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Yeah, our case today is mainly directed. So I'm discussing a simple case because it needs some interactions regarding uh some cases regarding the acute renal failure, how to deal with it with the ICU. Regarding the pharmacological, the dialysis, how the indication? When should we admit the patient? When should we solve the nephrology advise? When should we start the renal replacement therapy? And for how long and which modality to use of this is what are we going to discuss today? The case is a little bit, we will go into everything related to the ICU a little bit. So if there is none of you as an intensive care, if there is anything nonclear, I can clarify it for you. Ok. Should we start? So we're discussing a case of William, which is a 55 years old male patient known alcoholic liver disease. It day three of hospital admission to the ward with acute severe pancreatitis with act abdomen and pelvis with contrast on admission which showing um pancreatitis and started to Debra for the CCC protein and rising creatinine which showed 180 Millon from 85 85 was four months ago. He has a past medical history of being hypertensive on ace inhibitors and known CO PD and right-sided heart failure. So what we are going to discuss today, what are the possible causes for the deterioration, kidney functions for will if you can just share for me, what are the possib causes in your mind? This is the first issue. So I just need a end of diagnosis. What's going on? What could be the possibilities? Can we start just to think about it? Anybody has any ideas? Fine. So we have some steps regarding the answers regarding the antibiotics, dehydration, right-sided heart failure and also chronic liver disease causing kidney symptoms. Ok. Bye. These are brilliant issues. Anyone else nephrotic regarding his age? Ok. What would be the causes? Fine? OK. I will pause with you regarding the next question but we will get back to the answer. So do you think that this is acute or chronic or acute on top of chronic? Ok. So Steven is saying that you on top of chronic? Yeah, the same idea also fine. Ok. Can anybody share what to do just to give fluids or diuretics? Any ideas, fluids, diuretics, none of them good. So slow fluids. Fine. Ok. So let's start discussing the first three questions. So what are the possible causes of deteriorating kidney function? So we're having a multiple causes on this patient. We will start to take them one by one, starting from his case. He's knowing the current liver disease. So, causing a renal failure, there is a multiple causes. So being, having an abdominal pain with pancreatitis, he could develop a spontaneous bacteria perit. And this is a serious issue we have to think about and we have to rule it out just putting a needle inside his tummy and change of some amount of CC and send it to a blood culture bottle is a helpful issue. We have to think also regarding other causes of current liver diseases, causing renal failure. The hepato renal syndrome, which is a diagnosis of exclusion that we have to rule it out. Anyway, the other issue is the ascitis itself can cause some compartmental syndrome, increasing the intraabdominal pressure. The second cause, as you said is a cardiac cirrhosis. The right sided heart failure might be causing renal syndrome, which could be a type one, which is acute one and the chronic one and type five, which is a mixed issues. This issue, we have to measure out the BNP and the other issues. And the third issue could be the pancreatitis itself and the pancreatitis is causing it through the hypovolemia. So he has been in the work for three days. So we don't know if he's still continuous on his medications for diuretics. Yes or no. Some volume loss with the third space with the pancreatitis. This is the second issue. Renal causes, you know that the pancreatitis is causing systemic inflammatory response syndrome and this is causing a multiorgan dysfunction. This is one of the complications of the pancreatitis causing aal failure. And the third issue could be a postrenal with a massive ascitis, as I said is causing an acute chronic syndrome. The fourth issue could be a contrast induced nephropathy. So he received the contrast on admission. Ok. And the contrast sometimes causing affection of the kidney function, sometimes we will get this issue. Later, the first issue could be an hospital acquired infection, which could be adding as a sepsis caused to the renal impairment, right? And the other causes could be a drug induced as you discussed, which could be the ace inhibitors and piperacillin tazobactam. Uh The sound is clear. I for me it's clear. Uh Ahmed. Um Yes. Yeah. If you want me to repeat it back, if anything is not clear, I can repeat it back to you. Yes. OK. For what might still not clear. OK, I will repeat it back. So we are discussing William a 55 years old known as chronic liver disease and his day three of hospital admission with a severe pancreatitis. He did a contrast to admission for the ct abdomen and pelvis and he started a inactin for rising CRP and rising creatinine also 180 from 85 and this 85 millimoles was four months ago and he known hypertensive on ace inhibitor CO PD and rightsided heart failure. So the possible causes of kidney functions here that we discussed is a chronic liver disease might affect the renal failure with the three mechanisms. The first issue, the spontaneous bacterial peritonitis, just complaining of abdominal pain in a patient whose child see cirrhosis. So we have to rule out spontaneous bacterial peritonitis. Even if there is a pancreatitis. Sometimes it's not only raining, sometimes it's a perfect storm. So there could be a multiple causes. The second issue is the Brenal syndrome, which is a diagnosis of exclusion and the therapy issue in the sides itself. If it's causing increased intraabdominal pressure, it might cause an abdominal compartmental syndrome. Ok. The second cause could be acardiac cirrhosis which a cardio renal syndrome type one or type two, acute or chronic. Ok. And type five that could be mixed. We know that cardiorenal syndrome has a five types, ok. In this case, being a right sided heart failure. So we have a type one, acute heart failure that's causing and chronic issues it's dependent on and we, that's why we need to send the B and P the B type. Ok. The third issue with the pancreatitis itself. So the pancreatitis would say can cause a renal impairment or injury with multiple factors. The first factor is a prerenal element with the hypovolemia with, if he's using diuretics before a volume loss with the interstitial fluid loss. This is the first cause. The second cause the renal infection itself. The glomeruli tubules are in, have an injury with multiorgan dysfunction which is expected with the pancreatitis. It causes a systemic inflammatory response syndrome. It causes an inflammatory stool which might affect the lung and the kidneys. Ok. The third issue, as we discussed, the pancreatitis itself might cause a massive ascitis causing an abdominal compartmental syndrome. The fourth reason could be the contrast that he received. Ok, which might affect the kidney functions with the diagnosis, contrast induced nephropathy. Ok. Other