Diabetic Ketoacidosis (DKA) & Hyperglycemic Hyperosmolar Syndrome (HHS)

[Music] our ninja nerds in this video we're gonna talk about diabetic ketoacidosis and hyperglycemic hyperosmolar syndrome which are acute complications of diabetes alright so the first thing we have to talk about is the causes of DKA and HHS now I want you to remember these by the basic mnemonic here kind of like a tool that you can utilize is the six eyes now those six eyes come down to two big overarching themes one of the themes is that there is a decrease insulin supply so there's an insulin deficiency and what kind of individuals would an insulin deficiency be a problem an insulin deficiency would be a problem in an undiagnosed diabetic doesn't know that they have diabetes so they're not taking insulin that could be one reason or it could be a diabetic who's not taking their insulin they're not compliant with their insulin or they're not taking enough of their insulin that's one of the eyes all the other eyes the other remaining five eyes that I want you to remember are associated with this point where there's an increase insulin demand and more specifically there's some stress in the body that's causing an increase insulin demand and I'll explain that in the later okay now the five eyes are going to be infections and this is high-yield because this is the most common cause for increase insulin demand now what are some of the infections that are associated with this one is called pneumonia the other one is gonna be urinary tract infections so cystitis pyelonephritis and infections of the skin like cellulitis the next thing is inflammatory conditions of multiple tissues in the body which could also be type of some infections such as inflammation of the pancreas called pancreatitis or inflammation of the gallbladder inflammation of the gallbladder is called cholecystitis the other thing that I want you to remember is intoxication may be someone's drinking too much alcohol that could be a trigger so someone's drinking a little bit too much rose' right so if there's increased out Hall now not only if there's increased alcohol but what if someone is actually taking certain types of toxins we got a toxin symbol here like what may be cocaine or other types of medications like methamphetamines okay so this could be things like sympathy mimetic drugs like ADHD medications the next thing is I want you to remember infarction infarction I want you to remember two particular organs that can create this increase insulin demand one is an acute myocardial infarction so some type of infarction of the cardiac tissue or an infarction of the cerebral tissue so a cerebral vascular accident or a stroke the last I that I want you to remember is I at regenexx which is mean it was caused by the practitioner and sometimes this could be because we give a particular drug steroids so corticosteroids these are a big one because corticosteroids increase our blood glucose levels which increases insulin demand and the other thing is surgery surgery requires wound healing and that requires glucose and sometimes that can also cause problems as well and just generate stress on the body so we know the six eyes that are responsible for DKA or HHS insulin deficiency infection inflammation intoxication infarction and iatrogenic affects the insulin deficiency part it can lead to a specific pathological mechanism now how is this happening now remember whenever there's decreased insulin in the situations that we talked about remember from the diabetes lecture that means that we can't get glucose into our cells if we can't get glucose into our cells what happens to the ATP production it starts to drop where does our body start doing it starts tapping into the secondary fuel sources what's that secondary fuel source triglycerides now triglycerides are in adipose tissue and whenever adipose tissue is broken down like the triglycerides in the adipose tissue is broken down it's called lipolysis and we break the triglycerides down into what's called free fatty acids and there's also glycerol now these free fatty acids what happens to them is that they then get converted into acetyl co a well it's called beta oxidation we break down the free fatty acids into two carbon chains push it into a sea look away whenever you have increased beta oxidation you get increased acetyl co a production now acetyl co a wants to go into what's called the Krebs cycle but whenever there's so much of this acetyl co a the krebs cycle gets saturated so it starts shifting the acetyl co way into another metabolic pathway which is synthesizing ketone bodies and whenever we Kerr convert acetyl co a into ketone bodies it's called ketogenesis now the problem with this is that these ketone bodies like acetoacetate and beta-hydroxybutyrate can get into the bloodstream when these guys get into the bloodstream they have the ability to release protons and when they release protons that makes the blood more acidic and causes acidosis but a more specific type of acidosis that's important to remember here called ketoacidosis the next thing I want to remember because it's gonna come up in a little bit here