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Hello, everyone and welcome to medical education. It's great to have you. Um Today I am joined by Doctor Alastair Rankin and um he is gonna be chatting to us about acute kidney injury. Uh As always, please pop your questions in the chat. We'll get to them at the end of the talk throughout the talk though. Um Alastair will be asking questions. Please do respond in the chat with your answers. Ok. Again, at the end of our medical education event, the feedback form will be in your inbox. So that is in an hour's time, your feedback form will be in your inbox. Please complete it and your attendance certificate will be on your med profile. We will be sending the feedback on to Alista so that he can have a look through and maybe if you put on some suggestions of further teaching that he thinks he would fancy doing, maybe we can get him back again. Ok. So I am gonna pass you straight over to Alastair. Thank you. My name is Alastair Rankin. I'm a consultant in Renal medicine. I work at the University of Hospital Monklands, which is in Scotland and I'm also affiliated with the University of Glasgow. And today I'm gonna be discussing acute kidney injury or AK I So what I plan to do over the next 45 minutes is we're going to discuss what is a, we're going to come up with an approach to, to um approach patients with acute kidney injury. We've got four cases and then I'll leave plenty of times for questions. I think this might take an hour with questions. Um And I should say that I realize there's um people from all over the world joining here. So some of the approach to AKI may vary with resources from one hostel to the next or one country to the next. I'll try and give as much of a general approach as I can. So what is AK I, well, there's lots of definitions but you can think of it as a sudden reduction in kidney function that causes biochemical and or fluid imbalances. And it defined based on serum creatinine according to cao criteria which is an increase of 1.5 times baseline, baseline, which has either happened or assumed to have happened within seven days. You can also define AKI based in Oliguria. This is particularly relevant or useful for places such as intensive care and critical care where um they monitor your output very closely. And if a patient has oliguria for more than six hours, they can be assumed to have acute kidney injury without needing to wait for the creatinine results to come back. So the definition is based on creatinine. What is creatinine? What it's a waste product that's produced by muscle is chosen as a measure of kidney function because it's produced at a fairly constant rate of production and it's eliminated at a fairly constant rate of elimination in the normal state. So the creatinine goes up implies that the renal function has gone down. So if we take this life cycle of creatinine, there's a, a representative picture of the average Scottish male creatinine is produced in muscle, it's filtered in the kidneys and it's excreted in urine. And we can think of that then as a bathtub analogy and that the creatinine is produced at a constant rate that fills up the bath water, if it then drains at a constant rate, means the creatinine level stays constantly stays at the same level. Um because what's being produced is being excreted at the, at the same rate. However, if there's a reduction in the amount of creatinine that's excreted due to renal impairment, the creatinine level in the blood in the bath will rise and suddenly the more severe the obstruction or the more severe the impairment, the higher the creatinine level goes. Now, nephrologists like to make things complicated, but uh in a rare moment of clarity and quite unusually for nephrologists, the staging of AKI is actually quite simple because if your creatinine has increased two fold, it's stage two AKI. And if your creatinine has increased three fold, it's stage three AKI. There are some other parameters you can measure as well. But I think keeping that in your head gives you a good guide. So we've talked about creatin, I would hope you're all also familiar with eeg G fr or estimated glomerular filtration rate. And I'm gonna ask you what four things are used to calculate EEG G Fr. So thank you to anyone that's willing to put answers in the chat. Everyone else you're not willing to speak out. Please think about what things are involved and the answers are serum, creatinine sex age and controversially in some calculations, race is used as well. But the main driver of the EGFR is the creatinine and they're mathematically linked. So if creatinine goes up, the EGFR goes down, you might have heard of creatinine clearance as well. That's a similar measure. But this time incorporating a patient's weight, you can remember that a computer doesn't know the patient's weight. So if I take your bloods today, the computer will give me an eeg fr it doesn't know your weight. So that's an easy way to remember. Weight is not part of, of G. Fr. Egfr has several advantages. It accounts for patients age and sex. You can think of it roughly as a percentage of the remaining kidney function and that a normal G FR is approximately 100. So patients will come to my clinic and say, ok, doctor, last time I was here, kidney function is sitting at 30%. What is it today? Um For example, and it's used to categorize CKD stages in combination with proteinuria. But the more the lower the egfr the more severe staging of chronic kidney disease. Now there are disadvantages to EG FR and it's validated for KD, not for acute kidney injury. And in changing situations where such as acute kidney injury, where the creatinine is changing day on day. Most people prefer to use the creatinine, which we'll focus on. Um going forward that said, you know, creatinine goes up means EGFR goes down. So um it it can still be used, but for technical reasons, probably prefer creatinine. So how do you approach a patient with acute kidney injury? So let's say we have a 70 year old male patient with a