causes should be expected like a hospital acquired infection sepsis anywhere might affect the kidney function the last course. And number six, it could be a drug induced like the ace inhibitors and the pil in tazobactam clear for that or there is anything missed. Ok. Now we will check to the next question. Is it acute or chronic? No, we will check to the next question. So it's acute or chronic or acute on top of chronic. So basically, uh no one can predict how survive. So we have to know how to differentiate between the acute or chronic renal failure. So basically, we have to differentiate because it's have been four months ago. We do not know how was the probability of being that this is 85 and jumped it suddenly to 180 or it was gradually progressing because he has uh some causes causing chronic renal impairment and some causes might cause acute on top of chronic within the gap of four months. So how to differentiate between the acute and chronic renal impairment the per abdominal ultrasound is the first one to rule and this is one of the most predictable, it's assisting the size and echogenicity and corticomedullary differentiation. Ok. The second issue would be the hemoglobin because usually the chronic kidney diseases have an anemia of chronic kidney disease unlikely that the acute renal failure will have a normal hemodia. Ok. Unless it's diluted with IV fluid that we are giving or something else. The third issue, the third issue to differentiate between acute and chronic renal failure would be using the electrolytes. So the chronic renal impairment have a disturbance in the electrolyte balance, including the calcium and phosphorus and consequently, the parathyroid hormone. So if we send the calcium and phosphorus and the calcium is low and the phosphorus is high, this is pointing more to the chronic kidney disease also unless there is other causes causing hypocalcemia like the pancreatitis itself fine. But the combination of hypocalcemia and hyperphosphatemia is mostly going with the chronic kidney disease. So, these are the three issues to differentiate between acute and chronic. So nobody, as long as we don't have any criteria regarding his hemoglobin, his calcium and phosphorus, the assessment of size and ecogenicity on the ultrasound. So we cannot differentiate. Is it acute or chronic or acute on top of chronic, happy with that fine. So the third issue, what are we going to do? So, as we discussed, we will have to send a full blood count, we'll have to request a pelvic abdominal ultrasound. We have to request the calcium and phosphorus. Then we'll have to send the BNP. Then we will have to see if there is any signs of infections. The creactive protein, the procalcitonin if it's available in your hospital is an important issue. Ok. And consequently, the lactic acid also fine. This is to rule out if there is any sepsis or anything, stop any harmful do drugs like the Pillin aac, if it's not needed, we can switch to another antibiotics, stopping the ace inhibitors. This is the issue and we'll follow up just to the heart failure therapy. Ok. This is the answer to the third question. The first question that I'm discussing should be bring the nephrology on board. So how do you think about that? Should we just bring the nephrology asking him? We have a blah blah blah case of rising creatinine? Is that the best time or should we just wait more? I can just wait your answer. So I should come out. It just saying that nephrologist would help any other ideas? Ok. Based on the causes, wait for the hydration effect monitor closely. OK. Generally speaking. And uh if I'm calling the nephrologist, it's not every case of rising kidney function that we need to call for the nephrologist. Ok. So there is a certain criteria, I will just be sure enough in cases if there is an acute on top of chronic kidney disease This is the first issue. Ok. This is the first priority just to hold in first, the second issue, if the patient has a chronic kidney disease, plus or minus proteinuria or red cell costs, because this might point that the patient might need a biopsy. This is the second issue. The third issue is the patient has a chronic kidney disease with uncontrolled hypertension with more than four antihypertensive drugs. This is an indication for possibility of secondary causes to be ruled by the nephrologist. And if the patient has an uncontrolled hypertension with a hypokalemia because this might point to inherited disease, especially in the young age. If the patient is developing hypertension below the age of 30 years, the first issue that might help us in this case, if the GFR is below 30 we might be preparing the patient for hemodialysis. We need to call the nephrologist, the first issue with the progressive deterioration of the GFR which is not improving by the IV fluids or anything. So the nephrologist might be on board on this issue if the patient is not going to the ICU. Ok. So our first question, should we call the ICU team? So if I have the internal medicine ridge and I'm having this case or the surgery ridge was just covering, should we call the ICU team for? Now, does this patient need the hemodialysis now to go to the ICU for better monitoring or should we wait? Just give fluids or something else. Anybody has any ideas? Ok. So now immediately unless hemody an just informing them, ok, fine. I think we have to ask ourselves, what are the IC are going to do? What would the patient benefit from the ICU admission? And basically speaking for this case, we usually go for two issues. Number one that the patient needs a hemodynamic monitoring, giving the IV fluids. Yes or no. This is the first issue, but I think we agree that we are giving the patient fluids and fluids and fluids. So this is the indication for neurologist to resuscitate him. Ok. This is the first issue and the second issue. Does the patient need the hemodialysis? Yes or no. And this is the question. Also, I need to take your answers that the patient now needs hemodialysis or we can wait. I think we discussed before that we can wait or anybody has a different ideas. Good. All. So we can wait a little bit. Can we shift to the next slide, please soon? Yeah. So here we are discussing the causes of the renal failure per se. So generally speaking, apart from this case, this is like I'm putting that we have to rule out, think about how to think about the causes of renal failure. So here the anatomical wise that we can see that the kidney is formed anatomically of glomeruli cortex and the medulla glomeruli and tubules. And this is the point and this slide I am putting because there is some of the MC Qs. Sometimes it's asking that if you can see the blood supply reaching till the end. Ok. Fine. If the cortex and the glomeruli main, he is lying in the cortex of the kidney which having the blood ties the blood supply. So, may I just ask you from what you can see, which is the um one of the most common causes that could be necrotic part of the kidneys, the cortex or the medulla. What do you think? So, now we can see a section of the kidneys which is showing the glomeruli tubules in between and interstitial and the glomeruli is full of blood supply, reaching to the cortex for vein. And now we can see