is that one of the ketone bodies called acetyl acetate can actually get broken down and when it gets broken down it releases a particular molecule called acetone and the important thing about acetone is he can get sent to the lungs and then from the lungs he can get exhaled out that comes into play a little bit later that's one aspect and that's coming from the insulin deficiency the other part is the increased stress that's the infection the inflammation the infarction the iatrogenic effect and intoxication these cause stress on the body that stress stimulates our sympathetic nervous system what is the sympathetic nervous system release what kind of neurotransmitters epinephrine norepinephrine and epinephrine and norepinephrine these to actually stimulate glucagon production by the pancreatic alpha cells now with increased epinephrine norepinephrine and glucagon they love to act on to the liver when they go to the liver they promote two processes which is high-yield gluconeogenesis which is where I can take amino acids I can take glycerol and I can take lactic acid and convert it into glucose the other mechanism that it can promote is called glycogenolysis and glycogenolysis is where we take glycogen a big storage part of glucose and break it down into small glucose molecules that's called glycogenolysis but guess what else it can do it can also take this epinephrine and norepinephrine and glucagon it can also generate the lipolysis mechanism which can generate everything we talked about here now let's go back to this high glucose whenever there's elevated levels of glucose remember what we said it does in the kidney it gets filtered into the PCT the PCT can't deal with all that large volume of glucose and so because of it it can't reabsorb it and a lot of that glucose gets lost into the yarn well when glucose gets lost into the air and what does it draw with it water and as we draw water out into the urine what is that process called osmotic diuresis and also can pull sodium with it too which will come in later as we just Diaries tons of water and sodium out into the urine what can that lead to dehydration the next thing is as you have this excessive osmotic diuresis what does that mean that means you're decreasing the water concentration right as you decrease water concentration in the blood that means that all you're gonna have is little water in the blood and tons of this glucose tons of glucose in the blood with very little water is referred to as a hyperosmolar state and this is high-yield the last part that I want to talk about relevant to this is we have three components here that we basically encompassed ketoacidosis dehydration in hyperosmolarity and that's what we see responsible for DKA and HHS but more particularly for your exams DKA is more particularly seen with symptoms that are responsible from ketoacidosis and dehydration and variable hyperosmolarity but for exams remember these two the next thing is DKA occurs more acutely usually with an onset less than a day and for your exams remember it is most common in type 1 diabetics because of that insulin deficiency hyperglycemic hyperosmolar syndrome on the other hand we primarily see these two effects dehydration and hyperosmolarity on top of that usually the onset comes on a little bit more than a day in time and on top of that this is more commonly seen high-yield here with type 2 diabetes mellitus why do they not have as much of the ketoacidosis because in type 2 diabetics you still can produce a little bit of insulin so if you can produce a little bit of insulin there's not going to be as much ketoacidosis all right so now that we understand the three big things that happens with DKA and HHS now the first let's focus on is these ketone bodies how can these ketone bodies that we generate lead to particular clinical manifestations well you guys remember that ketone bodies they can act on a particular area in the actual brain stem called the chemo trigger zone and they can stimulate the chemo trigger zone whenever they're in high concentrations the chemo trigger zone is in an area of the medulla near the area post rima and that stimulates what's called the emetic Center in the medulla the emetic center in the medulla will then trigger reflex that causes some nausea like sensation and more particularly vomiting that's one of the things that you might see and those with elevated Etan bodies particularly DKA patients the other thing is ketone bodies remember these are things like their acids their keto acids so they can give off protons whenever they give off protons the problem with this is that this causes an acidosis now in acid states whenever there's high level of protons in the extracellular fluid and here we have a cell in its intracellular fluid what happens is the protons want to move because they're in so much concentration here and the extracellular fluid they want to move into the intracellular fluid so what happens is the protons move from the extracellular fluid into the intracellular fluid but in response to that our body takes potassium and pushes potassium out for every proton that comes in so now potassium is gonna