speaker: As we talked about before, these patients oftentimes have a sodium that is near normal on the lab.
Speaker: But if you correct the sodium, their sodium is actually going to be hypernatremic.
Speaker: So how do we correct sodium?
Speaker: So there's a formula that you can use.
Speaker: There's the 1.6 for every 100, which was calculated by using the osmoms of sodium and someone much more nerdy than I did than I am calculated what this was.
Speaker: And then there's another number that's 2.4 for every 100.
Speaker: This one's actually a little bit more physiologically accurate.
Speaker: What they did was they took
Speaker: They took people and gave them octreotide and turned their pancreas off and gave them a large bolus of glucose.
Speaker: And then they basically just checked their glucose and their sodium levels every 10 minutes to see what it was.
Speaker: And so that 2.4 for every 100 is actually a little bit more close to what's physiologically accurate.
Speaker: But I don't like doing advanced math in a pinch.
Speaker: I can, but I don't like to.
Speaker: And so what's right in between 1.6 and 2.4?
Speaker: Two.
Speaker: It's exactly right in between the two numbers.
Speaker: So I just use two.
Speaker: So for every 100 of glucose that's over 100, I know that I'm going to need to add two to the sodium.
Speaker: Okay.
Speaker: So if you measure what the actual or the corrected sodium is, that's how you should be choosing your choice of your IV fluids.
Speaker: There's literally almost zero literature that talks about fluid choice in HHS.
Speaker: The recommended guidelines from the ADA and this new set of guidelines that came from all those different diabetes organizations still say to use sodium.
Speaker: Normal saline in this circumstance and this is the one circumstance where I actually do agree with them significantly Normal saline may be the appropriate Fluid of choice in this patient population because they have that hyper nature in natremia That's corrected that we don't want to expose the brain to so by giving them normal saline and they're corrected sodium is let's say 160 and
Speaker: we're actually close to what they actually are in terms of their sodium, as opposed to giving them lactated ringers, which has a sodium level of 130, and plasmalite, which has a sodium level of 140.
Speaker: In the long run, probably not going to be super harmful in that circumstance.
Speaker: But when we're seeing sodiums that are corrected of 180 and 190 even, and the highest I've ever seen is 194, which made my anal sphincter tighten up a lot,
Speaker: LR would probably be significantly harmful and can certainly lead to those patients developing cerebral edema.
Speaker: So what I traditionally do now is I will correct their sodium and see what it is, and I will base my fluid choice on what their corrected sodium is.
Speaker: If their corrected sodium is only like 152, 153, then I don't necessarily feel like that normal saline is going to be my fluid of choice.
Speaker: I don't want to make them more hypernatremic.
Speaker: So then I will use plasmolyte in that circumstance.
Speaker: But that's the thing that we're actually going to be monitoring is their sodium levels.
Speaker: The reason why this is very important is because these patients are also going to be put on an insulin trip.
Speaker: However, I don't want to put them on a significantly high insulin.
Speaker: dosing for that insulin infusion because I don't want that corrected sodium to now become their true sodium.
Speaker: So if you think about it, if their true sodium is, let's just say one 30 and their sugar is 1600, right?
Speaker: So if you take those numbers two times 15, which is 30, so that patient's sodium is one 60.
Speaker: If I start them on an insulin infusion at 0.1 units per kilogram per hour, um,
Speaker: The next sugar, I might check in an hour because they may be, let's say they're insulin naive.
Speaker: Their next sugar might have dropped from 1600 to 1000.
Speaker: So it drops 600 points.
Speaker: Now, this is obviously, these are hypothetical situations.
Speaker: But now if I check their sodium and it's 150,
Speaker: Now I'm exposing that brain because now we have a significant problem with that sodium concentration.
Speaker: Now that brain is getting exposed to that 150 as opposed to that 130.
Speaker: So these patients, we certainly have to be careful about what their sodium levels are and their glucose levels.