this. So which part should be firstly affected if the patient is getting a decreased renal blood, the medulla. Yes. And this is one of the MC Qs that starting asking about this, that the medulla is the most necrotic part to be affected because it's very liable to hypoxemia. So this is the first issue. Can we meet chef to the next slide, please too. Yes. And this, this is how we need and this is like we are discussing how to discuss causes of acute renal failure. So we'll start with the prerenal causes if there is any causes of volume loss or anything that we need to discuss about. This is the first issue. If there is any strength secret that causes per se. As we discussed in the previous slide, the glomeruli uh might be affected with the chlamydia nephritis, multiple types or anything, any thrombosis inside the glomeruli. This is the next issue and the tubular injury itself which causing ischemia and toxins affecting the tubules. And this is called acute tubular necrosis and interstitial nephritis. And the fourth issue, which is usually a missed course. Yes. So the vas cocois, which is including any vasculitis, like the arthritis nodosa, which is affecting the kidney, any TRM or trig, which is affecting the kidneys also. And this is one of the reason if you're suspicious about a vasculitis that we need the nephrologist on board. Ok. Or there is a thrombosis or embolism like the cholesterol embolism like other causes of thrombosis in elderly age, if we have uh an aortic thrombosis. Ok. So, and uh the last item at the post three, of course. Ok. So basically speaking, how we would ask ourselves for any patient who is presenting to us with causes of acute renal failure, which should be a prerenal aal causes, which is including glomerular tubular interstitial and muscular and postrenal causes. We can shift to the next slide. So please, yeah, on this slide, we are discussing about the postrenal kidney injuries which could be anatomic w A ureteric obstruction, bladder obstruction or the urethral obstruction. You can see all of them are almost stones, tumor, fibrosis, benign prosthetic hyperplasia. And these issues can be easily discovered using the ultrasound, the bladder scan, the post medical history of the patient, any drugs that he's using any issues. So these are the issues for now. And if the patient is drinking a slight amount of urine density or something, this is consequently causing that there is any obstruction or anything, the most important issue for us. That's why I'm putting this slide that we are a little bit different in thinking from the internal medicine. So we're just also thinking of additional causes like the tumor lysis syndrome, which could be one of the post renal causes and the rhabdomyolysis that we need to think about. In addition to one of the sometimes acute abdominal compartmental syndrome, which with high intraabdominal pressure that can be affecting some patient might be causing a renal or postrenal obstruction of that causing acute kidney injury. So these are some of the factors that might be missed here. OK. And this is one of the factors that shouldn't be missed with us if we're thinking of the causes of the acute kidney injury. OK. I think we can shift to the next slide. OK. This next slide is highlighting two issues. How can we differentiate between three renal causes of renal failure and causes of renal failure? So you can see here, I put this slide just to come in for you. So you can see in some of the M CQ, it's discussing the blood urea nitrogen to the creatinine tissue if it's above 20 or below 20. Ok. But you know that the blood urine nitrogen is affecting how the volume state of the dehydration and everything and the protein uh diet or anything else. Ok. Gi bleeding. These are some of the limiting factors of the urine nitrogen. The second issue is the fraction of excretion of the sodium which you can see less than 1% or more than 2%. OK? And honestly speaking, the fur yeah, honestly speaking, the fena is not more used. OK? And sometimes it's coming in the in Q. So the 1% and the renal more than 2%. But honestly speaking, on the life outside, it's no more used for two reasons. The first issue because life is not straightforward. So sometimes you have a mixture between a prerenal causes and renal causes. This is the first issue. The second issue, there is a multiple factors that might limit the prerenal causes. Like the contrast use might cause a false high even if it's a prerenal cause. So you can sometimes see the patient who is dehydrated and volume behind. So the prerenal, so the fraction excretion of sodium should be less than 1%. And in addition, using the contrast induced might change the index of the fraction excretion on sodium to be more than 2%. OK? So this is the issues. The last issue is the infection excretion of the and this is an important issue, urine osmolality, this is important issue. And this is an important. You also just to differentiate with the prerenal, the urine osmolality is more than 500. And with the renal, it's less than 400. OK. The last issue with the urine sediment and cast type. So you can see in the prerenal, you can see um some highline costs and blunt cost. And in the renal you can see a granular cast. OK? The most important issue for me is the urinary sodium and this is the last point. So if it's the pre it's less than 20 sorry. So if it's I sodium, if the Urena it's less than 20 if it's renal, it's more than 40. So for me, the fractional excretion of urea, the Urena is sodium are anti costs. These are the three important issues and this is slide. This is the first issue that you need to concentrate on and these are most of the causes, the questions coming to the M CQ. OK. Fine. Online just discussing with the clinical cases to the urinary sodium is the most important for me. OK. Should we shift to the next slide soon? OK. So this slide is discussing the definition and staging of acute kidney injury using the rifle criteria and in the next slide. Uh so can you shake check next, please? Yes, this is the other staging system. It's called the system. OK. So rifle with the previous slide was just found in 2007. Ok. The Eggo criteria that we can see now is at 2012. Ok. Fine. I will just play a little game with you that we need to differentiate between the rifle system and the legal system. If anybody can check between the two slides, then we can see that there is some differences between the two slides. Can you see the slides? I will give you a minute just to find two or three differences between the right foot criteria and the criteria. Anybody can write anything for me from what can you see? I tried to put them on the same page but it was difficult a little bit. That's why we will exhaust. So if she can flip between the two slides for a while. So Stephen is writing the serum creatinine any other ideas? It's like playing, what's the difference between the two images? OK, guys. Any other ideas? Fine. So um so if we start at the previous slide, please. Yeah, so you will see on the rifle criteria. Thank you on the Rle Criteria. It's written here that it's from 1 to 7 days in the stage one. OK. Fine. Which is the first difference. And in criteria, it's written that it's only 48 hours. OK. So