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Focusing today on this. Let's start. Now, let's start with the case. Uh, we have a 38 year old female who has come to, er, with the chief complaint of abdominal pain for eight hours. And when you take history from the patients, uh she says that she's been having the pain since two days. It has been intermittent in the past and, but now it's more severe and constant and the pain is mainly on the epigastric region and it's radiating to the back and she also complains of some pain in the left iliac fossa. Uh, she has had one episode of non bilious vomiting in the morning and there is decreased urinary frequency and dark urine, bowel habits are all normal and, uh, you check the vitals and the vitals are pretty much normal. Ok. So when I, when you called, uh, from the, er, and when you handed over this case, uh, from the, uh, from the, er, to the surgical team, uh, what do you think first? Like what goes on in your head when you see such a presentation, what are the differentials that you would be thinking? Can I see the J the Johnson, I'll let you know if anything comes in so far or not. OK. OK. So we have a patient here with epigastric pain radiating to the back, right? So the first thing, the differential that comes to your mind is anything related to that anatomical area. So the most important thing that you would want to rule out or even when you take the vitals, you want to see if the patient is having uh aortic dissection. Typically with the, with the uh presentation like epigastric pain radiating to the back, you wanna rule out the most danger uh um uh differential diagnosis. So you can check the um uh BP in both the arms. You can check for radio radial delay, you can do a radio, you can check for radiofemoral delay and then you can carry out uh the investigations accordingly. And there so many differential diagnosis that we can think in this particular scenario. So you obviously because the topic is acute pancre penitis, we think of pancreatitis especially because the pain is in epigastric region rating to the back. Um You can think of gastric ulcer. Um So you have to rule out if uh you have to see if the patient has is showing any features of uh peritonitis or perforation peritonitis. And then because it is the female patient and she's also complaining of pain in the left iliac FSA. So you will obviously do a urine pregnancy test for the patient um because your differentials would be uh ectopic pregnancy and rupture. So you think of, so you can think of so many different things when you uh get such a history and then you can take a detailed history and then you will start examining the patient. So when we examine this particular patient, we find that the patient uh is agonized because of the pain and she's lying still in the bed. Um There is pallid in the conjunctiva. Uh There is guarding present on abdominal examination and you can see there is um uh a new find. There is tenderness, especially in the epigastric region. There's also rebound tenderness uh in the epigastric region and left iliac posa bowel sounds are present and other systemic examinations are all normal. Ok. So what do we make out of this? So again, um when you do examination, you think you keep your differentials in mind and then you examine the patient, right? Um So when you think of uh like when I said previously, when you think of aortic dissection, you would be looking for radio radial delay for that patient. And when you think of gastric ulcer, you wanna rule out perforation and you see if there is any rigidity, uh whe when you do a abdominal examination and just the nature of the patient itself like um then you on the left side, there's not only uh in the female patient, there is obviously ovaries and everything there's also the kidney, so you can even think of uh renal stones. So renal stone patients, usually you don't see them lying still on the bed, they'll be moving around, they'll be in severe pain, colicky pain as such, that patient won't be able to lie or sit in one place. Uh So you see, as you observe everything about the patient when you examine the patient. So this particular patient, we move on to labs and uh thankfully, the area has already done uh some labs and has given us the results and you see that uh the inflammatory markers in their raised um you see urine pregnancy test is negative and especially you see two particular enzymes, amylase and lipase to be elevated. You see amylase is 1003 99 and lipase is 350 this rings a bell like w we think first thing when we see these two enzymes elevated, we think of pancreatitis, right? And you see serum calcium is 8.1 you do other couple of blood tests for this for this patient. And uh because you thought about uh pa we thought about perforation, right? So we do a chest X ray for the patient to rule out air under the diaphragm. And thankfully, this patient does not have air under the diaphragm and we have ruled out proliferation in this case. And ultrasound shows there is uh the that means there are uh stones inside the gallbladder. And then you see the C CBD is also dilated, it is 12 millimeter and you see calcification in the uh eighth segment of the liver and bilateral minimal pleural effusion. And the diagnosis from ultrasound shows acute, mild biliary pancreatitis with cholelithiasis and choledocholithiasis. Um ok. So now what is acute pancreatitis, acute pancreatitis, acute in the sense that you know, it develops acutely within a short span of time and pancreatitis is inflammation of the pancreas. There's inflammation and autodigestion happening within the pancreas. Now, we'll come to what is autodigestion. How this occurs when we learn about what causes pancreatitis in the first place. And the difference between acute and chronic pancreatitis is that acute pancreatitis is the reversible form of inflammation. Um and the pancreas can regain