Speaker: So what the new guidelines recommend, which I love, I've been doing this for a number of years, is I don't start them on 0.1 units per kilogram per hour, which is what the 2009 guidelines said.
Speaker: I start them on 0.05 units per hour, units per kilogram per hour.
Speaker: And what that does is it slows the glucose dropping down.
Speaker: While they are continuing to get watered.
Speaker: I like to think about this as we're watering the brain a little bit.
Speaker: We're giving the water, giving the brain a little bit of water to allow it to rehydrate.
Speaker: Cause these patients can be anywhere between nine and 20 liters down.
Speaker: I need time for this to happen.
Speaker: If I just fix their glucose, which I can fix.
Speaker: If I have a patient who has glucose to 1600 in my emergency department, I could probably fix their glucose in like three or four hours.
Speaker: I don't want to do that in this circumstance because the next time I check the sodium on this person, it might be 170.
Speaker: I want to give their brain some time to get some of that water that I'm giving them with the IV fluids.
Speaker: And so by slowing the insulin infusion down and watching their glucose down, come down very slowly while they're continuing to get more of that free water from the plasma light or the normal saline that I'm giving them, it allows them to prevent them from developing cerebral edema, which is the most common complication that we see from patients with HHS.
Speaker: And I think as you mentioned earlier, George, right, it doesn't, people don't get into HHS in five hours.
Speaker: Right.
Speaker: But we shouldn't correct it in five hours.
Speaker: Exactly.
Speaker: I mean, it kind of, it takes, I mean, some time to get there and we want to be very careful and not overdoing it and causing more harm than benefits.
Speaker: I think that's an important take home message.
Speaker: You mentioned, obviously, that a lot of these patients with DKA especially have goose mild breathing.
Speaker: Patients with HHS might have significant mental status changes.
Speaker: Could you just give us a couple comments on respiratory support for patients with hyperglycemic emergencies?
Speaker: Sure.
Speaker: So, DKA should scare you when you're thinking about ventilation and respiratory support.
Speaker: The
Speaker: The problems with DKA are that these patients have a respiratory compensation for their metabolic acidosis.
Speaker: So if we take their respiratory compensation away, which is what happens with rapid sequence intubation when we make them apneic, we actually will watch their, if we had like a manometer that could check their pH or some kind of
Speaker: continuous pH checker, we would actually watch their pH.
Speaker: It wouldn't slowly decline.
Speaker: These patients will have an exponential decline in their pH because they now have nothing that is compensating for their metabolic acidosis.
Speaker: So can you do non-invasive positive pressure ventilation?
Speaker: The worry with non-invasive positive pressure ventilation is that these patients obviously are at high risk for aspiration and nausea and vomiting causing aspiration.
Speaker: So we certainly don't want to give them something that's going to make them insufflate their stomach and predispose them to that.
Speaker: However, if you give them antiemetics, and I've done this a number of times, you actually can give them a little bit of support with non-invasive positive pressure ventilation.
Speaker: which can actually help them with that Kussmaul respirations.
Speaker: You're not going to cause them to fix.
Speaker: You're not fixing them with this non-invasive positive pressure ventilation.
Speaker: What you're doing is you're actually giving them a little bit of pressure support that's going to help them with their breathing so that they won't subsequently tire out, which they sometimes do after a period of time.
Speaker: But the goal here is to allow them to do what they are doing for as long as they possibly can.
Speaker: Most of the time when I have to provide respiratory support is because they have some other disease processes going on that has precluded them from being able to support themselves.
Speaker: So for instance, they have an overwhelmingly large pneumonia or multi-lobar pneumonia that's caused them to become hypoxic.
Speaker: And I'm giving them oxygen.
Speaker: I'm putting them on high flow nasal cannula and their oxygen saturation is not improving or
Speaker: Their mental status is so uptunded that they're not protecting their airway.
Speaker: In this circumstance, you're not going to want to give them non-invasive positive pressure ventilation.
Speaker: If they're hypoxic, you can give them non-invasive positive pressure ventilation.
