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This on-demand session will cover the topic of Acute Kidney Injury (AKI) and is relevant to medical professionals. We will discuss the prevention and early detection of AKI, its consequences, the three main subtypes, various causes, how to investigate and treat depending on the cause, and finally, a case study to tie it all together. This session will bring attention to the burden of illness, cost, variability in how well we manage it, prevention and treatment methods, all relevant to medical professionals.
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Learning objectives

Learning Objectives: 1. Identify key symptoms associated with acute kidney injury (AKI). 2. Describe the different causes, types, and consequences of AKI. 3. Explain how to diagnose, investigate, and treat AKI effectively. 4. Recognize the importance of prompt recognition and treatment of AKI in order to improve outcomes. 5. Compare and contrast the two contrast agents (intravenous and intraarterial) used in imaging techniques and the potential consequences on the kidneys.
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The following transcript was generated automatically from the content and has not been checked or corrected manually.

Yeah. All right. I think we'll just get started and hopefully you can all hear me. Um It certainly seems to be coming through. Uh How do I get to the chat in here? Um So if anyone can hear me, please put it in the chat now. Uh So as we're strapping in, so my name's Don, I'm one of the tattoos. He's been a medicine for the last couple of months. I'm going to be talking to you about acute kidney injury. Uh Major declaration is that a lot of this is inspired by a fantastic talk at the Royal College of Physicians of Edinburgh by one of the renal physicians from Aberdeen called Laura Clark. Um You do see me looking down to my left is because this program is, let me see my notes. So I'll be looking away to my laptop in the left, but without further a do we'll get going. So main things will cover widely worry about AKI diagnosing, investigating and AKI treating an achy I depending on the cause and then a quick case sort of tie all nicely together. So, could I go is Kidney Disease International? Um Sort of guidelines to improve outcomes. Um And it's common up to one in 20 or in patient will have it and up to two thirds people in ICU will get, it has a heavy burden of illness and the cost of managing and AKI is high, especially if it progresses to end stage renal disease. Um amenable to early detection and can be prevented and actually, there's huge variability in how well we deal with it. Could I go? Who came up with the Achy I guidelines in 2012? Um they released guidelines for the entire world and they had previously come up with the guidance that you'll see on the right hand side there. So it's the same people. Um And I believe the AKI guidance is about to be updated. Um So, um the biggest thing to note is that generally the secular patient's are the more like they are to get naked eye. Why the immediate consequences of an Achy I, well, immediately it can be life threatening and we can get a rapid deterioration, real function leading to an acute renal failure. During admission, there's an increased risk of death. First, people who don't an increased risk of dialysis and increased length of state, which obviously, we'll circle back around and also increase the risk of death and longer term risk. You know, CKD has a higher chance developing higher chance of moving to end stage renal disease. And also even if the craftsman is normal on discharge. There is an increased risk of cardiovascular death and disease further down the line. We don't understand it. We've known it since 2005. It's one of the reasons that we care so much about preventing, especially in Scotland where are rates of cardiovascular death. And these are also very high uh, in the background. So I suppose what is the name when we are thinking about AKI? Well, we want to prevent it in the first place. If that's impossible, we want to prevent it progressing. And if that's impossible, we just need to support the kidneys long enough for them to recover all achy. I is sort of different in how it comes about and we'll speak more about that. But basically, the thing you, what we wish to prevent is a move to an acute tubular necrosis, um uh other cells and shutting down of the kidneys, that's what we want to prevent. We don't want it progressing any further than it actually has two. And that means the prevention isn't possible, then early treatment, early recognition then become the key. Here's start quite overview, the three main sort of subtypes will dive into this more. But basically, the thing to take home is there's prerenal, there's intrinsic issues with the kidneys or is post renal problem and that's the easiest way to think about it in the boxes. Um And there's lots of causes. So if we think about it within the boxes and then how we're gonna investigate within those boxes, it makes him much, much easier. So, prerenal a chi is the most common. You probably have thought that on the tape, lot of people come in dehydrated, lot of people come in a bit sick. Some people will have lost blood and their kidneys will have gone off. Uh None of this will have come as a massive shock to you. Over diaries is a common one and the heart failure patients' even just sort of the opposite of that. And under diaries is in the heart failure patients' and a subsequent sort of left and trick their failure can also cause lack of perfusion to the kidneys and hepatorenal syndrome in the liver disease, patient's as well. Um Also to note here and not something that you think in terms of the concept, but renovascular disease, renal