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Hello. Hello, Christine. This one. Good evening, everyone. Welcome to the weekly teachings hosted by U Me on Med All uh for all of you who don't know what um medic is. It's a group of junior doctors who work across the NHS. And we organize weekly teaching sessions every Thursday from 7 p.m. to 8 15, 8 30. And the topics we take are usually the cases or complaints we come across very commonly in the hospital. And so today we have doctor Pune who would be taking such a lesson for all of us. And without further ado I would like to hand it over to Pune. Hello, everyone. A very good afternoon. Good evening, good morning to everyone and all joining us from UK and across the world. I welcome you guys to the second session of these teachings today. It will be about A K I and uh I will start the presentation first. Uh My colleague is gonna put up a poll. We just wanna find out what people think A K I is in the first place. So if people can just drop, uh uh you know, just fill in the pool that would be nice just gonna be looking at my phone to make sure that I have a gauge of what you guys are holding about. Ok. So essentially what I'm gonna be presenting to you today about is A K I also known as acute kidney injury. Uh We're going to start off with the contents. What AKI is, what are the risk factors involved? What are the causes? What is the staging? What a few cases that we'll be discussing about? And then the complications, which is quite important, the treatment aspect about things that how do we approach an AKI patient? And then we'll talk about a few references that we got from. So essentially why do we need to know about api why is it so important to know about api firstly, it what is a a it's basically a drop in function or simply put the kidneys are not working properly. It is very prevalent and it's very common. You see this in almost one in every five adults and one in every three Children who are hospitalized due to any acute illness in NHS, an estimated about 47,000 deaths occur in a year just because A K I hasn't been treated optimally. And about 1 billion lbs of NHS funds are used towards treating AKI. So you can imagine how much of a burden this is on all the health services across the NHS. Simply put, if we do have a streamlined method of tackling AKI, when we, when we, when we, we actually see them in the hospital, it's going to help a lot in, you know, cutting down the cost saving patients lives and whatnot. So when I say drop in function or simply not working properly, what does it mean? It essentially means that we're looking at the estimated glomerular filtration rate, the GFR. So when we ask what, what, what does it mean by the AKI? It basically means that the functioning has dropped to such a level where there's a drop in the GFR. And it usually shows on the bloods clinically, we can see people come in with things like, you know, dehydration, confusion, decreased urinary output and uh on the bloods where we do urea and electrolyte bloods, we usually see a drop in the EGFR. What are the risk factors for? AKI? I firstly being over 65 makes you innately at risk of AKI I. So it's almost like double trouble. All the rest such as heart failure, diabetes, liver disease, dehydration, having any preexisting renal conditions like CKD also makes you at a higher risk of developing A K if you have any urary tract obstruction blocks, if you're under any infection or sepsis. Again, this will put you at a higher risk of developing A K. So when we come to the cause of acute kidney injury, we have three categories that we usually look for the prerenal, the post renal and the intrinsic. Why is this very, why is this important? It's mainly important so that we know what the cause is and we can reverse it. Acute kidney injury is something which happens over a very short time. It it occurs in acute, in onset and mo in most cases, it's reversible. If we do all that, it is, we can reverse it. If you're not able to reverse it, it usually progresses to other complications. So just to make sure that we don't go all the way there, we have to find out the cause and treat it as such. So, as you could see from the photo prerenal is anywhere where there's an interruption of the blood flow to the kidneys. And it can be anything like dehydration, heart failure, sepsis, vascular occlusion, intrinsic renal is all the conditions where it is only dealing with problems with the kidneys. So you have conditions like toxins, drugs, infections, acute tub necrosis, all of which will significantly impact the functioning of the kidneys, rendering them, you know, at a, at a, at a lesser baseline than normal post renal is where you have obstruction and obstruction of the flow of urine is going to cause a back, back flow. And you know, this is going to significantly impact the kidneys as well. So things like prostate cancer, cervical cancer BPH, all of these are basically uh under the post renal causes of A K. When we come to criterias, we have a few criterias in place. They have been used for quite some time now. And uh essentially what is, what is most easy and convenient to use is the KDIG, which is the kidney disease, disease, improving global outcomes. Uh This is