[Music] all right welcome back you guys to the fourth lesson in our series on the endocrine system and in this lesson we're gonna be talking about the differences between DKA and HHS and for those of you who don't know my name is Eddie Watson and this is ICU advantage if this is your first time to our channel and watching one of our videos and you'd be interested in more in depth critical care educational content such as this then we invite you to subscribe to our channel below make sure when you do you hit that Bell icon that way you'll be notified as soon as our new lessons become available as always I truly value the subscriptions the likes and the comments that you guys leave as they really go a long way to help support our channel and for that I do want to thank you guys alright so with that said let's go ahead and begin the lesson and let's start to talk about DKA and HHS and really DKA diabetic ketoacidosis and HHS which is hyperosmolar hyperglycemic State they're really both hyperglycemic emergencies that are similar in some sense but are also quite different from one another they essentially are both states of an acute hyperglycaemia in decompensated diabetic patients and what's really important for us to know is that they require quick intervention and close monitoring typically in the ICU we're gonna cover quite a bit of information here but hopefully at the end of this lesson you'll have a really good understanding of what each of these are as well as how we're gonna take care of these patients and so with that said let's go ahead and start right off with diabetic ketoacidosis so our first distinction when we talk about DKA is that this is going to occur almost primarily with type 1 diabetics now it can happen but it is pretty rare for it to occur in our type 2 diabetics and so our DKA is really defined as hyperglycemia hypovolemia ketone emia anion gap metabolic acidosis so I know that was a mouthful and we definitely will get into explaining that more here and just a bit but this is really our definition of what DK is but there really are some key characteristics that we're going to be looking for and identifying these patients with DKA the first of these is going to be a glucose level greater than 300 milligrams per deciliter we're also gonna see a bicarb that's less than 15 mil equivalents per liter although in moderate DKA we could see this less than 10 and in severe DK that can even be less than 5 we're also gonna see our patients with a pH that's less than 7.3 although once again for moderate DK this can be less than 7.2 and in severe DKA we're gonna often see this less than 7.1 and finally our patients are gonna have ketone emia & ketonuria present and what this means is that we're gonna see ketones in the blood and ketones in the urine so now that we know what these defining characteristics are let's talk about some of the causes for DK and the first and primary one that I want to talk about is really our patients who are newly diagnosed with type 1 diabetes and oftentimes that's how these patients are first diagnosed by having some sort of event that leads them into DKA other causes could also be things like insufficient administration of insulin as well as stressful events also things like infection trauma surgery or even pregnancy and alcohol intoxication can all lead our patients into decay and so what is it about these causes that leads our patient into the state of decay in order to really tell you about that we're gonna have to talk about the patho that goes into this so as we talk about the patho for this it's important to know that this can develop in less than 24 hours so oftentimes this DKA will develop very quickly in these patients so it's gonna be initiated by having either insufficient or absent levels of insulin and as a result of this glucose is not going to be able to be brought into their cells and as a result of this we're gonna see a couple things happen we're gonna see an increase in our fatty acid metabolism and as a result of this this is where we're gonna see our ketones we're also gonna see an increase in our liver gluconeogenesis and this is where we're gonna get glucose from our proteins and amino acids and so we're also gonna see the secretion of our counter regulatory hormones glucagon and the stress hormones and these stress hormones like we've talked about before those catecholamines the cortisol and growth hormone these are all released as a result of stress and what they do is they actually will decrease the effect of insulin and being able to lower our glucose levels but the important thing to know here is that our body is going to have more and more of this glucose in our blood but the cells are going to be deprived of glucose at the cellular level and so this is where we're gonna see the effects of these within our pathophysiology and we can organize this into two main components first we are going to see a fluid volume deficit with an electrolyte imbalance and we're also going to see an acid-base imbalance in our patients so first let's talk about this fluid volume deficit and this electrolyte imbalance so we know that due to the lack of insulin our glucose levels are going to be high in the blood and like we just talked about due to the stress response hormones we are going to further increase this glucose that is available as well as we're also going to see the production of