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Yeah. Right. I think we're alive now. Ok. So hi, everyone. Uh welcome to the next lecture in the Meath UK MLA series. Today's presentation will be on AK I acute kidney injury and it will be delivered by Doctor Ban Latiff. Uh My name is Chen. I and I'm from the med team. I'm one of the medical educators and I'd like to pass on to Doctor Latiff. Um Hello, everyone is, is my voice or her. Can you hear my voice? Can someone confirm if my voice can be heard? Ok, perfect. So, hi, my name is Wan. I am. I used to be one of the junior clinical fellows in uh General Internal Medicine and Geriatrics in the Royal Free London Hospital. I was a GP practitioner overseas. I am now back in my country and I'm presenting this lecture there. I used to present this lecture in the Royal Free Hospital. So if you guys are ready, let's just dive into the subject right away because I'm already late by five minutes, which I really apologize for that. I had to uh uh travel very quickly just to have a pla get a place to get internet connection. So I guess we can just dive right in. Um is my screen visible. Can everyone see the screen the acute kidney injury, please just confirm perfect. Ok, good. So acute kidney injury, we're gonna talk about that but we will start with the case. You have a 87 year old male presented to the ed with confusion and he was diagnosed with lower respiratory tract infection. This is his admission bloods which showed a creatinine of 250 a urea of 15 and an EGFR of 70. So the question would be, what is your comment on the blood tests? Of course, we are using the UK uh United Kingdom units for these ones. Uh If you're not familiar, these values are definitely raised, the creatinine is raised, the urea is raised and the EGFR is low. So the question is, what is your comment? We would say these are like abnormal blood tests. But the important question would be, is this an AK I is this an acute kidney injury? So put an answer in your mind and we will go to uh next segment. So the answer would be first, you have to match the criteria for an AK I and the C the criteria would be the following. You must have a rise in creatinine as the following. For example, you must have more than 26 micromole per liter, uh rise of creatinine within 48 hours or one. And a half times the baseline within seven days, as well as a urine output reduction of less than half a milliliter per kilogram of body weight per hour for six consecutive hours. In that case, we can say that we have an acute kidney injury. So this is based on the K ego, which is the kidney diseases, improving global outcomes guideline. Um So if we define the AKI, it would be as defined as the following. For example, it's a syndrome of uh decreased renal function. It's sudden and often reversible and it occurs over how much do you think? So take a guess how much do you think it occurs over? So it open over hours or days or even weeks depending on the cost. So how do we measure the AK, as we mentioned, we have the criteria, the same criteria as what we used to measure the AKI. So it's by serum creatinine and the urine output. And then the next one would be um the next thing we need to know is it has different et and it can be multifactorial. So it can have two causes responsible for the AK at the same time. So what about mortality from AK? Generally, the mortality is low if it is uncomplicated AK for which is around 7%. But if there is sepsis and multiorgan failure, that will be around 50 to 70%. And of course, the mortality depends on the cause of the AK and not the AK itself. So, sepsis is a different from just mild dehydration or dehydration in general. OK. Yeah. All right. So staging, how do we stage the AK I, first of all, you have stage one, stage two and stage three. So first stage one, as we mentioned, you must have a rise of at least 26.5 micromole per liter or in other other units which like the AER the American systems use uh milligram per deciliter, which is 0.3 or any rise of 1.5 to 1.9 of the baseline. And then the urine output should be less than half milliliter per kg per hour for 6 to 12 hours. And then if you want to go to stage two, you need to have a rise of the baseline of around 223 or let's say 2.9 of the baseline and the urine output has to be the same amount, but it should be more than 12 hours. That would be considered as AK stage two. And then if you want to stage three, you have the number which is 353.6 microm per liter or 4 mg per deciliter or any rise uh three times of the baseline or anyone who is indicated for a renal replacement therapy, these people or dialysis that would be considered a stage three AKI if we've taken into uh consideration the urine output, that would be less than 0.3 per milliliter per kg per hour for 20 for more than 24 hours or in an area of 12 hours. So these are the staging for um AK I So now as you know that we use creatinine a lot in our um staging and recognition and the criteria for AK I, we should also know the limitations of creatinine. So if any of you have, know anything about the limitations, you could share something in the comments. Yeah, sure. So, so uh Glena to go, go back to the slide that talks about the urine output. Is it that one? Um So now I'm gonna slide muscle to previous slide to this, please. Um Yeah, sure. Let's cover this slide. So that is the slide about the criteria for an AK, no problem. And I'm gonna move forward now. So that is the definition have a quick peek and please let me know when to move forward. OK, perfect. So we mentioned about the stages and now the limitation of creatinine. So somebody mentioned in the comment uh it was ni uh which was right. Um So creatinine is in thin individuals who have low muscle mass, you will have a lower creatinine in general. So if you measure AK I in these patients, you might have a big AK I but because of the low creatinine, it might be underestimated. And the same is true for people who have a big muscle mass, you might overestimate an AK when in fact, the AK is just very little. So that is our limitation of creatinine. Of course, creatinine is different from race to race, each uh group of race of people um can