Speaker: But if they're not protecting their airway, then certainly non-invasive positive pressure ventilation is not going to be helpful, and you're probably going to have to intubate them.
Speaker: But I try to avoid intubating these patients at all costs if I can.
Speaker: If I cannot, then there's two preferential methods of ventilation that I do with these patients for intubation.
Speaker: The first is I do ketamine only intubation.
Speaker: So I don't want to take away their respiratory drive.
Speaker: So I will give them ketamine only.
Speaker: I'll give them some viscous lidocaine or I will give them some nebulized lidocaine to prevent.
Speaker: nebulize the airway to anesthetize the airway.
Speaker: And then I will preferentially intubate those patients after inducing them with ketamine so that their respiratory drive isn't gone and they are still able to do that respiratory compensation.
Speaker: The second thing, if
Speaker: I'm really worried about them is I'll use something called VAPOX.
Speaker: And Scott Weingart talks about VAPOX, which is ventilator assisted pre-oxygenation.
Speaker: So I will use the ventilator with a non-invasive positive pressure ventilation mask to pre-oxygenate the patient.
Speaker: So put the BiPAP mask on or the CPAP mask on and put the patient on SIMV and
Speaker: give them a little bit of pressure support, give them a tidal volume, usually around 550.
Speaker: And then I will turn the respiratory rate down as low as I can.
Speaker: If I can make it to zero, great.
Speaker: If I have it at one, that's fine.
Speaker: But essentially the ventilator is just providing pressure support.
Speaker: So it's essentially like a non-invasive positive pressure ventilation.
Speaker: Then I will give them the RSI medications,
Speaker: So I'll give them the induction agent, I'll give them paralytic.
Speaker: And then as the paralytic kicks in, I'll give them a jaw thrust and I will turn the respiratory rate to about 12, 12 being a number that's arbitrary, but it's a number to hopefully give them enough time to not insufflate the stomach significantly.
Speaker: And so as the paralytic kicks in and they start to decrease the respirations, the ventilator will sense the fact that they're not giving themselves enough of a tidal volume and it'll kick in and start that respiratory rate at about 12.
Speaker: And after about a minute and that paralytic has kicked in, then I will go ahead and intubate the patient.
Speaker: And what that does is it gives me a little bit of that respiratory compensation.
Speaker: Again, not enough.
Speaker: but gives me a little bit of that respiratory compensation to give me some time to,
Speaker: to intubate the patient as opposed to if they had gone apneic where I would have seconds to intubate the patient with traditional RSI.
Speaker: So those are the two methods that I typically will use.
Speaker: I haven't had to use VAPOX a significant number of times because ketamine has worked very, very well for me.
Speaker: But the times when ketamine has failed, then I will preferentially try to use VAPOX if available.
Speaker: And as we mentioned earlier, the vast majority of patients we treat with decay especially don't need this type of support.
Speaker: Correct.
Speaker: But when they do, I think being overcautious and understanding what the underlying issues are is very important.
Speaker: So thanks for that excellent discussion.
Speaker: George, as we close, I wanted just to hear from you what are George Willis' top three common pitfalls and top three pearls that you can provide us as we close?
Speaker: Sure.
Speaker: So first and foremost, remember to look for the etiology.
Speaker: Think about those four eyes.
Speaker: That's a big pitfall is treating just the DKA or just the HHS and missing like a massive stroke, missing a massive myocardial infarction, massive pneumonia or overwhelming sepsis.
Speaker: So think about those four eyes.
Speaker: Number two, pitfall is do not, do not, do not forget to give these patients fluids.
Speaker: And if you're going to give them fluids, I still say giving them plasma light or lactated ringers in the case of DKA and then calculating that sodium for your patients with HHS.
Speaker: And then the last one is ventilatory support.
Speaker: Try not to do it.
Speaker: Don't just willy-nilly intubate these patients thinking that you have time.
Speaker: These patients are really sick.
Speaker: You should be intubating them with the thought processes.
