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Hyperglycemic Emergencies
15 Plays1 year ago
In this episode, Dr. Sergio Zanotti discuss the management of critically ill patients undergoing hyperglycemic emergencies. He is joined by Dr. George Willis, a practicing emergency medicine physician. 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. A recognized clinical educator, he holds a particular interest in endocrine emergencies, vascular emergencies, procedural education, and medical education.
Additional resources:
Hyperglycemic Crises in Adults with Diabetes: A Consensus Report. GE Umpierez, et al. Diabetes Care 2024: https://diabetesjournals.org/care/article/47/8/1257/156808/Hyperglycemic-Crises-in-Adults-With-Diabetes-A
Clinical Effects of Balanced Crystalloids vs Saline in Adults With Diabetic Ketoacidosis. WH Self, et al. JAMA 2020: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7670314/
Evaluation and Management of the Critically Ill Adult with Diabetic Ketoacidosis. B Long, GC Willis, S Lentz, et al. J Emerg Med 2020: https://pubmed.ncbi.nlm.nih.gov/32763063/
The SQuID protocol (subcutaneous insulin in diabetic ketoacidosis) Impacts on ED operational Metrics. Acad Emerg Med 2023: https://pubmed.ncbi.nlm.nih.gov/36775281/
Books mentioned in this episode:
Kintsugi: Finding Strength in Imperfection. By Celine Santini: https://bit.ly/3NCdAYB
Recommended
Transcript
Introduction to Critical Matters Podcast
00:00:06
Speaker
Welcome to Critical Matters, a sound podcast covering a broad range of topics related to the practice of intensive care medicine.
00:00:14
Speaker
Sound provides comprehensive critical care programs to hospitals across the country.
00:00:19
Speaker
To learn more about our programs and career opportunities, visit www.soundphysicians.com.
00:00:26
Speaker
And now your host, Dr. Sergio Zanotti.
Focus on Hyperglycemic Emergencies
00:00:32
Speaker
In today's episode of Critical Matters, we will discuss the management of critically ill patients with hyperglycemic emergencies.
00:00:39
Speaker
Our guest is Dr. George Willis, a practicing emergency medicine physician.
00:00:43
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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.
00:00:54
Speaker
a recognized clinical educator with a special interest in endocrine emergencies, vascular emergencies, procedural education, and medical education.
00:01:02
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.
00:01:12
Speaker
It is a true pleasure and an honor to have him with us today.
00:01:15
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George, welcome to Critical Matters.
00:01:17
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Sergio, thank you for having me.
00:01:19
Speaker
It is an absolute pleasure to be here.
Frequency and Causes of Hyperglycemic Emergencies
00:01:21
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?
00:01:30
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Sure.
00:01:31
Speaker
So to be honest with you, it's
00:01:34
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It's really increasing.
00:01:36
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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.
00:01:48
Speaker
Now I see so many hyperglycemic emergencies in my shift.
00:01:53
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It's, it's funny because my residents are like, Dr. Wells, I have a really good patient for you.
00:01:56
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And I'm like, I already know it's, it's gonna be a hyperglycemic emergency.
00:02:00
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.
00:02:12
Speaker
And we're starting to see, again, an increase in the diagnosis of diabetes.
00:02:16
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.
00:02:26
Speaker
So diabetic emergencies are much more common.
00:02:30
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.
00:02:45
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.
00:02:58
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And when they get diagnosed with diabetes, they're not.
00:03:01
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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.
00:03:09
Speaker
And so they would either ration their insulin, they take it like every other day or every three days.
00:03:17
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And unfortunately, especially with type one diabetics, they would wait too long to start their insulin that they would develop, start to develop DKA.
00:03:27
Speaker
And it started leading to, you know,
00:03:30
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.
00:03:45
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.
Risks and Complications of Hyperglycemic Emergencies
00:03:52
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.
00:04:09
Speaker
But these patients have real risk, right?
00:04:11
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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.
00:04:22
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Absolutely.
00:04:23
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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.
00:04:34
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We oftentimes think that we know what we're doing.
00:04:37
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And unfortunately, we actually make more mistakes with this management, especially with HHS.
00:04:44
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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
00:04:53
Speaker
HHS not adequately.
00:04:57
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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.
00:05:05
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We'll say, oh we have this patient with HHS but we fixed them in the emergency department.
00:05:09
Speaker
That is not a good thing.
00:05:11
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That's not something that you want to do.
00:05:14
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These patients need to be treated just as slow as they develop their disease process.
Terminology and Pathophysiology of Hyperglycemic Syndromes
00:05:20
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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.
00:05:29
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Absolutely.
00:05:30
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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.
00:05:42
Speaker
Could you just give us the current and accepted terminology of what is considered a hyperglycemic emergency?
00:05:49
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Sure.
00:05:50
Speaker
So DKA is still DKA.
00:05:52
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It's diabetic ketoacidosis.
00:05:54
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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.
00:06:03
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We've seen this this kind of evolution of HHS.
00:06:08
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And so
00:06:08
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When I was in training, we used to call it HONK, which I universally hated because it stands for hyperosmolar non-ketotic.
00:06:19
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Well, where's the hyperglycemia in that?
00:06:22
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The hyperglycemia is certainly going to be necessary.
00:06:25
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And some people say, well, HONK is actually not spelled H-O-N-K.
00:06:30
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It's spelled H-H-O-N-K.
00:06:32
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So it stands for hyperglycemic.
00:06:35
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hyperosmolar non ketotic syndrome.
00:06:38
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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.
00:06:51
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So the NK or the non ketosis is where that came from.
00:06:56
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Now we have developed it into HHS, which I love so much more.
00:07:02
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So it's the hyperglycemic hyperosmolar syndrome or state.
00:07:07
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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.
00:07:17
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I like syndrome a little bit more.
00:07:18
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It makes it seem like it's a formal diagnosis.
00:07:21
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But that's the current terminology now is still DKA and HHS, meaning hyperglycemic hyperosmolar syndrome.
00:07:30
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Perfect.
00:07:31
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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.
00:07:45
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It's really kind of triggered, I think, an interest in pathophysiology and critical illness.
00:07:51
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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?
00:08:01
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Sure.
00:08:02
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So this is this is I'm going to warn you, Sergio.
00:08:05
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I am a true endocrine nerd.
00:08:08
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True.
00:08:09
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Tried and true.
00:08:10
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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.
00:08:20
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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.
00:08:29
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So starting with DKA, the main premise for DKA is that the body thinks that it is hypoglycemic.
00:08:38
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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.
00:08:52
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And so as a result, the body thinking that it's hypoglycemic, it actually starts a process to make more glucose.
00:09:01
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So the primary hormone in that, the counter-regulatory hormone in that, there's three big ones, which are
00:09:09
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Cortisol, which is obviously a stress hormone, that cortisol is a glucocorticoid, so it's a glucose-containing steroid.
00:09:20
Speaker
But cortisol also has the role of turning off insulin.
00:09:25
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So even if the pancreas was capable of making insulin, which in type 1 diabetics usually isn't, the pancreas,
00:09:34
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cortisol is going to actually tell the pancreas to stop making insulin because, again, it thinks that it's hypoglycemic.
00:09:41
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So this is actually the thought-to-be mechanism for how type 2 diabetics develop DKA, the thought process being that
00:09:51
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Type two diabetics typically can make insulin, so they usually don't go into DKA.
00:09:56
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But when they have some stress or some event, usually it's either overwhelming sepsis or massive infection or myocardial infarction or stroke.
00:10:07
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Some other large stressor the.
00:10:10
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Cortisol that gets secreted in that high stress state causes the pancreas to not make any insulin.
00:10:18
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And subsequently, they end up going into DKA despite having a pancreas that's actually functioning.
00:10:24
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So there's cortisol.
00:10:25
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Then there's catecholamines, which causes the neuro glycopenic effects.
00:10:29
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So your increased heart rate, your increased blood pressure, diaphoresis, agitation, diabetes.
00:10:35
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And then the last one, which is the very important one, which is glucagon.
00:10:38
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So glucagon does a couple of things.
00:10:40
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One, it starts gluconeogenesis.
00:10:43
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So it starts the creation of more glucose.
00:10:46
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Second thing it does is it breaks down glycogen in the liver to, again, make more glucose.
00:10:52
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.
00:11:00
Speaker
And so it starts making ketone bodies to essentially feed the brain.
00:11:04
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And those ketone bodies being negatively charged are beta-hydroxybutyrate or beta-hydroxybutyric acid and acetoacetate or acetoacetic acid.
00:11:14
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And the large predominance of those ketone bodies in the blood and ketonemia is what actually leads to the keto acidotic state.
00:11:25
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So that in a nutshell is what's happening with DKA.
00:11:29
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And we'll get into the meat in the treatment, but essentially insulin and glucagon are polar opposites of each other.
00:11:37
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So when glucagon causes ketogenesis and ketoacidosis, insulin reverses everything that glucagon does.
00:11:44
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And so we'll get a little bit more into that when we get into treatment.
00:11:47
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Now, HHS is significantly
00:11:50
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different.
00:11:51
Speaker
So in this scenario, the body still makes insulin in most of these circumstances.
00:11:59
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But again, it's not making enough insulin.
00:12:03
Speaker
So what ends up happening is that is there is a significant
00:12:07
Speaker
elevation in the glucose level.
00:12:08
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And so, you know, we see HHS usually in patients who have blood sugars who are greater than a thousand.
00:12:15
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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.
00:12:25
Speaker
So there is no ketoacidosis.
00:12:27
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There's no ketone bodies that are being formed.