have different uh readings for creatinine. So our labs tend to correct these, they use their special equations. This is something I'm not gonna go into, into detail. So the risk factors, why would someone who is um uh going to be at risk for developing an AK I? So any guesses? So I'm gonna move forward. So anyone with a preexisting chronic kidney disease is at risk of developing AK I the higher, the higher the age, the more the risk, male sex and comorbidities which you might already know by now that diabetes, cardiovascular disease, malignancies, chronic liver and complex surgeries, these increase the risk of AKI and then we're gonna come to the causes. Um Yeah. So someone mentioned that be check statin C levels. Yep, that is one of the new substances which is not, not really new, but has not made their way into the textbooks of how to measure the uh um uh renal function. I don't think in practice, it's still used cystatin C levels, but it is the one that I use most often in research uh than uh in clinical practice. So, yep, cardiac conditions age and infections. So in general, I'm gonna go roughly through the causes of AKI. So your hypovolemia is very common and then you have sepsis and then you have drugs and obstruction. These are like very common causes of AKI. Of course, you have cardiogenic shock, you have hepatorenal syndrome and you have major surgeries. These are just like randomly gathered causes, but like the most common ones. But if you have ever come across an A Kr and textbook or in any um medical lectures, you would know that it is um classified as prerenal where there's decreased perfusion to the kidney. Um for whatever cause or you have a renal one where you have an entrance in renal disease, or you would have a postrenal which is an obstruction to the urine outflow. So these are like how the causes are um classified. So we're gonna come give you a couple of examples. So for example, if you have a prerenal, you would have, for example, decreased vascular volume um or dehydration, for example, as an hemorrhage or, and due to that and vomiting, sometimes the volume is fine, but the cardio output is not fine. In that case, uh for example, in a cardiogenic shock or an M I, sometimes the heart is pumping very fine, you have enough volume but your blood vessels are uh uh under uh pathologic stress. Like for example, vasodilatation from sepsis or sometimes you just have a renal vasoconstriction. Like for example, when you take necessary antiinflammatory drugs, which are known to be nephrotoxic So you don't prerenal does not necessarily mean reduced vascular volume. It could mean anything that interferes with the uh blood vessels going to the kidneys and then you have the renal ones. So it's either in the glomerulus, like for example, inflammation, glomerular nephritis. It could be the interstitium where for example, you might have an infection like pyelonephritis or it could be in the blood vessels like for example, vasculitis and then postrenal which is either an obstruction inside of the renal tract or an extrinsic compression. Like for example, a pelvic malignancy onto the uh ureters onto the renal tract which causes the obstruction and then uh an AK. So what are the early management steps of an AK I anyone can give us any clue, any hints. A couple of words will do just fine. Um So the chat is silent, stop nephrotoxic drugs. Definitely, that's one of them. But I wouldn't say that this is the very first step that we would do. The early steps would be something, let's say a bit more urgent fluid management, stop drugs. These are all correct. But what is the very first thing that I want to run into? Um when I see an AK and the blood results? So let's go forward. So the very early steps is first to check if there are any life threatening complications, what life threatening complications would you expect from an AK I, somebody mentioned BP, vitals, urine. Definitely, you will do all these treat the underlying cause, definitely treat the underlying cause. But before we move on to the course, before we do anything, the first thing is to check if there is any life threating complications and that would be a high Kalemia which is accompanying Akis. So you will treat it immediately if there is any potassium, more than 6.5 or there are changes due to hyperkalemia. Ok? And if there are any pulmonary edema and fluid overload in these cases, we try to manage these as early as possible and then we move on to the other things. So we're going to examine the patient for sure. If there's any signs of hypovolemia, we can quickly treat with fluids, which is a bo of 250 or 500 mL. You can give up to 2 L and then review. So you can also check the bladder quickly. It's a very quick exam. See if the bladder is palpable, if it was, you will catheterize and if there is no response, the best thing in medicine is always be a safe doctor and always involve somewhat more experience than yourself. So you seek an expert review and these are like the early steps of management of an AKI. So now that we have managed these things, um we have to monitor the patient. So how often do we monitor a patient with AK I first vitals on observations every four hourly. And then if the patient is not catheterized for obstruction, let's say it was due to dehydration. Um We will still consider putting a catheter just to measure the urine output. It's not a must have, but it's something we closely consider, especially in an AK which is difficult to manage. So, if there are signs of sepsis, we make sure to send for lactate and do the sepsis management. And of course, we monitor creatinine daily. What is important to know is that the creatinine levels lack 24 hour behind the clinical response. So if you are, if it is resolved today, it will take 24 hours to um uh get the creatinine match the clinical response. So it will be late by one day. So, investigate how do we investigate a patient with an AK. Um Do you guys have any ideas? Yup, ultrasound scan. Definitely ultrasound is definitely one of them correct. Check urine analysis. 