can you shift to the next slide? Yeah. So that's it. So you can see in stage one in the that the serum creatinine increased more than 26 miller within 48 hours. But on the criteria, it's 1 to 7 days. This is the first difference. OK. So you can see both of them are dealing with serum creatinine, both of them are dealing with the urine output. The criteria is a three stages. The rifle criteria is a five stages. OK. The second difference could be on the G fr. So in all the three stages in the rifle, it's used if you can go through to the biggest type piece. Yes. So you can see here the G fr is used. So you can see in the stage of risk, injury, failure, loss, and endstage renal disease. And you can see in the non part, you can see that the G fr more than 25 more than 50 more than 75%. These are one of the uses of the G fr in the criteria. You will not find any use of the G fr. OK. The third difference would be in the criteria. Would you mind to go to the next slide too? Yes, thank you. So, on the third one. So you can see initiation on the stage three, initiation of renal replacement therapy, I respective to the stage at time of initiation. This is one of the difference and it's not uses on the right criteria. OK. The first difference would be in the rightful criteria using a five stages. Yes. Thank you. So, using the lost and endstage renal disease, usually, if there is an irreversible acute kidney injury or persistent more than four weeks or it's more than three months, we label them as a loss at end stage renal disease. This is important, at least for me because if anyone is working in the intensive care unit, you will face this question a lot. So some of the families are being worried concerned if you're discussing with them that your patient will start a hemodialysis session in the intensive care unit. The next question after they hear everything from you, why are we doing the dialysis and everything? So they will start ask you for how long have you get the dialysis? And this issue being, the dialysis issue will be a lifelong issue. Yes or no. This is the point and this issue you have to discuss with them that if it is persistent more than three months, so likely to be an endstage renal disease. And at this point, you can just discuss with them that the dialysis might be a life long if it is around four weeks. So this would be left to the nephrologist to follow about because nobody can differentiate according to the cause and everything fine. And you can see here that the is increased with increased duration, just affecting and assuring how much the kidney has lost with progressive loss of the the creatinine, increased creatinine and loss of the GFR. So the more you're going deep, the more duration, the more you're likely to be dependent on the dialysis life. Fine. Now we can get back to the next slide. Yeah, next one, please. Yes. So now we get back to William. Ok. So three days later, William was not admitted, we agreed that just a few resuscitation that we can monitor him, his creatinine improved amylas and like this number are improved also and the abdominal pain got better. Then a follow up ct abdomen and pelvis showed just increased free fluid in the abdomen. But later on day 20 of the hospital admission, William developed a generalized abdominal distension, pain and tenderness, creatinine of 300 which shooted me more. Then the next day was 400. The patient started to be more i feverish, soft BP and more. I and the potassium went up to six miller at this patient. We requested a blood gas which the ph was 7.28 the pu two of 10 mo the P two of 10 and the bicarb of 20 in case anybody is not using these issues. So we're using the mi mode so we can multiply by 7.5 just to change it to a millimeter mercury for pu two and pu two. OK. We noted also that there is an increased oxygen requirement. So he's in 30 40% 10 L and the albumin is two, the lactate is six, the sodium is 128 and the chloride is 93. And the bedside nurse started to tell you that he is not tolerating his feeding also. So sometimes he's not tolerating particular amount, feeling nauseated, vomiting, something like that. So what are the could be the possible causes? Anybody has any ideas if we can get um back to the past history that we know that the patient has heart failure is the patient's CO PD. Yeah. Thank you so much is known chronic liver disease secondary to alcohol and he was on antibiotics and he's known hypertensive COPD heart failure. Thank you. So you can get back to the previous slide. Yes, good. So now we're discussing that the patient is deteriorating. Can anybody figure out what's going on? So, Ahan is writing that this could be heper mm I endstage renal disease, but we discussed that endstage renal disease should be more than three months just to decide that this is still on day 20. So we cannot verify worsening pancreatitis. I might agree with that also. Yes, good ideas. Ascitis. Yes. Pancreatic ascitis also. Good. What else? I think you're covering almost everything. So we're discussing that we have a CT which is showing increased free fluid and this increased the free fluid could be. Secondly, as you said, the pancreatic ascitis space, especially that the patient has a hypoalbuminemia with the crystalloid resuscitation. So there is a possibility part, this is the first issue, cardiac cirrhosis could be renal injury. So these are the causes of increasing free flu and spontaneous bacterial peritonitis also fine because he's having some abdominal pain. What could be the causes of the increased creatinine? So just to answer this question, we just to discuss, I need just to enumerate with you. What are the possible complications of pancreatitis? Can anybody just write for me a rapid knows what could be other than the pancreatitis? Uh other than the renal failure, what are other complications of the pancreatitis that the patient might be suffering from? So the patient is coming with a pancreatitis. So we have to list what are the possible complications? We have to start to search for them. We have to start to rule them out because basically we are not treating the pancreatitis. We're just supporting organs until the inflammatory storm subsides. Anybody has any ideas. What are the complications of pancreatitis? Yeah. So it can become necrotic but this is a little bit delayed issue. Fine, raise blood sugar. I agree it called a tertiary diabetes. Ok. Uh hypocalcemia. Yeah. Very good, fine five compartmental syndrome. Yes, very good. Excellent. Any other ideas. What about the blood gasses? The patient is suffering from a metabolic acidosis sepsis is a secondary issue to the pancreatitis. Could be. Yes. As I was mentioning that there is systemic failure, could we just go? Which system I think I can pick up? So the patient might suffer of acute respiratory syndrome. And the pancreatitis is one of the precipitating factors that we need to rule it out, especially that the patient is suffering of increased oxygen requirement. So we need to calculate something called oxygenation index or DQ mismatch. So how the patient, how is due to um than 30 40%? This is the second issue and I guess you mentioned almost everything, the abdominal compartmental i gastric residual volume because of