00:12:29
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And so, but the body's still
00:12:32
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predominantly increasing the amount of glucose due to stress levels and things like that.
00:12:38
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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.
00:12:50
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So these patients, this is where we see that pseudo hyponatremia that occurs very typically with hyperglycemia.
00:12:57
Speaker
And so that's what happens at the beginning.
00:12:59
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.
00:13:11
Speaker
And what the body's trying to do essentially there is to lower the glucose the best way that it can.
00:13:17
Speaker
Unfortunately, it's...
Clinical Management of Hyperglycemic Conditions
00:13:19
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
00:13:46
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You have two times the sodium.
00:13:48
Speaker
And then at the end, you have glucose divided by 18.
00:13:51
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.
00:14:03
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.
00:14:15
Speaker
They are very clearly in HHS.
00:14:17
Speaker
Well, that patient is simply hyperglycemic.
00:14:20
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.
00:14:32
Speaker
Most of the time it's a stupor or confusion, and then it progresses to obtundation or coma.
00:14:38
Speaker
So if you think about it from the sodium perspective, basically,
00:14:44
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.
00:14:58
Speaker
And so these patients who will be hyperglycemic with normal sodiums,
00:15:06
Speaker
that sodium is affecting the osmolarity so much that the brain is actually starting to be affected.
00:15:12
Speaker
And so that's the big pathophysiology for HHS.
00:15:16
Speaker
It's not really the glucose.
00:15:18
Speaker
The glucose is the cause, but the sodium is the problem.
00:15:21
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.
00:15:29
Speaker
And that's what ends up being the big problem.
00:15:32
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.
00:15:43
Speaker
But as that central nervous system starts to become affected, your thirst response is
00:15:48
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
00:16:11
Speaker
And I think also explains, obviously, why the treatment that really makes a difference is fluids and not necessarily the insulin.
00:16:18
Speaker
But I think there's a great, I mean, overview and explanation.
00:16:22
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.
00:16:31
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.
00:16:40
Speaker
So anybody can start a DKA protocol, I'm sure.
00:16:44
Speaker
But not every patient responds the same way.
00:16:46
Speaker
And understanding what might be going on and what you need to adjust, I think, is guided by pathophysiology first and foremost.
00:16:54
Speaker
You hit that nail right on the head.
00:16:56
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.
00:17:08
Speaker
And we'll talk about this a little bit.
00:17:09
Speaker
But when we get to diagnostic criteria, you focus so much on the fact that this patient has.
00:17:17
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
00:17:36
Speaker
I really encourage people to think outside the box with a lot of these diagnoses.
00:17:41
Speaker
But certainly if patients present very typically or classically, you certainly don't want to miss this diagnosis as well.
00:17:49
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.
00:18:00
Speaker
We should program ourselves to ask more questions, right?
00:18:03
Speaker
Always ask what else, what could be causing, what am I missing?
00:18:08
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.
00:18:14
Speaker
that we didn't really pay attention to that ultimately can cause significant harm to our patients.
00:18:20
Speaker
100%.
00:18:21
Speaker
Absolutely.
00:18:22
Speaker
So let's talk about clinical presentation and diagnosis.
00:18:25
Speaker
Let's start with DKA, diagnostic criteria.
00:18:28
Speaker
My understanding from reading some of your excellent review papers is that there's not a lot of agreement here.
00:18:35
Speaker
You can quote ADA, but the British say something different.
00:18:37
Speaker
Some people say, I mean, you know when you see it.
00:18:41
Speaker
I mean, can you tell us kind of how you think about this?
00:18:44
Speaker
Sure.
00:18:45
Speaker
So we'll talk about diagnostic criteria first, because interestingly, you
00:18:50
Speaker
Hot off the press in June of 2024, the ADA, the British Society of... The British Society.
00:19:01
Speaker
Now I'm forgetting the name.
00:19:02
Speaker
Give me a second.
00:19:03
Speaker
It's the British Society of...
00:19:08
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.
00:19:25
Speaker
This is the first time that anyone has really put together a joint set of criteria for the diagnosis of DKA and HHS.
00:19:35
Speaker
The ADA guidelines were based off of a study or a paper that was written by Katabji et al.
00:19:40
Speaker
in 2009.
00:19:41
Speaker
And we've been using that criteria since 2009.
00:19:46
Speaker
But so much has changed.
00:19:48
Speaker
We've we've developed so much different knowledge bases now with with with DKA.
00:19:53
Speaker
I'm so glad that they've actually made an adjustment.
00:19:56
Speaker
So these new criteria now.
00:19:58
Speaker
Excuse me.
00:20:01
Speaker
are the following one, um, the, the glucose definition.
00:20:06
Speaker
So it used to be a glucose greater than two 50.
00:20:08
Speaker
They've lowered that now to 200 and added the stipulation or a previous diagnosis of diabetes.
00:20:17
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.
00:20:28
Speaker
And that commonly is, um,
00:20:31
Speaker
seen in patients who are on diabetic medications.
00:20:34
Speaker
And so you are not
00:20:38
Speaker
I don't know if it's possible.
00:20:40
Speaker
It's certainly possible in my thought process that it could happen.
00:20:44
Speaker
It would be very difficult to happen.
00:20:46
Speaker
But you're not going to see a new onset diabetic come in and euglycemic DKA in most circumstances.
00:20:52
Speaker
So most of the euglycemic DKA that we see are typically patients who've already been previously diagnosed with diabetes.
00:20:58
Speaker
So I love the fact that they actually changed this as a diagnostic criteria for
00:21:03
Speaker
to lower the glucose and then add whatever glucose that they have.
00:21:07
Speaker
If they have a history of diabetes, they could be at risk for DKA.
00:21:11
Speaker
The second one's unchanged.
00:21:14
Speaker
They have to have ketonuria or ketonemia.
00:21:18
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.
00:21:30
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.
00:21:46
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.
00:21:56
Speaker
And beta-hydroxybutyrate is actually the predominant ketone body that's made.
00:22:02
Speaker
And so that acetoacetic level or acetoacetate level changes.
00:22:07
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.
00:22:19
Speaker
And then the last one is an anion gap metabolic acidosis.
00:22:23
Speaker
That one, again, is unchanged, pH less than 7.3 or a serum bicarb level of less than 18.
00:22:31
Speaker
So those are the diagnostic criteria for DKA.
00:22:37
Speaker
HHS, their definition for HHS really hasn't changed significantly since the 2009 paper that we discussed.
00:22:46
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.
00:22:57
Speaker
So that definition hasn't changed in years.
00:23:01
Speaker
They use for hyperosmolarity two different measures for osmolarity.
00:23:06
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.
00:23:19
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
00:23:37
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
00:23:53
Speaker
And then absence of acidosis.
00:23:55
Speaker
So that's unchanged.
00:23:58
Speaker
The thing that is a little frustrating is they used to have a diagnostic criteria for mental status.
00:24:04
Speaker
They've taken that out for some reason that I'm still unsure of why.
00:24:10
Speaker
In the grand scheme of things, again, we talked about the mental state.
00:24:13
Speaker
So these patients are going to come in with some element of altered mental status.
00:24:18
Speaker
But from the diagnostic criteria, they have taken that part out of the diagnostic criteria for HHS.
00:24:27
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.
00:24:37
Speaker
And we talked about the ways that people can present with type 2 diabetes.
00:24:43
Speaker
We're still more commonly going to see that in type one diabetics.
00:24:47
Speaker
These patients usually will present with abdominal pain and nausea and or vomiting.
00:24:53
Speaker
And all of those symptoms are traditionally as a result of the ketoacidosis that's present.
00:24:59
Speaker
It's not the hyperglycemia that's causing that.
00:25:01
Speaker
It is the ketoacidosis that's causing that.
00:25:04
Speaker
They may have an element of altered mental status when their pH starts to drop into the less than seven range.
00:25:12
Speaker
So you may see some element of altered mental status as well.
00:25:16
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.
00:25:27
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.
00:25:40
Speaker
So that's kind of the classic picture for DKA.
00:25:45
Speaker
For HHS, there's there's.
00:25:49
Speaker
Classically, you're going to see this in type two diabetics.
00:25:51
Speaker
Type one diabetics typically won't get high enough before they're developing DKA.
00:25:57
Speaker
So you won't typically see HHS in type one diabetics.
00:26:01
Speaker
It's more commonly going to be in type two diabetics.
00:26:04
Speaker
And you're going to probably see this more commonly in the elderly population.
00:26:09
Speaker
However, recently we've had an increase in childhood obesity and subsequent re
00:26:17
Speaker
terrifyingly, we've seen a larger number of type two diabetics getting diagnosed in the pediatric population.
00:26:26
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.
00:26:42
Speaker
So, but the classic presentation here, they typically are going to be missing your ketoacidosis symptoms.
00:26:51
Speaker
So they're not going to have the abdominal pain.
00:26:52
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.
00:27:01
Speaker
And then the again, getting back to the mental status.
00:27:05
Speaker
So the mental status in these patients is is frequently going to be significantly altered compared to their baseline.
00:27:13
Speaker
So it can be any type of neurologic symptom they can have.
00:27:17
Speaker
I've seen patients with HHS who've had stroke like symptoms.
00:27:19
Speaker
I've seen patients with HHS have paresthesias.
00:27:23
Speaker
But the classic.
00:27:24
Speaker
presentation for HHS is going to be some element of altered sensorium where they're globally confused.
00:27:32
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.
00:27:45
Speaker
So those are the kind of classic presentations for patients who present clinically.
00:27:50
Speaker
Perfect.
00:27:51
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?
00:28:04
Speaker
Sure.
