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Summary

This on-demand teaching session focuses on diabetic ketoacidosis for medical professionals. It covers a wide range of topics from recognizing and diagnosing to monitoring and treating the condition. The session also delves into the scientific basis behind ketoacidosis, detailing the pathogenesis and clarifying common misunderstandings. A few of the discussed symptoms include increased thirst, urinary frequency, vomiting, lethargy, and a fruity smell on the breath. Attendees can also expect to learn more about the role of insulin in potassium levels and the effects of dehydration on the body. The teaching aims to prepare practitioners for managing high-stress scenarios such as escalating deteriorating patients and factors requiring critical care input.

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Learning objectives

  1. Understand the pathogenesis of ketoacidosis, particularly focusing on the accumulation of ketones and glucose in our body and the role of the kidneys in excretion.
  2. Gain knowledge on the symptoms and signs of ketoacidosis, including increased respiration, nausea, vomiting, dehydration, and fruity breath.
  3. Learn about the situations that warrant suspicion of diabetic ketoacidosis, including the presence of the triad: increased thirst, increased urinary frequency, vomiting, and signs of shock or dehydration.
  4. Develop insights on the treatment approaches for ketoacidosis, including the role of insulin and the need for continuous monitoring and finding the cause of preconditions.
  5. Understand the necessary standards to consider in the resolution of diabetic ketoacidosis, as well as the signs that indicate necessary escalation of care or urgent critical care input.
Generated by MedBot

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Computer generated transcript

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The following transcript was generated automatically from the content and has not been checked or corrected manually.

Hello. Can you hear me now? OK. I'm so sorry about this. Uh So why would you guys like me to start again? So do I start explaining the pathogenesis again? I hope all of you can hear me now and also see the screen. OK. So, all right, perfect. So back to the pathogenesis. So like I was seeing, there is a lot of accumulation of ketones and glucose in our body, right? So the body is gonna try and excrete this. So when this excretion happens, it's in the kidneys, right? So, but along with the ketone and glucose, what happens is there's excretion of a lot of water. So that's why this leads to dehydration. So the main two things that happen in ketoacidosis is first, I mean it's there in the name itself. So one is accumulation of ketone bodies that leads to ketoacidosis. And the other one is dehydration. So these two are the most important uh I mean mechanisms that ha take place which are responsible for all the symptoms. So you have to treat the dehydration and you have to treat the keton. OK. Is it clear up till now? Is there anything you guys want me to repeat until this point. OK. Moving on. So now the mechanism of we know what's happening now. Now why we have symptoms is because so when there is excess of acid in the body, right? Different regions of our body get activated like your chemo receptor baro receptors, et cetera. So I'm not gonna go too much into detail, but I'll just mention a few things. So what happens is there's excess of acid. So the certain receptors in the brain get stimulated, right? So this will try and get this excess acid out of your body. So one is where there is your uh respiration will get increased so that you're excreting a lot of carbon dioxide out which will decrease the acid level of the blood. So that leads to your respiration like someone said, which is a very real like when someone asks you what happens, acidosis, you have to mention it gives you like that gives you the most important uh scoring. You cannot miss that. The next thing that's happening is the nausea and vomiting. Again, there are certain receptors in the brain that get activated. They're trying to, you know, push out this acid. So that leads to symptoms like nausea, vomiting, we also know that insulin has been pushing the potassium from the blood in and we also have the sodium when there, which is guided by insulin. So when there is no insulin working. So what has especially, this occurs in the intestine. It leads to para iris because your peristalsis is not taking place. So that leads to your abdominal pain. Ok? One more thing. So when we did two ketone bodies, one is the beta hydroxybutyrate and there is other keto respiration. So that is what gives you the fruity breath. Is it clear up to? Now, do you want me? OK. Since this, so we have in the intestine for the pals to take place, you have the sodium potassium pump. Ok. This is driven by insulin when you do don't have enough insulin. This pump take ileus or ileus, which