Let’s Talk LMCC
Diabetes Mellitus

S01E02

Susan Wang, Meryem Talbo, Alice Cheng, Katherine Lan, Esther Kang for the McGill Journal of Medicine1
Published online: May 5, 2023

1McGill University
mjm.med@mcgill.ca

Abstract

Welcome to the McGill Journal of Medicine (MJM) LMCC review. This podcast series was created to aid medical students studying for the Canadian Medical Council’s licensing exam. Each episode is created based on specific LMCC objectives and is divided into 2 parts. In part one we provide an overview of the topic with the help of experts in the field, followed by Part 2 where we review LMCC styled questions to help consolidate knowledge. In this episode, we welcome our expert advisor, Dr. Alice Cheng, Endocrinologist and Associate Professor at the University of Toronto to speak on LMCC Objective 37-2: Diabetes Mellitus. This episode was written by Susan Wang & Dr. Alice Cheng, edited by Esther Kang, Meryem Talbo and Katherine Lan. Please see our website www.mjmmed.com for more information, including a link to show notes.

     

Content overview

0:00 Introduction;

0:36 Episode overview;

0:57 Part 1: Overview of concepts;

2:15 Screening and presentation of complications of diabetes - macrovascular complications, microvascular complications, and neuropathies;

12:47 Glycemic control;

15:44 Glycemic-related emergencies in diabetes mellitus;

16:06 Acute hypoglycemia;

17:55 Hyperglycemic emergencies:diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS);

25:11 ABCDESSS of diabetes management;

28:24 Part 2: sample LMCC questions:Type 1 and Type 2 management, differentiating DKA vs HHS and their management;

37:00 Outro;

Glossary

Links and papers

Transcript

0:00 Esther Kang (EK): Welcome back to the MJM LMCC review. My name is Esther Kang and I'm excited to introduce the second episode in this new podcast series that was created to aid medical students studying for the Canadian licensing exam. Each episode is created based on specific LMCC objectives and is divided into 2 parts. In part one we provide an overview of the topic with the help of experts in the field, followed by Part 2 where we review LMCC styled questions to help consolidate knowledge. Here's Diabetes Part 2 with their host Susan Wang and our expert advisor, Doctor Alice Cheng.

0:36 Susan Wang (SW): Thank you Esther. This podcast is divided into 2 parts. First, we will do a quick overview of concepts and definitions, followed by Q&A with Dr. Cheng to go over example MCCQE Part I questions. Welcome back, Dr Cheng, to our podcast.

Dr Alice Cheng (AC): Thank you very much, Susan, it’s a pleasure to be back.

0:57 SW: So we’ve gone over the definition of Diabetes, its subtypes and some diagnostic criteria. Due to its prevalence, diabetes is often seen as a “bread and butter” disease that everybody gets at some point, but it is in fact quite an invasive systemic disease. What makes diabetes so scary?

Dr. C: So first of all, I’m not sure I would use the word “scary”, because I think that it’s important that we all get comfortable with diabetes and- and know the basics about it, because regardless of what specialty you’re in, you will undoubtedly encounter individuals living with diabetes. However, we have fantastic treatments now, for diabetes, so it really does not need to be “scary”. However if diabetes is not appropriately managed, then it is associated with complications and those complications can impact microvascular and macrovascular systems. So yes, there are definitely very real potential complications of diabetes, but on a very positive side, we have excellent therapies and management tools now, so it does not need to be scary, for sure.

SW: Well that’s very reassuring to know that we have great therapies now that can help to manage diabetes. So, that being said, what are the most typical presentations of diabetes-related vasculopathies?