00:28:05
Speaker
So whenever I think about patients who come in with hyperglycemia, I think of the four, what I call the four I's.
00:28:11
Speaker
And so those four I's are the very much the most common reasons why patients develop hyperglycemia.
00:28:19
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.
00:28:28
Speaker
So number one cause of hyperglycemia worldwide is infection.
00:28:33
Speaker
So these patients will have more commonly you're going to see urinary tract infections and pneumonias be the primary cause.
00:28:40
Speaker
But bacteremia, really any infection can do this.
00:28:44
Speaker
I've seen patients with new onset diabetes who have had fourniase.
00:28:49
Speaker
I've seen lots of septic patients who have developed new onset diabetes as well or worsened diabetes.
00:28:56
Speaker
hyperglycemia in patients who are already diabetic.
00:28:59
Speaker
So infection needs to be one of the things that we certainly consider.
00:29:05
Speaker
Number two is ischemia.
00:29:07
Speaker
So that can be myocardial ischemia.
00:29:10
Speaker
That can be
00:29:12
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
00:29:35
Speaker
So any infarction or ischemia is another eye to think about in terms of etiology.
00:29:44
Speaker
Third is infancy.
00:29:47
Speaker
So basically being pregnant.
00:29:49
Speaker
So obviously our patients who are in their age of childbearing age,
00:29:57
Speaker
They will they can present with hyperglycemia as well.
00:30:02
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.
00:30:18
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.
00:30:29
Speaker
And then the last I is insulin being insulin noncompliance.
00:30:33
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.
00:30:45
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.
00:30:56
Speaker
And so my diagnostic workup for the most part is going to be to look for any of these four eyes.
00:31:02
Speaker
You know, if a patient comes in with.
00:31:06
Speaker
Doc, I'm sorry.
00:31:08
Speaker
I have not been taking my insulin like I'm supposed to.
00:31:11
Speaker
I know that I'm in DKA because I haven't taken my insulin in like a week.
00:31:15
Speaker
I apologize, but unfortunately it was just too expensive.
00:31:18
Speaker
That may be a patient who may get very minimal workup from a diagnostic perspective.
00:31:24
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.
00:31:35
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.
00:31:43
Speaker
I'm getting a urine anyway to make sure they don't have an infection.
00:31:47
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.
00:32:00
Speaker
But then also, you know, having a low, very low threshold to getting blood cultures.
00:32:08
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.
00:32:17
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.
00:32:25
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,
00:32:35
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.
00:32:40
Speaker
And so I have a much, much more, much bigger workup in that patient population because of how sick those patients are.
00:32:50
Speaker
So that's, those are the big kind of, kind of infection or initial workups in patients who come in with hyperglycemic emergencies.
00:32:59
Speaker
And you talked about, obviously, other diagnostic criteria and the differences between measuring the different keto acids.
00:33:07
Speaker
I wanted to ask you, George, is there a role for end tidal CO2 here?
00:33:13
Speaker
Yes.
00:33:13
Speaker
One of my favorite things.
00:33:15
Speaker
So, you know, we can get I work at one of the ivory towers.
00:33:20
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.
00:33:29
Speaker
I can get with lights, with electrolytes.
00:33:31
Speaker
So I can get a rapid VBG with electrolytes and probably.
00:33:34
Speaker
Five minutes.
00:33:35
Speaker
So I can I can know if a person's in DKA relatively quickly.
00:33:39
Speaker
I know that most people don't practice in an ivory tower like I do.
00:33:44
Speaker
And they may not have access to a rapid point of care BBG or electrolyte panel.
00:33:49
Speaker
So what do you have access to that you can do relatively quickly?
00:33:53
Speaker
Because we'll get patients who come into the to our emergency department or in our critical care setting who are hyperglycemic.
00:34:00
Speaker
So you can do end-tidal CO2 and quickly rule out DKA.
00:34:05
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%.
00:34:17
Speaker
So it is a very useful tool.
00:34:21
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 โ
00:34:30
Speaker
high quote unquote, meaning it's greater than 600 milligrams per deciliter.
00:34:34
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.
00:34:44
Speaker
And within five minutes I can have an entitled CO2 level.
00:34:48
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.
00:34:56
Speaker
and then give them some fluids.
00:34:58
Speaker
I don't necessarily have to give them any insulin or any other anti-hyperglycemic therapy.
00:35:05
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.
00:35:15
Speaker
When the level is less than 27, it doesn't 100% rule in DKA, it just makes DKA more likely.
00:35:23
Speaker
It means that they have some type of acidosis process
00:35:26
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
00:35:54
Speaker
And I started the patient on fluids.
00:35:56
Speaker
I'm giving them insulin and I'm watching their entitled CO2 start to creep up.
00:36:01
Speaker
I know that I'm actually improving the patient and making them better.
00:36:04
Speaker
If it's not moving, I do two things.
00:36:08
Speaker
One is I may need to start increasing my treatment or I may need to look for some other etiology.
00:36:16
Speaker
Does this patient have a lactic acidosis?
00:36:17
Speaker
Does this patient have a toxic alcohol on board that I was unaware of?
00:36:22
Speaker
So I start to think about other diagnoses that may be going on concomitantly with the DKA.
00:36:28
Speaker
So I love the use of entitled CO2 in this patient population.
00:36:32
Speaker
Excellent.
00:36:33
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.
00:36:39
Speaker
And from what you described,
00:36:40
Speaker
It almost feels like a, a, akin to a D-dimer, right?
00:36:45
Speaker
It helps you rule out stuff, but it doesn't necessarily make the diagnosis.
00:36:49
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.
00:36:59
Speaker
Yep.
00:37:00
Speaker
Awesome.
00:37:00
Speaker
So let's talk about management.
00:37:02
Speaker
And you talked about the four eyes.
00:37:04
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.
00:37:21
Speaker
And it's almost similar to source control, right?
00:37:23
Speaker
We have to take care of that.
00:37:24
Speaker
First and foremost, otherwise we're not going to get anywhere with that patient.
00:37:29
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?
00:37:36
Speaker
Sure.
00:37:37
Speaker
So one of the things that I think is super important here is just what you're describing.
00:37:43
Speaker
Because, you know, we can basically give these patients fluids and...
00:37:48
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
00:38:03
Speaker
And then we stop all of those interventions.
00:38:05
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.
00:38:13
Speaker
What caused you to go back into decay?
00:38:15
Speaker
And it's because we missed the underlying etiology or the cause of these patients symptoms.
00:38:21
Speaker
And so, again, in a sick situation.
00:38:23
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.
00:38:34
Speaker
If they have anything that looks even remotely like they are septic in any way, obviously still following the sepsis guidelines, they're
00:38:45
Speaker
We want to start those patients on empiric antibiotics early.
00:38:48
Speaker
And so I have a low threshold in this patient population to starting these patients on empiric antibiotics.
00:38:55
Speaker
And again, we're looking for sources of ischemia.
00:38:58
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
00:39:12
Speaker
was refusing to take the patient to the cath lab.
00:39:15
Speaker
And I was who we got their sugar better.
00:39:17
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.
00:39:23
Speaker
But I need you to take this patient to the cath lab ASAP.
00:39:26
Speaker
And, you know, after some significant bargaining, um, I feel like I owe one of my children, um,
00:39:34
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.
00:39:43
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.
00:39:49
Speaker
So we took it to the cath lab and the patient, both all three of those patients had really good outcomes.
00:39:54
Speaker
So starting with source control is important.
00:39:58
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.
00:40:13
Speaker
But you have to treat those things as well.
00:40:15
Speaker
The one eye that you're obviously not going to treat is the
00:40:20
Speaker
the infancy.
00:40:21
Speaker
Obviously, if you have a pregnant lady, you're not going to get rid of the baby because she's in DKA.
00:40:26
Speaker
You're just going to treat that.
00:40:28
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.
00:40:35
Speaker
So those are the big kind of source control things that I do.
00:40:39
Speaker
Very, very low threshold to starting antibiotics.
00:40:42
Speaker
Again, looking for sources of ischemia and then treating the patient appropriately from there.
00:40:47
Speaker
Perfect.
00:40:48
Speaker
So let's talk a little bit more about DKA and go through the different aspects of treatment.
00:40:53
Speaker
And as you explained earlier, the pathophysiology kind of links to what we're doing.
00:40:59
Speaker
So we start with IV fluids.
00:41:01
Speaker
What are your thoughts on IV fluids for DKA?
00:41:04
Speaker
100% necessary.
00:41:06
Speaker
You have to do it the right way, though.
00:41:08
Speaker
We'll talk about why.
00:41:09
Speaker
Again, I'm going to go a little in the weeds.
00:41:11
Speaker
Endocrine nerds, that's me.
00:41:13
Speaker
So as we alluded to before, we talked about the osmotic diuresis.
00:41:16
Speaker
And the key thing to focus on with the osmotic diuresis is two things.
00:41:21
Speaker
One,
00:41:22
Speaker
glucose and water are like best friends.
00:41:25
Speaker
They go everywhere together, which includes out in the urine.
00:41:29
Speaker
So these patients have a very significant volume depletion that occurs intravascularly as a result of the osmotic diuresis.
00:41:38
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.
00:41:50
Speaker
So if
00:41:50
Speaker
you just said this patient classically looks like DKA.
00:41:53
Speaker
They tell me they're in DKA.
00:41:55
Speaker
They quack like they're in DKA.
00:41:57
Speaker
This patient's in DKA.
00:41:58
Speaker
I know they need insulin.
00:41:59
Speaker
I'm just going to go ahead and start an insulin drip.