previous myocardial infarction who's got a history of type two diabetes and they admitted to hospital with a fever admission blood show acute kidney injury because the creatinine went from 80 micromoles per liter to 300. If you're in the North America. Um or certainly United States of America, you'll use different units that be 0.9 to 3.4 mgs per deciliter. So there's acute kidney injury, what we're going to do? Well, I would argue every patient with acute kidney injection have four things reviewed early on in their hospital admission. I think they should have their fluid status, including the BP reviewed. They should have the medications, there should be a urine dipstick in consideration of quantifying the the protein in the urine and the consideration of renal imaging. And the reason why those four things are important is because you can approach acute kidney injury as prerenal renal and post renal causes. And there's lots of things we're taught in medical school that turn out to either not be useful in working as a doctor or turn out to actually be wrong. But thinking about renal dysfunction as prerenal, renal and postrenal is actually a very useful way of approaching things. And the fluid status and BP focuses on the prerenal. The medications crosses between the two. Some cause pre ai some cause reno aii urine dipstick is primarily looking for intrinsic glomerular renal disease and then post renal AKI I is excluded by renal imaging. So pre renal AKI is by far the most common cause of AKI making up more than 85% of hospital. Um and patient ak I So what are the causes of acute kidney injury? Thank you again to who puts answers in the chat. What I think are the main causes are listed here and if you take nothing else away from today, I think it's reasonable to remember that no BP equals no PP. And that hypotension shock, organ non perfusion is the most common cause of or certainly the most significant cause of prerenal AKI I, you can get volume depletion causing pre renal AKI. I even with a normal BP, similar sepsis and severe sepsis. You might not have septic shock or low BP, but you can still get an associated achy eye and renal artery stenosis is a slightly different entity, but it is before the kidney, the kidney sensors reduced blood flow to that kidney and can cause an achy eye. So when we're assessing a patient with pre AKI, I, we're gonna look for any episodes of low BP and that can be relatively low BP as an low for what is normal for them. We're gonna look for any history of volume depletion. Have they been vomiting, diarrhea, not eating and drinking any medications that would worsen pre AKI I? And do they have risk factors for pre ral AKI and risk factors for AKI I are hypertension d heart failure, diabetes, liver disease, and the more risk factors that are present, the less insult will be needed to, to cause the AKI eye. So for a 70 year old patient, the one that had the previous myocardial infarction type two diabetes had a low BP and it was usually high, had a history of reduced oral intake, had continued to take the ramipril and flusemide despite being volume deplete and in a blood glucose of 25 millimoles per liter. So very high hyperglycemic suggesting with osmotic diuresis, I think we can say it is very likely this would be a pre renal AKI. Now I mentioned medications. So, what medications are commonly associated with acute kidney injury? And there are several, but I'd like you to try and think of a few and then I'll give you my, er thoughts. So, RAAS inhibitors, ace inhibitors and angiotensin receptor blockers are probably one of the most common answers to get to this question. We need to remember these drugs are not nephrotoxic. They're probably the most evidence for protecting kidney function in the long term. So we don't like to use that phrase. But if their BP is low, they reduce um autoregulation of renal perfusion and can worsen acute kidney injury. As can any BP drug. If the patient's BP is low, that will be exacerbating the problem. Another big class of medications associated with AKI are nonsteroidal antiinflammatories. They can cause interstitial nephritis. They can also cause an ischemic hit to the kidneys. So they're definitely implicated in in, in ak trimethoprim doesn't actually cause acute kidney injury as such. It causes it blocks tubular excretion of, of creatinine. So it causes the blood creatinine level to rise er quite predictably. But the problem there is if patients on trimetin, you don't know how much of it is the trimethoprim effect and how much is true. AKI I, so it certainly gives the appearance of AKI and should be avoided or might be contributing to the case diuretics again, they are not nephrotoxic as such. They don't harm the kidneys except if a patient has volume depletion, if they have prerenal AKI, then the diuretics will make it harder for the patient's native kidneys to re retain the water work and could worsen uh volume depletion as part of it. Antibiotics such as aminoglycosides, gentamicin, amikacin are certainly linked to acute kidney injury. And increasingly we're seeing immune checkpoint inhibitors. So, novel cancer anticancer drugs um with really a whole host of immune side effects, uh unfortunately can cause interstitial nephritis and cause acute kidney injury. I think it's important to see at this point as well that iodinated ct contrast doesn't cause acute kidney injury or if it does, it, it is very, very rare. And certainly the most important thing is that if your patient has a reason for a contrast, enhanced CT scan, then we shouldn't deprive that patient of contrast. Um based on their, on their kidney function, the risk that patient is of AKI is much smaller than the risk of missing a diagnosis. If the, if the scan is truly indicated now, as well as medications that are associated with causing AKI or worsening it, there's also medications that need the dose reduced when a patient does have acute kidney injury. And again, there's several of these medications, I think ones to look out for are