those ketones in addition to that we also have the catabolism of protein stores which is again going to further elevate that glucose level and so now because we have all of this glucose in the blood glucose actually contributes to osmotic pressure and so as a result of this osmotic pressure and hyper osmolality that we're gonna see fluid shift from the intracellular to the extracellular space essentially pulling fluid into our vasculature and because of this osmotic pressure this is going to lead to osmotic diuresis and because we have this hypotonic loss of fluid due to this diuresis that this is going to cause this intracellular and extracellular fluid volume deficit and the electrolyte loss that goes along with it and so as we lose this water through the urine we're also going to lose our sodium our magnesium calcium and phosphorus in our patients potassium may either be low or high depending on a few different factors depending on if our patient is experiencing nausea or vomiting how their fluid status is as well as their acid-base imbalance which we're going to talk about here in a minute now for this volume deficit if this progresses far enough this can even lead our patients into hypovolemic shock in addition to this we're gonna see a decrease in the GFR rate in our kidneys for glucose which means we're gonna have a difficult time clearing glucose via the kidneys which is going to contribute to this cycle of progression that we see and then finally due to this volume deficit we could see the dehydration of cells in our brain which are going to lead us to the neurological symptoms that we see and we will talk about those signs and symptoms that we'll see in our patients here in a minute but next I want to move on and talk about this acid-base imbalance that we're going to see and so we know with our cells that they're gonna starve without glucose and so the body is going to attempt to use fats and proteins to produce glucose thinking that's what the cells need and so specifically as we're metabolizing these it's we're gonna see the production of ketone acids and this is going to cause a metabolic acidosis you're also going to see the production of acetone which will play an important role in one of the signs and symptoms that will pick up on here in a minute but if you remember we were just talking about the fluid volume deficit and the hypovolemia that our patients are going to be experiencing which this is going to lead to decreased tissue perfusion causing our cells to switch into a anaerobic metabolism to which a byproduct of that is going to be our lactic acid which is going to further worsen our metabolic acidosis and so because of this metabolic acidosis that this is where we're going to see an increase in our anti n gap and normally our anion gap we're gonna see is between 12 and 14 and what's happening is our body is normally maintaining a ratio of our sodium and potassium to our chloride and bicarb and so our calculation for this we normally add together our sodium and potassium then we add up our chloride and bicarb and we subtract that from the total of the sodium and the potassium and this is what gives us our anion gap oftentimes because of the low number you'll see the potassium eliminated from this calculation and we'll just subtract the chloride and bicarb our sodium and this calculation is how we determine our anion gap but once again because of this osmotic diuresis we're gonna see a low bicarb and we're not going to have the bicarb available to buffer this metabolic acidosis that we have going on and we'll see this reflected in an increase in this anion gap and so as a result of this decreased bicarb in this metabolic acidosis the respiratory system is going to attempt to compensate and so what it's going to do is attempt to blow off co2 by increasing our respiratory rate and increasing our tidal volume to try and bring that pH back up into a normal level if you want to understand this a little bit more I'm gonna link to a lesson that I did on our arterial blood gases which will explain this a little bit more for you guys this acidosis we're also gonna see spillover into an intracellular acidosis so the insides of our cells are going to be acidotic which is going to lead to a potassium shift and so it's going to move potassium from inside the cell outside and attempt to lower the pH of the cell and then because of this level of potassium in the blood the kidneys are going to work to excrete this as well as we're gonna lose that potassium as a result of that fluid volume loss and so this can become a problem later because as we administer insulin and these patients that we can induce a shift of potassium back into the cell and lead to a state of hypokalemia in these patients because we've excreted that potassium out at this point all right so this was a pretty complicated but interconnected pathology between this fluid volume deficit and electrolyte imbalance as well as this acid-base imbalance that we're going to see in our patients so next let's talk about some of the signs and symptoms that we are going to see in these patients the first thing I'm going to mention is acetone breath and that's a fruity smelling breath because of this acetone production which has a fruity smell to it we're also going to see something called Kussmaul respirations and essentially this is rapid deep breathing and this is a