00:42:02
Speaker
What happens is, is that intravascularly, the body will sense the insulin presence and it will start to pull glucose out
00:42:09
Speaker
out of the vascular system and into the tissue.
00:42:13
Speaker
Well, where glucose goes, water says, bring me too.
00:42:17
Speaker
And so it leaves the intravascular space, which can lead to circulatory collapse.
00:42:22
Speaker
Subsequently, these patients will get hypotensive and can go into cardiac arrest.
00:42:27
Speaker
So you don't want to just blanket start these patients on insulin until you've adequately hydrated them.
00:42:33
Speaker
So this is where I use ultrasound to my advantage.
00:42:35
Speaker
I will actually assess their volume status and see what I can see in terms of looking at their IVC.
00:42:41
Speaker
looking at some other objective measures intravascularly to see if I can get a sense of what their true vascular status is.
00:42:48
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.
00:42:59
Speaker
And in those patients, they may have a normal volume status.
00:43:03
Speaker
And so flu isn't necessarily as important in that patient.
00:43:07
Speaker
Or they may have developed myocardial ischemia from a massive myocardial infarction.
00:43:12
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.
00:43:19
Speaker
So in that circumstance, I may hold or give smaller volumes of fluids, but I want to assess what their volume status is.
00:43:28
Speaker
The vast majority of patients who are in DKA, though, are going to be very volume down.
00:43:34
Speaker
And again, we don't want to just start them on insulin.
00:43:36
Speaker
So IV fluids is going to be the most important thing to establish rehydration and replenishing the intravascular.
00:43:44
Speaker
Volume in terms of which IV fluids.
00:43:46
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.
00:43:58
Speaker
Now, the thing that I do like about their statement is that they don't bad mouth the
00:44:03
Speaker
balanced solutions.
00:44:05
Speaker
They just say you can use balanced solutions.
00:44:08
Speaker
And there is some literature out there that says that balanced solutions leads to a quicker resolution of the decay.
00:44:15
Speaker
So they at least acknowledge that balanced solutions are better.
00:44:18
Speaker
But I make the argument that balanced solutions should be our initial go-to.
00:44:22
Speaker
Now, obviously, if you don't have balanced solutions, normal saline is perfectly fine.
00:44:28
Speaker
It's just...
00:44:30
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
00:44:52
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,
00:45:06
Speaker
the thing that's being subtracted from sodium.
00:45:09
Speaker
And so that anion gap is going to close rather quickly, despite the fact that the acidosis is not actually moving or improving.
00:45:17
Speaker
And so these patients develop a non-anion gap hyperchloramic metabolic acidosis.
00:45:23
Speaker
And so to avoid that, you can start them on plasma light, which is my go-to or lactated ringers.
00:45:31
Speaker
Plasma light has a chloride concentration of 98, which is much more physiologic.
00:45:36
Speaker
Lactated ringers has a chloride concentration of 109.
00:45:39
Speaker
Again, closer to the physiologic status of the chloride concentration in the body.
00:45:45
Speaker
And so you don't develop that hyperchloremic non-anigap metabolic acidosis with balanced solutions versus normal saline.
00:45:52
Speaker
So I preferentially use...
00:45:55
Speaker
plasma light, um, LR is available at my hospital.
00:45:59
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.
00:46:12
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.
00:46:25
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.
00:46:36
Speaker
But also keeping them longer than they need to in the ICU also has a cost implication.
00:46:43
Speaker
Plus, I would argue that...
00:46:45
Speaker
The available literature in critical illness, general critical illness, supports the use of balanced solutions, right?
00:46:53
Speaker
Absolutely.
00:46:54
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.
00:47:06
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?
00:47:17
Speaker
So eventually, as you move your strategy, you have to figure that out, correct?
00:47:21
Speaker
Correct.
00:47:22
Speaker
So, yeah, so just to kind of go back to your previous point, the literature, the literature is really good here.
00:47:30
Speaker
The previous studies that were done were done on were done in like smaller numbers.
00:47:35
Speaker
So, you know, I think one of the studies had 25 patients.
00:47:38
Speaker
Another one had 49 patients.
00:47:40
Speaker
The largest study, which is the study that I absolutely adored,
00:47:45
Speaker
was done by Self et al.
00:47:47
Speaker
published in November of 2020.
00:47:48
Speaker
And it looked at the subgroup of patients who were in DKA from the SALT-D trial and the SMART trial.
00:47:57
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.
00:48:07
Speaker
So there's literature again that shows that
00:48:11
Speaker
You want to get these patients out of the ICU faster.
00:48:13
Speaker
You want to get them out of the hospital faster.
00:48:15
Speaker
You should start these patients on plasma light.
00:48:18
Speaker
Now, uh,
00:48:19
Speaker
There is currently as of, I think if I remember correctly, 2023, a D5 Plasmalite that is available.
00:48:29
Speaker
I had been under the impression that it was never going to happen.
00:48:33
Speaker
And I actually wrote a letter to the company to say, you should probably make this happen.
00:48:40
Speaker
I never heard back from them, but sure enough,
00:48:43
Speaker
Very shortly thereafter, there's dextrose, 5% plasma light.
00:48:50
Speaker
There are not a lot of hospitals that have it yet.
00:48:53
Speaker
I do believe that it will be coming down the pipe, but...
00:48:57
Speaker
D5 LR is available.
00:49:00
Speaker
So a lot of people know that there is a D5 LR and D5 is certainly available.
00:49:04
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.
00:49:16
Speaker
So the two bag method is something that's been well, well researched in the pediatric population.
00:49:23
Speaker
and has been shown to be helpful.
00:49:25
Speaker
In this circumstance, what you do is you actually start them on the fluid of choice that you have for them.
00:49:33
Speaker
So for instance, plasma light.
00:49:35
Speaker
And then on the second bag, you actually start them on a D10.
00:49:40
Speaker
And I use half normal saline.
00:49:43
Speaker
I don't like using D5W because I think it waters down the sodium.
00:49:47
Speaker
And I certainly don't want to affect the sodium significantly.
00:49:49
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.
00:50:02
Speaker
They've recently now studied this in the adult population and have also found it to be significantly helpful.
00:50:09
Speaker
So preferentially, what I typically will do is I'll start them on plasma light.
00:50:14
Speaker
start them on the insulin, which we'll talk about in a second.
00:50:17
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.
00:50:28
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.
00:50:44
Speaker
Awesome.
00:50:45
Speaker
So let's talk about insulin.
00:50:48
Speaker
Oh, insulin.
00:50:50
Speaker
We know insulin is the savior.
00:50:53
Speaker
This is the thing that's going to stop the ketoacidosis, stop the ketogenesis.
00:50:57
Speaker
So it's going to reverse everything that glucagon does.
00:51:02
Speaker
Now, how do we administer the insulin?
00:51:05
Speaker
So the classic teaching was the insulin infusion.
00:51:10
Speaker
Thankfully, we have gotten rid of the insulin bolus plus the insulin infusion.
00:51:15
Speaker
In pediatric population, again, bolus is completely contraindicated.
00:51:20
Speaker
In the adult population, you can go ahead and do it if you feel like it's necessary.
00:51:24
Speaker
In most circumstances, though, the literature has borne out that you don't have to start the insulin infusion.
00:51:29
Speaker
And then I'm sorry, the insulin bolus and then the insulin infusion.
00:51:33
Speaker
So do you have to start everybody on an insulin infusion?
00:51:37
Speaker
I'm a beat up two things here.
00:51:39
Speaker
One, you don't have to do everybody on an insulin infusion.
00:51:43
Speaker
And then the second thing we're going to talk about is the insulin titration protocols, which drives me up the wall.
00:51:49
Speaker
So from an insulin infusion,
00:51:53
Speaker
If they're in severe DKA, the literature has borne out that you still should start the patient on an insulin infusion.
00:51:58
Speaker
So if their pH is 7.1 or less, you should go ahead and start that patient on an insulin infusion.
00:52:06
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.
00:52:18
Speaker
What the squid or subcutaneous insulin uses is they use aspart or lispro insulin, which is an ultra rapid acting insulin.
00:52:28
Speaker
You give it subcutaneously.
00:52:29
Speaker
You still do it every hour.
00:52:31
Speaker
You do if their blood sugar is high, you start them on point two units per kilogram.
00:52:39
Speaker
And then if their blood sugar is closer to that 250 range, then you start them on point one units per kilogram.
00:52:46
Speaker
And the unfortunate thing with the squid protocol is it's exceptionally nurse intensive.
00:52:52
Speaker
So if you're in the ICU, this is probably a fine place to do it.
00:52:58
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.
00:53:09
Speaker
They're going to be Q1 hour finger sticks,
00:53:12
Speaker
They're going to be Q1 hour insulin and insulin boluses subcutaneously.
00:53:18
Speaker
But they found that comparing subcutaneous insulin versus the insulin infusion, the outcomes were pretty much the same.
00:53:26
Speaker
But they actually got out of the hospital and out of the emergency department faster when you did the subcutaneous insulin.
00:53:33
Speaker
So now I preferentially actually in patients who are your kind of, you know, classic insulin.
00:53:42
Speaker
Insulin non-compliance.
00:53:43
Speaker
There's no source of infection.
00:53:46
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.
00:54:07
Speaker
So like, yeah, it makes sense.
00:54:09
Speaker
I mean, to try to avoid the ICU, right?
00:54:11
Speaker
But once they go to our world in the ICU, you're almost as equally off just with the insulin drip.
00:54:18
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.
00:54:26
Speaker
But I do think it's important for people to be aware of that.
00:54:30
Speaker
Absolutely.
00:54:31
Speaker
100 percent.