100% fractional sodium. Absolutely. Blood your nitrogen. Definitely true. You guys have a good idea about how to go. First of all, we'll go to check a urine dipstick, which is a quick bedside examination. Ideally, before we put the catheter. So if there's hematuria and there's proteinuria, we wanna know how much of these we have because these may suggest an interesting renal disease, we'll check the urine specific gravity, which we expected to become high in dehydration. And then you will check the urine sodium. Normally, if you are dehydrated or in prerenal, ak, the body tends to um keep the sodium for itself. So you might have a low urine sodium in these cases. But in renal IK you'll have a urine sodium of more than 40. And then in prerenal, as I said, it will be low. So it will be around less than 20. That is the normal. So we check platelets if anyone has any, doesn't know why we check the platelets could write it down in the in the chat. So why do we check the platelets? Yes. Uh Abdul uh get the correct answer because we wanna check um if the patient has hemolysis because of a cause known as hemolytic uremic syndrome. And we also check liver function. Part of me, I have a terrible cough. So sometimes I might cough. Um So why do we check the liver function? Correct? And and the reason why we do the liver function? Yeah, some manner, correct answer. It would be to check for Hepato syndrome where you have liver failure, accompanying renal failure and creatinine kinase. You know, this is something found in the muscles. This can be found in AK I in a patient with a long life. So for example, in elderly patients where you have a patient who is dehydrated, had a fall due to dehydration, had delirium and started to lie down on the floor for six hours and with either a neighbor or a partner or someone else in the house finds out about it. So we check the creatinine K is to check if this is responsible for the AK I as well as to check for any uh Pernal ones. So we check the serum urea to creatinine ratio because it will be high in prerenal AK I and low in post renal. OK? Because the urea uh is go arises in a couple of conditions which is not just an AK but also rises in dehydration as well as in dry bleeds. So it would be expected that you can have a high urea in a prerenal AK and low in postrenal. Ok. So, investigation further, we will do investigate for intra diseases, not in every AK but only if indicated. For example, you would send the immunoglobulin levels, the para proteins, the complement and the autoantibodies like antinuclear antibodies, antinuclear cytoplasmic antibodies and anti basement membrane. Um ultrasound scan. We don't do it for every single patient with AK. Um But um if you're suspecting an obstruction, it would be good to do an ultrasound. Um But if the patient has responded already to your fluid management, then likely this has not been an obstruction and the ultrasound would not be indicated. So you might find small kidneys like less than nine centimeters that would suggest a CKD. And if you found asymmetry, that could suggest renal vascular disease. Ok. So now that if you me earlier, some of you mentioned that we stop nephrotoxic and we will do uh vitals and stuff for every patient, regardless of the cause of the AK, we will always try to optimize renal infection for everyone. And it will be done through the following. If the patient is septic, we will treat the sepsis. And if the patient is nephrotoxic, has any nephrotoxic medication, we will stop the nephrotoxic medications even if the cause is not these medications. Um So the following would be like nephrotoxic nonsteroidals, ac inhibitors, angiotensin receptor blockers and aminoglycosides. Most of the time, for example, in the elderly, you will have an aminoglycoside as the cause of the AK I in the elderly with a uti. Um so stop the drugs that may increase complications. Um for example, the following diuretics, especially the potassium sparing because um AKI can cause hyperkalemia as well as potassium sparing diuretics. So we wanna avoid that Metformin is not given during acidosis and in a low creatinine clearance and then you have some antihypertensives. So you check all drug dosages um for the renal impairment. Most of the time you have to liaise with the pharmacist and they have something called the renal drug handbook or sometimes the renal team. And the same thing can be found in the renal drug database.com where you check the doses for a patient with AK I and D. So you have to prescribe or represcribe the drugs to different doses which is appropriate for the AK I and of course, uh common sense would be to avoid radiological contrast, consider gastroprotection and consider nutritional support. These are not always, but you just consider doing an AKI. So when do you ask for advice from the renal team, you are not gonna ask them for every AK you are also not gonna um refer every AK I to the renal team. But in the following, it would be wise that for the renal team to be aware because they are specialist and they know how to advise you through a patient with AK that could be difficult. So for example, if the AK I has anything stage three, so stage one, you can manage stage two, you can manage even as a junior doctor, but anything stage three and stage three, I think it's recommended that you should contact the renal team. And if your AKI is not responding to treatment, it's good to uh consult the renal team. If you have complications like hyperkalaemia, acidosis and fluid overload. If you notice that hyperkalaemia is in gray and not as in black. The reason why I had to put it is because some textbooks recommend that you contact them for hyperkalaemia. But in practice, you don't really contact them, you just manage hyperkalaemia, which we're gonna come to on how to manage it. But acidosis, you definitely have to contact and fluid overload because it will be difficult to manage. And then if your patient has a difficult fluid balance for example, has hypoalbuminemia, heart failure or pregnancy, definitely tell the renal team. And if there is any interesting renal disease, the right person to manage this would be the renal team and not us, not even my consultant who would be a geriatric consultant would uh would want to manage a patient with intrinsic renal disease and would leave it for the