2:15 AC: So when we think about diabetes complications, we tend to divide them into microvascular and macrovascular complications. So let’s start off with the macrovascular. So as the name would suggest, these are typically large vessels. So we’re talking about heart, we’re talking about peripheral arterial disease, and we’re talking about brain cerebrovascular disease. So, brain, heart, legs, I guess. And in terms of what typically presents, from a heart perspective, interestingly the most common presentation is actually heart failure, which is not something that we often think about, it’s not something that we talked a lot about before. We used to mostly emphasize myocardial infarctions and atherosclerotic cardiovascular disease, which is definitely increased in those living with diabetes, but we now also know that heart failure, be it with preserved or reduced ejection fraction, is also much more common in those living with diabetes. And then, if we go to the brain, then obviously we’re talking about stroke, or TIAs (or transient ischemic attacks). And then if we’re talking about legs, or the peripheral arterial system, then we’re talking about things like intermittent claudication, or if it gets worse, more severe, acute blocks that can occur in the peripheral arterial system And which could then ultimately lead to things like amputation. So, large vessel disease is a very real potential complication of diabetes, hence it’s critical that we do everything that we can to reduce that risk, and we’ll talk about that later as we talk about management, but it’s also important that we screen for it. So how do we screen for it? Like with everything else:history, physical, and tests. So history is knowing to ask about questions such as:“Do you have chest pain?”, “Do you have shortness of breath?”, “Any reductions in your exercise tolerance?”, “Any pain in your legs when you’re walking?”, “Any sudden onset of weakness or loss of sensation on one side or the other?”. So make sure that we screen for it on history. And then physical exam, obviously listening for bruits, examining for any neurologic deficits, checking for pulses, etc. And then from a test perspective, the recommended screening test would be a resting ECG, at 3-5 year intervals for those over the age of 40 with diabetes, or long duration, or any evidence of end organ damage, or anybody that you’re worried about, really. Then you would do an ECG. And then if symptoms or signs would suggest potential atherosclerotic disease, then you would go on to more sophisticated testing, such as stress testing, or echocardiogram, or even pro-BNPs if you’re worried about heart failure. So therefore, your testing would then be directed by the findings from your history and physical.

5:15 SW: So now we’ve discussed macrovascular complications. What about the smaller vessels?

AC: So if we’re thinking about microvascular complications of diabetes, we’re thinking about eyes, we’re thinking about kidneys, and we are also thinking about the nerves. So let’s talk about the eyes first. So the diabetic retinopathy is probably the most diabetes-specific complication that we have, and interestingly, the diagnosis of diabetes, the glucose diagnostic criteria, are actually based on the increased risk of retinopathy. And the reason is because the other -opathies, like nephropathy, for example, could be caused by other things, but diabetic retinopathy is very specific to elevated glucose. People develop diabetic retinopathy with longstanding hyperglycemia and it can present as macular edema, or non-proliferative, or as it progresses, proliferative diabetic retinopathy, retinal capillary nonperfusion, and things that could ultimately lead to blindness. Now, the good news is that these days, blindness secondary to diabetes is far, far less common. Decades and decades ago, if you went to a diabetes clinic, you would definitely see people sitting in the waiting room who would be using the white cane, indicating that they’d lost vision. Nowadays, it’s actually very uncommon to actually see that in a typical waiting room. So again, very good news. And why is it that that has happened? It’s because we know that controlling blood sugars well, early, and consistently, will significantly reduce the risk of retinopathy. We also know that routine screening is critical. So it’s critical that people living with diabetes be seen by an eye care professional, for a dilated eye exam, at diagnosis for type 2 diabetes, and then 1-2 year intervals thereafter. In the case of type 1 diabetes, usually within 5 years after diagnosis, or if they’re diagnosed as a kid, then post-pubertal. And again, 1-2 year frequencies. So, screening for it is critical, and then of course preventing it. And sometimes I got patients asking me, well why do I have to go see the eye doctor? I see fine. And my answer is, by the time you don’t see fine, we’ve missed the boat. So therefore, screening is absolutely critical for retinopathy. On the kidney side of things, so diabetic nephropathy, or as we actually now more precisely call it, is chronic kidney disease in diabetes, it is very common. And it is diagnosed, or the criteria used is a reduced eGFR or estimated glomerular filtration rate (kidney function) below 60 and/or an elevated albumin-creatinine ratio which, an ACR, of greater than 2. And the reason why there’s 2 pieces to the puzzle is that the eGFR tells you about the function of the kidney, the ACR tells you about damage to the kidney. And either one being off is a problem. So therefore, the testing for it needs to be both. People need to have their eGFR, a blood test, based on the serum creatinine, on an annual basis, and they also need to have their urine tested for albumin creatinine ratio on an annual basis. So it’s an eGFR blood test annually and a urine ACR annually in order to determine if they have chronic kidney disease in diabetes. Now there’s certain risk factors that put people at higher risk, so, if you’ve had diabetes for longer, if you’ve had higher blood sugars for longer, if you also have high blood pressure, smoking, dyslipidemia, all of those things could increase your risk for developing CKD. But again, the very good news is we’ve got fantastic treatments to help prevent or help reduce the risk of developing and then obviously the earlier we screen and identify people, the better chances of us intervening and doing good things.

