COVID-19 | Crash Course in Medicine | In the ICU | Diabetic Ketoacidosis | @OnlineMedEd

this lesson is about the management of diabetic ketoacidosis and before we get started the management of DKA is almost exclusively protocol driven which means that your facility is going to have an order set that you just type in and the nurse executes so likely you will have a greater chance of harming that process if you try to mess with it rather than just letting it go the reason for this lesson though is because if there's not a protocol in place or if the protocol doesn't work you need to know how to intervene and why also you need to know the pitfalls that you can get into if you don't get out of the nurses way so this lesson is going to be about the things that you should do and the things that you shouldn't do and anticipate the problems that people fall into and I either end that is other diagnosing or getting them out of the unit DKA is managed in the unit and unlike most of the lessons in this series I'm going to dip back down into the basic sciences a little bit because it's going to justify the major pitfall insulin has nothing to do with a blood glucose let's start there a pata sites have on them insulin receptors they also want to other receptors to the scepters like glucagon and they can be influenced by other counter regulatory hormones kind of regulatory that oppose insulin such as epinephrine or the cytoplasmic receptor or the hormone cortisol back in metabolism we said that the parasites lived either in an insulin dominant world or a glucagon dominant world well that meant was the pancreas the endocrine pancreas always secretes a certain amount of insulin and glucagon and depending on what state the body is in one of those hormones would predominate in a well-fed state with lots of calories coming from the diet the insulin dominant state would predominate more insulin would be made in the fasting State the liver was responsible for making energy for everyone else that's the glucagon dominant state in type one diabetics those who get DKA and now also you glycemic DK in type twos but this is going to be about type one's in type one diabetes if the patient doesn't take their insulin there is no insulin signal which means that no matter how little glucagon is secreted by the pancreas that's the only signal of parasites here and when a pet asides here a glucagon dominant signal they think this is a poorly fed state I need to make energy for everyone else make energy for everyone else means gluconeogenesis initially the liver is going to use its own glycogen supplies glycogen a lysis to make that glucose but eventually it's going to need to do gluconeogenesis to do that it's going to need energy it's sent out fatty acids to be stored as triglycerides and adipocytes now in the glucagon dominance state the liver calls for those fatty acids back from the periphery in order to do fatty acid oxidation this generates high-energy compounds including acetyl co a used for citric acid cycle electron transport chain and any excess acetyl co a the parasites have after they're flush with ATP is used to make another transportable energy form ketones and so if a diabetic type one doesn't take their insulin there is no opposition to glucagon in so the liver the apat asides do what they're told to do in a glucagon dominant state increased gluconeogenesis glycogenolysis fatty acid oxidation and ketone synthesis the problem is in type 1 diabetes than any insulin skeletal muscle myocytes and adipocytes have no signal to decrease the systemic blood glucose which means the blood glucose is elevated and the liver is making more the real problem that causes is in the kidney this is a glomerulus this is the proximal convoluted tubules this is the rest of the nephron whose names you don't have to actually know missus cushon glucose is freely filtered and is supposed to be a hundred percent resorbed by the proximal convoluted tubules but the PCT is limited the numbers don't actually matter just the concept it's around two hundred and so if you've got three hundred high glucose all three hundred will be filtered two hundred will be resorbed which means that a hundred stays behind again it's not the number it's the fact that it just stays behind there is no mechanism other than at the proximal convoluted tubules to resort glucose glucose is osmotically active you lose glucose in the urine waters gonna follow it you lose volume patients who present in DKA are going to be immensely volume deplete that volume depletion is sensed by other sensors specifically arena and angiotensin aldosterone axis aldosterone is going to ensue Anette channels here to try to resorb sodium osmotically active in an attempt to hold on to that volume it doesn't work because the glucose wins and the volume the water goes with the glucose but resorbing excess sodium results in the wasting of potassium a failure of volume resorption but also wasting a body k which means that the total body k total body potassium of somebody in DKA will be deficient which means that in anyone who presents with DKA already you know your job is going to be to replete the volume with intravenous fluids and to replete potassium this only predisposes someone to DKA they're making ketones they're making extra sugar the parasites don't get the signal to do what they're supposed to do even those a bunch of blood glucose around that isn't a problem because the cells that need glucose like endothelial cells and neurons have glucose transporters that don't require an insulin signal in fact that's the problem with long term hyperglycemia they end up getting osmotic damage not for this discussion the