start accumulating in the extracellular fluid because of the acidosis the other thing that you want to remember you know in every cell you have sodium potassium ATPase is they pump 3 sodium out of the cell and 2 potassium into the cell these pumps are driven by insulin so in individuals who are insulin deficient can they stimulate these pumps no if they can't stimulate the pumps can you push potassium into the cell no so what happens the potassium starts building up into the extracellular fluid now that means that there's a net movement of potassium from the inside of the cell to the outside of the cell what's the problem with that this is happening in so many cells of the body that it leads to a decrease in the total body potassium but because a lot of this potassium can end up in the blood you might get either normal or possibly elevated serum potassium called hyperkalemia what's the problem with these whenever there's hyperkalemia hypokalemia Crees total body potassium and high serum potassium this can create arrhythmias now our arrhythmia is my presented with symptoms of palpitations or chest pain another thing is as you decrease total body potassium this can alter the peristaltic activity in this intestin if you alter the peristaltic activity into the small intestine this can lead to an ileus where there's no peristaltic contraction in that area of the small intestine and because of that this can lead to abdominal pain now that's one aspect the next thing is whenever there's increased protons in the blood these create acidic environments that stimulates peripheral chemoreceptors remember these they're located in the aortic bodies and the carotid bodies and they're connected to the vagus and claw so fragile nerve whenever it's stimulated it sends these impulses on the vagus nerve and glossopharyngeal nerve to the central nervous system and that creates a reflex that tries to increase respiratory rate why because if we increase respiratory rate the thought is that that's going to help us to breathe more co2 out of the body and if we drop co2 we get rid of some of that acid because that's the problem is acidosis but in attempts of doing this this creates a pathological sign which is extremely high yield which is when someone has deep and rapid respirations called Co smalls respiration the other thing is not only you trying to breathe off co2 to try to bring the pH back up but you're also breathing off that acetone from the acetoacetate remember that ketone body that breaks down into acetone this acetone as you breathe it off it gives off a particular smell or odor which we call a fruity breath odor and this is extremely high yield as well the last thing I want to talk about with the ketone bodies is that ketone bodies can do what's called increasing the anion gap now some of you might know that anion gap is defined as whenever you take the sodium minus the chloride plus the bicarb but you know there's another formula for this it's when you take the unmeasured anions - the unmeasured cations well guess what a ketone body is it's an unmeasured anion so if I have an increased number of unmeasured anions I take a large number subtract it by a small number what happens to my anti half it goes up and on top of that I have an acidic environment this is called Hagman so whenever someone has a high anion gap and acidosis due to a metabolic issue they call this high anion gap metabolic acidosis the next thing is that we have to talk about is dehydration which we see in both DKA and hyperglycemic hyperosmolar syndrome now the DKA you primarily see ketoacidosis right now dehydration what happens and why is this because we started to pee off lots of water now as we peel off lots of water that causes this dehydration now dehydration can present in two particular physical exam findings one is decreased skin tear so whenever we pull on their skin it doesn't return back to its normal position as quickly the other thing is that their mucous membranes will appear dry so you look in their mouth and if a really start to look dry in appearance the next thing is as you drop as you become dehydrated the total volume of blood because of the loss losing the water drops as you drop blood volume what do we say is directly proportional an increase in blood volume causes an increase in blood pressure right well in the same way a drop in blood volume causes a drop in blood pressure and this can cause hypotension the other thing is is that we're not getting enough blood perfusing particular organs like the kidneys this can lead to decreased renal perfusion and that can lead to decreased urine output okay that's important the next thing is whenever your blood volume drops remember those receptors the aortic sinus and the carotid sinus which are located in the aorta and then the carotid the bifurcation of the common carotid arteries they detect drops in blood volume but more particularly related to blood pressure when blood volume drops blood pressure drops that stimulates these baroreceptors they send signals to your central nervous system your central nervous system becomes activated and it basically activates the cardiac