9:24 SW: You also mentioned that neuropathies are a common complication of diabetes. Can you speak a little bit more on that?

AC: Sure. So the other complication that we typically define as microvascular, although that’s a little more grey-zone, is neuropathy, or nerve damage from diabetes. And that one is associated with longstanding hyperglycemia, although it’s not just elevated blood sugars, because neuropathy is a tricky one. That one can sometimes present before the diabetes diagnosis is even made, so there are other contributors to neuropathy. But the neuropathy, the classic one, is a distal symmetric polyneuropathy, so the classic one would be, these are your longest nerves, the ones to your toes, so it’s numbness and tingling in the feet - would be by far the most common. It’s a sensory neuropathy. If it's a small fibre neuropathy, you could have shooting, sharp pain, or burning sensation. If it’s a large fibre neuropathy, then it could be, again, numbness/tingling, loss of protective sensation, and you can imagine that if you have that loss of protective sensation, then you’re at risk of injuring yourself, so you know, we’ve all done this. We bought a new pair of shoes, we wore them for the first day, and we develop a blister. Now if you had diabetic neuropathy, you would not feel that blister, it would not hurt, and you could keep walking and keep using those shoes, and then you can imagine that a lot of damage could get done before you actually notice there’s a problem. It’s not uncommon that the patient says the story of “oh, I didn’t notice there was a problem until I saw blood in my shoe”. So that’s because they couldn’t feel the damage that was being done. Now that can then lead to infection, ulceration, and ultimately, amputation. Another kind of neuropathy, though, that people can get, is autonomic neuropathy, which would be of the autonomic system. So it could be things like bladder dysfunction, it could be things like bowel dysfunction, it could also be things like postural hypotension, postural dizziness, because they’re unable to sort of fix the autonomic system. And one of the more common autonomic ones, unfortunately, is gastroparesis, where the stomach fails to empty properly, and then people can get a lot of nausea/vomiting because the food just stays there and does not go down the system like it’s supposed to. Much less common would be things like cardiac autonomic neuropathy, where people can get resting tachycardia and heart rate variability. So what do we do about neuropathy? We do think that glycemic control can impact neuropathy, although that association is not as clear-cut as it is with the other micro- and macrovascular complications. History, physical exam, right? So, asking the right questions on history:do you get numbness/tingling/pain/burning in your feet? And then of course the other symptoms of the other neuropathies. Physical exam, examining people’s feet, at least on an annual basis. I typically do it at every visit. And then also, screening with a monofilament on the feet to determine if they can sense 10g of pressure, which is what the typical monofilament can apply, and if they fail to feel it, then that’s bad, then that means that they’re at high risk of developing ulceration and we need to be very careful about counseling for foot care.

12:47 SW: Given that these most long-term complications are tightly related to persistent hyperglycemia, I guess it’s pretty obvious that the main objective of diabetes management is then glycemic control. We’ve gone over some screening and follow-up for the specific complications, but what are the recommendations for glycemic monitoring?