result of that respiratory system attempting to compensate for the acidosis these patients oftentimes are going to have abdominal pain and nausea and vomiting you could also see an altered sense aureum these are going to be things like paresthesia which is the tingling prickling chilling burning sensation they could experience paresis or muscle weakness pleasure or paralysis or even aphasia which is the loss of an ability to either understand or express speech you're also going to see tachycardia polyuria which is excessive urination polydipsia which is going to be an excessive thirst and depending on the extent of our dehydration they could be lethargic stupor Asst or unconscious and so hopefully all these signs and symptoms make sense as a result of what we just talked about within this pathophysiology all right so we talked about quite a bit so far here for DKA but I actually want to move on right now and talk about our HHS and so like we talked about what DK that that's primarily going to be seen in our type 1 diabetics HHS is typically going to be seen in our type 2 diabetics but unlike type 1 which is oftentimes first diagnosed in children it's going to be pretty rare for us to see type 2 diabetes and children although lately we have been seeing an increase in our childhood obesity rates and this is actually leading to an increase in our seeing HHS and children now our HHS is really defined as a hyperglycemia with a profound dehydration in the absence of ketosis and we also have a set of defining characteristics for this as well and for HHS we're gonna see glucose levels that are usually in the range of 600 to 2,000 although typically they're around 1,100 you're also gonna see profound dehydration and that hyper osmolality and so the defining characteristic of this glucose level you're gonna see is going to be oftentimes much higher than what we see in DKA now for our causes they're actually going to be very similar to what we see in DKA so again stressful events infection trauma surgery but this is where you're often gonna have undiagnosed or untreated type 2 diabetes so now let's move in and talk about some of the paths though we're gonna see in HHS and a lot of it is actually going to be very similar to what we see in DKA with a few differences now the first is that the onset is often progressive and it's not quick like we see in dk and in fact we can even see this happen over weeks to months now in these patients because they have some insulin that's being secreted we're not gonna see that lipolysis and thus no overproduction of ketones and ketosis and so that means we're not gonna see the acetone breath we're not going to see koo smalls respirations and we're often not going to see abdominal pain and nausea and vomiting in these patients and because of the lack of these symptoms this often is going to keep our patients from seeking treatment earlier now because of the extremely high glucose levels that we talked about we're gonna see much higher osmotic pressure and therefore significantly higher diuresis than what we see in DKA and this is what's going to lead to that profound dehydration oftentimes our volume deficit in these patients is going to be 9 to 10 liters we are also going to see those decreased electrolytes due to the diaeresis and dehydration but more often than not we're gonna see a normal pH in these patients if we do see acidosis or the patients are acidic this is going to be due to lactic acid buildup from hypoperfusion not ketoacidosis like we'd see in DKA and those are essentially the differences in the path that we're going to see with HHS here now we already talked about some of the differences that we're going to see and our signs and symptoms but it is important to know that the CNS dysfunction and our mortality rates are often going to be worse with HHS due to that severe volume loss that they're experiencing and the fact that we're often dealing with chronically ill patients here and so that's going to contribute to this increase in mortality and so our concern for our patients dying is going to be a result of either CNS depression of either our cardiac respiratory centers cerebral edema cardiovascular collapse due to that profound dehydration we could see renal shutdown or even there at a high risk for vascular embolism so our risk of death in these patients is definitely increased compared to that of DKA all right so that pretty much gives you a good overview of DKA and HHS and some of the similarities as well as some of the key differences that we see with this and so now let's talk about our treatment for these hyperglycemic emergencies so our treatment for DKA and HHS it's almost identical and it revolves around four main areas the first is our fluid replacement next is treating the hyperglycemia the third is our electrolyte replacement and the last is treating the underlying disorder and so we'll start with this last one because it's the simplest as we really need to just determine whatever the precipitating event was and treat that oftentimes for both DK and HHS this event is going to be some sort of infection so now let's talk about our fluid volume replacement and both in DK and HHS that this is going to be our priority because we want to prevent that cardiovascular collapse and so initially we're going to treat this with our 0.9% normal saline and often we're going to start this with a rapid