Speaker: If I do this wrong, I will kill this person.
Speaker: So use VAPOX, use ketamine only.
Speaker: And if you can, you can use non-invasive positive pressure ventilation.
Speaker: Just make sure that you give these patients some...
Speaker: Some antiemetics to make sure that you're not going to miss anything from a pearls perspective.
Speaker: I still say if they want to eat cake, let them eat cake, give them some antiemetics.
Speaker: Remember, we don't want these patients to go hypoglycemic.
Speaker: So we want to make sure that they are maintaining their sugar a little bit greater than 200 to 250.
Speaker: And so I preferentially will allow them to eat.
Speaker: Same vein, number two, is monitor their potassium and use oral potassium to help replenish it.
Speaker: I think giving them oral potassium is much faster than giving them 10 mil equivalents through a peripheral IV or 20 mil equivalents through a central line if you have access to that.
Speaker: And then the last pearl...
Speaker: is I think using your sodium to guide your management will actually lead to better outcomes for HHS patients.
Speaker: So remember to think about that when you're managing these patients appropriately.
Speaker: Think about looking at their sodium and keeping an eye on just their sodium and focusing on just keeping the glucose just above 200 to 250.
Speaker: I think those are my big pearls.
Speaker: Excellent.
Speaker: We like to close the podcast traditionally, George, with a couple of questions unrelated to the clinical topic.
Speaker: Would that be okay?
Speaker: Sure, of course.
Speaker: So the first question relates to books.
Speaker: Is there any book or books that have influenced you significantly or books that you have gifted often to other people?
Speaker: So my probably favorite book is...
Speaker: A book called Kintsugai.
Speaker: So the the I'm going to give a shout out to a very good friend of mine named Ross Fisher, who practices pediatric surgical oncology in the in the United Kingdom.
Speaker: Kintsugai is the concept of taking gilded taking pottery.
Speaker: that's shattered and repairing it with gilded gold.
Speaker: And this book actually talks about how kintsugai can be applied to our lives when you have some type of adverse outcome.
Speaker: So you may have had a really bad patient encounter,
Speaker: or you may have unfortunately even had a patient who died as a result of some significant medical error that you did.
Speaker: And the direction that you go from there really defines you as a person because you could go down the path of, Oh my gosh, I'm,
Speaker: I am the worst doctor in the world, so I'm just going to give up on medicine.
Speaker: Or unfortunately, especially in this time of COVID, we had people who did subsequently commit suicide, unfortunately.
Speaker: And it's sad because those medical errors are things, you know, to err is human.
Speaker: It's a thing that we're all going to deal with at some point in time in our life.
Speaker: And obviously the goal is to minimize errors and certainly not cause significant errors that cause harm.
Speaker: But
Speaker: It may happen to you.
Speaker: What happens afterwards is really what defines you as a person.
Speaker: And so what this concept of kintsugai is, is that you have this broken person.
Speaker: The art of kintsugai doesn't make it so that it is perfect.
Speaker: Because if you look at a piece of pottery that's undergone Kintsugai, there's obviously, you know, shards and broken pieces and so on and so forth.
Speaker: But it's actually more beautiful than it was when it was first put together, when it was first, you know, shaped by the clay maker into this pot or this bowl.
Speaker: And so the Kintsugai concept is very similar to how you apply it to your life.
Speaker: You're not perfect, but now you are a better doctor as a result of this mistake.
Speaker: That is unfortunate, obviously, you know, and I'm not belittling the mistakes that were made or that the patient's lives don't matter.
Speaker: What I'm trying to kind of relay with this is that when you look at yourself differently,
Speaker: as a broken person, do you want to look at yourself as a broken person that's better now as a result of that mistake?
Speaker: Or do you want to look at yourself as a broken person who's going to now over order tests and, you know, over admit patients to the hospital because you're so nervous or scared that you're going to make a different, make, make a, a different mistake or a second mistake.
Speaker: So I have, I have applied Kintsugai on several occasions in my life.