in turn causes abdominal pain. Is that clear? And so you're losing a lot of water from your body, right? That's dehydration. So that leads to a dropping BP drops. What happened? And the baroreceptors get activated system gets activated, which in turn tries to increase your heart rate, increase the pumping mechanism which will try to bring the BP up. So when this is ha ha like sweating and sometimes some of them a bit of PPI as well, I always look out for signs of dehydration, like loss of skin ts membranes or if they are like acutely very confused urine output is significantly reduced. So all these would be signs of dehydration and then you would know what to manage immediately. I OK. Moving on is the connection bad. I'm so sorry, I'm trying to fix it. But is it better now? Ok. Moving on. So now, when do you suspect diabetic ketoacidosis? So we mentioned the trial earlier, right? So you should have features of the trial. And the next would be symptoms. So you had mentioned earlier, increased thirst, increased urinary frequency, vomiting, diarrhea, abdominal pain, lethargy confusion, some amount of visual disturbance, fruity smell of acid on the breath, acidotic breathing, which is the respiration dehydration, then signs of shock for dehydration. Again, you can divide into mild, moderate, no, only be clinically detectable. Moderate would be your dry skin and mucous membranes. You skin severe would be some prolonged capillary time along the dry skin and mucous membranes at your skin do. And also clinically when you see the patient, they just look relatively dehydrated. Ok. And X goes after severe dehydration probably lead to shock. So you will have tachy perfusion, lethargy, decreased level of cost, urine output, reduce BP. So all this means that the no diabetic and then they fill all known or unknown diabetic. They fill the criteria of my heart plus they have all these symptoms. You have the first suspicion should be diabetic ketoacidosis. Now, where should these patients be treated? So most often it happens in type one X, right? And type one is detected at an early age. So they can come with a complication at any point of time. So if they are less than 18 years, they have to pediatric team. So you should know that you have to refer to the pediatric team and if they're 18 and above, they would be by the medical team, biochemical changes. So when you're correcting, obviously, when we get insulin, because it's high glu you don't want to overcorrect it lead to a drop in glucose, right? And insulin all plays a role in the potassium. So what insulin does is it puts, what is the potassium? So your serum potassium be high in acidosis because insulin is low type it. You don't want to lead to hypokalemia all of a sudden as well. So that's why you need to constantly keep monitoring when you're treating, that would take you to acidosis. Not like you give one medication when you're done. Still you reach particular standards required, you have to continue monitoring your treatment. Ok. And then find the cause of pre was it because they weren't taking enough insulin? Were they new diagnosis of diabetes or was it the other uh like the infection inflammation, iatrogenic infarct? Was that one of the four the precipitation of DKA? So find the pre and treat that as well. Don't treat that. Then there's always a chance that this the minute you stop the DKA treatment, you go back to DK. So as you're stabilizing the patient, you should also try finding the cause and treat the cause as well. Ok. So now when I said you have to meet particular standards, what you mean is. So we know that if the bicap is less than 15, it's considered acidosis or if the PH is less than 7.3. So you want the bicap to be more than 18, you want the Ph to be more than 7.3 your blood ketones, which was more than three, that should become less than 0.6. So this is ideally what you would consider as resolution of diabetic ketoacidosis. So now escalation of this. So you're treating but your patient is just getting more and more unwell. So this would happen if the Ketose is mo more than six or the bicarb is less than five or the PH is less than seven or if the hypokalemia is less than 3.5 right? So because you have treated it, so you've overtreated it now and the potassium level has gone less than 3.5. So that will again need urgent critical care input. So for all of the GCS is really low or the new score is really high. Every uh sats are getting worse, BP is getting worse, an anion gap is getting worse. So, anion gap basically means that basically there's excess of H plus, right? So that would lead to an increase in the anion gap. OK. And then if the, if you know the precept is like a surgical cause, the patient has recently had surgery and then that has led to this or if the patient is really young and you have to also be cautious when you're giving fluid resuscitation, you can't give too much of it all of a sudden because that could cause cerebral edema. So you have to be slow and cautious