full abdomen and other issues. So now we cover the complications of the pancreatitis that we need to search about. Can anybody tell me what's their impression? What's your impression about the blood gasses? Can someone give me a full comment? D IC is a possible if there is a sepsis or infection ongoing and multiorgan system failure but unlikely from itself that the pancreatic go to the IC directly. Yeah, I agree with acidemia. So now we have an acidosis. So what's the comment of acidosis? Is it metabolic or respiratory? And what could be the causes of this acidosis are respiratory alkalosis? Yeah. Any other ideas? Fine. So I can just discuss with you. We will take it step by step. So we'll start. This is I agree that this is a metabolic acidosis, but let's go more deep. Ok. With the nephrologist, we are just going more deep regarding the metabolic acidosis. So we agree that the PH is less than 7.35. So this is a metabolic acidosis because the CU two of 10, it doesn't help because the patient has a previous COPD. So he might be a chronic retainer of CU two. That's why the cu two of 10 that we do not accept it per se, but we have to look first at the ph. So the PH is 7.28 and this is acidosis. This is the first tissue and the bicarb of 22 which could be normal, right? But if you put in mind that the patient has a chronic retainer being a COPD. So the usual picture of this patient that he has been living with, if he's a chronic retainer, that the C is around 10, and consequently, the kidneys started to retain some bicarb. So the bicarb is touching 30 or 30 something. So this is the usual compensation that you can look at it that there is ac two and bicarb inside the body. So the lung is responsible for the cu two balance. So the lung is failing with the COPD, the kidney is trying to compensate it just retaining bicarb. Now, so the ph is the final mirror of the balance between both of them. Now, we will look at the PH which is showing a metabolic acidosis because the bicarb originally with the case scenario was around 30 or something. And now it's dropping to 22. This is the first tissue. Ok. The second issue, this is a metabolic acidosis. The second issue for us would be which type of metabolic acidosis are we discussing? So, if this is a metabolic acidosis, we usually have uh two types. Does anybody know any of them? So, there is something called a high anion gap, metabolic acidosis. And the other type called a normal an gap, metabolic acidosis. Fine. So usually if we have renal failure, can anybody guess how to calculate this? Could be a high anion gap or normal anion gap, metabolic acidosis, any suggestions or anything? Right? So we can go that this patient has a high anion gap, metabolic acidosis. So usually the anion gap is calculated based on the sodium which is 128 minus the chloride, which is 93 plus the bicarbon the blood gas, which is 22. So if we 93 plus 22 which is 115 this is the first issue and the second issue would be minus the 128. So 128 minus 93 and it's minus 22 also. OK. So total, we will end up by a nine gap of 30. OK. This is the issue. The second issue that we need to discuss with that. There is an albumin of two and the albumin is one of the negative slight causes of the being a protein charge. OK. That might affect the anion gap measurement. So each drop on the albumin causes a full flow anion gap fine. So if we calculate the gap Yes. So if we calculated the gap that is 13, we have to add for it that this is a full slow on gap because of the hypo. So just to add to your knowledge, the hypoalbuminemia is consequently affecting the measurement of multiple issues inside your body. This is the major protein responsible for the osmotic pressure. The first issue, the second issue, the calcium measurement is affected by the albumin concentration. The phenytoin level is a affected by the albumin concentration. So if you measuring the phenytoin level for patient who has an epilepsy, you should put in your mind, the albumin concentration. And consequently, the third issue is the an gap. OK. So if we calculated for each drop of the albumin bef below four, OK, you increase at 2.5 to the gap. So if the albumin is two, we should increase it by five. So now the gap is 80. So what could be the causes of the high? An IG the first issue could be a renal failure. So highly gap, then there is it is acid that is added to the circulation. That could be a renal failure, which the kidney is defective on just senses of the bicarb. This is the first issue. So it's losing its function as a buffer. The second issue could be any K embodies inside your body which might be affected with the DK A might be with the starvation ketosis. Some of the alcohols are causing some K embodies and sodium glucose transporter inhibitors are causing AAA keto bodies inside your body. OK. The third issue that we can see the lactic acid is six. So this is an additional uh acid inside your body which causing I am I gap. So this is the third issue. And the fourth issue if there is any drugs that might cause adding acidosis, acetylsalicylic acid. This is an aspirin causing acidosis because it's an acid that citrate inside your body is a citric acid inside your body. And the paracetamol toxicity, it's affecting your liver and it's causing acidosis also fine and alcohol per se that methanol it a glycol, all of them are causing high osmolar gap with the metabolic acidosis. So on high gap, you're adding acids to your body. There is another type of normal, which is not our issues. It's mainly affected by drugs, renal tubular acidosis, diarrhea, saline infusion. This is the most important issue. There is some uh trust now are normal using saline inside the ICU as a whole because of this reason. Ok. So now back to our cases. So what we are going to do just if this ABG is showing to me. So this is a metabolic acidosis because the BH is 7.28. And the patient originally in in case scenario, the bicarb of 30 now it's 22. So there's a drop of bicarb. So this is a metabolic acidosis. Ok. This is the first issue. And the second question, is it a high anion gap or normal anion gap? So the anion gap 128 minus 93 plus 22 which is causing us plus 13, the normal anion gap is 3 to 7. OK. So if it's above seven, it's a high anion gap. OK. Sorry, the nine gap is seven plus or minus four. So it's from 3 to 11. So if it's above 11, so this is a high or nine gap. So 13 is high. So this is a higher nine gap and the correction with the hypo, this is 18. So this is definitely a high anion gap, metabolic a dose fine. This is the second issue. There is an advanced level called a gap gap. If you're having some metabolic alkalosis in addition to the metabolic acidosis, which might happen inside your body. Ok. Fine. This is the issue that might happen. But this is not our reason. Now, if we have to find it. Ok. So the next issue would be the question about CT abdomen and pelvis with IV contrast, we need to rule it out. So usually the surgeon is just asking, we need to rule it out if the pancreatitis. I think one of the comments is just was mentioning that the pancreatitis is deteriorating. How do you just verify it? So we need to rule out CT abdomen and pelvis. But we discussed before that there is an additional