Speaker: The book is by, um,
Speaker: Um, this, um, person named Celine Santini.
Speaker: Um, but it's, it's a wonderful book to read.
Speaker: I've given it out to a number of my mentees.
Speaker: Um, it's, it's a great concept to apply to life as well.
Speaker: Um, and, and one of the lectures that I do is called the success of failure.
Speaker: Um, and it applies this concept of Kintsugai, um, and how you grow from the mistakes that you make.
Speaker: Beautiful.
Speaker: I've heard the concept before.
Speaker: I think it's a Japanese pottery concept.
Speaker: Yep.
Speaker: And but I haven't heard of the book.
Speaker: So I definitely will put in the show notes and we'll check it out.
Speaker: Thanks for sharing that, George.
Speaker: Of course.
Speaker: The second question, could you share something you have changed your mind about over the last couple of years?
Speaker: So, um, this was, this is a hard question to think about because I could do this from the medical perspective, um, or I could do it from the life perspective.
Speaker: And I think I would prefer to do it from the life perspective.
Speaker: Um, this pertains to my kids, um, um,
Speaker: I originally, when I was, I would say probably in my early 20s, thought that having kids was going to be something that would that was going to be super easy.
Speaker: And this is going to be a two part answer because it's I've actually changed my mind twice.
Speaker: So I I'm a I'm a child of I'm a fourth child.
Speaker: I'm a third out of four children of my parents.
Speaker: And so when I was growing up, I always knew I wanted to have kids.
Speaker: And I believe that I wanted to have kids.
Speaker: a million kids.
Speaker: I was like, I could have eight kids.
Speaker: This would be easy.
Speaker: This would be fine.
Speaker: And then we started having kids and then my mind changed.
Speaker: And I was like, this is way, way, way harder than I thought it was going to be.
Speaker: My kids are wonderful kids.
Speaker: Don't get me wrong.
Speaker: But when we went from having two kids to three kids, we literally changed our mentality because now we went from man to man defense to zone defense.
Speaker: And that was literally the hardest transition out of all of the kids.
Speaker: The three to four was super easy because at that point in time, it's just like, it doesn't matter anymore.
Speaker: The, but my mind changed again when, um,
Speaker: We actually put our first one in college, which we did this year, and he stays at home.
Speaker: His college is 15 minutes down the road.
Speaker: But what you realize more and more is it's really a lot easier than than you thought it was like the second part where I thought, oh, my gosh, this is way harder.
Speaker: It's really only hard because you make it hard.
Speaker: Kids don't want your life to be difficult and they try not to make it as difficult as possible, despite what it seems like.
Speaker: But as as they've gotten older now.
Speaker: it's a lot easier.
Speaker: And now I miss it.
Speaker: I miss how young they were.
Speaker: And, and, you know, my daughter, I have two daughters now, one's nine and one's 11.
Speaker: Um, I miss when they were three and they were drawn all over the walls and ripping up papers and, and, and typing on my computer and spilling water on my computer.
Speaker: I miss those times now because life is short.
Speaker: Life is really, really short.
Speaker: Um, here I am now at 45 with, um,
Speaker: Four kids, one in college, one in every every type of school.
Speaker: And I am dreading the day when they're all gone.
Speaker: You know, me and my wife talk about it all the time.
Speaker: Oh, my gosh, we're going to be empty nesters in, you know, 10 years.
Speaker: And I'm like, no, no.
Speaker: I don't want to be empty nesters.
Speaker: I mean, I love you.
Speaker: You're my wife.
Speaker: I love you.
Speaker: And I can't wait to spend time with you, but I'm going to miss the kids when they're gone.
Speaker: And we're not going to see them as much.
Speaker: And so what it, what it has actually caused me to do is to think more and more about me as a child and as a, as a son of my parents, um,
Speaker: My parents probably feel the same way about me now as I am, you know, doing my own life and living my own life that they're like, I miss...
Speaker: my kids and miss my sons.