problem comes though when the apat asides were already primed to being the glucagon dominant state the only signal they have suffer an additional insult volume depletion may be enough but any stressor is going to increase counter regulatory hormones those that oppose insulins actions epinephrine goes up cortisol goes up counter regulatory hormones tell via pot asides do the same thing Luke agon does increase gluconeogenesis increased glycogen lysis increased fatty acid oxidation increase ketone Genesis increase glucose increase glycogen lysis increased burning of fatty acids increase in production of ketones and it is this the production of ketones that kills people yes the patient has an elevated blood sugar because it is diabetic ketoacidosis but the diabetic part the glucose part has nothing to do with what kills them ketones are the keto acids of diabetic ketoacidosis it is the keto acids and the acidosis that kills which means when you give insulin to DKA what you are doing is telling the apat asides just stop doing that you are turning off ketone production in the chronic management of type 1 diabetes you give insulin to control the blood sugar in DKA you give insulin to turn off the ketoacidosis to tell the apat asides stop making ketones so with that when you see somebody who might have DKA what you're looking for is diabetes elevated blood sugar ketones and acidosis to decide that you're going to get an arterial blood gas which will show you reduced pH I'm going to get a basic metabolic profile which will reveal an anion gap metabolic acidosis as well as an elevated blood glucose and then you need ketones urine ketones or serum ketones licensing exams like you to choose the serum beta hydroxy butyrate you've got an altered person of the low pH and I'm gap metabolic acidosis and elevated blood glucose and the dipstick is positive for ketones that counts and then if you look online you're going to see these charts to determine how severe the DKA is and in there they're going to include what the level of bicarbonate is whether or not there are ketones or an elevated blood sugar they've got diabetic ketoacidosis the bio carbs can be low the sugars high and there are ketones obviously what makes the difference is how acidotic and how volume depleted you look at that ABG you look at their meditation and their blood pressure if the ABG shows a pH greater than 7.2 they are completely alert and their blood pressure is normal they're not in DKA this is the DK you can manage on the floor and so I'm going to put it in parenthesis here or quotations floor DK a that actually means they've just got the green arrows they're predisposed to DK not in it yet if the pH is less than 7 they're probably obtunded and they're so volume deplete they are hypotensive this is severe of course volume depletion in total body K depletion can't happen if you have end-stage renal disease that's a caveat what I want you to hear is if DK a volume down K down in between is regular old DK a I'll go to the unit they're all treated the same way the only difference might be you're gonna give a little bit of bicarb to a pH less than 7 to get that pH up you make the diagnosis you know the severity you put them in the unit what orders do you put in here's the clinical stuff the management of diabetic ketoacidosis has three arms and you will not be surprised with what they are isn't they already got rectangles around them on the board and involves fluid management potassium management and insulin again unless they're in stage renal disease regardless of anything else on this board you know their volume deplete and they need volume resuscitation you're going to give two liters lactated ringers bolus now you can use normal saline but there's a theoretical risk of acidosis and they're already acidotic so I prefer lactated ringers but that's my practice pattern and then you're gonna turn after that two liters put it to 250 cc's per hour lots of volume what you want to do initially is give insulin you're going to give insulin reg you ten units IV once then start an insulin infusion you start at 0.1 units per kg per hour but wait can you give insulin you give insulin d50 to treat hyperkalemia because insulin is going to shift potassium into cells they start off total body potassium deplete in addition because of the acidosis the way the body handles that is by bringing in hydrogen ions to the cells and releasing potassium when you give insulin you're going to reverse the acidosis and shift K into cells both are going to shift K out of the blood and into cells but the cardiac myocytes feel is what's in the blood so you have to be careful not to induce hypokalemia leading to fatal arrhythmias so you must ensure that the potassium is good if the potassium is greater than five you can proceed if the potassium is less than three point five ever see what I mean by ever you need to hold insulin and give both Pio and IV potassium if you're in between you can go ahead with the insulin but also be sure to give potassium that's ten milli equivalents for a peripheral line or up to 20 ml equivalents per hour through a central line you're going to repeat this process that is assess and give potassium assess and give insulin on a repeated basis over time the fluids are going may change because the purpose of giving insulin is to reverse the ketoacidosis it may be that the insulin is given the anion gap does not close but the blood sugar falls down to near normal ranges ongoing insulin administration is going to lead to hypoglycemia so you may find yourself switching that 250 CCS per hour flight to the ringers to add extras containing solution D five half normal saline and