predominantly opiate medications. So if someone's on morphine, they will become much more likely to accumulate that drug and become drowsy and develop side effects. And that's true with, with just about all the opiates. Metformin needs dose reduced with a higher risk of uh lactic acidosis. Various antibiotics need lower doses, low, low molecular weight heparin. Sorry, I struggled there, gabapentin and, and there's many others. But as well as looking at what drugs can cause acute kidney injury, you need to be aware that many drugs, most drugs are really excreted and therefore need dose reduction in kidney function drops. Ok. So we talked about prerenal AKI, I'm going to skip past the kidneys. We want to talk about post Rno AI. And that's because it's, it's more straightforward inside the kidneys where things get complicated. So post Reno AKI, well, together with pre AKI that makes up the vast majority, there's a nephrologist in America. He's on Twitter with the hand at kidney boy. He's a really an excellent educator and there's lots of good educational content around nephrology. B commonly says 90% of AKI will be fixed by fluids and a fully a fully there being a urethral bladder catheter. And, and I think it's, it's true, the majority of in hospital acute kidney injury is either due to volume depletion and prerenal causes or obstruction. So, post renal AKI, how do we approach it? Well, when do we need to expect post renal AKI? And, and I think that the answer there is we need to expect it or think about it in everybody. There's no definite symptoms or ways you can exclude it without doing the, the test and doing the imaging. If something's very clear cause the AKI and it's getting better, then fine, let's, you know, if it fully resolves, you maybe don't need to pursue the imaging. But if someone's got severe AKI regardless of the cause, at some point, we need to get some kidney imaging. It's highest risk in people with older men due to prostate problems, patients, history of cancer or lymphoma because they can get obstruction from lymphadenopathy if they have history of urinary retention or urinary symptoms. And if they get history of renal stone disease, that's when you really need to think this, we need to push earlier on for, for excluding post renal AKI I, how do we exclude, exclude post, you know, a well, it requires the resources to do the imaging but that it's a very simple test in that you look at the kidneys on, on imaging. So either on ultrasound renal tract and that includes includes point of care, ultrasound with several studies showing medical students can be very quickly taught to exclude hydronephrosis with high sensitivity. Or you can do a CT scan, a ct kidneys, urinary bladder and that can be not in contrast and would um exclude hydronephrosis. You can also do a bladder scan or put a catheter in and that will actually also treat the most causes of obstructive AKI I, if it's bladder outlet obstruction, but it doesn't fully take postrenal causes out because there could still be upper tract dilatation and blockage. And I quite commonly hear when I'm taking referrals for, for RNA, the patient is passing urine so it can't be obstruction. Do you think that's true? Uh No, that's a loaded question, but it's definitely false. The majority of patients with post renal obstructive AKI I still pass urine and that's because it's a pressure effect. The bladder fills up to get a pressure and then passes urine. Uh So some urine comes out per urethra, but the back pressure on the kidneys is enough to affect the the tubular function. So if our 70 year old patient had a normal BP, had any volume depletion, had a one week history of difficulty passing urine, you put your hand in their tummy to uh uh to examine them and they had a full bladder and palpation. And your colleague managed to use some point of care. Ultrasound, showing bilateral hydronephrosis and a post void residual volume of 600 mils in the bladder. Then we can be confident this is post, you know, acute kidney injury. So I mentioned ultrasound. I mentioned imaging, this is hydronephrosis and what it looks like. So normally you should have the the kidney, the renal pelvis draining into the ureter. If there's an obstruction, somewhere, pressure builds up urine builds up urine appears black on ultrasound. And so we see the back pressure of uh, urine filling the renal pelvis and causing that dilatation. It's graded as mild, moderate and severe. The grading is very subjective and probably doesn't really matter. It's either present or, or not present. Um, but, but that's what it, what it looks like. And I've got a slight here saying rules of obstruction and II should point out these are my rules of obstruction. It might not be universally agreed. But if there's bilateral hydronephrosis, regardless of the the severity, then to my mind, that is the cause of the acute kidney injury until proven otherwise. And on the opposite side of things, if there's no hydronephrosis in a patient who still has ongoing acute kidney injury, then that is not the cause or it is not post you know, cause for the AKI. So we all are not, most people have two kidneys and can function quite well with one kidney. So it's really bilateral hydronephrosis we're concerned about or unilateral nephrosis. If the other kidney is shrunk in disease or, or thought to otherwise not be functioning at full capacity. So if someone report comes back as bila bilateral hydronephrosis, the first question you should be thinking is, is the bladder full because the bladders fill. Then we're thinking about bladder outlet obstruction, urinary retention. So we think about prostate pelvic mass. You put a catheter in, in that and that should fix the problem. If the bladder is empty, it must be higher up the urinary tract that the obstruction has occurred. And then we're thinking lymphadenopathy, kidney stones rich peritoneal fibrosis, putting a catheter in is not likely to fix the problem. And we need to be thinking about doing some other intervention through