renal team who are the experts in this one. So hypertension again, I wrote it in gray because that's what some textbooks recommend. But in practice, we never referred to the renal team just because the patient is hypertensive. So when you contact the renal team, um they're likely gonna ask you the following. So the each country might be different or each system you're gonna work with is different. But in the UK, you are expected to have all the information on the patient before you actually contact the team because if you don't, they're gonna ask you and if you don't know, you're gonna be fluster and you're gonna check left and right for information that you should have already known. Pardon me? So before you contact the renal team, make sure you have the following relevant information. This is true for the renal team and for all the other teams, you should always have your um relevant information prepared to you. So the clinical observation of the patient, the new score since admission, their fluid input and output your examination findings, like are they hypovolemic or hypervolemic and any of the patient has any comorbidities. You could tell them about the creatinine trend, the creatinine baseline, the potassium status and bicarbonate and lactate. And of course, you'll tell them about the, the uh hemoglobin and platelet count, which you know about that already. Why. Um they would ask you today, you were on dipstick. So you can always do a dipstick and then contact them afterwards. Um And then if you have an ultrasound scan result, you can always tell them about the ultrasound scan results. OK? And drugs, they will ask you if this patient has been given any drugs. Has the patient been given any nephrotoxic? If yes, what was the drug? And when was it given? So now we're gonna come to the um yeah, so now we're gonna come to the management of an AK um in more steps that's gonna follow the earliest steps that you mentioned. So the earlier was to exclude any life for complications. And now we're gonna come to the management. So you always have to treat the cause. Uh because as you know, you have the prerenal, renal and postrenal and if it was prerenal, likely sometimes if it was uh volume depletion, you will correct. So you, if the cause was not the volume, if it was the heart, you will try to increase the renal perfusion by circ by supporting the heart. So, cardic support via ionotrope. And if the patient who septic, you will treat sepsis. So, just something to know is that in prerenal AKI, the kidney will not be damaged unless the AKI is severe and sustained for a long period of time. That is why luckily, um for us and for the patient, when we treat an AK due to dehydration, it's rapidly going to respond to, to the fluid management and to the um and the renal function will come back very quickly and fairly normal without any damage to the kidney. Um And renal, as I mentioned, you have to discuss with the renal team if it was a postrenal, um depending on the cause, of course, again, but it could be a catheter, for example, the patient is in urine retention or if there is a urological obstruction, you need to um contact the urological team for either what the, what, what they recommend is gonna be a nephrostomy or any other urological intervention. Um That one however can lead to chronic renal injury over several weeks. So it can lead but it takes time. So in management of an AKI, you have four pillars of every AK management and that will be the following. First of all fluid balance, for everyone, you need to have the right fluid balance. We don't wanna oh put the patient into fluid overload if they were dehydrated. Um So I'm gonna talk about that in each, each of these one in detail, but fluid balance is one of the pillars. The other one would be to manage acidosis. The third one would be hyperkalaemia, the fourth and the last one would be primary recognition of anyone who might need dialysis or renal replacement therapy. So let's go to volume status. I am sure most of you would be familiar with the signs of hypovolemia. So it could be either low BP, low urine volume or nonvisible JVP in a patient which had previously high JVP or in a patient who lies down and you still cannot see a JVP when the patient is lying flat. So you might have poor tissue turgor, you might have a high pulse rate. And for example, daily weight loss. One thing to note is that sometimes hypovolemia will not be uh detected by low BP because low BP is not as sensitive as a postural drop, which is a postural drop in BP. And that is a known as orthostatic hypotension. So if a patient has orthostatic hypotension, then they are dehydrated even if their BP is normal or something with like over 100 20/80. So that was something I would say would be the giveaway regarding the BP and hypovolemia. So uh low BP, skin t and capillary changes may be late. So don't wait for this. As I said, low uh postural hypertension is a more sensitive indicator and when it comes to fluid overload, I'm sure, although you can think about signs and symptoms of fluid overload. So you might have an increased BP, maybe not, you might have a raised JVP. You might have basal lung reputations. You might have peripheral edema and they gallop rhythm. So these are the signs of fluid overload. So just one note would be raised. A VP does not reflect intravascular volume if you have a right sided heart failure, because that would be the reason for the raised A VP. So if the patient was hypovolemic, we would have to do fluid or gestation. And as we mentioned before, you know, perfusion simply improves with just volume replacement. So you give a 500 mils or 250 in elderly um over 15 minutes of a crystalloid and the crystalloids would be either uh something like a ring or lactate or a sodium chloride. So you have, you can repeat the bodos of 255 100 mL again and again, up until 2 L are given or until the patient is UIC. So we just need to care about in two groups of people. One of them would be in cardiac disease because you might have decreased renal perfusion. Despite adequate circulating volume. We mentioned that sometimes you do not have an issue with the blood volume, but with the heart pumping is