or if they are pregnant or if they're known to have like heart kidney issues or they're like elderly patients who are just not improving with your initial management, they're just getting worse. So you know that they need senior review or they would need ICU care. So always be prepared to call for help, like do what you need to do what is expected of you initially start it. But if it's not improving, you don't have to wait till it improves. Do not take to call for help. All right, has different policies. I believe this is what we follow in our trust until the senior comes. So main thing, what we need dehydration. So you keep the normal cell line right in the first half, don't give potassium because of giving normal cell line along with normal line, you'll have to start with insulin as well. So the insulin will be pushing the potassium into the cell. So you don't want potassium to be corrected. So after you give n normal saline in the first hour, depending on the potassium levels, if it's between 3.5 to 5.5 you can give some potassium along with the normal saline to maintain it in that range. Ok? It depends if your potassium levels are 5.5 and above, you don't have to give any more potassium. Just continue giving your saline and your insulin. Ok? Do the baseline injection, the blood ketones, the blood glucose, the PGS to check the ph full blood count to check what the pre in factors were. Whatever you're suspecting, you know, an ECG to check if the heart is ok. If there's any, in fact, if you suspecting an in fact in the brain, we have to do some see test to look for like an infection, digest infections. So these all this would be some baseline invest but you would do ask the patient to stabilize. The next thing you need to remember is so if they are non diabetic and they are insulin, do not stop that because you're giving a variable reading, you have to get long acting insulin along with the infusion simultaneously. And then once the patient is stabilized, you can stop the infusion slower, but you have to continue the long acting insulin, OK. Diagnosis, you have to continue this variable rate infusion till their comments on some long acting basal insulin. So like I mentioned earlier, so after you stabilize the patient in my horse to the college, you can get DS and review as well because if it's first diagnosis are always better to involve the DS. But obviously, the involvement will come after you stabilize the patient. OK. Targets. So as you're treating the target generally would be of the blood ketone patient by point mio poly in the bup by three double R reduction in the capillary goes by three millimoles per liter per hour. So when you keep checking every two hours, you these other parameters you're looking for. Is it? So that means you know, your treatment is working. If it's not like we mentioned earlier, you may need ICU treatment, you may need to get the senior involved. So be prepared. OK. By targets have not achieved right? Check the line if the canalized patient or not because you're giving fluids, you're giving insulin. But is it actually going into the body? Right? You need to check that check if the rate of the infusion is the right. That is. So this rate of the infusion again, there's like a separate criteria in every test. So you'll have these forms. So you can give it according to that and then once the glucose falls, you can. So again, when you're correcting the glucose levels, you don't want them to suddenly go into hypoglycemia, right? So if the glucose falls below, now, you can give like a long insulin and the fluids, you have to give a bit of glucoside just a little bit because you don't want to overcorrect. It's all about maintaining a OK, same thing with the potassium. So the minute to give insulin, it will reduce your levels, but you don't want sudden hypokalemia, right. So that's why I give a bit of potassium, a bit of sugar along with the correction of the potassium and the sugar. Ok. So this is pretty much the same thing I mentioned earlier. I'm not gonna go through this probably be a little too much. So now when would you stop this infusion that you're giving her the insulin infusion? Remember long acting basal insulin should be continued along with this and then this can be stopped once you've reached your target levels, but your basal insulin should continue. Ok. But that will also depend on if the patient is eating and drinking well, and you've reached these parameters. If you reach the parameters with the patient is not eating and drinking, well, you cannot stop it because again, that would cause issues. So only if the patient is eating and drinking, well, you stop and you've reached all the parameters patient are more stable. Now go back to the regular and get the DSN involved them to see if they wanna make any changes to the patient. So just one of the key, is it clear up till now? Uh on what is diabetic ketoacid? Does it happen? And the aims of the treatment? Have I lost connection? Hello. Can you hear me? Am