interventional radiology or urology such as nephrostomy or ureteric stents. Right. So we talked about prerenal, we've talked about post renal, let's get into the kidneys now and talk about intrinsic renal causes of AKI I and it's fair to say that intrinsic Raynaud disease is an uncommon cause of acute kidney injury, maybe 5% of cases. But some of these cases are medical emergencies that you don't want to miss because in these situations, time is kidney and the longer it takes to make the diagnosis and give the treatment, the the more likely that patient is um going to come to harm and potentially end up on dialysis the rest of their lives. So, consider intrinsic renal disease if there's no prerenal factors, if there's no obstruction, imaging, if there's blood and protein on the urine dip, and especially if it's systemic features of another disease. So what are the causes of renal intrinsic renal AKI? I again, please put them in the chat or have a think your yourselves. Um But what the main ones I think to consider is glomerulonephritis and that includes systemic vasculitis within it. So that's a umbrella term for inflammation within the glomeruli causing proteinuric achy eye myeloma, myeloma, kidney disease can cause intrinsic kidney disease. And interstitial nephritis is I think the other big one which is most commonly uh a drug effect or in a response to infection with inflammation in the, the uh interstitial of the kidney. And the most common drugs are nsaids, proton pump inhibitors and certain antibiotics. So, if a 70 year old patient with a history of type two diabetes and myocardial infarction had normal BP, had normal renal imaging and had blood and protein and dipstick. We've got to thinking well, we we can't explain this otherwise. Could this be an intrinsic cause of AKI in that situation? I think if you get access to a renal specialist, you can phone, that's exactly the sort of cases they want to know about. Again, if you had access to a likely task, you'd send the glomerulonephritis screen. And ultimately, that patient might end up needing a kidney biopsy. I'm not expecting non nephrologists to make decisions about kidney biopsies. I think it is worthwhile knowing that the big risk factor for that is bleeding. And so if you see a patient who's unwell after a kidney biopsy, we need to really be thinking about the, the risk of bleeding. And this table then shows the, the common tests are included in the G nephritis screen, um which the, the main one or perhaps the most common, most important one being ANCA which is split into MP and PR three antibodies. Um, because they are really very specific for, um, vasculitis, which is a very treatable condition. It is a, a condition that carries a high morbidity and mortality if it's not treated. And um, it's probably one of the higher yield results from a glom nephritis test test end. So that's one of the cases that we, we really don't want to miss. So we'll move on to some cases. Now, let's say case one is a 62 year old man with difficult to control. Type two diabetes presents with diarrhea and vomiting. And he was seen at diabetes clinic one month ago. So we can see his admission bloods on the, the right hand side of the screen show his sodium is low. His potassium is high, his urea is high. His creatinine has, has jumped um, more than double from er his previous bloods. And with that, as you'd expect, his EGFR has fallen, his BP is low. He's tachycardic and he's not passed any urine since survival. So, in this situation, what do we think is the most likely cause of acute kidney injury? We'll think about it as prerenal, renal and postrenal. So, could it be prerenal? Yes, definitely. He's got low BP, very clear history of volume loss and he's got risk factors for acute kidney injury, meaning his kidneys gonna be vulnerable to changes in fluid status. And that's his diabetes and his baseline C KD. Could it be intrinsic renal disease possibly. But I think there's some more likely things to consider first and we can go back to that possibility if it's not improving, it is worthwhile. Remembering he has diabetes. His d it's likely he's got baseline proteinuria. So if we dip his urine, there's protein in it, we need to bear in mind that that might be consistent with his previous results and not a new phenomenon. Could it be postrenal? Yeah, he does need imaging to exclude that. But actually there's, there's some much more likely causes in the the prerenal category. Now, that's the cause of the aci but what's actually the most concerning blood result? I hope you're all spotted. The most concerning blood result with the most eminent risk to him is his potassium of 7.2. A potassium greater than 6.5 is classified as life threatening hyperkalemia in in most guidelines. So you do an ECG it shows changes of hyperkalemia list two ecg changes of hyperkalemia. That was that exam question that came up in my finals exam. It's also in clinical practice. If you're referring somebody with hyperkalemia to renal, they'll be saying, what does the ECG show is there changes of hyperkalemia? Because that means they're much that the management is different and they're at higher risk of harm if we don't treat it quicker. So tall tinted T waves, prolonged pr interval, low flat P, uh P waves, broad QR S bradycardia and if it gets really severe, it gets sinusoidal. And the big ones there for, for me, when I'm taking referrals is, is the QR S Broad. And what's the heart rate if they're bradycardic? I think it quite commonly responds to, to treatment and it gets better if the QR S is broad, that's a higher risk for, um, cardiac arrest. And there's an example E CG, we can see where it's got a broadening of the QR S and certainly very tt waves in the, in the chest boots. So what's the management of hyperkalemia then? Well, it can get split into three rough categories. We can talk about stabilizing the myocardium. If there's E CG changes, shifting potassium temporarily into the cells and then actually removing the potassium from the body. And the way