essentially one of the most commonly used criterias where we divide A K into three stages, 12 and three. If you can see in the photograph, uh the, the picture I would say AK one is anywhere where serum creatinine has increased 1.5 to 2 folds on the baseline and of less than 0.5 ml of kg per hour of urine output in six consecutive hours. This AKI two is when the serum creatinine increases by two or three times from the baseline and or or when the pu output is less than 0.5 ML per kg per hour for 12 hours. And beyond that is AKI three, while the serum creatinine has increased out almost above three times from the baseline. So I've been talking quite a lot about baseline. So what is baseline? So when we talk about what is baseline, we have to understand that um our kidneys function at a rate which has been consistent over time. So they might be working at the optimal level, they might be working at a lesser than normal level, but they have been working since you were born essentially. So, baseline is anything where consistency of the kidney function has been showing over the past few years, I would say. So when you look at the some uh at the patient's bloods, for example, if the patient has come to the a and multiple times or he has, you know, he has come over a few years, you take a look at the urine electrolytes, you see how their GFR is performing, how their creatinine and ure are performing and you have a baseline about how the kidneys are performing over time. So all these serum creatinine increases are usually compared to all the previous bloods. So what do we do if you don't have previous bloods? Then what essentially we can do is we can look at the serum creatinine increase over the 48 hours or we can just tabulate according to the normal values as expected for the age and for the sex. And essentially this is what uh we usually use for, you know, uh staging A ps. So how do you approach an API? So when we approach an API especially if the patient is deteriorating or you know, his, his, his vitals are unstable, we start off with the A two, the approach and we take a good background. The important things that we need to look for is medications. Um I'll be explaining why in the next upcoming slides, comorbidities like we discussed earlier on about the risk factors and all the risk factors put them at a high risk. So we need to know what comorbidities, they have any family history of kidney conditions, any urinary or prostate issues or any recent interventions. These are a the, the history which, which we actually need to gather when we approach a patient. So we'll discuss a few cases first. Then I'll go about explaining the rest of our rest of API so firstly, we'll take a look at this case. Now. Uh John Doe, a 65 year old gentleman from Wales has traveled across Asia and his first to become becoming globe trotter. He presents to A&E with a reduced urine output two days after landing back in the UK, he says that he probably would opt to travel in the winter next time as the heat was just unbearable this time around. He has a background of hypertension as in onto for it. His pulse is 88 BP is 108 by 76 and respiratory rate is 16. You can see the baselines there and you can see his current is on the left side. Um So if anyone can tell me what, what stages are you in at the moment? Ok. OK. So there's a pull up which says prenatal renal and post renal. So what do we think uh might be the cause in this case? Do we think there's something going on renally, something going on renally or something going on post renal? So a lot of you guys have answered pre so can you guys also drop uh what do we think as the cause of, you know uh of the A K in this gentleman in this case? Ok. So in this case, John Doe um OK. So in this case, John Doe has traveled across Asia, this requires some amount of detective work. I would say if he picked up on that sentence while he did. Um Yeah, that's right. A lot of you guys have answered, right? So it is dehydration. So the most simplest cause of A K I would be dehydration. So in this case, um it's not wrong to say dehydration. And also there's an element of medication there that needs to be changed in terms of treatment of dehydration. So the condition is dehydration and what we need to do is probably suspend Ramipril, which I'll explain further and then we'll come back to this case. So don't worry about that, but all of you guys are on point. It is dehydration. Dehydration has caused John Doe to go into AKI. And right now if you guys can tell me what stage he's at. So dehydration is free renal. So you guys are right about that as well. There's a little bit of max going on into this. So um creatinine is 1 18. If you go back to the KDG criteria, you look at a KSH one, the serum creatinine increasing 1.5 to 2 fold from baseline. In this case, his baseline is 60. So if you multiply it two times, it's going to be 1 20. So below 1 20 he is in AKI I stage one, we'll go on to the next case now. So in this case, the same, you called to the ICU to see an acutely deteriorating patient va we we don't know much about her. Her file is missing. Her computer records are missing. We are told that she's being treated with some antibiotics on examination. She has dry mucus membranes