artery stenosis often triggered by someone who's had it for years and years and years without really knowing about it, I'm bitter and then their kidney function rapidly deteriorating. So what happens? Basically, the impaired kidney perfusion which then fires inappropriate physiological responses. Um The drop in blood pressure means the kidneys want to enhance it even water retention. Um And they're also be a firing of the sympathetic stimulation. The endpoint of that with the release of adrenalin, another source of counterregulatory hormones will cause vasodilation reduction of most of the body. Um But that will also include the effort arterial and it will dilate the Afrin arterial. Um, the rass system will then fire that will culminate in increase production of angiotensin two. And that will cause more surveys of construction, all the steroid release which again will hold more water. And the um, and there's also gonna be some immediate release basically holding onto water. Um There's sort of net point of that is that um your, all the body responding absolutely fine. And if you're a normal person with normal kidneys who's dehydrated, these functions will protect your kidneys and you will compensate. But if you're old, you're frail, you're on a nephrotoxic drug, you're really unwell, then it's only gonna be able to compensate so far. And then that's when we get an A K I. Um the other important thing to note as well is that the kidneys receive about 25% of cardiac output a minute. So that obviously other saying, if you're young, well, you will compensate and your heart rate will go up and your left ventricle will compensate appropriately and cardiac output will go up, especially in times of increased demand. But if whatever reason, as we said, you're diabetic, your failure older, then these aren't going to, this isn't gonna get occur. And actually about two thirds of pre renal AKI starting community and then brought into hospital. So we think it's only happened on the moment they ventured hospital. But actually these things, most of the time I've been brewing before they've come in to take it more simply, I don't know if this light will work. Um Generally, the tubular glomerular function remains unimpaired. This is a problem with the body that the kidneys have tried to competent. Haven't the danger is if this goes on for a prolonged period and ischemia curse at that point, we then enter into um intrinsic issue where the necrosis has caused a problem. Um And as you can see there, that's the sort of most common cause of an intrinsic aching. It's ischemia due to a prolonged prerenal achy I, which means the trivial start to break up and become destroyed. Other causes of that gentamicin is obviously the big one. some chemo methotrexate, ethylene glycol. I don't know if any of you guys saw the young guy who took the massive overdose of that and ended up in ICU for a couple of weeks. He ended up on 42. Um He had had a very, very bad achy I and then the one that they often use in hematology, um adversary in be the antifungal, there's also systemic diseases that will cause it. Um Any sort of him all Icis rhabdomyolysis and the myoglobin that ends up start getting chewed up by the tubules and then destroying them. Uric acid and tumor lysis syndrome. And the Bench Jones protein in, in myeloma can all cause it. And it's also the mechanism for which contrast from scans um causes an achy I as well, but we'll come onto that and why? It's a bit more controversial. Intrinsic. A high makes up about 30% of them. The other ones which are less common uh in traditional nephritis is basically an allergic reaction. The kidneys often penicillin, Sven atone, PPI NSAID cyclosporin drugs will cause it. I've never seen an infection cause it seems like the drugs cause it. And then the infiltrated disease like sarcoid and amyloidosis within this group, you also get the glomerular nephritis kids, they're less common. Um tend to be rapidly progressive, tend to have a urine dip that lights up with lots of protein. And then the vascular diseases where there tends to be some other problem that's pretty clear. You know, vasculitis is with odd rash is TTP with odd rashes and low platelets. Hos where they've had severe sort of diarrhea and equal oh and 57. Prior, exceptionally high BP are known sort of vascular path and they've thrown off often infarction or renal, they tend to be associated more pain. Um but just always something to consider that if they're not overly dry and it's all slightly odd, then it, and there's no obvious obstruction that this is where we'll be going. We'll speak more about that. But the main thing to sort of note with intrinsic is that it's completely dependent on the path of physiology, but generally there is some tubular damage. Um And there is depending on the path physio, we'll probably need to find a way to reverse that. The only real way of know exactly what is calling an intrinsic gay guys to take a renal biopsy. And as we know, that's not always possible. So often this is about discussing with the renal team and going through it with them and coming up with our best guess and working diagnosis as opposed to a, a completely clear diagnosis, if that makes sense, the talk about contrast. Um and why it's condo the Royal College of Radiologists, the Royal College of Emergency Medicine within the last month, have released a uh communiqu saying that this obsession with not doing scans with EGFR is under 30. If it's urgent. If it's emergent, if the patient is exceptionally well, you need to seek a diagnosis quickly, then it should be completely binned and that it should have no bearing on whether or not, you know, patient should get the scan. The sort of opinion from renal consultants is that actually intravenous contrast is less