we do that is with calcium salts. So there's ECG changes. So that's 10 mils, a 10% IV calcium chloride or 30 mils. If you're using calcium gluconate, it needs to be into a well functioning Benin because it can cause tissue necrosis and you do it slowly over 5 to 10 minutes. If it's a non cardiac arrest situation, we then want to temporarily shift or drive er potassium into the cells. We use that with insulin dextrose, it's the insulin, that's the, the work course there. The dextrose is just to stop hypoglycemia. You can also use nebulized salbutamol at a much higher dose than you would usually use for asthma and you can consider checking bicarbonate and treating er acidosis. But I think you, you would do that with a specialist input. Then none of those things actually change the total amount of potassium in somebody's body. So those treatments alone, if you give it four hours, the potassium will rebound. So they need to remove the potassium from the body. And that's using a potassium binder by treating the AKI and discussing with Reno to think about hemodialysis. Now, in more detail, you can see this uh flow chart is from the UK Kidney Association algorithm for hyp hyperkalemia treatment. It's a long but excellent guideline and this uh picture summarize it and you can find that on the internet and it is worth a read. So let's see, the ultrasound shows two normal kidneys with no hydronephrosis. The potassium is treated with medical management and BP improves with some IV fluids, crystalloid fluid. And actually, amazingly, he starts to pass urine. So he sees admission blood results there. His potassium is 7.2. He gets insulin dex shows an hour later the potassium has come down to much safer levels. So we're delighted the creatinine's got worse, but I mean, we, we don't necessarily care that still very, very soon to expect a change from that. We do the bloods again at four hours to make sure the potassium hasn't shot back up and rebound. And we're delighted to see it hasn't and actually, incredibly, he has started to pass urine and with that, his creatinine has started to fall. So this has clearly been a very um prerenal BP and volume depletion related um injury. And at 12 hours, he continues to improve towards his baseline. So that's a very quick response which we don't often see a as quick as that. But a good example case but different case then case two of four, this is an 85 year old man who's got one month of recurrent uti s and difficulty passing urine. He has some low back pain but otherwise has felt well, he's no vomiting, blood pressure's a little bit high and his urine dip is negative. His medications are listed there with vitamin D3, amLODIPine and a statin last year. His blood, his e knees were normal fast forward a year. His creatinine has gone from 70 to 800. His potassium's slightly high at 6.1 moderately elevated. So what is the cause of AKI I, we didn't really hear much prerenal triggers there. Could it be renal disease? I mean it, it could be, but I think there's something else that's much more likely. Could it be postrenal? Well, he's got lower urinary tract symptoms. He's got risk factors with his age and sex. So, yes, I think that's the priority to exclude a bedside ultrasound shows a full bladder with bilateral hydronephrosis. A catheter is inserted at 1.5 L comes out the first hour and later on, his psa is prostate specific antigen is checked and it's very high in the kind of metastatic range. And so we can call this postrenal A I. What happened next? He developed post obstructive polyuria. Um He produced 6 L of urine per day. His creatinine fell very, very quickly, which can often happen in this situation and his potassium went from being too high to too low subs needed potassium supplements. He was then transferred onto the urology ward for ongoing management of his volume status. He would need extra fluids to keep up with his urine output. And um for further investigation and treatment of his presumed prostate cancer. After any achy eye, the kidneys can wake up and produce what can be thought of as poor quality high volume urine. It's particularly common after obstruction and we just need to watch out for it at some point. If you're giving them loads of IV fluids, you'll start to drive that polyuria. So you can allow them to run a little bit negative, but you probably don't want someone more than a liter negative fluid balance in a day when they're recovering from acute kidney injury case. Three. So we got a 50 year old female previously. Well, not on any medications presents with two month history of weight loss, night sweats and muscle aches. They were recently referred to ear, nose and throat with nosebleeds. They now have noticed a fiery rash over the legs and they're a nonsmoker, but they've had recent shortness of breath and coughing up blood and their GP gave them antibiotics for lower respiratory tract infection. They've never had bloods done before, but they get bloods done on admission to hospital and they have abnormal kidney function with a creatinine of 450 other bloods show raised inflammatory markers with ACR P of 100 and 50. And the urine dip shows blood and protein on Dipstick. Ok. What's the cause of AK I could it be prerenal? There was a few things there, some general malaise, this could all be pneumonia and sepsis, but there's no history of volume loss and the BP is normal. So I'm not totally convinced that explains the kidney function. Could it be renal, intrinsic renal disease? Yes, I hope you all thought. Absolutely. It could be. There's the positive view in depth and there's some other features of systemic vasculitis expecting the audience to be different, er, levels of knowledge of vasculitis. It can affect just about any organ but commonly kidneys involved, commonly skins involved with a vasculitic rash and you know, upper respiratory tract as well. So lots of the story that this, this patient has described could be explained by vasculitis. Could it be post, you know? Well, I think you still want to get some imaging