possibility of contrast induced nephropathy, right? So what to do? Should we use the ct abdomen pelvis with contrast? Yes or no. Just give me a quick answer. Fine. Yes. With contrast, I agree with that. Anybody against fine. Can we shift to the next slide? Two, please? OK. So this is slide is discussing the history of contrast induced nephropathy, which is technically, I was just prove to you and this is slide that this is originally it's just a myth. This started at 1954. This is the first case report about acute anuria following IVP using the contrast. OK. The question now just to prove you there is some to highlight multiple issues which is important because we have to use the contrast to verify where are we going we have to use to rule out if there is a deteriorating pancreatitis. Yes or no. So the first issue that we need to use that the first uh uh issue that we are not quite sure that there is a big evidence of the contrast induced nephropathy. This is the issue. There is a multiple studies that has been done which didn't show any relation between the nephropathy and the use of the contrast and developing nephropathy. You will find some cases regarding that it should be within day 2 to 3 of using the contrast and other issues. But basically see this is a diagnosis of exclusion. This is the first issue and there is no lab diagnosis that we can detect by it that the patient kidneys are worse with using the contrast. This is the first issue. The second issue that the contrast that we are using now is much different than the contrast that we used at 1954. So the use of I dine which is around 50% concentration or something like this, but now it's much different. So you will find that multiple concentrations of the ID inside the contrast, which is around a 27 or 30% of concentration ID inside the contrast. So the contrast that we're using now is much different than the contrast have been used in 1954. This is the second issue. The third issue, I'm trying to tell you is the creatinine a good marker of the kidney injury. I mean, if we use the contrast and we find the creatinine is rising, that the creatinine is the best biomarker that she can tell you that there is an um genuine renal injury inside your body. Actually, it's not the best issue. And this is one of the limitations of the creatinine because basically the creatinine is one is just an inert material inside your body that is just secreted by the muscles in a fixed citrate in the normal condition. But if the kidney started to fail, there is some causes and it's mainly excreted through the proximal con you. OK. And it's measuring how the kidneys is able to as a glomeruli to filtrate your kidneys from the creatinine inside the proximate convoluted tubule. So this is the measurement of the creatinine inside your serum. If the kidney is uh failing to filtrate an inner material like the creatinine, this is that, that this means that there is a low glomerular filtration rate. And do you know about the uh calculation about the estimated G fr which is both age and sex muscle mass and everything? These are all issues affecting the creatinine inside your body. And the more that there is multiple factors, the more that this is affecting a low sensitivity of the measurement. The third issue, you need to know about that. There is some medications that might affect the creatinine measurement inside your body, either falsely increasing or falsely decreasing. And we cause we call a medication that might cause increased creatinine inside your body. So which means that these medications are blocking the tubular secretions of the creatinine inside your uh tubules. And thus, it's increased in the serum like the trim, the dil and tazobactam and dexamethasone sometimes causing increased creatinine. So these are called pseudo nephrotoxin because apparently they just block the creatinine secrets inside the proximal computed tute but they do not express a renal injury inside your body, right? The A S staying on the contrary, might cause increased excretion of the creatinine inside your tibs, which is the opposite side. OK. The last issue I need you to be about that. There is that's why we started to jump into other biomarkers inside your kidney, like the cystatin C, like the NGA L neutrophil gelatinase associated Lipo Kalem. These are all the new factors but I did not see any of the hospital using them, maybe one trusted using the cystatin C per se. So this is the issue. So long story short, how many cases have we seen with a contrast use that caused a contrast induced nephropathy? You will find it very mild. The second issue, how many cases that we call a contrast induced nephropathy as a diagnosis of in is to reach a hemodialysis also a very minor because even if we reach the hemodialysis, it's one or two sessions and it has been never for lifelong. The reason I'm highlighting this issue because I saw multiple cases which the one of the patient lost his life because of that. It has been a cardiology case with an old stenosis called a cardiorenal and kidney compensated with renal impairment and he was gone for the T and because of the uh renal impairment, he did not do a PC before the de so we ended up with a conditional shock and he died because he lost his chance of the surgery. That's not the issue. Now, we can shift to the next slide, please. Ok. So the next question that we're using now we need to admit the patient because of the deteriorating kidney functions, blah, blah, blah. So the next question should we ask ourselves if the patient needs uh renal replacement therapy now? Yes or no. So this is the first question. And I just in this slide, I think this is the most important slide. This is the one that the question should be asked. Should we initiate the renal replacement therapy inside the ICU now? Or we can delay it for a while and for how long we can delay it. So these are five studies done on the last just 10 years or something. Elena study and study, you will find that they both started in France at 2016 and they got contradictory results. So the Elena study was supporting the early initiation of renal replacement therapy. The study just supported the of replacement therapy. OK. So that's why we start to shift to other studies. The Ideal ICU which was done in 2018, released in the New England Journal of Medicine to start the API study, the studies and the three of us, the trials are both supporting that. Sometimes we can wait for the initiation of renal replacement therapy. But the next question for how long should we wait? Usually these start as a whole so that we can wait until ph 7.20. OK. And above around 4100 and 10 and the patient should wait. Even if he's oligo 72 hours, there is no estimated difference in mortality on waiting for this patient with this issue unless the patient have been hyperkalemia. So you will find one of the studies that showing that there is a high incidence of hyperkalemia. The ideal ICU which is more in the delayed icu. Ok, we can check to next please. Ok, this is slide. No need just to discuss anything. And the most important issue is the conclusion. So you will find that in severe acute kidney injury with patient of oligo more than 72 hours, the bone around 110 mg or 40 miller, no