of a hit to the kidneys than inter RTO contrast by a good number of factors. Um And so actually, whether or not intravenous contrast is the reason someone gets naked eye probably less likely than the reason that you got them, the scan. It be that the they're intraabdominal sepsis, be it their diverticular Perth be it um they're cracking pneumonia, that's probably more likely to be driving it than intravenous contrast as opposed to intra-arterial contract is well known to cause a KIS. Generally, we need 4 to 48 hours post scan and you generally get a clear dip with sediment. The agreed management generally is to avoid further hits the kidney. So I don't know if you've ever heard renal physicians speak about this, but we often talk about hits. Um, uh, the first hit would be being unwell, second hit would be getting a contrast scan. Your third hit would be getting started on Gentamicin as part of your IV triple 1/4 hit would be your ace inhibitor not being stopped when you came in. And the whole point is is that you avoid the hits as much as you can because actually, it's almost cumulative damage. I don't know the evidence bases for it, but you'll often hear people speak about it but avoid hypovolemia. They've proven no benefit between orals and IVF unless the oral pathway has a problem. So if you need someone to take a load of fluid quickly, um if they're willing to drink 500 mills at least her over the course of 30 minutes, the amazing trial showed no difference in outcomes between IVF. Normal's. If it's a less urgent scan, let's say it's a CT cap for malignancy there. An old person, they've fallen, they're a bit dry. Then you there, EGFR sitting at 27 then you probably want to give them some IV fluids gently withhold the race inhibitor with all the diuretics, with all the Metformin, withhold their SGTL two inhibitor. Again, none of this will come as a shock to you, but it's all, you know, the scan can go ahead and we shouldn't always, just until the far is above 30. Why would the number of 29 suddenly be much better than a number of 30? You know, it's the reference ranges of the croutons are probably that different day to day and to sort of have an arbitrary number without thinking about it, probably a little bit left. Um If in any doubt, speak to a senior, uh moving on post renal causes the urology, uh specialists, area of expertise about one in 10. Generally, it's got to be something that's big enough to call the bilateral obstruction of urinary tract. Um sort of above the bladder. So big sort of pelvic tumor's uh potentially stones or maybe kidney has infarct kidney on one side, infarcted and the other side now has a stone bleeding with subsequent clot formation. But generally, it tends to be in front of the bladder tends to be blood right flow obstruction. It tends to be BPH and older males. Um Neurogenic bladder can call it an can congenital, more operations, but in essence, the kidneys aren't draining and we need to change that around and we need to speak to a urologist. We need a catheter, we need a nephrostomy. We need a uh ultrasound green. All we need a bladder scan. We did CT QB depending on your point of view, but this is very much their area of expertise but always good one not to be missed. So, diagnosing AKI all of you will be familiar with this. It hasn't changed since 2012. However, we always, always, always forget about the 26.5 millimeter minimal increase were really, really bad for it. Um, sometimes the computer misses it. Um, and the people to fear this in our, the elderly population have small undetected rise of crap, especially if they're failing cachectic. Uh, they, they have a baseline cracking of 28. They're 90 they're not eating very well and all of a sudden that then goes up to 50 for, well, it's not quite double people are like, oh, well, you know, we don't really know what her baseline is. Well, technically she's an A Kr one and because she's so small, she's not gonna be producing a lot of creatinine. And actually this is a significant hit for her kidneys. Um, and if this is a younger person with an Egfr as a crown of 67 who has now gone up to 100 and 18, it would definitely raise eyebrows. Um, but because the EGFR stayed greater than 60 people tend to ignore it. And that correct. And it doesn't nicely mean you need to do anything for these patient's. But you certainly need to be aware that something could be rumbling and especially given the increase in mortality and morbidity. Um, it's something you'd be quite brave to ignore. The other thing to note is often urine output. Now, if I'm a 60 kg male, I should be producing, you know, 30 mils of urine an hour. Um, and minimum. And if I'm making less than that, then, you know, even for six hours, then, you know, technically people overnight are going to be an account. And I would ignore that. I would say this is urine output during daytime hours only. But it is just something always to be aware that if there is any doubt over someone's urine output, they're sick and the renal functions off, then you put Catherine and keep it on it. It's as simple as that and it's quite a good way to guide in that this often sort of the stages of achy, I often reflect the terms of increased risk and the increased risk of progression. Um The main thing to note with urine output as well is that obviously an ideal world, everyone would have this accurately documented. Everyone would be as compos mentis enough to fill out their own fluid charts. But sadly, that's not the case and nursing colleagues are too busy. Um So it is just something that the fluid charts are often wrong. There should always be handle with a pinch of salt and that often to know, incompetent people, it can become impossible to monitor. So it's just something to be aware that they may well be a