its functionality after the inflammation is all settled. But in chronic pancreatitis because there is severe, like there is repeated bouts of inflammation happening in that patient. Uh there would be because of repeated inflammation. There is fibrosis and calcification and pancreas loses part of its ability to function normal normally as before. And that is what happens in chronic pancreatitis and acute pancreatitis. Um it ranges from mild to severe in severity. Uh we can classify the pancreat is mild, moderate and severe. We'll come to that later as well. Now, about pancreatitis. Uh what is the most common cause of pancreatitis? Anybody? What is the most common cause that you see in patients with pancreatitis in acute pancreatitis. Uh, someone just said idiopathic, yeah, idiopathic alcohol, alcohol. Yes, gallbladder. Yes. All of these are all causes of the, uh, pancreatitis. Someone said gallbladder. Um, the gallstones, actually gallstones is the most common cause of pancreatitis. The most common causes, uh, gallstones, I would say for acute pancreatitis. And there is this popular pneumonic that we learn as med students. Um, it's called, I get smashed. I'm sure you all must have heard about that. The thing is most of the causes from there, especially the scorpion bite that we all remember is very rare. The most common ones are very few and the most common is obviously the gallstones and I would say why and how that happens. So we understand the pathophysiology. If you understand w what and how pancreatitis is caused, everything becomes very easy. So these are the most common cause. These are the causes of pancreatitis. OK. So can you see the image of pancreas here? I am. I don't know in zoom. How do I point things out? Can you see my arrow? Yeah, we can see her. OK. Great then. OK. So this is your gallbladder and coming out of this is the cystic duct, it joins with your common hepatic duct and forms the CBD. OK. Can you see the CBD? Uh CBD goes inside the pancreas, it joins with the main pancreatic duct and then the in it uh pours out into the second part of the duo So this is our basic structure and this ducts that you can see these are the pancreatic ducts and they have something called ductal cells. And this is the the bunch of these pancreas here and there, they have a lot of these acinar cells. So the cells of pancreas, they have these pancreatic enzymes inside them. And you know, these pancreatic enzymes are very important for the digestion. Uh protease is amylase lipase. So, proteases, they digest proteins, amylase, digest the carbs and lipase digest the fats. So these are required for us. A normal human beings and normal like all of us. So when we eat, what happens, these digestive enzymes are inside the pancreas. They are in an inactive form. Ok? So they're an inactive form. So they're not activated yet. And when they are activated, uh when they, they released into the duodenum and they get activated and then they help digest the food, right? That's what usually happens. Now, what happens if you have a stone in the gallbladder or gallstones and it gets obstructed moves your, gets obstruct none of the ducts. So either in the CBD or in the main pancreatic duct, even what happens is there is a backflow back pressure. So the uh the enzyme is not easily pouring out into the duodenum. When there is a back pressure, there is uh damage to the ductal cells, right? Um And then the the pancreatic enzymes, they're not meant to be released and while inside the pancreas, they're released now and that causes autodigestion. So, the pancreatic enzymes digest their own tissues and cells. Now. So that is the basis of pancreatitis right in uh when there is when gallstone is the cause of pancreatitis. So, this is an acute, the most common acute uh c the cause of acute pancreatitis would be gallstones. Now, if you see in this, uh we have cystic fibrosis as well. This is another cause of this also causes obstruction, but this is most common in chronic pancreatitis where you have repeated episodes of pancreatitis. So, cystic fibrosis, obviously a chronic condition and uh you have thick mucus production. Imagine. So instead of the g uh the gallstones, you have now thick mucus that is causing obstruction and damage to the ductal cells of pancreas and again, causing the release of all of these toxic enzymes and uh causing the autodigestion. And this leads to inflammation of the pancreas. In other cases where you have alcohol trauma and triglycerides. And all of these, there is direct cell injury to the acinar cells. The these the lobules can you see uh here there are these acinar cells and they obviously have enzymes inside them and when they are damaged, they release the enzymes and they undergo autodigestion and inflammation. So, when you have inflammation in your body, anywhere in your body, what happens, our immune system gets activated. So our immune system gets activated and you have raised white blood cells and the and there's also increased neutrophils and macrophages that are ready to fight. So these neutrophils and macrophages, they in turn, they start pumping out cytokines. So, cytokines, the most common ones in pancreatitis are uh interleukin 16 and TNF alpha. So this is the main basis, the pathophysiology of pancreas. Now, they in turn will cause a lot of things in uh in the, in the body of the patient leading to the complications. So that is um so when we come later to complications, I'll explain how this leads to the complications. So we can understand why this thing is happening in pancreatitis. Ok. So when there are these inflammatory markers released and these cytokines are out there, they are released into the bloodstream, right? And uh and the blood vessels, they, they, they erode the walls of the blood vessels and the blood vessels become more permeable, they start leaking out. So when they leak out fluid, what happens, they leak