AC: So controlling blood sugars is absolutely critical in diabetes management. But as we’ll talk about later, it’s not the only thing in diabetes management. But it is a critical component. So in order to do that, you gotta know what the blood sugars are, right? So what are we gonna follow? The A1C, which is a blood test, is still the most commonly used form of glycemic monitoring to give us an assessment of the level of control. And that’s typically done every 3 months, and if things are going well, then one could do it every 6 months. But that’s very infrequent, and it’s helpful for the person living with diabetes to know what their sugars are doing right now, so that they can make decisions about food, activity, etc. And that’s where self-monitoring of blood glucose can come in, so you can either do it with classic SMBG, self-monitoring, which is the finger poke and then a drop of blood on a test strip attached to a meter, which then gives you the sugar. The alternative is to measure glucose through different body fluid compartment, which would be the interstitial fluid, and then that would be a form of continuous glucose measurement, where someone wears a sensor on their skin, there’s a small filament that’s embedded in the interstitial fluid, and it’s constantly measuring the interstitial fluid glucose, and then sending that information to a device of some sort, or you can extract the information with a device through scanning. So those are sort of the most popular ways of measuring glucose, either self-monitoring blood glucose with a finger stick or wearing a sensor to get a continuous glucose measurement of the interstitial fluid. The frequency of the finger stick, of the SMBG, depends on what treatment you’re on. If you’re on insulin, you’re going to poke your finger more often, because you’re going to make decisions about the insulin based on the values. If you’re on drugs that can cause hypoglycemia, you’re going to test more often, but if you’re on drugs that do not cause hypoglycemia, you might only test once a week, because it’s more for information on other things. So the frequency of testing is very much dependent on the type of treatment. And then finally, there’s also ketone testing, which is not for everyone. Ketone testing would really be isolated to those living with type 1 diabetes and only to be used when they’re not feeling well. So it’s really to catch diabetic ketoacidosis, should that occur, so that they can take action earlier.

15:44 SW: Thank you, Dr Cheng, for going over the complications of diabetes and blood glucose monitoring. So now, what happens if there is an acute, extreme swing in blood glucose levels in someone with diabetes?

16:06 AC: So when we think about glycemic related emergencies in diabetes, we think about either acute hypoglycemia, low blood sugar, or we think about diabetic emergencies of hyperglycemia. So if we start off with hypoglycemia, acute hypoglycemia, that would be defined as Whipple’s triad in terms of the definition of hypo, so having symptoms of hypoglycemia, especially neuroglycopenic, having an actual low blood glucose and then responding to the administration of carbohydrates. Now, the levels of hypoglycemia are defined as mild, moderate or severe. And it’s severe hypoglycemia that’s probably the most worrisome. Severe hypoglycemia is defined as requiring third party assistance. So you’re so low that you cannot help yourself. You cannot treat yourself. And when there’s severe hypoglycemia, then there’s obviously a risk of seizure/loss of consciousness, because you’re not able to help yourself. Most important thing to do there is to avoid it from happening in the first place, which then, thinking about the treatments that are being offered, the kind of monitoring that’s being offered, and then of course, a lot of education for the individual, of recognizing symptoms and treating it as early as possible. If someone does in fact have severe hypoglycemia and requires assistance, if they’re awake and alert, then you can just give them juice, or dextrose tabs or glucose tabs, about 20 grams, to raise that glucose. However, if they’re unconscious, then you cannot give them anything orally, then that’s where glucagon administration would make sense, which now exists either as an IM injection, intramuscular injection, or as a nasal spray. So that’s on the acute hypoglycemia side of things.

17:55: On the high blood sugar side of things, the diabetic emergencies there, would be considered, would be either diabetic ketoacidosis, DKA, or hyperosmolar hyperglycemic state, known as HHS. Now both of these are medical emergencies, both of these are hyperglycemic emergencies. Diabetic ketoacidosis or DKA is typically seen in type 1 diabetes, and is a function of missing insulin with excess glucagon, which then results in the body making excess ketones in an attempt to find a fuel that works, and then with that, a lot of acid, and then people can get super sick. Hyperosmolar hyperglycemic state is a different scenario whereby there is such marked hyperglycemia that the person becomes extremely dehydrated and has too much, their blood becomes too thick, essentially, and then that can result in decreased level of consciousness, etc. So they don’t have an acid-base problem, they usually still got lots of insulin floating around, but the problem is their extreme marked hyperglycemia, dehydration, and then their kidneys shutdown, and that worsens the hyperglycemia. So these two are different causes of the hyperglycemic emergencies, but they share certain features. So if we think about the features that they share, it would be profound volume depletion. In both scenarios, people are extremely dry. So, giving fluids is critical in the management of DKA as well as HHS. The other thing is, both of these things usually have a trigger, and that trigger is usually some sort of acute illness, whether that’s an acute infection, or a cardiovascular event, or trauma of some sort, surgery… so there’s usually some sort of acute triggering event to allow the cascade to occur. And in both cases they present with marked hyperglycemia, really high blood sugars. So those are some of the similarities that they may present with, as well as a decreased level of consciousness, and nausea/vomiting, just feeling really, really lousy. However, the treatments of them are gonna be quite different. And to differentiate between DKA and HHS, in the case of DKA, because of the excess ketones and with them acid, the hallmark of DKA is an acidosis, a ketoacidosis. So they have a low pH, a low bicarb, an elevated anion gap, and also the presence of ketones. So low pH, low bicarb, high anion gap, as well as elevated ketones. That’s DKA. In the case of HHS, remember they’re still making insulin, so they don’t have ketones, they do not have an elevated anion gap, but they have very high blood sugars and their plasma osmolality is very high, greater than 320. And usually their kidneys are also not doing well because of profound volume contraction. Now the treatment of them are different. In both cases though, you’re going to give lots of fluids, because they’re so incredibly dry. In the case of :DKA though, their main problem is missing insulin, so you need to give them insulin in order to stop the ketone production. The other critical piece of treatment though is that you need to replace electrolytes, because during the time that they’ve been sick, they’ve been peeing, peeing, peeing, and usually losing lots of electrolytes in that process, and therefore you also need to replenish those electrolytes. In the case of HHS, they’re incredibly dry, so they need lots and lots of fluids, and often with the fluids, the kidneys wake up again, and then the kidneys will start to flush out the extra sugar. So they often do not require insulin, in the case of HHS. They just need lots and lots of fluids, and of course treatment of the underlying disorder.