and her blood show the following. As you can see, she's quite tachycardic. She is Spire cell, her BP is quite low. She has urine di positive g leucocytes and nitrates both are positive. Um You can see that you and these creatinine is quite high. UA is quite high. The EGFR is low. So again, what are we thinking in terms of stage of A P? And what do we think? What cause what, what do you think pre renal renal or post renal? So the first is up where the stage of A K I is there? So, and use your calculators phones. OK. So a lot of uh a lot of you guys have answered as AKI stage three, which is correct if you see the baseline, which is 62. And if we go back again to the Kdigo guidelines, AKI one is 1.5 to 2 times. AKI two is 2 to 3 times and AKI three is more than three fold of the baseline. So here if you, if you see 62 into three is well beyond 1 86 it's almost more than three times of her baseline. So she'll be in AKI stage three. So is there any confusion regarding staging of A P? So the next question would be, what cause do we think she has in this, in this case where urine dip, which shows positive leukocytes, positive micros, what do we think are the causes or just put up the causes so that you guys can reference? OK. So in this case, there's a mixed picture of things. It might be both prerenal and intrinsic renal. Um So what is happening here? Her, her, her nitrates are positive, her leucocytes are positive. So she's, she's battling a urinary tract infection most likely. And she's also septic and uh one of you guys have answered septic six. great job. So the patient is in sepsis. Also, it probably the patient is in zero sepsis. So, uh element of both prerenal and intrinsic renal is happening with her and she's in AKI stage three. So what can we do? Uh What can we do for her? This in itself again will be discussed later on. But any any thoughts on how to tackle her? I think one of you guys have already put in sepsis six, which is on point. You guys are right about that IV fluids, correct. Any other things that can be done we, we'll be discussing about how to assess fluid status as well because that is quite important. Ok. That's, that's fine. We'll go on to the next case, all the treatment I'll teach you. Uh, I'll, I'll, I'll let you guys know at the end because it'll be much more easier if you, if we go through the cases try to get uh, understanding about what stage, what, what cause it might be, why it comes under the causes and what staging is basically being done in these patients. One other note that I wanted to share with you guys is there might be some where we don't actually have uh basically in NHS throughout NHS, most of the trusts really have a system where the bloods are reported. A K one A K two and A K three based on the previous baseline bloods. So it usually makes things a little bit more easier for all of us. Uh But if not, we can always refer to the criteria and we can come to uh you know, an agreement about what, what stage the patient is on um the case. So Mike, a 23 year old builder presents to the same day emergency care with pain in his right flank. He has observed small amounts of blood in his urine says that he's been feeling chilly these days. He has not been feeling well and has been going to the washroom 7 to 8 times every day. Passing large amounts of urine and loose stools. He also says he has been throwing up every day and he is not able to keep his foot down. So again, what stage of A P is here? And is it a prerenal cause a renal cause? Or a post renal cause? OK. You're having quite a mixed uh answers here. OK. How is arm six stage one? OK. So, so I have purposefully made uh each case a little bit difficult so that everyone gets, you know, um gets a say in what what's happening with the cases. So for the people saying prerenal, what are we thinking? The diagnosis is in this case or what is the provisional diagnosis that we're thinking might have in this case? And for the people who are thinking renal and post renal, what are we thinking? This person might be having? You can just drop it on the checkbox. OK? It got one answer. One brave soul was answered both mixed with prerenal and renal dehydration with a TN in your arm. So wonderful. So a few answers there. So firstly, all of you guys are correct. Stage one is indeed the answer here. I think everyone has got a hang about how to, you know, see which stage the person is on based on the drugs. So the causes. So again, here a little bit of uh you know, I would say Sherlock Holmes a little bit. He has been vomiting, he's been passing large amounts of urine, large amount of stools. So, not only does he have dehydration, uh but here, here he has pain in his right flank. He's been feeling chilly so that in itself could lead to a differential diagnosis of renal stones or it could also lead to a differential diagnosis of uti ris as well. So not only will he have um the, the, the pre we know where he's dehydrated from vomiting and passing large amounts. But you'll also have the intrinsic renal where he has the infection. And even in this case, if further imaging, further bloods and further clinical analysis does show that he has a stone, you might also have a post renal as well. So it it was on purpose that I, you