but er, there's no risk factors unless and this is how, you know, medicine is difficult is I mean, if the hemoptysis is actually due to cancer and this is disseminated malignancy, then it, it, it could still be part of the the differential. But I think vasculitis is the real time dependent thing you don't want to miss. So it was discussed at the tertiary hospital with the renaud team and they said send an urgent gen screen that came back with an ANCA antibody. The pr three specificity that very elevated over 100 and 30. And this would be consistent with a diagnosis of ANCA associated pr three positive vasculitis. We don't need to get too much more into the, the further details of that, but it's an emergency transfer to the renal unit. They get IV steroids, they get riTUXimab. And there's some consideration with cyclophosphamide plasma exchange and potentially kidney biopsy and that will have all tried to happen quite quickly in an ID world. Ok. So the role of the urine dip, the urine dip, there's a bedside test. It's widely available. It's not perfect. But what we're trying to use it for is to differentiate between tubular causes and glomerular causes a previous AKI due to volume depletion should have a normal urine dip. Glomerulonephritis will have blood and protein on it. A negative urine dip. If it's completely bland means it's pretty unlikely to be glomeru nephritis causing acute kidney injury. If there's white blood cells and nitrates in it, it means we can think about infection but it's harder to interpret. And if it's from a catheter, then there's often a bit of blood and protein that's harder to interpret, especially if it's just going in. I think we don't want to miss acute renal failure with blood and protein and dipstick. So I'll do one more case. You'll be pleased. Now, we're getting towards the end 86 year old female admitted from a nursing home with a fall and a neck of femur fracture, right hip replacement seven days ago, has a new acute kidney injury and has been drowsy and vomiting. You were asked to see her for worsening hypoxia. When she was admitted, her creatinine was 100 not too bad. On the day of her operation, her creatinine was about 100 much the same five days after that or four days after that, she was found to have acute kidney injury with her creatinine rising to 400. So it's more than three times that's stage three achy high. And then two days after that, it continued to rise. You think? Well, what's the cause of this? AKI I and you go review the patient and you find out the blood pressure's normal now, but it was low during her operation and continued to be low in the recovery. She continued to take her Ramipril tablet, even with the low BP. And day two after the operation, she was given some nonsteroidal antiinflammatories for pain. And you realized that part of her uh antibiotic induction in theater included gentamicin. She then became drowsy, um a a few days ago and he thinks she's been on morphine for her hip replacement. And so has this opiate toxicity and then she probably started sleeping more and stopped eating and drinking. And this is all occurring with the baseline risk factors for acute kidney injury, including her advanced stage, her chronic kidney disease and her history of hypertension. Her urine dip is negative. So we're not worried about renal causes and everything is normal. So it's not post renal causes. So I think we're pretty confident this is prerenal AKI and there's multiple hits and I think that's important to be aware that um, it's really, really just one thing. It is often a, a combination of many things. And if you've only found one cause of pre AKI, you need to think, have you not found others or is there something else going on? But there's lots of reasons why this person would have acute kidney injury, um, predominantly prerenal cause. So pre I give fluids, that's the answer, isn't it? Well, we need to think about things. So you realize that actually she's been given IV Saline for the past four days. So after she had a bit drowsy, somebody started some fluids and then when her kidney in, she was noticed, uh they were sped up and um, so she's had 6 L of intravenous fluids over the past two days today. There's only been 50 mils, urine charted and her oxygen saturations are 92% on 60% humidified um oxygen. So she's got a big auction requirement uh to maintain the saturations. So, so what's going on here? Well, it's, it's pulmonary edema I think is the problem. So this person has definitely had prerenal AKI. I um but it's been, I identified a bit late. So the prenal part of it has been fixed, the hypotension has been fixed. The volume depletion has been fixed and they've now not been peeing. And actually, we've gone from being dry and volume delete to them at some point, passing through euvolemia to to fluid overload. And now um she's in pulmonary edema. So like the, the treatment is in this situation. Well, yeah, the chest X ray shows P edema. As we can see, she was given a high, high dose intravenous fides, 100 and 50 mgs. If you get bad kidney function, you need bigger doses to respond. But she really wasn't passing any urine if someone's very, it's very unlikely that FRS is going to work even in, in high doses. And the decision needs to be made whether uh this is a patient that's suitable for dialysis. So I'll put to you a question, what are the four main indications for acute dialysis? And you can put some answers in the chat and then I'll read out what I think. Ok, so we have P edema which is refractory. We have refractory hyperkalemia, refractory acidosis and symptomatic uremia. And by symptomatic uremia, we're really talking about pericarditis and uremic encephalopathy. I put 1/5 1 in which is toxin removal. There's particular toxins which an overdose are removed by dialysis lithium being one of them. And that's a, a bit more of AAA niche example. But by far the most, the two big reasons for an in dialysis is palmar edema and hyperkalemia chia. They're the two ones that we, we, we really worry