severe complication that would mandate immediate renal replacement therapy. And the additional delay beyond this level did not confer additional benefits but was associated with potential harm. So the patient usually if he's a ph of 7.257 0.30 or you got it for one day or something, the potassium is 5.5. Usually we do not trust for early initiation of renal replacement therapy. We can wait up until ph 7.20 and bone is around 110 mg or 40 millim and ur for more than 72 hours. Ok? Ok. Next slide please. OK. So this is the last slide that we might spend some issues. Um This issue is uh higher level for some of the one interested in the intensive care unit. So we'll just verify for this the modalities of the renal replacement therapy that is different? What's the difference between the continuous renal replacement therapy? Tr RT or C VVA HD or what's the difference between C DVH D or C DVH DF? OK. And what's the difference between, there are some cases that develop a peritoneal? You got a peritoneal dialysis. So, what's the difference between the hemo and peritoneal dialysis? Does each one has a different venous axis? Yes or no, continuous versus intermittent falls asleep. Which uh the appreciation of slow uh low efficiency dialysis. And what's the physics between the dialysis difference between what is meant by dialysis filtration or diafiltration? OK. So these are the three questions. So basically, just to make it simple, the hemodialysis is just you put a vascular axis which usually for a temporary dialysis GTA inside the internal jugular or inside the femoral vein. So we need a central vein. This is the first. OK. This can be applied through the intermittent hemodialysis that we're doing in the outpatient in the slip and in the CDH D. OK. The CRRT that we're doing inside the IG. The only difference for my, for us in the ITU that if the patient having an endstage renal disease and he has already an access through a fistula or anything which is mature and has been used. Can this patient go for the crr T? No, he cannot, why he cannot? Because the flow on the intermittent hemodialysis is very high. So it can be used through the fistula. But the flow inside this continuous renal replacement therapy, we're using a small fluid remover over the next 24 hours or something and slowly removing the blood that outside your body filtrating it and removing it back. This is slow filtration will cause the blood to clot inside the fistula and outside it. That's why it is, we need a temporary vascular. Even if the patient has a mature graft or fistula, he needs to insert a vascular. And this is one of the important application that you need to know. This is the first issue. The second issue. What is the peritoneal dialysis? So the peritoneal dialysis in short term, just using a glucose rich hypertonic dialysis fluid just to inject it inside a specific inside your peritoneal cavity and you just remove it again. It's not used for the other. So it's mainly in the pediatric population and some people are using it at home. So these are the indication and for some questions inside the MC Qs, the contraindications for the peritoneal dialysis is being if there is no stuff that is, has been trained for using the peritoneal dialysis. This is the first issue and the second issue if there is an evident infection of the catheter itself. Ok. But the peritonitis per se is a relative contraindications for the peritoneal dialysis. So still the peritoneal has its own, it's old tank of catheter inserted inside your peritoneum, you inject the glucoside dialysis, then you left it for a while, three or four hours, then you remove it back with all the toxin. And so you, this is the first issue. Now, we go to the other modalities of the hemodialysis called the intermittent hemodialysis that we use in the outpatient, the slip. And the CT, we said that the CRT is having it's only for temporary vascular access. This is the first difference. And what about the other dentist, which called the dialysis filtrations or diafiltration. So the dialysis per se. So the dialysis is just going just to remove a small particles outside your body and that causing us to the next question. So what are definition of small particles, medium or large particle or extra large? So we have a different classification. I know I did not put it because it's large, complicated issue and it's a large, I'm trying to explain it but it's not heavily associated. It's just for the one who's working in the intensive care. So the small particles is just the urea potassium phosphorus electrolytes and the medium particles like the creatinine. So both of them can be easily removed with the intermittent hemodialysis. But the large particles like the myoglobin. If there is a patient who's having rhabdomyolysis, it's better to be removed. So the continuous renal replacement therapy, this is the second difference. The third difference is in the type of filter itself. So the filter in the intermittent hemodialysis is a simple filter just removing small and medium particle. This one done in the outpatient but in the intensive care with using a different filter to remove large particle like the myoglobin. And it can also remove the small and medium particle with a small, less efficacy. But we are more important just to uh more effective to remove large particles and remove fluids. So you can remove easily fluids inside the intensive care. So you can cal it so you can control it how much ultrafiltration by the machine that can be removed by hour. So you can imagine within 24 hours, you can remove 45 or 6 L over 24 hours without affecting the hemodynamics or anything. Imagine this issue in a patient with a septic shock or anything who cannot tolerate just removal with the usual intermittent hemodialysis with a high flow because usually the flow on the intermittent hemodialysis machine is removing a 300 CC. All of a sudden if you remove it in a patient inside the intensive care unit or something applied for it, the patient will become severely hypotensive immediately the crrt in the ICU, we're removing a small amount of fluid around 100 cc for one hour and we'll determine it back. So it's not affecting the hemodynamics or anything. The last issue that needs to be highlighted that you need to know for the CRR T inside the ICU that we are using an anticoagulation. And this is consequently can be applied because originally, we're removing the blood outside the body and it very slowly. So there is a high possibility that it might clot inside the catheter itself or inside the extracorporeal, outside your body, the sedation. So the CRR T is using inside the ICU, we definitely you need to use an anticoagulation, ok. In the intermittent hemodialysis or even the sli we just going without any anticoagulation fine. So this is patients for now, the CRR T have a simple principle, it's called the conviction. And this is one of the MC Qs which just removing some particles, the blood with the plasma is just you moved out of the catheter. You can just imagine it. We put a temporary dialysis catheter with two ports. One of them is the outlet. So we just got some blood on a small flow. 100 CC started to anticoagulate it inside the filter and it's going through