accelerator and increases your heart rate and this is called reflex tachycardia the other thing is we never you have increased sympathetic activity this starts acting on your sweat glands and increasing your sweat production and this can lead to diaphoresis the last thing that we have to talk about is the hyperosmolarity and this is primarily something that we see in HHS right now hyperosmolarity how do we classify that whenever there's tons and tons of glucose in the blood but very very little water because we're peeing a lot of that out so what that means is in the blood it's really hyperosmolar tons of glucose very little water now as this blood is flowing through particular tissues such as the brain or central nervous system let's say right so brain and spinal cord or maybe muscles the water inside of the cells of the neurons in the brain or spinal cord in the the actual water inside of the muscle cells sees all this high glucose in the blood as it's passing through these tissues and it says I see lots of glucose I gotta go to where the glucose is so the water starts rushing out of the cells of the brain and the spinal cord neurons and out of these muscle cells that draws water out of these cells and into the blood by doing that you shrink these cells now if you shrink the cells of the central nervous system that ain't good and what can happen is this can cause an altered mental status where they start to become confused they start to become really lethargic then over time if it continues to get worse and not treated it can then progress to seizures and then worst case scenario they go into a coma the other thing is if it pulls water out of these muscle cells it can cause problems with the muscle cells where they're not gonna function properly and this can lead to weakness alright so the next thing we have to do and this is extremely important is figure out the labs for DKA and HHS so remember this start off with a CBC a CMP a CMP is going to give your kidney and liver function let's check an ABG which is gonna tell us our acid based Dallas sat as well let's get a UA ketones a serum osmolality and then we can add on lene EKG depending upon their potassium and their age and comorbidities so let's say that we do that and we get some of these things that we really want to focus on here the first thing is checking their glucose which is going to be a milligrams per do now in DKA i want you to remember that this is generally greater than 250 milligrams per deal while has an HHS it's super high greater than 600 milligrams per deal why is this because they both cost hyperglycemia DKA remember we said that this is more common a type 1 diabetics which are usually more commonly younger younger individuals might have better kidneys so they might be able to get rid of some of that excess glucose is the thought behind that and that might be why their glucose is a little bit lower okay pH remember DKA is the one that has the ketoacidosis so that pH we expect to be low anything less than 7.3 and it can get much lower with him HHS it doesn't cause that much ketoacidosis it shouldn't cause very much ketosis at all so because of that their pH should be greater than 7.3 bicarb we'll remember go back to this concept down here remember co2 Plus water yields carbonic acid which gets broken down into protons and bicarb remember what the ketones are doing they're increasing protons as you increase the protons what's gonna have to happen with this bicarb the bicarb is gonna have to combine with the protons so that we can make carbonic acid so if we utilize bicarb to make carbonic acid what happens with the bicarb concentration in those with ketoacidosis it should drop and we say that when it's less than 18 we can consider that with the DKA but again we shouldn't see much ketosis or ketoacidosis with HHS so that bicarb should be greater than 18 not bad right urine serum ketones we're gonna get this super simple DKA ketone production a lot of it so you're gonna expect for this to be positive and potentially elevated ketones in the urine and in their blood with HHS let's make it simple it should be negative we really wanted to be specific it's gonna be a very small production not enough for it to be considered abnormal anion gap now remember in those with DKA they produce those ketone bodies that increases the unmeasured anions that increases the anion gap so because of that their anion gap is going to be greater than 12 and HHS there's not that much ketone body production because they can still make a little bit of insulin because they're type 2 diabetics gents generally if that's the case then there's not going to be as much ketoacidosis and not much effect on that anion gap so their anion gap is going to be less than 12 the last thing is serum osmolality with DKA they can have hyperglycemia but depending on this case-by-case basis it can be variable there can be times where this serum osmolality can be normal and it can be super high what's more high yield is HHS hyperglycemic hyperosmolar they should have a super high osmolarity greater than 320 all right so the next thing we have to know is okay we treat the underlying