Speaker: And so it's caused me to go home more frequently and, and to go see them and call them more frequently than I used to.
Speaker: Now I live far away.
Speaker: I just moved to Texas three years ago.
Speaker: Um, my parents live in West Virginia.
Speaker: And so to get, to get home to them is a lot harder than it was when I was in Maryland.
Speaker: So I'm less, I'm there less now, um,
Speaker: So now I'm just spending more money to go there more frequently.
Speaker: So that's that's how having kids has changed my life.
Speaker: And I've changed my mind over these past few years.
Speaker: For sure.
Speaker: And I think that I'll tell you that I'm already an empty nester, but today my first granddaughter is three months old.
Speaker: Oh, wow.
Speaker: It starts again.
Speaker: So the cycle, it starts again.
Speaker: And somehow I find the granddaughter more fun because you can always give her back to the parents.
Speaker: Yeah.
Speaker: Give them back.
Speaker: That's exactly right.
Speaker: That's awesome.
Speaker: So the last, if we could just close with a, what would you want every listener to know?
Speaker: It could be a quote, a fact, or just a departing thought.
Speaker: Oh, wow.
Speaker: I would probably say I'm a little biased here because I am very faith-based and I'm going to say a quote that I think applies to
Speaker: globally.
Speaker: And it doesn't necessarily mean that you have to believe in God or believe in Jesus for whatever you think in your life.
Speaker: But one of the things that I always tell myself, and I think that everybody should apply to their life is, I say that I can do all things through Christ who strengthens me.
Speaker: This is a quote from the Bible, Philippians 4.13.
Speaker: And what it allows me to do is to think about
Speaker: what I am getting ready to endure or getting ready to go into, I say this before I have any procedure, any critical patient that's coming into the emergency department by EMS, cardiac arrest, you know, unresponsive, intubated, so on and so forth.
Speaker: I know that these are patients who are going to need my full attention.
Speaker: And if I'm distracted or if I am not feeling like I am at my best for whatever reason,
Speaker: It resets me to think no matter what's getting ready to happen in this room, God's got my back.
Speaker: And so I can go into that room as confident as I can be that I am going to do the best that I can to save this person's life.
Speaker: or to do this procedure and do it successfully without any complications.
Speaker: And by doing that, it allows me to reset my brain to calm down as much as I can.
Speaker: One of the things that I like to employ whenever I have a resuscitation is what I call the quiet room.
Speaker: As I tell everybody in the room, nobody's allowed to talk unless you are spoken to or asked a question, or if you have a very critical piece of information that you need to administer.
Speaker: And it calms the room down so much when you're doing that, that I find everybody's able to kind of reset in their own mind what's actually happening.
Speaker: So I say that before every single critical situation that I'm getting ready to put myself in.
Speaker: And they don't all have to be critical.
Speaker: Sometimes I even say it before I'm getting ready to put in like an ultrasound guided peripheral IV.
Speaker: I'll say, OK, I'm going to do this and say my little thing.
Speaker: I can do all things through Christ who strengthens me.
Speaker: And I'm usually able to get most things within the first try that it's usually not a problem.
Speaker: So I would say find that thing that gives you your zen, your moment of calm before you do anything else.
Speaker: And I promise you it will change the way that you look at those critical situations.
Speaker: Beautiful.
Speaker: I think George is the perfect place to stop.
Speaker: I appreciate your willingness to share your expertise and your enthusiasm for endocrine emergencies with our audience.
Speaker: Look forward to having you back on the podcast soon and to see you in person.
Speaker: Sergio, as always, it was a pleasure.
Speaker: Thank you for having me on and I look forward to next time.
Speaker: Thank you for listening to Critical Matters, a sound podcast.
Speaker: Make sure to subscribe to Critical Matters on Apple or Google Podcasts and share with your network.
Speaker: Sound's transforming the way critical care is provided in hospitals across the country.
Speaker: To learn more, visit www.soundphysicians.com.