not efficient. So that's why we have an AK and, and sometimes as we mentioned in sepsis because it's not low blood volume, but because there's vasodilatation in sepsis, so we have to treat the sepsis and not give too much fluid. So always and always examine before and after you have given fluid to a patient to check for adequate response and to check for further needs. Um And to check for the patient is might be at risk of fluid overload if you are ever unsure about it. Um or if the patient remains in shock, always get an expert help. So, uh we mentioned about the fluid recreation. So the choice of fluid would be crystalloids. You will have normal saline or sodium chloride 0.9% but this can cause hyperchloremic acidemia. Lately, all the guidelines and all the researchers point to that the better fluid would be either Hartman or will be r lactate, which is a more physiologic one. But in this one, because they contain a little bit of potassium around five millimoles. So you could have uh if you have hyperkalaemia, be careful in using uh Hartman, it's not contraindicated, but you need just to use it with care. Um No normal sign is still fine. It's very unlikely to cause hyperchloremic acidemia with just a couple of, with a couple of uh with around 2 L. It needs to be given for prolonged periods of time to cause hyperchloremic acidemia, but you have to know that it can cause. So, if the patient has septic shock, we mentioned that again, crystalloids are the choice colloid will be second line only under special advice. One colloid would be like an albumin solution. And if the patient has hemorrhage, again, it will be fluids and then blood whenever the uh blood components are available. So if hepatorenal syndrome, we prefer a solutions. But again, under a specialist advice, as a junior doctor, if you are gonna ever ever become one, you are likely never gonna prescribe a colloid. It will always be under someone more senior than yourself. But you have to know about this anyway. So if the patient has hypervolemic or fluid overload, why do you think the patient would be in fluid overload or in uh hypervolemia? If you could think about a couple of causes before I put on the slides, so it can occur. Because first, we might give aggressive fluid reation in a patient with a dehydration. A ky. That is also true because the brain systems will be activated to preserve more fluid. And then uh it can happen due to oliguria. The kidney is not uh diuresing the uh extra blood volume that we have. And then you have increased capillary permeability, like and sepsis. This can be the reasons why you might have this one. So we will try to monitor the patient's weight daily. So in part of our plan, we write, please dear nurses, please monitor the patient's weight daily. So we can check the response of the patient to the IV fluids and the other things that we are gonna give the patient. So um fluid restriction in some people, for example, and cardiac failure, we have to give fluid restriction. So we receive the fluid to around 1.5 L or 1 L or even less if we have to. And when you calculate how much fluid the patient gets, please, you have to also include anything that the patient takes orally from other things, not just water and meals, but also from medications and IV fluid volumes. Like for example, the patient is on an antibiotic that you use in 100 mL of fluid. This also needs to be taken into consideration and calculation. Ok. So as I mentioned, you tried to give antibiotics and minimal fluids and you consider concentrated nutritional support for the patients who are needing nutritional support. Um We have different forms where the nutrition is the the nutrition pack is more concentrated with less fluid in it. Ok. So my question would be for the team. Do we give diuretics or not in an AK? Can I get a yes or a no? You don't have to be right. You just have to participate. Loop diuretics can be given. That is true. So I am just gonna go ahead. Now we have an answer. So yes, you can be given but only in symptomatic fluid overload and they are ineffective and even could be harmful if it's used to treat oligouria in someone who has no fluid overload. So, renal replacement therapy or dialysis is in the following can be indicated AK I with fluid overload and oligo urea or anuria. And that needs urgent referral to the renal renal team or the critical care team where they will immediately dialyze the patient and uh the fluid volume will be removed. So the second pillar would be um aosis. So let's just check same. So no potassium sparing diuretics. Yep, that is true. We try to avoid potassium sparing diuretics as you mentioned earlier because it is one of the medications that can cause complications in an AK because AKI can cause hyperkalemia. That is also true. Uh But if we use anything that would be loop diuretics, something like furoside or Lasix. So now we reached acidosis. So you have mild, moderate and severe, mild would be something between the ph, between 7.30 to 7.36 and or the bicarbonate anything more than 20 if you have moderate, that's even less. So that's 7.20 to 7.29 or bicarbonate of 10 to 30. And then if you have severe, that would be anything less than 7.2 and the bicarbonate of 2010. So, how do we treat acidosis? And you can tell us. So this might be a true question. The answer might be actually quite simple. But how do you treat acidosis? Yep. So, um happy that manner. F for the true question and abigail as well. So basically, the treatment for acidosis would be to treat the underlying cause for the AK and when it comes to B yes, that's true ablative. So you treat the cause first, you don't give bicarbonate to treat acidosis. Treat the cause first and the acidosis might resolve by itself because if the treatment is delayed acidosis will persist and now the patient might need renal replacement therapy. So, medical management of acidosis which is via bicarbonate is actually controversial. It is not wrong but controversial. So some sources say bicarbonate will generate CO2 and that you need to have a adequate ventilation to get rid of the extra CO2 to prevent respiratory acidosis. So, in a patient who has has hypervolemic and fluid overload and