disease or remember they're dehydrated let's get them fluid so really the regimen that they say is let's start off with what's called normal saline and there's a type called 0.9% normal saline we're gonna refer to this as normal saline and what we're gonna do is we're gonna start off for the one maybe two liters of that normal saline and let's do it over an hour then what we're gonna do is we're gonna recheck their sodium and glucose particularly the corrected sodium let's say that we checked their sodium and their corrected sodium is low well then if the corrected sodium is low I don't want to go ahead and give them a lower amount of that saline the bafta the normal saline so what I'm gonna do is I'm gonna keep that normal saline the 0.9% and I'm just gonna go with 250 to 500 CCS per hour and then what I'll do is after I do that I'll recheck the next thing is let me check and see let's say that their sodium is normal okay so it's normal or we check it in their sodium is elevated if that's the case then I don't want to give them this high concentration saline so let's give me a lower dosage of the saline or a type of saline called half-normal saline and this is half of which is 0.45% normal saline if I do that I'm gonna go ahead and give them 250 to 500 CCS per hour and I'm gonna give it of that half-normal saline dosage and then after that we'll recheck let's say that I do that and their sodium is fine but their glucose is what I'm worried about and their glucose is a little low maybe it's like less than 250 and that's a little low and I don't want to overcorrect their glucose and cause it to drop too low so because of that what I might do is is I might give them a hundred and fifty to two hundred and fifty cc's of water and what I'm gonna do is I'm gonna give them that half-door normal saline so half normal saline but I'm just gonna add a little bit of glucose into it called dextrose and I'm gonna give what's called d5 so d5 is that dextrose a little bit sugar there okay and hope that that corrects their fluid abnormalities the next thing is the insulin we got to give them insulin to push that glucose into the cells so when I do that I'm gonna start them off at a zero point one unit per kilogram dosage and we're gonna do this as an IV push so we're gonna push this in then we're gonna switch them to a drip where we keep that rate zero point one units per kilogram of body weight per hour what we'll do is we'll recheck their glucose what you'll do is if the glucose is dropping let's say that it drops less than 200 milligrams per deal on that glucose then we might not want to give too much high dosage of that insulin let's drop the insulin dosage down and they say do anywhere from 0.02 to 0.05 units per kilogram per hour and then again you can recheck the next thing you want to remember is okay we correct the high glucose we correct the dehydration we also remember that we have that total body potassium depletion on top of that remember what insulin does it when we give insulin it pushes the potassium back into ourselves so our total body potassium yes it might be low but our hot we might have what's called hypokalemia because we're pushing the potassium into the cells so because of that we might want to give potassium but we base it upon their blood so if we do a BMP and we get their potassium it's less than 4.5 million spur liter let's get them some potassium let's do 22:40 milli equivalents per liter of potassium and then recheck it after that problem is those if we give too much insulin and it drops our potassium too low it pushes too much of the potassium inside of ourselves and the potassium drops to less than three point three let's stop the insulin drip so let's discontinue the insulin for a little bit and let's just go ahead and give them twenty to forty middle equivalents per liter recheck it and see if then we can still restart the insulin okay last thing to remember is because this person can be acidotic if the pH is less than 7% severely acidotic sometimes you can give what's called bicarbonate because it's a base and it's gonna try to bring the pH back up iein engineer so in this video we talked about DKA and HHS I hope this video made sense I hope that you guys did enjoy it if you guys did hit that like button comment down the comment section and please subscribe down in the description box we'll have links to our Facebook page around the Instagram account as well as our GoFundMe you guys want to go check that out we truly appreciate it as always the engineers love you and until next time [Music] [Music] you

Channel: Ninja Nerd

Views: 880,724

Keywords: DKA, diabetes, diabetic ketoacidosis, dka vs hhs, what is diabetic ketoacidos, hyperglycemia, ketoacidosis, medicine, HHS, Ninja Nerd Science, insulin, diabetes mellitus, high yield format, clinical presentations of DKA, health, hyperosmolar hyperglycemic syndrome, type 1 diabetes, dka vs hhs nursing, lecture, Ninja Nerd Medicine, Acute diabetic complications, endocrinology, diabetes pathology, diabetes pathophysiology, DKA vs HHNS, nonketotic state, HHNS

Id: jCf7W1U4JKE

Length: 28min 14sec (1694 seconds)

Published: Wed Apr 29 2020