sitting duck for an 80. I, we just don't know that you're not, has dried up or is not appropriate for the further kidneys, the level of production of urine at that moment in time, just always something to bear in mind. So, sort of on that point with cramping and muscle mass will affect it a lot. It's gonna overestimate big muscular chaps, go to the gym all the time and have massive protein meals. It's going to underestimate small changes in old frail and we're gonna miss it. Exercise generally increases creatine in just the muscle breakdown and turnover. Semester. Even trimethoprim will block tribulus secretion of creatinine is one of the reasons why tromethamine causes so many a kis hemoglobin problem and methyldopa, we're all sort of mess with crown an essay. Um I didn't know that before. I did this talk as well. Hyperglycemia DK will also falsely elevate it. And more interestingly, if people are really sick with sepsis, their credit production will notice that as their body seeks to sort of rationalize its metabolism and this will also have an endemic to states and fluid overload again, falsely reassuring us that the real function maybe okay. And hence why when these people are going into monitored environment, we need to keep an eye on urine output because actually creating and may remain what would appear to be static and maybe only move slightly up. But actually because we're producing this crap in, in from tissues and actually don't know how well the, the kidneys are actually clearing it. So important point. So enough with the background and onto a little case from my time and wish, uh this is one that I had my third block. Um, I think it's quite interesting is, is quite sort of not uncommon for the rest of us. So 45 year old fit and well female, she's been unwell for a week. She had fever, she had sort of poor input. She thought she had COVID um and had tested and been negative and thought she just retested it. And on the day of presentation, her husband points the back for like, and he's like, what is that? And she has large erythematous patch with associates, you know, has no idea how I got there. She hadn't cut, it had been a dog bite. She had been out walking, I don't know, just appeared, goes to a GP and has referred her up query DVT to medical receiving. Um, she is a secretary of private hospital in Glasgow. She normally park runs. There's her husband strength training this week, usually just in a binge of the weekend and she's a social smoker and in terms of drug history, she's not on any contraception. She takes about effects of phentermine. In the summer time, I saw her in May. So she was taking at that point and she's just been taking paracetamol and Ibuprofen for her fever D dimer was raised at 1500. Uh, the ultrasound doctor left leg should know DVT. And so the sho has gone ahead and started, uh some IV flu clocks with an impression of left leg cellulitis. Uh sho has added on HBO and see which is normal and hemoglobin platelets which are all normal COVID negative. And it looks like there's an infection brewing the right cells and CRP that high. She's pyrexic a little bit tacky. It's a little bit hypertensive, but she's not confused. She just feels a bit knackered. However, uh GP blood from two years ago showed a crown in 67 Egfr Great at 60 which is now up to 100 and eight and 47. Uh fluids had been started by the attitude on the night shift and Yuria has also, you know, almost doubled. So uh she was kept in wish I didn't have a hospital at home service, didn't have an open at service that was at the other end of Lanarkshire. Um And because of the AKI and the opposite arrangement, we decided to keep her in and also slightly old story. So the major question is, is this a suitable plan to investigate the AKI sh done much? But they probably paid the numbers game and I thought it was the most common. That's what we're going to do but arguably lazy. So the answer is, it depends. Uh if the attitude had reached the end of their um sort of work up and have been like, yeah, this is a pre really hypovolemic AKI, fantastic, great job done. Repeat the using these tomorrow. Keep going. However, there is nothing in the clerking book. They look like they'd only looked at the leg and had been very reassured by the ultrasound Doppler. Uh There's no fluid assessment documented. So it is a lazy bad medicine. Um So when we have an achy, I first thing we think about is shout. Is there a sepsis? Is there hypervolemia? Are they obstructed? What is the your analysis say? Don't get any responsible for what's going on your analysis. You're mostly looking for blood and protein to suggest an intrinsic cause or maybe just blood in case it's a stone and they're just obstructed. However, 30% a renal stone, would your blood on a urine dip? And so there's any doubt to you for the CTKUB nephro toxins often important to be. Have they been started on something recently? Has something been stopped recently? Have they had something recently in the background that might have done it? Major thing for obstruction other than the blood to potentially your analysis. Has someone put hand on their tummy? Has someone put hands superpubic lee, are they retaining in their bladder? Do they have pain in their flank? Um And if they're over met, over 50 in male. Is it their prostate? Have we done a bladder scan? And if there's any doubt, have we popped the catheter in? So, just things to think about, I mean, in her case, she might be a little bit septic, but it seems unlikely. Actually she's not that persistently tacky Arctic and actually she sort of more serving as opposed to being septic. She mentioned of low input, but we're not sure about hypovolemia doesn't sound like she's obstructed. But we don't know that for a fact, your analysis hasn't been done