SW: So we spoke about the generalities of management in both of these hyperglycemic emergencies. Are there any particular points that differentiate them, or that are really important to know for the management of DKA and HHS?

AC: So in the case of DKA, I already mentioned that it’s critical to replace fluids and it’s critical to give insulin, because that’s what's going to stop the ketone production, but the other piece that’s actually critical and if we think about what causes death, potentially, in people with DKA, and really no one should die of DKA anymore, and when it happens, it’s an electrolyte issue, because leading up to them showing up in hospital, they are even profoundly volume depleted, and they are usually very potassium depleted as well. However, their initial blood tests does not reflect that. Because they’re missing insulin, their potassium has actually shifted into the plasma, into the blood, so their serum potassium may actually look OK, when you measure it initially. But their total body potassium is super low. And once you give insulin therapy, which they need, the ketone production will stop, but then they’ll also start shifting the potassium back into the cells, which will then dramatically drop their plasma potassium, their blood potassium. So it’s absolutely critical to initiate potassium replacement early in the treatment of DKA, and it’s usually when you start the insulin infusion, you need to be starting potassium supplementation if the serum potassium is less than 5 or 5.5. Now normally 5 or 5.5 is on the higher end, so you’re thinking, why would I want to give potassium when their potassium is on the higher end? Well that’s because you’re giving insulin which will then shift the blood potassium into their cells, and remember their total body potassium is low, so it’s critical that you do that. So that part is really critical for preventing a completely preventable arrhythmia and potentially death. So fluids, yes, insulin, of course, but don’t forget about potassium, because that part is absolutely critical. On the HSS side, it’s all about fluids, fluids, fluids. Insulin is optional, but it’s critical on the HHS side to figure out why that developed in the first place. Because mortality, for people present with hyperosmolar hyperglycemic state is actually very high. But it’s high, not so much because of the HHS, it’s high because of the underlying cause of the HHS, which is often severe infection, or cardiovascular event. So it’s critical to actually identify the trigger point when it comes to HHS.

25:11 SW: So how do we manage diabetes to prevent these complications and emergencies from happening in the first place?

AC: The great news, and I alluded to this earlier, is that now, if one is diagnosed with diabetes or living with diabetes, we’ve got fantastic treatments, and we have a very good understanding of how to minimize the risk of developing complications of diabetes and then with that also potential emergencies of diabetes. And that’s with a multifactorial approach. So as I said earlier, treating sugar is important but it’s not the only thing. We now want to approach it with the ABCDESSS of diabetes management.

A is for A1C, so therefore, control the sugar

B is for blood pressure, control the blood pressure, typically <130/80.