the fluid into the interstitial space. And this is why we have third space fluid loss in pancreatitis. So a lot of fluid uh loss is happening because of so many cytokines that are released during pancreatitis and this inflammatory process and third phase uh third space fluid loss, they lead to hypovolemia. So patient is losing fluid and that is why in the treatment of pancreatitis, I'm sure we all know the mainstay of treatment is what like uh IV fluids, right? We give fluids to the patients because they are hypovolemic. They tend to get hypovolemic and a lot of complications happen, happen because of hypovolemia. Ok. So the presenting features are most common is abdominal pain, nausea, vomiting, tachycardia and all of the other symptoms. Ok. Now, um this image, this is one of the clinical signs. It's not very common. But can anyone say what is this sign called on clinical examination? We know that the patient will have epigastric pain. That's the classic, right? Epigastric pain radiating to the back and there will be tenderness and all. Uh and this particular sign. Can you see this Amos around the periumbilical area? Why does this happen? Like what is someone is saying something? I can't see the chart uh colon sign. Yes. Uh correct me. So this is colon sign. OK. So what happens in Collins sign? This is because of uh hemorrhagic pancreatitis, right? And the other one, what is the sign called? It is also because of uh hemorrhagic pancreatitis, but the uh hemorrhage is happening in the flank and this is great sign. Very good. Xy, no time. Um OK. So colons in greater sign. Why do, why do they happen? Ok. So I said when there is hypoalr, there is ischemia and um there is ischemia and there is necrosis happening in the pancreas. So, pancreatic tissues when they are necrosis, they also erode the uh blood vessels nearby the pancreas, right? The pa the blood vessels that run near the pancreas, they also get eroded. And the most common ones like all of these in uh vessels, they are also retroperitoneal like the pancreas itself. Pancreas is one of the retroperitoneal organs. So they bleed into the retroperitoneum and that is what presents us uh colon sign and greater sign. Ok. Now, how do we diagnose acute pancreatitis? It's very, very easy. So when you see patients day to day pancreatitis is something very, very common that we see in the ad in the, in the ad uh three things. Only three things you keep in mind. Ok. So the pain consistent with acute pancreatitis. So typically you see patients with epigastric pain radiating to the back, sometimes not radiating to the back but severe epigastric pain. And uh second one is you see raised infla uh raised amylase or lipase and it should be three times the upper limit. The normal level of amylase is uh 40 to 140. So three times the higher. So more than 420 you see that means this is pancreatitis. If you see uh just 300 or 250 it is still raised but you can't, but it doesn't come under like exactly you can't point that this is pancreatitis. OK? And the third thing is the radiological evidence or CD evidence of pancreatitis. So you have three main things. One is clinical, one is laboratory finding and the other one is an imaging. So three things for you to diagnose acute pancreatitis. You need at least two of three to do to be able to diagnose pancreatis. You don't always need a CT scan to diagnose pancreatitis. You just need this um the uh the clinical, the typical history and examination of the patient and uh the amylase and lipase to be raised three times the upper limit or just one. Usually we do amylase because that's the first thing to be elevated. But the problem with amylase is after like one or 21 to 2 days, it start uh it starts coming down, but lipase will still be raised in the blood. Uh So this is what you do in the labs. You order, if you're thinking of pancreatitis, then you want to order amylase lipase, uh CRP. And sometimes you can also do procalcitonin if you're thinking about infection uh infection in the patient. And uh uh interleukin one, we don't usually do this, but this is what is usually elevated in uh pancreatitis and radiological investigation. You don't need it actually, like I said before, you don't need CT scan or any scans to confirm pancreatitis. You just need those two other things. Um So X you can do x-rays have some sign, it's only textbook wise. Uh In reality, we don't actually, to be honest, see all of these signs. Uh And in the, so I'll just do just for you guys, I have just included the pictures. This is called colon cutoff sign. So can you see this abrupt cut off of the colon here at the splenic flexure? And that is because the inflammation from the pancreas, right when there's exudation because of all of these inflammatory process, uh they, when they extend into the re colic ligament, uh that is where they uh they cause spasm, spasm of the bowel there in this region near the spinach flexure. And that is why you can't see the colon from there. It's like abruptly cut off and there's something called sentinel loop sign. And that is when you see a segment of the bowel that's undergoing ileus because when there's an acute, when there's a, sorry, when there's a inflammation process going on, uh, your bowel just, uh tends to get stunned and it stops working for some time. And that's called ileus. And uh you can see this a Sentinel lobe. It's not very common though, it's not even important. Um, ultrasound. If the, if the, if the pancreatitis is because of gallstones and you think, uh there's history when you take history from the patients, they might give you a history like they have, they've had uh episodes of biliary colic, then you think this pancreatitis might be because of gallstone and you can do an ultrasound. And here you can see these gallstones and this pas shadows, atic shadows we call this and you always hear you can't see but you always have to see for CBD