that will be dependent on the anion gap if the gap does not close you continue to give glucose with insulin to close that gap over time the nurse is going to titrate the insulin infusion the goal is to titrate to effect I'll talk without effect is in just a minute this is why routine assessment of the blood glucose does matter you need to decide if the insulin infusion is too fast too slow or if you need to change fluids and all the while you're going to be monitoring the potassium and anytime the tascam goes three point five you stop the infusion and give hassium or they'll either be greater than five you keep going or in between and you give contaminant insulin and potassium you know that because you're going to follow the potassium how you follow these things well first you're gonna get a basic metabolic profile every four hours what this is going to give you information on is the potassium and the anion gap you also get a blood glucose from this the nurse is going to use the capillary blood stick in order to titrate the insulin infusion BMP you do get a blood glucose but this is not the one you use you're gonna get a potassium reported and then regardless of what the blood glucose is because you learned that in determining tonicity you should correct the sodium for the glucose in calculating an anion gap you should not the sodium minus the chloride minus the bicarb is going to give you the anion gap and the anion gap less than 12 is what you're shooting for in addition you're gonna get a blood glucose every hour and that is gonna help titrate the insulin fusion the goal is to decrease the blood sugar by 75 milligrams per deciliter every hour increase the infusion if it doesn't change decrease the infusion if it changes too much and it will also help decide if the blood glucose gets below 250 you're going to change the lactated ringers to d5 half normal and this is the protocol it's going to be followed but in addition you need to find out why they went into DKA that is you need to go hunting simply calling it medication non-compliance is insufficient because medication non-adherence non-compliance non adherence only predisposes them to DKA now it is possible that they were going to have some psychological event where they get really amped up or the volume depletion is enough to tip them over but you cannot assume then at the start and so what you do is go hunting there are four things you should look for the first is infection the second infarction the third much less often but it's easy to check for is elicits and the fourth is trauma anything that revs up the epinephrine to cortisol can tip them over the infection is easy to look for you're gonna culture them up blood urine and get a chest x-ray what you want to do those things after the initial fluid bolus you want to make sure that if they have a pneumonia it fluffs up because of the fluid if they have a UTI you get a diluted sample that isn't stagnant and concentrated it might look like a UTI you want to get good values to make sure that they're not infected infarction the one you worry about the most is of course myocardial so you'll cycle troponin and twelve leads because they are in the unit they're going to be on telemetry and of course you also need to use your eyes because diabetics glycated proteins micro vascular disease they can have risk for ischemia of any limb or organ lactic acid also helpful again only after the fluids to make sure it isn't a contaminated sample elicits not usually the cause but easy to test for the new tox and then trauma either physical or psychological way cue can ask them if they don't tell you you don't know and sometimes it is just medication non-adherence but that's not what you walk in with and the last part is how you get them out of the ICU that is how do you bridge you've gotten out of the nurses way he's got them down to a normal gap in your normal blood sugar what do you do first you ensure that the anion gap is closed not closing is closed the rasa dosis is resolved so they're awake and they can eat about putting themselves at risk you give them with the infusion still going a subcutaneous basal insulin and food the nurse then Wiens the drips and fluids before they're allowed to leave you ensure the gap remains closed before you step them down we covered DKA this justifies the three prong approach you give insulin to tell the POTUS i'ts to stop making ketones to turn off the keto acids to reduce the anion gap you give volume because of volume deplete and you monitor the potassium because their total body potassium down and your insulin intervention can make that potassium worse diagnose it with an ABG BMP and urine ketones start insulin IV then continuous insulin infusion always monitoring the potassium and the anion gap q4 no matter what the potassium is you're going to bomb them with fluids as the blue glucose comes down if the anion gap remains open you're going to switch the dextrose containing fluids the blood sugar is tested every hour and the titration and fluids change based on that once you have that process started you then look for the reason they went into DKA it's more than medication non-compliance until it isn't and then when you want to bridge them make sure the gap is already closed basal sub-q and food wean the drip wait make sure the gap stays closed with the drip off for more than an hour it's better to keep a patient in the unit for one more hour than have them leave reopen and need to come back that's DKA

Channel: OnlineMedEd

Views: 23,862

Keywords: Diabetic Ketoacidosis, ICU, COVID-19, Coronavirus, Medicine

Id: pCym_IxYayo

Length: 23min 2sec (1382 seconds)

Published: Fri Jul 10 2020