00:54:31
Speaker
Yeah, I think that's that.
00:54:33
Speaker
I'm sorry to cut you off, Sergei.
00:54:34
Speaker
No, no, go ahead.
00:54:37
Speaker
I think I think you hit the nail right on the head.
00:54:39
Speaker
I think a lot of times it's just easier to put the patients on the on the infusion.
00:54:45
Speaker
And in other than like the description that I said before.
00:54:50
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.
00:55:02
Speaker
So it's reasonable to just start the infusion.
00:55:05
Speaker
There's been a very few circumstances where I've done the squid protocol.
00:55:08
Speaker
And again, those patients, it is just simply a, I'm noncompliant for whatever reason,
00:55:14
Speaker
I just need a couple of doses of insulin and I will probably be fine.
00:55:18
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.
00:55:26
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.
00:55:33
Speaker
Excellent.
00:55:34
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.
00:55:46
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.
00:55:56
Speaker
But could you talk about that portion and how you transition to longer acting insulin?
00:56:02
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.
00:56:09
Speaker
So this is a great transition point because...
00:56:14
Speaker
I do.
00:56:16
Speaker
I do do this a lot in my emergency department because we are, we have a lot of busy ICUs.
00:56:23
Speaker
So one of the things that's really hit emergency medicine in the United States is a problem with boarding.
00:56:30
Speaker
And so we actually do transition a lot of patients.
00:56:32
Speaker
So this is actually very pertinent.
00:56:34
Speaker
So with DKA, as we alluded to earlier, the insulin is going to be the big, big, big fixer here.
00:56:43
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.
00:56:58
Speaker
I will transition those patients to getting ready to turn off the insulin infusion.
00:57:03
Speaker
In order to do that, though, they still need insulin in place.
00:57:07
Speaker
And so the classic insulin to start these patients on is glargine.
00:57:12
Speaker
Glargine is a long-acting insulin that lasts about 23 to 24 hours.
00:57:17
Speaker
The teaching is that it's 23 hours.
00:57:23
Speaker
But what Glargine does is Glargine is essentially like a basal...
00:57:29
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
00:57:55
Speaker
dose level at about two hours and then it maintains that dose level for the next 21 hours or 22 hours.
00:58:03
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.
00:58:16
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,
00:58:27
Speaker
give them the glargine and then I wait about two hours and then I can turn the insulin drip off.
00:58:34
Speaker
And then essentially that glargine has started the drip for me.
00:58:39
Speaker
Now that two hour period is certainly going to, um, they're still going to be on the drip and things like that.
00:58:47
Speaker
And the unfortunate thing is that sometimes, you know,
00:58:51
Speaker
Nurses get busy.
00:58:52
Speaker
That insulin drip is going to run for maybe three hours or maybe four hours.
00:58:56
Speaker
And oh, my gosh, I completely forgot to turn the insulin drip off.
00:58:59
Speaker
So there's a study that has recently come out and it needs to be repeated.
00:59:06
Speaker
And it's something that's in interest of mine is why wait?
00:59:11
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.
00:59:21
Speaker
And there's been safety.
00:59:23
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.
00:59:35
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.
00:59:45
Speaker
So you can start the glargine at the beginning of the insulin infusion.
00:59:49
Speaker
And when their acidosis corrects, you can just turn the drip off and the glargine's in the system.
00:59:57
Speaker
Obviously, once the patient...
01:00:00
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.
01:00:12
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?
01:00:20
Speaker
And they may actually still get better in the same amount of time.
01:00:24
Speaker
But you you lose that.
01:00:27
Speaker
You know, I forgot to turn the insulin drip off.
01:00:28
Speaker
Oh, my gosh.
01:00:29
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.
01:00:37
Speaker
So an interesting area of research.
01:00:39
Speaker
So we'll see what happens.
01:00:41
Speaker
But that's how I transition.
01:00:43
Speaker
Give them the glargine once the ketoacidosis has resolved and then wait two hours, turn the insulin infusion off.
01:00:51
Speaker
And then they can go on about, you know, being treated with the glargine that's in their system.
01:00:58
Speaker
Excellent.
01:00:59
Speaker
And I think it's important for our critical care listeners to talk about glargine because a
01:01:08
Speaker
Basically, we always kind of think dogmatically that long-acting drugs are not friends of the ICU.
01:01:14
Speaker
We have the illusion of control, so we use shorter-acting insulin, we have more control.
01:01:19
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?
01:01:26
Speaker
I mean, start early and have that on board.
01:01:30
Speaker
And as the ketosis resolves, you can transition a lot, a lot quicker.
01:01:34
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?
01:01:45
Speaker
And then you have a rebound and it just delays things.
01:01:48
Speaker
It doesn't help our patients.
01:01:50
Speaker
You mentioned hypokalemia, and I wanted to talk about electrolytes.
01:01:55
Speaker
Could you just tell us, I mean, how you think about electrolyte management in these patients?
01:02:01
Speaker
Sure.
01:02:01
Speaker
So as we know, insulin will also shift potassium and putting them on an insulin infusion is actually a treatment for refractory hyperkalemia.
01:02:11
Speaker
So if you start a patient on an insulin drip, you are going to potentially bottom out their potassium.
01:02:19
Speaker
What I love about the way that I treat potassium is that it actually works fast if you do it correctly.
01:02:27
Speaker
So
01:02:30
Speaker
Again, the guidelines have changed, which I again love.
01:02:33
Speaker
The old guidelines used to say that the numbers were 3.3 and 5.5.
01:02:42
Speaker
So what that essentially meant was that I'm sorry, 5.2, 3.3 and 5.2.
01:02:46
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.
01:02:53
Speaker
If it was between 3.3 and 5.2, you gave insulin and you gave supplemental potassium.
01:03:01
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.
01:03:09
Speaker
I hate those numbers because, one, they're very hard to remember.
01:03:12
Speaker
Two, I feel like that 3.3 threshold is a little bit on the lower side.
01:03:18
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.
01:03:33
Speaker
And if they have pHs of 7 or lower, they're
01:03:38
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.
01:03:58
Speaker
So when it's 3.3, if they have a pH that's less than 7, their potassium is in the toilet.
01:04:06
Speaker
So I like the 3.5 to 5.5.
01:04:09
Speaker
The numbers are easier to remember.
01:04:12
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.
01:04:23
Speaker
So in terms of how I treat potassium is I actually give it to them IV and orally.
01:04:30
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.
01:04:41
Speaker
And I have not found a single ounce of literature to show that to be true.
01:04:45
Speaker
I have anecdotal evidence that says that that's false.
01:04:48
Speaker
So I think it's fake news.
01:04:50
Speaker
I think it's certainly dependent on what else is going on with the patient.
01:04:54
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.
01:05:19
Speaker
the infusion that's going to lower their potassium.
01:05:24
Speaker
So I preferentially will give them oral and IV.
01:05:28
Speaker
I also make sure
01:05:30
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.
01:05:39
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.
01:05:51
Speaker
Another controversial electrolyte is phosphorus.
01:05:57
Speaker
So
01:06:00
Speaker
Oops, that was Alexa, sorry.
01:06:04
Speaker
Phosphorus is controversial because phosphorus, the thought process is that most patients who are in diabetic ketoacidosis are actually hypophosphatemic.
01:06:14
Speaker
The problem with phosphate is that one, it's hard to administer.
01:06:19
Speaker
The IV formulation comes with several other electrolytes with it, and it's not sufficient enough of that electrolyte being mainly potassium.
01:06:30
Speaker
But the amount of potassium that comes with that phosphorus is not sufficient to replenish the potassium that you're trying to replenish.
01:06:39
Speaker
So that's why I preferentially give the potassium by itself.
01:06:42
Speaker
And the oral formulation, one, is terrible tasting.
01:06:47
Speaker
So the question becomes, is it necessary?
01:06:50
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.
01:06:58
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.
01:07:16
Speaker
So certainly the muscles may be getting tired, especially with their breathing a lot.
01:07:20
Speaker
Those patients may have an element of respiratory depression if their phosphorus gets low.
01:07:25
Speaker
But if the phosphorus is low and they're experiencing symptoms, then they recommend going ahead and replenishing the phosphorus.
01:07:32
Speaker
But otherwise, there's no real need or indication to replenishing phosphorus.
01:07:38
Speaker
So I preferentially don't do it.
01:07:40
Speaker
I usually try to fix the acidosis as quickly as I can so that their breathing is slowed down.
01:07:47
Speaker
And then they subsequently can eat orally and hopefully replenish their own phosphorus.
01:07:56
Speaker
And then subsequently, they usually don't need anything from me.
01:08:01
Speaker
Excellent.
01:08:01
Speaker
Any comments on magnesium and sodium as we wrap up the electrolyte discussion?
01:08:06
Speaker
Sure.
01:08:07
Speaker
So sodium becomes much more important, especially when we get to HHS.
01:08:11
Speaker
With DKA, sodium, we kind of just watch the sodium.
01:08:15
Speaker
It gives us a little bit of an assessment of what their intravascular...
01:08:21
Speaker
Yeah.
01:08:41
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.
01:08:51
Speaker
Magnesium, again, primarily I'm looking at it in the scenario of potassium replenishment.
01:08:59
Speaker
So if the magnesium is low, they're not going to.
01:09:02
Speaker
they're not going to retain any of the potassium that I'm going to replace their electrolytes with.
01:09:08
Speaker
So if their magnesium is low, I want to check it and replenish it.
01:09:13
Speaker
If they are in stage renal, their magnesium can be high.
01:09:18
Speaker
But again, that's not a common patient population.