and doesn't look like there's anything on the meds, but we actually haven't checked. So I need to go and do all that and sort of reaching. So next thing you do volume assessment, obviously quite hard to do at times because you're not obviously formed a large part of that. And as we were discussing, it can be quite hard on the wards to actually do um that and the fact that the fluid exam is actually one of the harder medical exams to do and takes a bit of time is often done quite poorly, you know, often means that you're sort of flying a bit blind when you see these people the next day. So I'll sort of work through what I tend to do. So, if the patient is compos mentis, do they have a suggestion of poor, poor input in their history as I per output in their history, you know, have they had dark urine, have had low urine output. Have they not been going to lose much? Do we need to catheterize this patient if they're really unwell or they're confused just to monitor the urine output or can we get away with the skills and maybe even giving the patient the fluid output chart next to them so that they can keep a track of how it's bringing I/O. And is there a history of dark familiar obs? We just want to make sure they're not persistently hypertensive in tachycardic, but always bear in mind that are actually masking something else. Is the sepsis? Is this a bleed? Is there something else going on like a pancreatitis? And we've just erroneously believed that they're just dry? And thirdly the exam I tend to do, do they feel thirsty? Always is quite a good one. I tried to look at the tongue JVP. Is it moving around? Is the past juggler reflexes at the base of the neck? Also take the lung bases, check for edema, um check the pulse volume. And then if there's any doubt and we need to resuscitate with large amounts of fluids, I often will do the leg race test, which is where you take BP lying down, flip their legs up to four or five degrees, hold it there for, for 30 seconds and then recheck the BP. If there is uh an increase, reasonable increase in blood pressure, then you can be fairly certain that that's our backflow from the venous system of the legs suggest they're still dry and there's still room to fill them up. Um In HD use an ice use where I've worked previously. Um People have central lines in, they used to take um the oxygen saturations of blood returning to the superior vena cava. But I believe the evidence based for that is poor, but people will still do. And certainly in Glasgow, that's something that they used to do in the high dependency units. Um, but I wouldn't recommend that myself, sir to go the next step. What we're going to do in terms of investigations, we're going to do what we've done on the previous page. We're gonna exclude steps is an obstruction. You take a load of bloods, do we need to image them? Do we need a bladder scan them? Do we need to renal up, send them, do we need to do a ctkub, put a hand on their tummy, which do your analysis. And we have a look at the drug chart if the, your analysis shows any sort of protein percent for urine, a cr and when that comes back, the renal team will usually except under 100 millimoles of sort of a cr ratio in the context of being really unwell. But if there's any doubt, it needs to be disgusted. Renal. And the other thing with the drug chart as well is even if we're holding drugs at that point, we need to also think about do it adjusting the other. So, arenal drugs that are less nephrotoxic but are excreted there in Austin is done quite poorly. You know, we'll stop the ace inhibitor or stop the ARB, we'll stop the diuretic. But have we adjust the amoxicillin, have we adjusted? The Mets have adjusted team moving, especially team Acilin varies quite a lot in terms of dosing, especially when you get down to the EGFR is like under 30 under 10. Um So always a good one just to double check the pharmacy or to have a quick Google yourself. Um There's a few things we can do in terms of um sort of uh categorizing AKI. I know we've got the Codigo AKI 123 that we discussed. People used to use rifle and Akin. They were actually recommended in that paper. Um They're basically along the same lines. The first three of both of them are achy I 12 and three in essence, however, rifle goes one step further and also has a sort of severity in the first three, the RIF but also then has outcomes in L and E. So loss and end stage renal disease are the two. So the whole point is, it's trying to make you think that the closer and more serious the achy I the more likely they're going to slip into this or long term loss of renal function in chronic kidney disease, but also then going to require dialysis or a serious discussion about where we're going to take this when they're discharged. So, it's just another way of thinking about it. Um, and it's certainly not used as much as it certainly used to be. So, what does that mean for our patient? Well, they've got a kid ago, AKI one. They're at risk on the rifle criteria and they're stage one in akin. So fantastic. We have bulked up our clerk in booklet. We looked really clever. We've categorized it. We haven't actually done anything for this patient yet. So what do we need to do? So you go to see her, the Rob's have improved. The character is sort of starting to settle. Heart is down a bit. Blood pressure's down a bit. It's probably mostly because we've given them some antibiotics and there's 0.9% saline running in the background 100 miles an hour that the sh you started, she appears comfortable. She doesn't look septic. She doesn't look like she's about to go off. Her capillary feel time is really good. And she does report four days darker urine and she, she is like, yeah, I'm not producing as much and actually, I've only just been to the toilet