in pulmonary edema that might actually worsen the clinical picture. And some sources say um the sodium bicarbon has a sodium component in it. So that again can cause fluid overload and it's not good in some patients who are vulnerable, but um it can improve hyperkalaemia. So I don't think ever in practice, anyone uses um sodium bicarbonate for hyperkalaemia. Um even if it can be improved, more or less it's almost never given unless a senior um physician tells you to do so as a junior doctor like for or it has to be a specialized, like for example, the renal team or in the uh intensive care unit So the third pillar would be hyperkalaemia and that by itself is a topic deserves its own lecture. So that lecture is actually that we're giving is two lectures, one inside the other is going to be about hyperkalaemia. So the first thing that you do is you want to check if the patient has true hyperkalaemia. So how do we check if the patient has true hyperkalaemia or a full hyperkalaemia? Anything, any ideas? E CG um So E CG can detect if there is cardiac changes. E CG changes for hyperkalaemia. But how do you check if this is a true hyperkalaemia and not a false one or let's say a false reading. So, ecg changes, you can have hyperkalaemia and no ECG changes and that hyperkalaemia would again still be true. So, yeah, you can repeat that is one of the things. So we're gonna talk about how to differentiate hyperkalaemia true from the pseudohyperkalaemia in the following. So for example, first, just check the patient if the patient is well and if the patient as well and you have a hyperkalemia, you just feel like it's not reasonable, just repeat the test urgently because it might be an artifact and an artifact would be the following. So yeah, so Sonia mentioned some ECG changes that is peak P wave. I don't think you would have peak P wave. Um But we're gonna come to the ECG changes, you would have a peaked another wave. Let me I'll let you guess it's not P wave though. Um So these, the following conditions can cause a false hyperkalemia, which is not true. So that means if you repeat the test, um you will have a normal potassium level and yep, improper sampling is one of them, but more common than improper sampling. And more accurately is, for example, if the patient has hemolysis, if the sample is hemolyzed, you would have hyperkalaemia. So you need in your sample. And then if you have a difficult venu puncture, for example, the patient has a difficult vein and has cleaned the fist, cleaned the fist. Um These two can cause again, false hyperkalemia and then contamination. So most of the time when you take blood, especially if you are not a litus, you might not know the right order. So we have many patients needing, let's say full blood count and a renal function. Um So you have two bottles, the purple and the gold top. So the gold top goes first because if you go with the purple one, which is for a full blood count, it has something called EDTA ethylenediamine tetra acetic acid, which is an anticoagulant and that can interfere with the potassium levels. So it's better to do the gold one first. So you have an accurate level of potassium and then you can do the purple one for full blood count. Ok? If you have thrombocythemia, you have a lot of platelets, sometimes platelet leaks out of the platelet during clotting. And for example, delayed analysis. This is very rare to happen in the hospital, especially in AK and hyper hyperkalemia because these bloods will be sent normally and marked as urgent. So, in delayed analysis, again, just like the platelets, potassium leaks out of the rbcs and it can cause a false hyperkalemia when in reality, it is not. So as you mentioned, these are the things Yep abigail corrected the thing. It's actually peed T wave for the ECG. We're gonna come to that. So what other things contribute to having a hyperkalemia? The following things. Um If you have an AK and the patient is on a potassium sparing diuretic, this is gonna increase the hyperkalemia if you have rhabdomyolysis because of a fall with long lie. Um If you have metabolic acidosis, we all know in acidosis, potassium tends to come into the blood stream and escape the intracellular environment and excessive potassium therapy or intake. I would like to tell you about a funny story about intake. Uh This doesn't happen to me. It happened to one of my senior colleagues. They mentioned that we had a patient with AK and the AK. I was, I don't remember the cause but the cause was treated. Um it was resolved. The only thing that was not resolving was the potassium levels. So the bad potassium levels seem to stay high even many days after the AK has been resolved, which is very unusual for an AK I and this probably happens like one in 10,000 cases or one in a million who, who knows. Um So then one day, one of one that, that senior colleague of mine said, um why don't we go check and see what the patient drinks? So they go to check the patient's um things and they find that the patient has a juice called, I don't know the name of a brand, any brand, definitely not natural juices. These like uh I think that you find in the markets and stuff. So they check the content and it's filled with um substances that contain potassium, potassium, sorbate, potassium, citrate, potassium, et cetera, potassium, et cetera. So they ask the patient, could you please stop taking this? This could be the reason why you have um hyperkalaemia even though we no longer have the AK and uh lo and behold after they stop the juices that the patient drinks daily, his potassium levels go back to normal. So yeah, always think about intake, especially in these cases. OK? And uh then you have Addison's disease uh where you have low steroid hormones and you have corticosteroids. Um and then you have massive blood transfusion. These can cause hyperkalemia. So, burns can cause hyperkalaemia and drugs like ac inhibitors. So sorry about that. When we have hyperkalaemia, we go to examine the patient. The one thing that would say would stand out in a patient with hyperkalaemia would be about the pulse. So do they look unwell because if the patient has a complication of hyperkalaemia and they have a problem