about. And we see by far the most commonly and I see refractory, I mean, not responding to medical treatment. So you need to try some diuretic or, or try some medical management. But I think you can also consider refractory as meaning oliguric. So if the patient is the pulmonary edema but is passing lots of urine, I would be optimistic. You should be able to manage that patient with medical therapy, with diuretics. If they're not passing urine, that's not going to work and they need to go for dialysis. And similarly, if they're very hyperkalemic and they're not passing any urine, you could give them all the insulin dextrose you want, but it's likely to rebound unless we get rid of it somehow and probably more likely uh dialysis. I see in the wards and kidney wards, urine is like liquid gold and it, it really does guide things especially in acute kidney injury. And we see that also if someone's acute kidney injury is getting worse, the creatinine went up and up and up. But actually two days earlier, the patient went from passing no urine to lots of urine or some urine. Then that patient is going to recover and we just sit tight and wait. So, and the urine output is clearly critical. Now, dialysis is a big topic. It will vary a lot depending on countries resources settings. Um but just as an idea, your peritoneal dialysis using the, the tummy membranes where you put fluid into the tummy and drain it out and it takes the toxins out or hemodialysis where you get connected up to a line or a fistula and a machine cleans the blood and gives you it back. It can be done acutely as a short term thing where someone recovers native kidney function as they recover from acute kidney injury or it can be longer term, meaning that's what they need until, you know, until they get a transplant or something else is decided the dialysis doesn't fix the kidneys, it just removes the fluid and solutes and waste products. Um, while we're hopefully waiting for the native kidneys to recover, um and it's a fairly burdensome mortality. So for acute kidney injury requiring dialysis in the UK, there's about a 30% in nostril mortality. So, um the these patients by definition are unwell in a high risk situation, but there are lots of people throughout the world who live very full happy lives on long term maintenance, dialysis and, and manage to achieve health through that. But it, it's still a major undertaking. Now that patient, the last case was volume deplete and then became fluid overloaded. Um I'm not going into too much because we could probably do a full other session on how to prescribe IV fluids. But if anyone's on Twitter, there is, you know, which is an educational app that you can find on Twitter. And they've got pinned Tweet, which is should I give them more fluid? And it's really excellent summary of the, the key pitfalls in trying to prescribe IV fluids in acute kidney injury. It's written by this nephrologist in England, Jamie Willows who posts some really great educational content. He's a very smart guy. Um and the, the take home messages we're aiming for Euvolemia and then we're stopping. If someone's not passing urine, then we're going to get their volume restored. And then once we get to that Euvolemia and they've got normal BP and they're not volume deplete anymore, then more fluid just risks harm without any benefit. So we should then stop and match input and output. So with that, I'll finish, I'd be delighted to take any questions. I'm very grateful for you all joining and for your interaction. Um And yeah, please put any questions in the chat or email me here if you want to follow anything up. Thank you. Perfect. So, if you, that's lovely. Um, so we'll start, uh, if people want, but the questions in the chat, I can add these to our Q and AQ. Um, if you are now Alastair, I will be completely honest with you. Sometimes words are written that I can't quite pronounce. So you might be better asking the question that's written and then answering it because sometimes the words are a bit difficult for me. I'll be honest. So th this er, this question, it's on the chat already. So I'll uh I'll go through the Q and A section. So the first question is saying Egfr not validated for acute kidney injury. Is it because there isn't enough research papers or because there's, there's no evidence. Um It, it's, it's slightly different than that, to be honest, the idea is that Egfr is meant to be estimating glomerular filtration rate. Um uh and uh so if you take a situation where let's say somebody has normal kidney function and you remove their kidneys, so you surgically remove both kidneys, that patient has no glomeruli and therefore no filtration rate. But the computer will estimate that glomerular filtration rate to be normal. The next day, the creatinine will have increased by 100. So the computer will think the GFR has gone down slightly. So we'll estimate the GFR to be maybe four 25 and so on. But actually the whole time that the true glomerular filtration rate was, was zero. So it was estimating something that, that didn't exist. And so if somebody's completely anuric, you can assume functionally that regardless of what the computer tells you that EGFR is their actual GFR is um is zero. So it, it shouldn't be applied in, in acute kidney injury for that sort of theoretical reason. The, the the main studies that have looked at though are in chronic settings and that's how it was developed and validated. Um There's a bit of being uh being pedantic there though. So some of my nephrology colleagues will criticize referrals that come through and say there's AKI the EGFR has gone down. But as I said, um Egfr is mathematically linked to creatinine. So by definition, if somebody's creatinine goes up, the Egfr will fall in some people, their creatinine can actually double before that, Egfr is detected as a fall because it often it doesn't show results in, in the UK. For instance, it only shows Egfr greater than 60. So if someone's GFR falls from 100 to 61 it's not detected. Um that's quite a