dilatation as well. Ok. Now one question, if you're thinking that the gallstone is, I mean, sorry, the pancreatitis is because of gallstone, but you're not able to see, like in this picture, like you're not able to see the, even if you're seeing the CBD, you're not able to see the stones and you don't know if the stone is present or not, but you see some CBD dilatation like in the patient that we had in case one. what do you think is the next investigation that you can do that can be useful for you or for you to confirm that, that this patient is having gallstone pancreatitis? Yes, great. You can do an M RCP. So MCP is an MRI for the uh for the hepatobiliary system. And uh you see if there is any stone in the pancreatic ducts and if there is any, then what do we do to uh like uh not immediately though we have to stabilize the patient and everything. And what is the definite management because the gallstone is the one that's causing it, right. So what do we do then after MCP for the patient? Yes, great. So we do an ERCP, which is an endoscopic procedure. So you do an endoscopic retrograde cholangiopancreatography uh to go in into the um ductal system. I mean, so, so this HEP uh biliary ductal system and then remove the stone that's causing it. Let me just go back to this picture. Yeah. So we go, we uh we go from mouth, right? So we go into the duodenum and then we go retrograde from here and then we retrieve the stone. Now, while you go here now, in some patients, if you cause injuries and it can again lead to pancreatitis and that we call it uh because uh call it iogen pancreatitis because we are inducing it through some procedure that is also one of the causes. So, if the patient is undergoing ercp for any other purpose, even before pancreatitis, then uh they, they are prone to be having pancreatitis after that. OK. And the next CT scan, CT scan, as I said before is not required to confirm pancreatitis. Uh But uh CT definitely can show uh like nice features of pancreatitis. If you are thinking of complications of pancreatitis and want to see what uh like rule out complications, then you do CT scan. OK. So you see the enlargement of the pancreas, the pancreas, right? You see the enlargement of the pancreas and then irregular enhancement, shaggy, contour of the pancreas, thickening of the fascial lines. OK? And then you see a fluid collections. Can you see some collections here? OK. And uh it can either be intraperitoneal, retroperitoneal and you can see some retroperitoneal air as well. OK. Uh CT scan, uh you have again scoring for CT scan based on how severe this is. Uh you do you have a score called BT score or CT severity index score and it shows how much the pancreas has undergo necrosis, right? So you have a grading of the pancreatitis itself. Uh So the how it says how much of the inflammation it has? So inflammatory changes in the pancreas or does it have fluid collection? So, based on that you have ABCDE and then pancreatic necrosis. Uh you have percentages of pancreatic necrosis means how much of the tissue uh in the pancreas undergone necrosis and the maximum score is 10. So this is the uh this is the um the severity, the CT score in uh severity score, index, mild to moderate, intermediate and severe based on the scores. Ok. And then this is the most important bit more than the CT si because this is what we do day to day uh in practice uh clinical score. So you have Ranson scores and so many number of scores. Uh but we the most common score that we use uh especially not trust Glasgow Emory score. Uh an Apache score, Apache score is mostly used in the HD in the ITU when uh we want to know the prognosis of the patient and uh Apache score more than eight means it's severe acute pancreatitis. So, Glasgow score is the the score that we use on admission as well and also to monitor the progression of the patient. So it and also it's very easy to remember because it follows the pneumonic pancreas itself. So you have uh pa O2, so less than seven point and each everything earns one point. And uh if it's more than three, that means the patient is prone to be having acute uh severe pancreatitis. If it's less than three, then it's not safe. Yeah. Um A is uh more than 55. So, N for, just remember, neutrophils and then cells um the WBC, more than 15 C for calcium, less than 80 less than uh 8 mg per deciliter. So just remember the one of the causes of pancreatitis is hypercalcemia. So having really high calcium like in uh some cancers and hyperparathyroidism can lead to pancreas uh pancreatitis. But when once the patient has pancreatitis, one, it's it's severe. Then one of the complications can be hypocalcemia. So it can lead to hypocalcemia afterwards. And then R is for uh uh renal, you have increased bun and uh creatinine. So just bun here, serum urea more than 16 E for enzymes LDH, more than 600 A for albumin, uh less than 3.2 S for sugar glucose, more than 180 or uh 10 millimoles per liter. This is very easily done uh from the labs that you have and you can put it in your notes every day in the hospital. Actually, we are supposed to do that and then bicep score. Uh bicep score is another one. This is also like it's uh it's done bedside. So you, you just need your bun it if it's more than 25 impaired mental status, si S systemic inflammatory response syndrome, I'll tell you what is that? Uh And then age more than 60 pleural effusions. If you have features of pleural effusions, then and then you can see the interpretation here. If the score is three and above, then there's 5 to 20% totality. So sa is a systemic inflammatory response syndrome and most of the uh not most, but then mostly the patients ha of pancreatis, they tend to go towards this. This is what we have to aim to prevent so systemic inflammatory response syndrome. Uh I'm sure everybody knows. So you have four thing here. Um your temperature either less than uh 36 or more than 