with the cardiac rhythm, they would definitely look unwell. So if the patient has a fast irregular pulse or if they have chest pain or sudden weakness or palpitations or any sudden lightheadedness, which is again due to the cardiac arrhythmia, they might be truly hyperkalemic. So that's what we do an ECG. And as we mentioned earlier, the following things are gonna be found in the ECG. So you would have tall and tented T waves, you would have small T waves and you'll have a wide, curious complex and eventually it becomes sinusoidal. And of course, if you don't treat it, it will become ventricular fibrillation and eventually cardiac arrest. So that what is an ecg of what, what uh hyperkalemia would look like if you notice the big T waves um prominent in leads V one, V two and V three. Um And then you could almost see no P waves anywhere except for the T waves and the Q RSS. And you definitely have a broad QR S complex, which is more than three small squares and normally they should be less than three. So that is a hyperkalemic changes of CG. So as you mentioned to 10 to T waves, increased pr interval, small or absent P wave widen curs and then finally, sine wave pattern and then assisted So that is a sign with pattern of ECG. I've taken both of these ecgs. Oh, I'm sorry, the second one, the one that is currently from the Oxford handbook of Clinical Medicine. And yep, as you can see flattening of the P wave, prominent T waves. If you check um, the lead, uh see uh A V two and V five, you could see at wave as almost as high as a complex which is unusual. I know it might be difficult to read because this is a Sinewave VCG. Um But yeah, if you, but you can compare the T wave being high enough to almost match the height of the Curis, which is not usual. So when do we treat hyperkalaemia, do we treat any hyperkalaemia or all hyperkalaemia? Um If you could let me know in the chat. So when do you treat hyperkalaemia? And I just would like to say that this is irrelevant of whether the patient has an AK I or not because hyperkalaemia is a topic of its own. But it is true for a patient with AK as well. So, um OK, when the patient is hemodynamically unstable, well, that would be true if it is due to an arrhythmia, that is where the hyperkalaemia is um is responsible for that arrhythmia. But if the patient is hemodynamically unstable due to a different cause, for example, dehydration or an arrhythmia not related, then we do not treat the hyperkalemia just because of this. So absolutely. So rear gave the correct answer. When you have ECG changes, you definitely have to treat. That is one of them. And the other one is whenever you have any hyperkalaemia, more than 6.5 you will always treat and ECG changes and I in a potassium more than six millimoles per liter. So the most important region in significant hyperkalaemia is so I want that answer because that is the most important thing that I want you to take away for today's lecture. What is the most important step? The most important treatment for hyperkalaemia? What is the first step? What is the golden treatment that we give in hyperkalaemia? Correct? We changes definitely. So any potassium more than 6.5 and any changes in your potassium, more than six calcium gluconate, that is the correct answer. So the very first thing that we want to do is not to lower the potassium immediately. Um Neither is the IV fluid. It's definitely uh attempt to stabilizing the cardiac membrane to prevent the arrhythmia. The hyperkalaemia can wait, we can correct the hyperkalaemia. So, but metabolizing the cardio membrane is the very first step to hyperkalemia. So you can give 10% sorry, 10% of calcium chloride, around 10 mL or 30% of 10% calcium gluconate. Both are appropriate and many trusts you have both. But it's preferably to be given IV over a big vein over 5 to 10 minutes and not of a small one because they can irritate the vein and they are repeated as necessary for the ecg if the ecg changes persist. So this is cardioprotective uh for around 30 to 60 minutes. So now it gives us time um to correct the potassium levels. Ok. So you don't go for the potassium levels first. So there's some notes about these ones. So calcium chloride contains three times the amount of calcium for calcium gluconate. And there's concerns about the bioavailability of calcium gluconate and both salts of these ones have a risk of necrosis with extra conversation. So it's preferable to have a cannula in place and um um over a big vein. So after you have stabilized the cardi membrane, the next step, yeah, a lot of correct answers. Uh calcium gluconate, calcium gluconate or calcium. Yeah, perfect. Perfect. Yeah. So that is the most important step. And then the next step is reducing the potassium levels. So anyone can tell me how we can reduce the potassium levels. Somebody already mentioned Ventolin nebulizers, but I would say that we would not jump to Ventolin nebulizer as a first line. Anything else? If it is the only thing at your disposal? Then? Definitely. Yep, racing is one of them. Insulin is one of them. Perfect. So you have insulin dextrose. Um So the dose would be 10 units of solub insulin and 25 g of glucose. So that 25 g of glucose depends on which preparation you have. It would be either 50% and 50 mL or it would be 20% of 125 mL. Thankfully, in some of the trust, like for example, London Hospital, which I was working in, we are working with an electronic system of the APR. You don't have to remember these numbers. You just have to type hyperkalemia management and you, it brings you the insulin dextrose combo, you just have to prescribe it. So, but if not, then you have to know the numbers. Um So the way the how the way it works is that insulin stimulates intracellular uptake of potassium and it lowers the potassium by around roughly one unit over 30 to 60 minutes. So you have a potassium of 6.5 you would expect to drop to 5.5. OK. The one thing is you have to be careful for is that you have to monitor for hypoglycemia because it can happen um especially in renal impairment. It can happen in up to six hours after infusion. Um So you have to for the nurses kindly to monitor the blood glucose um for the next six hours. Sorry