01:09:21
Speaker
So I empirically give magnesium if I know that their potassium is very, very low.
01:09:27
Speaker
And again, they're very acidotic.
01:09:30
Speaker
If they are...
01:09:32
Speaker
you know, in that mild to moderate state and the potassium is pretty close to normal, I won't necessarily replenish the magnesium.
01:09:39
Speaker
I'll check it, but I won't empirically give it, um, unless they are very low and their pH is very low.
01:09:46
Speaker
What about bicarb?
01:09:49
Speaker
Ah, one of my pet peeves.
01:09:52
Speaker
So sodium bicarbonate has been shown over the years to be universally not a great medication to give.
01:10:01
Speaker
In the DKA patient, it is extremely controversial.
01:10:06
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.
01:10:20
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.
01:10:37
Speaker
I'm okay, doc.
01:10:37
Speaker
Doing good.
01:10:38
Speaker
Just sitting here playing my game.
01:10:40
Speaker
And they don't need bicarb.
01:10:42
Speaker
So I reserve sodium bicarbonate for three patient populations.
01:10:47
Speaker
One, profound hyperkalemia.
01:10:50
Speaker
So patient, you know, usually they're going to be acidotic.
01:10:53
Speaker
They're going to have pHs that are pretty low.
01:10:56
Speaker
But let's say that they are end-stage renal, for an example, and
01:11:02
Speaker
and their potassium is eight.
01:11:04
Speaker
And I'm not seeing like peaked T waves.
01:11:06
Speaker
I'm seeing significant prolongations of the QRS complex, maybe even a sine wave.
01:11:13
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.
01:11:20
Speaker
So I may need to repeat that calcium.
01:11:23
Speaker
But in the interim, I'm going to also get that
01:11:27
Speaker
potassium out of the serum.
01:11:30
Speaker
And so I'm going to give those, give those patients bicarb.
01:11:34
Speaker
Typically I don't give pushes of bicarb.
01:11:37
Speaker
I usually start patients on a sodium bicarbonate drip, which is three amps of sodium bicarbonate in a liter of D five.
01:11:44
Speaker
So that's my preferential way of giving sodium bicarbonate in that patient population.
01:11:48
Speaker
Yeah.
01:11:49
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.
01:12:05
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.
01:12:22
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.
01:12:29
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.
01:12:41
Speaker
And so in that circumstance, I am administering sodium bicarbonate, this time in pushes, and
01:12:48
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.
01:13:03
Speaker
So those are the three times that I will administer sodium bicarbonate.
01:13:07
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,
01:13:16
Speaker
I will start them on insulin, start them on fluids.
01:13:20
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.
01:13:30
Speaker
And so I always make the one of my favorite statements is treat the patient, not the number.
01:13:36
Speaker
So I don't there's no blanket number for me for what their acidosis level is for me to start sodium bicarbonate.
01:13:43
Speaker
I will treat the patient, not the number.
01:13:46
Speaker
I agree, and I think it ties back to your comments on pathophysiology, right?
01:13:52
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?
01:13:59
Speaker
Right, and if you think about the equation...
01:14:01
Speaker
If you administer sodium bicarbonate, all you're doing is increasing the carbon dioxide that they now have to subsequently breathe off.
01:14:10
Speaker
And so these patients most of the time are maximally compensating from a respiratory perspective.
01:14:16
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.
01:14:27
Speaker
Perfect.
01:14:28
Speaker
So as we close the discussion on DKA, any specific comments on euglycemic DKA or DKA in pregnancy?
01:14:36
Speaker
Sure.
01:14:37
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.
01:14:45
Speaker
So these patients are euglycemic.
01:14:47
Speaker
And so I still preferentially treat them with
01:14:52
Speaker
IV fluids, insulin still monitor their potassium.
01:14:55
Speaker
But the other thing that I want to make sure that I'm doing is making sure that their glucose is not dropping.
01:15:00
Speaker
And the way that I do that, again, I do this a little controversially.
01:15:05
Speaker
This may make some people and rub them the wrong way.
01:15:07
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.
01:15:14
Speaker
My question is,
01:15:16
Speaker
Why?
01:15:17
Speaker
What is the reasoning for that?
01:15:20
Speaker
I care more about them going hypoglycemic than them going hyperglycemic.
01:15:26
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.
01:15:33
Speaker
We allow them to eat.
01:15:34
Speaker
And so I make the argument that if they want to eat, let them eat.
01:15:38
Speaker
And if they're capable of eating, you should let them eat.
01:15:40
Speaker
So I let my DKA patients eat, and that prevents them from going hypoglycemic.
01:15:46
Speaker
I give them nausea medicine to prevent vomiting because certainly we don't want them to aspirate.
01:15:51
Speaker
But give them food and allow them to eat because, again, we're trying to prevent them from going hypoglycemic.
01:15:57
Speaker
I especially do this with euglycemic DKA.
01:16:00
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.
01:16:13
Speaker
And so what that does is, again, it prevents them from going hypoglycemic, which is what we really worry about with euglycemic DKA.
01:16:21
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.
01:16:30
Speaker
So my preferential treatment is to start them on the dextrose drip with IV fluids, and
01:16:38
Speaker
concomitantly with the insulin infusion.
01:16:41
Speaker
And I let them eat while they're getting both.
01:16:44
Speaker
I actually check finger sticks.
01:16:46
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.
01:16:58
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.
01:17:09
Speaker
And then the next one's a finger stick and then the next one's a BMP and so on and so forth.
01:17:13
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...
01:17:27
Speaker
maintain euglycemia or a little bit of hyperglycemia.
01:17:31
Speaker
So if their sugar is 250, for instance, and I start the dextrose, the D10 drip at 125 milliliters per hour,
01:17:40
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
01:18:04
Speaker
Then I leave the dextrose drip alone and let them continue to get treated.
01:18:08
Speaker
Remembering that insulin is treating the ketoacidosis.
01:18:11
Speaker
I don't care about the sugar unless it gets low.
01:18:14
Speaker
So that's what I do for euglycemic DKA.
01:18:17
Speaker
Pregnancy is a difficult beast.
01:18:21
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.
01:18:28
Speaker
So you may need to even use a higher dose of insulin in this patient population.
01:18:34
Speaker
I have given...
01:18:36
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.
01:18:42
Speaker
Usually I go 0.15, and then subsequently, if that doesn't work, I may need to go to 0.2.
01:18:48
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.
01:18:57
Speaker
There have been circumstances where I've started patients on the insulin drip, seeing that sugar is continuing to either go up or
01:19:05
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.
01:19:13
Speaker
So there are really, really...
01:19:17
Speaker
difficult patient population to kind of deal with.
01:19:21
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.
01:19:36
Speaker
So I'm just a little bit careful with the pregnancy population.
01:19:39
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.
01:19:49
Speaker
So you don't want the baby to develop hypoglycemia because that obviously leads to worse outcomes.
01:19:56
Speaker
So you really want to avoid hypoglycemia in this patient population.
01:20:00
Speaker
So I tend to have a little bit of a higher threshold for their glucose.
01:20:05
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.
01:20:15
Speaker
I'd rather them be a little bit hyperglycemic compared to hypoglycemic.
01:20:19
Speaker
Perfect.
01:20:21
Speaker
No, and I think it's important to recognize, like you said, also the eucalycemic decay are increasing.
01:20:26
Speaker
So having that discussion, I think, is also an important refresher for all our audience.
01:20:33
Speaker
Absolutely.
01:20:33
Speaker
Could you tell us, George, in terms of like management of HHS, kind of your approach and contrasting what would be different?
01:20:40
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.
01:20:50
Speaker
Absolutely.
01:20:50
Speaker
So the big difference with HHS being again, as we alluded to earlier, is the sodium is much more important in this circumstance.
01:20:59
Speaker
A lot of people mistakenly think that glucose is the large thing that we're supposed to be monitoring.
01:21:07
Speaker
Glucose, again, I don't care about.
01:21:10
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.
01:21:21
Speaker
The thing to be monitoring here is the sodium.
01:21:24
Speaker
As we talked about before, these patients oftentimes have a sodium that is near normal on the lab.
01:21:31
Speaker
But if you correct the sodium, their sodium is actually going to be hypernatremic.
01:21:38
Speaker
So how do we correct sodium?
01:21:40
Speaker
So there's a formula that you can use.
01:21:42
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.
01:21:55
Speaker
And then there's another number that's 2.4 for every 100.
01:21:59
Speaker
This one's actually a little bit more physiologically accurate.
01:22:01
Speaker
What they did was they took
01:22:04
Speaker
They took people and gave them octreotide and turned their pancreas off and gave them a large bolus of glucose.
01:22:12
Speaker
And then they basically just checked their glucose and their sodium levels every 10 minutes to see what it was.
01:22:19
Speaker
And so that 2.4 for every 100 is actually a little bit more close to what's physiologically accurate.
01:22:26
Speaker
But I don't like doing advanced math in a pinch.
01:22:30
Speaker
I can, but I don't like to.
01:22:31
Speaker
And so what's right in between 1.6 and 2.4?
01:22:34
Speaker
Two.
01:22:36
Speaker
It's exactly right in between the two numbers.
01:22:38
Speaker
So I just use two.
01:22:39
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.
01:22:47
Speaker
Okay.
01:22:48
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.
01:22:59
Speaker
There's literally almost zero literature that talks about fluid choice in HHS.
01:23:05
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.
01:23:15
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
01:23:43
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.
01:23:54
Speaker
In the long run, probably not going to be super harmful in that circumstance.
01:24:01
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,
01:24:14
Speaker
LR would probably be significantly harmful and can certainly lead to those patients developing cerebral edema.