properly in the last 84 hours, 15 minutes ago. She's like, okay sounding uh correctly like dehydration. So your assessor, she's got a dry tongue chest is clear JVP is not visible even on the tummy. There's no edema and she still feels thirsty and she's very important. Um Your night, as we said, sounds like it's picking up. It does sound like she's dehydrated. And your analysis, the nurses have kind of got views, doesn't show anything on it, not even sediment. Um, obs look like they're improving but does look like she's previously hypovolemic and actually there's no pain in her abdomen. There is no history of real students with her or family. She doesn't say she's had any pain, no weight loss, no hematuria. So we can sort of start excluding a renal cancer and a bladder scan doesn't seem to show a minimal residual volume. So sounding all quite encouraging. Um So, you know, time to make your money, time to sort of have a think about what the impression is. I'll give you a second to think about what you think this is. There's no trick questions. So I would probably say that this is a hypothalamic criminal attack secondary to concurrent left leg cellulitis. I would continue the IVF I think that seems reasonable, but I switched to plasmalyte. Um We'll come back to that. I can tell you the flu clocks, read a lot of time to be certain, but it's a Saturday currently and actually won't get one until Monday, but we'll put it in the plan anyway. I don't think it's necessarily urgent and if there is concerns over real life, put or no improvement, real function. Then this lady probably needs a castor. In the meantime, just gonna use bottles and she's agreed to keep the charts date yourself. We'll get some blood in the morning and my safety net. Let's speak to Renal. That all seems quite reasonable. Why have I switched to plasmalyte? One of my massive bugbears 0.9% in a ki I was always taught by Dr Clark family enough at university that give 0.9% in a key. I is um not fantastic. It causes the huge amount of chloride in it are not physiological cause a large about a renal visa construction and plasma. Another balance crystal, I don't really have that as much. It'll exacerbate a hyperkalemia. It will show a greater acidosis if they're unwell. Um And actually, it's shown in animal models to, to cause harm less. So in humans, the reason why we've been using ceiling for users because it's cheap, plentiful and it's sort of been plucked out of thin air. And actually now with the rise of more physiological fluid, that's similar prices, we should probably just be using plasma lights. Um Yes, it's one of my bugbears and I would highly recommend anyone watching this to go and have a read of that uh fantastic website, em crit IBCC forward slash fluids. Uh because there's even stuff greater than this including like Ph driven fluid resuscitation and all that jazz, which is where you're really starting to sort of see fluids as drugs and, you know, treating them appropriately rather than just writing what the person had done before. So, if you're bored or require some reading to get you off sleep tonight, I'd highly recommend going and having a read. Uh The only time you really need to use Saline rather than plasma and traumatic brain injuries. The only group of patient's where it's been shown to have benefit. Uh My personal press is that everyone should get balanced crystalloid. So with that in mind, um we'll move on and the next day the patient's bit better, a little bit wiped out by the cellulitis. Not surprising. So that's been quite good. CRP and white cells are high. Um She did have borderline temperature spike overnight of 37 9 blood culture repeated like team we're earning their cash um legs. I like see stop spreading and seems to have held at the marks. The nurse is very kindly puts on and you're not that's picked up. Well, she's been up and down to the toilet all through the night and she, she assures you that even though the chart hasn't been done properly, that is improving in color and void. Uh That is a new thing jab uh That's the second book's longest um uh um consult on the post take has been like, yeah, 40 hours of IV antibiotics and then we'll aim to, I've almost on oral antibiotics there. As I said, there's no hospital at home. No, no pat. And we'll keep going with the IVF for a French fires and then try and get push orals after that. Uh, using these are much improved croutons. 91. It's still not 67 or the baseline from two years ago, actually, uh, much improved. So they'll repeat them tomorrow. So, with that in mind, your next day I come in, um, consultants. Like, can you go see her? She straightforward. I'm like, yep. Sure, fantastic. Sounds like really, really quick one, as I'm seeing her phone call from biochem. Uh credit in shopped 152. She's in a kit to your potassium safe at 5.300 is 10.1. What do we do now? Well, in straight, we go back and repeat our assessment. So this time she looks usually make her chest is clear. JDB is actually now visible and we'll ride up the neck with a hand on the tummy. She's not overloaded and she's no longer thirsty. She's producing a good amount of urine but repeat urinalysis shown plus blood plus protein. Uh and very good people will have, have very, very quickly turned around. In microscopy have shown red cells, white cells in a bit of pyuria obs are continuing to improve. She's now been a pyrexic for 36 hours and actually heading towards normality again, no pain in the tummy, no bleeding bladder scan again, minimal residual volume uh is there Mondays the really come back, no obstruction look like normal size kidneys, white house and CRP improving and actually as his bone profile and repeating are also normal. So with the normal bone phosphate and magnesium, we can essentially remove CKD