know uh worded the the case like that. So all of you guys are correct. So next case, um Samuel, a 72 year old has been having back issues after a recent fall and has come to A&E due to not being able to bear the pain. He has been given analgesia and he's feeling much better. He says that he has noticed that he's been weighing lesser than the in the past few days. When reviewing his bloods, you see that he's an ay too uh background. He has prolapsed disc gout previous mi I hypertension BPH. He has quite a few medications going on allopurinol, paracetamol, Ibuprofen, Aspirin CISplatin and Alla uh you can see the bloods there. So if anyone can tell me again, what cause do you think the patient is in this case? So is it gonna be prerenal gonna be renal, post renal? Because we already know that he's in a, a two? OK. Wonderful. A lot of great answers here. See Leo. So which what are we suspecting here in under the renal cause? OK. So again, this case has been structured in such a way that you have a few answers, not only one. So he has been having quite a significant amount of pain, has been weighing less the past few days. He has a background of BPH and uh he's been on a lot of medications. So we do see that he is having a lot of drugs there that could impact the kidneys. I will be touching upon the nephrotoxic ducts soon. So we can understand why this patient is on a lot of medication that needs that needs to be stopped. But yes, for, for in this case, um a lot of medications might be the problem and he has been weighing lesser with the background of BPH. So what we can think about is probably progression of BPH, calling him post renal or we can also think about him not having or having too much medications, which again puts him under the intrinsic renal, intrinsic renal cause. So again, here, there are no, there's no right answer. There's all you know, work up towards the final diagnosis. So the last case here will be case five where Francis and his daughter are urgently transferred by air ambulance from Cambodia. His seven year old daughter has been trekking in the wild forest with him and she suddenly complained of a sharp pain in her left shin. Following that, she started to vomit become drowsy and lethargic. Her vitals are as such temperature. 7.6 heart rate is nine BP is going to the hypertensive side. So in this case, I want to know what the causes can be in this case. So there's gonna be a pole that's gonna be put up if you guys can just click on the pole. So we don't see this often in the UK but usually in the Asia and other tropical areas, we do see a lot of uh these cases where you know, people do come in to the hospital and when they are checked, their urine electrolytes are quite deranged, quite low, mainly because they've been bit by something. In this case, the options were insect, scorpion and snake. And the answer is actually all of the above. So all of them can actually cause AKI i in, in, in individuals. It irrespective of what kind of species it may be because all of them usually have toxins that the kidneys will actually get impacted by. And if you look back on the causes, do we think it's renal or in renal? So it's gonna be intrinsic renal toxins. So, all of them are right. All of them do cause um uh some amount of damage on the kidneys and might even lead to ATM or acute tub necrosis as well. So, what are the complications of A K I if not treated? Firstly, it can lead to hyperkalemia. So we as we all know when the kidneys do not function properly, a few things go wrong. So the metabolic byproducts are supposed to be excreted. The urea creatinine get accumulated in the body. It does not allow a lot of water to go out of the body or fluid to go to the body. So you start developing, developing edema edema, then can progress into an even dangerous form associated with a higher mortality like primary edema CKD, which can quickly turn into end stage renal failure if not, you know, treated in the proper time. And of course, all of these will lead to death. So these are the basically the complications of take care nephrotoxic. So just now when we were discussing about a few cases, there were a few medications that I put in. There was a purposeful reason behind which those were mentioned mainly because the nephrotoxic. So why are we talking mainly about nephrotoxic? As the name explains itself, these are toxic on the kidneys and these have to be stopped in any case where you see the patient being an API. So for example, if you go back to the case four Samuel is on a, on a lot of medications which can be nephrotoxic. So when I say nephrotoxin, the main ones that I need is a CE I inhibitors, arvs, uh NSA and you know, medications like CISplatin as well. So here he's on allopurinol, which is nephrotoxic, Ibuprofen aspirin CISplatin and all of these can be nephrotoxic. So these have to be substituted with again in case one and one of you guys had mentioned that hypertension might be the cause of, you know, A P, which is also correct at this, at this point of time, probably he has been on it for quite some time. But if he's a new starter or if something goes wrong in his body where the blood, you know, the medications have started exacerbating the cause of the kidney damage. Rain