01:24:22
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.
01:24:30
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.
01:24:38
Speaker
I don't want to make them more hypernatremic.
01:24:40
Speaker
So then I will use plasmolyte in that circumstance.
01:24:45
Speaker
But that's the thing that we're actually going to be monitoring is their sodium levels.
01:24:49
Speaker
The reason why this is very important is because these patients are also going to be put on an insulin trip.
01:24:54
Speaker
However, I don't want to put them on a significantly high insulin.
01:25:01
Speaker
dosing for that insulin infusion because I don't want that corrected sodium to now become their true sodium.
01:25:08
Speaker
So if you think about it, if their true sodium is, let's just say one 30 and their sugar is 1600, right?
01:25:16
Speaker
So if you take those numbers two times 15, which is 30, so that patient's sodium is one 60.
01:25:24
Speaker
If I start them on an insulin infusion at 0.1 units per kilogram per hour, um,
01:25:30
Speaker
The next sugar, I might check in an hour because they may be, let's say they're insulin naive.
01:25:36
Speaker
Their next sugar might have dropped from 1600 to 1000.
01:25:40
Speaker
So it drops 600 points.
01:25:42
Speaker
Now, this is obviously, these are hypothetical situations.
01:25:45
Speaker
But now if I check their sodium and it's 150,
01:25:49
Speaker
Now I'm exposing that brain because now we have a significant problem with that sodium concentration.
01:25:56
Speaker
Now that brain is getting exposed to that 150 as opposed to that 130.
01:26:00
Speaker
So these patients, we certainly have to be careful about what their sodium levels are and their glucose levels.
01:26:06
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.
01:26:16
Speaker
I start them on 0.05 units per hour, units per kilogram per hour.
01:26:22
Speaker
And what that does is it slows the glucose dropping down.
01:26:28
Speaker
While they are continuing to get watered.
01:26:30
Speaker
I like to think about this as we're watering the brain a little bit.
01:26:34
Speaker
We're giving the water, giving the brain a little bit of water to allow it to rehydrate.
01:26:39
Speaker
Cause these patients can be anywhere between nine and 20 liters down.
01:26:43
Speaker
I need time for this to happen.
01:26:46
Speaker
If I just fix their glucose, which I can fix.
01:26:49
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.
01:26:56
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.
01:27:03
Speaker
I want to give their brain some time to get some of that water that I'm giving them with the IV fluids.
01:27:08
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.
01:27:31
Speaker
And I think as you mentioned earlier, George, right, it doesn't, people don't get into HHS in five hours.
01:27:38
Speaker
Right.
01:27:38
Speaker
But we shouldn't correct it in five hours.
01:27:40
Speaker
Exactly.
01:27:41
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.
01:27:48
Speaker
I think that's an important take home message.
01:27:51
Speaker
You mentioned, obviously, that a lot of these patients with DKA especially have goose mild breathing.
01:27:57
Speaker
Patients with HHS might have significant mental status changes.
01:28:01
Speaker
Could you just give us a couple comments on respiratory support for patients with hyperglycemic emergencies?
01:28:08
Speaker
Sure.
01:28:09
Speaker
So, DKA should scare you when you're thinking about ventilation and respiratory support.
01:28:17
Speaker
The
01:28:19
Speaker
The problems with DKA are that these patients have a respiratory compensation for their metabolic acidosis.
01:28:26
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
01:28:41
Speaker
continuous pH checker, we would actually watch their pH.
01:28:45
Speaker
It wouldn't slowly decline.
01:28:47
Speaker
These patients will have an exponential decline in their pH because they now have nothing that is compensating for their metabolic acidosis.
01:28:57
Speaker
So can you do non-invasive positive pressure ventilation?
01:29:01
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.
01:29:10
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.
01:29:15
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.
01:29:26
Speaker
which can actually help them with that Kussmaul respirations.
01:29:29
Speaker
You're not going to cause them to fix.
01:29:32
Speaker
You're not fixing them with this non-invasive positive pressure ventilation.
01:29:35
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.
01:29:46
Speaker
But the goal here is to allow them to do what they are doing for as long as they possibly can.
Respiratory Support in Severe Pneumonia
01:29:54
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.
01:30:04
Speaker
So for instance, they have an overwhelmingly large pneumonia or multi-lobar pneumonia that's caused them to become hypoxic.
01:30:11
Speaker
And I'm giving them oxygen.
01:30:13
Speaker
I'm putting them on high flow nasal cannula and their oxygen saturation is not improving or
01:30:21
Speaker
Their mental status is so uptunded that they're not protecting their airway.
01:30:25
Speaker
In this circumstance, you're not going to want to give them non-invasive positive pressure ventilation.
01:30:32
Speaker
If they're hypoxic, you can give them non-invasive positive pressure ventilation.
01:30:35
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.
01:30:42
Speaker
But I try to avoid intubating these patients at all costs if I can.
01:30:48
Speaker
If I cannot, then there's two preferential methods of ventilation that I do with these patients for intubation.
01:30:56
Speaker
The first is I do ketamine only intubation.
01:31:00
Speaker
So I don't want to take away their respiratory drive.
01:31:04
Speaker
So I will give them ketamine only.
01:31:05
Speaker
I'll give them some viscous lidocaine or I will give them some nebulized lidocaine to prevent.
01:31:13
Speaker
nebulize the airway to anesthetize the airway.
01:31:17
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.
01:31:27
Speaker
The second thing, if
01:31:29
Speaker
I'm really worried about them is I'll use something called VAPOX.
01:31:34
Speaker
And Scott Weingart talks about VAPOX, which is ventilator assisted pre-oxygenation.
01:31:39
Speaker
So I will use the ventilator with a non-invasive positive pressure ventilation mask to pre-oxygenate the patient.
01:31:49
Speaker
So put the BiPAP mask on or the CPAP mask on and put the patient on SIMV and
01:31:57
Speaker
give them a little bit of pressure support, give them a tidal volume, usually around 550.
01:32:01
Speaker
And then I will turn the respiratory rate down as low as I can.
01:32:07
Speaker
If I can make it to zero, great.
01:32:08
Speaker
If I have it at one, that's fine.
01:32:11
Speaker
But essentially the ventilator is just providing pressure support.
01:32:14
Speaker
So it's essentially like a non-invasive positive pressure ventilation.
01:32:18
Speaker
Then I will give them the RSI medications,
01:32:22
Speaker
So I'll give them the induction agent, I'll give them paralytic.
01:32:26
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.
01:32:41
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.
01:32:55
Speaker
And after about a minute and that paralytic has kicked in, then I will go ahead and intubate the patient.
01:33:02
Speaker
And what that does is it gives me a little bit of that respiratory compensation.
01:33:06
Speaker
Again, not enough.
01:33:07
Speaker
but gives me a little bit of that respiratory compensation to give me some time to,
01:33:12
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.
01:33:20
Speaker
So those are the two methods that I typically will use.
01:33:24
Speaker
I haven't had to use VAPOX a significant number of times because ketamine has worked very, very well for me.
01:33:31
Speaker
But the times when ketamine has failed, then I will preferentially try to use VAPOX if available.
DKA Management Strategies
01:33:39
Speaker
And as we mentioned earlier, the vast majority of patients we treat with decay especially don't need this type of support.
01:33:45
Speaker
Correct.
01:33:46
Speaker
But when they do, I think being overcautious and understanding what the underlying issues are is very important.
01:33:53
Speaker
So thanks for that excellent discussion.
01:33:56
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?
01:34:09
Speaker
Sure.
01:34:09
Speaker
So first and foremost, remember to look for the etiology.
01:34:15
Speaker
Think about those four eyes.
01:34:17
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.
01:34:27
Speaker
So think about those four eyes.
01:34:30
Speaker
Number two, pitfall is do not, do not, do not forget to give these patients fluids.
01:34:36
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.
01:34:49
Speaker
And then the last one is ventilatory support.
01:34:53
Speaker
Try not to do it.
01:34:54
Speaker
Don't just willy-nilly intubate these patients thinking that you have time.
01:34:58
Speaker
These patients are really sick.
01:35:00
Speaker
You should be intubating them with the thought processes.
01:35:03
Speaker
If I do this wrong, I will kill this person.
01:35:06
Speaker
So use VAPOX, use ketamine only.
01:35:10
Speaker
And if you can, you can use non-invasive positive pressure ventilation.
01:35:14
Speaker
Just make sure that you give these patients some...
01:35:18
Speaker
Some antiemetics to make sure that you're not going to miss anything from a pearls perspective.
01:35:23
Speaker
I still say if they want to eat cake, let them eat cake, give them some antiemetics.
01:35:28
Speaker
Remember, we don't want these patients to go hypoglycemic.
01:35:32
Speaker
So we want to make sure that they are maintaining their sugar a little bit greater than 200 to 250.
01:35:38
Speaker
And so I preferentially will allow them to eat.
01:35:42
Speaker
Same vein, number two, is monitor their potassium and use oral potassium to help replenish it.
01:35:49
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.
01:35:59
Speaker
And then the last pearl...
01:36:02
Speaker
is I think using your sodium to guide your management will actually lead to better outcomes for HHS patients.
01:36:10
Speaker
So remember to think about that when you're managing these patients appropriately.
01:36:14
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.
01:36:22
Speaker
I think those are my big pearls.
01:36:26
Speaker
Excellent.
Kintsugai and Personal Growth
01:36:27
Speaker
We like to close the podcast traditionally, George, with a couple of questions unrelated to the clinical topic.
01:36:33
Speaker
Would that be okay?