I still connected guys? Ok. So now this is just one of the cases which we had come across in our hospital. So let's just walk through it together. Ok? I am really sorry. About the connection. I'm not quite sure why it's behaving the way it is. Ok. So, basically it's a 76 year old lady, right? She came with a fall and long life. And then when you did the blood glucose, you realized that it was 41. Ph was 6.9. So she's acidotic bicarb is less ketones were 6.2. Right? Oh, sorry. The bicarb level I jotted down here is wrong. So just assume that the bicarb was less than OK. So now you have her past medical history where she is a known type two diabetic who's on insulin, she does not take any regular dose, but her HP A1C was really high. So it means that her sugars were not under control. OK? She's had a recent total hip replacement. You don't know if this was just a ago or not, but you have arthritis. This is what's happening. OK. So now when she was investigated, we realized that she was having some sort of infection. She was confused when she presented to us. So we did do the rest of the screen. OK? Also because she had a long life, you have to do a creatinine kinase. So that was done, urine culture showed positive for cure. So here, what do you think are the risk factors for or to develop diabetic ketoacidosis? They're quite pointed of you. Yes. So phos thing is Gina, the age itself tells you that somebody older age group, right. She's noncom had a surgery. We don't know if it's recent or not. So we'll have to check that. That could be another precipitant right stroke earlier. But who knows she probably have, be having one right now, which is like precipitating cause she was confused to you. You're not able to get more history off of her, right? And then the next thing if you go to her infective markers were high, her urine culture has shown something so that again, could be another precipitative. So she has multiple factors that could have pre precipitated the DK. Yes, exactly the current illness infection. So, like we mentioned earlier, the main aim is in diabetic ketoacidosis to treat dehydration and ketoacidosis. And it is a continuous process to keep monitoring until your target levels are achieved. And the patient is ST OK. So now just overview of if there is a DK A in pregnancy, right? So again, pregnancy is occasionally one of the precipitants for diabetic ketoacidosis. So your mother and the baby both are at risk, right? So they can present with abdominal pain, but they may have only very modest elevation of glucose levels. Like the glucose levels may not be really high. But you know, the pregnancy is a risk factor for DK. So always all and if they present with abdominal pain, which is I can a common symptom of pregnancy itself, but you have to make sure that you've ruled out that the patient does not have. Ok. And this again, with the obstetric, the medical team together and again, keeping them at the high dependent. And I see. So treatment for is the same. Manage your dehydration, manage the insulin, you may just need to alter infusion rate in pregnancy because there is insulin resistance in pregnancy. So you may probably need to give higher infusion rates. Again, people who are already using insulin pumps in this what you should do. Uh I can start the continuous in, right? Make sure you get the seniors involved because you wouldn't know how to deal, discontinue the pump for a bit and start the standard DKA the DS since it more as soon as possible as well. Again, if they, there are patients who are on some SG SGLT two inhibitors, that is the sodium glucose cotransport type two inhibitor. I'm pretty sure I would have heard of agin Canagliflozin. You would have at least cyst being pre somewhere most often. If the like acutely unwell patient, you always hold this because again, there is a risk of if you pass, you're pushing the patient more into acidosis. So you hold this, you can restart it. I mean, if they're already in acidosis as well, suspend this medication, treat the acidosis based on the protocol, stabilize the patient. Once the patient is stabilized, you can always go back to the regular medications he was on. Ok. So that's it guys. I mean, do you have any questions? It can get a little confusing and difficult, but always remember, there will be guidelines in the hospital or diabetic ketoacidosis. So make sure you have the guideline with you and follow that. Keep monitoring the and whenever you feel you're not sure how to proceed further, do not hesitate to get senior help or even if you know how to treat, just involve the senior right at the beginning and tell them that this is what you're doing. Things go downhill. They're up to date and they, they're able to intervene. Ok. Any questions? Thank you guys. I will be Attach Week which will be hosted by one of my kindly to register for it. And also please do give and collect your certificates as well. I will be putting the link below. I really hope the session was useful too.