complicated answer. And in practice, it's actually OK to use both as long as you realize that the EGFR is no longer actually estimating glomerular filtration rate in an acute setting. Hope that answers the question. It was a slightly long answer. Sorry about that. How would you decide whether to stop or reduce the dose of above meds and AKI for nsaids. I usually switch to paracetamol a week copay. But for patients who are hypertensive, what do you do? So, if someone's AKI and they're on an NSAID, then, then we should stop. The NSAIDS. Clearly, nsaids are very effective medications, uh, for, for treating pain. And there's a, a movement and research paper suggesting they're underutilized in people with CKD. Um, but once somebody who's on an NSAID then develops AKI, I think that the NSAID has to, to stop. You have to assume it's uh implicated in, in some way and yet paracetamol, weak opiates, opioids. There are some opioids that aren't really excreted. For instance, our fentaNYL um is shorter acting is harder to give. That's either that's parenterally given or um given as fentaNYL in a patch, but it's not renally excreted, which can be preferable. But when someone's got abnormal kidney function and needing opioids for pain, it does become complex hypertensive patients. You, you the the risk of ace inhibitors in somebody is hypertensive is much less. Uh as long as that patient doesn't have renal artery stenosis. It's um there's theoretical reasons why it could actually be beneficial. Um It might cause changes in creatinine that make things uh things difficult. So, different specialists I think would, would use that differently uh in the settings. But um assuming you're talking about Aces and Arbs there, there, there's a risk to giving them into somebody in acute kidney injury with hypertension. But there's very specific scenarios when that's exactly what you do. An example of that being sclerodermic renal crisis where um ace inhibitors are are lifesaving in that even though the patient has terrible with acute kidney injury, but they have high BP. Uh there's also a paper in in DT from a few years ago, looking at treating severe hypertension with ace inhibitors even in the presence of uh AKI and in that situation, it it was felt to be safe. So the the main risk of ace inhibitors in acute kidney injuries in people with uh low BP. But practice will vary between specialists. The kidney stones question in AKI we've spoken about already. That's postrenal AKI eye that would cause obstruction and you would see hydronephrosis in both kidneys or one kidney uh shrunk in the other kidney hydronephrotic. So, next question in general practice, how do we treat AKI in heart failure? Um It's a good question. It's all questions are good questions obviously and it's I'll give a concise answer here but probably needs to, to discuss it in a broader context and and more time. Um if a patient has heart failure has decompensated and very clearly has um fluid overload, then that patient should get diuretics and they should get heart failure management, prioritizing the heart and their symptoms over changes in creatinine. Um If a patient has been fluid overloaded and has been diaries successfully, then actually there is some signal from trials that worsening kidney functions. So, rising creatinine at the end of diuresis is associated with improved survival and lower readmission rates at the hospital. Meaning that we expect to see AAA hemoconcentration and a hemodynamic rise in creatinine. If you effectively di someone the difficulty in practice, there is some people, we get it wrong and we over diurese them and actually dry them out and continuing to pursue diuretics. There will make things worse. So it is a high risk scenario. But, um, I think rising creatinine shouldn't put you off treating heart failure and treating especially with diuretics. Um, if you're competent, that patient is, is fluid overloaded. Um, which one is the fastest method for hyperkalemia? Well, we talked a bit about that at the time, but, um, the, the priorities of the ECG changes is the, the calcium and then probably it's the shifting the potassiums into cells would, would work quicker. So if you give somebody AAA an insulin, so 10 units or 30 minutes, you would expect the deer of that. Uh, potassium is the lowest potassium we get in response to that about 30 minutes after the infusion finishes. So it works within an hour. Cool. That is all the questions that II wasn't too rushed. No, thank you very much and I'm really sorry everyone. Um I'm not sure what was happening. I did see, um, maybe it was Wi Fi at our end. I do not know. Um, apologies for everyone. I will chop up the session so it won't look so stop and start, so it'll look more uh fluid. I'm so sorry. I've also got a cat meowing in the background who was just actually to say hello. It's one of those times, isn't it? And as you can see, there's a dog behind me too. Um Welcome to my home. We were all work from home at meal. Um Anyway, thank you, Alastair. That was an incredible talk and there's lots and lots of thank you in the chat. Um For all our delegates, your feedback form should be in your inbox. Now, please complete it, please, uh you know, complete the feedback, be honest. Um I know all our speakers really do love to have great feedback. Um but please be honest, er, and I will be passing that feedback on to Alistair as well and if there's anything you sort of think, oh, I would love to have some more teaching on. If Alastair to, to touched on something that you think I'd love to go into depth a little bit more. If we get a lot of that feedback, then we can actually approach Alistair and say, look, do you fancy giving it another go? But anyway, please fill out the feedback, your attendance certificate will be on your medal profile straight after you fill that out. All right, and hopefully we will see you again at another meal education event. So for now, Alastair and I will say goodbye. So thank you very much, everyone. Thank you. Thank you. Thanks again.