01:36:34
Speaker
Sure, of course.
01:36:35
Speaker
So the first question relates to books.
01:36:38
Speaker
Is there any book or books that have influenced you significantly or books that you have gifted often to other people?
01:36:45
Speaker
So my probably favorite book is...
01:36:51
Speaker
A book called Kintsugai.
01:36:53
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.
01:37:03
Speaker
Kintsugai is the concept of taking gilded taking pottery.
01:37:10
Speaker
that's shattered and repairing it with gilded gold.
01:37:14
Speaker
And this book actually talks about how kintsugai can be applied to our lives when you have some type of adverse outcome.
01:37:23
Speaker
So you may have had a really bad patient encounter,
01:37:28
Speaker
or you may have unfortunately even had a patient who died as a result of some significant medical error that you did.
01:37:35
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,
01:37:44
Speaker
I am the worst doctor in the world, so I'm just going to give up on medicine.
01:37:47
Speaker
Or unfortunately, especially in this time of COVID, we had people who did subsequently commit suicide, unfortunately.
01:37:56
Speaker
And it's sad because those medical errors are things, you know, to err is human.
01:38:04
Speaker
It's a thing that we're all going to deal with at some point in time in our life.
01:38:07
Speaker
And obviously the goal is to minimize errors and certainly not cause significant errors that cause harm.
01:38:12
Speaker
But
01:38:13
Speaker
It may happen to you.
01:38:15
Speaker
What happens afterwards is really what defines you as a person.
01:38:18
Speaker
And so what this concept of kintsugai is, is that you have this broken person.
01:38:26
Speaker
The art of kintsugai doesn't make it so that it is perfect.
01:38:31
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.
01:38:42
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.
01:38:55
Speaker
And so the Kintsugai concept is very similar to how you apply it to your life.
01:39:03
Speaker
You're not perfect, but now you are a better doctor as a result of this mistake.
01:39:10
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.
01:39:16
Speaker
What I'm trying to kind of relay with this is that when you look at yourself differently,
01:39:24
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?
01:39:31
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.
01:39:46
Speaker
So I have, I have applied Kintsugai on several occasions in my life.
01:39:51
Speaker
The book is by, um,
01:39:54
Speaker
Um, this, um, person named Celine Santini.
01:40:00
Speaker
Um, but it's, it's a wonderful book to read.
01:40:02
Speaker
I've given it out to a number of my mentees.
01:40:05
Speaker
Um, it's, it's a great concept to apply to life as well.
01:40:10
Speaker
Um, and, and one of the lectures that I do is called the success of failure.
01:40:15
Speaker
Um, and it applies this concept of Kintsugai, um, and how you grow from the mistakes that you make.
01:40:21
Speaker
Beautiful.
01:40:22
Speaker
I've heard the concept before.
01:40:23
Speaker
I think it's a Japanese pottery concept.
01:40:26
Speaker
Yep.
01:40:26
Speaker
And but I haven't heard of the book.
01:40:28
Speaker
So I definitely will put in the show notes and we'll check it out.
01:40:30
Speaker
Thanks for sharing that, George.
01:40:32
Speaker
Of course.
01:40:33
Speaker
The second question, could you share something you have changed your mind about over the last couple of years?
Parenting and Emotional Journeys
01:40:39
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.
01:40:50
Speaker
And I think I would prefer to do it from the life perspective.
01:40:53
Speaker
Um, this pertains to my kids, um, um,
01:40:57
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.
01:41:08
Speaker
And this is going to be a two part answer because it's I've actually changed my mind twice.
01:41:15
Speaker
So I I'm a I'm a child of I'm a fourth child.
01:41:22
Speaker
I'm a third out of four children of my parents.
01:41:25
Speaker
And so when I was growing up, I always knew I wanted to have kids.
01:41:28
Speaker
And I believe that I wanted to have kids.
01:41:32
Speaker
a million kids.
01:41:32
Speaker
I was like, I could have eight kids.
01:41:34
Speaker
This would be easy.
01:41:35
Speaker
This would be fine.
01:41:36
Speaker
And then we started having kids and then my mind changed.
01:41:39
Speaker
And I was like, this is way, way, way harder than I thought it was going to be.
01:41:44
Speaker
My kids are wonderful kids.
01:41:46
Speaker
Don't get me wrong.
01:41:49
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.
01:41:57
Speaker
And that was literally the hardest transition out of all of the kids.
01:42:01
Speaker
The three to four was super easy because at that point in time, it's just like, it doesn't matter anymore.
01:42:08
Speaker
The, but my mind changed again when, um,
01:42:13
Speaker
We actually put our first one in college, which we did this year, and he stays at home.
01:42:19
Speaker
His college is 15 minutes down the road.
01:42:21
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.
01:42:32
Speaker
It's really only hard because you make it hard.
01:42:35
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.
01:42:42
Speaker
But as as they've gotten older now.
01:42:46
Speaker
it's a lot easier.
01:42:47
Speaker
And now I miss it.
01:42:48
Speaker
I miss how young they were.
01:42:52
Speaker
And, and, you know, my daughter, I have two daughters now, one's nine and one's 11.
01:42:56
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.
01:43:05
Speaker
I miss those times now because life is short.
01:43:09
Speaker
Life is really, really short.
01:43:11
Speaker
Um, here I am now at 45 with, um,
01:43:14
Speaker
Four kids, one in college, one in every every type of school.
01:43:21
Speaker
And I am dreading the day when they're all gone.
01:43:25
Speaker
You know, me and my wife talk about it all the time.
01:43:27
Speaker
Oh, my gosh, we're going to be empty nesters in, you know, 10 years.
01:43:30
Speaker
And I'm like, no, no.
01:43:33
Speaker
I don't want to be empty nesters.
01:43:34
Speaker
I mean, I love you.
01:43:35
Speaker
You're my wife.
01:43:36
Speaker
I love you.
01:43:36
Speaker
And I can't wait to spend time with you, but I'm going to miss the kids when they're gone.
01:43:41
Speaker
And we're not going to see them as much.
01:43:43
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,
01:43:54
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...
01:44:05
Speaker
my kids and miss my sons.
01:44:07
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.
01:44:14
Speaker
Now I live far away.
01:44:15
Speaker
I just moved to Texas three years ago.
01:44:18
Speaker
Um, my parents live in West Virginia.
01:44:20
Speaker
And so to get, to get home to them is a lot harder than it was when I was in Maryland.
01:44:24
Speaker
So I'm less, I'm there less now, um,
01:44:28
Speaker
So now I'm just spending more money to go there more frequently.
01:44:32
Speaker
So that's that's how having kids has changed my life.
01:44:35
Speaker
And I've changed my mind over these past few years.
Faith in Critical Medical Situations
01:44:38
Speaker
For sure.
01:44:39
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.
01:44:46
Speaker
Oh, wow.
01:44:47
Speaker
It starts again.
01:44:48
Speaker
So the cycle, it starts again.
01:44:50
Speaker
And somehow I find the granddaughter more fun because you can always give her back to the parents.
01:44:57
Speaker
Yeah.
01:44:59
Speaker
Give them back.
01:45:00
Speaker
That's exactly right.
01:45:01
Speaker
That's awesome.
01:45:02
Speaker
So the last, if we could just close with a, what would you want every listener to know?
01:45:09
Speaker
It could be a quote, a fact, or just a departing thought.
01:45:13
Speaker
Oh, wow.
01:45:16
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
01:45:29
Speaker
globally.
01:45:29
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.
01:45:39
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.
01:45:50
Speaker
This is a quote from the Bible, Philippians 4.13.
01:45:54
Speaker
And what it allows me to do is to think about
01:45:59
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.
01:46:16
Speaker
I know that these are patients who are going to need my full attention.
01:46:20
Speaker
And if I'm distracted or if I am not feeling like I am at my best for whatever reason,
01:46:29
Speaker
It resets me to think no matter what's getting ready to happen in this room, God's got my back.
01:46:36
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.
01:46:44
Speaker
or to do this procedure and do it successfully without any complications.
01:46:48
Speaker
And by doing that, it allows me to reset my brain to calm down as much as I can.
01:46:55
Speaker
One of the things that I like to employ whenever I have a resuscitation is what I call the quiet room.
01:47:00
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.
01:47:11
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.
01:47:21
Speaker
So I say that before every single critical situation that I'm getting ready to put myself in.
01:47:26
Speaker
And they don't all have to be critical.
01:47:28
Speaker
Sometimes I even say it before I'm getting ready to put in like an ultrasound guided peripheral IV.
01:47:32
Speaker
I'll say, OK, I'm going to do this and say my little thing.
01:47:35
Speaker
I can do all things through Christ who strengthens me.
01:47:37
Speaker
And I'm usually able to get most things within the first try that it's usually not a problem.
01:47:42
Speaker
So I would say find that thing that gives you your zen, your moment of calm before you do anything else.
01:47:52
Speaker
And I promise you it will change the way that you look at those critical situations.
01:47:57
Speaker
Beautiful.
01:47:58
Speaker
I think George is the perfect place to stop.
01:48:01
Speaker
I appreciate your willingness to share your expertise and your enthusiasm for endocrine emergencies with our audience.
01:48:10
Speaker
Look forward to having you back on the podcast soon and to see you in person.
01:48:15
Speaker
Sergio, as always, it was a pleasure.
01:48:17
Speaker
Thank you for having me on and I look forward to next time.
01:48:20
Speaker
Thank you for listening to Critical Matters, a sound podcast.
01:48:24
Speaker
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01:48:30
Speaker
Sound's transforming the way critical care is provided in hospitals across the country.
01:48:34
Speaker
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