38. Uh your W BC less than 4000 or more than 12,000, your heart rate more than 90 the patient's uh respirator rate more than 22 I guess. So, if two or more is present, then you diagnosed that. I mean you, that, that, that's confirmed the patient have uh a systemic inflammation going on in there. Ok. Um Now, before we move on to the complications bit and the CT the, the cla not ct the classification, um a small question, a 48 year old male patient presents with severe epigastric pain for one day duration. After binging on alcohol, he had eight episodes of non bilious, vomiting, he's tachycardic and um uh fever of 38 °C. The CRP is th 375 amylase is 3000, 100 lipase is 1000. He was diagnosed with acute pancreatitis. He's admitted in the it for treatment and CT shows uh more than 70% necrosis. Creatinine is 44 mg per deciliter urea is 45. GFR is 45 an ad showed ba two of 7.3 lactate is three. He was found to have severe acute pancreatitis. Now, which of the following is an appropriate marker for severe pancreatitis. Like what among this is uh making you say that this patient is having a severe acute pancreatitis? Oh With, so I just um shared a pool for it. Ok. Yeah, I'll let you know the answer at the end. OK. Thank you. So far, majority have said CT scan necrosis greater than 70%. Uh A few people, both the said raised lipase or amylas greater than 3000 or renal failure greater than 48 hours. OK. Ok. Thank you. Say um the answer is renal failure more than 48 hours. Um Congratulations to those who got this right. Um So why do you think this is the answer renal failure more than 48 hours and not any of these? So, um the severity right there is uh like I said before, pancreatitis can be classified into mild, moderate and severe. Um The severity based on the complications. So the complications, renal failure is one of the systemic complication. And if it's present for more than 48 hours, then we classify the that. So when we come to classify, I mean complications, I'll explain in detail about why this is the answer. And in the same patient, what would be your preferred feeding technique? Would you want an NG feeding? A TPN? An NG feeding or percutaneous gastrostomy? The next ball is out as well? Ok. So at the moment, we're kind of 5050 between TPN and Nasojejunal feeding. Um Oh no. OK. So I'm so sorry. The right answer is uh na nasogastric feeding. OK. So why is, why do you think um sorry, can you think of why the nasogastric feeding is the preferred one and not the others? Ok. So in patients with the pancreatitis, um you know that they, they, they have the severe abdominal pain and they're throwing up, they're not able to eat and we want to. And previously we were taught like few years back that the treatment for pancreatitis is you keep the, the first thing that you put in the chart is keep the patient little by mouth and then uh give IV fluids for the patient and pain uh management. And so and so, but now it has shifted towards starting early enteral feeding. So a lot of meta-analysis and a lot of uh trials have been done on uh feeding the patient and they found out that nasogastric feeding, I mean, starting the bowel back to how it was like even oral feeding, like, you know, normal uh intake is better like it's better compared to the others, especially CPN. Like why? So what happens when the, when you're not using your bowel, when you're not using a bowel for a long period of time? What happens? So the structure and the function of the intestinal mucosa, it get, it gets altered and it gets atrophied over time, right? When you're not using your bowel properly. And what happens? What is inside the bowel? There is bacteria, there is, there, there happen something called translocation of the bacteria and that can lead to infection and sepsis which we don't want in patients with pancreatitis, which is why nasogastric feeding has shown so much improvement uh in patients with pancreatitis. And it's recommended that you start feeding the patient within 48 hours of admission. OK. So moving on now we will learn about uh some. So why not NJ feeding? Yes, that's a very good question. Um So it, they have done a trial on this as well. So NJ feeding versus NG feeding, they have found that NG feeding was much better probably because they also got to move the duodenum as well. And duodenum we know we want that to move. That is also that's very close to pancreas, right? We don't want any damage or anything to happen to the duodenum as well. So that could be the reason of why uh nasogastric feeding is much better than NJ feeding. OK. So next, we have uh classifications ATLA we have, this is called Atlanta classification is one standard classification that we have for pancreatitis. And this is uh for local complication. This is not the classification for mild, moderate and severe, but this is the local complications of what happens during a pancreatitis. So we know that like I said before, there is this inflammatory cascade that's activated. And then they did uh all of these cytokines has been pumped out and they cause the blood vessels to leak and there is hypovolemia um and uh third space fluid loss, right? So when all of this, uh when the fluid leak happens uh near the in the pancreas itself, uh there is edema, right. So this uh flu. So there is this pancreatic vessels and then there is fluid leakage into the interstitial space. You have edema happening and edema collects urine there in the pancreatic tissues. And that is called acute pancreatic fluid collections. OK. This one and this is when it happens within four weeks of the disease progression. So, pancreatic uh pancreatitis has started and in the first four weeks when the edema happens, that is when that is w what we call acute pancreatic fluid collections only collections, they're not organized yet. They're just edema here and there. OK. Now, when the same thing ha after four weeks, they have