about that. And you have salbutamol um inhalation via nebulization. So it can cause again, intracellular potassium shift, but you would need high doses. So for so for asthma, you might need 5 mg um to inhale or to sorry, not inhale uh to, to nebulize and then inhale. Um but you might need 1020 mg via nebulizer. And that makes it inappropriate for, if you can guess it would be for patients with tachycardia. So patients with ischemic heart diseases, you can only use 10 mg and it's preferably to avoid it in tachyrhythmia. And then you have calcium b sorry, potassium binding resins like for example, you have calcium resonium, which is 15 g per eight hourly, which three times a day per oral or as enema. And you have something called lokelma, which is something also used by the renal team or by other trusts. Um It's the scientific name would be the sodium zirconium, cyclosilicate again, 10 g three times a day orally for three days. And then you have er so btex calcium, this is again another potassium binder. We can use all three depending on the potassium. Hello. So if we do not correct the underlying pathology, um then renal replacement will be indicated eventually. Um the options would be either hemodialysis and hemofiltration or just peritoneal dialysis. So, what possible indication we would have for renal replacement therapy? Anyone can guess correct. Insulin dextrose. So what indications do we have for renal replacement therapy? Progression to C KD. That's a tricky one. Yeah, definitely stage three AKI that is one of them uremia. That is true. Complicated uremia, fluid overload. That is definitely true. Not every fluid overload, but some fluid overload, especially in pulmonary edema, life threating pulmonary edema, electrolyte, imbalance, acidosis, fluid overload. Perfect. That is true. Resistant hyperkalaemia acidosis, less than 7.2. Correct. That is all true. So, the following would be the indications of fluid overload, unresponsive to medical treatment if you have severe or prolonged acidosis and if you have a recurrent or persistent hyperkalemia despite medical treatment, and then of course, uremia with complications like uremic pericarditis or uremic encephalopathy, which of course, as we mentioned, both AK and the complications of uremia are more common in patients who already have CKD. So, complications of renal replacement therapy, it's not a uh uh risk free treatment. You would have first of all risk of dialysis insertion and the maintenance, the catheter insertion and the maintenance. And then of course, you might have hypertension from the procedure, you might have bleeding because the patient might need anticoagulation. Of course nutritional drug clearance. That's why if you remember that we might have to consider um nutritional supplementation for patients who undergo AKI not for everyone though. Um They goal is, as we mentioned before is timely recognition. If you remember the fourth pillar was to recognize who might need a renal replacement therapy because we do not want to give it as a treatment when complications happen. We in fact want to prevent further complications. So going back to our case, we have an 87 year old man presented to the ed with confusion. He was diagnosed with lower tract infection. His admission blood showed the following. If you remember the question, I said, what's going on? Is this an AK or not? Now, we should be able to answer the question. The answer would be we don't know without previous creatinine baseline because that patient might have already existing CKD and now presenting with the same thing. Um So the following would might help you in recognizing the features of AKI versus a chronic kidney disease. So AKI is normally of short duration of symptoms. Thankfully, in most of the trust, you have access to the patients, previous records, uh previous admissions. So you have all the blood um investigation line next to each other. Um So you can compare and then the labs of AK I that is, that is uh consistent with uh AK I would be a low urinary sodium as you mentioned, especially in uh prerenal AK, which is the more common one than renal and postrenal AK. And then you have high serum uric creatinine ratio and then high urine specific gravity on ur analysis. And of course, you would have the absence of markers of chronic kidney disease, for example, like anemia of chronic disease, uh sorry anemia due to CKD, not of chronic diseases, you would have elevated parathyroid hormone and small kidneys on ultrasound scans. So, thank you for your time. I am sorry that I got delayed by a couple of minutes for the lecture. If you have any questions please. This stage is free, right? So if there are no questions, I think we can end it there. Thank you to Doctor Petite for that very comprehensive presentation. Uh Thank you all for joining us today. Uh Just to know if you want to recap the lecture or any of the other previous lectures in the UK MLA series. Um I believe that they are all available. If you kind of search the me of international profile on Medal and you'll be able to access all the recordings um as well to all attendees. It'd be really helpful. If you could fill in the feedback forms, it will be sent to you shortly after this is over. Um It'd be really helpful if you could just give this back to us. So we know where to improve for future events, but otherwise we can end there. And thank you all very much. Um If I may just add uh these are my references that I use for this lecture, I use the Oxford handbook series and the Davidson's principle and practice of internal medicine and a lot of other online sources. But these are like the main two sources that I depended on. So if you're interested to go into more detail and reading about the topic of both AK A and hyperkalaemia, please, you can uh see these sources or you can. Um And of course, I have no problem with you being provided with lecture slides. So that would be, you can contact the Meath team and they would provide you with my slides. Um I have no problem with that. So, thank you very much. Thank you for attending. Thank you for your time. Thank you Chennai for organizing this. Thank you Meath International as well. It was a pleasure.