bolus of one to three liters within the first hour depending on the patient's blood pressure and their serum sodium level and then from there we're going to continue infusing fluids until that volume is restored and so once our patient serum glucose begins to come back down we'll often switch this normal saline to a d5 half ns and we're really doing this to prevent hypoglycemia in these patients typically for DK once we reach about 250 is when we're going to do this although we may do this higher in patients with HHS in order to prevent that cerebral edema risk now as we talk about our next one here the treating of the hyperglycemia that is gonna involve IV insulin and this is one of the big reasons why these patients may require frequent monitoring and therefore care in the ICU now with this insulin treatment we're typically going to be requiring more for these patients that are in HHS due to the really high glucose that we see and we are gonna see different protocols that really vary from facility to facility for these insulin infusions but ideally our goal is to decrease our glucose level by 50 to 70 per hour once again like we just talked about we're gonna switch the patient to the d5 half an s but we're also going to decrease our insulin and rate at that time again trying to prevent hypoglycemia and it's really important that we do keep the insulin infusion going until we have a normal pH and this is really to avoid that intracellular hypokalemia which we'll talk about more as we talk about our electrolyte replacement so once again we're typically going to see these deficits present both in our patients with dk and HHS and if you remember this is a result of that osmotic diuresis like I said earlier who might see a worsening of our patients hypokalemia due to an acidosis that they have going on while we're treating them and the reason for this is like I talked about with that intracellular acidosis the cells are going to shift that potassium outside in order to maintain a normal pH within the cell and so typically what you'll see in your patients for every point one drop in their pH that you're gonna see their potassium level rise by 0.6 as a result of this potassium shift and so once again the body is going to be excreting this excess potassium as well as we're going to be losing it due to that osmotic diuresis and so as we administer our insulin that that actually draws potassium back into the cell which can cause a hypokalemia for our patients and so it's going to be really important that we monitoring our patients potassium level frequently as well as administering potassium and our goal here is to avoid those cardiac arrhythmias that are going to be associated with that hypokalemia we're also going to be monitoring their magnesium level calcium level and phosphorous level because as we rehydrate them it could further dilute those levels and so typically we're gonna be administering and replacing our magnesium and calcium based on our patient serum level but typically our foss is going to correct on its own with our volume replacement but sometimes we are going to be giving foss to them as well important to remember though in our renal patients we want to be avoiding this phosphorus replacement finally based on our patient's bicarb level and the severity of their acidosis we also need to be assessing for replacing their bicarb this is going to be primarily for our patients with a pH less than 7 and again as we give the bicarb and raise that pH that's going to cause that potassium to go back into the cells and so we're going to really need to monitor for that hypokalemia again all right so that pretty much sums up our treatment here like I said it's pretty much the same for DKA and HHS and it's really revolving around making sure we get the fluids back controlling their hyperglycemia replacing the electrolytes and really treating whatever the underlying disorder was if we can do all that we can get our patients back into a much better more hemodynamically stable picture and ultimately get them on their way to recovery alright well we covered quite a bit of information here the pathways for DK and HHS are pretty complex but I hope in talking through this that some of this make sense for you guys and you can see how these signs and symptoms really are a result of what's happening within this pathophysiology that we see with these processes along with that hopefully you're able to really distinguish between DK in HHS because while they are similar in a lot of ways there are some very key differences that hopefully you'll be able to pick up on and recognize all right and with that said that's gonna conclude this lesson and I do want to thank you guys so much for watching I really hope that you guys found this lesson useful and if you did please leave a comment for us or hit the like button as it really does support our channel here and the next lesson in this series we're actually going to take a look at the differences between diabetes insipidus and the syndrome of inappropriate antidiuretic hormone di versus SIADH so if you haven't already subscribed to our channel that will you'll be notified when that lesson becomes available and in the meantime head on over and check out the last series of lessons that we did in which we did a great review of heart failure as always thank you guys so much for watching and you have a great day