C is for cholesterol, typically an LDL <2.0

D is for drugs to protect the heart, which I’ll come back to,

E is for exercise/eating

S is for smoking cessation, and then if we tack on a couple more,

S, which is for screening for complications and

S, self-management,

Then we’ve got the full checklist for what to do every time we see someone living with diabetes, so that we ensure we accomplish all of that multifactorial approach. Now there’s a fantastic study called the STENO-2 study, which is an older study now, but that clearly demonstrated that this approach will not just reduce complications but save lives. So it is critical that we think about this multifactorial approach. Now, if we flip back to the drugs to protect the heart, what am I talking about? I’m talking about ACE inhibitors or ARBs for heart and kidney protection, statins for heart and brain protection, aspirin, if they’re secondary prevention patients for, I guess, heart and brain protection, and then GLP-1 receptor agonists or SGLT-2 inhibitors for heart, kidney and brain protection. And these medications are to be used regardless of their original reasons for existence. So regardless of the blood pressure, regardless of the LDL, regardless of the A1C, we are to use these organ-protecting therapies, in the right patients, in order to do just that, provide organ protection. And as a bonus, it’s also going to help the blood pressure, the lipids, the A1C, etc, etc. So this multifactorial approach is absolutely critical to help prevent complications. DES’s, there was also the E part, which was exercise and eating, so what that’s referring to is the importance of learning about proper dietary choices as well as the importance of physical activity. There’s also the S, which is self-management, which also then emphasizes the importance of a multidisciplinary approach to diabetes management, and therefore involving colleagues, from our dietitian colleagues, our nursing colleagues, our other colleagues to also help educate the patients, so another critical piece to the management of diabetes.

28:24 SW: Thank you so much Dr Cheng, for going over the complications and emergencies in diabetes with us. Now we will go over some sample LMCC questions. A 21 year-old previously healthy man presents to your office with polyuria, polydipsia, weight loss, ongoing for the last several months. He is overweight but has lost about 10 lbs over the last few months. His blood pressure is 121/79. A fasting blood glucose reveals a value of 18.2 mmol/L, and LDL-c of 1.9 mmol/L. Blood work is positive for anti-glutamic acid decarboxylase with undetectable C-peptide levels. Nobody in his family has diabetes of any kind. What is the first line therapy in this individual?

a. Sulfonylurea

b. Lifestyle intervention according to Diabetes Canada Guidelines, follow up in 3 months

c. Insulin therapy

d. Metformin

e. Glucagon injections

AC: So in this case, the red flags are his hyperglycemic symptoms, polyuria/polydipsia, but the biggest red flag is the weight loss. So weight loss to me means that there is a catabolic state that’s happening, and I am worried about insulin deficiency. Absolute insulin deficiency, causing this unintentional weight loss. Now of course, his blood sugar is high, and then on top of that, he has positive anti-GAD antibodies and an undetectable C-peptide… All of this put together favors very much a type 1 diabetes diagnosis, where he’s missing insulin. So in someone who’s missing insulin, the critical treatment, without question, is starting insulin. Should he also have lifestyle intervention? Of course. This would be simultaneous. However, what’s going to avoid him going into hospital and getting sicker is going to be insulin. So replace the insulin that his pancreas is no longer making, whilst at the same time, referring him for diabetes education to get all of the other stuff that needs to happen. But this gentleman has type 1 diabetes, and absolutely must be started on insulin therapy right away.

30:38 SW: For the next question, we have a 45 year-old lady who presents to your office with polyuria and polydipsia ongoing for the last several months, also. Her BMI is 29.6 kg/m2. Her blood pressure is 150/80. A fasting blood glucose reveals a value of 14.2 mmol/L, and she has an LDL-c of 2.5 mmol/L. Her blood work is negative for anti-GAD with a high C-peptide level. Her family history is positive for a mother with type 2 diabetes. What is your first step in management?

a. Prescribe a statin

b. Prescribe an ACE inhibitor or ARB

c. Prescribe metformin

d. Involve a multi-disciplinary team for counseling on diet, physical therapy, and self-management

e. All of the above

AC: So in this woman, yes she has hyperglycemia, but she is presenting with an elevated BMI, elevated sugar, a negative anti-GAD, high C-peptide meaning high insulin levels, and a family history of type 2 diabetes, so it really is in keeping with a type 2 diabetes diagnosis. So for her, the ABCDES approach is critical to think about, therefore I would actually do E, all the above. And the reason is because she’s age over 40, and she therefore deserves a statin, her blood pressure is elevated, therefore deserves the ACE or ARB, the metformin is to help address her hyperglycemia, and of course involving the multidisciplinary team is critical to help with the E part, the exercise, eating and just understanding her diabetes. So, for her, I would say E, all of the above.