from the from the equation unless it's very, very mild. Um apart from the Malays, she actually feels okay. So what's going on? So differential time, time to earn your money and see what you think. So, in terms of this or three meat, uh prerenal pushing on an intrinsic, it doesn't sound like it's prerenal. Um It doesn't sound like she's bleeding, does not accept this and it looks like we fixed her hypertension, hypovolemia. She's got no tummy pain. If you're really worried, you potentially chucker anomalies, make sure she's not got panic attacks, but doesn't really sound like that. Um She's not get any pain. The normal renal ultrasound, there is plus blood, but there wasn't before. There's not a history pain, no history, weight loss pushed. It does sound strange given that there's um that there's no sort of residual volume and weirdly doesn't sound like a vasculitis. The normal platelets, no rash basically make it all sound um slightly less likely. So, what we think we're thinking intrinsic is it an tribulus necrosis is an interstitial nephritis? Is this a weird and wonderful Gloria crisis rapidly progressive or actually does she have renovascular disease and has the cellulite is actually throwing that off. We don't know. So we proceed for it. When do we consider intrinsic AKI? Um We'll talk to in terms of this patient, she's not really had nonspecific constitutional symptoms of the previous few weeks. It all sounds quite acute. It doesn't sound like she was expecting to have to come into hospital. Often. The ones who happen vaguely unwell for about a month or so usually aren't shocked when something happens. There's no sediment in her. You um she's not anemic, she's not got thrown cytosis and CRP is coming down appropriately and she doesn't have any rash or joint symptoms. But but but she hasn't improved fluid read us and she does to be appear to be in Euvolemia. So um that is where you'll be getting your money on that, something's going on. So what we do with intrinsic AKI, well, we speak to the renal team and who do renal want us to speak about in terms of AKI. Well, they want to know about severe AKI AKI threes, low platelets, any suspicion of intrinsic kidney disease. As is the case of this patient? Uncertainty. And then all of you re a plus the factory hyperkalemia overload really unwell, failing to improve or renal failure. Uh sorry, liver failure or heart failure. Basically, anyone who's complex, what they need to know is I need to know the history, the patient, the examination, the patient, the fluid stated with fluid charts in case they disagree with you. Um The obs and or previous instability periods of prolonged blue BP. New af what the BP was like with Sass, the ultrasound result and a urine dipstick amongst all those things, they should be able to come up with a sort of plan that satisfies all parties. They'll probably come and have a look at the patient is very good here in Fife. That wasn't the case in, in Whishaw Renal were actually on another site. So a lot this is being done over the phone and done blind. So it's really important that you get all your information ready so that they know. Uh and that also sort of includes the middle of the night because you don't want to have to call your doctor back in from Edinburgh. Um If you just give her all the information on over the phone, so you discussed with renal and renal like, yep, sounds like something we need to be seeing. Um So they say Papa Catherine will come and see her. Uh Actually when we're doing a wardrobe tomorrow, um it does sound like she's usually make, let's stop the flu clocks and switch to clean and see how she goes with that daily use knees in a book and renal profile. So let's just stop her fluids, make sure she didn't come to harm from that all sensible. So next day with all that cellulitis is improving, it's now retreating. Patient feels better they remain the eight ft brow using these are stabilizing. Um And actually she's pretty some good volumes of urine. She is now starting to get a little bit and it's about being hospital now that she feels a bit better. So the day after that lasted two clinda uh po white cells now normalized CRP is really nicely and renal function is actually now improving, um almost heading in the right direction. So we'll pop back, see her and they're like, yep, we think she probably did have hypokalemic premium this but actually it looks like it probably was the flu clocks giving her an acute interstitial nephritis. She's rapidly recovering. She's not driving her urine output as steady as she goes and we'll try and get her way home. Uh once things have improved for a second day, which thankfully they did. So when can we discharge achy is well, contrary to popular belief, you don't need really function to normal. This can take weeks to months to occur. Then we just want a prolonged improvement or stabilization. I mean, sure, they're not going to re fall down again. When you're doing the discharge letter. You want to communicate the calls on the severity of the achy IGP so that they know and can try and prevent it happens again, especially if it's someone frail or housebound and you want to give him a very clear timeframe for follow up and repeat using these and always, always safety net with discussed Arenal if there are any issues with the renal function in community and as always, if there's any doubt, run it past renal prayers discharge because they'll be the ones picking up the pieces of GP and they won't. Thank you. It's a bit of a mess. Um, on them going home. That leads us home nicely to, when do we restarted nephrotoxic meds again. Not really appropriate with this patient, but it's important. There's no right or wrong answer. We go with cardioprotective drugs first, the ace inhibitor. Um the ARB um if there