become organized. OK. And uh they have, they walls around it a around these collections and that is when we call them pancreatic pseudo, I'm sure we all have heard of this very, very common. Um So after four weeks, we call this pseudocyst. Now why it is pseudo or false cyst? Because true cyst, they are covered with uh epithelial cells, right? So false cyst, I mean, the pseudocyst uh these are all uh surrounded by granulation tissues. That is why we call them pseudocyst. The most important thing is this pseudocyst, we have to prevent it from getting infected. Now, patients with pseudocyst, they present like any other patients pancreatitis, they may not be severely unwell clinically. So uh when you see that when you find that the patient has pseudocyst or like any patient pancreatitis, the most important thing is we have to prevent this from getting infected because if this gets infected, it's very difficult to treat. And the same thing. So now we have uh this is one part OK. That is fluid collections, uh not organized. First, that is called a pexy and becomes organized after four weeks, that's called psy. Now we have the other counterpart which is necrosis. So in the first four weeks, you have acute necrotic collections. So what happens? So two things contribute to the necrosis of the pancreas. So the one thing they all know autodigestion happens. So when there's autodigestion, uh and inflammation of their own pancreatic tissues that leads to necrosis. And the other thing that contributes to necrosis is because of hypovolemia and there is decreased pancreatic perfusion like and then there is less perfusion, right. So there is the uh ischemia and necrosis. Uh so that can cause nec uh necro necrotic tissues in the pancreas as well. So, necrosis are here and there, they're not forming any collections. This is in less than four weeks and after four weeks, they become organized and they're encapsulated. And that is when we call this world of necrosis. Now, this is very easy to get infected. And this, it's a very critical situation. And when you see that if you have done a CT scan and you see this world of necrosis, then it's very important that you prevent um like you uh the patient from getting any infection and again, infection, why does the patient have infection? And why are these patients prone to get infections again? So they have all of these inflammatory cascade and things going on? There's hypovolemia when there's hypovolemia, what happens there is decreased tissue perfusion to end organs and all of uh not end organs, all of the organs, all of the vital organs inside our body. When there is the uh decreased uh blood perfusion to the bowels, what happened to the bowels? There's ischemia in the bowel wall and they undergo necrosis and then there's translocation of the bacteria from the bowel and that is the main source of infection for patients with pancreatitis. And that is why it's very, very important for us to uh resuscitate these patients with fluids. Ok. Now, these are the local complications that we saw and this is the regional complications. So, again, the same process, right? So, leakage inflammatory cascade and then third space fluid loss. So patients can have ascitis, pancreatic ascitis. So and uh pleural effusion. So same thing happening in the lungs and these fluids, they are rich in amylase. They're rich in pancreatic enzymes and they're very um concentrated and uh toxic. And if they come in contact with the bowel, they can lead to perforation of the bowel even. And the most common site would be transverse colon because that's newer to the pancreas. Uh And uh if they, the same thing, if they come in contact with the, uh they can cause um uh with the vessels, they can cause erosion of the vessels. And the most common artery to get eroded is the uh um splenic artery and gastroduodenal artery. And uh uh uh superior mesenteric, mesentary veins and portal vein, thrombosis are also common in the patients that if the complications spreads, that is and that can lead to portal hypertension, all the same, the same process going on. So, the the inflammatory process now that's becoming regional and that can spread to systemic as well when it gets in the systemic blood circulation. So, when it gets in systemic blood circulation and there is hypovolemia. So there is less blood supply to all of the organs and the most common common organs to get uh affected by hypovolaemia and ischemia is the heart and the kidneys. So, in heart, what happens when there is uh perfusion? When there's, when there's hypovolemia itself, what do we have? We get shock, I mean, not we the patients, sorry, the patients, uh the patients with pancreatitis, they tend to have hypovolemic shock. In hypovolemic shock, the patients are hypotensive and tachycardic, right. Uh And so the heart is affected and because of hypovolemia, there is less perfusion to the kidneys and the patients are prone to have acute kidney injury. And this we call it prerenal AK. Uh just remember that the patients with the uh pancreatitis, they tend to have AK and you will see that, that uh by AK, what do we mean? How do we diagnose this? So just two simple things, uh decreased urinary output and you will see raise creatinine and bun or urea. Um this is very, very important to treat and the patient again is fluid prestation for the patient. So uh the patients can have kidney injury, the patient can have ARDS in the lungs because again of the uh you know, the, you know, the third space fluid loss and the interstitial edema going on in the lungs and the alveoli getting filled with the fluids causing diffuse alveolar uh edema and ARDS. Um so the organ, so they can be organ failure in the patients. And there is Atlanta classification a criteria for mild, moderate and severe pancreatitis. So, in miles, there is absence of organ failure and absence of local complications. So you will not have any