32:20 SW: The next question involves a 44 year-old man with type 2 diabetes. He presents to the ER with a decreased level of consciousness and some tonic-clonic movements. He had sick contact at home and developed a cough and fever 2 days ago. He is very hypotensive, tachypneic, and does not respond appropriately to your questions. His capillary refill is >3 seconds. His blood work shows plasma osmolality 326 mmol/kg, blood glucose of 40 mmol/L, pH 7.42, bicarbonate 22 mmol/L, and an anion gap of 8 mmol/L. What is his diagnosis?

a. Acute hypoglycemia

b. Diabetic ketoacidosis

c. Hyperosmolar hyperglycemic state

d. Hypovolemic shock

AC: So in this individual, he’s obviously presenting very sick. You’ll notice the marked hyperglycemia as well as the hyperosmolar state, and the lack of an acidosis. So therefore, to me, the answer is C, hyperosmolar hyperglycemic state, for the very reasons that I just said. He’s hyperosmolar, he’s hyperglycemic, and he does not have DKA because he does not have acidosis. So he has HHS.

33:38 SW: Our last case presents a 44 year-old man living with type 1 diabetes. He presents to the ER with a decreased level of consciousness nausea, vomiting and abdominal pain. He had sick contact at work and developed a cough and fever 2 days ago. He is mildly hypotensive, tachycardic, tachypneic, but he responds to your questions appropriately. His capillary refill is <3 seconds. Blood work shows plasma osmolality 318 mmol/kg, blood glucose of 28 mmol/L, pH 7.2, bicarbonate 11 mmol/L, anion gap of 14 mmol/L, and potassium of 4.8 mmol/L. What is the first step in his management?

a. Give insulin at 0.1 U/kg/h until plasma glucose is 8 mmol/L.

b. Give KCl 40 mEq PO x 1

c. Give sodium bicarbonate 50 mmol IV x 1

d. Give IV NS at 500 cc/hour for 4 hours, then 250 cc/hour for 4 hours, then as required.

e. Give insulin at 0.1 U/kg/h until plasma glucose is 14 mmol/L.

AC: So this patient is presenting with diabetic ketoacidosis. He lives with type 1 diabetes, he has a classic presentation, most importantly though, he has evidence of acidosis and it’s an anion gap metabolic acidosis. Presumably he also has positive ketones, so he has DKA. So in this case, I think the correct answer based on the stem is to start by giving fluids, but at the same time, I would say that it’s critical we also initiate insulin therapy to actually stop the ketone production, and to also administer potassium, because the insulin therapy will shift the potassium from his blood into his cells, and make him profoundly hypokalemic, which of course puts him at risk of an arrhythmia. So I think that the correct initial treatment is fluid resuscitation, but very quickly thereafter, it would also include insulin and potassium replacement as well.

35:48 SW: Thank you Dr Cheng. So, here’s our last question:two patients are admitted with very similar symptoms but different concerns. One has DKA and the other HHS, how would you proceed to distinguish the two and what clinical signs or symptoms will help you make the appropriate diagnosis and treatment?

AC: So I think the thing would be the kind of diabetes that the person has to begin with, the other differentiator would be the presence of absence of acidosis,the presence or absence of ketones, and the, well the level of hyperglycemia would be the same, so it really would be those three main differentiators, would be the diagnosis of diabetes, type 1 or type 2, ketones, acidosis, I guess anion gap would be part of that picture, would really help make that differentiation.

SW: Great, thank you so much, Dr. Cheng, for joining us in our first episodes of the LMCC series. To learn more about Dr. Cheng, see the episode description, where you will also find more information on different definitions and additional resources related to the topics covered in this episode.

AC: Thank you very much for having me Susan, this was great.

37:00 EK: We hope you enjoyed this episode. For details about the LMCC objectives, diabetes resources, and information about our expert advisor, Dr Cheng, please check out the episode descriptions below. As this is a podcast made in the spirit of learning, we would love to hear your feedback. Let us know what you think about our episodes by sending us an email at mcgilljmed.podcast@gmail.com. And stay tuned for our next episode, on Medical Law and Ethics with Dr Carolyn Ells.



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