are liver patient, you probably want to start their, their spiro first, especially if you've got ascites. Um You want to repeat the fluid assessment after that, you know, they might have been on a whacking great big dose of your meta night and they may not actually need to go back onto that. It could be reduced, it could be rationalized. Um You may need to get a GP or the heart feel nurses involved to help with this. And then you want to go from there, titrate other diuretics, repeat the fluid assessment just be guarded by patient's symptomology. Um Often what you'll see is combatant source of cardiorenal syndrome. Your may just need to accept deterioration in real function with these patient's. There are no easy answers. It's, you know, it's a dual organ failure. Um You know, and something that young fit patient would end up in icu with, but you know, we're just having to accept because they're old and frail. Um and you may just need to offload them to, you know, to improve the real profusion. Again, this is head against the land of senior consultant level decisions. Um The decisions that you may have to make in the heat of the moment at night or in discussion with the intensive ists but not something that we should be doing alone. And so we should always discuss the senior before doing this. So final couple of slides, how do we prevent achy? I always bear to think who's at risk of an achy. I so age of 78/75 hypertension hadlima generally um in terms of how long it's prolonged for the higher the channel progressing, taking I septus, the more severe the sepsis, the more the chance, the worst, the renal function, the more the chance vascular disease, heart failure, diabetes. John, this never talks about COVID 19. Absolutely awful for it. And then as we were saying, it's the ICU admission, you know, nearly two thirds will get it. So in terms of prevention, you want to stop the drugs, the need health emission. As we were saying before, you want to do regular food assessment on your in patient's sick day rules are quite controversial. There's little evidence that they actually benefit patient's, everyone has a different interpretation of what illnesses. Some people will be like profusely knowledge of vomiting, diarrhea, other people will be attached the sniffles. It's uh sort of very much patient belief led part medicine and that's reflected in the fact, the evidence is quite poor. The danger, of course, with them, especially in heart failure is they thought heartfelt patient stops the BMS 92 and two and the spiral 25 is that they're gonna come back in public. Um, and that's benefiting new one. So it's something that we should persevere with. But actually we, it's when people come into hospital that we just get keep and make sure that the correct drugs are stopped at the correct times. And that actually, we should realize that just because they've had the race inhibitor for the last three days and get the diuretic going, that it's probably a little bit on us that it's not straightforward. And that in an ideal set of circumstances, these people be getting phone appointments with their GPS when they start to get unwell. But unfortunately, don't work in a system like that. Suit wrapping up what we're taking home with us today. Stop nephrotoxic on a mission of patient somewhere making eyes are common. They're preventable and actually categorizing them, helps us get a cause on how to treat them. If it's prerenal, we treat the underlying cause. We really fill the patient ideally, fluids and prevent progression to tribulus necrosis. We should be suspicious friend if the patient is not dry or their background, constitutional symptoms in the weeks prior and speak to reno and post renal. Always, always, always image of the bladder scan or ultrasound. If there's suspicion discussed with urology, if there's any suspicion, uh if there's any doubt and their kidney function getting worse, put a Catherine uh achy is include even a small rising Crafton in greater than 27. That's not to be forgotten about special old frail wheeled ladies use shout sepsis, hypovolemia, obstruction, urinalysis and toxins to help identify cause. Generally the sicker are more come over the patient, the more likely they are developing an achy i and therefore the increase in mortality in cardiovascular discuss hyperkalemic and oliguric patient's with a senior, a renal or non straightforward patient's of the renal team. And if there's pushing a dip, send it urine, I'll be in crested inr issue. That is all for me. Thank you very much for listening and being through patient. And we would very much appreciate if you could fill out some feedback just as we're approaching the halfway point in our course of lectures. And it would be a huge help to me maybe and fatima to be guided on what you guys want to hear as opposed to us guessing what you want to hear. Um We'll also send you a little sort of feedback thing as well um to everyone who's in the chat. So if you just do one of those, um primarily this day, we'd be very, very, very grateful. So, no, thank you very much for time. Does anyone have any questions? And if not, no pressure at home and if you want to put it into the chat, you're more than welcome to. Sure. Well, that's right, Erin, rushing, uh, in to do anything but you're more than welcome to email the, um, Dominic dot Coats to any chest dot Scott. And I'm happy to answer or signpost or send you anything else. Um, the one thing I would say is that em crypt, um, fluids website is absolutely fantastic and I'd recommend everyone take a look at some point. Um, I is fascinating and something that I feel we do not speak enough about in this hospital. Thanks very much for your time, folks looking for us feedback and, um, we'll be seeing you back shortly. Tues today.