might be a contributory factor to causing his AKI or making it even more severe. So when we come back to nephrotoxic, all of these medications are too much to memorize a few things that we need to take into consideration will be ace inhibitors. Like I said, Arbs, um nss, you know, and if you can see in the list, there are a few antibiotics as well. This has to be quite keenly observed because it has a significant role when I come to the management. So what do we do when we see a patient with A K and coming with the treatment? Now, which is probably the most important aspect of things. So when we see a person in AKI one, firstly, we need to take a good history and examination. We're gonna first assess the fluid status of the patient mainly because we need to know whether he's overloaded with fluid or if he requires fluid. In AKI one, we want to supplement the kidneys with some amount of fluid just so that it has a temporary relief. Sometimes the causes are decreased distribution, fluids or you know, in cases where the patient is in sepsis or is he's hypotensive because he has lost a lot of blood, which are, you know, causes of AKI. In that case is we want to assess the fluid status and if he's hypovolemic, you know, give him IV fluids. So how do we do that? So in fluid status, we're going to look at the BP, see whether it's hypertensive or not heart rate edema, look at the legs, look for peripheral edema, look at the JVP and the skin. If you see that the patient is hypovolemic, uh definitely, definitely, even if it's, I would say you vole, there is a role of hydration. So start him on IV fluids. And here what are the important things we have to do is restrict hourly fluid balance. So every trust has their own guidelines on treating, treating a care mainly because it's so prevalent. And you know, it's been seen in so many patients across England. So follow your trust guidelines, do obviously review them, but most of them will also have guidelines on how to go about with a KIS based on the stage. So this is part, this is basically my trust guidelines where probably what we do at this kind of state is give strictly strict hourly fluids, fluid balance and then we'll see the patient if you feel that the patient is deteriorating, if you feel that the patient might go into further determination and you need to know how much fluids he is, it is going in and how much fluids is exiting. You probably need to put a catheter in because not only will it give us the proper amount of fluid being excreted, but it will help us basically calculate the amount of IV fluids going in the negative balance, the positive balance and then we can treat going ahead. The most important step in a care would be trying to reverse all the damage that has been done if the patient is on any potential drugs and we'll have to repeat the UN A within the next 24 hours to make sure that we know what kind of a trend the the person is on. So at this stage, AKI two will basically involve all of these steps in AKI one and then it'll go forward again. So AKI two in A K two, we do everything that is in A K one that I just said along with that, there comes a role of ultrasound of kidneys. Why? Because sometimes on initial management, we might not find any, you know, relief, the the person might still be in A K I or might be progressing worse in A K I two. In that case, you need some amount of imaging such as ultrasound, ultrasound of the kidneys. And if you have an AC N on a renal pain, it's definitely uh pertinent to discuss with them and send for further investigations because they might want to escalate, especially if the patient has a lot of comorbidities or if the patient is already CKD. So A K or CK D or if he has significant comorbidities, you want to basically escalate it to the renal team or the A N and send in a few blood tests which are specialized via clinically relevant in A I three. Few things that you'd already have done by A K one and A K two would be probably the urine dipstick test. You have already stopped the nephrotoxic drugs such as the Aci inhibitors and the Aib blockers. You'd already have done a serum creatinine test within 24 hours. And based on A K two, you have already done A US scan of the urinary tract as well and a discussion with a. So the most important thing here as junior doctors would be sitting down with the pharmacist and reviewing the medication. Why? Because most of the times, if you see the prerenal renal and post renal causes, most of the times prerenal is almost 55% of all the cases causing, you know, causative of A K. So medication review, especially in people above 65 is gonna take AAA huge role in treating the patients and simply just suspending nephrotoxic can basically give a huge, you know, relief to all these patients in terms of repeating bloods and finding out that they're actually improving. So this is what we do in A K three. So a simple, uh you know, I would say a simple protocol that most of the trust follow would be an ABC D even for A K A. So as you can see here, it's a quite a useful mnemonic that we can all use first. A would be address the drugs like we all discussed niaarb contrast and the G site, all of them have to be stopped. Um If you see one case early on that, we discussed