of these complications, like not necrosis and no, none of these and also none of the uh organ system failure. And that is mild and moderately severe or moderate. You will have local complications and transient organ failure less than 48 hours. So if you find, if we find out that the patients ha is going towards organ failure and we treat it early, we can prevent them going into severe or persistent organ failure, which is more than 48 hours. So the, so to answer the question that we had earlier, so patients with the renal failure of more than 48 hours, that is when we term it as severe. So it can be any organ uh failure going on for more than 48 hours. Ok. Now that we have finished the complications, the management of the acute pancreatitis. I can't stress enough. Like how important the fluid resuscitation is the most important thing that we start in the patient with pancreatitis once you think this is pancreatitis. Um so the crystalloid, many uh there have been many uh trials done and it shows that crystalloid is the best that you like plasma light and ringer lactate which is similar to our plasma. And uh the solution has to be given to 250 to find a ML per hour in the 1st 12 hours, uh 12 to 24 hours. And uh there are also been researches that have shown normal salina is not recommended not to be given to patients with the pancreatitis because it can trigger the uh hyperchloremic metabolic acidosis. Now, patient with pancreatitis already in a state of metabolic acidosis, you don't want to add more to it, right? So we don't give them normal saline, we either give them plasma light or crystalloid some good crystalloid solution. And um how do you monitor the response? How, how, how much fluid resuscitation do you have to get? So you have to maintain a urine output of more than 0.5 ml per kg body weight per hour. And you can also do a lactate and see if it's like reducing, if it's not uh raising up and you can do a bedside b and hematocrit level as well to see like these are all the signs to see if you're they are doing adequate fluid resuscitation. And it's also very, very important to keep in mind to not over uh like uh overly give the fluids because already the patient is undergoing third space fluid loss, right? And they have a sight is going on here. And if you uh like if you push in, so like liters and liters of fluid and not looking at the response of the patient, then uh it can add on to more of these ascitis and it can increase the abdominal pressure. And when what happens when the intraabdominal pressure increases, what do we call that? Uh is there's a term right? We call when the abdominal pressure is increased. Uh So we have some things, a complication is called abdominal compartment syndrome. And it's um and it's very dangerous, obviously because it have abdominal hypertension, yeah, increase abdominal pressure. It's also called abdominal compartment syndrome. So if the pressure goes up above 20 mmhg, so you we pressure, we measure it through the bladder actually. And if it goes really high, what happens. So the pressure, it starts pushing the uh you can just imagine. So it pushes the diaphragm. So what happens? The patient will be tachy neck and when it pushes on the SVC, OK. I mean on the in vena cava, the vena cava, uh there is decreased, return to the heart and then the pa there is uh hypotension in the patient. Ok. And then uh if it presses on the renal veins, they will be ak. So if you see these things, these three features in the patient, then you have to uh think of uh abdominal compartment syndrome, measure the pressure and uh act immediately because it can be life threatening. And the next important thing in the treatment is analogies. Yeah, pain management has to be immediately started. These patients will be in so much pain and pain management plays very important role in recovery. I mean, I mean, they are full process of treatment and we follow the who analog take ladder. You start from your uh non opioids and adjuvant and then you climb up the ladder slowly to your weak opioids, like your uh traMADol and codeine and stronger opioids later like morphine, fentaNYL, buprenorphine and so on and then enteral nutrition. And this during this uh when you're working in the hospital, right? So we have pain team. So if you're not able to control the pain, if you're not, uh if you're not very sure, always feel free to contact the pain team and always escalate when you're struggling with some patient, you don't know what to do. After a certain point. I can't stress enough how important escalation is, especially in patient and pancreas when you think something is wrong with the patient, right? And when you assess a patient, um you, when you go on a patient like the first case that we caught, right? When we go and see a patient, we always do an ABCD assessment on the patient. When you get a hand off from the nurse uh from uh uh about a patient who's already in the ward uh for being treated for acute pancreatitis. But then the nurse is calling you saying that now the BP is going down, uh going down the patient is appear to be ha appearing to be having some fever. Uh then uh when you go and assess the patient, always do a thorough ABCD assessment. So you don't miss out on anything. Ok. The next thing is enteral nutrition. I have spoken about it already as well. So uh it has been shown that NG feeding is very safe and tolerated compared to the NJ feeding and parenteral nutrition. Also, it's very important that you start enteral feeding uh as early as 48 hours of admission because that has shown to reduce the mortality, multiple organ failure and infection when compared to late enteral feeding, an antibiotic. So do you think uh antibiotic is needed for all the patients with anti uh with pancreatitis? Do you think we should give antibiotics to the patient with pancreatitis? Uh We don't, actually there's an answer. No, very good. So