a certain filter specific similar may have been great removing all the solutes and all the water that we can remove then get it back. This is called the conviction. OK. Simply that you can apply. No one will ask you to explain the conviction. But you have to know that the principle of removal is conviction in the crrt. But the principle of removal in the intermittent hemodialysis is just an infusion, right? Plus the issue that we need to highlight is the anticoagulation back itself to anticoagulation inside the renal replacement therapy. The crr t we're using a citrate and this is the first choice. And the second choice would be a heparin and low molecular weight of heparin. And the third choice. And plus, which is almost non applied in the prostate gland and the AP pros, but it's not used because it's causing vasodilatation hypotension, which we don't need A I you some strong pain. So, forget about it. So the citrate is the first choice unless there is a patient is have a liver cirrhosis or he has a severe hyperglycemia that is not corrected or has a massive blood transfusion. Why that? Because there is something called a citrate toxicity that might happen with a patient whose liver cirrhosis and he's having a renal failure like our patient and we started to use the citrate inside the circuit as an anticoagulation. So, does anybody know what is the citrate? I can start to pick it up for that. So the citrate is an inner material it's causing it's sharing in the coming from the pyruvate if we go back to the chemistry from the first year of the college. So the pyruvate. So the acetyl coenzyme is going to the citrate and the citrate is going into Krebs cycle. Actually, if you remember the Krebs cycle from the biochemistry, it's called a citric acid cycle. So the citrate is going into Krebs cycle and it ended up into sodium into a bicarbon. Ok. So if there is any patient who's getting a citrate either through the filter itself. This is the first tissue and this citrate or a massive blood transfusion. So the blood transfusion, they are adding citrate as just uh preservative material. So, more than six or seven units within 24 hours, the patient is able to get a citrate overload. So the patient is getting high citrate overload and the liver has a liver cirrhosis. So the citrate is not metabolized. So the citrate keep accumulating inside your body. This might cause something called a crate toxicity inside the ICU. How the citrate is working inside your body as an anticoagulant because it attach it to the calcium and the calcium is a procoagulant if you go back to the physiology. So the coagulant factors are around 13 factors. The calcium is factor four of the coagulation factor. So straight attach it to the calcium and it goes into the filter just to causing anticoagulation through just attention to the calcium. And consequently, it's an an that the citrate start to accumulate. Ok. So what could be the signs of citrate toxicity? As we said, it attach it to the calcium. So it causes a high and as we said before, also the citrate is citric acid. So it causes some high anion gap, metabolic acidosis because we're adding citrate. Ok. And the therapy issue could be some metabolic alkalosis because high citrate is changing to a bicarb and this is causing a metabolic alkalosis and the metabolic acidosis and signs of hypocalcemia, which you all know about neurological issues. Carpal spasm and tetany, QT and negative and factors all these issues. So we treat it. We switch to another of low molecular weight using IV calcium to replace the calcium chloride or gate, you know about all these issues and that's it. Um I hope everything is fine. Uh I hope I did try it. Um I think that's it. Uh So this is the last slide as far as I remember. Yes. So if there is any questions, uh I'm much appreciative. I hope it was clear enough, but I tried to cover all the aspect inside the ICU for each intensive care physician needs to know about the chapter of acute renal failure from A to Z for a patient who is suffering multiple comorbidities. We're trying to rule out what's happening for him. If there is any questions, you're more than welcome to start. Perfect. Thank you very much. Do you want to turn on your camera now? Thank you very much. Does anyone have any questions, please pop them in the chat? Um Sorry about the um er slides there. I'm not sure what was going on, but hey, I've learned an awful lot really. I know it's a lot of information to learn about, but I try to make it simple as much as I can. Well, I'm not medical at all. So like I'm but it does, it amazes me time and time again when I listen to these talks, just how intricate our body is, right? And if something's not working, the impact that that has on our body, it's just phenomenal. I'm happy that you're enjoying this my code. Well, yeah, but I'm not medical so the others might not have enjoyed it. Does anyone have any questions? Please put them in the chat because I can't ask any. I don't know what I'm talking about and it looks like they're quiet, although there was a lot of interaction wasn't there. So, uh I think it, I think they did love the challenge of your talk. Um, and they seem to have learned, I think when it's interactive, it appears that the learning is higher cos it's, they can't just switch off. So there we go. Thank you. There you go. Um He says an excellent session. So that's brilliant. Does anyone have any questions at all? Um, obviously your feedback will ah ha be in your inbox now? Um Please complete that I will be passing all that feedback on to Ahmed as well. Um Please come for more with a good internet. You've been asked to come back Ahmed. Have you got any other talks up your sleeve? What again can you hear? OK. Yes. If you can come back with any other talks, I think they would love it for sure. Yeah. So in your feedback form, if there's things that you would like further teaching on in this particular subject. Pop any feedback form, let us know because like I said, I will be passing all this onto Ahmed. And if he feels there's something additionally that he can teach on that he would like to teach on, we can arrange another session and we can get some more teaching for you. Hopefully metal education, we are looking for speakers. We do want this to continue to grow. We love metal education. We love the ethos behind it that it's for everyone and it's open access and it's free and, and so we are growing the um what we're gonna be doing, hopefully, you know, it's summer now. So we will be growing that again. September, October, November. Ok. Um The last slide was very busy information to discuss next time. Ok. So it looks like you've got lots and lots of thank yous. So, um, er Ahmed and I will say goodbye. If there's no questions, we'll say goodbye. Um, like I said, fill out your feedback form, I'll pass it on and your certificate will be on your medical account once you've filled that out. Our next event that I have scheduled in is on anesthesia. It's not live yet and that is in August. So please look out for that. Follow us, uh follow me education at the top there and Ahmed's talk will be on catch up if um, er, in a couple of days time. Alright, so thank you ever so much everyone and do take care.