where a patient was in zero sepsis and being treated with antibiotics. And if you look at the slide where we actually have necro toxics, you'll see that a few of these antibiotics are actually nephrotoxic. And they also have to be discussed with the pharmacist on how to tweak their dose because all of them will have X adjusted doses. So in in cases where you find yourself that you're having to give antibiotics to a patient with API it is definitely worth you to, you know, have a chat with the pharmacist or go to your local guidelines about the, we have adjusted doses of uh antibiotics. The second one would be boosting the BP IV fluids with regular fluid assessment. You will definitely want to uh, give IV fluids to patients with AKI. But at the same time, you have to be cautious because some of uh some people, especially ones with heart failure or people who are a little bit in a geriatric age group can easily become fluid overloaded. And at that time, it becomes quite difficult to, you know, uh move about with management. The third one would be calculating fluid balance. Uh input output shot is very, very important to know how much of fluids going in, how much of fluids are going out. And in that sense, a catheter would be the best useful tool uh in that place. A urine dip is definitely important. We need to know what whether an infection is going on, whether there's blood, whether there's proteins exiting and based on the urine dip. And you know, further scans, we can think about maybe doing a biopsy in the future along with the renal if needed. Last one be which is exclude obstruction. So, post renal causes sometimes uh doing a renal us S or CTK would be worthy to find out any causes of obstruction because once you obviously relieve the obstruction, uh the A K has been, why are we doing so much in terms of A K, like I said, firstly, there's a huge burden. Secondly, it is reversible. So if we do reverse this, it doesn't progress further and lead to all the complications as simple as that. So the next one would be a few differences between AKI. That's a CKD in A K I, it's reversible. In CKD. It may be nonreversible. Uh sorry, not, not m nonvisible. It's actually nonreversible. So you see CKD, uh it can even be from infants if they have some congenital diseases. In A K, you see a steep decline in function. Whereas in CKD, there's usually a gradual decline in function. So A K I presents with sudden onset, severe symptoms of short duration uh which usually become normal or resolved once the whatever uh you know, uh whatever is the causative is removed or it's, it's dealt with once that is done. Uh usually A K gets resolved. But the CK D, most of the people with CK D, they're usually asymptomatic too, very severe CK D. And it's usually a long process over many years in CK D. What happens is poin which is secreted by the kidneys also becomes uh decreased or get affect, also gets affected. So usually you see anemic chronic normocytic anemia in people with CKD. Whereas in A K I, you see the HP to be usually normal because it hasn't had that much of A time to significantly affect the physiology of kidneys. Yet in imaging, the renal us is likely to be normal. Whereas in CKD, the renal us will show evidences of some amount of some degree of, you know, scarring or large kidneys, things like that in different conditions. So these are my references. I hope this has been useful for you guys and just uh I just hope that one slide you guys can take away from this presentation will be this because I do know that it's quite frightening once you see patients with AKI and don't know how to go about. The first thing we can just go to is just this ac of A K and I'm sure you guys will do a great job. So thank you so much for attending the today. Uh Just take any doubts. Uh If there's any doubts as well have the next week session also. So next week it's gonna be about the range elect lights and I'm sure that's gonna be very use to everyone as well. If you have any doubts, please drop it in the chat Boxx. I I'm happy to take any questions. OK. So we have a question here which is more reliable to check renal function, creatinine. Uh Wonderful question. So GFR is what we check usually for the renal function. So a drop in EGFR does mean that there's something going on with the kidneys, but serum creatinine is more specific. So in Fr there's a problem with it. In the sense, you do see a lot, there might be a large individual with a very poor fr there might be a very small individual with a very good TFR because it's some, some amount of is is also based on the, the weight of the person. So in terms of looking at kidney injury and AKI treatment, we go more for the creatinine because EGFR can easily be misconstrued especially when there's weight differences. So EGFR is usually taken in account when we are trying to look for initial signs of A P but we usually look for serum creatine when we want to categorize the patient and then repeat blood. We obviously want to see any improvement in both. Mm mm Any other questions? Oh Thank you everyone for being so wonderful today. Um I think I'll stop the broadcasting if you have any, you know any other questions, sir. All right. Thank you, everyone. Have a wonderful evening.