we don't actually give antibiotics to all the patients. We only use antibiotics when it's required. So that is when the patient is having severe acute pancreatitis and developing sepsis. And uh if the in like the necrosis that we talked about, right? If that is infected, then definitely the patient has to be started on antibiotics. And uh if they have si s and they are like prone and there you think of the patients having sepsis, then yes, we start antibiotics for the patient. Also, prophylaxis is only given when there are these specific infectious marker. Like procalcitonin and they are raised. So, procalcitonin is a marker, particularly raised when there is bacterial infection going on. And uh we prefer a broad spectrum antibiotic that covers gram positive, gram negative and anaerobes like imipen opine. And I'm sure every trust they have their drug guidelines for antibiotics. And we can always refer to those BNF and also uh call the microbiology department as well if you have any doubts uh of what antibiotic exactly to pre uh like what to prescribe for these patients. And then another one is somatostatin and octreotide, the use of these uh in treating pancreatitis. So what are these? So somatostatin and its analog called octu. They are inhibitors of exocrine pancreatic secretion. So, um these exocrine um uh uh secretions, these are the uh pancreatic enzymes that causes the autodigestion, right. So some uh researchers have come up that if you stop these enzymes which is causing autodigestion that, that might help in progression of the disease. But it's still very controversial to use this in the practice and researches are still going on on this. And last is the surgical intervention. So, we know that the most common cause is gallstone. And if you have diagnosed that this patient is having gallstone pancreatitis, then you obviously go treat that. So first you've treated the patient with fluid resuscitation and everything. Uh pain management patient is very stable and all, then you go for E RCP, you remove the stones and then the first thing that's what is causing the stones in the uh CBD and the ducts is the gallstone, right? Uh is the gallbladder stones. Uh So you have to, the patient at some point, they have to undergo laparoscopic cholecystectomy. And that's the gold standard. And um uh we al always make sure the patient is very stable before you uh they undergo the surgical interventions. And the other surgical intervention is when the patient is having infected necrosis, they need to undergo necrosectomy. And it's preferred that it's done minimally invasive. So, either percutaneous or endoscopic and again. So this patient, you can't just take them uh when you find out that this patient have uh has infected necrosis, you, they need to be stabilized before taking them to theater and open necrosectomy is associated with high morbidity and mortality. So that's what we always a minimally invasive technique and it's always in a step up approach, right. So you have to stabilize the patient and then um go for the procedure and the key points are uh treat the organ system failure accordingly. Uh and always try and prevent the next step. That is a complication. So, if the patient already has local complications, try and prevent the regional and systemic the mainstay of treatment, especially like the three important things is fluid resuscitation, analgesia, early enteral feeding mo mobility of the patient, everything plays a role and uh treat the primary course. And a tiny quiz at the end. I'm so sorry to bore you guys for so long. I'm sure not across an hour. Has it been an hour? Just slightly over? But I'm sure it'll be done soon. Ok. We just send the new pull in. Ok. So your majority of said gallstones, right? That's the correct answer. Next one. Oh, here you have to choose three options. So, according to the poll, I don't think they'll be able to choose three or you can put in the chat box to anybody. Yes. So some people said all of the above. Um and some uh most of them said Emily is three times normal. Ok. It's all the diagnostic right that we learned the three important things. So obviously, one is amylase three times normal or amylase or uh lipase three times normal. And then uh you have clinical sign, epigastric pain, radiating to the back and imaging showing pancreatitis. These are the three things that you need for diagnosis. And if you have any two out of three, then you can uh diagnose the patient with acute pancreatitis. Uh It is not all of the above. I'm so sorry because vomiting and tachycardia. Um it, the patient always doesn't need to have vomiting and tachycardia. So the last B is out here majority smoke IV fluids. Yes, IV fluids is correct. But the correct answer is uh manage with ABCD principles because when you manage with ABCD principles, you do find the patients hypovolemic and that, you know, they have pancreatitis and you will obviously give IV fluids. But remember that every patient that you go assess, uh you have to start with your ABCD because this covers everything you will be giving IV fluids when you follow the ABCD principles. And the last thing to take home message is that this pancreatitis is a lifethreatening disease. We don't, we obviously we don't take it lightly. Um Patient can derate very quickly than you think. Always follow the ABCD protocol when you assess the patients and scoring is very important to assess the progression of the disease and escalate early. Thank you very much. Any, if anybody has any questions, please feel free to ask them. I know it just feedback from on the chart as well. Thank you so much. We'll just give it like two more minutes in case someone has any questions. But otherwise, thank you everyone for joining and thank you. And that was a great, thank you for joining and thank you for hosting the session. Sorry about any technical issues, but I'm glad you started it. Yes.